Category Archives: Biological Chemistry

What is N95? ——The knowledge about face masks

Facing the outbreak of the new coronavirus, all kinds of face masks were sold out in the blink of an eye. More and more people seem to start to realize the importance of face masks.  But, do face masks really work? and how they work?

The answer largely depends on what type of face mask you are wearing.

Classification of Face Masks

According to the design of the face masks, the general ranking of the protective ability is (high to low): N95 masks> surgical masks> ordinary medical masks> ordinary cotton masks. But in the case of the new coronavirus, the most effective type of face masks are medical-surgical masks and masks filtering 95% or more of non-oily particles, such as N95, KN95, DS2, FFP2, etc. At present, China’s medical face masks are mainly divided into three types: medical protective masks with the highest protection level, medical-surgical masks commonly used in invasive operating environments such as operating rooms, and ordinary disposable medical masks.

 

How Face Masks Work?

Usually, medical face masks are made of non-woven fabrics, and its raw materials are mainly Polypropylene. And polypropylene layers are arranged to form an SMS structure.

SMS structure makes face masks capable to block floating particles while allowing airflow in and out the face masks. In this structure, the key material that brings the virus filtering effect is a high density, electrostatic layer lies in the middle: melt-blown non-woven fabric. When small particles like viruses get close to the melt-blown nonwoven fabric, it will be immediately captured by the electrostatic field and adsorbed on the surface of the non-woven fabric, and therefore prevent the virus gets into the body.
Yicheng Zhu

Revolution of Orthopedic Surgery – Bioactive Glass Composite Pore-forming Strategy

The use of adhesives to replace traditional invasive internal fixation tools (such as steel plates and nails) will revolutionize orthopedic surgery. The ideal bone cement should be able to immediately fix the fracture site, while providing a space and microenvironment suitable for bone cell growth and promoting fracture healing.

Cyanoacrylate (commonly known as universal glue) is currently the only medical glue with excellent instant adhesive strength and biocompatibility, but its polymerization product is non-degradable and cannot support the growth of new bone tissue through the adhesive layer, which hinders Because of bone healing, it cannot yet be used as a bone cement.

Recently, with the support of the Ministry of Science and Technology, the National Natural Science Foundation of China, and the Chinese Academy of Sciences, Qiu Dong’s group at the has proposed a bioactive glass composite pore-forming strategy to help cyanoacrylate bonding Agents are used for internal fixation of fractures to promote fracture healing. Bioactive glass has excellent osteoconductivity, osteoinduction, and can promote the regeneration of bone tissue.

To prove that the bioactive pore‐forming adhesive is not only strong and instant bonded but also facilitates cell ingrowth and displays excellent bioactivity, they conducted bone‐fracture healing experiments. In the experiment, the bioactive pore‐forming adhesive (PSC1/PEG4/OCA5) was compared with commercial adhesive (OCA) and pore‐forming adhesive (PEG5/OCA5) by applying all to a circular bone piece which was fixed within freshly formed cranial fractures in a group of mice.

Figure 1. The scheme of a mouse cranial fracture with the craniotomy location (Source)

The stability of the circular bone piece and bone healing effect were evaluated at 12 weeks post‐operation. The ratio of bone volume (BV) within the circular gap over the total volume (TV) within the circular gap was quantified as shown in the figure 2 below. After 12 weeks, BV/TV of the PSC1/PEG4/OCA5 group was 0.76 ± 0.06, which was significantly higher than that of the PEG5/OCA5 group (0.47 ± 0.10), the OCA group (0.40 ± 0.06), and the group with no adhesive treatment (0.26 ± 0.05). These findings supported that the adhesive with pores for bone ingrowth was crucial for new bone formation.

Figure 2. quantitative analysis of new bone formation (Source)

ARS (Alizarin Red S) can detect calcium which is a characteristic evidence to bone‐like structures. As shown in Figure 3, the Ca content in the bioactive pore‐forming adhesive (OD = 0.084 ± 0.008) was around two-fold higher than those in the merely pore‐forming adhesive (OD = 0.046 ± 0.004) and CA adhesive (OD = 0.041 ± 0.001). As a result, these findings were consistent with the statement that the PSC BG can promote osteogenic differentiation that is of importance for bone regeneration.

