Medicine Medical Science Thread

Remove this Banner Ad

Snake_Baker

Snake_Baker

The one true King of the North
30k Posts 10k Posts HBF's Milk Crate - 70k Posts TheBrownDog Podcaster Bay 13: Flog of the Year BeanCoiNFT Investor
Apr 24, 2013
81,024
153,169
Arden Street Hill
AFL Club
North Melbourne
Other Teams
Essendon Lawn Bowls Club
Brazilian Wasp Venom Kills Cancer Cells Without Harming Normal Cells


A newly published study shows how Brazilian wasp venom selectively kills cancer cells without harming normal cells.

The social wasp Polybia paulista protects itself against predators by producing venom known to contain a powerful cancer-fighting ingredient. A Biophysical Journal study published September 1 reveals exactly how the venom’s toxin–called MP1 (Polybia-MP1)–selectively kills cancer cells without harming normal cells. MP1 interacts with lipids that are abnormally distributed on the surface of cancer cells, creating gaping holes that allow molecules crucial for cell function to leak out.

“Cancer therapies that attack the lipid composition of the cell membrane would be an entirely new class of anticancer drugs,” says co-senior study author Paul Beales, of the University of Leeds in the UK. “This could be useful in developing new combination therapies, where multiple drugs are used simultaneously to treat a cancer by attacking different parts of the cancer cells at the same time.”

MP1 acts against microbial pathogens by disrupting the bacterial cell membrane. Serendipitously, the antimicrobial peptide shows promise for protecting humans from cancer; it can inhibit the growth of prostate and bladder cancer cells, as well as multi-drug resistant leukemic cells. However, until now, it was not clear how MP1 selectively destroys cancer cells without harming normal cells.

Beales and co-senior study author João Ruggiero Neto of São Paulo State University in Brazil suspected that the reason might have something to do with the unique properties of cancer cell membranes. In healthy cell membranes, phospholipids called phosphatidylserine (PS) and phosphatidylethanolamine (PE) are located in the inner membrane leaflet facing the inside of the cell. But in cancer cells, PS and PE are embedded in the outer membrane leaflet facing the cell surroundings.

The researchers tested their theory by creating model membranes, some of which contained PE and/or PS, and exposing them to MP1. They used a wide range of imaging and biophysical techniques to characterize MP1’s destructive effects on the membranes. Strikingly, the presence of PS increased the binding of MP1 to the membrane by a factor of 7 to 8. On the other hand, the presence of PE enhanced MP1’s ability to quickly disrupt the membrane, increasing the size of holes by a factor of 20 to 30.

“Formed in only seconds, these large pores are big enough to allow critical molecules such as RNA and proteins to easily escape cells,” Neto says. “The dramatic enhancement of the permeabilization induced by the peptide in the presence of PE and the dimensions of the pores in these membranes was surprising.”

In future studies, the researchers plan to alter MP1’s amino acid sequence to examine how the peptide’s structure relates to its function and further improve the peptide’s selectivity and potency for clinical purposes. “Understanding the mechanism of action of this peptide will help in translational studies to further assess the potential for this peptide to be used in medicine,” Beales says. “As it has been shown to be selective to cancer cells and non-toxic to normal cells in the lab, this peptide has the potential to be safe, but further work would be required to prove that.”

Publication: PE and PS Lipids Synergistically Enhance Membrane Poration by a Peptide with Anticancer Properties,” Biophysical Journal, Volume 109, Issue 5, p936–947, 1 September 2015; doi:10.1016/j.bpj.2015.07.033

https://scitechdaily.com/brazilian-wasp-venom-kills-cancer-cells-without-harming-normal-cells/
 
Rarely do we need medicine to attack cancer growths

All we need do is support the immune system. It does a better and healthier job

Cbt treatment has been shown time and time again to restore connection with the rogue cells

Allowing the immune system to do it's job an establish total control.

A healthy diet of real food feeds the immune system the fuel it needs.

