AwesomeCapital

Saturday, July 6, 2024

Dead body found wrapped in sleeping bag on NYC sidewalk next to trash bags

A dead body was found wrapped in a sleeping bag that was placed atop a dolly on a Manhattan sidewalk Friday evening, police said.

The grim discovery was made after cops were called to investigate a “suspicious package” outside of 207 East 27th Street in Kips Bay about 5 p.m., according to the NYPD.

The sleeping bag was left among several black trash bags placed on the sidewalk for garbage collection.

“It looked like whoever did it went through a lot of trouble to make sure it was wrapped up and stuck out in the open,” local Ted Oehmke told The Post.

“But I was pretty surprised to see it sitting there in the regular garbage as if sanitation was gonna pick it up and take it away,” said Oehmke, who posted video and photo on social media of officers surrounding the sleeping bag.

Oehmke said he believes he saw the top of the head as he walked by the scene.

“I see people sleeping around here all the time,” he said. “It looked like it could be just a, it’s like another body on the ground. The people I see around here, they’re not dead but they look like they could be half the time so I guess it wasn’t really that much of a shock.”

Another local said the abandoned body left her unnerved.

“It’s not something you see in this area a lot so that’s a little scary,” Marina Alves said.

The identity of the person, including age and gender, is not yet known.

It is also unknown if foul play was involved in the death, pending an examination by the Office of Chief Medical Examiner, police said.

https://nypost.com/2024/07/06/us-news/nyc-dead-body-found-in-sleeping-bag-atop-dolly-on-manhattan-sidewalk/

"Think About It Very Carefully": Author Don Winslow Posts Curious Message To Mark Warner

by Jonathan Turley,

Last night, President Joe Biden refused to take a cognitive or neurological test despite widespread concerns over his physical and mental decline. ABC’s George Stephanopoulos pressed the President on his low polling and efforts of Democrats to get him to drop out of the race. He specifically mentioned the effort of Sen. Mark Warner (D., Va.) to organize members to pressure him to end his campaign. Biden took a not-so-subtle dig at Warner. However, it was nothing compared to a curious posting by author and Democratic activist Don Winslow, who appeared to threaten Warner on X (formerly Twitter).

When the story broke in the Washington Post, Winslow posted a curious and ominous response:

It is not clear what Winslow meant by Warner knowing what he was talking about when asking if he was “sure you want to go down this road?”

The message has caused a bit of a stir on the Hill. For the denizens of the Beltway, it sounds extortive and threatening. The suggestion is that Winslow has something on Warner.

While some have asked whether this could be viewed as a threat criminally, it is clearly not sufficient for a charge. Warner is a public figure and this comment could just be a reference to political backlash or the lack of an alternative.

His asking Warner “Are you sure you want to go down this road?” could be a reference to the political implications of the resulting chaos, including making Kamala Harris the presidential candidate. Harris is even less popular than Biden according to some polls. While some polls show her doing slightly better than Biden against Trump, other polling shows that she would do considerably worse.

However, it is the follow up of “Think about it very carefully” that has got tongues wagging in D.C.

Whatever the intended meaning, the posting shows the depth of the division on the issue. Those divisions are only likely to deepen further after the refusal to take a test to put these concerns to rest.

Notably, Biden has insisted that the public can simply observe him. However, that position stands in contradiction to the frivolous privilege claims made by the Administration to withhold the audiotape from the interview with Special Counsel Robert Hur. That was an interview that the President was prepared for in advance and held in ideal conditions with staff. It is an opportunity for the public to hear him under questioning to reach the very conclusions that Biden suggested in the interview.

As for Winslow’s posting, it may just be an incautious, poorly worded message rather than extortion or blackmail. We have all made postings that we regretted.

The real issue for Democrats is how to address this looming issue without tearing the party apart. I have tried to drill down on the legal implications of swapping out the top of the ticket or the entire ticket. It is uncharted territory when it comes to the federal election laws on the use of past contributions as well as some states with restrictive rules on ballot changes.

https://www.zerohedge.com/political/think-about-it-very-carefully-author-don-winslow-posts-curious-message-mark-warner

NYS public-campaign-finance fraud exposes state board’s utter incompetence

New York state’s new public-campaign-funding scheme couldn’t be more ripe for fraud and abuse.

