Long-term Alterations Research Articles

The effects of social defeat stress on hippocampal glial cells and interleukin-6 in adolescence and adulthood.

Adolescent social stress has been associated with the vulnerability to developing psychopathological disorders in adulthood that are accompanied by brain inflammatory processes. The purpose of this study is to investigate the dynamic changes of the hippocampal neuroinflammatory mediators, including microglia, astrocyte, and interleukin-6 (IL-6) levels in mice experiencing social defeat stress during adolescence. Adolescent mice were divided into the control group and stress group. Mice in the stress group were exposed to chronic intermittent social defeat for a total of 12 days, and control mice were reared in normal conditions. The hippocampal microglia, astrocyte, and IL-6 levels were measured 24 h and 3 weeks after the end of stress exposure. Microglia activation characterized by increased ionized calcium-binding adapter molecule 1 positive cell numbers or staining area in the CA1 and CA3 regions of the hippocampus were observed 24 h after the end of stress, which did not last into the adulthood. No short-term or long-term alterations of the number of hippocampal CA1 and CA3 glia fibrillary acidic protein astrocytes were found in mice experiencing adolescent social defeat, whereas IL-6 levels were only increased 3 weeks after the end of stress. These data suggested that exposure to chronic social defeat stress led to short-term and long-term neuroinflammatory changes in the hippocampus.

Long-term alterations of ERP systems: lasting through relinquishment and regeneration

PurposeThis paper highlights how technical devices last in organizations. Instead of focusing on the usual implementation or short-term post-implementation phases, this study aims to explore what happens to established technical devices.Design/methodology/approachThe authors build on a 10-year in-depth longitudinal case study examining a CRM package, a type of Enterprise Resource Planning system specialized in customer relationship management, in a door-drop advertising company. This case is based mainly on 35 interviews and four weeks of non-participant observation, made over three different periods.FindingsDrawing on the literature on drift and maintenance, this study investigates two tensions foregrounding lasting: one regarding the degree of human intervention on the technical device (object being maintained vs object maintaining itself) and one regarding the relationship to the initial expectations towards the technical device (relinquishment of certain hopes vs regeneration of interests). This case combines these tensions and allows to highlight four alterations in the CRM system to show how apparently stable devices keep on changing.Social implicationsIn a time of resource exhaustion, it is important to reflect upon our relationships to information technology and their modalities of lasting. By stressing that uses emerge from relinquishment and reduction, the authors wish to help organizations move towards more sustainable engagement with their technical devices in the long run.Originality/valueLasting is not just a matter of being maintained in a context of threat but also builds upon the capacities of a technical device to maintain itself. The self-alteration dynamics that the authors come up with, shedding and ramification, offer a dedramatized interpretation of maintenance that complements studies on institutional maintenance. The results also contribute to studies on technological drift. The authors stress that drifts are triggered by ties that run out, in particular, discontinuation of maintenance in the system. The durability of technical devices in organizations thus does not consist in always more uses or functionalities, but is also made of reductions and relinquishment.

Cannabis in Adolescence: Lasting Cognitive Alterations and Underlying Mechanisms.

Cannabis consumption during adolescence is an area of particular concern, owing to changes in the social and political perception of the drug, and presents a scientific, medical, and economic challenge. Major social and economic interests continue to push toward cannabis legalization as well as pharmaceutical development. As a result, shifting perceptions of both legal and illicit cannabis use across the population have changed the collective evaluation of the potential dangers of the product. The wave of cannabis legalization therefore comes with new responsibility to educate the public on potential risks and known dangers associated with both recreational and medical cannabis. Among these is the risk of long-term cognitive and psychological consequences, particularly following early-life initiation of use, compounded by high-potency and/or synthetic cannabis, and heavy/frequent use of the drug. Underlying these cognitive and psychiatric consequences are lasting aberrations in the development of synaptic function, often secondary to epigenetic changes. Additional factors such as genetic risk and environmental influences or nondrug toxic insults during development are also profound contributors to these long-term functional alterations following adolescent cannabis use. Preclinical studies indicate that exposure to cannabinoids during specific windows of vulnerability (e.g., adolescence) impacts neurodevelopmental processes and behavior by durably changing dendritic structure and synaptic functions, including those normally mediated by endogenous cannabinoids and neuronal circuits.

Parental obesity-induced changes in developmental programming.

