Biology environment human body

Why do Mosquitoes Bite Some More Than Others?

Monsoon can take a toll on human health. From manageable disease like cold and flu, to fatal diseases like dengue, malaria and chikungunya, monsoon brings along with it health complications that can put us at risk. While it might not be possible to avoid mosquito bites, as despite using ways like using mosquito repellents and avoiding mosquito-breeding, the vector succeeds in transmitting these diseases.

In a group, you must have noticed there is always someone who will complain about mosquitoes attacking them the most. That’s because, according to a report by Huff Post mosquitoes are selective insects, and some people are more likely to get bites than others.

There are certain factors which contribute to this effect. In one controlled study by the Journal of Medical Entomology, the bugs landed on people with blood Type O nearly twice as frequently as those with Type A. The researchers noted this has to do with secretions we produce, which tips mosquitoes off on a person’s blood type.

Entomology professor at the University of Florida, Jonathan F. Day said that more research needs to be conducted on mosquitoes’ potential preference for certain blood types over others. However, he agreed that mosquitoes do pick up on some cues we give off that make the bugs more likely to land on certain people.

“These cues let them know they are going to a blood source,” Day said. “Perhaps CO2 is the most important. The amount of CO2 you produce, like people with high metabolic rates ― genetic, other factors ― increases the amount of carbon dioxide you give off. The more you give off, the more attractive you are to these arthropods.”

The next question which pops up is what separates us from the nonliving entities that give off carbon dioxide, like cars? Mosquitoes look for primary cues in conjunction with what Day calls “secondary cues.”

Lactic acid — the stuff that causes our muscles to cramp during exercise — is one of those secondary cues, for example. Lactic acid is released through the skin, signaling to mosquitoes that we are a target, Day said.

Mosquitoes also have other qualities that help them pick up on secondary cues. “Mosquitoes have excellent vision, but they fly close to the ground to stay out of the wind,” Day said. “They are able to contrast you with the horizon, so how you’re dressed matters. If you have on dark clothes, you are going to attract more because you’ll stand out from the horizon, whereas those wearing light colors won’t as much.”

A mosquito also takes in “tactile cues” once it has landed on you.

“Body heat is a really important tactile cue,” Day said. “That comes into play with genetic differences or physiological differences. Some people tend to run a little warmer — when they land, they’re looking for a place where blood is close to the skin.” That means those whose temperatures are a little higher are more likely to get the bite.

Lifestyle or other health factors may also play a role, said Melissa Piliang, a dermatologist at Cleveland Clinic. “If body temperature is higher, you’re exercising and moving around a lot, or if you’re drinking alcohol, you are more attractive to mosquitoes,” Piliang said. “Being pregnant or being overweight also increases metabolic rate.”

Huff Post also said that one study showed that people who consumed just one can of beer were more at risk of attracting mosquitoes than those who didn’t. Of course, drinking outside is a popular summer and fall activity. “If you’ve been moving around all day doing yardwork and then you stop around dusk and drink a beer on your patio, you’re definitely at risk of bites,” Piliang said.

mosquitoes biting a person
Biology human body

Can body’s own immune system fight cancer?-turns out- YES!!

I was watching Netflix series- “Alexa & Katie” which is about the high school journey two best friends one of whom suffers from leukemia (blood cancer). Watching it really motivated me to find out more about the life threatening disease- cancer which kills many people every year.

While surfing I came across this article about a novel research that optimizes that our body’s own immune system can fight cancer.

Before jumping on to the article, first, let’s look at what is cancer?

Cancer is a disease in which some of the body’s cells grow uncontrollably and spread to other parts of the body. 

Cancer can start almost anywhere in the human body, which is made up of trillions of cells. Normally, human cells grow and multiply (through a process called cell division) to form new cells as the body needs them. When cells grow old or become damaged, they die, and new cells take their place.

Sometimes this orderly process breaks down, and abnormal or damaged cells grow and multiply when they shouldn’t. These cells may form tumors, which are lumps of tissue. Tumors can be cancerous.

