Fat in poop linked with early presence of colorectal cancer

October 27, 2016

colorectalOct 27: Paving the way for a fast, noninvasive method that could lead to the early diagnosis of colorectal cancer, researchers have identified a suite of molecules in faeces that signifies the presence of precancerous polyps. ‘The exciting part is being able to see differences in the stool,’ said one of the researchers Herbert Hill, Professor at Washington State University. ‘This could lead to a noninvasive, more comprehensive early-warning detection method for colorectal cancer, but a lot of research needs to be done before it can be actually realised,’ Hill noted. Colorectal cancer is the second most common cancer worldwide. Nearly 1.4 million new cases were diagnosed in 2012, according to the World Cancer Research Fund International. Though early detection is key to successful treatment, most screening tests are limited in diagnostic capability or ease of application. Colonoscopy, for example, is a known lifesaver but is costly and unappealing to many people who might otherwise undergo testing. More people would be willing to provide a stool sample than undergo a biopsy through a colonoscope, Michael Williams from Washington State University, noted.

In addition, colonoscopes can only extend a limited distance into the large intestine, potentially missing some polyps. ‘With our new test, it could be possible to diagnose cancer occurring throughout the entire colon,’ he said. The researchers discovered the molecular fingerprint for colon cancer using a technology called ion mobility-mass spectrometry. They first identified metabolic products from normal colon tissue in both humans and mice. The scientists then compared this normal profile to that found in cancerous colon tissues from humans and research mice with polyps in their colons that mimic those in humans. In both cases, the scientists found that colon cancer caused significant changes in fat metabolism, especially for lipids and fatty acids. These abnormalities created a molecular fingerprint that was similar in humans and mice, said Hill. Next, the researchers examined droppings from transgenic and control mice to see if the molecular fingerprint could be found in feces as well. Here is how vitamin D helps to fight colorectal cancer.

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Agencies
January 25,2020

Washington D.C., Jan 25: A new study conducted by a team of researchers reveals why individuals who have a history of early life adversity (ELA) are disproportionately prone to opioid addiction.

The study conducted examined how early adversities interact with factors such as increased access to opioids to directly influence brain development and function, causing a higher potential for opioid addiction.

The study was lead by UCI researchers and was published in Molecular Psychiatry.

Tallie Z. Baram, MD, PhD, the Danette Shepard Chair in Neurological Sciences at the UCI School of Medicine and one of the senior researchers for the study, was on the take that the widely known factor genetics that plays major role in addiction vulnerability, cannot be solely held responsible for the recent rise in opioid abuse.

To further clarify, the researchers simulated ELA in rats by limiting bedding and nesting materials during a short, postnatal period of time.

In female rats, this led to striking opioid addiction-like characteristics including an increased relapse- behaviour, for example.

As observed in addicted humans, the rats were willing to work very hard (pay a very high price) to obtain the drug.

Baram said: "Ultimately, we found that conditions during sensitive developmental periods can lead to vulnerability to the addictive effects of opioid drugs, especially in females, which is consistent with the prevalence of ELA in heroin-addicted women."

These findings can be used to highlight the importance given to sex differences in future ELA-related studies on opioid addiction, and in future prevention or intervention strategies being developed to address the growing opioid crisis.

The study conducted examined how early adversities interact with factors such as increased access to opioids to directly influence brain development and function, causing a higher potential for opioid addiction.

The study was lead by UCI researchers and was published in Molecular Psychiatry.

The study found that unpredictable, fragmented early life environments may lead to abnormal maturation of certain brain circuits, which profoundly impacts brain function and persists into adolescence and adulthood.

Tallie Z. Baram, MD, PhD, the Danette Shepard Chair in Neurological Sciences at the UCI School of Medicine and one of the senior researchers for the study, was on the take that the widely known factor genetics that plays major role in addiction vulnerability, cannot be solely held responsible for the recent rise in opioid abuse.

To further clarify, the researchers implanted ELA in rats by limiting bedding and nesting materials during a short, postnatal period of time.

In female rats, this led to striking opioid addiction-like characteristics including an increased relapse- behaviour, for example.

As observed in addicted humans, the rats were willing to work very hard (pay a very high price) to obtain the drug.

Baram said: "Ultimately, we found that conditions during sensitive developmental periods can lead to vulnerability to the addictive effects of opioid drugs, especially in females, which is consistent with the prevalence of ELA in heroin-addicted women."

These findings can be used to highlight the importance given to sex differences in future ELA-related studies on opioid addiction, and in future prevention or intervention strategies being developed to address the growing opioid crisis.