In the lead-up to the June 25 primaries, the state’s Public Campaign Finance Board doled out more than $8.6 million in matching-fund payments to 69 state legislative candidates — with no real guardrails to prevent shady candidates from ripping off the taxpayers.

The board looks to be as feckless as the Cannabis Control Board, which not-so-coincidentally was also launched under Gov. Andrew Cuomo.

In a fit of responsible local journalism, The New York Times has chronicled, how Dao Yin, a Flushing Democrat who filed to run for state Assembly, apparently used straw donors to scam the system out of $162,800 in taxpayer-financed matching funds.

Naturally, New York funds the most generous statewide public-matching-funds system in the nation: A single $50 donation nets $600 in public funds while a maximum $250 contribution garners $1,800.

For contributions between $5 and $250 from legislative district residents, the public match is 12-to-1 for first $50, 9-to-1 for next $100 and 8-to-1 for the following $100.

And the board’s “oversight” doesn’t seem to go much beyond sending out the checks.

The Times’ review of Yin’s contribution cards found a host of red flags:

At least 48 alleged donors who said they never heard of Yin denied making the alleged contributions and said their signatures were forged; some said they no longer resided at the addresses listed.

Almost $28,000 in cash coming from small donors.

Most of his his donations, 80%, came in cash — about 15 times the average cash share of contributions for Assembly candidates participating in the system.

Multiple “donor” records missing key required contact information or with other errors.

Dao Yin was the campaign treasurer, chief fundraiser and candidate.

The board liaison to the Yin campaign missed all of this — and took Yin’s word that he sent so-called “good-faith” letters to validate questionable donors.

To be fair, the city Campaign Finance Board may have been as lax: For his 2020 borough president and 2021 City Council campaigns, he got over $1 million in city matching funds.

(The city board also needs to complete its 2023 City Council campaign audits, too, as the 2025 election season is upon us.)

The state idiocy was baked in from the start:

An April 2018 Siena poll found that nearly two-thirds of New York voters opposed public funding of state elections when told it would cost an estimated $100 million every two years — at least.

But Cuomo and the Legislature went ahead anyway, creating a commission to devise the system in March 2019.

They stacked it with political operatives, such as election lawyer and former de Blasio fixer Henry Berger and state Democratic Party boss Jay Jacobs — for whom Cuomo suspended a state regulation that prevented political party bosses from serving in “policy making” posts in state government.

Today, the PCFB chair and vice chair are former state lawmakers Barbara Lifton (D) and Brian Kolb (R): That is, bipartisan patronage posts.

But the geniuses also left basic guardrails missing, such as:

Expenditure limits.

Mandatory post-election audits of every campaign.

Sufficient staff to review and monitor campaign filings.

The board has no independent subpoena power to pursue rogue campaigns.
Hundreds of millions of dollars in taxpayer money for political appointees to dole out is a magnet for the corrupt.

The state program is a boon for incumbent lawmakers and their unscrupulous challengers — and another needless drain on taxpayers’ wallets.

https://nypost.com/2024/07/06/opinion/nys-public-campaign-finance-fraud-exposes-state-boards-utter-incompetence/

Oxytocin as possible treatment for obesity and postnatal depression

Scientists have identified a gene which, when missing or impaired, can cause obesity, behavioural problems and, in mothers, postnatal depression. The discovery, reported today in Cell, may have wider implications for the treatment of postnatal depression, with a study in mice suggesting that oxytocin may alleviate symptoms.

Obesity and postnatal depression are significant global health problems. Postnatal depression affects more than one in 10 women within a year of giving birth and is linked to an increased risk of suicide, which accounts for as many as one in five maternal deaths in high income countries. Meanwhile, obesity has more than doubled in adults since 1990 and quadrupled in adolescents, according to the World Health Organization.

While investigating two boys from different families with severe obesity, anxiety, autism, and behavioural problems triggered by sounds or smells, a team led by scientists at the University of Cambridge, UK, and Baylor College of Medicine, Houston, USA, discovered that the boys were missing a single gene, known as TRPC5, which sits on the X chromosome.

