The Gary Null Show - 09.07.20

Curcumin suppresses aldosterone-induced CRP generation in 

Hebei University of Chinese Medicine (China), September 2, 2020

 

According to news reporting from Shijiazhuang, People’s Republic of China, research stated, “Aldosterone regulates the initiation and development of atherosclerosis which is identified as a chronic inflammatory disease by promoting the generation of C-reactive protein in vascular smooth muscle cells.”

Our news correspondents obtained a quote from the research from Hebei University of Chinese Medicine: “Curcumin is the most active ingredient of turmeric with anti-inflammation and antioxidation effects. Here, the effect of curcumin on aldosterone-induced C-reactive protein generation in vascular smooth muscle and the molecular mechanisms involved were explored. Primary rat vascular smooth muscle cells and hyperaldosteronism model rats were used in this study. The amount of C-reactive protein, reactive oxygen species, and the signaling pathway-related molecules generated were estimated. We found that curcumin inhibited aldosterone-induced C-reactive protein generation in vascular smooth muscle cells by interfering with the reactive oxygen species-ERK1/2 signal pathway.”

According to the news reporters, the research concluded: “The results provide new evidence for the potential anti-inflammatory and cardiovascular protective effects of curcumin.”

 

 

Meta-analysis finds DHA and EPA have similar anti-inflammatory effects

Laval University (Quebec), August 26, 2020

 

According to news originating from Quebec City, Canada, research stated, “Recent data from randomized clinical trials (RCTs) suggest that DHA may have stronger anti-inflammatory effects than EPA. This body of evidence has not yet been quantitatively reviewed.”

Our news journalists obtained a quote from the research from Laval University, “The aim of this study was to compare the effect of DHA and EPA on several markers of systemic inflammation by pairwise and network meta-analyses of RCTs. MEDLINE, EMBASE, and The Cochrane Library were searched through to September 2019. We included RCTs of 7 d on adults regardless of health status that directly compared the effects of DHA with EPA and RCTs of indirect comparisons, in which the effects of DHA or EPA were compared individually to a control fatty acid. Differences in circulating concentrations of C-reactive protein (CRP), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-a) and adiponectin were the primary outcome measures. Data were pooled by pairwise and network meta-analysis and expressed as mean differences (MDs) with 95% CIs. Heterogeneity was assessed (Cochran Q statistic) and quantified (I2 statistic) in the pairwise meta-analysis. Inconsistency and transitivity were evaluated in the network meta-analysis. The certainty of evidence was assessed using the GRADE (Grading of Recommendations Assessment, Development, and Evaluation) approach. Eligibility criteria were met by 5 RCTs (N=411) for the pairwise meta-analysis and 20 RCTs (N=1231) for the network meta-analysis. In the pairwise meta-analysis, DHA and EPA had similar effects on plasma CRP [MDDHA versus EPA=0.14 mg/L (95% CI: -0.57, 0.85); I2=61%], IL-6 [MDDHA versus EPA=0.10 pg/mL (-0.15, 0.34); I2=40%], and TNF-a [MDDHA versus EPA=-0.10 pg/mL (-0.37, 0.18); I2=40%]. In the network meta-analysis, the effects of DHA and EPA on plasma CRP [MDDHA versus EPA=-0.33 mg/L (-0.75, 0.10)], IL-6 [MDDHA versus EPA=0.09 pg/mL (-0.12, 0.30)], and TNF-a [MDDHA versus EPA=-0.02 pg/mL (-0.25, 0.20)] were also similar. DHA and EPA had similar effects on plasma adiponectin in the network meta-analysis.”

According to the news editors, the research concluded: “Results from pairwise and network meta-analyses suggest that supplementation with either DHA or EPA does not differentially modify systemic markers of subclinical inflammation.”

 

 

 

Common cold combats influenza

Yale University, September 4, 2020

 

As the flu season approaches, a strained public health system may have a surprising ally—the common cold virus.

Rhinovirus, the most frequent cause of common colds, can prevent the flu virus from infecting airways by jumpstarting the body's antiviral defenses, Yale researchers report Sept. 4 in the journal The Lancet Microbe.

The findings help answer a mystery surrounding the 2009 H1N1 swine flu pandemic: An expected surge in swine flu cases never materialized in Europe during the fall, a period when the common cold becomes widespread.

A Yale team led by Dr. Ellen Foxman studied three years of clinical data from more than 13,000 patients seen at Yale New Haven Hospital with symptoms of respiratory infection. The researchers found that even during months when both viruses were active, if the common cold virus was present, the flu virus was not.

"When we looked at the data, it became clear that very few people had both viruses at the same time," said Foxman, assistant professor of laboratory medicine and immunobiology and senior author of the study.

Foxman stressed that scientists do not know whether the annual seasonal spread of the common cold virus will have a similar impact on infection rates of those exposed to the coronavirus that causes COVID-19.

