Cellular senescence is a phenomenon characterized by the cessation of cell division. In their experiments during the early 1960s, Leonard Hayflick and Paul Moorhead found that normal human fetal fibroblasts in culture reach a maximum of approximately 50 cell population doublings before becoming senescent. This process is known as "replicative senescence", or the Hayflick limit. Hayflick's discovery of mortal cells paved the path for the discovery and understanding of cellular aging molecular pathways. Cellular senescence can be initiated by a wide variety of stress inducing factors. These stress factors include both environmental and internal damaging events, abnormal cellular growth, oxidative stress, autophagy factors, among many other things.

The physiological importance for cell senescence has been attributed to prevention of carcinogenesis, and more recently, aging, development, and tissue repair. Senescent cells contribute to the aging phenotype, including frailty syndrome, sarcopenia, and aging-associated diseases. Senescent astrocytes and microglia contribute to neurodegeneration.

Cellular mechanisms

Stress response and DNA damage
Mechanistically, replicative senescence can be triggered by a DNA damage response due to the shortening of telomeres. Cells can also be induced to senesce by DNA damage in response to elevated reactive oxygen species (ROS), activation of oncogenes, and cell-cell fusion. Normally, cell senescence is reached through a combination of a variety of factors (i.e., both telomere shortening and oxidative stress). The DNA damage response (DDR) arrests cell cycle progression until DNA damage, such as double-strand breaks (DSBs), are repaired. Senescent cells display persistent DDR that appears to be resistant to endogenous DNA repair activities. The prolonged DDR activates both ATM and ATR DNA damage kinases. The phosphorylation cascade initiated by these two kinases causes the eventual arrest of the cell cycle. Depending on the severity of the DNA damage, the cells may no longer be able to undergo repair and either go through apoptosis or cell senescence. Such senescent cells in mammalian culture and tissues retain DSBs and DDR markers. It has been proposed that retained DSBs are major drivers of the aging process. Mutations in genes relating to genome maintenance has been linked with premature aging diseases, supporting the role of cell senescence in aging (see DNA damage theory of aging).

Depletion of NAD+ can lead to DNA damage and cellular senescence in vascular smooth muscle cells.

Although senescent cells can no longer replicate, they remain metabolically active and commonly adopt an immunogenic phenotype consisting of a pro-inflammatory secretome, the up-regulation of immune ligands, a pro-survival response, promiscuous gene expression (pGE), and stain positive for senescence-associated β-galactosidase activity. Two proteins, senescence-associated beta-galactosidase and p16Ink4A, are regarded as biomarkers of cellular senescence. However, this results in a false positive for cells that naturally have these two proteins such as maturing tissue macrophages with senescence-associated beta-galactosidase and T-cells with p16Ink4A.

Senescent cells can undergo conversion to an immunogenic phenotype that enables them to be eliminated by the immune system. This phenotype consists of a pro-inflammatory secretome, the up-regulation of immune ligands, a pro-survival response, promiscuous gene expression (pGE) and stain positive for senescence-associated β-galactosidase activity. The nucleus of senescent cells is characterized by senescence-associated heterochromatin foci (SAHF) and DNA segments with chromatin alterations reinforcing senescence (DNA-SCARS). Senescent cells affect tumour suppression, wound healing and possibly embryonic/placental development and a pathological role in age-related diseases.

Role of telomeres
Telomeres are DNA tandem repeats at the end of chromosomes that shorten during each cycle of cell division. Recently, the role of telomeres in cellular senescence has aroused general interest, especially with a view to the possible genetically adverse effects of cloning. The successive shortening of the chromosomal telomeres with each cell cycle is also believed to limit the number of divisions of the cell, contributing to aging. After sufficient shortening, proteins responsible for maintaining telomere structure, such as TRF2, are displaced, resulting in the telomere being recognized as a site of a double-strand break. This induces replicative senescence.  Theoretically, it is possible upon the discovery of the exact mechanism of biological immortality to genetically engineer cells with the same capability. The length of the telomere strand has senescent effects; telomere shortening activates extensive alterations in alternative RNA splicing that produce senescent toxins such as progerin, which degrades tissue and makes it more prone to failure.

Role of oncogenes
BRAFV600E and Ras are two oncogenes implicated in cellular senescence. BRAFV600E induces senescence through synthesis and secretion of IGFBP7. Ras activates the MAPK cascade which results in increased p53 activation and p16INK4a upregulation. The transition to a state of senescence due to oncogene mutations are irreversible and have been termed oncogene-induced senescence (OIS).

Interestingly, even after oncogenic activation of a tissue, several researchers have identified a senescent phenotype. Researchers have identified a senescent phenotype in benign lesions of the skin carrying oncogenic mutations in neurofibroma patients with a defect that specifically causes an increase in Ras. This finding has been highly reproducible in benign prostate lesions, in melanocytic lesions of UV-irradiated HGF/SF-transgenic mice, in lymphocytes and in the mammary gland from N-Ras transgenic mice, and in hyperplasias of the pituitary gland of mice with deregulated E2F activity. The key to these findings is that genetic manipulations that abrogated the senescence response led to full-blown malignancy in those carcinomas. As such, the evidence suggests senescent cells can be associated with pre-malignant stages of the tumor. Further, it has been speculated that a senescent phenotype might serve as a promising marker for staging. There are two types of senescence in vitro. The irreversible senescence which is mediated by INK4a/Rb and p53 pathways and the reversible senescent phenotype which is mediated by p53. This suggests that p53 pathway could be effectively harnessed as a therapeutic intervention to trigger senescence and ultimately mitigate tumorigenesis.

p53 has been shown to have promising therapeutic relevance in an oncological context. In the 2007 Nature paper by Xue et al., RNAi was used to regulate endogenous p53 in a liver carcinoma model. Xue et al. utilized a chimaeric liver cancer mouse model and transduced this model with the ras oncogene. They took embryonic progenitor cells, transduced those cells with oncogenic ras, along with the tetracycline transactivator (tta) protein to control p53 expression using doxycycline, a tetracycline analog and tetracycline responsive short hairpin RNA (shRNA). In the absence of Dox, p53 was actively suppressed as the microRNA levels increased, so as Dox was administered, p53 microRNA was turned off to facilitate the expression of p53. The liver cancers that expressed Ras showed signs of senescence following p53 reactivation including an increase in senescence associated B-galactosidase protein. Even if the expression of p53 was transiently activated or deactivated, senescence via SA B-gal was observed. Xue et al. show that by briefly reactivating p53 in tumors without functional p53 activity, tumor regression is observed. The induction of cellular senescence was associated with an increase in inflammatory cytokines as is expected based on the SASP. The presence of both senescence and an increase in immune activity is able to regress and limit liver carcinoma growth in this mouse model.

Signaling pathways
There are several reported signaling pathways that lead to cellular senescence including the p53 and p16Ink4a pathways. Both of these pathways are activated in response to cellular stressors and lead to cell cycle inhibition. p53 activates p21 which deactivates cyclin-dependent kinase 2(Cdk 2). Without Cdk 2, retinoblastoma protein (pRB) remains in its active, hypophosphorylated form and binds to the transcription factor E2F1, an important cell cycle regulator. This represses the transcriptional targets of E2F1, leading to cell cycle arrest after the G1 phase.

p16Ink4a also activates pRB, but through inactivation of cyclin-dependent kinase 4 (Cdk 4) and cyclin-dependent kinase 6 (Cdk 6). p16Ink4a is responsible for the induction of premature, stress-induced senescence. This is not irreversible; silencing of p16Ink4a through promotor methylation or deletion of the p16Ink4a locus allows the cell to resume the cell cycle if senescence was initiated by p16Ink4a activation.

Senescence-associated secretory phenotype (SASP) gene expression is induced by a number of transcription factors, including C/EBPβ, of which the most important is NF-κB. Aberrant oncogenes, DNA damage, and oxidative stress induce mitogen-activated protein kinases, which are the upstream regulators of NF-κB.

Characteristics of senescent cells
Senescent cells are especially common in skin and adipose tissue. Senescent cells are usually larger than non-senescent cells. Transformation of a dividing cell into a non-dividing senescent cell is a slow process that can take up to six weeks.

Senescent cells affect tumor suppression, wound healing and possibly embryonic/placental development, and play a pathological role in age-related diseases. There are two primary tumor suppressor pathways known to mediate senescence: p14arf/p53 and INK4A/RB. More specifically p16INK4a-pRb tumor suppressor and p53 are known effectors of senescence. Most cancer cells have a mutated p53 and p16INK4a-pRb, which allows the cancer cells to escape a senescent fate. The p16 protein is a cyclin dependent kinase inhibitor (CDK) inhibitor and it activates Rb tumor suppressor. p16 binds to CDK 4/6 to inhibit the kinase activity and inhibit Rb tumor suppressor via phosphorylation. The Rb tumor suppressor has been shown to associate with E2F1 (a protein necessary for transcription) in its monophosphorylated form, which inhibits transcription of downstream target genes involved in the G1/S transition. As part of a feedback loop, increased phosphorylation of Rb increases p16 expression that inhibits Cdk4/6. Reduced Cdk4/6 kinase activity results in higher levels of the hypo-phosphorylated (monophosphorylated) form of Rb, which subsequently leads to reduced levels of p16 expression.

The removal of aggregated p16 INK 4A positive senescent cells can delay tissue dysfunction and ultimately extend life. In the 2011 Nature paper by Baker et al. a novel transgene, INK-ATTAC, was used to inducibly eliminate p16 INK4A-positive senescent cells by action of a small molecule-induced activation of caspase 8, resulting in apoptosis. A BubR1 H/H mouse model known to experience the clinicopathological characteristics of aging-infertility, abnormal curvature to the spine, sarcopenia, cataracts, fat loss, dermal thinning, arrhythmias, etc. was used to test the consequences of p16INK4a removal. In these mice p16 INK4a aggregates in aging tissues including the skeletal and eye muscle, and adipose tissues. Baker et al. found that if the senescent cells are removed, it is possible to delay age-associated disorders. Not only does p16 play an important role in aging, but also in auto-immune diseases like rheumatoid arthritis that progressively lead to mobility impairment in advanced disease.

In the nervous system, senescence has been described in astrocytes and microglia, but is less understood in neurons. Because senescence arrests cell division, studies of senescence in the brain were focused mainly on glial cells and less studies were focused on nondividing neurons. Analyzing single nucleus RNA-Seq data from human brains suggested p19 as a marker for senescent neurons, which are strongly associated with neurons containing neurofibrillary tangle.

SASP

The secretome of senescent cells is very complex. The products are mainly associated with inflammation, proliferation, and changes in the extracellular matrix. A Senescence Associated Secretory Phenotype (SASP) consisting of inflammatory cytokines, growth factors, and proteases is another characteristic feature of senescent cells. There are many SASP effector mechanisms that utilize autocrine or paracrine signalling. SASP induces an unfolded protein response in the endoplasmic reticulum because of an accumulation of unfolded proteins, resulting in proteotoxic impairment of cell function. Autophagy is upregulated to promote survival.