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Agencies
April 17,2020

Washington DC, Apr 17: In recent research, scientists have linked the emotional, social and psychiatric problems in children and adolescents with higher levels of genetic vulnerability for adult depression. The study implies that the genetics passed from parents may be linked with psychiatric problems in children and adolescents and may also leading to depression in adults.

University of Queensland scientists made the finding while analysing the genetic data of more than 42,000 children and adolescents from seven cohorts across Finland, the Netherlands, Norway, Sweden and the UK.

Professor Christel Middeldorp said that researchers have also found a link with a higher genetic vulnerability for insomnia, neuroticism and body mass index.

"By contrast, study participants with higher genetic scores for educational attainment and emotional well-being were found to have reduced childhood problems," Professor Middeldorp said.

"We calculated a person's level of genetic vulnerability by adding up the number of risk genes they had for a specific disorder or trait and then made adjustments based on the level of importance of each gene We found the relationship was mostly similar across ages," Middeldorp added.

The results indicate there are shared genetic factors that affect a range of psychiatric and related traits across a person's lifespan.

Middeldorp said that around 50 per cent of children and adolescents with psychiatric problems, such as attention deficit hyperactivity disorder (ADHD), continue to experience mental disorders as adults, and are at risk of disengaging with their school community among other social and emotional problems.

"Our findings are important as they suggest this continuity between childhood and adult traits is partly explained by genetic risk," the Professor said.

"Individuals at risk of being affected should be the focus of attention and targeted treatment," Middeldorp continued.

"Although the genetic vulnerability is not accurate enough at this stage to make individual predictions about how a person's symptoms will develop over time, it may become so in the future, in combination with other risk factors. And, this may support precision medicine by providing targeted treatments to children at the highest risk of persistent emotional and social problems," Middeldorp added.

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Agencies
June 17,2020

Leading physicians are celebrating a small dose of good news that arrived Tuesday about dexamethasone, a cheap and widely used steroid shown to be able to save lives among COVID-19 patients, but also cautioning against releasing study results by press release during a global health emergency, like in the case of the latest dexamethasone study by University of Oxford.

"It will be great news if dexamethasone, a cheap steroid, really does cut deaths by one-third in ventilated patients with COVID19, but after all the retractions and walk backs, it is unacceptable to tout study results by press release without releasing the paper", Atul Gawande, surgeon and CEO of Haven Healthcare, tweeted.

"Bottom line is, good news," Dr. Fauci, America's foremost infectious diseases expert told a US newswire on Tuesday, soon after the dexamethasone results were announced in the UK.

Fauci, who has long championed the therapeutics-first view said that dexamethasone is a "significant improvement" in the available therapeutic options currently available.

On Medical Twitter and Facebook, doctors broadly agree that dexamethasone use aligns well with the way COVID19 attacks the body's immune system. Fauci said the results in the Oxford study make "perfect sense" in that context.

"We should see the number of people who actually survive go up, if the study holds up," virologist and epidemiologist Dr. Joseph Fair told a television network.

Global coronavirus cases crossed 8 million on Tuesday. In the US, Texas and Florida are facing a new wave of cases after lifting lockdown orders earlier than medical experts recommended. Amidst the relentless graph upwards, the dexamethasone study results injected hope for better survival rates among those most seriously ill.

World Health Organization chief scientist Soumya Swaminathan welcomed the results from the randomised control trial.

Dr Eugene Gu, Founder and CEO of CoolQuit tweeted that he is "genuinely impressed" with the UK dexamethasone trial. This may be a "game changer", he wrote.

"There's no conflict of interest as dexamethasone is a generic steroid. The mechanism of action makes sense because steroids can reduce cytokine storms and overactive immune systems that makes COVID-19 so deadly. The number needed to treat is 8 ventilated patients which is great."

The Oxford study found that dexamethasone reduced deaths by 35 percent in patients who needed treatment with breathing machines and by 20 percent in those only needing supplemental oxygen. Dexamethasone was one of 5 drugs studied in a large clinical trial in the United Kingdom named RECOVERY, short for Randomised Evaluation of COVID-19 Therapy.

Peter Horby, chief investigator of the University of Oxford clinical trial, said dexamethasone is the first drug to be shown to improve survival in COVID-19. Details of the study have not been released. The trial organisers said they made their announcement via a news release because of "the public health importance of these results." According to Horby's public comments, there was a lot of initial resistance to studying steroids.

During the study, 2,104 patients were randomly selected to be given 6 milligrams of dexamethasone once a day (either by mouth or by intravenous injection) for 10 days. That group was compared with 4,321 patients who received the usual care alone.

Researchers estimated that dexamethasone would prevent one death for every eight patients treated while on ventilators and one for every 25 patients on extra oxygen alone.

UK experts have called the study results a breakthrough in the fight against the virus. The researchers have promised they would publish the results soon.

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