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Researchers from the Centenary Institute and the University of Sydney have developed a unique nasal vaccination approach that provides significant lung immunity and protection against the SARS-CoV-2 Covid virus.

The findings were reported in the prominent journal Nature Communications. The novel vaccination technique has been successfully tested in mice and has the potential to be a significant tool for improving protection against COVID-19 infection and limiting viral dissemination.

Lead author of the study, Dr Anneliese Ashhurst, research fellow in the University of Sydney’s Faculty of Medicine and Health and the Centenary Institute said that while current COVID-19 vaccines are critical, there were some limitations, including the waning of immunity post-vaccination and infection, combined with the impact of new viral variants evolving.

“Current vaccines against SARS-CoV-2 substantially reduce mortality and severe disease, but protection against infection is less effective. Vaccinated individuals are still catching COVID-19 and can spread the infection, so breakthrough infections are still occurring,” said Dr Ashhurst.

“To stop viral spread and to prevent this virus from mutating we need a new vaccine approach that blocks COVID-19 transmission,” she said.

In the mice study, the new vaccine was delivered nasally, making its way through the respiratory tract, adhering to the tissues of the nasal cavity, airways and lungs. Testing showed the generation of high levels of protective antibodies in the airways and increased T-cell responses in the lungs (T-cells help destroy SARS-CoV-2 infected cells).

Covid vaccine test

Significantly, none of the vaccinated mice became infected with COVID-19.

“Our vaccine differs from most current COVID-19 vaccines in that it enables generation of an immune response directly in those areas of the body that are likely to be the first point of contact for the virus – the nose, airway and lungs. This may help explain the vaccine’s effectiveness,” said Dr Ashhurst.

Senior study author, Professor Emeritus Warwick Britton AO, Head of the Centenary Institute’s Tuberculosis Research Program, said that the new vaccine strategy could play a key role in the fight against many diseases.

“Our vaccination findings have shown exciting potential in pre-clinical studies, improving protection against SARS-CoV-2 infection. The approach developed here could help break the COVID-19 infection cycle and will likely influence future coronavirus vaccine related studies,” Professor Britton said.

He added that adapted versions of the new nasal vaccine could also be potentially applied to other viral or bacterial respiratory diseases such as influenza, avian flu, SARS and MERS.

Also Read: Baby vaccination responses linked to birth delivery method: Research

According to a recent study, children with a severe type of epilepsy should take the flu vaccination due to the higher risk of seizures caused by an influenza infection. The risk of severe neurological symptoms and complications, such as worsening seizures, declining language and motor skills, and even death, led the Murdoch Children’s Research Institute and the University of Melbourne researchers to conclude that the safe administration of the seasonal influenza vaccine should be a priority in people with SCN1A-positive Dravet syndrome.

According to Murdoch Children’s paediatric neurologist Dr Katherine Howell, the decision for parents to vaccinate their children with this syndrome is complex since seizures can be caused by both illness and immunisation. Despite the fact that the condition has been connected to a high prevalence of extended seizures during infections, Dr. Howell claims that the consequences of influenza have yet to be studied.

The research, published in Neurology, included children with SCN1A-positive Dravet syndrome who had a confirmed flu infection at The Royal Children’s and Austin Hospitals. Researchers observed that 21 children were infected with the flu 24 times, with brain abnormalities occurring in 88% of those cases.

All presented to the hospital, with 75% healing promptly, but one in every five infections resulted in death or long-term brain damage. They each got 60 influenza injections, with the majority of them tolerating the vaccine well.
“Concerns about giving the flu vaccine and incomplete routine immunisations are common in this patient group due to the risk of seizures after vaccination,” Dr Howell said.

However, because this syndrome is also associated with a high risk of seizures during infections, it highlights the critical need to protect patients from the complications of vaccine-preventable infections like the flu. Our research highlights that the benefits of flu vaccines for these children far outweigh the risks of seizures being triggered following vaccination.”

SCN1A-positive Dravet syndrome, the most common severe form of genetic epilepsy, affects one in every 15,000 children.
Fraser Caddy, 4, of Melbourne, started having seizures as a baby and was subsequently diagnosed with SCN1A-Dravet syndrome. Renae noted that her child now gets an annual flu vaccination to avoid experiencing long seizures, which are usually caused by sickness. Fraser spent four days in the hospital after having a two-hour seizure due to the virus when he was 11 months old.

