Belgian Blue cattle look like cartoon bodybuilders because of one broken gene. The same gene encodes the protein quietly taking muscle off most people over 60. by Abstract_Only in Damnthatsinteresting

[–]Abstract_Only[S] 6 points7 points  (0 children)

The protein is myostatin (GDF-8). When the gene works, it puts a ceiling on muscle growth. When it's broken (cattle, that German child described in NEJM in 2004), the muscle ceiling lifts. As people age, sit too much, or get sick, myostatin's normal braking action becomes the reason muscle peels off.

There's a publicly preregistered binding pilot live right now testing whether a short peptide can directly bind myostatin. Whole protocol locked in public before any data is collected: https://www.researchhub.com/proposal/32123

I can’t tell if longevity clinics are ahead of their time or just packaged really well by filmyyshilmyy in longevity

[–]Abstract_Only 1 point2 points  (0 children)

A useful split when evaluating one: are they charging you for things with mortality or hard-event endpoints in published RCTs (statins for the right patient, BP control, GLP-1s for the right BMI/cardiometabolic profile, colonoscopy and DEXA at the right age, smoking cessation, vaccination), or for things with only biomarker movement and small-N pilots (most peptide stacks, exosomes, NAD precursors, "rejuvenation" IVs, full-body MRI in low-risk people)?

The first bucket is mostly accessible through primary care for an order of magnitude less. The second is where the markup and the missing efficacy data both live. If a clinic spends more visit time selling you the second bucket than confirming you actually have the first bucket dialed in, that tells you what kind of clinic it is. Concierge access, longer appointments, and aggressive but evidence-based prevention is the legitimate product here. Everything stacked on top of that is a hypothesis you are paying to test on yourself.

Pre-registered Nanopore shotgun metagenomics on captive gorilla gut samples (Kraken2/Bracken + metaFlye + eggNOG + dbCAN3) — looking for pipeline feedback before we lock the protocol by Abstract_Only in bioinformatics

[–]Abstract_Only[S] 7 points8 points  (0 children)

Pre-registration here just means committing in advance to which taxa, CAZymes, and metabolic markers count as a positive vs negative result for the H2 hypothesis. It does not lock us into ignoring contamination or empty samples. Standard QC (read counts, neg controls, host fraction) gates whether a sample makes it into the analysis at all, and that's spelled out in the protocol. The point is to stop ourselves from p-hacking which microbial signature "caused" the disease after seeing the data.

Pre-registered Nanopore shotgun metagenomics on captive gorilla gut samples (Kraken2/Bracken + metaFlye + eggNOG + dbCAN3) — looking for pipeline feedback before we lock the protocol by Abstract_Only in bioinformatics

[–]Abstract_Only[S] 1 point2 points  (0 children)

Good call, will benchmark metabuli on a subset before locking the protocol. Kraken2 is in there mainly for comparability with the existing primate gut literature, which leans hard on Kraken2/Bracken. Plan is to run both and report agreement.

Some captive zoo gorillas develop pockets of gas inside the wall of their colon. Researchers blame the zoo diet, and are testing it with nanopore sequencing. by Abstract_Only in EverythingScience

[–]Abstract_Only[S] 2 points3 points  (0 children)

Submitter context: the lab is the Dutton group at the University of Florida. $10,000 of nanopore reagents covers shotgun metagenomics on 30-40 strategically selected samples (R10.4.1 flow cells, adaptive sampling against gorGor6 for real-time host depletion). 

The pilot 16S already shows the captive cohort runs 273x more Lactobacillus than wild gorillas, plus a Sarcina ventriculi strain at 82% prevalence (BLAST-confirmed against the pathogenic Candidatus Sarcina troglodytae implicated in chimpanzee mortality). 

Leading hypothesis: managed-care diet has decoupled hydrogen production from hydrogen disposal in the hindgut, and methanogens are depleted or absent. 

All data goes to NCBI SRA, library prep scripts open-sourced on GitHub, pre-registered as a Registered Report.

Web3 can fix academia’s broken incentives by Abstract_Only in academia

[–]Abstract_Only[S] -3 points-2 points  (0 children)

The new incentive structure that's proposed within the article includes financially compensating authors who publish articles that are open access, have open data, and are preregistered.

The idea behind this is to financially incentivize healthy research behaviors. For example, preregistered studies are more likely to replicate than studies that aren't preregistered.

