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UNC School of Medicine researchers have achieved significant advances in the intriguing disciplines of cellular reprogramming and organ regeneration, and their results might have a significant influence on the development of future therapies for shattered hearts.

In a study published in the journal Cell Stem Cell, researchers at the University of North Carolina in Chapel Hill discovered a more efficient and effective technique to convert scar tissue cells (fibroblasts) to become healthy cardiac muscle cells (cardiomyocytes).

The fibrous, stiff tissue that causes heart failure after a heart attack or as a result of cardiac disease is created by fibroblasts. Researchers are looking into possibly treating or one day curing this widespread and deadly illness by converting fibroblasts into cardiomyocytes. Surprisingly, a gene activity-controlling protein called Ascl1, which is well recognised to be an essential protein involved in converting fibroblasts into neurons, turned out to be the key to the new cardiomyocyte-making approach. Ascl1 was once assumed to be neuron-specific by researchers.

Li Qian, PhD, senior author of the study and associate director of the McAllister Heart Institute at the UNC School of Medicine, said, “It’s an out-of-the-box finding, and we expect it to be useful in developing future cardiac therapies and possibly other kinds of therapeutic cellular reprogramming.”

In the past 15 years, researchers have created a number of methods to convert adult cells into stem cells and then drive those stem cells to differentiate into other types of adult cells. In recent years, researchers have discovered strategies to reprogramme cells directly from one mature cell type to another. It has been hoped that once these techniques are as safe, effective, and efficient as possible, clinicians will be able to provide a direct injection to patients to transform harmful cells into helpful ones.

“Reprogramming fibroblasts has long been one of the important goals in the field,” Qian said. “Fibroblast over-activity underlies many major diseases and conditions including heart failure, chronic obstructive pulmonary disease, liver disease, kidney disease, and the scar-like brain damage that occurs after strokes.”

In the new study, Qian’s team used three currently used approaches to reprogramme mice fibroblasts into cardiomyocytes, liver cells, and neurons. This team also included co-first authors Haofei Wang, PhD, a postdoctoral researcher, and MD/PhD student Benjamin Keepers. Their goal was to document and contrast the variations in gene activity patterns and variables that control gene activity during these three separate reprogrammings.

Unexpectedly, the scientists discovered that converting fibroblasts into neurons activated a group of genes related to cardiomyocytes. They quickly discovered that Ascl1, one of the master-programmer “transcription factor” proteins employed to create the neurons, was the cause of this activation.

The researchers added Ascl1 to the three transcription factor cocktails they had been using to create cardiomyocytes to see what would happen because Ascl1 activated cardiomyocyte genes. They were shocked to see that it significantly increased reprogramming efficiency–the percentage of effectively reprogrammed cells–by more than ten times. In reality, they discovered that only Ascl1 and another transcription factor known as Mef2c remained from their original cocktail of three factors.

Using biomarkers detected in blood samples, researchers developed a method to detect amyloid buildup in the brain, a hallmark of Alzheimer’s disease.

Alzheimer’s disease is a neurological illness that causes the brain to gradually lose neurons and synapses.

One of the primary causes of Alzheimer’s disease is the accumulation of amyloid b (Ab) in the brain, where it forms plaques. Alzheimer’s disease is mostly seen in individuals over 65 years of age, and cannot currently be stopped or reversed. Thus, Alzheimer’s disease is a major concern for nations with ageing populations, such as Japan.

A team of scientists from Hokkaido University and Toppan, led by Specially Appointed Associate Professor Kohei Yuyama at the Faculty of Advanced Life Science, Hokkaido University, have developed a biosensing technology that can detect Ab-binding exosomes in the blood of mice, which increase as Ab accumulates in the brain. Their research was published in the journal Alzheimer’s Research & Therapy.

When tested on mice models, the Ab-binding exosome Digital ICATM (idICA) showed that the concentration of Ab-binding exosomes increased with the increase in age of the mice. This is significant as the mice used were Alzheimer’s disease model mice, where Ab builds up in the brain with age.

In addition to the lack of effective treatments of Alzheimer’s, there are few methods to diagnose Alzheimer’s. Alzheimer’s can only be definitively diagnosed by direct examination of the brain–which can only be done after death.

