The injury pattern and outcomes among elephant attack survivors presenting to the emergency department: A retrospective observational study.

BACKGROUND: Human-elephant conflicts (HECs) are becoming a disturbing public health concern in eastern India. This study highlights the pattern of injuries, epidemiological factors, and outcomes among the victims who survived an elephant attack (EA). METHODS: This retrospective observational study was conducted in a tertiary care hospital. Data were retrieved from the medical records of EA victims who presented to the emergency department of the hospital over five years (January 2019-January 2024). Data regarding sociodemographic characteristics, injury mode, injury pattern, radiological findings, emergency procedures, and outcome variables (admission, length of intensive care unit and hospital stay, and death) were collected. RESULTS: In total, 45 EA victims were included in this study. The mean participant age was 45.8 ± 14.57 years. Of the total participants, 35 (78 %) were men. Most EAs [n = 18 (40 %)] occurred in the forest area and during the early morning hours between 4am and 8am [n = 18 (40 %)] of the winter season [n = 37 (82 %)] and were unprovoked [38 (84 %)]. Of the total injuries, 26 (67 %) injuries were due to the direct mode of EA and 13 (33 %) were due to the indirect mode. The most common mechanism of EA was using the trunk and foot [20 (51 %)], followed by the tusk [6 (15 %)]. The median ISS in victims was 20 (13-29). The median AIS score of chest injuries was 1 (0-3). Thirteen (29 %) patients were positive on e-FAST. Of the total EA victims, 12 (26 %) were admitted to the intensive care unit (ICU) and 17 were admitted to the wards. Severe chest injury (AIS score ≥ 3) (p = 0.003), direct mode of injury, and polytrauma (ISS > 16) were identified as significant factors contributing to ICU admission. The median ICU stay of the victims was 6 (3-8) days, and the median length of hospital stay was 7 (0.5-11) days. One inpatient mortality was noted. CONCLUSION: Middle-aged men were the most common victims of EA occurring during the early morning hours. Extremity and soft tissue injuries were most common, followed by chest and abdominal injuries. Severe chest injury resulted in ICU admission and extended hospitalization.

MST1 selective inhibitor Xmu-mp-1 ameliorates neuropathological changes in a rat model of sporadic Alzheimer's Disease by modulating Hippo-Wnt signaling crosstalk.

Alzheimer's disease (AD), the most prevalent form of dementia, is characterized by progressive cognitive impairment accompanied by aberrant neuronal apoptosis. Reports suggest that the pro-apoptotic mammalian set20-like kinase 1/2 (MST1/2) instigates neuronal apoptosis via activating the Hippo signaling pathway under various stress conditions, including AD. However, whether inhibiting MST1/2 has any therapeutic benefits in AD remains unknown. Thus, we tested the therapeutic effects of intervening MST1/2 activation via the pharmacological inhibitor Xmu-mp-1 in a sporadic AD rat model. Sporadic AD was established in adult rats by intracerebroventricular streptozotocin (ICV-STZ) injection (3 mg/kg body weight). Xmu-mp-1 (0.5 mg/kg/body weight) was administered once every 48 h for two weeks, and Donepezil (5 mg/kg body weight) was used as a reference standard drug. The therapeutic effects of Xmu-mp-1 on ICV-STZ rats were determined through various behavioral, biochemical, histopathological, and molecular tests. At the behavioral level, Xmu-mp-1 improved cognitive deficits in sporadic AD rats. Further, Xmu-mp-1 treatment reduced STZ-associated tau phosphorylation, amyloid-beta deposition, oxidative stress, neurotoxicity, neuroinflammation, synaptic dysfunction, neuronal apoptosis, and neurodegeneration. Mechanistically, Xmu-mp-1 exerted these neuroprotective actions by inactivating the Hippo signaling while potentiating the Wnt/ß-Catenin signaling in the AD rats. Together, the results of the present study provide compelling support that Xmu-mp-1 negated the neuronal dysregulation in the rat model of sporadic AD. Therefore, inhibiting MST/Hippo signaling and modulating its crosstalk with the Wnt/ß-Catenin pathway can be a promising alternative treatment strategy against AD pathology. This is the first study providing novel mechanistic insights into the therapeutic use of Xmu-mp-1 in sporadic AD.