Considering cytokines, SASP molecules IL-6 and IL-8 are likely to cause senescence without affecting healthy neighbor cells. IL-1beta, unlike IL-6 or IL-8, is able to induce senescence in normal cells with paracrine signaling. IL-1beta is also dependent on cleavage of IL-1 by caspase-1, causing a pro-inflammatory response. Growth factors, GM-CSF and VEGF also serve as SASP molecules. From the cellular perspective, cooperation of transcriptional factors NF-κB and C/EBPβ increase the level of SASP expression. Regulation of the SASP is managed through a transcription level autocrine feedback loop, but most importantly by a continuous DDR. Proteins p53, p21, p16ink4a, and Bmi-1 have been termed as major senescence signalling factors, allowing them to serve as markers. Other markers register morphology changes, reorganization of chromatin, apoptosis resistance, altered metabolism, enlarged cytoplasm or abnormal shape of the nucleus. SASPs have distinct effects depending on the cellular context, including inflammatory or anti-inflammatory and tumor or anti-tumor effects. While considered a pro-tumorogenic effect, they likely support already tumor-primed cells instead of shifting healthy cells into transformation. Likewise, they operate as anti-tumor protectors by facilitating the elimination of damaged cells by phagocytes. The SASP is associated with many age-related diseases, including type 2 diabetes and atherosclerosis. This has motivated researchers to develop senolytic drugs to kill and eliminate senescent cells to improve health in the elderly. The nucleus of senescent cells is characterized by senescence-associated heterochromatin foci (SAHF) and DNA segments with chromatin alterations reinforcing senescence (DNA-SCARS).

Clearance of senescent cells by the immune system
Due to the heterogeneous nature of senescent cells, different immune system cells eliminate different senescent cells. Specific components of the senescence-associated secretory phenotype (SASP) factors secreted by senescent cells attract and activate different components of both the innate and adaptive immune system.

Natural killer cells (NK cells) and macrophages play a major role in clearance of senescent cells. Natural killer cells directly kill senescent cells, and produce cytokines which activate macrophages which remove senescent cells. Senescent cells can be phagocytized by neutrophils as well as by macrophages. Senolytic drugs which induce apoptosis in senescent cells rely on phagocytic immune system cells to remove the apoptosed cells.

Natural killer cells can use NKG2D killer activation receptors to detect the MICA and ULBP2 ligands which become upregulated on senescent cells. The senescent cells are killed using perforin pore-forming cytolytic protein. CD8+ cytotoxic T-lymphocytes also use NKG2D receptors to detect senescent cells, and promote killing similar to NK cells.

Aging of the immune system (immunosenescence) results in a diminished capacity of the immune system to remove senescent cells, thereby leading to an increase in senescent cells. Chronic inflammation due to SASP from senescent cells can also reduce the capacity of the immune system to remove senescent cells. T cells, B cells, and NK cells have all been reported to become senescent themselves. Senescent-like aging CD8+ cytotoxic T-lymphocytes become more innate in structure and function, resembling NK cells.  Immune system cells can be recruited by SASP to senescent cells, after which the SASP from the senescent cells can induce the immune system cells to become senescent.

Chimeric antigen receptor T cells have been proposed as an alternative means to senolytic drugs for the elimination of senescent cells. Urokinase receptors have been found to be highly expressed on senescent cells, leading researchers to use chimeric antigen receptor T cells to eliminate senescent cells in mice.  Chimeric antigen receptor natural killer cells have been proposed as an allogeneic means of eliminating senescent cells.

Transient senescence
It is important to recognize that cellular senescence is not inherently a negative phenomenon. During mammalian embryogenesis, programmed cellular senescence plays a role in tissue remodeling via macrophage infiltration and subsequent clearance of senescent cells. A study on the mesonephros and endolymphatic sac in mice highlighted the importance of cellular senescence for eventual morphogenesis of the embryonic kidney and the inner ear, respectively.

They serve to direct tissue repair and regeneration. Cellular senescence limits fibrosis during wound closure by inducing cell cycle arrest in myofibroblasts once they have fulfilled their function. When these cells have accomplished these tasks, the immune system clears them away. This phenomenon is termed acute senescence. Senescence of hepatic stellate cells could prevent progression of liver fibrosis, although this has not been implemented as a therapy, and would carry the risk of hepatic dysfunction.

The negative implications of cellular senescence present themselves in the transition from acute to chronic senescence. When the immune system cannot clear senescent cells at the rate at which senescent cells are being produced, possibly as a result of the decline in immune function with age, accumulation of these cells leads to a disruption in tissue homeostasis.

Cellular senescence in mammalian disease
Transplantation of only a few (1 per 10,000) senescent cells into lean middle-aged mice was shown to be sufficient to induce frailty, early onset of aging-associated diseases, and premature death.

Biomarkers of cellular senescence have been shown to accumulate in tissues of older individuals. The accumulation of senescent cells in tissues of vertebrates with age is thought to contribute to the development of ageing-related diseases, including Alzheimer's disease, Amyotrophic lateral sclerosis, type 2 diabetes, and various cancers.

Progeria is another example of a disease that may be related to cell senescence. The disease is thought to be caused by mutations in the DNA damage response, telomere shortening, or a combination of the two. Progeroid syndromes are all examples of aging diseases where cell senescence appears to be implicated.

List of progeroid syndromes

 Hutchinson–Gilford progeria syndrome
 Rothmund–Thomson syndrome
 Werner syndrome
 Bloom syndrome
 Cockayne syndrome
 Xeroderma pigmentosum
 Trichothiodystrophy
 Xeroderma pigmentosum-Cockayne syndrome
 Restrictive dermopathy
 Mandibuloacral dysplasia
 Fanconi anaemia
 Seckel syndrome
 Ataxia telangiectasia
 Dyskeratosis congenita
 Hoyeraal-Hreidarsson syndrome
 Néstor-Guillermo progeria syndrome

Senolytic drugs
Targeting senescent cells is a promising strategy to overcome age-related disease, simultaneous alleviate multiple comorbidities, and mitigate the effects of frailty. Removing the senescent cells by inducing apoptosis is the most straightforward option, and there are several agents that have been shown to accomplish this. Some of these senolytic drugs take advantage of the senescent-cell anti-apoptotic pathways (SCAPs); knocking out expression of the proteins involved in these pathways can lead to the death of senescent cells, leaving healthy cells.

Organisms lacking senescence
Cellular senescence is not observed in some organisms, including perennial plants, sponges, corals, and lobsters. In other organisms, where cellular senescence is observed, cells eventually become post-mitotic: they can no longer replicate themselves through the process of cellular mitosis (i.e., cells experience replicative senescence). How and why cells become post-mitotic in some species has been the subject of much research and speculation, but it has been suggested that cellular senescence evolved as a way to prevent the onset and spread of cancer. Somatic cells that have divided many times will have accumulated DNA mutations and would be more susceptible to becoming cancerous if cell division continued. As such, it is becoming apparent that senescent cells undergo conversion to an immunologic phenotype that enables them to be eliminated by the immune system.

See also
Ageing
Senolytic
Apoptosis
Mitotic catastrophe
Necrosis
Senescence
DNA damage
DNA repair
Cell cycle
Telomeres
Progeroid syndromes
Carcinogenesis

References

Further reading

External links

Ageing processes
Cell biology
Cells
Cellular processes
Senescence


TCP NAT traversal and TCP hole punching (sometimes NAT punch-through) in computer networking occurs when two hosts behind a network address translation (NAT) are trying to connect to each other with outbound TCP connections.  Such a scenario is particularly important in the case of peer-to-peer communications, such as Voice-over-IP (VoIP), file sharing, teleconferencing, chat systems and similar applications.

TCP hole punching is an experimentally used NAT traversal technique for establishing a TCP connection between two peers on the Internet behind NAT devices.  NAT traversal is a general term for techniques that establish and maintain TCP/IP network and/or TCP connections traversing NAT gateways.

Terminology
In the following, the terms host, client and peer are used almost interchangeably.

 local endpoint, internal endpoint
 the local IP:port as seen locally by the host and the internal part of the NAT.
 public endpoint, external endpoint
 the external IP:port mapped by the NAT, as seen by the network and the external part of the NAT.
 remote endpoint
 the IP:port of the other peer as seen by the network, or the external parts of both NATs.

Description
NAT traversal, through TCP hole punching, establishes bidirectional TCP connections between Internet hosts in private networks using NAT. It does not work with all types of NATs, as their behavior is not standardized.
When two hosts are connecting to each other in TCP, both via outbound connections, they are in the "simultaneous TCP open" case of the TCP state machine diagram.

Network Drawing
{| style="border: 1px black solid;"
|  Peer A ←→ Gateway A (NAT-a) ← .. Network .. → Gateway B (NAT-b) ←→ Peer B
|}

Types of NAT

The availability of TCP hole punching depends on the type of computer port allocation used by the NAT.
For two peers behind a NAT to connect to each other via , they need to know a little bit about each other. One thing that they absolutely need to know is the "location" of the other peer, or the remote endpoint. The remote endpoint is the data of the IP address and a port that the peer will connect to. So when two peers, A and B, initiate TCP connections by binding to local ports Pa and Pb, respectively, they need to know the remote endpoint port as mapped by the NAT to make the connection.
When both peers are behind a NAT, how to discover the public remote endpoint of the other peer is a problem called NAT port prediction. All TCP NAT traversal and hole punching techniques have to solve the port prediction problem.

A NAT port allocation can be one of the two:
 predictable the gateway uses a simple algorithm to map the local port to the NAT port. Most of the time a NAT will use port preservation, which means that the local port is mapped to the same port on the NAT.
 non predictable the gateways use an algorithm that is either random or too impractical to predict.

Depending on whether the NATs exhibit a predictable or non-predictable behavior, it will be possible or not to perform the TCP connection via a TCP simultaneous open, as shown below by the connection matrix representing the different cases and their impact on end-to-end communication:

{| class="wikitable"
|-
|
! A predictable
! A non-predictable
|-
! B predictable
| YES
| YES
|-
! B non-predictable
| YES
| NO
|}

 YES: the connection will work all the time
 NO: the connection will almost never work

Techniques

Methods of Port Prediction (with predictable NATs)

Here are some of the methods used by NATs to allow peers to perform port prediction:

 The NAT assigns to sequential internal ports sequential external ports: If the remote peer has the information of one mapping, then it can guess the value of subsequent mappings. The TCP connection will happen in two steps, at first the peers make a connection to a third party and learn their mapping. For the second step, both peers can then guess what the NAT port mapping will be for all subsequent connections, which solves port prediction. This method requires making at least two consecutive connections for each peer and requires the use of a third party. This method does not work properly in case of Carrier-grade NAT with a lot of subscribers behind each IP addresses, as only a limited number of ports are available and allocating consecutive ports to the same internal host may be impractical or impossible.

 The NAT uses the port preservation allocation scheme: the NAT maps the source port of the internal peer to the same public port. In this case, port prediction is trivial, and the peers simply have to exchange the port to which they are bound through another communication channel (such as UDP, or DHT) before making the outbound connections of the TCP simultaneous open. This method requires only one connection per peer and does not require a third party to perform port prediction.