Further investigation revealed that both boys inherited the gene deletion from their mothers, who were missing the gene on one of their X chromosomes. The mothers also had obesity, but in addition had experienced postnatal depression.

To test if it was the TRPC5 gene that was causing the problems in the boys and their mothers, the researchers turned to animal models, genetically-engineering mice with a defective version of the gene (Trpc5 in mice).

Male mice with this defective gene displayed the same problems as the boys, including weight gain, anxiety, a dislike of social interactions, and aggressive behaviour. Female mice displayed the same behaviours, but when they became mothers, they also displayed depressive behaviour and impaired maternal care. Interestingly, male mice and female mice who were not mothers but carried the mutation did not show depression-like behaviour.

Dr Yong Xu, Associate Director for Basic Sciences at the USDA/ARS Children's Nutrition Research Center at Baylor College of Medicine, said: "What we saw in those mice was quite remarkable. They displayed very similar behaviours to those seen in people missing the TRPC5 gene, which in mothers included signs of depression and a difficulty caring for their babies. This shows us that this gene is causing these behaviours."

TRPC5 is one of a family of genes that are involved in detecting sensory signals, such as heat, taste and touch. This particular gene acts on a pathway in the hypothalamus region of the brain, where it is known to control appetite.

When the researchers looked in more detail at this brain region, they discovered that TRPC5 acts on oxytocin neurons -- nerve cells that produce the hormone oxytocin, often nicknamed the 'love hormone' because of its release in response to displays of affection, emotion and bonding.

Deleting the gene from these oxytocin neurons led to otherwise healthy mice showing similar signs of anxiety, overeating and impaired sociability, and, in the case of mothers, postnatal depression. Restoring the gene in these neurons reduced body weight and symptoms of anxiety and postnatal depression.

In addition to acting on oxytocin neurons, the team showed that TRPC5 also acts on so-called POMC neurons, which have been known for some time to play an important role in regulating weight. Children in whom the POMC gene is not working properly often have an insatiable appetite and gain weight from an early age.

Professor Sadaf Farooqi from the Institute of Metabolic Science at the University of Cambridge said: "There's a reason why people lacking TRPC5 develop all of these conditions. We've known for a long time that the hypothalamus plays a key role in regulating 'instinctive behaviours' -- which enable humans and animals to survive -- such as looking for food, social interaction, the flight or fight response, and caring for their infants. Our work shows that TRPC5 acts on oxytocin neurons in the hypothalamus to play a critical role in regulating our instincts."

While deletions of the TRPC5 gene are rare, an analysis of DNA samples from around 500,000 individuals in UK Biobank revealed 369 people -- around three-quarters of whom were women -- that carried variants of the gene and had a higher-than-average body mass index.

The researchers say their findings suggests that restoring oxytocin could help treat people with missing or defective TRPC5 genes, and potentially mothers experiencing postnatal depression.

Professor Farooqi said: "While some genetic conditions such as TRPC5 deficiency are very rare, they teach us important lessons about how the body works. In this instance, we have made a breakthrough in understanding postnatal depression, a serious health problem about which very little is known despite many decades of research. And importantly, it may point to oxytocin as a possible treatment for some mothers with this condition."

There is already evidence in animals that the oxytocin system is involved in both depression and in maternal care and there have been small trials into the use of oxytocin as a treatment. The team say their work provides direct proof of oxytocin's role, which will be crucial in supporting bigger, multi-centre trials.

Professor Farooqi added: "This research reminds us that many behaviours which we assume are entirely under our control have a strong basis in biology, whether that's our eating behaviour, anxiety or postnatal depression. We need to be more understanding and sympathetic towards people who suffer with these conditions."

This work was supported by Wellcome, the National Institute for Health and Care Research (NIHR), NIHR Cambridge Biomedical Research Centre, Botnar Fondation and Bernard Wolfe Health Neuroscience Endowment.