Cancerous tumors spread into, or invade, nearby tissues and can travel to distant places in the body to form new tumors (a process called metastasis). Cancerous tumors may also be called malignant tumors. Many cancers form solid tumors, but cancers of the blood, such as leukemias, generally do not.

Armed with the basics of cancer let’s move on to the research article,

A groundbreaking study led by engineering and medical researchers at the University of Minnesota Twin Cities shows how engineered immune cells used in new cancer therapies can overcome physical barriers to allow a patient’s own immune system to fight tumors. The research could improve cancer therapies in the future for millions of people worldwide.

The research is published in Nature Communications, a peer-reviewed, open access, scientific journal published by Nature Research.

Instead of using chemicals or radiation, immunotherapy is a type of cancer treatment that helps the patient’s immune system fight cancer. T cells are a type of white blood cell that are of key importance to the immune system. Cytotoxic T cells are like soldiers who search out and destroy the targeted invader cells.

While there has been success in using immunotherapy for some types of cancer in the blood or blood-producing organs, a T cell’s job is much more difficult in solid tumors.

“The tumor is sort of like an obstacle course, and the T cell has to run the gauntlet to reach the cancer cells,” said Paolo Provenzano, the senior author of the study and a biomedical engineering associate professor in the University of Minnesota College of Science and Engineering. “These T cells get into tumors, but they just can’t move around well, and they can’t go where they need to go before they run out of gas and are exhausted.”

In this first-of-its-kind study, the researchers are working to engineer the T cells and develop engineering design criteria to mechanically optimize the cells or make them more “fit” to overcome the barriers. If these immune cells can recognize and get to the cancer cells, then they can destroy the tumor.

In a fibrous mass of a tumor, the stiffness of the tumor causes immune cells to slow down about two-fold — almost like they are running in quicksand.

“This study is our first publication where we have identified some structural and signaling elements where we can tune these T cells to make them more effective cancer fighters,” said Provenzano, a researcher in the University of Minnesota Masonic Cancer Center. “Every ‘obstacle course’ within a tumor is slightly different, but there are some similarities. After engineering these immune cells, we found that they moved through the tumor almost twice as fast no matter what obstacles were in their way.”

To engineer cytotoxic T cells, the authors used advanced gene editing technologies (also called genome editing) to change the DNA of the T cells so they are better able to overcome the tumor’s barriers. The ultimate goal is to slow down the cancer cells and speed up the engineered immune cells. The researchers are working to create cells that are good at overcoming different kinds of barriers. When these cells are mixed together, the goal is for groups of immune cells to overcome all the different types of barriers to reach the cancer cells.

Provenzano said the next steps are to continue studying the mechanical properties of the cells to better understand how the immune cells and cancer cells interact. The researchers are currently studying engineered immune cells in rodents and in the future are planning clinical trials in humans.

While initial research has been focused on pancreatic cancer, Provenzano said the techniques they are developing could be used on many types of cancers.

“Using a cell engineering approach to fight cancer is a relatively new field,” Provenzano said. “It allows for a very personalized approach with applications for a wide array of cancers. We feel we are expanding a new line of research to look at how our own bodies can fight cancer. This could have a big impact in the future.”

Honestly, let’s hope that this approach of treating cancer is able to save lives of millions of people affected with cancer

Biology Evolution human body

New microevolutinary change :Median artery in the human forearm

The median artery is the main vessel that supplies blood to the forearm and hand, when first formed in the mother’s womb, but it disappears once two arteries seen in adults develop.

The radial and ulnar arteries usually replace the median artery during developmental stages in the womb, so most adults obviously don’t have a median artery, but increasing numbers of cases retain it, so a person can have all three arteries.

The median artery is now present in about 35% of people and researchers predict that people born 80 years from now will all carry a median artery if the trend continues.