Many studies support the link between parental obesity and the predisposition to develop adult-onset metabolic syndromes that include obesity, high blood pressure, dyslipidemia, insulin resistance, and diabetes in the offspring. As the prevalence of obesity increases in persons of childbearing age, so does metabolic syndrome in their descendants. Understanding how parental obesity alters metabolic programs in the progeny, predisposing them to adult-onset metabolic syndrome, is key to breaking this cycle. This review explores the basis for altered metabolism of offspring exposed to overnutrition by focusing on critical developmental processes influenced by parental obesity. We draw from human and animal model studies, highlighting the adaptations in metabolism that occur during normal pregnancy that become maladaptive with obesity. We describe essential phases of development impacted by parental obesity that contribute to long-term alterations in metabolism in the offspring. These encompass gamete formation, placentation, adipogenesis, pancreas development, and development of brain appetite control circuits. Parental obesity alters the developmental programming of these organs in part by inducing epigenetic changes with long-term consequences on metabolism. While exposure to parental obesity during any of these phases is sufficient to alter long-term metabolism, offspring often experience multiple exposures throughout their development. These insults accumulate to increase further the susceptibility of the offspring to the obesogenic environments of modern society.

Platelets and Sera from Donors of Convalescent Plasma after Mild COVID-19 Show No Procoagulant Phenotype.

Coronavirus disease-2019 (COVID-19) is associated with increased thromboembolic complications. Long-term alteration in the coagulation system after acute COVID-19 infection is still a subject of research. Furthermore, the effect of sera from convalescent subjects on platelets is not known. In this study, we investigated platelet phenotype, coagulation, and fibrinolysis in COVID-19 convalescent plasma (CCP) donors and analyzed convalescent sera-induced effects on platelets. We investigated CCP donors who had a history of mild COVID-19 infection and donors who did not have COVID-19 were used as controls. We analyzed phosphatidylserine (PS) externalization, CD62p expression, and glycoprotein VI (GPVI) shedding both in platelet-rich plasma (PRP) and after incubation of washed healthy platelets with donors' sera using flow cytometry. Coagulation and fibrinolysis systems were assessed with thromboelastometry. Forty-seven CCP donors (22 males, 25 females; mean age (±SD): 41.4 ± 13.7 years) with a history of mild COVID-19 infection were included. Median duration after acute COVID-19 infection was 97 days (range, 34-401). We did not find an increased PS externalization, CD62p expression, or GPVI shedding in platelets from CCP donors. Sera from CCP donors did not induce PS externalization or GPVI shedding in healthy platelets. Sera-induced CD62p expression was slightly, albeit statistically significantly, lower in CCP donors than in plasma donors without a history of COVID-19. One patient showed increased maximum clot firmness and prolonged lysis time in thromboelastometry. Our findings suggest that procoagulant platelet phenotype is not present after mild COVID-19. Furthermore, CCP sera do not affect the activation status of platelets.

Comparison of Clinical, Biochemical, and Sonological Parameters in Adolescents with and without Polycystic Ovarian Syndrome

Objectives The Pediatric Endocrine Society consensus criteria was developed in 2015 to diagnose adolescent PCOS. There are no Indian studies that use these criteria for diagnosis and then compare the clinical characteristics with those of normal controls. The objective of this study was to compare the clinical and biochemical profile in adolescents with and without PCOS and to study the ovarian morphology in adolescents with and without PCOS. Materials and Methods We conducted a prospective case–control study on 60 adolescents who attended the outpatient department/adolescent immunization clinic. Group A included 30 adolescent girls with PCOS diagnosed as per the consensus criteria and Group B included 30 adolescents without PCOS. All participants were clinically evaluated and called empty stomach in the follicular phase for metabolic (Serum TSH, prolactin, FSH, LH, and testosterone) and endocrinal workup (2-hour OGTT, lipid profile) followed by ultrasonic examination. Results In group A, 40% were overweight and 36.7% were obese and in group B, 20% were overweight and 20% were obese. There were no significant differences noted in gonadotropin levels in two groups. Mean testosterone levels were higher in PCO adolescents. The mean ovarian volume and ovarian follicle number were significantly higher in adolescents with PCOS. We found that if ultrasound criteria were added to the diagnosis, there would be about 7% lesser PCOS diagnosis. Conclusion PCOS alters the fat distribution and lipid distribution in the body. These are features that lead to long-term metabolic alterations and life-threatening diseases. All PCOS adolescents thus be screened for these abnormalities and advised lifestyle modifications to keep these parameters under control.