It's simple s**t



 
Thegibbsgamble said:
Rarely do we need medicine to attack cancer growths

All we need do is support the immune system. It does a better and healthier job

Cbt treatment has been shown time and time again to restore connection with the rogue cells

Allowing the immune system to do it's job an establish total control.

A healthy diet of real food feeds the immune system the fuel it needs.

It's simple s**t
Click to expand...

CBT? Cognitive Behavioural Therapy, utensil and Ball Torture or something else?

Back on track, it's not simple s**t. Cancer cells are very clever at either disguising themselves or switching off the normal immune systems ability to destroy them. For example Melanoma uses the PD-1 pathway to hide from T cells. This stops T cells from attacking Melanoma and allowing Melanoma to grow and spread. Pembrolizumab (Keytruda) stops this and results in about a 50% remission rate in metastatic melanoma. This is an incredible improvement and thanks to it we have Roughie playing again. As the basic biology of each cancer is understood more specific and effective therapies will become available.

No matter how much you feed/boost the immune system, if it can't see the tumour cells then it ain't going to attack them.

As for CBT for cancer therapy I can't see either form resulting in a reliable cure.
 

Log in to remove this ad.

  • Thread starter
  • Banned
  • #4
Thegibbsgamble said:
Rarely do we need medicine to attack cancer growths

All we need do is support the immune system. It does a better and healthier job

Cbt treatment has been shown time and time again to restore connection with the rogue cells

Allowing the immune system to do it's job an establish total control.

A healthy diet of real food feeds the immune system the fuel it needs.

It's simple s**t
Click to expand...

Not sure if this is a pisstake.
 
  • Thread starter
  • Banned
  • #7
Molecule that acts on human cells might provide hope for 'irresistible' cold cure

Date: May 14, 2018
Source: Imperial College London

Researchers have lab-tested a molecule that can combat the common cold virus by preventing it from hijacking human cells.

Early lab-based tests with human cells have shown the molecule's ability to completely block multiple strains of cold virus, and the team hope to move to animal and then human trials. The results of initial tests are published today in the journal Nature Chemistry.

The common cold is caused by a family of viruses with hundreds of variants, making it nearly impossible to become immune to or vaccinate against all of them. On top of that, the viruses evolve rapidly, meaning they can quickly gain resistance to drugs.

For these reasons, most cold remedies rely on treating the symptoms of the infection -- such as runny nose, sore throat and fever -- rather than tackling the virus itself.

However a new molecule, developed by researchers at Imperial College London, targets N-myristoyltransferase (NMT), a protein in human cells. Viruses 'hijack' NMT from human cells to construct the protein 'shell', or capsid, which protects the virus genome.

All strains of the virus need this same human protein to make new copies of themselves, so the molecule should work against all of them. Additionally, the molecule also works against viruses related to the cold virus, such as polio and foot and mouth disease viruses.

The molecule targets a human protein and not the virus itself, making emergence of resistant viruses highly unlikely.

Lead researcher Professor Ed Tate, from the Department of Chemistry at Imperial, said: "The common cold is an inconvenience for most of us, but can cause serious complications in people with conditions like asthma and COPD. A drug like this could be extremely beneficial if given early in infection, and we are working on making a version that could be inhaled, so that it gets to the lungs quickly."

There have been previous attempts to create drugs that target human cells rather than the viruses, but many have the side effect of being toxic. The researchers showed that the new molecule completely blocked several strains of the virus without affecting human cells. Further study is needed to make sure it is not toxic in the body.

The research team included the labs of Professor Roberto Solari and Professor Seb Johnston at Imperial's National Heart & Lung Institute, Dr Aurelie Mousnier from Imperial and Queen's University Belfast, structural biologists at the University of York, and colleagues at the Pirbright Institute.

Professor Tate said: "The way the drug works means that we would need to be sure it was being used against the cold virus, and not similar conditions with different causes, to minimise the chance of toxic side effects."

The medicinal chemistry team in the Tate group at Imperial, led by Dr Andy Bell (who previously invented Viagra as a researcher at Pfizer), were originally looking for compounds that targeted the protein in malaria parasites. Screening large libraries of compounds, they found two hits and were surprised to discover that they worked best together.

