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Category Archives: Transhuman News

3576 – Gene ResultCXCL8 C-X-C motif chemokine ligand 8 [ (human)]

Posted: November 23, 2022 at 5:04 am

Envelope surface glycoprotein gp120 env HIV-1 CN54, JRFL, and Ada Env (gp120) upregulates IL-6, CCL2, CCL4, CXCL8, and IL-1b through TLR4 and CCR5 induction in monocyte derived macrophages and hepatic stellate cells because treatment with an anti-TLR4 antibody mitigated the response PubMed env HIV-1 JRFL Env (gp120) upregulates IL8 in ARPE-19 cells PubMed env HIV-1 ADA infection decreases production of CXCL8 (IL8), CCL2 (MCP-1), and IL6 at a basal level or after Fc receptor, complement receptor 3, or bacterial stimulation in primary human macrophages PubMed env HIV-1 IIIB Env (gp120) upregulates production of TNF (TNF-a), IL-17A, CCL2 (MCP1), CCL5 (RANTES), IL6, IL10, CXCL8 (IL8), CXCL1 (GRO-a), and CCL1 (I309) in stimulated monocyte derived macrophages PubMed env Interleukin 8 (IL-8) gene expression is enhanced in monocytes treated with HIV-1 gp120 PubMed env Curcumin, a potent and safe anti-inflammatory compound, inhibits HIV-1 gp120-mediated upregulation of the proinflammatory cytokines TNF-alpha and IL-6, and the chemokines IL-8, RANTES, and IP-10 in primary human genital epithelial cells PubMed env HIV-1 gp120 upregulates the expression of interleukin 8 (IL8) in human B cells PubMed env HIV-1 gp120 upregulates the expression of IL-6 and IL-8 via the p38 signaling pathway and the PI3K/Akt signaling pathway in astrocytes PubMed env The binding of soluble HIV-1 gp120 to TLR2 or TLR4 results in upregulation of the TNF-alpha and IL-8 production through NF-kappaB activation PubMed env HIV-1 gp120-mediated increases in IL-8 production in astrocytes are mediated through the NF-KappaB pathway PubMed env In endometrial epithelium-derived cells, gp120 from CCR5-tropic HIV-1 increases the release of monocytes/chemokines-attracting chemokines (IL-8 and GRO) and proinflammatory cytokines (TNF-beta and IL-1alpha) PubMed Envelope transmembrane glycoprotein gp41 env The binding of soluble TLR2 to HIV-1 MA, CA, or gp41 inhibits the nuclear translocation of NFKB p65 subunit and downregulates CXCL8 (IL-8) and CCR5 expression, leading to inhibition of HIV-1 infection in cells PubMed env Evidence suggests HIV CA (p24) binds TLR2 and blocks activation by HIV MA (p17) and/or gp41 BUT DOES NOT block activation via Pam3CSK4 suggesting that HIV manipulates innate immune signaling through a TLR2-dependent mechanism PubMed env Exposure of TZM-bl 2 cells to CA (p24) for 1h prior to HIV gp41 decreases CXCL8 (IL-8) production yet has little to no effect on the inhibition of Pam3CSK4 (a synthetic bacterial TLR2/1 ligand) production of CXCL8 (IL-8) PubMed env Exposure of human T cells to HIV gp41 increases extracellular CXCL8 (IL-8) levels but to a lesser extent than CA (p24) and gp41 PubMed env A synthetic peptide corresponding to the immunosuppressive domain (amino acids 574-592) of HIV-1 gp41 inhibits activation of PBMCs and upregulates the expression of IL-8 in peptide-treated PBMCs PubMed env The interaction between HIV-1 gp41 fusion peptide and lymphocyte membrane is blocked by interleukin-8 and abolished by pre-treating the cells with heparin sulfate (HS) PubMed Nef nef HIV-1 Nef induces IL6 and CXCL8 (IL8) expression in a PIK3-PKC dependent, AKT independent manner PubMed nef HIV-1 Nef induces IL6 and IL8 expression through the NF-kappaB pathway PubMed nef HIV-1 Nef treatment induces IL6 and IL8 production in SVGA cells and primary human fetal astrocytes PubMed nef HIV-1 Tat and Nef combination treatment induces release of both IL-6 and IL-8 in human mesenchymal stem cells PubMed nef HIV-1 Nef expression by immature human and macaque dendritic cells (DCs) upregulates IL-6, IL-12, TNF-alpha, CXCL8, CCL3, and CCL4 release, but without upregulating co-stimulatory and other molecules characteristic of mature DCs PubMed Pr55(Gag) gag MVA-gag induces a significant release of cytokines such as IL-2R, IL-6, IL-8, TNF-alpha, IFN-gamma, MCP-1, MIP-1alpha, MIP-1beta, and RANTES by the infected monocyte-derived dendritic cells in comparison with uninfected cells PubMed Tat tat HIV-1 Tat upregulates CXCL8 mRNA and protein expression in CRT-MG human astroglioma cells PubMed tat HIV-1 Tat upregulates (CXCL8) IL8 protein expression in human monocytes and monocyte-derived dendritic cells in a TLR4-CD14-MD2 dependent manner PubMed tat HIV-1 Tat and Nef combination treatment induces release of both IL-6 and IL-8 in human mesenchymal stem cells PubMed tat HIV-1 Tat-induced upregulation of IL-8 in a time-dependent manner involves NF-kappaB and AP-1 transcription factors, activation of the p38 MAPK beta subunit, and PI3K/Akt pathway in astrocytes PubMed tat HIV-1 Tat upregulates IL-8 expression in astrocytes, monocytes, monocyte derived macrophages, Jurkat T-cells, HeLa cells, and human brain endothelial cells, an effect that likely contributes to the immune dysregulation observed during HIV-1 infection PubMed tat HIV-1 Tat downregulates the expression of adiponectin protein and upregulates the expression of IL-6, IL-8, and MCP-1 proteins in human SGBS preadipocytes PubMed tat HIV-1 Tat protein upregulates expression of IL-6 and IL-8 in human breast cancer cells by an NF-kappaB-dependent pathway PubMed tat HIV-1 Tat upregulates IL-8 and VEGF production and release from polymorphonuclear leukocytes (PMNL), indicating that PMNL recruitment by Tat is linked to angiogenesis PubMed tat