"It is impossible to predict how two viruses will interact without doing the research," she said.

To test how the rhinovirus and the influenza virus interact, Foxman's lab created human airway tissue from stem cells that give rise to epithelial cells, which line the airways of the lung and are a chief target of respiratory viruses. They found that after the tissue had been exposed to rhinovirus, the influenza virus was unable to infect the tissue.

"The antiviral defenses were already turned on before the flu virus arrived," she said.

The presence of rhinovirus triggered production of the antiviral agent interferon, which is part of the early immune system response to invasion of pathogens, Foxman said.

"The effect lasted for at least five days," she said.

Foxman said her lab has begun to study whether introduction of the cold virus before infection by the COVID-19 virus offers a similar type of protection.

 

 

Highly fluorinated chemicals can increase risk for diabetes and coeliac disease in children

Orebro University (Sweden),  September 4, 2020

 

Tuulia Hyötyläinen and Matej Orešič, both researchers in biomedicine, have published two studies on the connection between highly fluorinated chemicals—per- and polyfluoroalkyl substances (PFASs) – and two diseases in children: type 1 diabetes and coeliac disease (US spelling celiac, or gluten intolerance). Both are autoimmune diseases, which arise from an abnormal immune response to the body's healthy cells or tissues.

The studies are based on a combination of comprehensive metabolomics (analysis of small molecules, i.e. metabolites, in a body), analysis of PFAS, and the system's biology approach to integrate complex data acquired in the study. The data comes from a group of expectant mothers and children.

Type 1 diabetes is one of the most common chronic diseases among children and younger people in the Nordic countries. Over the past decades, the number of cases has markedly increased. However, the incidence curve has flattened in recent years.

Some children are genetically predisposed for type 1 diabetes, but only a fraction of them, around one-tenth, develop the disease. It is clear that some environmental trigger is needed to initiate the progression to this autoimmune disease. For example, viral infections and diet are suspected to have an influence.

Tuulia Hyötyläinen and Matej Orešič show in this study, published in Environment International, how PFAS impacts lipid metabolism and risk of type 1 diabetes in new-born children. The study includes expectant mothers exposed to these harmful substances at various levels, which are then transferred from the expectant mother to the fetus.

Within the same study, these findings were further confirmed in another prospective clinical study involving children at-risk for type1 diabetes, as well as in two studies in mice (experimental models of type 1 diabetes).

"We show that children exposed to the high levels of PFAS during the prenatal stage have a certain lipid profile. We have previously identified this profile to be associated with an increased risk for type 1 diabetes and the development of the disease in children," explains Matej Orešič.

In another study published in Environment Research, Tuulia Hyötyläinen and Matej Orešič show a connection between PFAS and coeliac disease.

"These results show that high exposure to PFAS in the womb and in first years of life can accelerate the development of coeliac disease in children," says Tuulia Hyötyläinen.

PFAS consists of some 5,000 man-made chemical substances in extensive use in society. They are used in a wide range of products, such as coatings in clothing, furniture, adhesives and food packaging as well as in fire-fighting foam.

"Exposure to harmful chemicals in early life, including prenatally, may offer an explanation for the changing incidence of these autoimmune diseases in developed countries and can be connected to other health risks," says Matej Orešič.

The increase of type 1 diabetes has flattened in many industrial countries, especially in the Nordic countries. A possible explanation is the stricter PFAS regulation.

 

T cells need methionine 

University of Michigan School of Medicine, September 2 2020. 

 

Research reported on September 2, 2020 in Nature revealed a mechanism used by cancer cells to evade the immune system.

“Abnormal epigenetic patterns correlate with effector T cell malfunction in tumors, but the cause of this link is unknown,” Yingjie Bian of the University of Michigan School of Medicine and colleagues wrote. “Here we show that tumor cells disrupt methionine metabolism in CD8+ T cells, thereby lowering intracellular levels of methionine and the methyl donor S-adenosylmethionine (SAM) and resulting in loss of dimethylation.”

Dr Bian and colleagues sought to determine why immune cells known as T cells stop combatting tumors and other related questions. They found that low methionine levels were associated with T cell impairment. 

Other research has investigated the effects of starving tumor cells of methionine. However, this also starves T cells of the amino acid, thereby diminishing their function. "You have competition between tumor cells and T cells for methionine,” explained senior author Weiping Zou, MD, PhD, who is a Professor of Surgery, Pathology, Immunology and Biology at the University of Michigan in Ann Arbor. “The T cells also need it. If you starve the tumor cells of methionine, the T cells don't get it either. You want to selectively delete the methionine for the tumor cells and not for the T cells."