Post-Injury Buprenorphine Administration Is Associated with Long-Term Region-Specific Glial Alterations in Rats.

Traumatic brain injury (TBI) is a major leading cause of death and disability. While previous studies regarding focal pathologies following TBI have been done, there is a lack of information concerning the role of analgesics and their influences on injury pathology. Buprenorphine (Bup), an opioid analgesic, is a commonly used analgesic in experimental TBI models. Our previous studies investigated the acute effects of Buprenorphine-sustained release-Lab (Bup-SR-Lab) on diffuse neuronal/glial pathology, neuroinflammation, cell damage, and systemic physiology. The current study investigated the longer-term chronic outcomes of Bup-SR-Lab treatment at 4 weeks following TBI utilizing a central fluid percussion injury (cFPI) model in adult male rats. Histological assessments of physiological changes, neuronal damage, cortical and thalamic cytokine expression, microglial and astrocyte morphological changes, and myelin alterations were done, as we had done in our acute study. In the current study the Whisker Nuisance Task (WNT) was also performed pre- and 4w post-injury to assess changes in somatosensory sensitivity following saline or Bup-SR-Lab treatment. Bup-SR-Lab treatment had no impact on overall physiology or neuronal damage at 4w post-injury regardless of region or injury, nor did it have any significant effects on somatosensory sensitivity. However, greater IL-4 cytokine expression with Bup-SR-Lab treatment was observed compared to saline treated animals. Microglia and astrocytes also demonstrated region-specific morphological alterations associated with Bup-SR-Lab treatment, in which cortical microglia and thalamic astrocytes were particularly vulnerable to Bup-mediated changes. There were discernable injury-specific and region-specific differences regarding myelin integrity and changes in specific myelin basic protein (MBP) isoform expression following Bup-SR-Lab treatment. This study indicates that use of Bup-SR-Lab could impact TBI-induced glial alterations in a region-specific manner 4w following diffuse brain injury.

Involvement of Lateral Habenula Dysfunction in Repetitive Mild Traumatic Brain Injury-Induced Motivational Deficits.

Affective disorders including depression (characterized by reduced motivation, social withdrawal, and anhedonia), anxiety, and irritability are frequently reported as long-term consequences of mild traumatic brain injury (mTBI) in addition to cognitive deficits, suggesting a possible dysregulation within mood/motivational neural circuits. One of the important brain regions that control motivation and mood is the lateral habenula (LHb), whose hyperactivity is associated with depression. Here, we used a repetitive closed-head injury mTBI model that is associated with social deficits in adult male mice and explored the possible long-term alterations in LHb activity and motivated behavior 10-18 days post-injury. We found that mTBI increased the proportion of spontaneous tonically active LHb neurons yet decreased the proportion of LHb neurons displaying bursting activity. Additionally, mTBI diminished spontaneous glutamatergic and GABAergic synaptic activity onto LHb neurons, while synaptic excitation and inhibition (E/I) balance was shifted toward excitation through a greater suppression of GABAergic transmission. Behaviorally, mTBI increased the latency in grooming behavior in the sucrose splash test suggesting reduced self-care motivated behavior following mTBI. To show whether limiting LHb hyperactivity could restore motivational deficits in grooming behavior, we then tested the effects of Gi (hM4Di)-DREADD-mediated inhibition of LHb activity in the sucrose splash test. We found that chemogenetic inhibition of LHb glutamatergic neurons was sufficient to reverse mTBI-induced delays in grooming behavior. Overall, our study provides the first evidence for persistent LHb neuronal dysfunction due to an altered synaptic integration as causal neural correlates of dysregulated motivational states by mTBI.