Figure 3. The optical density of eluents from ARS‐stained adhesives (Source)

The bioactive bone cement has good clinical transformation prospects and can provide new ideas and methods for clinical fracture treatment. At the same time, the above-mentioned composite pore-forming strategy can also be used for substances other than bioactive glass to increase matrix materials and functions. Material compatibility.

 

-Xinyue Yang

Posted on Mar.2nd, 2020

Deep Brain Stimulation on Patients with Parkinson Disease

Deep Brain Stimulation (DBS) is a form of neurological stimulation and is used as a form of treatment for those suffering from Parkinson’s Diesease (PD). PD is a neurodegenerative brain disorder which hinders dopaminergic neurons, resulting in impaired mobility. DBS involves a surgical process of implanting a small battery operated device and a electrodes into the brain.

Figure 1 – Deep Brain Stimulation Retrieved from – GAPS

This study published in August 2006 highlights the efficacy of DBS. 156 patients were randomly paired (78 pairs) and were subjected to different treatments. One was subjected to treatment from pharmaceuticals and the other underwent DBS. To test the efficacy of DBS, the patients’ quality of life was assessed using the Parkinson’s Disease Questionaire (PDQ-39). Additionally, numerous symptoms associated with PD were measured using the Unified Parkinson’s Disease Rating Scale, part III (UPDRS-III).

Efficacy of DBS

Out of the 78 pairs of patients, the patient who underwent DBS in 50 of the pairs saw an improvement in their PDQ-39 and UPDRS-III scores compared to their partner who was only provided with pharmaceutical drugs.

Figure 2 – How DBS and Pharmaceuticals affected the PDQ-39 and UPDRS-III scores in patients immediately after treatment. In 50 of the 78 pairs, those who underwent DBS showed improvement in their scores compared to their partners who took medication. Data from Deuschl et al.

Furthermore, the patients were assessed again in six months. Those who underwent DBS saw a 25% increase (a lower score) to their PDQ-39 score, while there we no significant changes to those who took medication.

Figure 3 – PDQ-39 Scores immediately after treatment (baseline), and 6 months after treatment. Error Bars represent standard deviation. Data adapted from Table 3 of Deuschl et al.

Benefit of DBS Compared to Medication on Treating Depression

There are additional benefits of DBS on other aspects of PD. This study published in March of 2005 highlights how DBS is able to treat depression, which is a symptom associated with PD. Patients who were treated by DBS noted a decrease in depression-like symptoms 1 month after treatment, and up to 1 year. In contrast, medication can only treat depression in the short-term.

Figure 4 – A visual interpretation of depression Retrieved from – ConsumerReport

So why is DBS better than Prescription Medication?

The results of both studies indicate that DBS is capable to treating PD with a higher efficacy compared to medication. Additionally, medication is kept constant and can be used to treat one specific issue. In contrast, the strength of DBS can be altered (stronger/weaker pulses) to treat different symptoms that may arise. Consequently, DBS results in long-term benefits, while medication is only able to provide short-term benefits.

-Jackson Kuan

Re-wiring Your Brain For Sugar Craving

Have you ever wondered why we have desires for sweet food but not bitter food? Dr. Li Wang and other scientists at Columbia University have discovered that mammalian brains for tasting can be re-patterned or erased by performing a series of experiments on mice. This study has significance for future studies in eating disorders and weight management.

The taste sensory system 

Mammalians have a developed sensory system for identifying tastes and associating tastes with mechanisms of reward and aversion. This sensory system has two main parts: the tongue and the brain. There are many sensory neurons in our tongues. These sensory neurons, the detectors of the five basic tastes (sweet, sour, salty, bitter and umami), signal our brains and turn on the amygdala of the brains responsible for identifying and interpreting tastes. Dr. Li Wang and her team have confirmed that neurons in the sweet-responsive cortex project to a different area compared to those in the bitter-responsive cortex. The strong segregation of neuron projection transmits desirable, or aversive taste signals, as shown in Figures 1 and 2. Therefore, we cannot stop eating sweets since our amygdala associate sweets with appetitive, desirable signals.