HIV-1 Tat upregulation of IL-8 is linked to the cell cycle and involves NF-kappa B, RelA, c-rel, and CREB-binding protein PubMed tat Upregulation of IL-8 by HIV-1 Tat is implicated in the pathogenesis of Kaposi's sarcoma PubMed tat HIV-1 Tat downregulates IL-8 expression in the Raji B-cell line, however in the presence of PMA+PHA Tat induced IL-8 expression PubMed tat Upregulation of IL-8 by HIV-1 Tat in astrocytes is inhibited by the MEK1/2 inhibitor UO126, indicating a role for MEK1/2 in Tat-mediated chemokine induction PubMed Vpr vpr Treatment of human primary astrocytes with HIV-1 Vpr upregulates secretion of IL6, CXCL8 (IL8), MCP-1, and MIF and downregulates secretion of serpin E1, a serine proteinase inhibitor (known as PAI-1) PubMed vpr HIV-1 Vpr downregulates the expression of IL8 in human monocyte-derived dendritic cells PubMed vpr HIV-1 Vpr induced upregulation of CXCL8 (IL8) involves PI3K/Akt mediated activation of NFKB1 (NF-kappa-B) in astrocytes PubMed vpr HIV-1 Vpr-mediated upregulation of CXCL8 (IL8) involves NFKB1 (NF-kappa-B) PubMed vpr HIV-1 Vpr enhances the secretion of CXCL8 (IL8) from human fetal astrocytes PubMed vpr HIV-1 Vpr upregulates the expression of CXCL8 (IL8) mRNA in human fetal astrocytes PubMed vpr HIV-1 Vpr upregulates the expression fo CXCL8 (IL8) mRNA in SVGA in a dose-dependent manner PubMed vpr HIV-1 Vpr upregulates the expression of CXCL8 (IL8) mRNA in SVGA astrocytes in a time dependent fashion PubMed vpr HIV-1 Vpr enhances the secretion of CXCL8 (IL8) from SVGA astrocytes in a time dependent fashion PubMed vpr HIV-1 involves the JUN (AP-1) transcription factor in the induction of CXCL8 (IL8) in astrocytes PubMed vpr HIV-1 Vpr involves the CEBPD (C/EBP-delta) transcription factor in the induction of CXCL8 (IL8) in astrocytes PubMed vpr Vpr-mediated upregulation of CXCL8 (IL8) involves MAPK8 (JnK-MAPK) in astrocytes PubMed vpr Vpr-mediated upregulation of CXCL8 (IL8) in astrocytes involves p38-MAPK11 (beta isoform of p38-MAPK) PubMed vpr HIV-1 Vpr regulates interleukin 8 (CXCL8 (IL8)) expression, with reports showing both up- and downregulation of CXCL8 (IL8) PubMed capsid gag CXCL8-induced upregulation of HIV-1 p24 levels and 2-LTR circles is inhibited by CXCR1 or CXCR2 neutralization in HIV-1-infected monocytes-derived macrophages PubMed gag The binding of soluble TLR2 to HIV-1 MA, CA, or gp41 inhibits the nuclear translocation of NFKB p65 subunit and downregulates CXCL8 (IL-8) and CCR5 expression, leading to inhibition of HIV-1 infection in cells PubMed gag Treatment with chemokine CXCL8 significantly upregulates HIV-1 CA (p24) levels in supernatants of both HIV-1-infected monocytes-derived macrophages as well as microglia in a dose-dependent manner PubMed gag Evidence suggests HIV CA (p24) binds TLR2 and blocks activation by HIV MA (p17) and/or gp41 BUT DOES NOT block activation via Pam3CSK4 suggesting that HIV manipulates innate immune signaling through a TLR2-dependent mechanism PubMed gag Simultaneous exposure of TZM-bl2 cells with HIV CA(p24) and MA (p17) decreases MA (p17)- induced production of CXCL8 (IL-8) in a dose-dependent manner PubMed gag Exposure of TZM-bl 2 cells to CA(p24) for 1h prior to HIV gp41 or MA (p17) decreases CXCL8 (IL-8) production yet has little to no effect on the inhibition of Pam3CSK4 (a synthetic bacterial TLR2/1 ligand) production of CXCL8 (IL-8) PubMed gag Exposure of human T cells to HIV CA (p24) increases extracellular CXCL8 (IL-8) levels in a dose dependent manner and to a greater extent than gp41 but to a lesser extent than MA (p17) exposures. PubMed gag PLA-p24-loaded human monocyte-derived dendritic cells enhance the secretion of MIP-1beta, IL-6, IL-8, and TNF-alpha in comparison with PLA-loaded cells alone PubMed integrase gag-pol The formation of 2-long terminal repeat circles, a measure of viral genome integration, is higher in CXCL8-treated, HIV-1-infected monocytes-derived macrophages and microglia, suggesting the interaction between HIV-1 IN and CXCL8 PubMed gag-pol IL-8 decreases HIV-1 reverse transcription and viral integration during the early infection, suggesting the interaction between HIV-1 IN and IL-8 PubMed matrix gag Evidence suggests HIV CA (p24) binds TLR2 and blocks activation by HIV MA (p17) and/or gp41 BUT DOES NOT block activation via Pam3CSK4 suggesting that HIV manipulates innate immune signaling through a TLR2-dependent mechanism PubMed gag Simultaneous exposure of TZM-bl2 cells with HIV CA(p24) and MA (p17) decreases MA (p17)- induced production of CXCL8 (IL-8) in a dose-dependent manner PubMed gag Exposure of TZM-bl 2 cells to CA(p24) for 1h prior to HIV MA(p17) decreases CXCL8 (IL-8) production yet has little to no effect on the inhibition of Pam3CSK4 (a synthetic bacterial TLR2/1 ligand) production of CXCL8 (IL-8) PubMed gag Exposure of human T cells to HIV MA (p17) increases extracellular CXCL8 (IL-8) levels in a dose dependent manner and to a greater extent than CA (p24) and gp41. PubMed gag The binding of soluble TLR2 to HIV-1 MA, CA, or gp41 inhibits the nuclear translocation of NFKB p65 subunit and downregulates IL-8 and CCR5 expression, leading to inhibition of HIV-1 infection in cells PubMed gag Surface plasmon resonance analysis reveals that HIV-1 p17 binds IL-8 PubMed nucleocapsid gag HIV-1 NC upregulates IL8 in HEK 293T cells PubMed reverse transcriptase gag-pol IL-8 decreases HIV-1 reverse transcription and viral integration during the early infection, suggesting the interaction between HIV-1 RT and IL-8 PubMed