Assessment of the natural flow regime and its variability in a tributary of Ganga River: Impact of land use and land cover change

Accurate assessment of hydrological processes in a catchment including the estimation of virgin or natural flow regime of the rivers is critical to maintaining healthy river ecosystems, particularly in the developing nations that currently face the challenges of limited quantity and poor quality of available water. In this work, we aim to estimate the natural river flow and its variability due to land use and land cover (LULC) alterations over a period of ∼43 years (1970–2013–14) in the Ramganga River Basin (RRB), a sub-basin of the most fertile and densely populated basin in the world i.e., the Ganga River Basin. Hydrological modeling of the RRB was performed using the Soil and Water Assessment Tool (SWAT) and its performance was evaluated by performing statistical analysis (e.g. coefficient of determination and Nash–Sutcliffe efficiencies). The simulated flows exhibited good agreement with the observed flows at the three flow monitoring stations in the RRB - Katghar, Chaubari, and Dabri. Upon achieving a good model performance, the natural flows for the 2013-14 LULC scenario were estimated by removing all existing flow interventions (e.g. dams and barrages) and irrigation usage. Average annual natural flows were observed to be higher by at least ∼40% than the average annual existing flows (i.e., flows estimated with current managed conditions) for the three stations. Historical LULC information for the basin was obtained from the object-based image classification of CORONA satellite images (1970). The annual average natural flows for the 1970 scenario were observed to be lower (3–12%) than the 2013-14 scenario which could be attributed to a significant increase in urban settlements and a reduction in the area coverage by barren land and shrubs and bushes. Overall, our work provides valuable insights into the natural flow regime and its variability due to anthropogenic activities and long-term LULC alterations in the RRB which may inform future strategies for sustainable water resources management in the basin.

Site-specific decreases in DNA methylation in replicating cells following exposure to oxidative stress.

Oxidative stress is a common feature of inflammation-driven cancers, and it promotes genomic instability and aggressive tumour phenotypes. It is known that oxidative stress transiently modulates gene expression through the oxidation of transcription factors and associated regulatory proteins. Neutrophils are our most abundant white blood cells and accumulate at sites of infection and inflammation. Activated neutrophils produce hypochlorous acid and chloramines, which can disrupt DNA methylation by oxidizing methionine. The goal of the current study was to determine whether chloramine exposure results in sequence-specific modifications in DNA methylation that enable long-term alterations in transcriptional output. Proliferating Jurkat T-lymphoma cells were exposed to sublethal doses of glycine chloramine and differential methylation patterns were compared using Illumina EPIC 850K bead chip arrays. There was a substantial genome-wide decrease in methylation 4 h after exposure that correlated with altered RNA expression for 24 and 48h, indicating sustained impacts on exposed cells. A large proportion of the most significant differentially methylated CpG sites were situated towards chromosomal ends, suggesting that these regions are most susceptible to inhibition of maintenance DNA methylation. This may contribute to epigenetic instability of chromosomal ends in rapidly dividing cells, with potential implications for the regulation of telomere length and cellular longevity.

Genetically proxied therapeutic prolyl-hydroxylase inhibition and cardiovascular risk.

Prolyl hydroxylase (PHD) inhibitors are in clinical development for anaemia in chronic kidney disease. Epidemiological studies have reported conflicting results regarding safety of long-term therapeutic haemoglobin (Hgb) rises through PHD inhibition on risk of cardiovascular disease. Genetic variation in genes encoding PHDs can be used as partial proxies to investigate the potential effects of long-term Hgb rises. We used Mendelian randomization to investigate the effect of long-term Hgb level rises through genetically proxied PHD inhibition on coronary artery disease (CAD: 60 801 cases; 123 504 controls), myocardial infarction (MI: 42 561 cases; 123 504 controls) or stroke (40 585 cases; 406 111 controls). To further characterize long-term effects of Hgb level rises, we performed a phenome-wide association study (PheWAS) in up to 451 099 UK Biobank individuals. Genetically proxied therapeutic PHD inhibition, equivalent to a 1.00g/dl increase in Hgb levels, was not associated (at P < 0.05) with increased odds of CAD; odd ratio (OR) [95% confidence intervals (CI)] = 1.06 (0.84, 1.35), MI [OR (95% CI) = 1.02 (0.79, 1.33)] or stroke [OR (95% CI) = 0.91 (0.66, 1.24)]. PheWAS revealed associations with blood related phenotypes consistent with EGLN's role, relevant kidney- and liver-related biomarkers like estimated glomerular filtration rate and microalbuminuria, and non-alcoholic fatty liver disease (Bonferroni-adjusted P < 5.42E-05) but these were not clinically meaningful. These findings suggest that long-term alterations in Hgb through PHD inhibition are unlikely to substantially increase cardiovascular disease risk; using large disease genome-wide association study data, we could exclude ORs of 1.35 for cardiovascular risk with a 1.00g/dl increase in Hgb.