Ab accumulation in the brain can be measured by cerebrospinal fluid testing or by positron emission tomography; however, the former is an extremely invasive test that cannot be repeated, and the latter is quite expensive. Thus, there is a need for a diagnostic test that is economical, accurate and widely available.

Previous work by Yuyama’s group has shown that Ab build-up in the brain is associated with Ab-binding exosomes secreted from neurons, which degrade and transport Ab to the microglial cells of the brain. Exosomes are membrane-enclosed sacs secreted by cells that possess cell markers on their surface.

The team adapted Toppan’s proprietary Digital Invasive Cleavage Assay (Digital ICATM) to quantify the concentration of Ab-binding exosomes in as little as 100 uL of blood. The device they developed traps molecules and particles in a sample one-by-one in a million micrometer-sized microscopic wells on a measurement chip and detects the presence or absence of fluorescent signals emitted by the cleaving of the Ab-binding exosomes.

Human clinical studies using the technique are presently underway. This highly sensitive idICA technology is the first ICA application that allows for the highly sensitive detection of exosomes that retain specific surface molecules from a small amount of blood without the need to learn special techniques; because it is applicable to exosome biomarkers in general, it can also be adapted for use in the diagnosis of other diseases.

A new understanding of how some visually handicapped individuals might begin to see gives a fresh perspective on the brain’s capabilities. According to recent research, the adult brain has the capacity to recover partially from hereditary blindness.

The researchers were looking at a therapy for Leber congenital amaurosis, often known as LCA. The phrase is used to describe a category of hereditary retinal illnesses that are characterised by significant vision impairment at birth.

The condition, which stems from mutations in any of over two dozen genes, causes degeneration or dysfunction in the retina’s photoreceptors. Administering chemical compounds that target the retina, called synthetic retinoids, can restore a notable amount of vision in children with LCA. The UCI team wanted to find out if the treatment could make a difference for adults who have the condition.

“Frankly, we were blown away by how much the treatment rescued brain circuits involved in vision,” said Sunil Gandhi, professor of neurobiology and behavior and the corresponding author. Gandhi is a fellow of UCI’s Center for the Neurobiology of Learning and Memory and a member of the Center for Translational Vision Research. “Seeing involves more than intact and functioning retinae. It starts in the eye, which sends signals throughout the brain. It’s in the central circuits of the brain where visual perception actually arises.” Until now, scientists believed that the brain must receive those signals in childhood so that central circuits could wire themselves correctly.

Working with rodent models of LCA, the collaborators were surprised by what they found. “The central visual pathway signaling was significantly restored in adults, especially the circuits that deal with information coming from both eyes,” Gandhi said. “Immediately after the treatment, the signals coming from the opposite-side eye, which is the dominant pathway in the mouse, activated two times more neurons in the brain. What was even more mind-blowing was that the signals coming from the same-side eye pathway activated five-fold more neurons in the brain after the treatment and this impressive effect was long-lasting. The restoration of visual function at the level of the brain was much greater than expected from the improvements we saw at the level of the retinae. The fact that this treatment works so well in the central visual pathway in adulthood supports a new concept, which is that there is latent potential for vision that is just waiting to be triggered.”

The finding opens exciting research possibilities. “Whenever you have a discovery that breaks with your expectations about the possibility for the brain to adapt and rewire, it teaches you a broader concept,” Gandhi said. “This new paradigm could aid in the development of retinoid therapies to more completely rescue the central visual pathway of adults with this condition.”

Gandhi and first author Carey Huh, PhD, who initiated the project, teamed with Krzysztof Palczewski, Distinguished Professor of ophthalmology. Palczewski, director of the Center for Translational Vision Research, is renowned for his work on retinoids and the visual cycle.

People with psychotic disorders, such as schizophrenia, are 2.5 times more likely to acquire dementia than individuals who do not have a psychotic disorder, according to one research.

The new systematic review and meta-analysis, published in Psychological Medicine, discovered that psychotic illnesses may be more closely related to dementia than other mental health problems such as depression or anxiety.