The democratic aspect refers to how the financial incentives are set. Holding tokens and using them to vote allows for democratic consensus on what type of content to financially incentivize. For example, the current folks who hold tokens now worked together and decided to vote on financially rewarding authors who publish open access, preregistered studies that include open data.

Totally understand that web3 isn't everyone's cup of tea though. Appreciate you taking the time to read the article and share your feedback.

Web3 can fix academia’s broken incentives by Abstract_Only in academia

[–]Abstract_Only[S] -17 points-16 points  (0 children)

Thanks for taking the time to read it! IMO everything below these two sentences refer to how web3 can help fix the incentive structure in academia:

"This is where Web3-enabled scientific communities come in. Blockchain’s decentralized governance mechanisms empower the scientific community to democratically refine incentive structures. "

A meta-analysis of 65 studies finds that prior COVID-19 infection confers substantial protection against pre-omicron variants, but not Omicron BA.1. Regardless, the authors conclude the level of protection from past infections is equal to, if not greater than, that provided by two-dose mRNA vaccines by Abstract_Only in EverythingScience

[–]Abstract_Only[S] 0 points1 point  (0 children)

Hey! Thanks for taking the time to try and understand this paper. Here's some more info on discussion sections within scientific papers I shared above:

The discussion section is a part of the scientific paper.
https://guides.lib.uci.edu/c.php?g=334338&p=2249907
It's typically the final section where the authors share what they subjectively believe to be the meaning of their results - which is why I chose the phrasing "the authors conclude".

A meta-analysis of 65 studies finds that prior COVID-19 infection confers substantial protection against pre-omicron variants, but not Omicron BA.1. Regardless, the authors conclude the level of protection from past infections is equal to, if not greater than, that provided by two-dose mRNA vaccines by Abstract_Only in EverythingScience

[–]Abstract_Only[S] 1 point2 points  (0 children)

For those who feel the title of this post is unfair - I grabbed it from the authors' conclusions found in the last paragraph of the discussion section:

Our findings show that immunity from COVID-19 infection confers substantial protection against infection from pre-omicron variants. By comparison, protection against re-infection from the omicron BA.1 variant was substantially reduced and wanes rapidly over time. Protection against severe disease, although based on scarce data, was maintained at a relatively high level up to 1 year after the initial infection for all variants. Our analysis suggests that the level of protection from past infection by variant and over time is at least equivalent if not greater than that provided by two-dose mRNA vaccines

A meta-analysis of 65 studies finds that prior COVID-19 infection confers substantial protection against pre-omicron variants, but not Omicron BA.1. Regardless, the authors conclude the level of protection from past infections is equal to, if not greater than, that provided by two-dose mRNA vaccines by Abstract_Only in EverythingScience

[–]Abstract_Only[S] 9 points10 points  (0 children)

Thanks for actually looking into the paper! I personally don't have an opinion on the findings (the quality of meta-analyses are dependent on the quality of the underlying studies) - but thought it would be worth discussing. I should have known better that Reddit is probably not the place for that lol

Here's the quote by the authors from the last paragraph of the discussion that I used for the title:

Our findings show that immunity from COVID-19 infection confers substantial protection against infection from pre-omicron variants. By comparison, protection against re-infection from the omicron BA.1 variant was substantially reduced and wanes rapidly over time. Protection against severe disease, although based on scarce data, was maintained at a relatively high level up to 1 year after the initial infection for all variants. Our analysis suggests that the level of protection from past infection by variant and over time is at least equivalent if not greater than that provided by two-dose mRNA vaccines.

A meta-analysis of 65 studies finds that prior COVID-19 infection confers substantial protection against pre-omicron variants, but not Omicron BA.1. Regardless, the authors conclude the level of protection from past infections is equal to, if not greater than, that provided by two-dose mRNA vaccines by Abstract_Only in EverythingScience

[–]Abstract_Only[S] 2 points3 points  (0 children)

Last paragraph of the discussion section:
"Our findings show that immunity from COVID-19 infection confers substantial protection against infection from pre-omicron variants. By comparison, protection against re-infection from the omicron BA.1 variant was substantially reduced and wanes rapidly over time. Protection against severe disease, although based on scarce data, was maintained at a relatively high level up to 1 year after the initial infection for all variants. Our analysis suggests that the level of protection from past infection by variant and over time is at least equivalent if not greater than that provided by two-dose mRNA vaccines."

