Basic – ASSET https://assetonline.org Sat, 27 Dec 2025 22:45:31 +0000 en-US hourly 1 https://wordpress.org/?v=6.9 https://assetonline.org/wp-content/uploads/2021/03/cropped-icon-32x32.png Basic – ASSET https://assetonline.org 32 32 Plasticity and Vulnerability: The Impact of Modern Societal Challenges on the Developing Prefrontal Cortex and Substance Abuse https://assetonline.org/plasticity-and-vulnerability-the-impact-of-modern-societal-challenges-on-the-developing-prefrontal-cortex-and-substance-abuse/ Sat, 27 Dec 2025 22:45:31 +0000 https://assetonline.org/?p=6008 The transition from childhood to adulthood is marked by a profound neurological renovation that renders the adolescent brain both exceptionally plastic and uniquely vulnerable. This discussion explores the intersection of pubertal neurobiology with the modern digital landscape, specifically examining how social media, and current societal challenges influence the developing teenage/young adult mind. There exists significant developmental mismatch between the subcortical limbic system, responsible for emotional processing and reward-seeking, and the prefrontal cortex (PFC), responsible for executive function and impulse control which remains under construction until the mid-twenties, explaining the heightened emotional reactivity and increased sensation-seeking characteristic of puberty. Social media platforms are engineered to exploit this neural vulnerability. Likes, Streaks, Emojis, Reactions and infinite scrolling function trigger surges of dopamine in the ventral striatum (VS), leading to binge scrolling creating a feedback loop where the brain’s reward system overrides the PFC’s ability to disengage, leading to a state of cognitive depletion and diminished self-regulation. Neurobiologically, peer rejection activates the same brain regions as physical pain (the anterior cingulate cortex). Consequently, the adolescent brain is hyper-tuned to peer pressure and the need for social validation. The desire for social conformity is driven by a need to maximize neural rewards associated with self-esteem. In the digital sphere, this manifests as a constant, exhausting pressure to curate a perfect online persona, often at the expense of authentic emotional development. Conversely, the fear of social exclusion serves as a potent driver of behavioral aberrations. Neuroimaging shows that social rejection activates the anterior cingulate cortex and the insula, the same regions responsible for processing physical pain. To avoid this distress, the young brains may prioritize matching expectations of the group like engaging in binge drinking or vaping, as a survival mechanism to maintain social inclusivity. The neurobiology of substance abuse is particularly dangerous during this window since the adolescent brain is still undergoing synaptic pruning and myelination. Substances like nicotine, THC, and alcohol hijack the still-developing dopamine pathways, potentially hard-wiring the brain for addiction more effectively than in adults. Puberty-driven changes in the amygdala lead to heightened emotional volatility. When combined with the stress of social hierarchies, adolescents and young adults may turn to substances as a form of chemical coping to manage social anxiety or the pressure to perform, creating a dangerous feedback loop. Hence understanding that the teenage/adolescent brain is critical towards designing interventions that focus on strengthening inhibitory control and fostering positive reinforcement that reward healthy decision-making towards the greater goals of life.

Authors List :
Sreyashi Samaddar
Presenting Author :
Sreyashi Samaddar
Affiliations :
Brooklyn College, CUNY
Email :
sreyashi.samaddar@gmail.com
Key Words (5 Words Maximum) :
Neurodevelopment, Plasticity, Substance Abuse, Reward
]]> A Comparative study about Glycemic Index and Diabetes https://assetonline.org/a-comparative-study-about-glycemic-index-and-diabetes/ Thu, 25 Dec 2025 20:03:48 +0000 https://assetonline.org/?p=5941

