Too Hot, Too Cold, Too Old: The dying phone battery
Too Hot, Too Cold, Too Old: The dying phone battery
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You hiked for an hour in the cold to reach the top of the hill, which is covered in fresh and crisp snow, and the sun is making everything glitter. You take out your phone to capture the aesthetic view, only for it to die on you when you need it the most! Not just that, the phone battery also drains faster if you hike on a hot summer afternoon. Like us, phones also hate extreme temperatures and age with time.
Batteries are energy storage devices for electricity. When you charge a battery, it converts the electricity into chemical energy and stores it until you need it. All batteries, whether used in remotes, mobile phones, or electric cars, have the same construction. They have two electrodes (named anode and cathode) and an electrolyte in between.
Phones use Lithium-ion batteries that have graphite (anode) and Lithium-cobalt-oxide (cathode) as the electrodes and a Lithium salt in organic solvent as the electrolyte. It also has a porous plastic material to prevent short circuits between the two electrodes and protect it from thermal runaway (like the phone catching on fire). In a fully charged state, lithium ions are concentrated at the graphite anode by intercalating into the graphite structure. During phone use, they migrate from the anode to the cathode through the electrolyte, while the electrons move through the electronic circuit and power the phone. When the phone is plugged in, the lithium ions migrate back from the cathode to the graphite anode, restoring the charged state. Although the main chemical reaction recharges the phone battery, other side reactions physically damage the battery. The Lithium ion, instead of intercalating in the graphite, sometimes gets deposited on the surface of the graphite anode. This creates an irreversible layer of Lithium atoms on the anode (lithium plating). Over time, charging-discharging cycles create a thick layer that permanently consumes the Lithium atoms, thus reducing the battery's performance. The electrolyte also breaks down and gets deposited over the graphite layer, increasing the battery’s resistance.
At cold temperatures, the organic solvent in the electrolyte becomes more viscous, slowing down the movement of the Lithium ions and the electrons. This increases the resistance of the phone battery, and it does not read the voltage (charge percentage) accurately. This causes the phone to slow down or die on the spot, but it recovers as soon as it is put in a warm pocket. When the phone heats up during use, charging, or on a hot summer afternoon, the rate of all chemical reactions increases, discharging the battery quickly. The unwanted reactions, like breaking down the electrolyte, also increase damaging the battery irreversibly.
Lithium-ion batteries are not just used in phones, but also in electric vehicles. Unlike phones, the performance of vehicles is not drastically affected by driving in extreme temperatures. This is due to the inbuilt battery thermal management system (BTMS) that regulates the temperature in the proximity of the battery. Since phones are not equipped with such systems, you can feel the dramatic effect of temperature.
Unfortunately, modern phone batteries are glued to the phone. When the battery gets old and its performance degrades, the entire phone needs to be replaced. However, this is not the end, and we can look forward to improvements in battery technology that can be lighter, longer-lasting, and cheaper to manufacture. Until technology catches up, rely only on your eyes and mind to capture the glittering snow, and not on the cold phone.
Cortisol: Built for predators, stuck with deadlines
Often referred to as the ‘stress hormone’, cortisol has other roles to play. It is responsible for waking you up in the morning, regulating metabolism and blood pressure, and keeping you alert. Cortisol follows a 24h cycle, peaking and dipping throughout the day. Its level starts rising in the early morning (around 2-3 am) and peaks in the morning to wake you up. It gradually decreases during the day and reaches the lowest level at midnight, when your body relaxes into sleep. A slight increase in cortisol level can affect these peaks and dips. During periods of stress, this early morning slow rise of cortisol is enough to wake you up. This is why sleep feels fragile during times of stress. You wake up around 3 a.m. and can’t get back to sleep. All because of the cortisol that is trying to get you ready for the day.