 The NAT uses "endpoint independent mapping": two successive TCP connections coming from the same internal endpoint are mapped to the same public endpoint. With this solution, the peers will first connect to a third party server that will save their port mapping value and give to both peers the port mapping value of the other peer. In a second step, both peers will reuse the same local endpoint to perform a TCP simultaneous open with each other. This unfortunately requires the use of the SO_REUSEADDR on the TCP sockets, and such use violates the TCP standard and can lead to data corruption. It should only be used if the application can protect itself against such data corruption.

Details of a typical TCP connection instantiation with TCP Hole Punching

We assume here that port prediction has already taken place through one of the methods outlined above, and that each peer knows the remote peer endpoint. Both peers make a POSIX connect call to the other peer endpoint. TCP simultaneous open will happen as follows:

 Peer A sends a SYN to Peer B
 Peer B sends a SYN to Peer A

 When NAT-a receives the outgoing SYN from Peer A, it creates a mapping in its state machine.
 When NAT-b receives the outgoing SYN from Peer B, it creates a mapping in its state machine.
 Both SYN cross somewhere along the network path, then:
 SYN from Peer A reaches NAT-b, SYN from Peer B reaches NAT-a
 Depending on the timing of these events (where in the network the SYN cross),
 at least one of the NAT will let the incoming SYN through, and map it to the internal destination peer
 Upon receipt of the SYN, the peer sends a SYN+ACK back and the connection is established.

Interoperability requirements on the NAT for TCP Hole Punching

Other requirements on the NAT to comply with TCP simultaneous open

For the TCP simultaneous open to work, the NAT should:
 not send an RST as a response to an incoming SYN packet that is not part of any mapping
 accept an incoming SYN for a public endpoint when the NAT has previously seen an outgoing SYN for the same endpoint

This is enough to guarantee that NATs behave nicely with respect to the TCP simultaneous open.

TCP Hole Punching and Carrier-grade NAT (CGN)

The technique described above works fine within a CGN. A CGN can also make use of a port overloading behavior, which means that distinct internal endpoints with the same port value can be mapped to the same public endpoint. This does not break the uniqueness of the } quintuple and, as a result, is acceptable. TCP port preservation can also lead to cases where the CGN ports are overloaded and is not an issue for protocol soundness.
Port overloading for TCP allows the CGN to fit more hosts internally while preserving TCP end-to-end communication guarantees.

See also

 Hole punching (networking)
 ICMP hole punching
 Port Control Protocol (PCP)
 UDP hole punching

References

Internet security
Peer-to-peer file sharing
Transmission Control Protocol
VoIP software


Integrator complex subunit 3 is a protein that in humans is encoded by the INTS3 gene.

References

Further reading


Serine/threonine-protein kinase WNK2 is an enzyme that in humans is encoded by the WNK2 gene.

The protein encoded by this gene is a cytoplasmic serine-threonine kinase that contains cysteine in place of the lysine found at the conserved ATP-binding location in subdomain II of protein kinases. Since this protein does have kinase activity, it is possible that another lysine in the kinase subdomain I can substitute for the missing conserved lysine.

References

Further reading


Pregnancy-specific beta-1-glycoprotein 10 is a protein that in humans is encoded by the PSG10 gene.

References

Further reading


HMS Expedition was a 70-gun third-rate ship of the line built at Portsmouth Dockyard in 1677/79. She was in active commission during the War of the English Succession participating in the battles of Beachy Head and Barfleur. She was rebuilt in 1699. Again, for the War of Spanish Succession she was in commission for the operation at Cadiz then returned to England where she sat for two years. She was in the Mediterranean for the Battle of Marbella in 1705. She then went to the West Indies and fought in Wager's action off Cartagena in 1708. She was rebuilt in 1709-14 to the 1706 Establishment. She spent her time split between the Baltic and as guard ship at Portsmouth before being broken at Portsmouth in 1736. She was rebuilt in 1736/40 at Deptford Dockyard.

She was the third vessel to bear the name Expedition since it was used for a 20-gun French ship, captured in 1618 and listed until 1652.

She was the first vessel to bear the name Prince Frederick in the English and Royal Navy.

HMS Expedition was awarded the battle honours "Barfleur 1692", and "Marbella 1705".

As HMS Prince Frederick, she was awarded the battle honours "Finisterre 1747", "Louisburg 1758", and "Quebec 1759".

Construction and Specifications
She was ordered in April 1677 to be built at Portsmouth Dockyard under the guidance of Master Shipwright Daniel Furzer. She was launched on 10 September 1679. Her dimensions were a gundeck of  with a keel of  for tonnage calculation with a breadth of  and a depth of hold of . Her builder's measure tonnage was calculated as 1,068 tons (burthen). Her draught was .

Her initial gun armament was in accordance with the 1677 Establishment with 70/62 guns consisting of twenty-six demi-cannons (54 cwt, 9.5 ft) on the lower deck, twenty-six 12-pounder guns (32 cwt, 9 ft) on the upper deck, ten sakers (16 cwt, 7 ft) on the quarterdeck and four sakers (16 cwt, 7 ft) on the foc’x’le with four 3-pounder guns (5 cwt, 5 ft) on the poop deck or roundhouse. By 1688 she would carry 70 guns as per the 1685 Establishment . Her initial manning establishment would be for a crew of 460/380/300 personnel.

Commissioned Service

Service 1679-1699
She was commissioned in 1689 under the command of Captain John Clements. She partook in the Battle of Beachy Head in Centre (Red) Squadron on 30 June 1690 . In 1691 she was under command of Captain Edward Dover until his death on 16 November 1695. She fought in the Battle of Barfleur in Blue Squadron, Van Division from 19 to 22 May 1692 . Captain John Shovell was in command in November 1695 until he died on 11 April 1697. Captain James Stewart took over in April 1697. She was in action on 23 August 1697. In 1699 Captain Lord Archibald Hamilton was her commander. She was paid off in May 1699. She would be rebuilt at Chatham in 1699.

Rebuild Chatham Dockyard 1699
She was ordered rebuilt after the end of the War of the English Succession at Chatham Dockyard under the guidance of Master Shipwright Daniel Furzer, Jr. She was launched/completed in 1699. Her dimensions were a gundeck of  with a keel of  for tonnage calculation with a breadth of  and a depth of hold of . Her builder's measure tonnage was calculated as 1,116 tons (burthen). She probably retained her armament as stated in the 1685 Establishment, though it is unclear if her armament was changed to the 1703 Establishment later. It is known that when completed her gun armament total at least 70 guns.

Service 1702-1709
With the outbreak of the War of Spanish Succession (1702-1712), she was commissioned under Captain John Knapp for service in Rear-Admiral Sir Stafford Fairborne's Squadron for the expedition to Cadiz, Spain. Admiral Fairborne's Squadron was detached to reconnoiter Corunna for French ships on the 22nd of July. Finding nothing they rejoined Sir George Rooke's Fleet at sea on 8 August. The Fleet arrived at the Bay of Bulls (north of Cadiz) on the 12th. After may meeting and indecision the Fleet departed on 18 September. On 21 September it was learned that a French Fleet and Spanish treasure ships were in the vicinity of Vigo Bay. On the 11th a council of war was held to determine the ships that would initially enter the bay. HMS Expedition was not chosen and remained off the entrance of the Bay of Vigo. She returned to England. In July 1704 she was lying at Portsmouth with no captain assigned.

In 1705 she was commissioned under Captain Thomas Coale sailing in Rear-Admiral Thomas Dilke's squadron. She fought at the Battle of Marbella on 10 March 1705. During the action two French ships the Magnanime (74) and the Lys (86) were driven ashore and burnt, three French ships were taken, the 60-gun Arrogant, the 66-gun Ardent and the 66-gun Marquis. In 1706 she sailed to Brazil.

She was under Captain Edward Windsor in 1707 as Commodore Charles Wager's Flagship for operations in the West Indies. The small squadron sailed from Plymouth on 10 April 1707. In 1708 she came under Captain Henry Long remaining as Wager's Flagship. With the intent of attacking the Spanish Treasure prior to it arriving at Havana, Cuba, Commodore Wager sailed in January 1708 to intercept these vessels. After two months it was discovered that the ships would not sail before 1 May. He returned to Port Royal, then sailed again on 14 April. The vessels were sighted on 28 May making for Cartagena, Venezuela. She fought in Wager's Action at Cartagena on 28 May 1708. Two Spanish 64-gun vessels were destroyed, and a 44-gun vessel was taken. After the action the captains of Portland and Kingston were court martialed and dismissed from their ships and never served againClowes (1898), Chapter XXIII, pages 373-376.

She arrived at Portsmouth on 11 March 1709 to be dismantle for rebuilding.

Rebuild Portsmouth 1709-1714
She was ordered rebuilt under the 1706 Establishment at Portsmouth under the guidance of Master Shipwright Richard Stacey. Her keel was laid on 11 March 1709 and launched on 16 August 1714. She was renamed Prince Frederick in honour of King George I's son Prince Frederick, the Prince of Wales on 2 January 1715. Her dimensions were a gundeck of  with a keel of  for tonnage calculation with a breadth of  and a depth of hold of . Her builder's measure tonnage was calculated as 1,110 tons (burthen).

Her armament was under the 1703 Establishment as 70 guns wartime/62 guns peacetime consisting of twenty-four/twenty-two 24-pounder guns of 9.5 feet in length on the lower deck, twenty-six/twenty-four demi-culverins of 9-foot length on the upper deck, twelve/ten 6-pounder guns of 8.5-foot length on the quarterdeck, and four/two 6-pounder guns of (2/2) 9-foot length and (2/0) of 7.5-foot length, with four 5.5 foot 3-pounder guns on the poop deck or roundhouse. She may have carried her demi-cannons on the lower deck for a few years more.

She was completed at a cost of £11,834.14.1.75d.

Service 1718-1736
She was commissioned as HMS Prince Frederick in 1718 under the command of Captain Covill Mayne for service with Sir John Norris's Fleet in the Baltic sailing on 28 April returning to England in October. Later in 1718 she was under Captain Robert Haward as Flagship of Rear-Admiral James Mighells in Home Waters. She was fitted for operations in the Baltic for the Spring of 1719, 1720 and 1721. In May 1719 Captain Edward St Lo was in command as the Flagship of Rear-Admiral Francis Hosier for service in the Baltic. On 16 April 1720 she again sailed for the Baltic with Sir John Norris, returning in November. She again returned to the Baltic in 1721 to cruise off Reveal. After peace was declared in 1721, Sir John Norris returned with his Fleet, anchoring at the Nore on 20 October . In 1723 she was fitted as a guard ship under the command of Captain Edward Falkingham on guardship duties at Portsmouth. She was again fitted for service in the Baltic in the Spring of 1726. In the Spring of 1727, she was fitted for service in the Mediterranean. She was off the coast of Spain in 1727. Her breaking was completed at Portsmouth in June 1736.