The interplay between hippo signaling and mitochondrial metabolism: Implications for cellular homeostasis and disease.

Mitochondria are the membrane-bound organelles producing energy for cellular metabolic processes. They orchestrate diverse cell signaling cascades regulating cellular homeostasis. This functional versatility may be attributed to their ability to regulate mitochondrial dynamics, biogenesis, and apoptosis. The Hippo pathway, a conserved signaling pathway, regulates various cellular processes, including mitochondrial functions. Through its effectors YAP and TAZ, the Hippo pathway regulates transcription factors and creates a seriatim process that mediates cellular metabolism, mitochondrial dynamics, and survival. Mitochondrial dynamics also potentially regulates Hippo signaling activation, indicating a bidirectional relationship between the two. This review outlines the interplay between the Hippo signaling components and the multifaceted role of mitochondria in cellular homeostasis under physiological and pathological conditions.

Enhancing the degradation rate and biomineralization nature of antiferromagnetic Fe-20Mn alloy by groove pressing.

The Fe-Mn alloys are potential candidates for biodegradable implant applications. However, the very low degradation rates of Fe-Mn alloys in the physiological environment are a major disadvantage. In this study, the degradation rate of a Fe-20Mn alloy was improved using the groove pressing (GP) technique. Hot rolled sheets of 2 mm thickness were subjected to GP operation at 1000°C. Uniform fine-grained (UFG) Fe-Mn alloys were obtained using the GP technique. The influence of GP on the microstructure, mechanical properties, degradation behavior in simulated body fluid (SBF), surface wettability, biomineralization, and cytocompatibility was investigated and compared to the annealed (A Fe-Mn) and rolled (R Fe-Mn) sample. The groove-pressed Fe-Mn (G Fe-Mn) alloy had a grain size of approximately 40 ± 16 µm whereas the A Fe-Mn and R Fe-Mn samples had grain sizes of 303 ± 81 and 117 ± 14.5 µm, respectively. Enhanced strength and elongation were also observed with the G Fe-Mn sample. The potentiodynamic polarization test showed the highest Icorr, lowest polarization resistance, and lowest Ecorr for the G Fe-Mn sample among all other samples indicating its higher degradation rate. The weight loss data from immersion tests also shows that the percentage of weight loss increases with time indicating the accelerated degradation behavior of the sample. The static immersion test showed an enhancement in weight loss of 0.46 ± 0.02% and 1.02 ± 0.05% for R Fe-Mn and G Fe-Mn samples, respectively, than A Fe-Mn sample (0.31 ± 0.03%) after 56 days in immersion in SBF. The greater biomineralization tendency in UFG materials is confirmed by the G Fe-Mn sample's stronger hydroxyapatite deposition. When compared to the A Fe-Mn and R Fe-Mn samples, the G Fe-Mn sample has a better wettability, which promotes higher cell adhesion and vitality, showing higher biocompatibility. This study demonstrates that Fe-20Mn processed by GP has potential applications for the manufacture of biodegradable metallic implants.

Amelioration of Amyloid-ß Induced Alzheimer's Disease by Bacopa monnieri through Modulation of Mitochondrial Dysfunction and GSK-3ß/Wnt/ß-Catenin Signaling.