During any ‘external threat’ (being attacked by a lion, going down on a roller coaster, or seeing a work email on a weekend marked ‘urgent’), the brain fires up signals in two phases, 1) the fast neuronal signal that takes seconds, and 2) the slower hormonal signal that takes a few minutes. Both signals reach the adrenal gland and produce two hormones- adrenaline (fast) and cortisol (slow). Adrenaline causes the immediate ‘fight-or-flight’ response, increasing the heart rate and sweating. Cortisol that is released in minutes maintains the high energy level. It temporarily slows down non-essential functions like digestion, growth, immune response and reproduction. It prioritizes supplying energy over storing it. It releases stored glucose and increases blood sugar level, so that the brain and muscles have enough energy to deal with the ‘external threat’.
Once the threat passes, cortisol does not get cleared away immediately. The half-life of cortisol (the time in which cortisol levels to reduce by half) is around 60-90 minutes, taking time for the levels to return to normal. This is why you feel alert and unsettled after a stressful event has passed. After reaching the normal level, the organs and systems affected by the increased cortisol revert to their regular functioning.
Cortisol is an important hormone evolved to protect against natural threats like running away from predators or falling off cliffs. However, modern-day stress has a slow-burning effect and never seems to go away. Continuous stress from work, financial worries, unexpected life-changing events, or the news keeps your body in a state of ‘threat’. This creates a continuous increase in cortisol, leading to sleep disruption, indigestion, a compromised immune system, and brain fog. Over time, chronic stress and high cortisol often lead to anxiety, heart disease, and depression.
The functioning of cortisol hasn’t changed in thousands of years, but the world that we live in has changed. Although you don’t have an apex predator chasing you down the road, you do have worries about job security or loans. Stress throws the cortisol clock out of sync, leaving you tired and feeling miserable. Simple lifestyle changes like regular exercise, prioritizing good sleep, and limiting artificial light can reduce the ‘stress’ signal and keep excess cortisol in check.
The Rise of Superbugs: Understanding Antibiotic Resistance
The Rise of Superbugs: Understanding Antibiotic Resistance
Penicillin was discovered in 1928 as a drug that kills bacteria. It took years of research before it could be mass-produced and made commercially available by 1945. Penicillin revolutionized the field of medicine and saved lives by killing the root cause of infectious diseases such as scarlet fever, pneumonia, syphilis, and other infections resulting from open wounds. Modifications to the chemical structure of penicillin led to the development of a class of penicillin-type antibiotics that are more effective against a wider range of infectious bacterial species. It has been less than a century since the discovery of penicillin, and now we see bacteria evolving to be resistant to antibiotics.
How do antibiotics work?
Bacteria are unicellular organisms. In most cases, bacteria survive in colonies where they exchange information via chemical signals. Antibiotics attack the parts or the functions of the bacteria that are responsible for their survival.
Disrupting cell walls: Some bacteria have cell walls that protect them against physical stress. Drugs like penicillin disrupt the cell walls and prevent their rebuilding. This causes the bacteria to swell up and ultimately burst. However, not all bacteria have a cell wall and they remain resistant to penicillin. It is important to know the kind of bacterial infection before treatment with penicillin.
Blocking essential functions: All living cells, including bacteria, have cellular machinery that produces and recycles complex molecules like proteins and nucleic acids. A certain class of antibiotics blocks the bacterial cell from performing these essential functions by binding to the machinery. Bacteria develop resistance to these antibiotics by actively pumping drugs out, producing chemicals that attack the drug itself, or changing the working of their machinery.
Leaking cellular content: Cell membranes are made of lipid bilayers that keep the aqueous interior of the bacterial cells from leaking out. Some antibiotics act like detergents, damaging the cell membrane. The bacteria rapidly lose important ions and molecules, leading to their death. Such antibiotics cause physical damage to the cell membrane. It is difficult to develop resistance to these antibiotics as it would require the bacteria to rebuild the entire cell membrane. Although this class of antibiotics is the last resort against antibiotic-resistant bacteria, some of these drugs are known to cause kidney problems.
Why is antibiotic resistance a global threat?