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3576 - Gene ResultCXCL8 C-X-C motif chemokine ligand 8 [ (human)]

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Genome Insight and Kun-hee Lee Child Cancer & Rare Disease Project Team of SNUH (Seoul National University Hospital) Made an Agreement About a…

Posted: at 4:59 am

Genome Insight and Kun-hee Lee Child Cancer & Rare Disease Project Team of SNUH (Seoul National University Hospital) Made an Agreement About a Pediatric Cancer Whole Genome Collaborative Study Business Wire

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China Runs Police Outpost In New York City – technocracy.news

Posted: at 4:53 am

The long arm of Chinas police reaches into other countries where Chinese citizens reside, encouraging them to return to the homeland to face criminal prosecution. The first in the U.S. was New York City. This is reminiscent of Chinas Confucius Centers at universities nationwide that spied on academia. TN Editor

Chinese authorities have opened at least one overseas police service station in the United States as part of the Chinese Communist Partys (CCP) global transnational repression, according to the human rights groupSafeguard Defenders.

These operations eschew official bilateral police and judicial cooperation and violate the international rule of law,and may violate the territorial integrity in third countries involved in setting up a parallel policing mechanism using illegal methods, the Spain-based group said in a recent report.

Thereport, titled 110 Overseas: Chinese Transnational Policing Gone Wild, examined the initiative, which was begun by 10 pilot provinces in 2018. These stations also are called 110 Overseas, named after the countrys police emergency services phone number.

An outpost in New York City was among the first batch of 30 overseas police service stations in 21 countriesset up by the Public Security Bureau in Fuzhou, the capital city of the southern coastal province of Fujian. Other Chinese cities also set up their own outposts abroad.