BACKGROUND: Alzheimer's disease (AD) is the most prevalent dementia, affecting a large number of populations. Despite being under scrutiny for decades, an effective therapeutic option is still not available. METHODS AND RESULTS: This study explores the therapeutic role of a nootropic herb Bacopa monnieri (BM) in AD-like pathological conditions produced by injecting preformed amyloid-ß42 (Aß42) fibril bilaterally into hippocampus of Wistar rats, and ethanolic extract of BM is orally administered for 4 weeks. Assessment of behavioral changes reveals that BM treatment ameliorates Aß42-induced cognitive impairment and compromised explorative behavior. Supplementation of BM also reduces oxidative stress biomarkers, proinflammatory cytokines, and cholinesterase activity in the AD rats. Additionally, BM treatment restores Bcl-2-associated X protein (Bax)/ B-cell lymphoma 2 (Bcl-2) imbalance, increases neurotrophic factors expression, and prevents neurodegeneration validated by quantifying Nissl-positive hippocampal neurons. Interestingly, BM administration eliminates amyloid plaques in the hippocampal region and normalizes the Aß42-induced increase in phospho-tau and total tau expression. Mechanistic investigations reveal that BM interacts with glycogen synthase kinase (GSK-3ß) and restores Wnt/ß-catenin signaling. CONCLUSION: BM has been used in diet as a nootropic herb for several centuries. This study highlights the anti-Alzheimer activity of BM from the behavioral to the molecular level by modulating mitochondrial dysfunction, and GSK-3ß mediates the Wnt/ß-catenin signaling pathway.

Could Vitamins Have a Positive Impact on the Treatment of Parkinson's Disease?

Parkinson's disease (PD) is the second most common progressive neurodegenerative disorder after Alzheimer's disease. Pathophysiologically, it is characterized by intracytoplasmic aggregates of α-synuclein protein in the Lewy body and loss of dopaminergic neurons from substantia nigra pars compacta and striatum regions of the brain. Although the exact mechanism of neurodegeneration is not fully elucidated, it has been reported that environmental toxins such as MPTP, rotenone, paraquat, and MPP+ induce oxidative stress, which is one of the causative factors for it. To date, there is no complete cure. However, the indispensable role of oxidative stress in mediating PD indicates that antioxidant therapy could be a possible therapeutic strategy against the disease. The deficiency of vitamins has been extensively co-related to PD. Dietary supplementation of vitamins with antioxidant, anti-inflammatory, anti-apoptotic, and free radical scavenging properties could be the potential neuroprotective therapeutic strategy. This review summarizes the studies that evaluated the role of vitamins (A, B, C, D, E, and K) in PD. It will guide future studies in understanding the potential therapeutic role of vitamins in disease pathophysiology and may provide a framework for designing treatment strategies against the disease.

Lethal Neurotoxicity in Lambda-Cyhalothrin Poisoning: A Rare Case Report.

ABSTRACT: Agricultural poisons (insecticides and pesticides) are the most common types of poison implicated in the morbidity and mortality associated with acute poisoning. Suicidal ingestion is more frequent than accidental or homicidal poisonings. Pyrethroids are considered relatively safer than other insecticides. Lambda-cyhalothrin (LCH) belongs to the fourth-generation, type II synthetic pyrethroid. To the best of our knowledge, fatalities after LCH exposure have not yet been reported in the literature. Here, we describe a case of LCH poisoning in a 54-year-old male farmer after an accidental pipe burst in a sprayer while spraying in the field. The patient died 10 days after poisoning due to severe neurotoxicity resulting in bilateral parieto-occipital and brainstem infarcts. The histopathological features of the brain associated with LCH poisoning have been discussed in this report.

Detrimental Effects of Alcohol-Induced Inflammation on Brain Health: From Neurogenesis to Neurodegeneration.

Alcohol consumption is known to cause several brain anomalies. The pathophysiological changes associated with alcohol intoxication are mediated by various factors, most notable being inflammation. Alcohol intoxication may cause inflammation through several molecular mechanisms in multiple organs, including the brain, liver and gut. Alcohol-induced inflammation in the brain and gut are intricately connected. In the gut, alcohol consumption leads to the weakening of the intestinal barrier, resulting in bacteria and bacterial endotoxins permeating into the bloodstream. These bacterial endotoxins can infiltrate other organs, including the brain, where they cause cognitive dysfunction and neuroinflammation. Alcohol can also directly affect the brain by activating immune cells such as microglia, triggering the release of pro-inflammatory cytokines and neuroinflammation. Since alcohol causes the death of neural cells, it has been correlated to an increased risk of neurodegenerative diseases. Besides, alcohol intoxication has also negatively affected neural stem cells, affecting adult neurogenesis and causing hippocampal dysfunctions. This review provides an overview of alcohol-induced brain anomalies and how inflammation plays a crucial mechanistic role in alcohol-associated pathophysiology.