By inventing a novel way to combine the two, they created a molecule, codenamed IMP-1088, which is more than a hundred times more potent than previous molecules targeting the protein in humans.
 
Scientists successfully transplant lab-grown lungs into pigs

For the first time, researchers have created lungs in the lab and successfully transplanted them into pigs.

These bioengineered lungs, described online August 1 in Science Translational Medicine, developed healthy blood vessels that allowed pigs to live for several weeks after surgery without medical complications. That’s a significant improvement from previous efforts: Lab-grown lungs implanted in rodents failed within hours, before the lungs could develop the complex blood vessel network necessary for long-term survival.

If the new procedure can be adapted for humans, with bioengineered lungs grown from a patient’s own cells, that could reduce the risk of organ rejection and slash wait times for organ transplants. In the United States, where about 1,500 people currently are on a waiting list for a lung transplant, the average wait is a few months.

“This study really brings the whole research field to the next level,” says Xi “Charlie” Ren, a biomedical engineer at Carnegie Mellon University in Pittsburgh not involved in the work.

For the study, immunologist Joan Nichols at the University of Texas Medical Branch at Galveston and colleagues built lungs for four pigs by first using a sugar and detergent mixture to strip the cells from lungs of donor pigs. That left sterilized, pearly white, lung-shaped scaffolds made of the intercellular proteins. (In humans, researchers envision using donated organs or 3-D printing made-to-fit lung scaffolding.) The researchers then repopulated each scaffold with blood vessel and lung tissue cells from the pig destined to receive that organ.

Each engineered lung grew for 30 days inside a bioreactor tank, pumped full of nutrient cocktails that helped cells stick to the scaffold and multiply in the right spots. The researchers then replaced the left lung of each pig with the bioengineered version.

After surgery, Nichols’ team allowed one pig to survive for 10 hours, another for two weeks, a third for a month and the fourth for two months. At each pig’s demise, the researchers did an autopsy on the animal to see how the new lungs integrated into the pigs’ bodies over time. None of the animals was given immunosuppressant drugs, and none of the transplants was rejected. Inside a pig’s body, the bioengineered lung’s blood vessels plugged into to the animal’s natural circulatory system, supplying the organ with oxygen and nutrients to survive.

The animals’ post-op recovery was “pretty amazing,” Ren says. The pig that lived two months after surgery didn’t experience any breathing problems, and its lung transplant was colonized by bacteria that inhabit normal pig lungs — signs that the tissue was developing normally and integrating well into the body.

Read more: https://www.sciencenews.org/article/scientists-transplant-lab-grown-bioengineered-lungs-pigs


 
High fat intake: longer life, no greater risk of cardiovascular disease.
High carb intake: shorter life, increased risk of cardiovascular disease.

Associations of fats and carbohydrate intake with cardiovascular disease and mortality in 18 countries from five continents (PURE): a prospective cohort study

Link: https://t.co/j2kfEHyU7T
 
Some more "big data". Keep playing sports people.

Association between physical exercise and mental health in 1·2 million individuals in the USA between 2011 and 2015: a cross-sectional study
Published:August 08, 2018DOI:https://doi.org/10.1016/S2215-0366(18)30227-X

Summary

Background

Exercise is known to be associated with reduced risk of all-cause mortality, cardiovascular disease, stroke, and diabetes, but its association with mental health remains unclear. We aimed to examine the association between exercise and mental health burden in a large sample, and to better understand the influence of exercise type, frequency, duration, and intensity.

Methods

In this cross-sectional study, we analysed data from 1 237 194 people aged 18 years or older in the USA from the 2011, 2013, and 2015 Centers for Disease Control and Prevention Behavioral Risk Factors Surveillance System survey. We compared the number of days of bad self-reported mental health between individuals who exercised and those who did not, using an exact non-parametric matching procedure to balance the two groups in terms of age, race, gender, marital status, income, education level, body-mass index category, self-reported physical health, and previous diagnosis of depression. We examined the effects of exercise type, duration, frequency, and intensity using regression methods adjusted for potential confounders, and did multiple sensitivity analyses.