The Chinese police authorities division in New York opened on Feb. 15, according to Dongnan News, a media outlet backed by the Fujian provincial government. The center, called Fuzhou Police Overseas Service Station, is located at 107 East Broadway, inside the headquarters of the American ChangLe Association (ACA), a nonprofit with close ties to the Chinese regime.

Safeguard Defenders identified 54 overseas police service stations across five continents, including in cities fromTorontotoDublin.

The total number of such stations is unclear.

There is no complete list of such 110 Overseas police service stations available, the report states. [T]he number is undoubtedly larger and such stations more widespread.

Established in 1998, the ACA is one of the most influential communities for immigrants from Fujian Province in the United States, according to its website.

The ACA cooperated with Fuzhous Public Security Bureau to set up the Fuzhou police service station this year, the associations chairman said in April during an event at the groups office while hosting the deputy Chinese consulate general in New York, Wu Xiaoming, Dongnan Newsreportedat the time. Wu, according to the report, recognized the associations contribution to promoting Sino-U.S. friendship and supporting Chinas peaceful reunification.

The New York community group, as with many purportedly grassroots Chinese organizations, is linked to the Chinese Communist Partys sprawling united front system. That refers to a network of thousands of overseas groups loosely overseen by the United Front Work Department, a powerful Party agency that works to advance the regimes interests abroad, including by carrying out foreign influence operations,suppressing dissident movements, gathering intelligence, and facilitating the transfer of technology to China.

The ACA maintains close ties to the regime and hasbeen praised for its efforts in supporting CCP and its leaders. Photos displayed on its website include acertificate of appreciationfrom the Chinese consulate in New York in 2015. The consulate praised the ACA for playing an active role in organizing overseas Chinese nationals to welcome Chinese leader Xi Jinping when he traveled to New York to attend United Nations meetings at that time.

The groups former president, Zhang Zikuo, in 2019 attended an official ceremony in Beijing to mark the 70th year of CCP rule over China as a representative of overseas Chinese nationals in the United States, according to a 2020reportby the Fuzhou City Federation of Returned Overseas Chinese.

In May 2020, Zhang, then-president of the ACA, attended an online seminar organized by the United Front Department of Fuzhous Changle District, during which they had an in-depth study of the spirit of the two sessions, the report reads. Two sessions refers to annual meetings held by the regimes rubber-stamp legislature and political advisory body.

Ostensibly, the overseas police service stations serve administrative purposes, with many tasks the report said that would be traditionally considered of a consular nature.

For example, the New York stations most popular service was assisting overseas Chinese in renewing drivers licenses without having to return to the country, according to an Augustreportby Dongnan News.The report said that from March 1 to April 27, 36 applications completed an online physical examination at the station and had their drivers licenses renewed.

The stations make overseas Chinese feel the care and love of the motherland, ACA Chairman Lu Jianshun told Dongnan News. The report mentions that Lu also is a staff member at the New York station.

Safeguard Defenders, however, saidsuch 110 overseas have a more sinister goal, as they contribute to resolutely cracking down on all kinds of illegal and criminal activities involving overseas Chinese.Some of the stations have already been implicated in collaborating with Chinese police in carrying out policing operations on foreign soil, the group said.

One example provided in the report was the successful return of a Chinese fugitive surnamed Xia, who was accused of fraud and fled to Serbia.

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Trilateral Commission: The secret circle that controls governments

Posted: at 4:53 am

This is a flashback article reposted by its author, Jon Rappoport. As documented in Technocracy Rising: The Trojan Horse of Global Transformation, the Trilateral Commission and its members were the main drivers to implement Technocracy on a global scale. Technocracy is a replacement economic system for capitalism and free enterprise, and the assigned agent of change is the United Nations with Sustainable Development. TN Editor

Who is in charge of destroying economies?

One group has been virtually forgotten. Its influence is enormous. It has existed since 1973.

Its called the Trilateral Commission (TC).

Keep in mind that the original stated goal of the TC was to create a new international economic order.

In the run-up to his inauguration after the 2008 presidential election, Obama was tutored by the co-founder of the Trilateral Commission, Zbigniew Brzezinski.

In 1969, four years before birthing the TC with David Rockefeller, Zbigniew Brzezinski wrote: [The] nation state as a fundamental unit of mans organized life has ceased to be the principal creative force. International banks and multinational corporations are acting and planning in terms that are far in advance of the political concepts of the nation state.

Goodbye, separate nations.

Any doubt on the question of TC goals is answered by David Rockefeller himself, the founder of the TC, in his Memoirs (2003): Some even believe we are part of a secret cabal working against the best interests of the United States, characterizing my family and me as internationalists and of conspiring with others around the world to build a more integrated global political and economic structureone world, if you will. If that is the charge, I stand guilty, and I am proud of it.