Diabetes care is a fundamental health issue all over the world and plays a crucial role as a dietary approach in managing blood glucose concentrations. Glycemic index (GI) measures the impact of carbohydrate-rich diets on blood glucose, but there are inadequate methods available for GI evaluation. The objective of this study was understand the glycemic index of foods like unripe banana and ripe banana by employing the phenol-sulphuric acid test to estimate the carbohydrate content in the sample. The unripe banana extract was obtained by the process of crushing, subsequent extraction using saline solution, and enzymatic hydrolysis of the sample by amylase. The total carbohydrate levels in the extract were determined by employing the phenol-sulphuric acid test by measuring the absorbance of the sample at 490nm using a colorimeter. Analysis of the results showed that the concentration of digestible sugars in unripe bananas was low compared to that in ripe bananas. This indicated that the glycemic index in unripe bananas was low. The phenol-sulphuric acid method was found to be a reliable technique in the quantitative analysis of carbohydrates in food materials. The results observed in this study justify the consumption of low GI foods by diabetics.

Authors List :
Zikra Shahid, Kainaat Mahmood, Fakhra Tabassum
Presenting Author :
Zikra Shahid, Kainaat Mahmood
Affiliations :
A.B.K. High School (Girls), Aligarh Muslim University, Aligarh, India, 202001, A.M.U. Girls School, Aligarh, India, 202001
Email :
sumbulshahid7500@gmail.com
Key Words (5 Words Maximum) :
Glycemic Index, Diabetes, Glucose, Carbohydrate, Food Consumption
]]> Adverse Drug Reactions and Pharmacogenomics https://assetonline.org/adverse-drug-reactions-and-pharmacogenomics/ Thu, 25 Dec 2025 20:02:04 +0000 https://assetonline.org/?p=5943 Adverse drug reactions (ADRs) are unintended, harmful responses to medications occurring at normal therapeutic doses and represent a significant challenge in clinical practice and public health. They contribute substantially to patient morbidity, mortality, prolonged hospital stays, and increased healthcare costs worldwide. ADRs may arise due to predictable, dose-dependent effects related to a drug’s pharmacological action (Type A reactions) or unpredictable, dose-independent effects such as hypersensitivity or idiosyncratic responses (Type B reactions). Several factors influence the occurrence of ADRs, including age, genetic predisposition, comorbidities, polypharmacy, and drug–drug interactions. In vulnerable populations such as children, the elderly, and patients with chronic diseases, the risk of ADRs is particularly high. Effective identification, assessment, and prevention of ADRs are therefore critical components of patient safety. Pharmacovigilance systems play a central role in monitoring ADRs through spontaneous reporting, post-marketing surveillance, and clinical studies, enabling early detection of safety signals and regulatory interventions. Healthcare professionals have a vital responsibility to recognize, document, and report suspected ADRs to improve drug safety profiles. Advances in pharmacogenomics and data-driven monitoring tools offer promising strategies for predicting and minimizing ADRs in the future. Overall, understanding ADRs is essential for optimizing therapeutic outcomes, enhancing patient safety, and promoting rational drug use in modern healthcare systems.

Authors List :
Ayesha fatima, Humera Quadriya, Shagufta Tarannum, Fehmida Begum, Majid Mohiuddin
Presenting Author :
Ayesha fatima
Affiliations :
Anwarul Uloom College
Email :
ayeshafatimaaa37@gmail.com
Key Words (5 Words Maximum) :
ADR, Drug, Morbidity, Risk Factor
]]> Circadian Rhythm Regulation and its Impact on Intestinal Microflora https://assetonline.org/circadian-rhythm-regulation-and-its-impact-on-intestinal-microflora/ Thu, 25 Dec 2025 09:04:59 +0000 https://assetonline.org/?p=5889