Figure 1. b and c show the active bitter taste cortex and active sweet taste cortex respectively. Source: “Nature Journal”

 

Figure 2. Licks per second (Licks rate) of mice upon photostimulation of the sweet and bitter cortexes. Adapted from “Nature Journal

Rewiring the brain on taste

Dr. Wang and her team rewound the brain of mice on taste by using a drug to silence the neurons in the sweet-responsive cortex and the bitter-responsive cortex, respectively. The team used licks per second to quantify and verify the appetitive and aversive responses of the mice upon photo-stimulating the sweet and bitter cortexes independently. The team found out that by silencing the neurons in the sweet cortex, the lick rate decreased, according to Figure3. This showed that the mice could not recognize sweet when the neurons were silenced by the drug. This confirmed that the taste specific neurons are essential to recognize tastes.

Figure 3 also showed another interesting phenomenon that the team made the animals think they were tasting sweet, even when the animal was drinking water. In Figure3, without the presence of the sweet neuron silencer, the lick rate of the mice with their sweet cortex stimulated was two times higher compared to the mice without the stimulation. The increase in the lick rate in Figure 3. showed that neurons in the amygdala control an animal’s sensory perception of taste.

Figure 3. Photostimulated sweet cortex in the presence or absence of sweet neuron inhibitor. Adapted from “Nature Journal”

The finding that animals’ brains can be manipulated and rewound to change the perceptions of taste has implications in future studies in weight management and eating disorders. By using small drugs to target these taste-specific neurons, we may say no for eating more and more sweets.

Reference

Li Wang. The coding of valence and identity in the mammalian taste system. Nature Journal, 2018; 558, 127-131. DOI: https://www.nature.com/articles/s41586-018-0165-4

Pricia

2020-03-02

 

Don’t Let Stress Get The Best of You

You may have heard of the saying, “diamonds are made under pressure”, especially from people working last-minute to meet deadlines. However, a study found that the stress accompanying our seemingly never-ending tasks actually decreases our ability to produce high-quality work, or to perform well on exams.

The study showed that upon chronic stress, neurons shrink in the hippocampus, which is the region in the brain that controls our memory; this equates to a weaker memory. Furthermore, neurons end up growing in the amygdala, which is the region in the brain that reinforces our fears; this translates to an increase in anxiety levels.

Figure 1. Chronic stress promotes the growth of neurons in the amygdala (a), and leads to the shrinkage of neurons in the hippocampus (b). Created by Athena Wang. Adapted from Davidson and McEwen (2012).

Therefore, instead of studying a week before exams when stress levels are the highest, you should space out your studying throughout the semester to retain as much information as possible while also being more calm.

ACUTE VS. CHRONIC STRESS

A bit of stress can be good for us; acute stress triggers our fight-or-flight response, and helps us overcome short-term stressors. However, chronic stress weakens our immune system, and leads to even more troubles, such as mental health and cardiovascular problems. Therefore, stress should be dealt with before it escalates.

WAYS TO RELIEVE STRESS

Good time-management skills are important, so that you don’t end up with a plethora of assignments due at the same time. Designate and follow the allotted times for your tasks, and hopefully having a better control over your time will decrease stress.

Another way is to practice mindfulness. This type of meditation makes you embrace your current situation and not dwell on unnecessary worries, which then allows you to feel less stressed. Lastly, incorporate enjoyable activities in your schedule to improve your mood and help you relax.

The next time you’re feeling stressed out, don’t let it get the best of you. Take a deep breath, and remember that you’ve got this!

Any additional tips? I would love to hear your thoughts in the comments below.

-Athena Wang

Stress and Grey Hair: An Answer to a Biological Mystery

Everyone has heard that too much stress will cause grey hair. This is easily seen in former president of the United States, Barack Obama, whose hair could not escape the stress of the Oval Office! But what exactly links grey hair and stress? This year, researchers at Harvard University found that the nervous system eliminates pigment-regenerating stem cells responsible for coloring our hair!