“The seizures have gone from monthly to weekly, but they are much shorter now, resolving after a few minutes rather than a couple of hours,” she said. But if he has a viral infection he will seize for as long as his temperature is high and may need a lot of medication and even intubation to get his seizures under control. “It can take Fraser up to four days to get back to normal after he experiences a severe seizure so anything we can do to avoid him getting sick we will do.” Renae said all his influenza vaccines had been well-tolerated with no seizures.

“The research is reassuring for parents that it’s beneficial for children with this condition to have the flu shot to try and avoid an onset of seizures caused by an infection, which are damaging and terrifying to watch,” she said.
University of Melbourne Professor Ingrid Scheffer said the findings would change clinical practice.

“Identifying safe strategies and strongly encouraging influenza vaccination in children and adults with SCN1A-Dravet syndrome is critical,” she said. “Prior to influenza vaccination, vaccine providers should review the child’s regular anti-seizure medications and ensure a seizure management plan is in place. The use of additional anti-seizure medications in the post-vaccination period, such as benzodiazepines, is now recommended to reduce the risk of seizures following a vaccine and is becoming routine practice.”

According to new study, adopting some of the tactics used to successfully treat the juvenile condition spinal muscular atrophy may enable the creation of medicines to slow the muscle degeneration that occurs with age. The study poster was exhibited at Neuroscience 2022, the Society for Neuroscience’s annual meeting. The survival motor neuron protein, which is distributed throughout the body and is necessary for keeping motor neuron cells alive and transmitting correct signals from the central nervous system to muscles, lies at the core of both illnesses.

Spinal muscular atrophy (SMA) is caused by a gene mutation that results in lower quantities of this protein, and gene therapy is one of three clinically accessible SMA treatments. The initial gene therapy recipients are already six years old.
Based on years of SMA research demonstrating the relevance of survival motor neuron protein to neuromuscular integrity, Ohio State University researchers are investigating linkages between the protein and sarcopenia, or the age-related loss of skeletal muscle mass and strength.

Their recent mouse study reveals a definite function for survival motor neuron (SMN) protein in muscle ageing: The protein levels in the spinal cords and motor neurons of advanced-age mice were 22% and 55% lower, respectively, than in middle-aged animals, and these protein decreases were followed by decreased muscle function.

“We found that SMN protein and aging are related – there is a decline in the protein with age and it correlates with a decline in neuromuscular function,” said first author Maria Balch, a postdoctoral scholar in neuroscience at Ohio State’s College of Medicine. “Based on what we know about SMA and therapeutics, we have a background in targeting SMN protein – and it’s possible that could be something down the line that could be applied to age-induced neuromuscular decline.”

The survival motor neuron protein is produced by two genes, SMN1 and SMN2. SMN1 is essential for motor neuron survival and function because it conducts the majority of the effort in producing the full-length protein. SMN2, which largely produces a shortened version, contributes slightly to full-length protein synthesis and may be regarded of as a helper – having more copies of the SMN2 gene is related with milder types of SMA.

The Ohio State researchers discovered that mice modified to express higher-than-normal quantities of the SMN protein had greater overall neuromuscular resilience and recovered from nerve damage faster. “That raised some questions,” said senior Ohio State author Arthur Burghes, a professor of biological chemistry and pharmacology and molecular genetics who developed the mouse model that advanced SMA research. “Different people get different amounts of weakness with age. Why are some people completely resistant to it, and other people are more susceptible?

“With aging and sarcopenia, there is an increased chance of injury due to falling. So it’s an important problem.” Though the researchers assume that a mix of genetics and behaviour is at work, there is a potential that the problem may be solved by enticing the ageing body to generate more SMN protein based on what they’ve discovered so far. This new study assessed a variety of parameters in mice divided into three age groups: 6-10 months, 21 months, and 27 months, which correspond roughly in human years to 35-50, 55, and above 70.

Researchers discovered other trends in older mice, in addition to the natural decrease in protein levels in the spinal cord and motor neurons with age: reductions in the number of motor units, or motor neurons plus the muscle cells they stimulate, as well as a decline in the function of muscles responding to nerve stimulation.
In terms of prospective therapeutic options, the viral-mediated gene therapy now in the clinic for newborns with SMA is unlikely to be effective for adults due to the enormous amount of virus required. The team is looking at different ways to boost SMN output.