Findings

Individuals who exercised had 1·49 (43·2%) fewer days of poor mental health in the past month than individuals who did not exercise but were otherwise matched for several physical and sociodemographic characteristics ( W=7·42 × 10 10, p<2·2 × 10 −16). All exercise types were associated with a lower mental health burden (minimum reduction of 11·8% and maximum reduction of 22·3%) than not exercising (p<2·2 × 10 −16 for all exercise types). The largest associations were seen for popular team sports (22·3% lower), cycling (21·6% lower), and aerobic and gym activities (20·1% lower), as well as durations of 45 min and frequencies of three to five times per week.

Interpretation

In a large US sample, physical exercise was significantly and meaningfully associated with self-reported mental health burden in the past month. More exercise was not always better. Differences as a function of exercise were large relative to other demographic variables such as education and income. Specific types, durations, and frequencies of exercise might be more effective clinical targets than others for reducing mental health burden, and merit interventional study.
 

(Log in to remove this ad.)

Possible breakthrough: AIDS cure hope emerges following stem cell procedure with HIV patient

A HIV-positive man in Britain has become the second known adult to be cleared of the AIDS virus after he received a bone marrow transplant from a HIV-resistant donor, his doctors say. Almost three years after receiving stem cells from a donor with a rare genetic mutation that resists HIV infection — and more than 18 months after coming off antiretroviral drugs — highly sensitive tests show no trace of the man's previous HIV infection.
Click to expand...
 
Over the last decade or so stem cells have thus far not lived up to there hype with neurological injury such as strokes or cord injury for a number of reasons (difficult to identify cell lines, unknown maturation factors and not turning into the cell you want, etc)

This article describes a non stem cell way of regenerating neurons from glia (supporting cells) in the brain. https://www.news-medical.net/news/2...elps-stroke-patients-develop-new-neurons.aspx

The researchers used a gene encoding neural transcription factor NeuroD1 that turns mouse glia into mouse neurons, with functional nervous activity. So far tested in rats and mice with strokes. The same team has shown the same effect in animal models of dementia. This could be really big if these results can be replicated in humans and leads to functional benefit. To me it's more elegant than using stem cells and is the first time I have seen a proposed therapy for completed strokes that I believe could actually work.

Chucking a bunch of stem cells into a damaged brain always seemed like putting random code in a malfunctioning computer and hoping it fixes it.
 
I've heard of this concept for staving off death a while back, and it might be coming close to being a reality :thumbsu:

www.theguardian.com

Humans put into suspended animation for first time

Groundbreaking trial in US rapidly cools trauma victims with catastrophic injury to buy more time for surgery
www.theguardian.com www.theguardian.com
 
Does anyone have a link to the study showing woman with a history of more than 2 former male partners have 250% chance of passing across an std if oral sex is performed?

It was a relatively recent study or within this decade.
 
Danger2Jenkins said:
Does anyone have a link to the study showing woman with a history of more than 2 former male partners have 250% chance of passing across an std if oral sex is performed?

It was a relatively recent study or within this decade.
Click to expand...
No, but I got 'crabs' from Sandra Wiley in 1976.
 
Collections of misfolded Tau proteins in neurons have been recognised in dementia, including that associated with chronic traumatic encephalopathy (CTE)
In tau-associated forms of dementia disease progression correlates with the spread of tau deposits throughout the brain. This is thought to occur because of misfolded, disease-associated (pathological) tau entering healthy neurons. Pathological tau interacts with normal (physiological) tau already present in the neuron and acts as a template for the misfolding of the normal protein, thus propagating tau pathology across neurons. This is prion behaviour. To what degree tau proteins are causative is yet to be determined, however more evidence accumulates to suggest these re one of the keys.

Because of their apparent role in dementia there is great interest in working out the mechanisms that allow pathogenic tau to exit one neuron and enter the next. This paper from Nature https://www.nature.com/articles/d41586-020-00874-z shows that tau uses a lipoprotein receptor, LRP1, to enter neurons and furthermore the loss of LRP stops tau entering into neurons.