Antibiotic-induced microbiota depletion in normally-reared adult rats mimics the neuroendocrine effects of early life stress

Early life stress induced by maternal separation (MS) causes neuroendocrine, behavioral, and metabolic alterations that are related to gut dysbiosis. MS also increases microglial activation and decreases neurogenesis. Whether these long-term alterations are maintained or worsened in the absence of gut microbiota remains unknown. Hence, this study evaluated the effect of MS symptomatology after antibiotic-induced microbiota depletion (AIMD) in adult rats. Control and maternally separated (3 h per day from postnatal day one to 14, MS180) rats were subjected to AIMD for one month, then assessed for behavioral, metabolic, and neuroendocrine responses. Effects of MS180 and AIMD on gut microbiota were confirmed by qPCR. The data indicate that MS180 caused a passive coping strategy in the forced swimming test and decreased hippocampal neurogenesis. In addition, fasting glucose, cholesterol, and corticosterone levels increased, which correlated with a decrease in Lactobacillus spp counts in the caecum. AIMD also increased immobility in the forced swimming test, decreased hippocampal neurogenesis, and augmented corticosterone levels. However, it had no effects on glucose homeostasis or plasma lipid levels. Furthermore, the MS180-induced long-term effects on behavior and neurogenesis were not affected by microbiota depletion. Meanwhile, the metabolic imbalance was partially reversed in MS180 + AIMD rats. These results show that AIMD mimics the behavioral consequences of MS180 but may prevent metabolic imbalance, suggesting that gut dysbiosis could be part of the mechanisms involved in the maintenance of the long-term consequences of early life stress.

Neonatal Streptococcus pneumoniae infection induces long-lasting dysbiosis of the gut microbiota in a mouse model.

Early life is a "critical window" for gut microbiota development, antibiotic use during this period exerts a profound effect on gut microbial dysbiosis and asthma. In clinical practice, antibiotics are usually used in patients with bacterial infections, we previously showed that neonatal S. pneumoniae pneumonia promoted adult-onset asthma in mice model, while it remains unclear whether neonatal S. pneumoniae infection have long-term effects on gut microbiota. Neonatal BALB/c mice were inoculated with 5*106 CFU D39 to establish non-lethal S. pneumoniae pneumonia model. At 2, 3, 8 weeks of age, feces in the cecum were prepared for 16S rRNA sequencing, lungs were collected for histopathologic and lung function analysis. S. pneumoniae-infected neonatal mice exhibited histopathologic lesions in their lungs and increased airway hyperresponsiveness, obvious alterations in alpha and beta diversities in the entire gut microbiota, and changes of the community structure during the breastfeeding period, infancy, and adulthood. Furthermore, gut microbial composition was modified after neonatal S. pneumoniae infection, with a decreased relative abundance of Lactobacillus in the breastfeeding period and infancy; in adulthood, the relative abundance of Allobaculum diminished while that of Proteobacteria was augmented. Neonatal S. pneumoniae infection induced a long-term alteration in microbial community composition.

Morphological, cellular, and molecular basis of brain infection in COVID-19 patients

Although increasing evidence confirms neuropsychiatric manifestations associated mainly with severe COVID-19 infection, long-term neuropsychiatric dysfunction (recently characterized as part of "long COVID-19" syndrome) has been frequently observed after mild infection. We show the spectrum of cerebral impact of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, ranging from long-term alterations in mildly infected individuals (orbitofrontal cortical atrophy, neurocognitive impairment, excessive fatigue and anxiety symptoms) to severe acute damage confirmed in brain tissue samples extracted from the orbitofrontal region (via endonasal transethmoidal access) from individuals who died of COVID-19. In an independent cohort of 26 individuals who died of COVID-19, we used histopathological signs of brain damage as a guide for possible SARS-CoV-2 brain infection and found that among the 5 individuals who exhibited those signs, all of them had genetic material of the virus in the brain. Brain tissue samples from these five patients also exhibited foci of SARS-CoV-2 infection and replication, particularly in astrocytes. Supporting the hypothesis of astrocyte infection, neural stem cell-derived human astrocytes invitro are susceptible to SARS-CoV-2 infection through a noncanonical mechanism that involves spike-NRP1 interaction. SARS-CoV-2-infected astrocytes manifested changes in energy metabolism and in key proteins and metabolites used to fuel neurons, as well as in the biogenesis of neurotransmitters. Moreover, human astrocyte infection elicits a secretory phenotype that reduces neuronal viability. Our data support the model in which SARS-CoV-2 reaches the brain, infects astrocytes, and consequently, leads to neuronal death or dysfunction. These deregulated processes could contribute to the structural and functional alterations seen in the brains of COVID-19 patients.