Rebuild Deptford Dockyard 1736-1740
She was ordered rebuilt in 1736 at Deptford Dockyard under the guidance of Master Shipwright Richard Stacey. Her remains were moved from Portsmouth to Deptford and her keel was laid in December 1736. She was launched on 18 March 1740. Her dimensions were a gundeck of  with a keel of  for tonnage calculation with a breadth of  and a depth of hold of . Her builder's measure tonnage was calculated as 1,224 tons (burthen).

Her armament was under the 1733 Establishment as 70 guns consisting of twenty-six 24-pounder guns on the lower deck (LD), twenty-six 12-pounder guns on the upper deck (UD), fourteen 6-pounder guns on the quarterdeck (QD), and four 6-pounder guns on the foc’x’le (Fc). After her great repair in 1742/43 her 6-pounder guns were reduced by six guns (four from the QD and two from the Fc) and she was rerated as a 64-gun third rate ship.

She was completed for sea on 11 June 1740 at an initial cost to include fitting of £23,378.16.5d.

Service 1740-1784
With the outbreak of the War of Austrian Succession (1740–48), she was commissioned in the Spring or early Summer 1740 under the command of Captain George Clinton for service with Sir John Norris's Fleet. However, in the late summer/early fall of 1740, she was placed under Captain Lord Audrey Beauclerk for service in the West Indies. She sailed on 26 October 1740 for the West Indies as part of Rear-Admiral Sir Chaloner Ogle's Fleet escorting 9,000 troops for an operation at Cartagena, Venezuela. On 27 December, while sailing towards St Kitt's, four large ships were sighted and Admiral Ogle order six ships of the line to give chase. By 4pm the strangers hoisted French colours and by 10pm The Prince Frederick caught the French ships. The vessels were hailed then a gun was fired and answered with a broadside from the French vessels. Prince Frederick and Orford fought for 90 minutes when Weymouth arrived. The captain of the Weymouth expressed his conviction they were French, so Captain Beauclerk signalled the Orford to desist, though the French continued to fire their guns. The British re-engaged for a further 30 minutes. During the action Prince Frederick had lost four killed with nine wounded. The British ships then rejoined Admiral Ogle and arrived at Jamaica on 9 January and fell under the command of Vice-Admiral Edward Vernon.

She took part in the operations around Cartagena during March/April 1741. She was involved in the general attack carried out on the 23rd of March which included a naval bombardment of the Spanish Fortifications. Captain Beauclerk was killed on 24 March 1741. The naval bombardment was ceased on the 24th. Captain the Honourable Edward Boscawen took command following the death of Captain Beauclerk . With mush dissent between the Army commander, General Wentworth and Vice-Admiral Vernon, the operation was abandoned by 16 April 1741.

In 1742 she was under command of Captain Curtis Barnet for service in the Bay of Biscay during July 1742. She underwent a fitting at Portsmouth for 6,161.6.11d between October 1742 and April 1743. When completed she flew the Broad Pennant in the Bay of Biscay in October 1743. Captain Harry Norris took command in 1744 for service with Sir John Norris's Fleet in the English Channel and Bay of Biscay during 1745/46. She took four privateers during this time: Madonna la Portiere – 9 July 1745; Le Jupiter – 20 July 1745; La Fortune – 18 February 1746; and L’Intrepide – 5 January 1746. She partook in the Battle of Finisterre on 3 May 1747. Twelve of the fourteen French men-of-war were taken. All vessels were incorporated into the Royal Navy.

She was under the temporary command of Captain William Holburne sailing with Vice-Admiral Sir Peter Warren's Fleet in April 1748. She underwent a survey on 29 January 1749 then placed in Ordinary at Chatham. On 23 April 1751 she underwent another survey. Under Admiralty Order 2 May 1751 she underwent a great repair at Chatham costing 16,284.12.11d between January 1751 and February 1752. She was recommissioned in April 1755 under the command of Captain Jervis Porter for service with Rear-Admiral Sir Edward Hawke's Fleet. In April 1756 she was sent to Admiral Hawke's Fleet as a reinforcement after the outbreak of the Seven Years War (1756-1763). In 1757 under Captain William Harman, she sailed for the Leeward Islands. In 1758 she was under Captain Robert Man and sailed for North America on 29 January 1758. In August 1758 Captain Robert Routh took command for the capture of Fortress Louisburg in Cape Breton. She was at the capture of Quebec on the Saint Lawrence in New France (Canada). In 1760 she was with the Western Squadron. Captain Routh died on 3 October 1760.She was surveyed on 3 February 1760 with no repair required. In October 1760, Captain Jervis Maplesden took command remaining with the Western Squadron. She was off Brest in 1761 and the blockade of the Basque Roads in 1762, then returned to Robert Man's squadron off Brest. With the end of the Seven Years War, she was paid off in March 1763. She was surveyed on 25 April 1763 with no repairs required.

Disposition
She was fitted as a temporary Lazerette at Chatham for £1,730.18.10d between June and July 1764., then transported to Stangate Creek. She was sold under Admiralty Order (AO) 27 August 1784.

Notes

Citations

References

 Colledge (2020), Ships of the Royal Navy, by J.J. Colledge, revised and updated by Lt Cdr Ben Warlow and Steve Bush, published by Seaforth Publishing, Barnsley, Great Britain, © 2020,  (EPUB), Section K (Kent)
 Winfield (2009), British Warships in the Age of Sail (1603 – 1714), by Rif Winfield, published by Seaforth Publishing, England © 2009, EPUB
 Winfield (2007). British Warships in the Age of Sail (1714 - 1792). by Rif Winfield, published by Seaforth Publishing, England © 2007, EPUB
 Lavery, Brian (2003) The Ship of the Line - Volume 1: The Development of the Battlefleet 1650-1850. Conway Maritime Press.
 Clowes (1898), The Royal Navy, A History from the Earliest Times to the Present (Vol. II). London. England: Sampson Low, Marston & Company, © 1898
 Clowes (1898), The Royal Navy, A History from the Earliest Times to the Present (Vol. III). London. England: Sampson Low, Marston & Company, © 1898
 Thomas (1998), Battles and Honours of the Royal Navy, by David A. Thomas, first published in Great Britain by Leo Cooper 1998, Copyright © David A. Thomas 1998,  (EPUB)

External links

Ships of the line of the Royal Navy
1670s ships


The Radio Research Laboratory (RRL), located on the campus of Harvard University, was an 800-person secret research laboratory during World War II. Under the U.S. Office of Scientific Research and Development (OSRD), it was a spinoff of the Radiation Laboratory (Rad Lab) at MIT, and set up to develop electronic countermeasures to enemy radars and communications, as well as electronic counter-countermeasures (ECCM) to circumvent enemy ECM. The RRL was directed by Frederick E. Terman and operated between 1942 and 1946.

The RRL was engaged in both analysis and hardware development. They made significant contributions to the basic understanding of methods, theories, and circuits at very-high and ultra-high frequencies for radio systems, particularly in signals intelligence gear and statistical communications techniques. However, unlike the Rad Lab, the RRL never released significant details on its accomplishments; ECM and ECCM have always been closely guarded secrets by all nations.

The RRL conducted considerable work on chaff, light-weight aluminum strips dropped in clouds from aircraft to confuse enemy radars. Fred L. Whipple, an astronomer, made detailed analytical studies of this and devised a formula giving radar cross-section at a given wavelength per kilogram of chaff.

An example of RRL hardware development was Tuba (aka 'Project Tuba'), a giant ECM system generating continuous 80-kW signals in the range of 300-600 MHz to jam German Lichtenstein radars. The power tube (called Resnatron) for Tuba was developed at the RRL by David H. Shone and Lauritsen C. Marshall. Tuba used a horn antenna built of mesh wire 150 feet long and driven through 22- by 6- inch waveguides, possibly the largest ever built. Tuba was placed in operation in mid-1944 on the south coast of England. The radiated energy was such that it lit fluorescent bulbs a mile away and jammed radars throughout Europe.

The RRL staff did document some of the general theory that they developed. After the war, this was released in a two-volume publication Very High-Frequency Techniques, edited by Herbert J. Reich (McGraw-Hill, 1947).

References
 Louis Brown, A Radar History of World War II, Inst. of Physics Publishing, p. 293, 1999
 Steve Blank, Google Tech Talk: https://www.youtube.com/watch?v=hFSPHfZQpIQ
 Raymond C. Watson Jr.; Radar Origins Worldwide, Trafford Publishing, pp. 203–205, 2009
 United States. Radio Research Laboratory, Harvard University. Records of the Radio Research Laboratory : an inventory, Harvard University Archives

Harvard University
University and college laboratories in the United States
Radiation
Radar


The Museum of Trade Ceramics is located in Hoi An, central Vietnam. It is a museum showcasing the origins and history of the town and the region in the context of historic trade and relationships with foreign nations such as China, India, Japan, the Philippines and Thailand.  The building housing the museum is itself an attractively restored traditional wooden house of Hoi An's old quarter, which, on account of design similarity and a historically significant local Japanese trading community, is likened to those of Kyoto.

Literature

External links

 The New York Times | Museum of Trade Ceramics

Museums in Hoi An
Ceramics museums


Carbonic anhydrase 7 (CA7) is an enzyme that in humans is encoded by the CA7 gene.

Function

Carbonic anhydrases are a large family of zinc metalloenzymes that catalyze the reversible hydration of carbon dioxide. They participate in a variety of biological processes, including respiration, calcification, acid-base balance, bone resorption, and the formation of aqueous humor, cerebrospinal fluid, saliva, and gastric acid. They show extensive diversity in tissue distribution and in their subcellular localization. The cytosolic protein encoded by this gene is predominantly expressed in the salivary glands. Alternative splicing in the coding region results in multiple transcript variants encoding different isoforms.

References

Further reading

External links
 PDBe-KB provides an overview of all the structure information available in the PDB for Human Carbonic anhydrase 7


EBD may refer to:

 on-board diagnostics, an automotive term referring to a vehicle's self-diagnostic
 end of business day, end of day


Carbonic anhydrase-related protein 11 is a protein that in humans is encoded by the CA11 gene.

Function

Carbonic anhydrases (CAs) are a large family of zinc metalloenzymes that catalyze the reversible hydration of carbon dioxide.  They participate in a variety of biological processes, including respiration, calcification, acid-base balance, bone resorption, and the formation of aqueous humor, cerebrospinal fluid, saliva, and gastric acid.  They show extensive diversity in tissue distribution and in their subcellular localization.  CA XI is likely a secreted protein, however, radical changes at active site residues completely conserved in CA isozymes with catalytic activity, make it unlikely that it has carbonic anhydrase activity. It shares properties in common with two other acatalytic CA isoforms, CA VIII and CA X.  CA XI is most abundantly expressed in brain, and may play a general role in the central nervous system.

Interactions

CA11 has been shown to interact with RIPK1.