I had to look up some papers about CTE and tau proteins This paragraph is lifted from this paper https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4526170/ It is a reasonably concise description of the relationship of head trauma and tau proteins.

Although all cases of neuropathologically verified CTE have been associated with repetitive mild brain trauma, the pathophysiological mechanisms critical to developing a latent and progressive neurodegeneration and tauopathy after repetitive mTBI, including concussion and subconcussion, are only beginning to be identified. When the semisolid brain, suspended in cerebrospinal fluid (CSF) inside a boney skull, is subjected to the rapid acceleration, deceleration and rotational forces associated with impact injury, the brain elongates and deforms, stretching the microstructural elements, including neurons, glial cells and blood vessels. These stretch forces predominantly affect long fibers, specifically axons and blood vessels (54, 61) and are most severe where the direction of axons changes or where a change in tissue-density occurs (e.g. around blood vessels or at the gray-white matter interface) (16, 26, 80). Experimental studies of acceleration-deceleration injuries in gyrencephalic animals further demonstrate that axonal injury and vascular disruption is most severe at focal stress points of the brain—particularly the perivascular region and the depths of the cerebral sulci (17, 87). Moreover, the early and predominant involvement of the superior and dorsolateral frontal lobes in CTE affecting former football players parallels the high frequency of impacts to the top of the head compared with those to the front, back and side of the head (35, 62). Functional MRI data in football players also shows activation impairments in dorsolateral prefrontal cortex that is associated with significantly higher numbers of head collisions to the top-front of the head (94).

Pathological studies of concussion and post-concussion syndrome in human subjects have found that multifocal traumatic axonal injury is often perivascular (6, 60, 77). Other changes found in acute and subacute concussion are microvascular injury and microhemorrhages (60, 77), astrocytosis, most severe in the cerebral white matter and brainstem white matter tracts, and clusters of activated microglia, most prominent in the white matter around small vessels (59, 77). Less common changes include focal clusters of p-tau in NFTs, pre-tangles and neurites or stage I CTE (60).

It is known from the experimental literature that acceleration-deceleration injury causes tau protein, normally associated with microtubules in axons, to become abnormally phosphorylated, misfolded, aggregated and cleaved, all of which generate neurotoxic tau peptide fragments (1, 12, 46, 47, 59, 101). Nevertheless, how this combination of factors: axonal injury, breach of blood–brain barrier, neuroinflammation and aggregation of abnormally truncated and hyperphosphorylated proteins, including p-tau and TDP-43, develop into a progressive deterioration remains to be determined.

There are most likely additional factors that play a role in the initiation of p-tau pathology in CTE, including genetic susceptibility or resistance, gender, physiological stress, additional environmental exposures and age at exposure. Studies have suggested that children and adolescents experience prolonged recovery rates after TBI compared with adults (24) as well as poorer outcomes (29). Animal models have shown that stress can lead to increased tau phosphorylation (72, 90). Environmental influences, such as alcohol, opiates or performance-enhancing drugs, could also play a role in tau aggregation, deposition and propagation. P-tau immunoreactivity in opiate user brains has been shown to be significantly higher than in controls (2). Glucocorticoids have also been associated with increased tau phosphorylation and greater cognitive deficits in rodent models (33, 89).
 
Last edited:
* The human mouth is the 2nd most dirty of any creature. The Komodo dragon being the worst.

There are studies now that say wearing a mask is like having a petri dish for bacterial growth that promotes bacterial pneumonia and can kill you.


Neurosurgeon Expresses Concerns Over Wearing Masks



The importance of these findings is that a drop in oxygen levels (hypoxia) is associated with an impairment in immunity. Studies have shown that hypoxia can inhibit the type of main immune cells used to fight viral infections called the CD4+ T-lymphocyte.

This occurs because the hypoxia increases the level of a compound called hypoxia inducible factor-1 (HIF-1), which inhibits T-lymphocytes and stimulates a powerful immune inhibitor cell called the Tregs. . This sets the stage for contracting any infection, including COVID-19 and making the consequences of that infection much graver. In essence, your mask may very well put you at an increased risk of infections and if so, having a much worse outcome.