“We know in the field of SMA that targeting an increase in SMN protein can be approached from different directions.
If we can determine that this is a viable therapeutic target in aging, there’s a lot of research we can lean on to help drive the direction of age-related therapeutics,” Balch said.

Predictions of the disease’s future prevalence are a crucial component of health policy-makers budget preparation and of significant interest to persons with a family history of cardiovascular disease (CVD). Researchers from Japan have now forecast a decline in CVD incidence through 2040 using new statistical modelling techniques. Governments need projections of disease rates to determine how much money will be needed for healthcare in the future and for what health priorities. However, due to the wide range of variables that affect disease rates, it might be difficult to make precise projections.

According to a research that will be published in The Lancet Regional Health – Western Pacific, between 2020 and 2040, there may be a decrease in coronary heart disease (CHD) and stroke mortality in Japan. “Key elements that must be considered include population ageing and population growth or reduction,” says Eri Kiyoshige, the study’s principal author. “When it comes to cardiovascular problems, additional variables such as rising diabetes, cholesterol levels, and body mass index lately observed in Japan play a vital influence.” Previous research that attempted to predict future CHD and stroke in Japan did not take into account the country’s 47 prefectures.

As a consequence, in addition to more typical statistical modelling, the researchers employed a Bayesian age-period-cohort model that takes into consideration Japanese population estimates as well as the number of CHD and stroke fatalities in Japan from 1995 to 2019. (for all men and women over 30 years of age). These were used to population forecasts for the years 2020 to 2040 in order to anticipate changes in CHD and stroke mortality more precisely than traditional modelling could.

“This model predicted that the number of national-level cardiovascular deaths in Japan will decrease from 2020 to 2040,” says Chris Kypridemos, one of the authors of the study. “Rates are also predicted to decline in most prefectures over this same time period, although some regional differences are predicted in 2040.”

The findings indicate that considerable decreases in death rates in the Japanese population can be expected to compensate for the negative consequences of an ageing population. Furthermore, changes in population size will have only a minor impact at the national and regional levels.

However, as CVD deaths decline and life expectancy rises, there is likely to be an increase in healthcare spending for dementia and frailty, as well as a possibly higher burden of residential care, all of which must be considered when estimating overall future healthcare expenses. These findings are likely to help health policymakers make more accurate funding choices, thereby improving health care at the national and regional levels in Japan.

Changes in gut function caused by weight gain are linked to an increase in the severity of asthma, according to research that will be presented at the Society for Endocrinology annual conference in Harrogate. Gaining weight, according to the study, is connected with higher levels of inflammation, indications of gut permeability, and less effective asthma control. These findings suggest not only to weight loss as a viable therapy option for individuals with severe asthma symptoms, but also to the stomach as an additional therapeutic target for improving asthma control in obese patients.

It has previously been proven that gaining weight modifies the nature of the bacteria in the gut, perhaps increasing gut permeability. A “leaky gut” can let deadly pathogens into the circulation, triggering inflammatory responses throughout the body. Obesity has been linked to an increase in the severity of chronic inflammatory disorders such as asthma. Although it is common, poorly treated asthma can have serious side effects such as tiredness, lung infections, and an increased chance of life-threatening asthma episodes. There has been no previous research on how increasing intestinal permeability may affect asthma management.

Cristina Parenti and colleagues at Nottingham Trent University studied the symptoms of 98 people with severe asthma, as well as the relationship between body weight and gut permeability. Patients with a lean-to-obese body mass index (BMI) reported their symptoms using the Asthma Control Questionnaire-6. Blood tests were used to measure asthma-related inflammatory markers and gut permeability markers (lipopolysaccharide binding protein (LPB) and calprotectin) (granzyme-A, IL-5, IL-6, CCL-4). LBP levels were significantly higher in individuals with poorly controlled asthma, and they increased with body weight. Rising LBP concentrations are associated with increased levels of inflammatory markers related to asthma.

Lead investigator, Cristina Parenti, commented, “We have found a significant link between gut permeability, being overweight and poor asthma control, particularly in people with obesity. This suggests that dietary interventions to improve gut barrier function may be an effective, alternative treatment target for asthma patients who are overweight or have obesity.”