Senior author Dr Jean Stafford (MRC Unit for Lifelong Health & Ageing at UCL) said: “We found that having a diagnosis of a psychotic disorder is linked to a much higher risk of developing dementia later in life.”

“Our findings add to evidence that protecting people’s mental health throughout life could help to prevent dementia.”

The study is the first high-quality systematic review looking at a range of psychotic disorders and their association with dementia risk. Schizophrenia and other related psychotic disorders are severe illnesses that involve symptoms such as hallucinations and delusions, and social withdrawal. Many people also experience impairments in cognitive and functional skills.

The researchers pulled together evidence from 11 studies from nine countries on four continents, which included close to 13 million participants in total.

They found that across multiple different psychotic disorders, and regardless of the age at which someone first developed their mental illness, there was a higher risk of dementia later in life. Some studies included people diagnosed with psychotic disorders while young adults, with follow-up periods of multiple decades. They also found that people who have had a psychotic disorder tend to be younger than average at dementia diagnosis, with two studies finding that people with psychotic disorders were much more likely to be diagnosed with dementia while still in their 60s.

The findings add to the list of modifiable risk factors for dementia. UCL researchers have previously found that four in 10 dementia cases could be prevented or delayed by targeting risk factors from across the lifespan. The current study’s joint senior author, Dr Vasiliki Orgeta (UCL Psychiatry), previously found that PTSD increases the likelihood of dementia, and while depression and anxiety also increase the risk, these latest findings suggest that psychotic disorders have the strongest association with dementia risk.

The researchers were not able to confirm the cause of the association, whether it is due to the mental illness itself, or perhaps because psychotic disorders increase the likelihood of conditions that in turn increase the risk of dementia. Some of the association may be because psychotic symptoms could be early markers of dementia for some people, but the fact that some of the studies had very long follow-up periods and included people experiencing psychosis at young ages suggests this is not the only explanation.

Dr Orgeta said: “People with psychotic disorders are more likely to have other health conditions such as cardiovascular disease or obesity, which can increase the risk of dementia, while they are also more likely to have a poor diet, smoke or use drugs, which may harm their health in ways that could increase their likelihood of developing dementia.”

Lead author Sara El Miniawi (UCL Psychiatry), who completed the research as her MSc dissertation, said: “Cognitive impairment and hallucinations can be symptoms of both dementia and psychotic disorders, so it is possible there could be a link between the two illnesses. This impairment could also limit people’s cognitive reserve, and increase their vulnerability to dementia symptoms.”

The researchers were not able to determine whether effective treatment for psychotic disorders could mitigate the dementia risk, or whether antipsychotic medication could be a factor, as there was limited and conflicting evidence.

Sara El Miniawi added: “As people with psychotic disorders face a higher risk of numerous other health conditions, managing their overall physical and mental health is very important, and here we found that health professionals working with them should also be watchful for any signs of cognitive decline.”

The cerebellum is most known for its function in motor control. According to researchers at the University of Basel, the cerebellum is also important in recalling emotional experiences.

The research was published in the journal PNAS. Positive and negative emotional events are particularly strongly remembered. This phenomena is critical to human existence since we must remember harmful circumstances in order to avoid them in the future. Previous research has revealed that the amygdala, a brain region crucial in emotion processing, plays a key role in this phenomena.

Emotions activate the amygdala, which in turn facilitates the storage of information in various areas of the cerebrum.

The current research, led by Professor Dominique de Quervain and Professor Andreas Papassotiropoulos at the University of Basel, investigates the role of the cerebellum in storing emotional experiences. In a large-scale study, the researchers showed 1,418 participants emotional and neutral images and recorded the subjects’ brain activity using magnetic resonance imaging.

In a memory test conducted later, the positive and negative images were remembered by the participants much better than the neutral images. The improved storage of emotional images was linked with an increase in brain activity in the areas of the cerebrum already known to play a part. However, the team also identified increased activity in the cerebellum.

The cerebellum in communication with the cerebrum

The researchers were also able to demonstrate that the cerebellum shows stronger communication with various areas of the cerebrum during the process of enhanced storage of the emotional images.