Fatal intracranial bleedings in a viper bite: A case report.

Viper bite envenomation represents a significant occupational hazard among agricultural workers in India. The viper bite envenomation is usually suspected when a patient presents with predominant local symptoms at the bitten site, including pain, swelling, and necrosis. Further, systemic findings such as diffuse intravascular coagulation, hypotension, and shock may alert physicians of viper bite envenomation rather than a neurotoxic snake bite. However, cerebral complications are rare in viper bites but may potentially fatal. Central nervous system involvement in a viper bite is either due to neurotoxins or hemorrhagins present in the venom, which may induce cerebral thrombosis, ischemia, infarction, and hemorrhage. Here we present a case of a previously healthy adult male who succumbed to extensive subarachnoid, intracerebral, and intraventricular hemorrhages involving bilateral cerebral hemispheres following viper snake bite envenomation. This report highlights the importance of anticipating cerebral complications in viper bite envenomation, a rare occurrence. It also emphasizes the need for early antisnake venom administration to prevent and control systemic envenomation and its complications.

Age-related Mitochondrial Dysfunction in Parkinson's Disease: New Insights Into the Disease Pathology.

Aging is a progressive loss of physiological function that increases risk of disease and death. Among the many factors that contribute to human aging, mitochondrial dysfunction has emerged as one of the most prominent features of the aging process. It has been linked to the development of various age-related pathologies, including Parkinson's disease (PD). Mitochondria has a complex quality control system that ensures mitochondrial integrity and function. Perturbations in these mitochondrial mechanisms have long been linked to various age-related neurological disorders. Even though research has shed light on several aspects of the disease pathology, the underlying mechanism of age-related factors responsible for individuals developing this disease is still unknown. This review article aims to discuss the role of mitochondria in the transition from normal brain aging to pathological brain aging, which leads to the progression of PD. We have discussed the emerging evidence on how age-related disruption of mitochondrial quality control mechanisms contributes to the development of PD-related pathophysiology.

Cellular senescence in the aging brain: A promising target for neurodegenerative diseases.

Aging is inevitable. Along with reduced ability to maintain the homeostasis of various biological processes, aging gradually deteriorates overall health. Extensive research on the aging brain has identified cellular senescence as a critical risk factor of neurodegeneration and cognitive decline. Associations of cellular senescence with neurodegenerative diseases like Alzheimer's disease, Down syndrome, Parkinson's disease, and multiple sclerosis are evident in an extensive body of literature generated over decades of research on aging. Cellular senescence triggers neurodegeneration via a complex interplay of mechanisms including neuroinflammation, mitochondrial dysfunction, oxidative stress burden, deranged protein homeostasis, and compromised nuclear and blood-brain-barrier integrity. Thus, cellular senescence can serve as a primary therapeutic target for various neurodegenerative diseases. This review summarizes the concept of cellular senescence, its role in the aging brain, and how it mediates neurodegeneration in several neurodegenerative disorders. Further, we have also highlighted senolytic therapeutics discovered and employed to ameliorate cellular senescence-associated degenerative diseases. This review can aid in providing directions for repurposing senolytic compounds and finding more therapeutic strategies targeting cellular senescence for the management and treatment of neurodegenerative diseases.

Self-Poisoning With Safer Insecticide: A Case Series on Imidacloprid Poisoning.