Short- and Long-Term Effects of Suboptimal Selenium Intake and Developmental Lead Exposure on Behavior and Hippocampal Glutamate Receptors in a Rat Model.

Selenium (Se) is an essential trace element required for normal development as well as to counteract the adverse effects of environmental stressors. Conditions of low Se intake are present in some European countries. Our aim was to investigate the short- and long-term effects of early-life low Se supply on behavior and synaptic plasticity with a focus on the hippocampus, considering both suboptimal Se intake per se and its interaction with developmental exposure to lead (Pb). We established an animal model of Se restriction and low Pb exposure; female rats fed with an optimal (0.15 mg/kg) or suboptimal (0.04 mg/kg) Se diet were exposed from one month pre-mating until the end of lactation to 12.5 µg/mL Pb via drinking water. In rat offspring, the assessment of motor, emotional, and cognitive endpoints at different life stages were complemented by the evaluation of the expression and synaptic distribution of NMDA and AMPA receptor subunits at post-natal day (PND) 23 and 70 in the hippocampus. Suboptimal Se intake delayed the achievement of developmental milestones and induced early and long-term alterations in motor and emotional abilities. Behavioral alterations were mirrored by a drop in the expression of the majority of NMDA and AMPA receptor subunits analyzed at PND 23. The suboptimal Se status co-occurring with Pb exposure induced a transient body weight increase and persistent anxiety-like behavior. From the molecular point of view, we observed hippocampal alterations in NMDA (Glun2B and GluN1) and AMPA receptor subunit trafficking to the post-synapse in male rats only. Our study provides evidence of potential Se interactions with Pb in the developing brain.

T cell perturbations persist for at least 6 months following hospitalization for COVID-19.

COVID-19 is being extensively studied, and much remains unknown regarding the long-term consequences of the disease on immune cells. The different arms of the immune system are interlinked, with humoral responses and the production of high-affinity antibodies being largely dependent on T cell immunity. Here, we longitudinally explored the effect COVID-19 has on T cell populations and the virus-specific T cells, as well as neutralizing antibody responses, for 6-7 months following hospitalization. The CD8+ TEMRA and exhausted CD57+ CD8+ T cells were markedly affected with elevated levels that lasted long into convalescence. Further, markers associated with T cell activation were upregulated at inclusion, and in the case of CD69+ CD4+ T cells this lasted all through the study duration. The levels of T cells expressing negative immune checkpoint molecules were increased in COVID-19 patients and sustained for a prolonged duration following recovery. Within 2-3 weeks after symptom onset, all COVID-19 patients developed anti-nucleocapsid IgG and spike-neutralizing IgG as well as SARS-CoV-2-specific T cell responses. In addition, we found alterations in follicular T helper (TFH) cell populations, such as enhanced TFH-TH2 following recovery from COVID-19. Our study revealed significant and long-term alterations in T cell populations and key events associated with COVID-19 pathogenesis.

Origin of multiple principal slip zones in a fault gouge zone within granitoids

Fault zones in crystalline rocks generally possess a relatively narrow (<50-cm-thick) fault core (i.e., a fault gouge layer/zone). However, the Geumwang Fault, a major strike-slip fault developed in granitic rocks in Korea, has a wider (∼24-m-thick) fault core with several gouge layers. Here we conduct detailed field and microanalytical investigations on the fault core of the Geumwang Fault. Results showed that some of the gouges are primary gouges in which seismic slip was localized as the principal slip zones (PSZs), whereas others are secondary gouges that formed by the injection of fluidized gouge material into fractures. Within the PSZs, the presence of amorphous carbon and graphite implies that frictional heat generated by coseismic slip triggered siderite decomposition. It was likely the consequence of gouge fluidization induced by thermal pressurization under fluid drained conditions. In addition, the gouge fluidization seems to neutralize the foliation of the PSZ. This process, together with weakening of the damage zone by long-term alteration, may facilitate subsequent seismic slip occurred along foliated breccia or the fault core boundary rather than the former neutralized PSZs, thereby widening the Geumwang Fault. We propose that coseismic fluidization of PSZ by thermal pressurization can act as a potential mechanism to widen the fault core and generate multiple gouge layers in crystalline rocks.