Antibiotic resistance is a result of evolution and natural selection. In all living systems, random mutations occur regularly. Some of these mutations have an advantage and function better than others in surviving. These mutations get passed on to further generations. Bacteria in large colonies also undergo similar mutations. Some of these mutations help them survive against antibiotics. Since bacteria have a short lifecycle, these mutations occur and are passed on very quickly to new generations, giving rise to "superbugs" that are resistant to almost all antibiotics. Bacteria also have a unique way of sharing pieces of genetic information with other members of the colonies. Consequently, the existing bacteria also develop resistance.
Misuse of antibiotics without identifying the causative bacteria, not completing the full antibiotic dose, and overuse of antibiotics in agriculture and livestock are major reasons leading to antibiotic resistance. Bacterial infections spread easily from one place to another via air, water, the food supply chain, and human travel. Antibiotic resistance is particularly problematic as it cannot be contained in one area and is a rising global concern.
Do we have an escape plan?
The rapid rise of antibiotic resistance is a race against time. Without new technology, we risk returning to a pre-penicillin world, where even minor cuts could result in deadly infections. Greater awareness is needed across hospitals, pharmacies, and educational institutions to ensure antibiotics are prescribed at the appropriate dose and duration, and only when clinically justified. Regulatory reforms are needed in countries where antibiotics are available over the counter, often at low doses. Without proper identification of the bacterial strain, such low doses risk prolonging illness and worsening its severity. Meanwhile, alternatives such as bacteriophages, which selectively destroy bacteria without harming human cells, and membrane-disrupting peptides are emerging as promising solutions.
All these approaches cannot eliminate the occurrence of antibacterial resistance, which is a natural process. We just need to slow the spread long enough for science to develop the next generation of treatments.
Is Your Thyroid Calling for Attention?
Feeling low, tired, and noticing sudden weight gain? Chances are, it’s not your lifestyle, but your body’s biology that needs attention!
The thyroid is a small, butterfly-shaped gland in the neck above the collarbone that plays a major role in metabolism and mood regulation. It produces two hormones, triiodothyronine and thyroxine, commonly known as T3 and T4. (Yes, these are the ones reported in blood work.) The numbers 3 and 4 refer to the number of iodine atoms in each hormone. That’s why iodine is important for healthy thyroid function. The thyroid produces almost 20 times more T4 than T3. T4 is converted into T3 inside tissues. The amount of T4 and T3 in the bloodstream signals the pituitary gland in the brain to produce thyroid-stimulating hormone (TSH, also reported in blood work). TSH tells the thyroid how much T4 and T3 to produce. This forms a feedback loop between the pituitary and thyroid glands to control T3 and T4 levels in the body.
In certain cases, malnutrition, hormonal imbalance, and inflammation affect the feedback loop between the pituitary and thyroid. The thyroid gland produces either too much or too little of the T3/T4 hormones. Low T3/T4 level (called hypothyroidism) causes an increase in TSH and slows down metabolism, causing sudden weight increase and tiredness. Other symptoms include dull skin, hair fall, irregular menstrual cycle, mood changes, sensitivity to cold, and constipation. To test hypothyroidism, the hormone levels of T3/T4 and TSH are measured. Once confirmed, the patient is prescribed an appropriate dose of synthetic T4 hormones (levothyroxine) to compensate for the lack of natural T4 in the body. This brings back the feedback loop in the normal range, and the symptoms of hypothyroidism disappear.
In the opposite case of overproduction of T3/T4 by the thyroid gland, called hyperthyroidism, the body’s metabolism increases, causing the patient to lose a lot of weight, experience anxiety, insomnia, and heat intolerance. The excess T3/T4 production causes the pituitary gland to decrease TSH, which shows up in the blood work. To bring back the feedback loop to normal, the patients of hyperthyroidism are prescribed Methimazole, which blocks the production of T3/T4 hormones by the thyroid gland.