The intricate relationship between circadian rhythms and intestinal microflora has gained significant attention in recent years. Circadian rhythms, regulated by an internal clock, orchestrate various physiological processes, including sleep-wake cycles, hormone secretion, and metabolism. Emerging evidence suggests that these rhythms also influence the composition and function of gut microbiota. The gut microbiome, in turn, produces metabolites that modulate host circadian clocks, creating a bidirectional feedback loop. Disruptions to this delicate balance, often caused by modern lifestyle factors like irregular sleep patterns, jet lag, and artificial light exposure, can lead to circadian rhythm disorders and gut dysbiosis. This dysregulation has been linked to various diseases, including metabolic syndrome, inflammatory bowel disease, and neurodegenerative disorders. Key microbial metabolites, such as short-chain fatty acids (SCFAs) and bile acids play a crucial role in modulating host circadian rhythms. SCFAs, produced by bacterial fermentation, can entrain peripheral clocks and influence gene expression. Conversely, host circadian clocks regulate gut motility, immune function, and secretion of antimicrobial peptides, shaping the gut microbiome. Understanding the complex interplay between circadian rhythms and intestinal microflora offers promising therapeutic avenues for managing circadian-related disorders. Chronotherapeutic strategies, such as time-restricted eating and targeted probiotics, may help restore rhythmic harmony and promote overall well-being.

Authors List :
Syed Burhan Uddin, Humera Quadriya, Fehmida Begum, Shagufta Tarannum, Majid Mohiuddin
Presenting Author :
SYED BURHAN UDDIN
Affiliations :
Anwarul Uloom College
Email :
smuzzu7860@gmail.com
Key Words (5 Words Maximum) :
Intestinal microflora, Internal Clock, Physiological Processes, Short chain fatty acids
]]> Pathogenic rickettsiae encode a secreted lipase that facilitates intracytosolic colonization in host cells https://assetonline.org/pathogenic-rickettsiae-encode-a-secreted-lipase-that-facilitates-intracytosolic-colonization-in-host-cells/ Wed, 24 Dec 2025 21:35:33 +0000 https://assetonline.org/?p=5880

Key cellular processes for the rickettsial obligate intracellular lifestyle, include internalization by phagocytosis, regulation of intracellular trafficking, and evasion of lysosomal destruction to establish an intracytosolic replication niche, remain poorly defined. Recent reports showed that rickettsial phospholipases play an important role in vacuolar escape, but their functions are dispensable depending on the host cell-type. Here, we report the identification of a putative lipase with a Serine hydrolase motif (GXSXG) in the R. rickettsii genome, which we named RLip (Rickettsia Lipase). Sequence comparison shows that the Serine hydrolase motif is conserved among RLip molecules of other Rickettsia species. Our work reveals that RLip harbors a lipase activity, and its recombinant expression is cytotoxic to yeast and mammalian cells. We further demonstrate that RLip expression is induced during R. rickettsii or R. parkeri infection, while its expression was minimally detected during R. montanensis (non-pathogenic) infection. Fractionation of R. rickettsii-infected host cells, shows the presence of RLip in the cytoplasmic fraction, while being minimally retained by the bacteria. Infection studies in HMEC-1 cells using R. parkeri wild type (WT) or R. parkeri rlip::Tn (non-functional RLip), demonstrate that lack of RLip function significantly impairs rickettsial evasion from bactericidal phagolysosomal fusion, suggesting that RLip plays a critical role in the escape from membrane-bound vacuoles to facilitate the intracytosolic colonization of pathogenic Rickettsia species