“The median artery offers benefits because it increases overall blood supply and can be used as a replacement in surgical procedures in other parts of the human body,” said senior author Professor Maciej Henneberg, a researcher in the Biological Anthropology and Comparative Anatomy Research Unit at the University of Adelaide and the Institute of Evolutionary Medicine at the University of Zurich.

“This is microevolution in modern humans and the median artery is a perfect example of how we’re still evolving because people born more recently have a higher prevalence of this artery when compared to humans from previous generations.”

In the study, Professor Henneberg and colleagues aimed to investigate the prevalence of persistent median arteries in postnatal humans over the last 250 years and to test the hypothesis that a secular trend of increase in its prevalence has occurred.

They found a total of 26 median arteries in 78 upper limbs (a prevalence rate of 33.3%) obtained from Australians aged 51 to 101 years.

“Our study into the prevalence of the artery over generations shows that modern humans are evolving at a faster rate than at any point in the past 250 years,” said lead author Dr. Teghan Lucas, a researcher in the Department of Archaeology at Flinders University and the School of Medical Sciences at the University of New South Wales.

“Since the 18th century, anatomists have been studying the prevalence of this artery in adults and our study shows it’s clearly increasing.”

“The prevalence was around 10% in people born in the mid-1880s compared to 30% in those born in the late 20th century, so that’s a significant increase in a fairly short period of time, when it comes to evolution.”

“This increase could have resulted from mutations of genes involved in median artery development or health problems in mothers during pregnancy, or both actually,” he added.

“If this trend continues, a majority of people will have median artery of the forearm by 2100.”

“When the median artery prevalence reaches 50% or more, it should not be considered as a variant, but as a normal human structure,” the authors said. al. find that the prevalence of the persistent median artery in postnatal life approximately tripled over the last 125 years.

Biology Covid-19 human body

Covid 19’s lingering problem : Heart damage

Massachusetts General Hospital pathologist James Stone can tell that most of the hearts he’s examined from COVID-19 patients are damaged from the first moment he holds them. They’re enlarged. They’re heavy. They’re uneven.

What he can’t tell—at least until he starts looking at samples of the tissue under a microscope—is exactly how those hearts were damaged, and whether it is a direct result of SARS-CoV-2 infection.

Early in the pandemic, other clinicians noted that even some patients who didn’t have preexisting heart conditions experienced cardiovascular damage while fighting COVID-19 infections, pointing to a possible causative link. Researchers had found, for example, that 8–12 percent of hospitalized COVID-19 patients had elevated levels of muscle contraction–regulating proteins called troponins—a sign of heart damage—and that these patients had an increased risk of mortality compared with those who didn’t have excess troponins. And early observations of patients in China who suffered reduced ejection fraction—the amount of blood getting pumped out of the heart each time it contracts—led researchers to suggest that these individuals were likely experiencing myocarditis, a severe form of inflammation that can weaken the heart and is commonly associated with infections.

But Stone and his collaborators’ analysis of heart tissue from 21 patients who died of COVID-19, published today (September 24) in the European Heart Journal, shows that while 86 percent of the patients did have inflammation in their hearts, only three had myocarditis. Several had other forms of heart injury, such as right ventricular strain injuries.

“The problem we identified in this study is that there’s other types of myocardial injury in these patients that is also causing elevated troponins,” says Stone. His international team sought to determine the mechanisms through which the disease damaged the heart and found that some conditions “really haven’t been talked about at all in the [COVID-19] papers that have previously been published.”

The pathologists observed a median of 20 slides from each heart, which is more than are included in most other studies regarding COVID-19’s cardiac effects. George Abela, a cardiologist at Michigan State University who was not involved in the study, tells The Scientist in an email, “This provides a more in-depth view of the extent of injury.”

The researchers expected to find some macrophages, a type of white blood cell that indicates inflammation, as pathologists had observed macrophages in the hearts of SARS patients during the 2003 outbreak. But Stone says he was surprised to see just how common these were—18 out of 21 COVID-19 patients’ hearts harbored macrophages that exhibited this type of inflammation. “It was really quite extensive,” he says.