Patrick Wood, author of Trilaterals Over Washington, points out there are only 87 members of the Trilateral Commission who live in America. Obama appointed eleven of them to posts in his administration.

For example:

Here is a stunning piece of forgotten history, a 1978 conversation between a US reporter and two members of the Trilateral Commission. (Source:Trilateralism: The Trilateral Commission and Elite Planning for World Management; ed. by Holly Sklar, 1980, South End Press, Pages 192-3).

The conversation was public knowledge at the time.

Anyone who was anyone in Washington politics, in media, in think-tanks, had access to it. Understood its meaning.

But no one shouted from the rooftops. No one used the conversation to force a scandal. No one protested loudly.

The conversation revealed that the entire basis of the US Constitution had been torpedoed, that the people who were running US national policy (which includes trade treaties) were agents of an elite shadow group. No question about it.

And yet: official silence. Media silence. The Dept. of Justice made no moves, Congress undertook no serious inquiries, and the President, Jimmy Carter, issued no statements. Carter was himself an agent of the Trilateral Commission in the White House. He had been plucked from obscurity by David Rockefeller, and through elite TC press connections, vaulted into the spotlight as a pre-eminent choice for the Presidency.

The following 1978 conversation featured reporter, Jeremiah Novak, and two Trilateral Commission members, Karl Kaiser and Richard Cooper. The interview took up the issue of who exactly, during President Carters administration, was formulating US economic and political policy.

The careless and off-hand attitude of Trilateralists Kaiser and Cooper is astonishing. Its as if theyre saying, What were revealing is already out in the open, its too late to do anything about it, why are you so worked up, weve already won

NOVAK (the reporter): Is it true that a private [Trilateral committee] led by Henry Owen of the US and made up of [Trilateral] representatives of the US, UK, West Germany, Japan, France and the EEC is coordinating the economic and political policies of the Trilateral countries [which would include the US]?

COOPER: Yes, they have met three times.

NOVAK: Yet, in your recent paper you state that this committee should remain informal because to formalize this function might well prove offensive to some of the Trilateral and other countries which do not take part. Who are you afraid of?

KAISER: Many countries in Europe would resent the dominant role that West Germany plays at these [Trilateral] meetings.

COOPER: Many people still live in a world of separate nations, and they would resent such coordination [of policy].

NOVAK: But this [Trilateral] committee is essential to your whole policy. How can you keep it a secret or fail to try to get popular support [for its decisions on how Trilateral member nations will conduct their economic and political policies]?

COOPER: Well, I guess its the press job to publicize it.

NOVAK: Yes, but why doesnt President Carter come out with it and tell the American people that [US] economic and political power is being coordinated by a [Trilateral] committee made up of Henry Owen and six others? After all, if [US] policy is being made on a multinational level, the people should know.

COOPER: President Carter and Secretary of State Vance have constantly alluded to this in their speeches. [a lie]

KAISER: It just hasnt become an issue.

This interview slipped under the mainstream media radar, which is to say, it was buried.

US (and other nations) economic and political policy run by a committee of the Trilateral Commissionthe Commission created in 1973 by David Rockefeller and his sidekick, Zbigniew Brzezinski.

When Carter won the presidential election (1976), his aide, Hamilton Jordan, said that if after the inauguration, Cy Vance and Brzezinski came on board as secretary of state and national security adviser, Weve lost. And Ill quit. Lostbecause both men were powerful members of the Trilateral Commission and their appointment to key positions would signal a surrender of White House control to the Commission.

Vance and Brzezinski were appointed secretary of state and national security adviser, as Jordan feared. But he didnt quit. He became Carters chief of staff.

Now consider the vast propaganda efforts of the past 40 years, on so many levels, to install the idea that all nations and peoples of the world are a single Collective.

From a very high level of political and economic power, this propaganda op has had the objective of grooming the population for a planet that is one coagulated mass, run and managed by one force. A central engine of that force is the Trilateral Commission.

How does a shadowy group like the TC accomplish its goal? One basic strategy is: destabilize nations; ruin their economies; send millions and millions of manufacturing jobs off to places where virtual slave labor does the work; adding insult to injury, export the cheap products of those slave-factories back to the nations who lost the jobs and further undercut domestic manufacturers, forcing them to close their doors and fire still more employees.

And then solve that economic chaos by bringing order.

What kind of order?

Eventually, one planet, with national borders erased, under one management system, with a planned global economy, to restore stability, for the good of all, for lasting harmony.

The top Trilateral players, in 2008, had their man in the White House, another formerly obscure individual like Jimmy Carter: Barack Obama. They had new trade treaties on the planning table.

After Obama was inaugurated for his first term, he shocked and astonished his own advisors, who expected him, as the first order of business, to address the unemployment issue in America. He shocked them by ignoring the number-one concern of Americans, and instead decided to opt for his disastrous national health insurance policyObamacare.