Keywords: Phagocytosis, Rickettsia Lipase, Pathogenic

Authors List :
Mohammad Sadik, Imran Moin, Saif Ullah, Andrew C. Krusenstjerna, Mathilde Gonin, Erin D. Goley, M. Sayeedur Rahman, and Oliver H. Voss
Presenting Author :
Mohammad Sadik
Affiliations :
University Of Maryland, Baltimore
Email :
Msadik@som.umaryland.edu
Key Words (5 Words Maximum) :
Rickettsia, Host-pathogen interaction, Lipase
]]> Prolonged Use of Major Antidiabetic Drugs in Type 2 Diabetes and Their Associated Side Effects https://assetonline.org/prolonged-use-of-major-antidiabetic-drugs-in-type-2-diabetes-and-their-associated-side-effects/ Mon, 22 Dec 2025 21:21:09 +0000 https://assetonline.org/?p=5845 Type 2 diabetes mellitus (T2DM) is a chronic metabolic disorder requiring long-term pharmacotherapy. While antidiabetic medications effectively manage blood glucose, prolonged use may lead to significant adverse effects. This presentation focuses on major drug classes commonly prescribed in outpatient settings: metformin, sulfonylureas, thiazolidinediones, SGLT2 inhibitors, and insulin. Long-term metformin use can cause vitamin B12 deficiency; sulfonylureas may lead to hypoglycemia and weight gain; thiazolidinediones are associated with fluid retention, weight gain, and fracture risk; SGLT2 inhibitors can cause genital infections and volume depletion; prolonged insulin therapy may result in hypoglycemia and lipohypertrophy. Emphasis is placed on regular monitoring, patient education, and individualized therapy to minimize risks and optimize outcomes. Understanding the balance between efficacy and safety is crucial for improving quality of life in patients with T2DM on long-term pharmacotherapy.

Authors List :
Sufiya Kouser, Kaiser Jamil
Presenting Author :
Sufiya Kouser
Affiliations :
Shadan Women's College of Pharmacy
Email :
kj.bmmrc@gmail.com
Key Words (5 Words Maximum) :
T2DM, antidiabetic drugs, pharmacotherapy
]]> Preventing Aggregation of SOD1-D90A ALS-causing Mutant Using No-Mo-Aggregate-81 (NMA81) https://assetonline.org/preventing-aggregation-of-sod1-d90a-als-causing-mutant-using-no-mo-aggregate-81-nma81/ Mon, 16 Dec 2024 05:10:31 +0000 https://assetonline.org/?p=5682 Single mutations in the SOD1 protein, such as A4V and D90A, are known to induce aggregation of Superoxide dismutase 1 (SOD1) proteins, which is often universal for an amyotrophic lateral sclerosis (ALS) diagnosis. The D90A mutation is the most common of the ALS-causing point mutations and is known to show significant aggregation potential. This in silico inquiry was conducted on the D90A variant of the SOD1 protein, to create a molecule that could potentially inhibit aggregation. Through qualitative examination of the structures, it was determined that the residue Tryptophan 32 is an ideal target for the proposed small molecule. It differs sterically from the D90A mutant to the wild-type and is also distant from the dimerization and allosteric sites. These properties make it unlikely that the small molecule will interfere with the enzyme’s regular function when bound. No-Mo-Aggregate-81 (NMA81), a novel small molecule that specifically targets the Trp 32 residue, is proposed as potential treatment to prevent aggregation of the SOD1 proteins. Reduced aggregation of SOD1 is expected to be associated with decreased severity of ALS.