As they analyzed the hearts further, the pathologists noted that only three patients had myocarditis, while four showed signs of heart injury due to right ventricular strain and another four had small blood clots in the vessels in the heart. It’s not clear why patients experience such inconsistent cardiac issues.

Abela says these findings have implications for treatment. For example, if the patient has right heart failure, a condition where the right side of a patient’s heart is not pumping enough blood to the lungs, a device that mechanically helps the heart pump blood might help, rather than drugs that target the inflammation or infection, which could be used to treat myocarditis.

Because so many of the hearts were infiltrated by macrophages, the researchers say that it may be difficult to discern who is experiencing myocarditis, which is characterized by different inflammatory cells—lymphocytes—while patients are alive. The two cell types would appear similar on tests that image the hearts of living patients. So, the team looked back at the patients’ medical records to see if they could find patterns in clinical tests that would reveal the type of heart damage when it still might be treatable. The three patients with myocarditis all had both troponin levels above 60 ng/mL and abnormal ECG readings while in the hospital. Only 15 percent of the patients without myocarditis had this combination.

The findings need to be replicated in larger groups of patients but could help doctors determine the best course of treatment for heart damage due to COVID-19, Stone says. The study is “giving the cardiologists and the ICU doctors that are taking care of these patients a roadmap of the changes that are going on in the heart.”

“Novel disease entities like SARS-CoV-2 reinforce the tremendous importance of continuing our efforts at continuing to facilitate autopsy evaluations,” says Allan Jaffe, a cardiologist at the Mayo Clinic, in an email. “This consortium of hospitals have added substantially to our knowledge of Covid disease.”


Ebola virus : A deadly havoc in people and not bats!!! Why???

The Ebola virus causes a devastating, often fatal, infectious disease in people. Within the past decade, Ebola has caused two large and difficult to control outbreaks, one of which recently ended in the Democratic Republic of the Congo.

When a virus brings serious disease to people, it means that humans are not good hosts for the virus. Viruses depend on a living host for their survival and have natural reservoirs — a hosting animal species in which a virus naturally lives and reproduces without causing disease. Bats are likely a natural reservoir for the Ebola virus, but little is known about how the virus evolves in bats.

Like most other RNA viruses, Ebola’s molecules are structured in a way that makes them more prone to genomic errors and mutations than other types of viruses. Because of this, Ebola and similar viruses have a remarkable ability to adapt to and replicate in new environments.

In the study, the research team, led by Alex Bukreyev, a UTMB virologist in the departments of pathology and microbiology and immunology, working with the team of Raul Andino, University of California, San Francisco, investigated how the Ebola virus adapts to both bat and human cells. They assessed changes in mutation rates and the structure of Ebola virus populations repeatedly in both bat and human cell lines using an ultra-deep genetic sequencing.

“We identified a number of meaningful differences in how the Ebola virus evolves when placed in a human cell line relative to a bat cell line,” Bukreyev said. “For instance, the RNA editing enzyme called ADAR within bat cells play a greater role in the replication and evolution of the Ebola virus than do such enzymes in human cells. We found that the envelope protein of Ebola virus undergoes a drastic increase in certain mutations within bat cells, but this was not found in human cells. This study identifies a novel mechanism by which Ebola virus is likely to evolve in bats.”

The study suggests that the Ebola virus and bats can live together harmoniously because of the bat cell’s ability to induce changes in the virus that make it less capable of harm. Bukreyev said that the study’s findings validate the ultra-deep genetic sequencing used in this study as a predictive tool that can identify viral mutations associated with more adaptive evolution. This technology can be very useful in studying, and perhaps shaping, the evolution of emerging viruses, like SARS-CoV-2, the virus responsible for COVID-19.


Biology human body

Can dual handedness boost your brain???

Only one percent of the global population is ambidextrous i.e., they have the ability to write with both the hands simultaneously. Leonardo da Vinci, Ben Franklin, Albert Einstein are some of the genius in history who are capable of writing with both their hands.