Thyroid function is also affected by autoimmune conditions such as Hashimoto’s and Grave’s disease. Hashimoto’s is a common cause of hypothyroidism in people with sufficient iodine intake. In this condition, the body produces antibodies (Anti-thyroid peroxidase (Anti-TPO) and/or Anti-thyroglobulin) that attack the thyroid gland, thus decreasing the production of T3/T4 hormones and increasing TSH. Hashimoto’s is confirmed by blood work showing the presence of the Anti-TPO antibodies in the blood. It is not a life-threatening condition and can be easily managed with levothyroxine medication.
In Graves’ disease, the immune system produces antibodies against the thyroid gland, such that it does not recognize the TSH that is secreted by the pituitary gland. This causes an overproduction of T3/T4, leading to a decrease in TSH and causing hyperthyroidism. Graves’ disease is confirmed by the presence of TRAb and TSI antibodies, which affect the TSH sensitivity of the thyroid gland. Grave’s disease can be managed by taking Methimazole in a proper dose, which stops the production of T3/T4 by the thyroid gland.
The thyroid gland may be small, but it plays a major role in keeping the body functioning. Thyroid issues related to it remain one of the most underdiagnosed issues, with women at a high risk of developing thyroid issues throughout their lifetime. The good news? Once diagnosed, most thyroid problems can be managed with proper medication. If you experience symptoms like tiredness, sleep problems, or unexplained weight changes, do not dismiss them as age or stress related. See your doctor and get your bloodwork done- your body might be calling for attention and proper care.
Spatial omics: The (W)hole in one
Spatial omics profiles biomolecules by their location in tissue. This spatial data reveals new insights into intercellular interactions and signaling. In the last decade, spatial omics has become popular with disease researchers and has enabled many commercial brands. Three main analytical techniques offer varied biomolecular coverage and spatial resolution: Next Gen Sequencing (NGS), microscopic imaging, and mass spectrometry.
The NGS methods can spatially map the transcriptome (RNA expression) on a tissue sample. The RNAs from the tissue conjugate to complementary DNA fragments on a slide that act as spatial barcodes. The spatially barcoded RNAs are then amplified and sequenced. During the data analysis, the whole transcriptome can be mapped back to specific regions of the tissue using the barcodes. With new advancements, NGS-based transcriptomics can be combined with proteomics and epigenomics (DNA and histone modifications) to study mechanisms of health and disease.
The microscopy-based omics methods use fluorescence signals from targeted biomolecules as a readout of their quantity and spatial coordinates. The biomolecules of interest (RNAs or proteins) are sequentially imaged using fluorescence in situ hybridization (FISH). For transcriptomics, DNA strands labelled with a fluorophore are introduced into the sample. They bind to their complementary RNAs only, which are imaged using a fluorescence microscope. Before continuing with the next round of imaging, the previous fluorophores must be removed to avoid false readings. This is achieved by either photobleaching the fluorophores or stripping away the fluorophore-labelled DNA. For proteomics, proteins are immunolabelled with antibodies. The secondary antibodies are generally tagged with barcoded DNA strands.
Another technique for spatial proteomics uses mass spectrometry in combination with a microscope. Proteins on the tissue are marked using metal ions tagged to antibodies. Then, a laser ablates the sample at the precise location of the metal atom, and it is detected using a mass spectrometer. Alternatively, laser-assisted microdissection can isolate specific regions of interest from a tissue, and these samples can be further analyzed for proteomic studies.
All these methods produce large data sets. With the fast-paced development of AI-based platforms, one can perform complex data analysis, improve data quality, and integrate different datasets. It can produce a final image or a 3D model with colocalized information from the multimodal spatial omics. Such studies have potential in translating into clinical applications for disease diagnosis, monitoring, and designing personalized precision medication for patients.
Spatial omics has come a long way since pathologists inferred spatial context in tissues primarily using H&E staining. Today’s state-of-the-art spatial omics are rapidly growing to facilitate understanding of human health and the molecular mechanisms of sustaining life.
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