Is there a significant long-term shift in phytoplankton in small pelagic fish diets along India's southwest coast?

The two main small pelagic fishes along the southwest coast of India in the eastern Arabian Sea, the Indian oil sardine (Sardinella longiceps) and the Indian mackerel (Rastrelliger kanagurta) were studied to see if there was any notable long-term alteration in phytoplankton in their diets. The basic oceanographic features and the long-term sea surface warming in the study region are first examined using satellite data, which reveals clear seasonality in the wind, sea surface temperature, sea surface salinity, and chlorophyll-a as well as long-term ocean surface warming. We then considered a recent gut content data set of Indian oil sardine and Indian mackerel from the 2010–2011 period from two landing places along India's southwest coast, which was compared with numerous historical data sets to find out if there was any long-term phytoplankton compositional change in the diet. The recent data revealed the same dominant phytoplankton as those collected decades ago, such as Coscinodiscus, Nitzschia, Pleurosigma, and Thalassiosira in sardines and Coscinodiscus, Thalassiosira, Ceratium, Dinophysis, Protoperidinium, and Pyrophacus in mackerel. This suggests the lack of any significant long-term qualitative shift of phytoplankton in the Indian oil sardine and Indian mackerel over the last several decades. However, several phytoplankton genera found present in the recent data were absent in the historical data, including 10 genera for mackerel and 17 for Indian oil sardine. These recent phytoplankton records are intriguing, and we feel they could be an early sign of long-term phytoplankton compositional or relative abundance shift, although additional research is needed to confirm this.

Arthrogenic Muscle Inhibition Following Anterior Cruciate Ligament Injury.

Arthrogenic muscle inhibition (AMI) is a common impairment in individuals who sustain an anterior cruciate ligament (ACL) injury. The AMI causes decreased muscle activation, which impairs muscle strength, leading to aberrant movement biomechanics. The AMI is often resistant to traditional rehabilitation techniques, which leads to persistent neuromuscular deficits following ACL reconstruction. To better treat AMI following ACL injury and ACL reconstruction, it is important to understand the specific neural pathways involved in AMI pathogenesis, as well as the changes in muscle function that may impact movement biomechanics and long-term structural alterations to joint tissue. Overall, AMI is a critical factor that limits optimal rehabilitation outcomes following ACL injury and ACL reconstruction. This review discusses the current understanding of the: (1)neural pathways involved in the AMI pathogenesis following ACL injury; (2)consequence of AMI on muscle function, joint biomechanics, and patient function; and (3)development of posttraumatic osteoarthritis. Finally, the authors review the evidence for interventions specifically used to target AMI following ACL injury.

Predicted changes in the distribution of Antarctic krill in the Cosmonaut Sea under future climate change scenarios

Antarctic krill (Euphausia superba) are the key species of the ecological system in the Cosmonaut Sea. Long-term habitat alterations in krill due to climate change have been considered in recent decades. However, there is still a lack understanding about krill distribution. The MaxEnt model was used to forecast the suitable distribution area of krill for this study, which is based on data from the Coupled Model Intercomparison Project in its sixth phase (CMIP6) in the near future and far future. A total of 145 occurrence points and 15 environmental factors were selected to build the MaxEnt model. The current suitable habitat regions for krill were mostly detected in the western and central regions of the Cosmonaut Sea, which accounted for 10.07% of the total area. The most important environmental variables that influenced krill distribution were minimum surface solar radiation downward (ssrdmin), the mean temperature (tem) and the mean northward velocity (v). In the near future and far future, the suitable area of krill was seen to decline under all shared socioeconomic pathways (SSPs), with the smallest reduction under SSP1-2.6 and the greatest reduction under SSP5-8.5. The suitable area for krill dropped quicker from the near future to the far future than the present to the near future. Krill habitats were expected to shift to the poles. The tem continued to rise in the future under all SSP scenarios, particularly under the high radiative forcing scenario. The increase in water temperature is the main reason for the decrease in suitable areas for Antarctic krill. Our results show the future distribution of krill in the future and provide a reasonable reference for the ecological protection policy of the Cosmonaut Sea.