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A functionalised dipeptide that self-assembles to form wormlike micelles at high pH can be treated as a surfactant. By varying salt concentration, the self-assembled structures and interactions between them change, resulting in solutions with very different shear and extensional viscosity. From these, gel noodles with different mechanical properties can be prepared.

Hierarchical self-assembly is an effective means of preparing useful materials. However, control over assembly across length scales is a difficult challenge, often confounded by the perceived need to redesign the molecular building blocks when new material properties are needed. Here, we show that we can treat a simple dipeptide building block as a polyelectrolyte and use polymer physics approaches to explain the self-assembly over a wide concentration range. This allows us to determine how entangled the system is and therefore how it might be best processed, enabling us to prepare interesting analogues to threads and webs, as well as films that lose order on heating and "noodles" which change dimensions on heating, showing that we can transfer micellar-level changes to bulk properties all from a single building block.

Pneumatic probes such as five-hole probes (5HP) have many advantages and can measure flow angles, total and static pressure, velocity and Mach number. In most applications, pressure transducers are connected to the probe head by lengths of tubes, allowing a simple, miniaturised, low-cost probe construction. Such “steady” probes therefore measure a “pneumatically-averaged” flow field, which is of sufficient accuracy for many purposes. However, this paper demonstrates that when the probe incidence angle fluctuates, pneumatic averaging causes errors in the indicated total and static pressure. The aim of this paper is to understand these pneumatic averaging errors and to demonstrate practical means to post-correct data. A quasi-steady model provides an analytical framework to explain the effect of unsteady flow on 5HPs. Total and static pressure coefficients have a largely symmetric response to positive and negative incidence, causing a bias error in the pneumatic average. The steady calibration cannot account for these effects, leading to erroneous measurements. These errors are demonstrated by comparing 5HP and Kiel-shrouded pitot traverses in the shedding wake of a D-shaped body. The 5HP overestimates total pressure loss and drag coefficients by up to 44% and 60% respectively. Similar pneumatic-averaging errors will have affected a substantial body of data in the literature. A post-correction method is demonstrated that can be applied to historical data. Estimates of unsteady flow angles are obtained from a low-cost unsteady computation. The quasi-steady model accurately corrects the 5HP data, reducing errors by an order of magnitude. Similar corrections are obtained using simple correlations based on the root-mean-squared angle fluctuation.

This review describes the authors' experiences in offering gender-affirming primary care and hormonal care using an evidence-based, interprofessional, and multidisciplinary approach. The authors offer references for best practices set forth by organizations and thought leaders in transgender health and describe the key processes they developed to respectfully deliver affirming care to transgender and nonbinary patients.

Hierarchical self-assembly is an effective means of preparing useful materials. However, control over assembly across length scales is a difficult challenge, often confounded by the perceived need to re-design the molecular building blocks when new material properties are needed. Here, we show that we can treat a simple dipeptide building block as a polyelectrolyte and use polymer physics approaches to explain the self-assembly over a wide concentration range. This allows us to prepare interesting analogues to threads and webs, as well as films that lose order on heating and “noodles” which change dimensions on heating, showing that we can transfer molecular-level changes to bulk properties all from a single building block.

Supplemental Digital Content is available in the text., Objective: The full spectrum of coronavirus disease 2019 (COVID-19) infection ranges from asymptomatic to acute respiratory distress syndrome, characterized by hyperinflammation and thrombotic microangiopathy. The pathogenic mechanisms are poorly understood, but emerging evidence suggest that excessive neutrophil extracellular trap (NET) formation plays a key role in COVID-19 disease progression. Here, we evaluate if circulating markers of NETs are associated with COVID-19 disease severity and clinical outcome, as well as to markers of inflammation and in vivo coagulation and fibrinolysis. Approach and Results: One hundred six patients with COVID-19 with moderate to severe disease were enrolled shortly after hospital admission and followed for 4 months. Acute and convalescent plasma samples as well as plasma samples from 30 healthy individuals were assessed for markers of NET formation: citrullinated histone H3, cell-free DNA, NE (neutrophil elastase). We found that all plasma levels of NET markers were elevated in patients with COVID-19 relative to healthy controls, that they were associated with respiratory support requirement and short-term mortality, and declined to those found in healthy individuals 4 months post-infection. The levels of the NET markers also correlated with white blood cells, neutrophils, inflammatory cytokines, and C-reactive protein, as well as to markers of in vivo coagulation, fibrinolysis, and endothelial damage. Conclusions: Our findings suggest a role of NETs in COVID-19 disease progression, implicating their contribution to an immunothrombotic state. Further, we observed an association between circulating markers of NET formation and clinical outcome, demonstrating a potential role of NET markers in clinical decision-making, as well as for NETs as targets for novel therapeutic interventions in COVID-19.

Myocardial tissue in optimal cutting temperature (OCT) fixation and cryostat sectioning was tested as a means of storing and preparing tissue for myofilament function analysis in relation to conventional liquid nitrogen freezing and dissection. Actomyosin interaction, Ca2+ force activation, and passive compliance were tested. The study concluded that OCT storage and cryostat sectioning do not interfere with the actomyosin cross-bridge dynamics or Ca2+ activation but that absolute tension values suffer and may not be investigated by this method.