There is another danger to wearing these masks on a daily basis, especially if worn for several hours. When a person is infected with a respiratory virus, they will expel some of the virus with each breath.

If they are wearing a mask, especially an N95 mask or other tightly fitting mask, they will be constantly rebreathing the viruses, raising the concentration of the virus in the lungs and the nasal passages. We know that people who have the worst reactions to the coronavirus have the highest concentrations of the virus early on. And this leads to the deadly cytokine storm in a selected number.

People with cancer, especially if the cancer has spread, will be at a further risk from prolonged hypoxia as the cancer grows best in a microenvironment that is low in oxygen. Low oxygen also promotes inflammation which can promote the growth, invasion and spread of cancers. Repeated episodes of hypoxia has been proposed as a significant factor in atherosclerosis and hence increases all cardiovascular (heart attacks) and cerebrovascular (strokes) diseases.

It gets even more frightening. Newer evidence suggests that in some cases the virus can enter the brain. In most instances it enters the brain by way of the olfactory nerves (smell nerves), which connect directly with the area of the brain dealing with recent memory and memory consolidation. By wearing a mask, the exhaled viruses will not be able to escape and will concentrate in the nasal passages, enter the olfactory nerves and travel into the brain.

pjmedia.com

Neurosurgeon Expresses Concerns Over Wearing Masks [Correction]

pjmedia.com pjmedia.com

Article also disputes Neurosurgeons opinion.
 
Covertackle said:
* The human mouth is the 2nd most dirty of any creature. The Komodo dragon being the worst.


Neurosurgeon Expresses Concerns Over Wearing Masks

There are studies now that say wearing a mask is like having a petri dish for bacterial growth that promotes bacterial pneumonia and can kill you.

The importance of these findings is that a drop in oxygen levels (hypoxia) is associated with an impairment in immunity. Studies have shown that hypoxia can inhibit the type of main immune cells used to fight viral infections called the CD4+ T-lymphocyte.

This occurs because the hypoxia increases the level of a compound called hypoxia inducible factor-1 (HIF-1), which inhibits T-lymphocytes and stimulates a powerful immune inhibitor cell called the Tregs. . This sets the stage for contracting any infection, including COVID-19 and making the consequences of that infection much graver. In essence, your mask may very well put you at an increased risk of infections and if so, having a much worse outcome.

There is another danger to wearing these masks on a daily basis, especially if worn for several hours. When a person is infected with a respiratory virus, they will expel some of the virus with each breath.

If they are wearing a mask, especially an N95 mask or other tightly fitting mask, they will be constantly rebreathing the viruses, raising the concentration of the virus in the lungs and the nasal passages. We know that people who have the worst reactions to the coronavirus have the highest concentrations of the virus early on. And this leads to the deadly cytokine storm in a selected number.

People with cancer, especially if the cancer has spread, will be at a further risk from prolonged hypoxia as the cancer grows best in a microenvironment that is low in oxygen. Low oxygen also promotes inflammation which can promote the growth, invasion and spread of cancers. Repeated episodes of hypoxia has been proposed as a significant factor in atherosclerosis and hence increases all cardiovascular (heart attacks) and cerebrovascular (strokes) diseases.

It gets even more frightening. Newer evidence suggests that in some cases the virus can enter the brain. In most instances it enters the brain by way of the olfactory nerves (smell nerves), which connect directly with the area of the brain dealing with recent memory and memory consolidation. By wearing a mask, the exhaled viruses will not be able to escape and will concentrate in the nasal passages, enter the olfactory nerves and travel into the brain.

pjmedia.com

Neurosurgeon Expresses Concerns Over Wearing Masks [Correction]

pjmedia.com pjmedia.com

Article also disputes Neurosurgeons opinion.
Click to expand...

They ARE a problem if someone contracts Sars-CoV-2 and continues to wear them as they recycle the viral load back in through the mouth.
 
You must log in or register to reply here.

Remove this Banner Ad

Back
Top