Obama never had any intention of trying to dig America out of the crash of 2008. That wasnt why he was put in the Oval Office. He could, and would, pretend to bring back the economy, with fudged numbers and distorted standards. But really and truly, create good-paying jobs for many, many Americans? Not on the TC agenda. Not in the cards.

It was counter-productive to the TC plan: further undermine the economy

So that, one day, a student would ask his teacher, What happened to the United States? And the teacher would say, It was a criminal enterprise based on individual freedom. Fortunately, our leaders rescued the people and taught them the superior nature of HARMONY AND COOPERATION.

The rough, uneven, and challenged nationalism surfacing in a number of countries is evidence that many people are waking up from the Trilateral-induced trance

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Steve Jackson Games Forums – Powered by vBulletin

Posted: at 4:53 am

General information about Steve Jackson Games.

General talk and questions about Steve Jackson Games. Some staff members may have continuing threads here.

Discussion and suggestions about these forums, and requests for help.

Questions and discussions about our online store.

Discussion of our digital offerings, and of digital game support in general.

Discussions of Munchkin games and all things munchkinly!

Discussion of Steve Jackson's original RPG, The Fantasy Trip.

General discussion about roleplaying, or about games OTHER than the above.

Play RPGs online by posting in threads.

If it's a board or card game that isn't Munchkin-related, you can discuss it here.

General discussion about board games and dice games.

General discussion about card games.

General discussion about miniatures.

General talk about the hobby, including finding games or gamers.

Talk about the gaming industry; the business side of things. If it's about making games, it goes here.

Gaming and science fiction conventions.

Buy, sell, announce eBay auctions, whatever. Moderation is irregular; expect ads and spam if you visit this group.

Heres a place to post "game group wanted" or "opponent wanted" messages.

All times are GMT -6. The time now is 03:53 AM.

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Human genetic clustering – Wikipedia

Posted: at 4:44 am

Human genetic clustering refers to patterns of relative genetic similarity among human individuals and populations, as well as the wide range of scientific and statistical methods used to study this aspect of human genetic variation.

Clustering studies are thought to be valuable for characterizing the general structure of genetic variation among human populations, to contribute to the study of ancestral origins, evolutionary history, and precision medicine. Since the mapping of the human genome, and with the availability of increasingly powerful analytic tools, cluster analyses have revealed a range of ancestral and migratory trends among human populations and individuals.[1] Human genetic clusters tend to be organized by geographic ancestry, with divisions between clusters aligning largely with geographic barriers such as oceans or mountain ranges.[2][3] Clustering studies have been applied to global populations,[4] as well as to population subsets like post-colonial North America.[5][6] Notably, the practice of defining clusters among modern human populations is largely arbitrary and variable due to the continuous nature of human genotypes; although individual genetic markers can be used to produce smaller groups, there are no models that produce completely distinct subgroups when larger numbers of genetic markers are used.[2][7][8]

Many studies of human genetic clustering have been implicated in discussions of race, ethnicity, and scientific racism, as some have controversially suggested that genetically derived clusters may be understood as proof of genetically determined races.[9][10] Although cluster analyses invariably organize humans (or groups of humans) into subgroups, debate is ongoing on how to interpret these genetic clusters with respect to race and its social and phenotypic features. And, because there is such a small fraction of genetic variation between human genotypes overall, genetic clustering approaches are highly dependent on the sampled data, genetic markers, and statistical methods applied to their construction.

A wide range of methods have been developed to assess the structure of human populations with the use of genetic data. Early studies of within and between-group genetic variation used physical phenotypes and blood groups, with modern genetic studies using genetic markers such as Alu sequences, short tandem repeat polymorphisms, and single nucleotide polymorphisms (SNPs), among others.[11] Models for genetic clustering also vary by algorithms and programs used to process the data. Most sophisticated methods for determining clusters can be categorized as model-based clustering methods (such as the algorithm STRUCTURE[12]) or multidimensional summaries (typically through principal component analysis).[1][13] By processing a large number of SNPs (or other genetic marker data) in different ways, both approaches to genetic clustering tend to converge on similar patterns by identifying similarities among SNPs and/or haplotype tracts to reveal ancestral genetic similarities.[13]

Common model-based clustering algorithms include STRUCTURE, ADMIXTURE, and HAPMIX. These algorithms operate by finding the best fit for genetic data among an arbitrary or mathematically derived number of clusters, such that differences within clusters are minimized and differences between clusters are maximized. This clustering method is also referred to as "admixture inference," as individual genomes (or individuals within populations) can be characterized by the proportions of alleles linked to each cluster.[1] In other words, algorithms like STRUCTURE generate results that assume the existence of discrete ancestral populations, operationalized through unique genetic markers, which have combined over time to form the admixed populations of the modern day.