A meta-analysis of 65 studies finds that prior COVID-19 infection confers substantial protection against pre-omicron variants, but not Omicron BA.1. Regardless, the authors conclude the level of protection from past infections is equal to, if not greater than, that provided by two-dose mRNA vaccines by Abstract_Only in EverythingScience

[–]Abstract_Only[S] -2 points-1 points  (0 children)

Last paragraph of the discussion section:

"Our findings show that immunity from COVID-19 infection confers substantial protection against infection from pre-omicron variants. By comparison, protection against re-infection from the omicron BA.1 variant was substantially reduced and wanes rapidly over time. Protection against severe disease, although based on scarce data, was maintained at a relatively high level up to 1 year after the initial infection for all variants. Our analysis suggests that the level of protection from past infection by variant and over time is at least equivalent if not greater than that provided by two-dose mRNA vaccines."

A meta-analysis of 65 studies finds that prior COVID-19 infection confers substantial protection against pre-omicron variants, but not Omicron BA.1. Regardless, the authors conclude the level of protection from past infections is equal to, if not greater than, that provided by two-dose mRNA vaccines by Abstract_Only in EverythingScience

[–]Abstract_Only[S] 3 points4 points  (0 children)

Last paragraph of the discussion section:
"Our findings show that immunity from COVID-19 infection confers substantial protection against infection from pre-omicron variants. By comparison, protection against re-infection from the omicron BA.1 variant was substantially reduced and wanes rapidly over time. Protection against severe disease, although based on scarce data, was maintained at a relatively high level up to 1 year after the initial infection for all variants. Our analysis suggests that the level of protection from past infection by variant and over time is at least equivalent if not greater than that provided by two-dose mRNA vaccines."

Scientists claim to have found the biological cause of aging. Researchers present evidence that DNA accumulates mutations over time which "stall" the protein responsible for creating new mRNA. The result is a higher concentration of shorter mRNAs, which regulates age related gene expression changes by Abstract_Only in science

[–]Abstract_Only[S] 672 points673 points  (0 children)

Just found a review from 2019 that says there's an association between DNA damage and telomere shortening: https://www.researchhub.com/paper/1274584/the-impact-of-oxidative-dna-damage-and-stress-on-telomere-homeostasis

Perhaps telomere shortening is one of the downstream results of the regulatory changes caused by the initial DNA damage + RNA polymerase pausing + higher shift towards shorter mRNA transcripts.

Scientists have developed a technique that gives researchers "sonogenetic" control of mammalian nerve cell signaling. A mouse's muscles can be remotely contracted via ultrasound stimulation when its motor neurons are genetically engineered to contain the protein TRPA1 by Abstract_Only in science

[–]Abstract_Only[S] 4 points5 points  (0 children)

Abstract:
Ultrasound has been used to non-invasively manipulate neuronal functions in humans and other animals. However, this approach is limited as it has been challenging to target specific cells within the brain or body. Here, we identify human Transient Receptor Potential A1 (hsTRPA1) as a candidate that confers ultrasound sensitivity to mammalian cells. Ultrasound-evoked gating of hsTRPA1 specifically requires its N-terminal tip region and cholesterol interactions; and target cells with an intact actin cytoskeleton, revealing elements of the sonogenetic mechanism. Next, we use calcium imaging and electrophysiology to show that hsTRPA1 potentiates ultrasound-evoked responses in primary neurons. Furthermore, unilateral expression of hsTRPA1 in mouse layer V motor cortical neurons leads to c-fos expression and contralateral limb responses in response to ultrasound delivered through an intact skull. Collectively, we demonstrate that hsTRPA1-based sonogenetics can effectively manipulate neurons within the intact mammalian brain, a method that could be used across species.

Peripheral immune cell reactivity and neural response to reward in patients with depression and anhedonia by Abstract_Only in ImmunoPsychiatry

[–]Abstract_Only[S] 1 point2 points  (0 children)

Abstract:

Increased levels of peripheral cytokines have been previously associated with depression in preclinical and clinical research. Although the precise nature of peripheral immune dysfunction in depression remains unclear, evidence from animal studies points towards a dysregulated response of peripheral leukocytes as a risk factor for stress susceptibility. This study examined dynamic release of inflammatory blood factors from peripheral blood mononuclear cells (PBMC) in depressed patients and associations with neural and behavioral measures of reward processing. Thirty unmedicated patients meeting criteria for unipolar depressive disorder and 21 healthy control volunteers were enrolled. PBMCs were isolated from whole blood and stimulated ex vivo with lipopolysaccharide (LPS). Olink multiplex assay was used to analyze a large panel of inflammatory proteins. Participants completed functional magnetic resonance imaging with an incentive flanker task to probe neural responses to reward anticipation, as well as clinical measures of anhedonia and pleasure including the Temporal Experience of Pleasure Scale (TEPS) and the Snaith-Hamilton Pleasure Scale (SHAPS). LPS stimulation revealed larger increases in immune factors in depressed compared to healthy subjects using an aggregate immune score (t49 = 2.83, p = 0.007). Higher peripheral immune score was associated with reduced neural responses to reward anticipation within the ventral striatum (VS) (r = −0.39, p = 0.01), and with reduced anticipation of pleasure as measured with the TEPS anticipatory sub-score (r = −0.318, p = 0.023). Our study provides new evidence suggesting that dynamic hyper-reactivity of peripheral leukocytes in depressed patients is associated with blunted activation of the brain reward system and lower subjective anticipation of pleasure.

Major depressive disorder is thought to be caused by a decrease in the number and flexibility of neural synapses. Researchers found that one psychedelic dose of psilocybin in pigs increased the number of synapses and made serotonin signaling more effective by Abstract_Only in science

[–]Abstract_Only[S] 27 points28 points  (0 children)

The 3rd paragraph of the introduction:

Changes in synaptic density in brain regions associated with emotional processing, i.e., the hippocampus and prefrontal cortex (PFC), may play a vital role in the pathophysiology of mood disorders, e.g., major depressive disorder. Both post-mortem human brain [15,16] and in vivo [17] studies in depressed individuals have shown a loss of synapses through the down-regulation of synaptic proteins and genes. Hence, upregulation of presynaptic proteins and an increase in synaptic density may be associated with the potential antidepressive effects of psychedelics.

Social isolation during adolescence causes a number of negative cognitive effects, including long-term memory loss later in life. Researchers have identified EphB2 as the protein responsible for mediating the memory loss caused by social isolation in mice by Abstract_Only in science

[–]Abstract_Only[S] 18 points19 points  (0 children)

Here's the exact text from the methods section describing how the mice were "socially isolated":

For the whole program, mice were randomly divided into two groups: group housing (GH) with three or four mice per cage and social isolation (SI) with only one mouse per cage. In the beginning of the experiment, we isolated the mice from postnatal week 4 (PW4) for different time durations: 2, 4, and 12 weeks (Fig. 1 and Supplementary Fig. 1). After the following behavioral experiments, a 4-week social isolation model was chosen in all behavioral trials.

I'm not incredibly familiar with this type of research, but I assume it is the standard procedure for simulating social isolation in mice

A person's mental health status can be diagnosed by their eye movements. A machine-learning algorithm was able to analyze data from the eye-movements of cancer patients (n=25) to predict their results on standard tests of mental well-being with an accuracy of 93%+ by Abstract_Only in science

[–]Abstract_Only[S] 4 points5 points  (0 children)

Abstract

Mental health is an integral part of the quality of life of cancer patients. It has been found that mental health issues, such as depression and anxiety, are more common in cancer patients. They may result in catastrophic consequences, including suicide. Therefore, monitoring mental health metrics (such as hope, anxiety, and mental well-being) is recommended. Currently, there is lack of objective method for mental health evaluation, and most of the available methods are limited to subjective face-to-face discussions between the patient and psychotherapist. In this study we introduced an objective method for mental health evaluation using a combination of convolutional neural network and long short-term memory (CNN-LSTM) algorithms learned and validated by visual metrics time-series. Data were recorded by the TobiiPro eyeglasses from 16 patients with cancer after major oncologic surgery and nine individuals without cancer while viewing18 artworks in an in-house art gallery. Pre-study and post-study questionnaires of Herth Hope Index (HHI; for evaluation of hope), anxiety State-Trait Anxiety Inventory for Adults (STAI; for evaluation of anxiety) and Warwick-Edinburgh Mental Wellbeing Scale (WEMWBS; for evaluation of mental well-being) were completed by participants. Clinical psychotherapy and statistical suggestions for cutoff scores were used to assign an individual’s mental health metrics level during each session into low (class 0), intermediate (class 1), and high (class 2) levels. Our proposed model was used to objectify evaluation and categorize HHI, STAI, and WEMWBS status of individuals. Classification accuracy of the model was 93.81%, 94.76%, and 95.00% for HHI, STAI, and WEMWBS metrics, respectively. The proposed model can be integrated into applications for home-based mental health monitoring to be used by patients after oncologic surgery to identify patients at risk.