It receives information from the cingulate gyrus – a region of the brain that is important in the perception and evaluation of feelings. Furthermore, the cerebellum sends out signals to various regions of the brain, including the amygdala and hippocampus. The latter plays a central role in memory storage.

“These results indicate that the cerebellum is an integral component of a network that is responsible for the improved storage of emotional information,” says de Quervain.

Although an improved memory for emotional events is a crucial mechanism for survival, it does have its downsides: in the case of very negative experiences, it can lead to recurring anxiety. This means that the findings, which have now been released, may also be relevant in understanding psychiatric conditions such as post-traumatic stress disorder.

Basel research on emotions and memory.

The current study forms part of a large-scale research project conducted by the Research Platform Molecular and Cognitive Neurosciences (MCN) at the University of Basel and the University Psychiatric Clinics (UPK) Basel. The aim of this project is to gain a better understanding of emotional and cognitive processes and to transfer results from basic research to clinical projects.

Pancreatic ductal adenocarcinoma is the most common and lethal kind of pancreatic cancer (PDAC). Patients with PDAC have a 5-year survival rate of only 7.1%.

Every cancer is unique. PDAC is distinguished by significant tumour desmoplasia, or fibrous connective tissue inside the tumour, which is induced by fibroblast infiltration and the extracellular matrix they secrete.

The main component of the matrix is type I collagen or Col 1, a protein broadly used in the body to form the basic structure of bone, skin, blood vessels and connective tissues. The effect of Col 1 on PDAC development and its response to therapy has been a matter of intense debate among researchers, with some arguing that Col 1 promotes tumor growth and spread and others contending that it restricts tumor growth and protects the cancer cells from immune attack.

In a new study, published October 5, 2022, in Nature, co-first authors Hua Su, PhD, a postdoctoral fellow in the lab of senior author Michael Karin. PhD, Distinguished Professor of Pharmacology and Pathology at University of California San Diego School of Medicine, and Fei Yang, PhD, a scientist working with Beicheng Sun, MD, PhD, at Nanjing University School of Medicine, settle the debate by showing that it is not the amount of Col 1 present in the tumor that matters, but its quality and nature.

Specifically, they report that Col 1 that has been cleaved by matrix metalloproteases (enzymes that break down matrix proteins, such as collagen) stimulates tumor growth while intact and non-cleaved Col 1 inhibits tumor growth.

“Moreover,” said Su, “cleaved Col 1 activates a signaling pathway that stimulates energy production in pancreatic cancer cells by binding to a receptor protein called DDR1. Non-cleaved Col 1 inhibits this pathway by inducing the degradation of DDR1.”

The research was conducted using mice models and a novel culture system in which PDAC cells were plated on extracellular matrix that contained either cleaved or non-cleaved Col 1.

The authors said the findings have important clinical implications.

The relative amounts of cleaved versus non-cleaved Col 1 in the human PDAC stroma or connective tissue strongly affect patient survival after surgical resection. Patients whose tumors were enriched in cleaved Col 1 and whose cancerous cells expressed high levels of DDR1 fared poorly, with most succumbing to their disease within two years of surgery.

This patient group represented 75 percent of the 106 patients analyzed as part of the study, using cancer specimens provided by Beicheng Sun, MD, PhD, and colleagues at the Affiliated Drum Tower Hospital of Nanjing University Medical School in China.

In contrast, the 25 percent of patients whose tumors mainly contained non-cleaved Col 1 with low levels of DDR1 expression experienced much better survival prospects.

“This work is important because it provides a simple way for patient stratification and suggests that patients with high levels of cleaved Col 1 and DDR1 expression need more aggressive post-surgery treatments,” said Karin.

“It also provides evidence that the most effective therapy for this group of patients should include inhibitors of DDR1 or key components of its signaling pathway whose activation results in increased number of mitochondria, the cellular power plants, in PDAC cells.”

According to a recent prediction, primary liver cancer was one of the top three causes of cancer mortality in 46 countries in 2020, and the number of primary liver cancer diagnoses and fatalities might climb by more than 55% every year by 2040.