Where model-based clustering characterizes populations using proportions of presupposed ancestral clusters, multidimensional summary statistics characterize populations on a continuous spectrum. The most common multidimensional statistical method used for genetic clustering is principal component analysis (PCA), which plots individuals by two or more axes (their "principal components") that represent aggregations of genetic markers that account for the highest variance. Clusters can then be identified by visually assessing the distribution of data; with larger samples of human genotypes, data tends to cluster in distinct groups as well as admixed positions between groups.[1][13]

There are caveats and limitations to genetic clustering methods of any type, given the degree of admixture and relative similarity within the human population. All genetic cluster findings are biased by the sampling process used to gather data, and by the quality and quantity of that data. For example, many clustering studies use data derived from populations that are geographically distinct and far apart from one another, which may present an illusion of discrete clusters where, in reality, populations are much more blended with one another when intermediary groups are included.[1] Sample size also plays an important moderating role on cluster findings, as different sample size inputs can influence cluster assignment, and more subtle relationships between genotypes may only emerge with larger sample sizes.[1][8] In particular, the use of STRUCTURE has been widely criticized as being potentially misleading through requiring data to be sorted into a predetermined number of clusters which may or may not reflect the actual population's distribution.[8][14] The creators of STRUCTURE originally described the algorithm as an "exploratory" method to be interpreted with caution and not as a test with statistically significant power.[12][15]

Modern applications of genetic clustering methods to global-scale genetic data were first marked by studies associated with the Human Genome Diversity Project (HGDP) data.[1] These early HGDP studies, such as those by Rosenberg et al. (2002),[4][16] contributed to theories of the serial founder effect and early human migration out of Africa, and clustering methods have been notably applied to describe admixed continental populations.[5][6][17] Genetic clustering and HGDP studies have also contributed to methods for, and criticisms of, the genetic ancestry consumer testing industry.[18]

A number of landmark genetic cluster studies have been conducted on global human populations since 2002, including the following:

Clusters of individuals are often geographically structured. For example, when clustering a population of East Asians and Europeans, each group will likely form its own respective cluster based on similar allele frequencies. In this way, clusters can have a correlation with traditional concepts of race and self-identified ancestry; in some cases, such as medical questionnaires, the latter variables can be used as a proxy for genetic ancestry where genetic data is unavailable.[9][4] However, genetic variation is distributed in a complex, continuous, and overlapping manner, so this correlation is imperfect and the use of racial categories in medicine can introduce additional hazards.[9]

Some scholars[who?] have challenged the idea that race can be inferred by genetic clusters, drawing distinctions between arbitrarily assigned genetic clusters, ancestry, and race. One recurring caution against thinking of human populations in terms of clusters is the notion that genotypic variation and traits are distributed evenly between populations, along gradual clines rather than along discrete population boundaries; so although genetic similarities are usually organized geographically, their underlying populations have never been completely separated from one another. Due to migration, gene flow, and baseline homogeneity, features between groups are extensively overlapping and intermixed.[2][9] Moreover, genetic clusters do not typically match socially defined racial groups; many commonly understood races may not be sorted into the same genetic cluster, and many genetic clusters are made up of individuals who would have distinct racial identities.[7] In general, clusters may most simply be understood as products of the methods used to sample and analyze genetic data; not without meaning for understanding ancestry and genetic characteristics, but inadequate to fully explaining the concept of race, which is more often described in terms of social and cultural forces.

In the related context of personalized medicine, race is currently listed as a risk factor for a wide range of medical conditions with genetic and non-genetic causes. Questions have emerged regarding whether or not genetic clusters support the idea of race as a valid construct to apply to medical research and treatment of disease, because there are many diseases that correspond with specific genetic markers and/or with specific populations, as seen with Tay-Sachs disease or sickle cell disease.[3][25] Researchers are careful to emphasize that ancestryrevealed in part through cluster analysesplays an important role in understanding risk of disease. But racial or ethnic identity does not perfectly align with genetic ancestry, and so race and ethnicity do not reveal enough information to make a medical diagnosis.[25] Race as a variable in medicine is more likely to reflect social factors, where ancestry information is more likely to be meaningful when considering genetic ancestry.[2][25]

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Human genetic clustering - Wikipedia

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Human Genome Project Fact Sheet

Posted: at 4:44 am

A special committee of the U.S. National Academy of Sciences outlined the original goals for the Human Genome Project in 1988, which included sequencing the entire human genome in addition to the genomes of several carefully selected non-human organisms.

Eventually the list of organisms came to include the bacterium E. coli, bakers yeast, fruit fly, nematode and mouse. The projects architects and participants hoped the resulting information would usher in a new era for biomedical research, and its goals and related strategic plans were updated periodically throughout the project.

In part due to a deliberate focus on technology development, the Human Genome Project ultimately exceeded its initial set of goals, doing so by 2003, two years ahead of its originally projected 2005 completion. Many of the projects achievements were beyond what scientists thought possible in 1988.