Authors List :
Ahad Asghar, Jasmine Jacobs, Karen Sabu Jose, Carrie (Roanna) Lu, Devnand Nambiar, Arjun Stenger, Hannah Zemans-Ronthal
Presenting Author :
Ahad Asghar, Arjun Stenger
Affiliations :
University of Western Ontario
Email :
ahadasghar2004@gmail.com
Key Words (5 Words Maximum) :
ALS, protein aggregation, in-silico, drug design
]]> Red Queen’s Muscle: Mitophagy and Cytoskeletal Dynamics in Sarcopenia, Muscle Wasting, and Critical Illness https://assetonline.org/red-queens-muscle-mitophagy-and-cytoskeletal-dynamics-in-sarcopenia-muscle-wasting-and-critical-illness-2/ Mon, 16 Dec 2024 05:07:43 +0000 https://assetonline.org/?p=5695 Mitophagy, the selective autophagic degradation of mitochondria, is a conserved quality control mechanism essential for cellular and mitochondrial homeostasis. Its dysfunction contributes to various human diseases, but the precise role of microtubule (MT) network dynamics in regulating mitophagy under stress remains poorly understood. Inspired by Lewis Carroll’s concept of the Red Queen’s race, which symbolizes maintaining equilibrium under constant demand, this study examines how cytoskeletal dynamics influence mitophagy across two distinct stress platforms: burn serum and lipopolysaccharide (LPS)-induced conditions.
In this cross-platform investigation, we utilized C2C12 myocyte cell lines expressing mRuby-tubulin, GFP-EB1 (a marker of MT plus ends), and mito-Keima or mitoKaede. These tools enabled live-cell monitoring of MT synthesis speed, network formation, and mitophagy flux. Stress models were created using rat-derived burn serum (30% body surface area) and LPS (1 μg/mL) to mimic critical illness conditions. MT synthesis rates were tracked via EB1 motion, basal and stress-induced MT network formation were analyzed, and mitophagosome maturation was assessed through ratiometric imaging of mitophagy reporters.
Under both burn serum and LPS-induced stress conditions, MT synthesis rates decreased significantly compared to controls. Basal MT network formation showed no differences between stressed and control groups; however, MT deficiencies became evident following CCCP-induced mitophagy. Mito-Keima and mitoKaede analyses revealed impaired vesicle trafficking, characterized by defective autophagosome/mitophagosome/lysosome interactions and diminished mitophagosome maturation. These findings indicate that MT network abnormalities manifest primarily under conditions of increased mitophagy flux demand, where robust cytoskeletal dynamics are critical for maintaining functionality. This study introduces the concept of the “Red Queen’s race” as a framework for understanding the interplay between cytoskeletal dynamics and mitophagy regulation. The analogy underscores the need for continuous, vigorous MT synthesis to sustain equilibrium, particularly under stress. The observed cytoskeletal dysfunction in both burn and LPS stress models highlights a shared mechanism linking stress-induced MT defects to inadequate mitophagy responses. By bridging these two distinct platforms, this work reveals that stress-induced cytoskeletal defects disrupt mitophagy flux through impaired vesicle trafficking and maturation, offering a unifying perspective on the impact of MT network dysfunction in critical illness. These insights provide a novel understanding of how cytoskeletal dynamics govern mitochondrial quality control, emphasizing the potential for targeting mitophagy maturation as a therapeutic strategy across diverse pathological conditions.

Authors List :
Shingo Yasuhara, Hiroki Ogata, Sora Kikuchi, Hiroyuki Morinaga, Jingyuan Chen, Yoh Sugawara, Maryam Khan, Asiya Karim, Erica Yasuhara, Alyssa Yasuhara, Asahi Adachi, Yurika Sakai, Mohammed Khan
Presenting Author :
Shingo Yasuhara
Affiliations :
Harvard Medical School, Massachusetts General Hospital, Shriners Hospitals for Children
Email :
shingoyasuhara136@gmail.com
Key Words (5 Words Maximum) :
autophagy, mitophagy, mitochondria, cytoskeleton, sarcopenia
]]> Global Trends and Risk Factors on Obesity https://assetonline.org/global-trends-and-risk-factors-on-obesity/ Mon, 16 Dec 2024 04:56:33 +0000 https://assetonline.org/?p=5687 The prevalence of obesity has surged globally, becoming a significant public health challenge. According to recent findings from Global Burden of Disease (GBD) studies and World Health Organization (WHO) reports, obesity rates have nearly tripled since 1975. The latest global obesity statistics shows that in 2023, over 1 billion people worldwide were classified as obese, including: 650 million adults (≥18 years old); 340 million adolescents (5–19 years old) and 39 million children (<5 years old). The prevalence in countries like the United States and Saudi Arabia exceeds 40%.. Rapid urbanization and dietary shifts have escalated obesity rates in nations like India, China, and Brazil. Obesity is emerging as a problem in urban areas due to increased access to processed foods and sedentary lifestyles. Obesity is a complex condition influenced by a combination of genetic, behavioral, environmental, and physiological factors. Understanding these risk factors is crucial for developing effective prevention and management strategies. Below are the primary risk factors for obesity: (i) Type 2 Diabetes Mellitus (T2DM), (ii) Cardiovascular Diseases (CVDs), (iii) Hypertension, (iv) Osteoarthritis, (v) Certain cancers (e.g., breast, colon) (vi) Dietary Habits: (most important parameter), (vii) Endocrine and Metabolic Factors (Hormonal Imbalances: conditions like hypothyroidism, Cushing’s syndrome, and polycystic ovarian syndrome (PCOS) can slow metabolism and promote fat accumulation), (viii) Insulin Resistance (Hyperinsulinemia can lead to increased fat storage and weight gain, creating a vicious cycle of obesity and metabolic dysfunction), (ix) Biological Factors (Gut Microbiota: an imbalance in gut bacteria (dysbiosis) can influence energy metabolism and fat storage, increasing obesity risk), (x) Epigenetics (Environmental exposures during critical developmental periods can alter gene expression and predispose individuals to obesity). Obesity arises from an interplay of genetic susceptibility, unhealthy behaviors, and environmental factors. Targeting these risk factors through lifestyle modifications, policy changes, and individualized healthcare interventions is essential for prevention and management.