ABSTRACT: Imidacloprid (IMI) is a systemic insecticide that belongs to the neonicotinoid group of insecticides. It is highly effective against sucking, boring, and root-feeding insects. Besides, it has a favorable toxicological profile on humans. Currently, IMI is the largest selling insecticide in the world by replacing organophosphates and carbamates. It acts as nicotinic acetylcholine receptor agonist in the central nervous system of insects. To date, there is no specific antidote available for IMI poisoning. Despite a better safety profile on humans, severe toxicity from IMI poisoning is not uncommon. Here, we report a series of 4 cases who were admitted to our tertiary care center with a history of IMI poisoning.

Ball of Death: A Fatal Case Report on Accidental Death of a Child After Crude Bomb Explosion.

ABSTRACT: Crude bombs are country-made explosive weapons, usually prepared from locally available materials such as firecrackers or explosives used in mines. These are generally concealed inside the fruits, such as jackfruit, pineapple, and watermelon, to kill wild boars or other animals by poachers in India. Occasionally, crude bombs are remodeled resembling fruit or a ball and placed on the fields, where animals usually raid their crops. Such crude bombs may result in accidental explosions and contribute to the death of unintended targets, including humans. Despite these sporadic incidents reported in media, scientific data are lacking. Here, we report a young child who sustained injuries after an accidental explosion of such a crude bomb. It exploded when the child apparently mistook it for a ball and grasped it firmly while playing with his brother. This case is the first to report the accidental death of a child after the crude bomb's fatal explosion to the best of our knowledge. This report also briefly overviews the emerging menace of crude bombs in India.

Pattern of injuries due to wild animal attack among patients presenting to the emergency department: A retrospective observational study.

PURPOSE: The human-wildlife conflicts (HWCs) causing nuisances and injuries are becoming a growing public health concern over recent years worldwide. We aimed to study the demographic profile, mode of injury, pattern of injury, and outcome of wild animal attack victims presented to the emergency department. METHODS: This retrospective cross-sectional study was conducted in the emergency department of a tertiary-care hospital in Eastern India. Data were retrieved from the medical records from May 2017 to May 2021. Patients of all ages and genders attacked by wild animals and secondary injuries were included in this study. Patients with incomplete data, injuries due to the attack of stray and domestic animals and trauma due to other causes were excluded. Demographic profile, mode of injury, the pattern of injury, injury severity score (ISS), radiological pattern, and outcome were recorded. Statistical analysis with R (version 3.6.1.) was conducted. RESULTS: A total of 411 wild animal attack victims were studied, of which 374 (90.9%) were snakebite injuries and 37 (9.1%) were wild mammalian (WM) attack injuries. The mean age of WM attack victims was 46 years, and the male-to-female ratio was 4:1. Elephant attack injury (40.5%) was the most common WM attack injury reported. Most WM attacks (43.2%) occurred between 4:00 a.m. to 8:00 a.m. The median ISS was 18.5 (13-28), where 54.2% of patients had polytrauma (ISS>15). Elephant attack was associated with a higher ISS, but the difference was not significant compared to other animal types (p = 0.2). Blunt trauma was common pattern of injury in the elephant attack injury cases. Lacerations and soft tissue injuries were common patterns in other animal attacks. Among snakebites, neurotoxic was the most common type (55.4%), and lower extremity was the most common site involved. CONCLUSION: The young male population is the major victim of HWCs; and elephant is the most common animal involved. There is a need to design scientifically sound preventive strategies for HWCs and to strengthen the preparedness in health establishments to manage victims effectively.

Bacopaside-I Alleviates the Detrimental Effects of Acute Paraquat Intoxication in the Adult Zebrafish Brain.