Barack Obama’s hair color at the start of his presidency versus seven years after. Credits: DailyMail.com

the root of the problem

When you are stressed, your body responds in three distinct ways: the activation of your immune system, the activation of your sympathetic nervous system (SNS), and the release of cortisol, an energy-stimulating hormone. All these responses put your body into a “fight or flight” mode; increasing heart rate and blood pressure. The challenge for Zhang’s team was to sort through these three responses and determine which caused grey hair.

Zhang’s team tackled this problem by performing a series of experiments on black-furred mice. They first tested if immune system activation was the cause by seeing if the fur greyed under stress, even when the immune system was deactivated. They indeed found that stressed immune-deficient mice still greyed, indicating that stress causes greying, independent of an immune response.

They also ran similar experiments using mice mutated to not respond to cortisol or noradrenaline, a molecule involved in SNS activation. The idea being that if  a response was involved, stress should not cause the fur to grey if it was removed. In mice lacking response to cortisol, the fur still greyed; however, in mice lacking the response to noradrenaline, their fur remained black! This indicated that the SNS was the main driver in hair greying.

Figure 1. The results of the experiments described above are shown. Note that mice unable to respond to SNS activation do not grey under stress. “Control” refers to unmutated mice. Also note that a different type of control (non-stressed vs stressed) was ran in the immune-deficient case. (Sample size = 6 for each condition, standard error bars). Credits: Adapted from Zhang et al.’s data.

Zooming in further…

With the culprit in hand, Zhang’s team didn’t just stop there! Through further experimentation, they illustrated that the SNS over-stimulates MeSC, the stem cells involved with hair pigmentation. During hair growth, these MeSC cells transform into pigment-producing cells and color the hair. Under stress, the SNS causes these MeSC cells to transform at an abnormally high rate, quickly depleting these cells and leading to grey hair.

The reason behind this link?

In truth, the reason why this MeSC and SNS interaction exists is unclear. Zhang’s team suggests an evolutionary perspective. Since octopuses, a distant relative to mice and humans, can modify pigmentation of their skin using the SNS, they hypothesize that this interaction was simply conserved. Whatever the reasons may be, this just further shows that the mystery has yet to be completely solved!

-Kenny Lin

Antibiotics found to kill bacteria in a new way!

 

Fig1.Antibiotics source

Antibiotic is the most powerful “weapon” to fight against bacterial infections. However, according to the World Health Organization, there are more than 700000 people die every year due to antibiotic resistance. On Feb 13th, 2020, Research team from the David Braley center for Antibiotic Discovery, University of McMaster posted an article on nature. Newly found corbomycin and complestatin would kill bacteria in a brand-new way. The discovery of these new groups of antibiotics would be the clinical candidate in the fight against antimicrobial resistance.

Fig2,Antibiotic resistance strategies in bacteria. source:Courtesy of E. Gullberg.

 

Antibiotics are the revolution of the pharmaceutical study in the 20th century. They are the most important type of antibacterial agent which either kills or inhibit the growth of bacterial cell walls. Alexander Fleming discovered modern antibiotic medicine – penicillin in 1928, which saved thousands of people’s life.

What does old antibiotics also bring you?

The enormous benefits of antibiotics also lead to new problems such as over-usage and resistance. Bacteria soon formed resistance toward these antibiotics and caused the ineffectiveness of the medicine. The resistance of antibiotics had become a new-rise problem. The World Health Organization announced: “serious threat is no longer a prediction for the future, it is happening right now in every region of the world and has the potential to affect anyone.”

Fig2.image of corbomycin

Fig2.image of corbomycin. source

The newly found corbomycin and complestatin have brand new way to attack bacteria. It is discovered from a glycopeptide family, and the new approach appears no significant resistance toward bacteria. “Antibiotics like penicillin kill bacteria by preventing the building of the wall, but the antibiotics that we found actually work by doing the opposite – they prevent the wall form being broken down. This is critical for cell to divide.” Said Beth Culp, a PhD candidate in biochemistry at McMaster.

Why do we know about these?