Supplementing with methionine restored T cell immunity in tumor-bearing mice and colon cancer patients. "There are still a lot of mechanistic details we have not worked out, particularly the detailed metabolic pathways of methionine metabolism,” Dr Zou remarked. “We also need to understand how metabolism pathways may be different from tumor cells and T cells. We hope to find a target that is relatively specific to tumor cells so that we do not harm the T cells but impact the tumor."

 

 

 

Green tea could hold the key to reducing antibiotic resistance

University of Surrey (UK), September23, 2020

 

Scientists at the University of Surrey have discovered that a natural antioxidant commonly found in green tea can help eliminate antibiotic resistant bacteria.

The study, published in the Journal of Medical Microbiology, found that epigallocatechin (EGCG) can restore the activity of aztreonam, an antibiotic commonly used to treat infections caused by the bacterial pathogen Pseudomonas aeruginosa.

P. aeruginosa is associated with serious respiratory tract and bloodstream infections and in recent years has become resistant to many major classes of antibiotics. Currently a combination of antibiotics is used to fight P. aeruginosa.

However, these infections are becoming increasingly difficult to treat, as resistance to last line antibiotics is being observed.

To assess the synergy of EGCG and aztreonam, researchers conducted in vitro tests to analyse how they interacted with the P. aeruginosa, individually and in combination. The Surrey team found that the combination of aztreonam and EGCG was significantly more effective at reducing P. aeruginosa numbers than either agent alone.

This synergistic activity was also confirmed in vivo using Galleria mellonella (Greater Wax Moth larvae), with survival rates being significantly higher in those treated with the combination than those treated with EGCG or aztreonam alone. Furthermore, minimal to no toxicity was observed in human skin cells and in Galleria mellonella larvae.

Researchers believe that in P. aeruginosa, EGCG may facilitate increased uptake of aztreonam by increasing permeability in the bacteria. Another potential mechanism is EGCG's interference with a biochemical pathway linked to antibiotic susceptibility.

Lead author Dr Jonathan Betts, Senior Research Fellow in the School of Veterinary Medicine at the University of Surrey, said:

"Antimicrobial resistance (AMR) is a serious threat to global public health. Without effective antibiotics, the success of medical treatments will be compromised. We urgently need to develop novel antibiotics in the fight against AMR. Natural products such as EGCG, used in combination with currently licenced antibiotics, may be a way of improving their effectiveness and clinically useful lifespan."

Professor Roberto La Ragione, Head of the Department of Pathology and Infectious Diseases in the School of Veterinary Medicine at the University of Surrey, said:

"The World Health Organisation has listed antibiotic resistant Pseudomonas aeruginosa as a critical threat to human health. We have shown that we can successfully eliminate such threats with the use of natural products, in combination with antibiotics already in use. Further development of these alternatives to antibiotics may allow them to be used in clinical settings in the future."

 

 

Research discovers links among poor sleep, high blood pressure, gut microbiome

University of Illinois, September 3, 2020

 

In the first study of its kind, University of Illinois Chicago researchers have found associations among disrupted sleep, elevated blood pressure and changes in the gut microbiome. 

The research aimed to determine whether a 28-day period of disrupted sleep changed the microbiota in rats. The gut microbiota refers to the collection of microorganisms living in the intestines. The researchers also sought to identify biological features associated with undesirable arterial blood pressure changes. 

The results were published in Physiological Genomics. 

Using rats, the researcher disrupted their sleep periods. Rats are nocturnal, so the experiments were designed to interfere with their daytime sleep periods. 

Telemetry transmitters measured the rats' brain activity, blood pressure and heart rate. Fecal matter also was analyzed to examine changes in the microbial content. 

The research idea was generated by several of the paper's authors who are or have been health care providers with night-shift schedules. 

"When rats had an abnormal sleep schedule, an increase in blood pressure developed -- the blood pressure remained elevated even when they could return to normal sleep. This suggests that dysfunctional sleep impairs the body for a sustained period," Maki said. 

Undesirable changes also were found in the gut microbiome -- the genetic material of all bacteria living in the colon. 

Contrary to her initial hypothesis, Maki found that the gut microbiome changes did not happen immediately, but instead took a week to show unfavorable responses such as an imbalance among different types of bacteria including an increase in microbes associated with inflammation. 

"When the sleep disruption stopped, everything did not come back to normal immediately," Maki said. "This research shows a very complex system with the presence of multiple pathological factors." 

This was initial research, and studies will continue to examine pathways involving the gut microbiome and metabolites produced by gut bacteria. The researchers will see exactly how sleep characteristics are changed and how long blood pressure and gut microbiome alterations persist. Researchers will then determine how this information translates to humans. 

"We hope to find an intervention that can help people who are at risk for cardiovascular disease because of their work and sleep schedules. People will always have responsibilities that interrupt their sleep. We want to be able to reduce their risk by targeting the microbiome with new therapies or dietary changes," Fink said.