References

External links

Further reading


Long-lived fission products (LLFPs) are radioactive materials with a long half-life (more than 200,000 years) produced by nuclear fission of uranium and plutonium. Because of their persistent radiotoxicity, it is necessary to isolate them from humans and the biosphere and to confine them in nuclear waste repositories for geological periods of time.

Evolution of radioactivity in nuclear waste
Nuclear fission produces fission products, as well as actinides from nuclear fuel nuclei that capture neutrons but fail to fission, and activation products from neutron activation of reactor or environmental materials.

Short-term
The high short-term radioactivity of spent nuclear fuel is primarily from fission products with short half-life.
The radioactivity in the fission product mixture is mostly short-lived isotopes such as 131I and 140Ba, after about four months 141Ce, 95Zr/95Nb and 89Sr take the largest share, while after about two or three years the largest share is taken by 144Ce/144Pr, 106Ru/106Rh and 147Pm.
Note that in the case of a release of radioactivity from a power reactor or used fuel, only some elements are released. As a result, the isotopic signature of the radioactivity is very different from an open air nuclear detonation where all the fission products are dispersed.

Medium-lived fission products
After several years of cooling, most radioactivity is from the fission products caesium-137 and strontium-90, which are each produced in about 6% of fissions, and have half-lives of about 30 years. Other fission products with similar half-lives have much lower fission product yields, lower decay energy, and several (151Sm, 155Eu, 113mCd) are also quickly destroyed by neutron capture while still in the reactor, so are not responsible for more than a tiny fraction of the radiation production at any time. Therefore, in the period from several years to several hundred years after use, radioactivity of spent fuel can be modeled simply as exponential decay of the 137Cs and 90Sr. These are sometimes known as medium-lived fission products.

Krypton-85, the 3rd most active MLFP, is a noble gas which is allowed to escape during current nuclear reprocessing; however, its inertness means that it does not concentrate in the environment, but diffuses to a uniform low concentration in the atmosphere. Spent fuel in the U.S. and some other countries is not likely to be reprocessed until decades after use, and by that time most of the 85Kr will have decayed.

Actinides

After 137Cs and 90Sr have decayed to low levels, the bulk of radioactivity from spent fuel come not from fission products but actinides, notably plutonium-239 (half-life 24 ka), plutonium-240 (6.56 ka), americium-241 (432 years), americium-243 (7.37 ka), curium-245 (8.50 ka), and curium-246 (4.73 ka). These can be recovered by nuclear reprocessing (either before or after most 137Cs and 90Sr decay) and fissioned, offering the possibility of greatly reducing waste radioactivity in the time scale of about 103 to 105 years. 239Pu is usable as fuel in existing thermal reactors, but some minor actinides like 241Am, as well as the non-fissile and less-fertile isotope plutonium-242, are better destroyed in fast reactors, accelerator-driven subcritical reactors, or fusion reactors. Americium-241 has some industrial applications and is used in smoke detectors and is thus often separated from waste as it fetches a price that makes such separation economic.

Long-lived fission products
On scales greater than 105 years, fission products, chiefly 99Tc, again represent a significant proportion of the remaining, though lower radioactivity, along with longer-lived actinides like neptunium-237 and plutonium-242, if those have not been destroyed.

The most abundant long-lived fission products have total decay energy around 100–300 keV, only part of which appears in the beta particle; the rest is lost to a neutrino that has no effect. In contrast, actinides undergo multiple alpha decays, each with decay energy around 4–5 MeV.

Only seven fission products have long half-lives, and these are much longer than 30 years, in the range of 200,000 to 16 million years. These are known as long-lived fission products (LLFP). Three have relatively high yields of about 6%, while the rest appear at much lower yields. (This list of seven excludes isotopes with very slow decay and half-lives longer than the age of the universe, which are effectively stable and already found in nature, as well as a few nuclides like technetium-98 and samarium-146 that are "shadowed" from beta decay and can only occur as direct fission products, not as beta decay products of more neutron-rich initial fission products. The shadowed fission products have yields on the order of one millionth as much as iodine-129.)

The 7 long-lived fission products

The first three have similar half-lives, between 200 thousand and 300 thousand years; the last four have longer half-lives, in the low millions of years.
Technetium-99 produces the largest amount of LLFP radioactivity. It emits beta particles of low to medium energy but no gamma rays, so has little hazard on external exposure, but only if ingested. However, technetium's chemistry allows it to form anions (pertechnetate, TcO4−) that are relatively mobile in the environment.
Tin-126 has a large decay energy (due to its following short half-life decay product) and is the only LLFP that emits energetic gamma radiation, which is an external exposure hazard. However, this isotope is produced in very small quantities in fission by thermal neutrons, so the energy per unit time from 126Sn is only about 5% as much as from 99Tc for U-235 fission, or 20% as much for 65% U-235+35% Pu-239. Fast fission may produce higher yields. Tin is an inert metal with little mobility in the environment, helping to limit health risks from its radiation.
Selenium-79 is produced at low yields and emits only weak radiation. Its decay energy per unit time should be only about 0.2% that of Tc-99.
Zirconium-93 is produced at a relatively high yield of about 6%, but its decay is 7.5 times slower than Tc-99, and its decay energy is only 30% as great; therefore its energy production is initially only 4% as great as Tc-99, though this fraction will increase as the Tc-99 decays. 93Zr does produce gamma radiation, but of a very low energy, and zirconium is relatively inert in the environment.
Caesium-135's predecessor xenon-135 is produced at a high rate of over 6% of fissions, but is an extremely potent absorber of thermal neutrons (neutron poison), so that most of it is transmuted to almost-stable xenon-136 before it can decay to caesium-135. If 90% of 135Xe is destroyed, then the remaining 135Cs's decay energy per unit time is initially only about 1% as great as that of the 99Tc. In a fast reactor, less of the Xe-135 may be destroyed.135Cs is the only alkaline or electropositive LLFP; in contrast, the main medium-lived fission products and the minor actinides other than neptunium are all alkaline and tend to stay together during reprocessing; with many reprocessing techniques such as salt solution or salt volatilization, 135Cs will also stay with this group, although some techniques such as high-temperature volatilization can separate it. Often the alkaline wastes are vitrified to form high level waste, which will include the 135Cs.Fission caesium contains not only 135Cs but also stable but neutron-absorbing 133Cs (which wastes neutrons and forms 134Cs which is radioactive with a half-life of 2 years) as well as the common fission product 137Cs which does not absorb neutrons but is highly radioactive, making handling more hazardous and complicated; for all these reasons, transmutation disposal of 135Cs would be more difficult.
Palladium-107 has a very long half-life, a low yield (though the yield for plutonium fission is higher than the yield from uranium-235 fission), and very weak radiation. Its initial contribution to LLFP radiation should be only about one part in 10000 for 235U fission, or 2000 for 65% 235U+35% 239Pu. Palladium is a noble metal and extremely inert.
Iodine-129 has the longest half-life, 15.7 million years, and due to its higher half life, lower fission fraction and decay energy it produces only about 1% the intensity of radioactivity as 99Tc. However, radioactive iodine is a disproportionate biohazard because the thyroid gland concentrates iodine. 129I has a half-life nearly a billion times as long as its more hazardous sister isotope 131I; therefore, with a shorter half-life and a higher decay energy, 131I is approximately a billion times more radioactive than the longer-lived 129I.

LLFP radioactivity compared
In total, the other six LLFPs, in thermal reactor spent fuel, initially release only a bit more than 10% as much energy per unit time as Tc-99 for U-235 fission, or 25% as much for 65% U-235+35% Pu-239. About 1000 years after fuel use, radioactivity from the medium-lived fission products Cs-137 and Sr-90 drops below the level of radioactivity from Tc-99 or LLFPs in general. (Actinides, if not removed, will be emitting more radioactivity than either at this point.) By about 1 million years, Tc-99 radioactivity will have declined below that of Zr-93, though immobility of the latter means it is probably still a lesser hazard. By about 3 million years, Zr-93 decay energy will have declined below that of I-129.

Nuclear transmutation is under consideration as a disposal method, primarily for Tc-99 and I-129 as these both represent the greatest biohazards and have the greatest neutron capture cross sections, although transmutation is still slow compared to fission of actinides in a reactor. Transmutation has also been considered for Cs-135, but is almost certainly not worthwhile for the other LLFPs. Given that stable Caesium-133 is also produced in nuclear fission and both it and its neutron activation product  are neutron poisons, transmutation of  might necessitate isotope separation.  is particularly attractive for transmutation not only due to the undesirable properties of the product to be destroyed and the relatively high neutron absorption cross section but also because  rapidly beta decays to stable . Ruthenium has no radioactive isotopes with half lives much longer than a year and the price of ruthenium is relatively high, making the destruction of  into a potentially lucrative source of producing a precious metal from an undesirable feedstock.

References

Nuclear technology
Nuclear chemistry
Nuclear physics
Inorganic chemistry
Radiobiology
Fission products


Tomosynthesis, also digital tomosynthesis (DTS), is a method for performing high-resolution limited-angle tomography at radiation dose levels comparable with projectional radiography. It has been studied for a variety of clinical applications, including vascular imaging, dental imaging, orthopedic imaging, mammographic imaging, musculoskeletal imaging, and chest imaging.

History
The concept of tomosynthesis was derived from the work of Ziedses des Plantes, who developed methods of reconstructing an arbitrary number of planes from a set of projections. Though this idea was displaced by the advent of computed tomography, tomosynthesis later gained interest as a low-dose tomographic alternative to CT.

Reconstruction
Tomosynthesis reconstruction algorithms are similar to CT reconstructions, in that they are based on performing an inverse Radon transform. Due to partial data sampling with very few projections, approximation algorithms have to be used. Filtered back projection and iterative, expectation-maximization algorithms have both been used to reconstruct the data.

Reconstruction algorithms for tomosynthesis are different from those of conventional CT because the conventional filtered back projection algorithm requires a complete set of data. Iterative algorithms based upon expectation maximization are most commonly used, but are  computationally intensive. Some manufacturers have produced practical systems using off-the-shelf GPUs to perform the reconstruction in a few seconds.

Differences from other imaging modalities
Digital tomosynthesis combines digital image capture and processing with simple tube/detector motion as used in conventional computed tomography (CT). However, though there are some similarities to CT, it is a separate technique. In modern (helical) CT, the source/detector makes at least a complete 180-degree rotation about the subject obtaining a complete set of data from which images may be reconstructed. Digital tomosynthesis, on the other hand, only uses a limited rotation angle (e.g., 15-60 degrees) with a lower number of discrete exposures (e.g., 7-51) than CT. This incomplete set of projections is digitally processed to yield images similar to conventional tomography with a limited depth of field. Because the image processing is digital, a series of slices at different depths and with different thicknesses can be reconstructed from the same acquisition. However, since fewer projections are needed than CT to perform the reconstruction, radiation exposure and cost are both reduced.