The current study comprised just a limited number of people with severe, uncontrolled asthma. The researchers plan to engage additional participants in the study, look at the results in people with well-controlled asthma across a variety of BMIs, and see if focusing on the stomach can benefit people with asthma management.
“Our preliminary findings indicate that increased gut permeability is likely to be a factor in worsening asthma symptoms in obese patients, so it will be interesting to see if dietary interventions can improve symptoms for these patients,” Cristina Parenti concluded.

Every year on November 14, people throughout the world observe World Diabetes Day to promote awareness of the health dangers that diabetes poses and how to avoid them. Sir Frederick Banting and Charles Best, two renowned scientists, are honoured on this day for their vital contributions to the development of insulin.

The major goal of World Diabetes Day, however, is to raise public awareness of the hazards of diabetes, present problems, and the best ways to solve them in order to provide modern treatment that is sustainable.

Date and history of World Diabetes Day 2022:

World Diabetes Day is marked yearly on November 14 to promote awareness of the chronic disease’s ramifications. The International Diabetes Federation founded the day in 1991 with the backing of the World Health Organization, and it was designated as a United Nations holiday in 2006.

Theme for World Diabetes Day 2022:
Between the years 2021 and 2023, the subject of World Diabetes Day will be “Access to Diabetes Care.”

The Importance of World Diabetes Day 2022:
The major purpose of this day is to raise worldwide diabetes awareness through campaigns viewed by over 1 billion people. It also supports IDF advocacy efforts throughout the year. It contributes to understanding the relevance of taking concerted action to combat diabetes.

A UN Resolution in 2007 established the blue circle logo for World Diabetes Day. This emblem, which acts as a symbol of diabetes awareness, unites the diabetes community worldwide.

According to a recent mouse research, the bacteria that assist break down food actually instruct the stomach how to do their job better. According to the researchers, bacteria appear to be able to control which of the gut’s genes are activated, and this interaction may lead to a remodelling of the epithelial cells lining the gut to fit the diet. According to the researchers, bacteria appear to be able to control which of the gut’s genes are activated, and this interaction may lead to a remodelling of the epithelial cells lining the gut to fit the diet.

“The gut is a wonderful link between an animal and the world it lives in, and it receives information from both the nutrition and the bacteria it houses,” said John Rawls, Ph.D., director of the Duke Microbiome Center and professor of molecular genetics and microbiology at Duke. The findings were published in the open access journal Cellular and Molecular Gastroenterology and Hepatology on May 6. To begin parsing the instructions sent by microorganisms to gut cells, Duke researchers compared mice grown without gut microbes to those raised with a normal gut microbiome.

The researchers concentrated on the interaction between RNA transcription (DNA being transcribed to RNA) and the proteins that switch this copying process on or off in the small intestine, which is where most fat and other nutrients are absorbed. While both germ-free and normal mice were able to metabolise fatty acids in a high-fat diet, the researchers discovered that germ-free mice employed a whole distinct collection of genes to deal with the high-fat meal.

“We were shocked to see that the gene playbook used by the gut epithelium to respond to dietary fat differs depending on whether or not microorganisms are present,” Rawls said. The researchers also discovered that microorganisms can aid in fat absorption in the stomach.

“It’s a really consistent conclusion across numerous studies, from our lab and others, that microorganisms actually improve lipid absorption,” said Colin Lickwar, Ph.D., senior research associate in Rawls’ lab and the paper’s lead author. “And, to some extent, this influences systemic processes such as weight growth.” The germ-free mice showed an increase in the activation of genes involved in fatty acid oxidation, which is the actual burning of fatty acids to supply fuel for the gut’s cells.

“We usually conceive of the gut as merely performing its job, absorbing food nutrients through the epithelium to share with the rest of the body,” Rawls added.

“What we believe is happening in germ-free mice is that the stomach consumes more fat than it would if the microorganisms were there.” This might be due to changes in the makeup of the gut’s epithelial cells.
“A number of recent articles have shown that there is a significant ability to affect the broader architecture of the gut as well as particular gene programmes,” Lickwar added. “The gut has an amazing amount of flexibility.” We don’t fully understand it, but this article sheds some light on it.”

The researchers concentrated their efforts on HNF4-Alpha, a transcription factor known to control genes involved in lipid metabolism and genes that respond to microorganisms.