“We hypothesized that if the genes that made these antibiotics were different, maybe the way they killed the bacteria was also different”, Culp explained. The “unique approach” to kill bacteria is a new mechanism that is worthy of studying. Scientists might be able to find the new family of antibiotics which have a completely different way to attack bacteria. These new antibiotics will be the revolution of modern biochemistry which will be powerful to fight against antibiotic-resistant.

 

Scientists believed that the observation of corbomycin and complestatin would open the “new door” in the field of antibiotics. People will be able to investigate more antiobiotics to fight against resistance in the glycopeptide family. This study will eventually benefit thousands of people suffering in antibiotic-resistant and give them hope to survive!

–Vicky Gu

 

Revised: Should you be worried?—An Outbreak of Novel Coronavirus!

Since December 2019, an unexplained pneumonia epidemic has occurred in Wuhan City, Hubei Province, China. An investigation found that these were related to Wuhan’s “South China Seafood Market”. Wuhan organized a multi-disciplinary expert consultation survey and used laboratory testing to identify pneumonia in Wuhan as viral pneumonia. On January 8, 2020, a new coronavirus was initially identified as the pathogen of the epidemic. With the outbreak of this novel coronavirus, it is crucial to know how this virus spread and evolved, more importantly, how we can take precautions against it.

The spread of the novel Coronavirus

Sources: National Health Commission of the People’s Republic of China; local governments. Note: Data as of 9 p.m E.T., Jan. 27

The outbreak of this infectious disease was first occured in Wuhan in December, 2019 and then spreaded globally since the huge flow og people in Wuhan during lunar new year. According to the New York Timesthere are more than 4,500 people in Asia infected the coronavirus as well as many other are suspected. At least 106 people have died as of Jan. 27, 20.

Evolutionary sources of coronavirus  and molecular pathways for infecting humans

To analyze the evolutionary source and possible natural host of the novel coronavirus, the researchers in this paper analyzed genetic evolution by comparing the novel coronavirus with collected large amount of coronavirus data. It was found that the novel coronavirus of Wuhan belongs to Betacoronavirus which is a RNA virus that parasitizes and infects higher animals (including humans). It is adjacent to the SARS virus and the SARS-like virus group in the position of the evolutionary tree. Therefore, Wuhan coronavirus and SARS or SARS-like coronavirus may share common ancestor. As the evolutionary neighbors and outgroups of Wuhan coronavirus have been found in various types of bats, it is speculated that the natural host of Wuhan coronavirus may also be bats and Wuhan coronavirus is likely to have unknown intermediate host vectors during the transmission from bat to human.

Phylogenetic tree (Source)

The authors used molecular computational simulation methods to perform structural docking studies on Wuhan coronavirus S-protein and human ACE2 protein, and found that although 4 of the 5 key amino acids that bind to ACE2 protein in Wuhan coronavirus S-protein have changed, the amino acids after the change have perfectly maintained the interaction between SARS virus S-protein and ACE2 protein. This result indicates that Wuhan coronavirus infects human respiratory epithelial cells through the molecular mechanism of S-protein interaction with human ACE2 protein, predicitng that Wuhan coronavirus has strong ability to infect humans.

Cα RMSD of 1.45 Å on the RBD domain compared to the SARS-CoV S-protein structure (Source)

Tips for prevention of coronavirus (source):

  • Wash your hands with soap for at least 20 seconds and avoid touching you mouth, nose and eyes with unwashed hands.
  • Keep a safe distance with people who are sick
  • Cover your cough or sneeze with tissue and throw the tissue in the trash
  • Clean frequently touched surfaces

-Xinyue Yang

Posted on Jan. 27th. 2020

Revised: Is Your Headache “Normal”?

If you experience a sudden and severe headache, be careful! It could be an intracranial aneurysm. An intracranial aneurysm is the ballooning of a weakened blood vessel in the brain, which causes an intense headache upon rupturing. In 2011, a study suggested that nonsteroidal anti-inflammatory drugs (NSAIDs) may be an alternative to surgical repair, which is currently the only treatment for aneurysms.

Unruptured aneurysm (left) vs. Ruptured aneurysm (right)
(Credit: Mayo Clinic)

How can NSAIDs help combat aneurysms?