In a recent article in the Elsevier-published Journal of Hepatology, researchers demand that measures to control the disease be given priority. Senior author Isabelle Soerjomataram, MD, PhD, International Agency for Research on Cancer (IARC/WHO), Cancer Surveillance Branch, Lyon, France, stated: “Liver cancer generates a large burden of disease globally each year.” Major risk factors for the disease include hepatitis B and C viruses, alcohol use, excess body weight, and metabolic diseases including type 2 diabetes. It is also completely preventable if control efforts are addressed.

“In light of the availability of new and improved global cancer incidence and mortality estimates, we wanted to provide the most up-to-date assessment of the burden of liver cancer and develop an essential tool for national liver cancer control planning,” explained lead author Harriet Rumgay, PhD candidate, International Agency for Research on Cancer (IARC/WHO), Cancer Surveillance Branch, Lyon, France. “In this analysis we describe where liver cancer ranks among all cancer types for cancer diagnoses and deaths in nations across the world. We also present predictions of the future liver cancer burden to 2040.”

Researchers took information on primary liver cancer cases and fatalities from the GLOBOCAN 2020 database of the International Agency for Research on Cancer, which generates estimates of cancer incidence and mortality for 36 cancer types in 185 nations worldwide. United Nations population forecasts were used to determine the projected change in the number of cancer cases or deaths by the year 2040.

According to the findings, 830,200 people worldwide would die from liver cancer in 2020, with an anticipated 905,700 more receiving liver cancer diagnoses. These statistics show that liver cancer is currently one of the top three cancer mortality causes in 46 nations and one of the top five cancer death causes in almost 100 nations, including numerous high-income nations.

Eastern Asia, Northern Africa, and South-Eastern Asia had the greatest incidence and fatality rates for liver cancer. If present rates do not change, researchers project that over the next 20 years, the number of new cases and fatalities from liver cancer will increase by more than 55% annually. The number of cases that are expected to increase will raise the demand for resources to manage patient care for liver cancer.

The discovery that liver cancer incidence and fatalities will keep rising year after year concerned the researchers. They warn that governments all over the world must achieve at least a 3% annual decline in liver cancer incidence and mortality rates through preventative efforts in order to avoid this increase in cases and deaths.

These figures give an overview of the global burden of liver cancer and show how vital it is to enhance and strengthen existing liver cancer preventive strategies.

According to Dr Soerjomataram, “we are at a turning point in liver cancer prevention as accomplishments in controlling the hepatitis B virus and hepatitis C virus will be reflected in rates of liver cancer in the next several decades. These measures need to be maintained and strengthened, particularly in light of the COVID-19 pandemic’s impact on some hepatitis B and C virus control initiatives.

The authors urge public health officials to strengthen current measures to prevent liver cancer, such as immunisation, testing, and treatment for hepatitis B virus; population-wide testing and treatment for hepatitis C virus, to prepare for the anticipated rise in demand for resources to manage the care of liver cancer patients throughout the cancer pathway, including improved access to palliative care due to the predicted growing number of liver cancer patients.

Without a significant reduction in liver cancer rates through primary prevention, Dr Soerjomataram warned that by 2040, “the number of people diagnosed with or dying from liver cancer annually could climb by over 500,000 cases or deaths.”

Also Read: Wear, tear from stress can increase risk of cancer mortality: Study

When we are awake, we assume that our thoughts are always racing with ideas. We keep our own dynamic mental stream, which is like a never-ending river stream.

A thought may lead to another, whether or not it is relevant to our actions, and it may ebb and flow between our inner and outside worlds. But how can the brain maintain such a thought-related state all the time? It absolutely cannot be done, according to a recent research published in the Proceedings of the National Academy of Sciences, since our brains must periodically “go offline,” which we perceive as mental gaps.

Re-analyzing a previously gathered dataset, researchers from the University of Liege, EPF Lausanne & University of Geneva asked healthy subjects to describe their mental state as it was just prior to receiving an auditory probe (beep) while lying still in the MRI scanner. The options were environmental perceptions, thoughts influenced by stimuli, ideas unaffected by stimuli, and mental lapses. Using this experience-sampling technique, good photos were gathered.