“We thought that it might represent an interface or a crossroads between interpreting information that comes from either microbial sources or from dietary fat,” Lickwar said.

“It’s certainly complicated, but we do appear to identify that HNF4-Alpha is important in simultaneously integrating multiple signals within the intestine,” Lickwar said.”For every way that germ-free animals seem unusual, that teaches us something about the large impact of the microbiome on what we consider to be ‘normal’ animal biology,” Rawls said.

A recent study discovered that nitrogen-containing bisphosphonates (N-BPs) like alendronate, which are often used to treat postmenopausal osteoporosis, are associated with decreased risks of pneumonia and death from pneumonia. The study’s findings have been published in the Journal of Bone and Mineral Research.

The research comprised 4,041 hip fracture patients who got N-BPs and 11,802 who did not. N-BPs were related with a 24% decreased incidence of pneumonia compared to no therapy across a median follow-up duration of 2.7 years (69 versus 90 cases per 1,000 people per year).

A similar link was seen with pneumonia mortality, with N-BPs being associated with a 35% decreased risk (23 versus 35 per 1,000 patients per year for the N-BP and non-N-BP groups, respectively).
Previous animal investigations show that N-BP therapy causes a high concentration of N-BPs in the respiratory system.

“Together with its anti-inflammatory and immune-modulatory properties, this may explain why N-BPs were associated with reduced risk of pneumonia, as revealed in our study,” said senior author Ching-Lung Cheung, PhD, of The University of Hong Kong. He added that studying the potential of N-BPs for treating symptoms of COVID-19 may be warranted.

A recent study from the University of South California demonstrates that a specific pattern of white matter connectivity has been found in the brains of autistic people. It is also distinct from the pattern seen in those with Developmental Coordination Disorder (DCD).

According to the study, which was published in the journal ‘Scientific Reports,’ roughly 85 percent of autistic persons have had or are at risk of being diagnosed with DCD, a disorder that interferes with learning and motor control. DCD can impede daily tasks such as typing, dressing, and walking, reducing one’s social involvement and enjoyment.

Distinguishing between the brain activity patterns of autism spectrum disorder (ASD) and DCD populations is critical because the widespread comorbidity of ASD and DCD confounds previous autism research, which was thought to be exclusively investigating its core social-communication symptoms at the time it was conducted.

“As the scientific community has learned more about DCD, we realised that white matter disparities previously observed in the autism literature might really be attributable to this underlying motor comorbidity,” stated senior author Lisa Aziz-Zadeh. “In reality, that’s exactly what our team discovered: many earlier research findings are likely not representing autism’s core symptoms, but rather co-occurring DCD.”

Aziz-Zadeh is an associate professor in the USC Dornsife College of Letters, Arts, and Sciences’ Brain and Creativity Institute and the Department of Psychology. She is the director of the USC Center for the Neuroscience of Embodied Cognition, which manages research projects funded by the National Institutes of Health, the US Department of Defense, and the Intelligence Advanced Research Projects Activity of the Office of the Director of National Intelligence.
Aziz-Zadeh and colleagues employed diffusion weighted MRI, a method for evaluating functional brain connections, on children and teenagers aged 8 to 17 years old who were randomly allocated to one of three research groups: those with ASD, those with suspected DCD, and those who were normally developing.

The photos were evaluated, compared, and connected with physical and social behaviour assessments performed by the participants. The researchers discovered that numerous structural brain connection patterns previously associated with autism also overlap with DCD. The team was able to identify three white matter pathways with distinctly different connectivity, distinct from the DCD and typically developing groups: the longitudinal fibres and u-fibers of the mid-cingulum, the corpus callosum forceps minor/anterior commissure, and the left middle cerebellar peduncle. These disparities were also connected to autistic participants’ emotional performance and/or autism severity. Children with DCD had distinct white matter patterns in the left cortico-spinal and cortico-pontine tracts.

“These findings show that we can use advanced imaging to differentiate between autism’s hallmark social symptoms and other motor-related symptoms at the level of brain anatomy,” said Emily Kilroy, the study’s first author and a former postdoctoral scholar in Aziz-lab Zadeh’s during the data collection period. “Of course, people are much more than their brain structure,” says the researcher, “but this level of clarity and precision at the anatomical level brings us one step closer to understanding the molecular foundation and presentation of autism.”