In India, there is an ambidextrous school where nearly 300 students are ambidextrous. They can write in high speed and utmost accuracy and most surprisingly they are able to write in six different languages like Hindi, English, Urdu, Sanskrit, Arabic and Roman.

But a question arises , ” Does Ambidextrousness improve the brain function and memory??”

Studies show that although teaching people to be ambidextrous is popular for centuries, this practice does not improve brain function, and it may even harm our neural development leading to dyslexia and dyscalculia, which are serious learning disabilities.

Research in Sweden found ambidextrous children to be at a greater risk for developmental conditions such as attention-deficit hyperactivity disorder. Another study revealed that these people performed worse than left or right-handers on a range of skills, especially in math, memory retrieval and logical reasoning. Also ambidextrous people are at a higher risk for schizophernia than the rest of the population (usually have the LRRTM1 gene which is linked with schizophrenia).

Biology human body

Gut microbes love a good workout

Exercise can have great effects on the trillions of microbes that live in our gut. Together the community of gut microbiome can weigh up to 2 kilograms (4.4 pounds).

Lucy Mailing, a nutritional scientist , performed a research on how exercise affects the gut microbiome at the University of Illinois Urbana-Champaign. The research showed that the microbes in active people made more short-chain fatty acids (SCFs) that are good for health. One of these was butyrate (BYOO-turayt). Studies have shown it can protect against certain cancers, fight inflammation and regulate genes that promote health. It may even enhance sleep. Our gut bacteria make such SCFAs from the fiber found in nuts, grains and many vegetables.

Riley Hughes studies nutritional biology at the University of California, Davis. She summarised research on exercise, diet and the microbiome in the January 2020 Frontiers in Nutrition. She says, “Multiple studies have found that exercise increases butyrate and other beneficial SCFAs. Athletes have more SCFAs in their gut than non-athletes.

Studies of how our gut and brain communicate are relatively new. But scientists have already discovered that childhood and adolescence are unique windows for recruiting these microbes. Regular exercise and a good diet during these early life stages create a healthy microbiome.

The final take home message remains the same : Exercise is good for you.

Biology human body

Bravo! the mystery resolved – “Brain clearing out the dead neurons”

In an average human body, tens of billions of cells die everyday. The dead and the dying cells must be quickly removed to prevent the development of inflammation, which could trigger the death of the neighbouring cells. Recently, the researchers at Yale School of Medicine have directly imaged the death of neurons in mice, as well as how the body clears them out afterwards.

Further down the line, these findings might even inform treatments for age-related brain decline and neurological disorders-once we know more about how brain clean-up is supposed to work, scientists can better diagnose what happens when something goes wrong.

The team focused on the “glial cells” responsible for doing the clean-up work in the brain, they used a technique called 2Phatal to target a single brain cell for apoptosis (cell death) in a mouse and then followed the route of glial cells using fluorescent markers.

Three types of glial cells – microglia, astrocytes, and NG2 cells – were shown to be involved in a highly coordinated cell removal process, which removed both the dead neuron and connecting pathways to the rest of the brain. The researchers observed one microglia engulf the neuron body and its main branches (dendrites), while astrocytes targeted smaller connecting dendrites for removal. They suspect NG2 may help prevent the dead cells debris from spreading.

The researchers also demonstrated that if one type of glial cell missed the dead neuron for whatever reason, other types of cells would take over their role in the waste removal process – suggesting some sort of communication is occuring between the glial cells.

Another interesting finding from the research was that older mouse brains were less efficient in clearing out dead neural cells, even though the garbage removal cells seemed to be just as aware that a dying cell was there.

New treatments might one day be developed that can take over this clearing process on the brains behalf – not just in elderly people, but also those who have suffered trauma to the head, for example.

Neurologist Elyiyemisis Damisah from Yale School of Medicine says, ” Cell death is very common in diseases of the brain. Understanding the process might yield insights on how to address cell death in an injured brain from head trauma to stroke and other conditions.”

For the first time scientists captured video of brain clearing out dead neuron