Paraquat (PQ), an environmental neurotoxicant, causes acute fatal poisoning upon accidental or intentional ingestion (suicidal cases) worldwide. To date, an effective remedy for PQ toxicity is not available. In this study, we have evaluated the therapeutic efficacy of Bacopaside-I (BS-I), an active compound found in the plant extract of Bacopa monnieri (Brahmi), against acute PQ intoxication using zebrafish as a model organism. Adult zebrafish were injected with a dose of either 30 mg/kg or 50 mg/kg PQ. PQ-intoxicated zebrafish showed an increased rate of mortality and oxidative imbalance in their brain. Also, the proliferation of neural cells in the adult zebrafish brain was inhibited. However, when BS-I pretreated zebrafish were intoxicated with PQ, the toxic effects of PQ were ameliorated. PQ treatment also affected the expression of particular genes concerned with the apoptosis and dopamine signaling, which was not altered by BS-I administration. Our results highlight the efficiency of BS-I as a novel therapeutic agent for PQ intoxication. It further compels us to search and evaluate the molecular mechanisms targeted by BS-I to develop a potent therapy for acute PQ intoxication.

Induction of oxidative stress and apoptosis in the injured brain: potential relevance to brain regeneration in zebrafish.

Recent findings suggest a significant role of the brain-derived neurotrophic factor (BDNF) as a mediator of brain regeneration following a stab injury in zebrafish. Since BDNF has been implicated in many physiological processes, we hypothesized that these processes are affected by brain injury in zebrafish. Hence, we examined the impact of stab injury on oxidative stress and apoptosis in the adult zebrafish brain. Stab wound injury (SWI) was induced in the right telencephalic hemisphere of the adult zebrafish brain and examined at different time points. The biochemical variables of oxidative stress insult and transcript levels of antioxidant genes were assessed to reflect upon the oxidative stress levels in the brain. Immunohistochemistry was performed to detect the levels of early apoptotic marker protein cleaved caspase-3, and the transcript levels of pro-apoptotic and anti-apoptotic genes were examined to determine the effect of SWI on apoptosis. The activity of antioxidant enzymes, the level of lipid peroxidation (LPO) and reduced glutathione (GSH) were significantly increased in the injured fish brain. SWI also enhanced the expression of cleaved caspase-3 protein and apoptosis-related gene transcripts. Our results indicate induction of oxidative stress and apoptosis in the telencephalon of adult zebrafish brain by SWI. These findings contribute to the overall understanding of the pathophysiology of traumatic brain injury and adult neurogenesis in the zebrafish model and raise new questions about the compensatory physiological mechanisms in response to traumatic brain injury in the adult zebrafish brain.

Epidemiology and patterns of road traffic fatalities in India pre- and post-motor vehicle (Amendment) act 2019: An autopsy-based study.

BACKGROUND: Road traffic accidents (RTAs) are a preventable cause of death. The government of India enacted the motor vehicle amendment (MVA) act on September 01, 2019, to curtail the alarming trend of RTAs and their associated fatality. The study objective was to compare the epidemiology and pattern of fatal RTAs before and after the MVA Act 2019 of India. METHODS: An autopsy-based cross-sectional study was conducted at the Department of Forensic Medicine and Toxicology (FMT) of a tertiary-care hospital from March 2019 to February 2020. The sample comprised 75 fatal RTA victims who underwent postmortem at FMT. Patients were studied in two groups: One pre-MVA group (n = 47) and one Post-MVA group (n = 28). The data were obtained from medical records and inquest reports with autopsy correlation. Data pertaining to sociodemographic profile, mechanism, injury profile including injury-severity-score (ISS) and survival-time was recorded. RESULTS: There was a 40.4% decline in mortality among RTA victims (P = 0.057) in the post-MVA group. The case fatality rate also declined during post-MVA implementation months compared to pre-MVA months (1.61 vs. 1.96). A significant correlation was noted between the ISS and survival-time of victims (P < 0.001, r = -0.522). The mean age of patients was 39.87 ± 17.44 years. Heavy motor vehicles along with motorized two-wheeler were the most common offending-vehicle. The median ISS of all victims was 41 (33-57). Head injury was the most common cause of death (60%). CONCLUSION: Study results signal-toward early triumph of the new MVA act, probably due to enhanced adherence to safety gears and constructive behavioral change.

Neuronal Hippo signaling: From development to diseases.