Applications

Breast
Digital breast tomosynthesis (DBT) is Food and Drug Administration (FDA) approved for use in breast cancer screening. The benefit for screening has been debated, but consensus is being reached that the technology is improving sensitivity compared to two-view digital mammography at the cost of a slightly reduced specificity (increased recall rates). Because the data acquired are 85 - 160 micron typical resolution, much higher than CT, DBT is unable to offer the narrow slice widths that CT offers (typically 1-1.5 mm). However, the higher resolution detectors permit very high in-plane resolution, even if the Z-axis resolution is less. Another interesting property of breast tomosynthesis is that image quality may vary substantially through the imaging volume.

Photon-counting breast tomosynthesis has been investigated, and spectral imaging applications, such as breast density measurement and lesion characterization, have been investigated on that platform.

Chest

Musculoskeletal imaging
Tomosynthesis has a much more limited depth of field than does CT. For this reason, it likely will not be able to replace CT for the evaluation of the deeper organs of the body. However, since bones are often near the skin, multiple musculoskeletal applications of tomosynthesis have been studied, most of which have mostly been used in research with limited use in everyday practice.

Evaluation of fractures
Tomosynthesis has been compared to both radiography and CT for the evaluation of healing fractures, especially in the presence of hardware. In a study of patients with wrist fractures, digital tomosynthesis was shown to enable detection of more fractures than radiography while simultaneously providing lower metal artifact than radiography.

Evaluation of erosions in rheumatoid arthritis
Tomosynthesis has been compared to digital radiography, with CT as the standard, for the detection of erosions associated with rheumatoid arthritis. The radiation dose of digital tomosynthesis was very close to that of digital radiography. However, tomosynthesis showed sensitivity, specificity, accuracy, positive predictive value, and negative predictive value of 80%, 75%, 78%, 76%, and 80%, compared to digital radiography were 66%, 81%, 74%, 77%, and 71%. The slight benefit digital tomosynthesis in this application may or may not justify the slightly increased cost of the modality compared to digital radiography.

Electronics
Tomosynthesis is also used for x-ray inspection of electronics, particularly printed circuit board assemblies and electronic components. Tomosynthesis is usually used where a CT slice is required at high magnification, where conventional CT would not allow the sample to be located close enough to the x-ray source.

References

External links
Digital Tomosynthesis: Advanced Breast Cancer Imaging Technique, by Max Wiedmann, UCSB

X-ray computed tomography
Breast cancer


Tolloid-like protein 2 is a protein that in humans is encoded by the TLL2 gene.

This gene encodes an astacin-like zinc-dependent metalloprotease and is a subfamily member of the metzincin family. Unlike other family members, a similar protein in mice does not cleave procollagen C-propeptides or chordin.

References

Further reading


Translocation protein SEC62 is a protein that in humans is encoded by the SEC62 gene.

Function

The Sec61 complex is the central component of the protein translocation apparatus of the endoplasmic reticulum (ER) membrane. The protein encoded by this gene and SEC63 protein are found to be associated with ribosome-free SEC61 complex. It is speculated that Sec61-Sec62-Sec63 may perform post-translational protein translocation into the ER. The Sec61-Sec62-Sec63 complex might also perform the backward transport of ER proteins that are subject to the ubiquitin-proteasome-dependent degradation pathway. The encoded protein is an integral membrane protein located in the rough ER.

References

Further reading


Tetraspanin-6 is a protein that in humans is encoded by the TSPAN6 gene.

The protein encoded by this gene is a member of the transmembrane 4 superfamily, also known as the tetraspanin family. Most of these members are cell-surface proteins characterized by the presence of four hydrophobic domains. The proteins mediate signal transduction events that play a role in the regulation of cell development, activation, growth and motility. This encoded protein is a cell surface glycoprotein and is highly similar in sequence to the transmembrane 4 superfamily member 2. The use of alternate polyadenylation sites has been found for this gene.

References

Further reading


BTB/POZ domain-containing protein TNFAIP1 is a protein that in humans is encoded by the TNFAIP1 gene.

This gene was identified as a gene whose expression can be induced by the tumor necrosis factor alpha (TNF) in umbilical vein endothelial cells. Studies of a similar gene in mouse suggest that the expression of this gene is developmentally regulated in a tissue-specific manner.

References

Further reading


Tensin-1 is a protein that in humans is encoded by the TNS1 gene.

The protein encoded by this gene localizes to focal adhesions, regions of the plasma membrane where the cell attaches to the extracellular matrix. This protein crosslinks actin filaments and contains a Src homology 2 (SH2) domain, which is often found in molecules involved in signal transduction. This protein is a substrate of calpain II. A second transcript from this gene has been described, but its full length nature has not been determined.

References

External links
 TNS1 Info with links in the Cell Migration Gateway

Further reading


Putative tyrosine-protein phosphatase TPTE is an enzyme that in humans is encoded by the TPTE gene.

Function

TPTE is a member of a large class of membrane-associated phosphatases with substrate specificity for the 3-position phosphate of inositol phospholipids. TPTE is a primate-specific duplicate of the TPTE2 (TPIP) inositol phospholipid phosphatase; TPTE itself is predicted to lack phosphatase activity. TPTE and TPTE2 are the mammalian homologues to the subfamily of voltage sensitive phosphatases.

References

Further reading


The 1926 college football season was the first in which an attempt was made to recognize a national champion after the season.

Stanford, coached by Pop Warner, was the top team in the U.S. under the new Dickinson System and was awarded the Rissman Trophy. Unbeaten Stanford (10–0) faced unbeaten Alabama (9–0) in the Rose Bowl, and the two teams played to a 7–7 tie.  Seven years later, Parke H. Davis, a renowned football historian and football rules committee member, declared Lafayette (9–0), where he had previously coached, an "Outstanding Nationwide Team" in Spalding's Official Foot Ball Guide.  Davis' work has been criticized for having a heavy Eastern bias, with little regard for the South and the West Coast.

Conference and program changes

Conference changes
Five new conferences began play in 1926
Buckeye Athletic Association – a conference active through the 1938 season
Pacific Northwest Conference – an active NCAA Division III conference now known as the Northwest Conference
Midwest Athletic Association – a conference of HBCUs active through the 1966 season that was also later known as the Midwest Conference and the Midwestern Conference
Texas Collegiate Athletic Conference – a conference active through the 1955 season
Michigan Collegiate Conference – a conference active through the 1932 season; most members now part of the Mid-American Conference

Membership changes

Program changes
 Kent State Normal College officially changed their nickname from the Silver Foxes to their present moniker, the Golden Flashes.

September
September 18 A few schools opened their seasons early, as Stanford beat Fresno State 44–0.  On September 25 Stanford beat visiting Caltech, 13–0 and USC defeated Whittier 74–0;
Brown beat the University of Rhode Island, 14–0 and Pennsylvania (which had all 9 of its games scheduled at home in Philadelphia) shut out Franklin & Marshall, 41–0.  Lafayette beat Muhlenberg College 35–0
In the South, defending Rose Bowl champion Alabama beat Millsaps College (Jackson, Miss) 54–0.  Tennessee defeated Carson-Newman, 13–0.

October
October 2  Navy opened its season with a 17–13 win over Purdue, while Army started with a 21–0 win over Mercy College of Detroit.  Brown beat Colby College (of Maine), 35–0 and Pennsylvania beat Johns Hopkins, 40–7.  Lafayette won again, beating Schuylkill (which later was merged with Albright College) 47–0;

Stanford defeated Occidental 19–0 and USC defeated Santa Clara 42–0.

Alabama played Vanderbilt at Nashville and won 19–7; Tennessee beat North Carolina, 34–0.

Ohio State opened its season with a 40–0 win over Wittenberg University, while Michigan started with a 42–3 win over visiting Oklahoma State.  Northwestern opened its season with a 34–0 win over visiting South Dakota.  Notre Dame tuned up with a game against Wisconsin's Beloit College, winning  77–0.  In the Missouri Valley, Kansas State beat Texas, 13–3.

October 9 At Annapolis, Navy's football team played a doubleheader, albeit with two different squads.  The varsity beat a weak Drake University team, 24–7, and the reserves beat Richmond, 26–0.  Army defeated West Virginia's Davis & Elkins College, 21–7.  Lafayette beat Pittsburgh, 17–7 and Pennsylvania beat Swarthmore, 44–0.

Ohio State played Ohio Wesleyan and won 47–0 and Northwestern beat Minnesota's Carleton College, 31–3.  Michigan crushed Michigan State, 55–3, in a conference game.
Notre Dame won at Minnesota, 19–7

Stanford had a 7–3 victory over an amateur team, the Olympic Club (from San Francisco).  USC defeated a strong Washington State team, 16–7

Alabama beat Mississippi State 26–7 at a game in Meridian, Mississippi, while Tennessee won at LSU, 14–7.  Kansas State won at Creighton 12–0.

October 16 In New York, Columbia University hosted Ohio State in an intersectional game, and lost, 32–7.
Brown defeated Bates College 27–14 in Providence, while in Philadelphia, Pennsylvania hosted Chicago and won 27–0.  Navy won at Princeton 27–13, while Army played a strong Syracuse team and won 27–21.   Lafayette beat Dickinson 30–7.

Stanford defeated Nevada 33–0, and USC beat Occidental, 28–6

At Atlanta, Alabama beat Georgia Tech 21–0.  Tennessee had beaten Maryville the day before, 6–0.  Notre Dame beat visiting Penn State, 28–0. In Western Conference play, Michigan beat Minnesota, 20–0, Northwestern defeated Indiana 20–0, and Illinois beat Iowa 13–6.  Kansas State defeated Kansas, 27–0.

October 23 Brown played its first Ivy opponent, winning 7–0 at Yale.  Pennsylvania beat Williams College, 36–0.  Navy beat Colgate, 13–7, and Army beat Boston University 41–0.  Lafayette defeated Albany, 30–7.

Notre Dame won at Northwestern, handing the Wildcats their first defeat, 6–0, with Rockne's reserves scoring on a touchdown pass.  Alabama had a 2–0 win over Sewanee; Tennessee beat Centre College, 30–7.  In Pacific Coast Conference games, Stanford won 29–12 at Oregon, and USC beat California at Berkeley, 27–0.  In Western Conference play,  Ohio State beat Iowa 23–6 and Michigan beat Illinois 13–0.Kansas State went to 5–0–0, winning at Oklahoma, 15–12.

October 30 Navy (5–0–0) and Michigan (4–0–0) played in Baltimore in an intersectional match of unbeatens.  Though the Wolverines were heavily favored, Navy blocked a field goal and held Michigan 2 yards from goal in the first half; Hamilton of Navy kicked a field goal, made a key interception to set up a touchdown, and added the point after for a 10–0 win.