Authors List :
Kaiser Jamil
Presenting Author :
Kaiser Jamil
Affiliations :
Professor, Head of Genetics Department Bhagwan Mahavir Medical Research Centre Mahavir Marg, A.C. Guards, Hyderabad- 500004, TS India
Email :
kj.bmmrc@gmail.com
Key Words (5 Words Maximum) :
Obesity, risk factors , insulin resistance, diet, metabolic disorders
]]> Fluid Dynamics and the Brain: A New Hypothesis for the Developmental Origin of Brain Asymmetry https://assetonline.org/fluid-dynamics-and-the-brain-a-new-hypothesis-for-the-developmental-origin-of-brain-asymmetry/ Fri, 13 Dec 2024 04:45:06 +0000 https://assetonline.org/?p=5645 The human brain exhibits striking left-right asymmetry in both its functions and anatomy, but the mechanisms underlying this asymmetry during embryonic development remain poorly understood. Here, we propose a novel hypothesis, combining computational fluid dynamics with mouse developmental biology, suggesting that directional fluid flow around the early embryo may contribute to the establishment of left-right asymmetry in the brain. In contrast to the brain, the mechanisms underlying left-right asymmetry in the visceral organs, such as the heart and liver, are well-established. In contrast to the brain, visceral organs such as the heart and lungs exhibit clear left-right asymmetry. In mammals, the first symmetry-breaking event occurs in the embryonic node, where ciliary rotation drives leftward fluid flow. This flow generates subtle asymmetries in force distribution near the node, which are subsequently amplified and integrated into downstream gene regulatory networks. Although this left-right symmetry breaking is typically considered independent of brain asymmetry, little is known about its potential influence on the brain. Through our investigation in mouse embryos, we discovered that the node is connected to the large extraembryonic space, the yolk sac cavity. This observation led us to hypothesize that cilia-driven flow at the node could extend beyond the node, inducing global fluid movement that may contribute to the establishment of left-right asymmetry in non-visceral organs, including the brain. Given the challenges of directly measuring fluid dynamics within the yolk sac cavity, we employed computational fluid dynamics to simulate cilia-driven flow. We examined how the spatial patterns of ciliary rotation influence fluid dynamics and whether such directional flow could propagate across the entire embryo. Our simulations suggest that nodal cilia can indeed induce a global flow, potentially contributing to LR asymmetry in the brain. This presentation will address our ongoing efforts to validate this hypothesis through in vivo measurements of fluid dynamics.

Authors List :
Kana Ishimatsu, Olivier Pourquie, Jonathan Touboul
Presenting Author :
Kana Ishimatsu
Affiliations :
Department of Mathematics, Brandeis University; Department of Pathology, Brigham and Women's Hospital
Email :
kanaishimatsu@brandeis.edu
Key Words (5 Words Maximum) :
Fluid dynamics, left-right asymmetry, developmental biology, mouse embryo
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