In contrast to the other states, mental blanking episodes were recorded much less frequently and recurred much less frequently over time, according to the researchers. The researchers also discovered, using machine learning, that during episodes of mind-numbing, our brains arranged so that all brain regions were in constant communication with one another.

The high amplitude of the fMRI global signal, a surrogate for low cortical arousal, further distinguished this ultra-connected brain pattern. To put it another way, when we describe mind blanking, our brains appear to be in a state that is comparable to deep sleep, except that we are awake.

Mind blanking is a relatively new mental state within the study of spontaneous cognition. It opens exciting avenues about the underlying biological mechanisms during waking life. It might be that the boundaries of sleep and wakefulness might not be that discrete as they appear to be after all”, says the principal investigator Dr Demertzi Athena, FNRS researcher at GIGA ULiege. “The continuously and rapidly changing brain activity requires robust analysis methods to confirm the specific signature of mind blanking”, continues Dr Van De Ville Dimitri.

The strict neurofunctional profile of mind blanking, according to the researchers, might explain why people are unable to report mental content because their brains are unable to discriminate signals in an instructional manner. This research demonstrates that instantaneous non-reportable mental experiences may occur during awake, establishing mind blanks as a relevant mental state throughout the current experience as we await clarification of the underlying processes.

Also Read: Wear, tear from stress can increase risk of cancer mortality: Study

According to specialists, the wear and strain on the body produced by chronic and lifelong stress might increase the risk of cancer death rates.

The term “allostatic load” refers to the cumulative consequences of stress over time.

“As a response to external stressors, your body releases a stress hormone called cortisol, and then once the stress is over, these levels should go back down,” said Dr. Justin Xavier Moore, epidemiologist at the Medical College of Georgia and Georgia Cancer Center. “However, if you have chronic, ongoing psychosocial stressors, that never allow you to ‘come down,’ then that can cause wear and tear on your body at a biological level.”

Investigators, led by Moore, performed a retrospective analysis of more than 41,000 people from the National Health and Nutrition Examination Survey, or NHANES, collected between 1988-2019. That database includes baseline biological measures of participants — body mass index, diastolic and systolic blood pressure, total cholesterol, hemoglobin A1C (higher levels indicate a risk for diabetes), albumin and creatinine (both measures of kidney function) and C-reactive protein (a measure of inflammation) — that the researchers used to determine allostatic load. Those with a score of more than 3 were categorized as having high allostatic load.

Then they cross-referenced those participants with the National Death Index, maintained by the National Center for Health Statistics and the Centers for Disease Control and Prevention, to determine which people died from cancer and when, Moore explained.

“To date, there has been limited research on the relationship between allostatic load and cancer among a current, nationally representative sample of US adults,” Moore and his colleagues write in the journal SSM Population Health. “Examining the association of allostatic load on cancer outcomes, and whether these associations vary by race may give insight to novel approaches in mitigating cancer disparities.”

The researchers found that, even without adjusting for any potential confounders like age, social demographics like race and sex, poverty to income ratio and educational level, those with a high allostatic load were 2.4 times more likely to die from cancer than those with low allostatic loads.

“But you have to adjust for confounding factors,” Moore explains. “We know there are differences in allostatic loads based on age, race and gender.”

In fact, in previous research he and his colleagues observed that when looking at trends in allostatic load over 30 years among 50,671 individuals, adults aged 40 and older had greater than a 100% increased risk of high allostatic load when compared to adults under 30. Further, regardless of the time period, Black and Latino adults had an increased risk of high allostatic load when compared with their white counterparts. Much of that, Moore says, can be attributed to structural racism — things like difficulty navigating better educational opportunities or fair and equitable home loans.

“If you’re born into an environment where your opportunities are much different than your white male counterparts, for example being a black female, your life course trajectory involves dealing with more adversity,” he said.

Even when controlling for age, the researchers found that people with high allostatic load still have even 28% increased risk of dying from cancer. “That means that if you were to have two people of the same age, if one of those people had high allostatic load, they are 28% more likely to die from cancer,” Moore says.

Adjusting for sociodemographic factors including sex and race and educational level, high allostatic load led to a 21% increase; and further adjusting the model for other risk factors like whether participants smoked, previously had a heart attack, or been previously diagnosed with cancer or congestive heart failure, led to a 14% increase.