In Los Angeles, another big game between unbeatens matched Stanford and Southern California (USC), both 5–0–0, faced off.  USC scored first, but Dick Hyland blocked the extra point; after a second Trojan touchdown, the kick failed, and USC had a 12–0 lead.  Stanford scored, but the extra point kick hit the upright, and it was 12–6 at halftime. Biff Hoffman's pass to Dick Hyland tied the game for Stanford, and George Bogue's point after kick proved to be the winning margin in Stanford's 13–12 win.  Lafayette and Washington & Jefferson were both 5–0–0 when they met in Philadelphia; the Presidents lost to Lafayette, 16–10

At Champaign, Illinois (4–1–0) hosted unbeaten (5–0–0) Pennsylvania, and won 3–0, while at Atlanta, Notre Dame beat Georgia Tech 12–0.  Alabama defeated LSU, 24–0 and Tennessee won at Mississippi State, 33–0.  Army won at Yale, 33–0 and Brown won at Dartmouth, 10–0.  Ohio State won at the University of Chicago, 18–0., and Northwestern won its rematch with the Hoosiers at Indiana, 21–0.
Kansas State went to 5–0–0 in beating Arkansas, 16–7.

November

November 6
Navy played an easy opponent in West Virginia Wesleyan College, winning 53–7.  Army won its sixth straight, a 55–0 whitewash of Franklin & Marshall.  Lafayette won again, beating Rutgers 37–0; Brown beat Norwich College, 27–0 and Pennsylvania beat Penn State, 3–0.

Alabama beat Kentucky 14–0 and Tennessee beat Sewanee 12–0.  Stanford beat Santa Clara 33–14, while USC was idle.  Michigan beat Wisconsin, 37–0, Northwestern beat Purdue 22–0, and Illinois won at Chicago 7–0.  Ohio State defeated Wilmington, 13–7.  Notre Dame won at Indiana, 26–0.  In Milwaukee, Kansas State suffered its first defeat, losing to Marquette, 14–0.

On Armistice Day (November 11, USC (5–1–0) and Oregon State (4–0–0) played at Portland, Oregon.  USC won 17–7.

November 13 In Yankee Stadium, Notre Dame and Army, both 6–0–0, faced off in another battle of powerhouses.  The Fighting Irish handed the Cadets their first defeat, 7–0.  In Columbus, Ohio State (6–0–0) hosted conference rival Michigan (5–1–0).  The visitors won by a point, 17–16.
Tennessee (7–0) and Vanderbilt (6–1) faced off in Nashville, and the Vols suffered their first defeat, 20–3.  Stanford (8–0–0) hosted Washington State (7–1–0) in another big PCC game, and won, 29–10.

Northwestern, meanwhile, beat Chicago 38–7.  Illinois defeated Wabash 27–13
Navy defeated Georgetown University, 10–7, and Lafayette recorded a fourth shutout, over Susquehanna, 68–0;  Alabama beat Florida, 49–0;  Kansas State lost again, at Nebraska, 3–0.  Brown won at Harvard, 21–0 and Pennsylvania beat Columbia 3–0.

November 20  Navy played Loyola College of Baltimore, winning 35–13, and Army beat  Ursinus, 21–15.  Lafayette completed its season with a 35–0 win in its annual game against Lehigh
Brown defeated New Hampshire, 40–12, to extend its record to 9–0–0.

Ohio State closed its season with a 7–6 win at Illinois, while Michigan recorded the same score in a rematch against the Gophers at Minnesota.  Northwestern defeated Iowa, 13–6.  All three schools finished 7–1–0, with Michigan and Northwestern being 5–0 in Western Conference play.

Notre Dame beat Drake, 21–0.  Kansas State, after winning its first five, lost its next three, including a 3–2 defeat by visiting Iowa State; the Wildcats' final record was 5–3–0.  USC defeated Idaho, 38–6.  Stanford closed the regular season with its traditional finale against California.  Though the Golden Bears had the home field, they were also having their first losing season since 1916, when their program began.  California lost, 41–6.

On Thanksgiving Day, November 25, Alabama hosted Georgia winning 33–6, and USC crushed Montana, 61–0.  Pennsylvania closed its season with a 10–10 tie with Cornell.

On November 27, Notre Dame was shocked by Carnegie Tech, 19–0.  The 1926 Army-Navy game took place in Chicago.  Navy, at 9–0–0, was unbeaten, while Army (7–1–0) had a single loss, to Notre Dame.  The two teams played to a 21–21 tie.  In Providence, Brown and Colgate tied, 10–10.

December 4 In Los Angeles, Notre Dame closed its season with a 13–12 win over USC.

At season's end, there were two "unbeaten and untied" teams, the Indians (later, "the Cardinal") of Leland Stanford University, and the Crimson Tide of the University of Alabama.  Alabama, which had won the Rose Bowl the previous year, was invited to return to Pasadena to face Stanford's PCC champion team.

Rose Bowl

United Press called the 1927 Rose Bowl "the football championship of America", and the game was considered the most exciting in the series up to that time. The crowd of 68,000 set an attendance record. Stanford's George Bogue missed an 18-yard field goal attempt in the first quarter, then threw a touchdown pass to Ed Walker and kicked the point after to put Stanford up, 7–0. Stanford held that lead through most of the rest of the game, but in the final minutes, they were forced to punt on fourth down. Frankie Wilton's kick was blocked, and Alabama took over 14 yards from goal. Four plays later, and with a minute left, Jimmy Johnson carried the ball for a touchdown, making it 7–6. The two-point conversion, and overtime, were decades in the future. Stanford's only hope was to block the point after, but Alabama ran the play quickly and Herschel Caldwell's kick tied Stanford, and took away a Stanford victory in the final minute.

Conference standings
For this article, major conferences defined as those including multiple state flagship public universities.

Major conference standings

Independents

Minor conferences

Minor conference standings

Dickinson System
The AP sportswriters' poll would not begin continuously until 1936. (although, the first time was a one instance publishing in 1934)  Frank G. Dickinson, an economics professor at the University of Illinois, had invented the Dickinson System to rank colleges based upon their records and the strength of their opposition.  The system was originally designed to rank teams in the Big Nine (later the Big Ten) conference.  Chicago clothing manufacturer Jack Rissman then persuaded Dickinson to rank the nation's teams under the system, and awarded the Rissman Trophy to the winning university.

Although Dickinson retroactively applied the system to the 1924 and 1925 seasons, the year 1926 was the first in which the trophy was awarded at season's end.  The system awarded 30 points for a win over a "strong team", and 20 for a win over a "weak team".  Losses were awarded points (15 for loss to a strong team, 10 for loss to a weak team).  Ties were treated as half a win and half a loss (22.5 for a tie with a strong team, 15 for a tie with a weak team).  An average was then derived by dividing the points by games played.

Final Dickinson rankings
Professor Dickinson's rating metrics were unfavorable to Alabama, which won all nine of its regular season games, but were given an average rating of 16.67, less than the average for wins over weak (20.00 point) contenders. Alabama was the only Southern team in the 1926 rankings.

Awards and honors

All-Americans

The consensus All-America team included:

Statistical leaders
Team scoring most points: Haskell, 558
Player scoring most points: Fred Koster, Louisville, 124, or Mayes McClain, Haskell, 253
Total offense leader: Gibby Welch, Pitt

References


Cysteine-rich secretory protein 2 is a cysteine-rich secretory protein that in humans is encoded by the CRISP2 gene.

References

External links

Further reading


Gay's the Word may refer to:

 Gay's the Word (musical), a musical by Ivor Novello with lyrics by Alan Melville
 Gay's the Word (bookshop), a gay bookshop in London


Testis-specific Y-encoded-like protein 1 is a protein that in humans is encoded by the TSPYL1 gene.

References

Further reading


Tetratricopeptide repeat protein 1 is a protein that in humans is encoded by the TTC1 gene.

Interactions
TTC1 has been shown to interact with HSPA4.

References

Further reading


I'm Sorry That Sometimes I'm Mean is Kimya Dawson's debut solo album, released in 2002.

Track listing

References

Kimya Dawson albums
2002 debut albums
Sanctuary Records albums
Rough Trade Records albums


Tetratricopeptide repeat protein 3 is a protein that in humans is encoded by the TTC3 gene.

References

Further reading


The Rock2Wgtn Festival was a two-day music festival. It is the second major music festival to be held in New Zealand, the first being the Big Day Out, but Rock2Wgtn is the first purely metal/rock festival. It is also the first two-day festival, as the Big Day Out is held over a single day. It was held at the Westpac Stadium, informally known as The Cake Tin due to the shape of the building.

Rock2Wgtn 2008

The Rock2Wgtn Festival was held Easter 2008. The headliners were Kiss and Ozzy Osbourne.  The other bands to play were Whitesnake, Lordi, Alice Cooper, and Poison.

New Zealand bands The Valves, Sonic Altar, and The Symphony of Screams played support over the 2 nights.

The special effects were supplied by Weta Workshop who have previously supplied effects for movies such as The Lord of The Rings.

Attendance over the 2 days was around 50,000. The event was not a commercial success, and it was noted that Kiss bassist/vocalist Gene Simmons insisted on large volumes of free tickets being given out in order to obviate the appreciably noticeable empty seats at the venue.

Band Line Ups (as of show)

Future

The 2008 Rock2Wgtn was the last one of its kind in Wellington, with it being announced that the next Rock2Wgtn will be in another city (with the name being changed to suit). On the promoters website, http://www.capitalc.co.nz/, an image is shown with the text "In 2009 we are bringing it on again! Not Wellington... not easter... new artists!", along with a new logo that says "Rock2????". However mid-2009 it got changed to Rock22010 with no word on delays. Still stating New Artist, New City, New Date.  As of September 2011 the Rock2Wgtn website doesn't even exist.

References

External links
Official Website
Relevant article about the event
Another article about the event
Osbournes leave NZ
Review of the event

Heavy metal festivals in New Zealand
Rock festivals in New Zealand
Festivals in Wellington


U2 small nuclear ribonucleoprotein auxiliary factor 35 kDa subunit-related protein 1 is a protein that in humans is encoded by the ZRSR1 gene.

References

Further reading

Proteins


Upstream-binding protein 1 is a protein that in humans is encoded by the UBP1 gene.

References

Further reading


UDP glucuronosyltransferase 1 family, polypeptide A cluster (UGT1A) is a human gene locus which includes several UDP glucuronosyltransferases.

The UGT1A locus includes thirteen unique alternate first exons followed by four common exons. Four of the alternate first exons are considered pseudogenes. Each of the remaining nine 5' exons may be spliced to the four common exons, resulting in nine proteins with different N-termini and identical C-termini. Each first exon encodes the substrate binding site, and is regulated by its own promoter.

References

Further reading

Gene clusters


Cytochrome b-c1 complex subunit 6, mitochondrial is a protein that in humans is encoded by the UQCRH gene.

Its gene product is a subunit of the respiratory chain protein Ubiquinol Cytochrome c Reductase (UQCR, Complex III or Cytochrome bc1 complex; E.C. 1.10.2.2), which consists of the products of one mitochondrially encoded gene, MTCYTB (mitochondrial cytochrome b) and ten nuclear genes: UQCRC1, UQCRC2, Cytochrome c1, UQCRFS1 (Rieske protein), UQCRB, "11kDa protein", UQCRH (cyt c1 Hinge protein), Rieske Protein presequence, "cyt. c1 associated protein", and "Rieske-associated protein".

References

Further reading


Knock-Knock Who? is Kimya Dawson's second solo album, released concurrently with My Cute Fiend Sweet Princess in 2004.