Inflammation is a major problem for intracranial aneurysms, as it can lead to their growth and rupture – but there is a solution! NSAIDs reduce inflammation by inhibiting the enzymes that promote inflammation and enlarge intracranial aneurysms. The study tested NSAIDs in mice and found decreased formation of intracranial aneurysms in the mice. 

Risks associated with NSAIDs and surgical repair

Although this treatment seems promising, long-term use of NSAIDs may lead to cardiovascular and gastrointestinal side effects. There are two surgical options to treating aneurysms: endovascular coiling and clipping. A major risk for coiling is that it may develop vasospasm, which occurs when the vessel constricts and leads to tissue death; whereas clipping increases the risk of infection and death, as it is an open surgery.

Two surgical procedures: Coiling an unruptured aneurysm (left) vs. Clipping a ruptured aneurysm (right)
(Created by Athena Wang)

Lifestyle changes to prevent rupture

With around 3% of the population having unruptured aneurysms, it is beneficial to know what lifestyle changes can prevent these ruptures. Eating a healthier diet, exercising regularly, and avoiding recreational drugs can all decrease risk factors that trigger ruptured aneurysms.

How is this headache different from a “normal” one?

Normal headaches such as those caused by tension or migraines is less intense than that of an aneurysm, which is described as a thunderclap headache. More importantly, this headache may be accompanied by a stiff neck, vomit, or even a loss of consciousness.

So, the next time you feel like you’re having the worst headache of your life, seek help fast – it could be an aneurysm!

-Athena Wang

Revised: Embarassed of Asian Glow? Don’t Worry, The Future is Promising

Ever find yourself beet red after one small drink? You’re not alone! Over one-third of East Asians and eight percent of the world population experience this awkward phenomenon; however, a solution is in the works. Just last month, researchers from Weill Cornell Medical College have solved this problem by experimenting with targeted gene therapy on mice.

What does asian glow look like? A before and after comparison. (Credits: Wikimedia Commons)

The Dangers of Asian Glow

Apart from causing embarrassment, asian glow comes with more serious consequences than just flushing red. The red glow is caused by a deficiency in the ALDH2 enzyme, a key component in detoxifying alcohol. When you drink alcohol, your body converts the alcohol into acetaldehyde. Normally, acetaldehyde is further converted to a safer compound by ALDH2; however in individuals with asian glow, ALDH2 does not function, causing acetaldehyde to build up. Since acetaldehyde is a cancer-causing agent, its accumulation drastically increases the risk of developing esophageal cancer by six to ten folds.

Conversion of alcohol to acetate is stopped in people with asian glow. This leads to toxic buildup of acetaldehyde. (Credits: Me – created with Notability)

A Glowing Solution…

Matsumura’s team reasoned if a lack of ALDH2 enzyme was the problem, maybe they could simply add it back in.

“We hypothesized that a one-time administration of a […] virus […] expressing the human ALDH2 coding sequence […] would correct the deficiency”

They tested their idea on three strains of mice: mice with functional ALDH2, mice lacking ALDH2, and mice with a non-functional version of ALDH2. The latter two simulated the asian flush syndrome seen in humans. After introducing all the mice with the ALDH2 gene and feeding them alcohol, the researchers carefully monitored acetaldehyde levels in the blood.

Their hard-work paid off! In the two strains deficient for ALDH2 function, acetaldehyde levels and abnormal behavior associated with alcohol consumption were back to near-normal levels. Furthermore, they found that one dose was enough to confer persistent and long-term protection.

From Mice to Humans: A Complicated Decision

Matsumura’s team emphasize that a long-lasting treatment for ALDH2 deficiency currently does not exist. Although making the jump from mice to humans will be challenging, they assure that virus-mediated gene therapy shows the most promise in becoming an effective therapy. The million-dollar question is whether the risks of the glow outweigh the benefits of reduced alcohol consumption seen in affected individuals. To this Matsumura’s team say:

“the overall burden […] on human health, particularly […] cancer, supports […] gene therapy.”

What do you think?

-Kenny Lin