President Bill Clinton and Francis Collins, M.D., Ph.D., (NHGRI Director) at a June 2000 event at the White House celebrating the draft human genome sequence generated by the Human Genome Project. Dr. Collins served as the de facto leader of the International Human Genome Sequencing Consortium, the group that sequenced the human genome during the Human Genome Project. (NHGRI Photo Archive)

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Abstracts | International Congress of Human Genetics 2023

Posted: at 4:44 am

The International Scientific Programme Committee (ISPC) invites you to contribute to the programme by submitting an abstract for possible inclusion in the 14th International Congress of Human Genetics (ICHG) 2023 programme.

Please follow the abstract guidelines below, to help you through the submission process.

Abstract GuidelinesUse Arial Font 11, single line spacing and full justification for the borders.

Abstract Title:A brief title that clearly indicates the content of the contribution (maximum of 30 words).

Please avoid abbreviations in the abstract title. Abbreviations may be used if they refer to gene names using the standardised nomenclature, and in the body of the abstract if defined when first used. Do not use capitals or capitalise words that are not nouns.

Example:Title: This is an important African contribution to the field in terms of the APOL1 gene

Abstract Content:Please ensure that your abstract summarises your entire contribution in one paragraph (maximum of 300 words). Do not use section headings, but ensure that the content is structured.

Diagrams, illustrations, tables, references and graphics are NOT permitted.

Qualities of a good abstract embodies the following structure:

Check grammar and spelling, sentence construction and punctuation before submission. Ensure that abbreviations are defined when used for the first time and then use the abbreviation in the rest of the abstract. Only use abbreviations if the term is used two or more times. Ask another person to carefully proofread and check your abstract for flow and content, as well as the details above.

Note: Abstracts not in the correct format will be returned to the submitting author.

Keywords:Please indicate at least 3 keywords for your abstract. These terms will be used to help people locate your abstract using the Conference App.

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Abstracts | International Congress of Human Genetics 2023

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Dwarf tomato seeds to launch to space station aboard SpaceX resupply flight – CNN

Posted: at 4:43 am

Dwarf tomato seeds to launch to space station aboard SpaceX resupply flight CNN
Three Experiments Heading to Space Station Aim to Support Deep-Space Missions | Science Mission Directorate Science@NASA
Space tomatoes and prescription yogurt incubator rocket to the ISS today TechCrunch
Microgravity tomatoes, yogurt bacteria, and plastic eating microbes are headed to the ISS Popular Science
From tomatoes to medical kit, what NASA sends in ISS resupply mission Hindustan Times
View Full Coverage on Google News

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Dwarf tomato seeds to launch to space station aboard SpaceX resupply flight - CNN

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Atopic eczema – NHS

Posted: at 4:30 am

Atopic eczema (atopic dermatitis) is the most common form of eczema, a conditionthat causes the skin to become itchy, dry and cracked.

Atopic eczema is more common in children, often developing before their first birthday. But it may also develop for the first time in adults.

It's usually a long-term (chronic) condition, although it can improve significantly, or even clear completely, in some children as they get older.

Atopic eczemacauses the skin to become itchy, dry, cracked and sore.

Some people only have small patches of dry skin, but others may experience widespread inflamed skin all over the body.

Inflamed skin can become red on lighter skin, and darker brown, purple or grey on darker skin. This can also be more difficult to see on darker skin.

Although atopic eczema can affect any part of the body,it most often affects the hands, insides of the elbows, backs of the knees and the face and scalp in children.

People with atopic eczema usuallyhave periods when symptoms are less noticeable, as well as periods when symptoms become more severe (flare-ups).

See a GP if you have symptoms of atopic eczema. They'll usually be able to diagnose atopic eczema by looking at your skin and asking questions, such as:

Typically, to be diagnosed with atopic eczema you should have had an itchy skin condition in the last 12 months and 3 or more of the following:

The exact cause of atopic eczema is unknown, but it's clear it is not down to one single thing.

Atopic eczema often occurs in people who get allergies. "Atopic" means sensitivity to allergens.

Itcan run in families, and oftendevelops alongside other conditions, such asasthma and hay fever.

The symptoms of atopic eczemaoften have certaintriggers, such as soaps, detergents, stress and the weather.

Sometimesfood allergies can play a part, especially in young children with severe eczema.

You may be asked to keep a food diaryto try to determine whether a specific food makes your symptoms worse.

Allergy testsare not usually needed, although they're sometimes helpful in identifyingwhether a food allergy may be triggering symptoms.

Treatment for atopic eczema canhelp to relieve the symptoms and many cases improve over time.

Butthere's currently no cure andsevere eczema often has a significant impact on daily life, whichmay be difficult tocope with physically and mentally.

There's also an increased risk of skin infections.

Many different treatments can be used to control symptoms and manage eczema, including:

Eczema is the name for a group of skin conditions that cause dry, irritated skin.

Other types of eczema include:

Page last reviewed: 05 December 2019Next review due: 05 December 2022

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