Track listing
 "Nobody's Hippie"
 "Great Crap"
 "My Bike"
 "Jest's Birthday"
 "Time to Think"
 "The Sound of Ataris"
 "So Nice So Smart"
 "For Boxer"
 "I'm Fine"
 "Stink Mama"
 "Red White & Blue Dream (Oops!)"
 "Once Upon a Time"

References

Kimya Dawson albums
2004 albums
Important Records albums


Wnt7b is a signaling protein that plays a crucial role for many developmental processes including placental, lung, eye, dendrite, and bone formation along with kidney development. The primary role of Wnt7b is to establish the cortico-medullary axis of epithelial organization.

Protein Wnt-7b is a protein that in humans is encoded by the WNT7B gene.

Function
The WNT gene family consists of structurally related genes that encode secreted signaling proteins. These proteins have been implicated in oncogenesis and in several developmental processes, including regulation of cell fate and patterning during embryogenesis. This gene is a member of the WNT gene family. It encodes a protein showing 99% and 91% amino acid identity to the mouse and Xenopus Wnt7A proteins, respectively. Among members of the human WNT family, this protein is most similar to WNT7A protein (77.1% total amino acid identity). This gene may play important roles in the development and progression of gastric cancer, esophageal cancer, and pancreatic cancer.

Role in kidney
Wnt7b is a key paracrine signaling factor secreted by the ureteric epithelium that establishes the cortico-medullary axis of the mammalian kidney. Wnt7b is a signaling protein that plays a crucial role for many developmental processes including placental, lung, eye, dendrite, and bone formation along with kidney development. The primary role of Wnt7b is to establish the cortico-medullary axis of epithelial organization. The establishment of the cortico-medullary axis plays an essential role for the development of the medullary component of the kidney. Wnt7b regulates orientation of cell divisions in renal medullary collecting duct epithelium, in which is the major structure driving renal medulla formation. There are two interstitial regulators that are explicitly linked to medullary development; Pod1 which encodes a transcription factor expressed in the renal interstitium while p57Kip2 encodes a cyclin-dependent kinase inhibitor which is linked to Beckwith-Wiedemann syndrome. Pod1, p57Kip2 and integrin α3 (ITGA3) are three factors that are involved in renal medullary morphogenesis. The knockout of Pod1 results in no renal medullary formation while p57Kip2 and Itga3 knockouts resulted in a reduced renal medulla. Removal of Wnt7b activity leads to a failure of medullary development while other aspects of kidney development including ureteric branching, development of the renal cortex, and nephrogenesis are unaffected. The absence of renal medulla also affects the plane of epithelial cell division along with little proliferative growth of the loop of Henle. Wnt7b null allele will result in fatality due to the diminution of placental function leading to the failure to initiate organogenesis.

References

Further reading


Saint Ida may refer to several Catholic saints:

 Itta (died 652), wife of Pepin of Landen and mother of Saint Begga
 Saint Ita (also known as Ida), an Irish nun
 Ida of Herzfeld (c. 788–813), widow of a Saxon duke
 Ida of Lorraine (1040–1113)
 Ida of Toggenburg
(c. 1140 – c. 1226)


Zinc finger protein 7 is a protein that in humans is encoded by the ZNF7 gene.

Interactions
ZNF7 has been shown to interact with RPL7.

References

Further reading

External links

Transcription factors


Garrett Glaser is a retired news reporter who was one of the first US television journalists to "come out" publicly as a homosexual.

His coming out occurred during the course of a speech he made before a large group of TV and radio executives at the 1992 convention of the Radio/TV News Directors Association being held in San Antonio, Texas. Although Glaser co-founded the Electronic Media Task Force of the National Lesbian/Gay Journalists Association (NLGJA) in 1990 and was later out to fellow journalists, he was not out to the public at large. That changed in 1994 when Glaser disclosed his sexual orientation during a live report on the Channel 4 News at KNBC-TV Los Angeles as he was reporting on the death of Elizabeth Glaser (no relation), an AIDS activist who founded the Pediatric AIDS Foundation.

Several months earlier, the Los Angeles Times had published a story on the front page of its "Calendar" section about Glaser's status as one of the few openly gay TV reporters in the nation,

Earlier, in an unrelated case, Glaser had become embroiled in a public spat with Los Angeles Times media columnist Howard Rosenberg over Glaser's coverage of the disappearance of music superstar Michael Jackson for KNBC.

Glaser also worked as a TV anchor, reporter or producer at CNBC, Entertainment Tonight,  WABC-TV New York. WPLG-TV Miami. WVEC-TV Norfolk VA. WXYZ-TV Detroit. WPTA-TV Fort Wayne IN. WHLW-AM Radio Lakewood NJ and WVNJ AM-FM Radio Newark NJ. He started as a researcher at WCBS-TV's News Election Unit and as a broadcast transcriber for the CBS Evening News With Walter Cronkite at CBS News headquarters in New York in 1976. He also freelanced as a crime reporter for The Villager and a feature writer for the SoHo Weekly News.

Career in corporate communications
In 2005, Glaser left journalism and became a corporate media trainer and CSR (Corporate Social Responsibility) consultant for two US PR and lobbying firms.

Among the corporate clients he counseled were Nestle, McDonald's, H&M, Samsung, Nikon, and Continental AG.

In 2007, he formed Glaser Media, a media training consultancy hired by Fortune 500 companies to train executives to communicate more effectively with news reporters.

Notes

External links

American LGBT rights activists
Living people
American television journalists
1953 births
LGBT Jews
American LGBT journalists
CNBC people
Jewish American journalists
American male journalists
21st-century American Jews
SoHo Weekly News alumni


Zinc finger protein 19 is a protein that in humans is encoded by the ZNF19 gene.

The protein encoded by this gene contains a zinc finger, a nucleic acid-binding domain present in many transcription factors. This gene is located in a region next to ZNF23, a gene also encoding a zinc finger protein, on chromosome 16.

References

Further reading

External links

Transcription factors


Lac La Biche may refer to:
Lac La Biche, Alberta, a hamlet (formerly a town) in northeastern Alberta,
Lac La Biche County, the specialized municipality comprising the former town and the former Lakeland County,
Lac la Biche (Alberta), the lake adjacent to the community, or
Lac La Biche Airport, an airport within Lac La Biche County.

Several provincial electoral districts have also borne the name:
Lac La Biche (provincial electoral district), from 1952 to 1971,
Lac La Biche-McMurray, from 1971 to 1986,
Athabasca-Lac La Biche, from 1986 to 1993,
Lac La Biche-St. Paul, from 1993 to 2012,
Lac La Biche-St. Paul-Two Hills, from 2012 to 2019,
Fort McMurray-Lac La Biche, from 2019 to present.


Duane Garrison Hunt (September 19, 1884—March 31, 1960) was an American prelate of the Roman Catholic Church. He served as bishop of the Diocese of Salt Lake City in Utalh from 1937 until his death in 1960.

Biography

Early life and education
Raised in a Methodist family, Duane Hunt was born on September 19, 1884, in Reynolds, Nebraska, to Andrew Dixon and Lodema Esther (née Garrison) Hunt. He attended Cornell College in Mount Vernon, Iowa, where he earned a Bachelor of Arts degree in 1907. He then taught at public high schools in Iowa until 1911, when he enrolled at the University of Iowa Law School. However, his poor eyesight forced him to withdraw from law school in 1912.

Hunt then entered the graduate school at the University of Chicago, in the field of public speaking. During his studies, he began to examine and question Methodism, his birth religion. He decided to convert to Catholicism, and was baptized at St. Thomas Church and Convent in Chicago in 1913. Shortly after his graduation from the University of Chicago, he moved to Salt Lake City, where he served as a faculty member of the speech department at the University of Utah from 1913 to 1916. Hunt resigned from his teaching post in order to study for the priesthood. He studied at St. Patrick's Seminary in Menlo Park, California, from 1916 to 1920.

Priesthood
On June 27, 1920, Hunt was ordained a priest for the Diocese of Salt Lake by Bishop Joseph Glass in the Cathedral of the Madeleine. He worked as a missionary in Vernal, Utah for eight months before becoming a curate at the cathedral, where he also served as director of the choir from 1923 to 1937. Hunt was named a papal chamberlain in December 1924, and raised to the rank of domestic prelate in April 1930. He became rector of the Cathedral of the Madeleine in 1925 and chancellor of the diocese in 1926. Hunt also served as vicar general of the diocese.

From 1927 to 1949, Hunt was the weekly speaker on NBC's "Catholic Hour," a radio program in which he discussed Catholic doctrine. He served as editor of the diocesan newspaper, The Intermountain Catholic,  from 1926 to 1934. Despite his poor eyesight, he ranked among the best tennis players in Utah and coached the first diocesan baseball league in 1928.

Bishop of Salt Lake
On August 6, 1937, Hunt was appointed the fifth bishop of the Diocese of Salt Lake City by Pope Pius XI. He received his episcopal consecration on October 28, 1937, from Archbishop John Mitty, with Bishops Robert Armstrong and Thomas Gorman serving as co-consecrators. Hunt was the first Methodist convert to become a Catholic bishop.

During his tenure, Hunt established fifteen parishes throughout the state. He also invited such religious institutes as the Carmelites, Sisters of Charity of the Incarnate Word, and Trappists to serve in Utah. An apologist, he authored several defenses of the Catholic Church.  These included The Continuity of the Catholic Church, which refuted Church of Jesus Christ of Latter Day Saints (LDS) claims against Catholicism.

Death and legacy
Hunt died from a heart ailment on March 31, 1960, at age 75 at Holy Cross Hospital in Salt Lake City. His funeral was attended by LDS Church president David O. McKay.

External links

 The Intermountain Catholic
 The Continuity of the Catholic Church

References

1884 births
1960 deaths
People from Jefferson County, Nebraska
Converts to Roman Catholicism from Methodism
Roman Catholic bishops of Salt Lake City
20th-century Roman Catholic bishops in the United States
University of Iowa College of Law alumni
Cornell College alumni
University of Chicago alumni
University of Utah faculty
Catholics from Nebraska


Zinc finger protein 22 is a protein that in humans is encoded by the ZNF22 gene.

References

Further reading

External links

Transcription factors


Zinc finger protein 33B is a protein that in humans is encoded by the ZNF33B gene.

References

Further reading

External links

Transcription factors


Austin Wakeman Scott (August 31, 1884 – April 10, 1981) was a professor of law at Harvard University who wrote a ten-volume treatise covering many topics of personal trusts such as the formation and termination of express trusts, resulting and constructive trusts, and the conflicts of interest encountered in the administration of trusts.  Many of Professor Scott's dictums for fiduciaries have been incorporated in the Uniform Prudent Investor Act (UPIA). His four-volume book, The Law of Trusts, was published in 1939.

He graduated from Rutgers University in 1903 with an A.B. and received his LL.B. in 1909 from Harvard Law School.

References

External links

1880s births
1981 deaths
American legal writers
Harvard Law School faculty
Rutgers University alumni
Harvard Law School alumni