Hippo signaling pathway is a highly conserved and familiar tissue growth regulator, primarily dealing with cell survival, cell proliferation, and apoptosis. The Yes-associated protein (YAP) is the key transcriptional effector molecule, which is under negative regulation of the Hippo pathway. Wealth of studies have identified crucial roles of Hippo/YAP signaling pathway during the process of development, including the development of neuronal system. We provide here, an overview of the contributions of this signaling pathway at multiple stages of neuronal development including, proliferation of neural stem cells (NSCs), migration of NSCs toward their destined niche, maintaining NSCs in the quiescent state, differentiation of NSCs into neurons, neuritogenesis, synaptogenesis, brain development, and in neuronal apoptosis. Hyperactivation of the neuronal Hippo pathway can also lead to a variety of devastating neurodegenerative diseases. Instances of aberrant Hippo pathway leading to neurodegenerative diseases along with the approaches utilizing this pathway as molecular targets for therapeutics has been highlighted in this review. Recent evidences suggesting neuronal repair and regenerative potential of this pathway has also been pointed out, that will shed light on a novel aspect of Hippo pathway in regenerative medicine. Our review provides a better understanding of the significance of Hippo pathway in the journey of neuronal system from development to diseases as a whole.

Anomalous Coulomb Drag between InAs Nanowire and Graphene Heterostructures.

Correlated charge inhomogeneity breaks the electron-hole symmetry in two-dimensional (2D) bilayer heterostructures which is responsible for nonzero drag appearing at the charge neutrality point. Here we report Coulomb drag in novel drag systems consisting of a two-dimensional graphene and a one-dimensional (1D) InAs nanowire (NW) heterostructure exhibiting distinct results from 2D-2D heterostructures. For monolayer graphene (MLG)-NW heterostructures, we observe an unconventional drag resistance peak near the Dirac point due to the correlated interlayer charge puddles. The drag signal decreases monotonically with temperature (∼T^{-2}) and with the carrier density of NW (∼n_{N}^{-4}), but increases rapidly with magnetic field (∼B^{2}). These anomalous responses, together with the mismatched thermal conductivities of graphene and NWs, establish the energy drag as the responsible mechanism of Coulomb drag in MLG-NW devices. In contrast, for bilayer graphene (BLG)-NW devices the drag resistance reverses sign across the Dirac point and the magnitude of the drag signal decreases with the carrier density of the NW (∼n_{N}^{-1.5}), consistent with the momentum drag but remains almost constant with magnetic field and temperature. This deviation from the expected T^{2} arises due to the shift of the drag maximum on graphene carrier density. We also show that the Onsager reciprocity relation is observed for the BLG-NW devices but not for the MLG-NW devices. These Coulomb drag measurements in dimensionally mismatched (2D-1D) systems, hitherto not reported, will pave the future realization of correlated condensate states in novel systems.

The emerging role of Hippo signaling in neurodegeneration.

Neurodegeneration refers to the complex process of progressive degeneration or neuronal apoptosis leading to a set of incurable and debilitating conditions. Physiologically, apoptosis is important in proper growth and development. However, aberrant and unrestricted apoptosis can lead to a variety of degenerative conditions including neurodegenerative diseases. Although dysregulated apoptosis has been implicated in various neurodegenerative disorders, the triggers and molecular mechanisms underlying such untimely and faulty apoptosis are still unknown. Hippo signaling pathway is one such apoptosis-regulating mechanism that has remained evolutionarily conserved from Drosophila to mammals. This pathway has gained a lot of attention for its tumor-suppressing task, but recent studies have emphasized the soaring role of this pathway in inflaming neurodegeneration. In addition, strategies promoting inactivation of this pathway have aided in the rescue of neurons from anomalous apoptosis. So, a thorough understanding of the relationship between the Hippo pathway and neurodegeneration may serve as a guide for the development of therapy for various degenerative diseases. The current review focuses on the mechanism of the Hippo signaling pathway, its upstream and downstream regulatory molecules, and its role in the genesis of numerous neurodegenerative diseases. The recent efforts employing the Hippo pathway components as targets for checking neurodegeneration have also been highlighted.