Moore and colleagues further examined the relationship between allostatic load and cancer mortality specifically among each racial/ethnic group (e.g., non-Hispanic Black, non-Hispanic white, and Hispanic adults). However, allostatic load was not as strongly related when broken down by race categories. These findings could be explained by the sheer size of the original sample.

“Epidemiologically, when looking at 41,000 people, there are many cancer related-death events,” Moore explains. “However, it is more difficult to ascertain a relationship between x (allostatic load) and y (cancer death) when you essentially have less datapoints to measure.” For example, limiting the sample to just non-Hispanic Blacks would mean analyzing a sample of just 11,000 people, so the relationship may look diminished or attenuated.

“The reason race even matters, is because there are systemic factors that disproportionately affect people of color,” he said.

“But even if you take race out, the bottom line is that the environments in which we live, work and play, where you are rewarded for working more and sometimes seen as weak for taking time for yourself, is conducive to high stress which in turn may lead to cancer development and increased morbidity and mortality.”

In the United States, cancer is the second leading cause of death and it was responsible for an estimated 1.9 million cases and nearly 609,000 deaths in 2021.

Also Read: Covid case update: India records 2,529 cases

India recorded 2,529 new COVID cases in the last 24 hours, informed the Ministry of Health and Family Affairs on Thursday.

India’s active caseload currently stands at 32,282 which accounts for 0.07 per cent of the total cases. A total of 3,553 patients recovered in the last 24 hours and the cumulative tally of recovered patients (since the beginning of the pandemic) was recorded at 4,40,43,436 on Thursday.

The national COVID-19 recovery rate is at 98.74 per cent, the health ministry said.

The daily positivity rate was recorded at 2.07 per cent, while the weekly positivity rate is 1.38 per cent.

Covid vaccines

“COVID-19 vaccination for the age group 12-14 years was started on 16 March, 2022. So far, more than 4.10 Cr (4,10,49,845) adolescents have been administered with the first dose of COVID-19 vaccine. Similarly, the COVID-19 precaution dose administration for age group 18-59 years also started from 10th April 2022 onwards,” read an official statement.

The last 24 hours saw a total of 1,22,057 COVID-19 tests being conducted. India has so far conducted over 89.62 crores (89,62,68,264) cumulative tests, said officials.

Earlier, ‘COVID Vaccination Amrit Mahotsava’, launched on July 15 this year to give an impetus to Precaution Dose as part of the national COVID vaccination drive, concluded after administering over 15.92 crores of precaution doses, according to the Ministry of Health and Family Welfare.

The Ministry of Health said that over 13.01 lakh Special COVID vaccination camps were organized during these 75 days.

“In 75 days, across all states and UTs, 11,104 camps were organized at bus stations, 5,664 camps at railway stations, 511 camps at airports, over 1,50,004 camps at various schools and colleges, 4,451 camps at routes of religious yatras, and over 11,30,044 camps were organized at various private and government workplaces and industrial establishments,” the statement from the ministry read.

The Ministry said that more than 76.18 lakh first dose, 2.35 crore second dose and 15.92 crore precaution dose had been administered in this period of 75 days.

“More than 24.73 lakh doses per day have been administered, including 20.68 lakh doses precaution dose per day,” it said, adding that with the intervention of 75 days long free vaccination campaign, 27 per cent of the eligible population have now received their precaution dose as it was only 8 per cent earlier at the start of the initiative.

Under the COVID Vaccination Amrit Mahotsava, all States and UTs were urged to run the campaign as a ‘Jan Abhiyan’ with massive mass mobilization, through a camp approach. Multiple special vaccination camps in the routes of Char Dham Yatra (Uttarakhand), Amarnath Yatra (Jammu and Kashmir), Kanwar Yatra (all States and UTs of North-India) as well as major Melas and congregations were organized.

Further, Special Vaccination Camps were organized at office complexes, industrial establishments, railway stations, inter-state bus stations, schools and colleges.

Also Read: “DO NOT use them”: WHO issues alert on four cough syrups made by India’s Maiden Pharmaceuticals