Journal Reference:

Yongxiang Li, Tessa M. Cacciottolo, Na Yin, Yang He, Hesong Liu, Hailan Liu, Yuxue Yang, Elana Henning, Julia M. Keogh, Katherine Lawler, Edson Mendes de Oliveira, Eugene J. Gardner, Katherine A. Kentistou, Panayiotis Laouris, Rebecca Bounds, Ken K. Ong, John R.B. Perry, Inês Barroso, Longlong Tu, Jonathan C. Bean, Meng Yu, Kristine M. Conde, Mengjie Wang, Olivia Ginnard, Xing Fang, Lydia Tong, Junying Han, Tia Darwich, Kevin W. Williams, Yongjie Yang, Chunmei Wang, Shelagh Joss, Helen V. Firth, Yong Xu, I. Sadaf Farooqi. Loss of transient receptor potential channel 5 causes obesity and postpartum depression. Cell, 2024; DOI: 10.1016/j.cell.2024.06.001

https://www.sciencedaily.com/releases/2024/07/240702135557.htm

T cells and genes related to immune disorders

Researchers led by Yasuhiro Murakawa at the RIKEN Center for Integrative Medical Sciences (IMS) and Kyoto University in Japan and IFOM ETS in Italy have discovered several rare types of helper T cells that are associated with immune disorders such as multiple sclerosis, rheumatoid arthritis, and even asthma. Published July 4 in Science, the discoveries were made possible by a newly developed technology they call ReapTEC, which identified genetic enhancers in rare T cell subtypes that are linked to specific immune disorders. The new T cell atlas is publicly available and should help in the development of new drug therapies for immune-mediated diseases.

Helper T cells are kind of white blood cell that make up a large part of the immune system. They recognize pathogens and regulate the immune response. Many immune-mediated disease are caused by abnormal T cell function. In autoimmune diseases like multiple sclerosis, they mistakenly attack parts of the body as if they were pathogens. In the case of allergies, T cells overreact to harmless substances in the environment like pollen. We know of several common T cells, but recent studies have shown that rare and specialized types of T cells exist, and they might be related to immune-mediated diseases.

Within all cells, including T cells, there are regions of DNA called “enhancers”. This DNA does not code for proteins. Instead, it codes for small pieces of RNA, and enhances the expression of other genes. Variations in T cell enhancer DNA therefore lead to differences in gene expression, and this can affect how T cells function. Some enhancers are bidirectional, which means that both strands of the DNA are used as templates for enhancer RNA. The researchers from several different laboratories at RIKEN IMS, as well as colleagues at other institutes, teamed up to develop the new ReapTEC technology and look for connections between bidirectional T cell enhancers and immune diseases.

After analyzing about a million human T cells, they found several groups of rare T cell types, accounting for less than 5% of the total. Applying ReapTEC to these cells identified almost 63,000 active bidirectional enhancers. To figure out if any of these enhancers are related to immune diseases, they turned to genome-wide association studies (GWAS), which have reported numerous genetic variants, called single-nucleotide polymorphisms, that are related to various immune diseases.

When the researchers combined the GWAS data with the results of their ReapTEC analysis, they found that genetic variants for immune-mediated diseases were often located within the bidirectional enhancer DNA of the rare T cells that they had identified. In contrast, genetic variants for neurological diseases did not show a similar pattern, meaning that the bidirectional enhancers in these rare T cells are related specifically to immune-mediated diseases.

Going even deeper into the data, the researchers were able to show that individual enhancers in certain rare T cells are related to specific immune diseases. Overall, among the 63,000 bidirectional enhancers, they were able to identify 606 that included single-nucleotide polymorphisms related to 18 immune-mediated diseases. Lastly, the researchers were able to identify some of the genes that are the targets of these disease-related enhancers. For example, when they activated an enhancer that contained a genetic variant related to inflammatory bowel disease, the resulting enhancer RNA triggered upregulation of the IL7R gene.

“In the short-term, we have developed a new genomics method that can be used by researchers around the world,” says Murakawa. “Using this method, we discovered new types of helper T cells as well as genes related to immune disorders. We hope that this knowledge will lead to a better understanding of the genetic mechanisms underlying human immune-mediated diseases.”

In the long-term, the researchers believe follow-up experiments will be able to identify new molecules that can be used to treat immune-mediated diseases.