BackgroundBooster vaccine doses offer protection against severe COVID-19 caused by omicron but are less effective against infection. Characteristics such as serological correlates of protection, viral abundance, and clearance of omicron infection in triple vaccinated individuals are scarce.MethodsWe conducted a 4-week twice-weekly SARS-CoV-2 qPCR screening shortly after an mRNA vaccine booster in 368 healthcare workers. Spike-specific IgG levels and neutralization titers were determined at study start. qPCR-positive participants were sampled repeatedly for two weeks and monitored for symptoms.ResultIn total 81 (cumulative incidence 22%) omicron infections were detected, divided between BA.1, BA.1.1 and BA.2. Increasing post-booster antibody titers were protective against infection (pConclusionWe report a high incidence of omicron infection despite recent booster vaccination in triple vaccinated individuals. Increasing levels of vaccine-induced spike-specific WT antibodies entail increased protection against infection and reduce viral load if infected. High viral load and secretion of live virus for up to nine days may facilitate transmission in a triple vaccinated population.

Candida albicans cell wall glycoproteins, and in particular their mannose-rich glycans, are important for maintaining cellular integrity as well as host recognition, adhesion, and immunomodulation. The asparagine (N)-linked mannose outer chain of these glycoproteins is produced by Golgi mannosyltransferases (MTases). The outer chain is composed of a linear backbone of ∼50 α1,6-linked mannoses, which acts as a scaffold for addition of ∼150 or more mannoses in other linkages. Here, we describe the characterization of C. albicans OCH1, MNN9, VAN1, ANP1, MNN10, and MNN11, which encode the conserved Golgi MTases that sequentially catalyze the α1,6 mannose outer chain backbone. Candida albicans och1Δ/Δ, mnn9Δ/Δ, and van1Δ/Δ mutants block the earliest steps of backbone synthesis and like their Saccharomyces cerevisiae counterparts, have severe cell wall and growth phenotypes. Unexpectedly, and in stark contrast to S. cerevisiae, loss of Anp1, Mnn10, or Mnn11, which together synthesize most of the backbone, have no obvious deleterious phenotypes. These mutants were unaffected in cell morphology, growth, drug sensitivities, hyphal formation, and macrophage recognition. Analyses of secreted glycosylation reporters demonstrated that anp1Δ/Δ, mnn10Δ/Δ, and mnn11Δ/Δ strains accumulate glycoproteins with severely truncated N-glycan chains. This hypo-mannosylation did not elicit increased chitin deposition in the cell wall, which in other yeast and fungi is a key compensatory response to cell wall integrity breaches. Thus, C. albicans has evolved an alternate mechanism to adapt to cell wall weakness when N-linked mannan levels are reduced.

Background: Emerging data support detectable immune responses for months after severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and vaccination, but it is not yet established to what degree and for how long protection against reinfection lasts. Methods: We investigated SARS-CoV-2-specific humoral and cellular immune responses more than 8 months post-asymptomatic, mild and severe infection in a cohort of 1884 healthcare workers (HCW) and 51 hospitalized COVID-19 patients. Possible protection against SARS-CoV-2 reinfection was analyzed by a weekly 3-month polymerase chain reaction (PCR) screening of 252 HCW that had seroconverted 7 months prior to start of screening and 48 HCW that had remained seronegative at multiple time points. Results: All COVID-19 patients and 96% (355/370) of HCW who were anti-spike IgG positive at inclusion remained anti-spike IgG positive at the 8-month follow-up. Circulating SARS-CoV-2-specific memory T cell responses were detected in 88% (45/51) of COVID-19 patients and in 63% (233/370) of seropositive HCW. The cumulative incidence of PCR-confirmed SARS-CoV-2 infection was 1% (3/252) among anti-spike IgG positive HCW (0.13 cases per 100 weeks at risk) compared to 23% (11/48) among anti-spike IgG negative HCW (2.78 cases per 100 weeks at risk), resulting in a protective effect of 95.2% (95% CI 81.9%-99.1%). Conclusions: The vast majority of anti-spike IgG positive individuals remain anti-spike IgG positive for at least 8 months regardless of initial COVID-19 disease severity. The presence of anti-spike IgG antibodies is associated with a substantially reduced risk of reinfection up to 9 months following asymptomatic to mild COVID-19. De tre första författarna delar förstaförfattarskapetDe fem sista författarna delar sistaförfattarskapet

Heterochromatin spreading, the expansion of repressive chromatin structure from sequence-specific nucleation sites, is critical for stable gene silencing. Spreading re-establishes gene-poor constitutive heterochromatin across cell cycles but can also invade gene-rich euchromatin de novo to steer cell fate decisions. How chromatin context (i.e. euchromatic, heterochromatic) or different nucleation pathways influence heterochromatin spreading remains poorly understood. Previously, we developed a single-cell sensor in fission yeast that can separately record heterochromatic gene silencing at nucleation sequences and distal sites. Here we couple our quantitative assay to a genetic screen to identify genes encoding nuclear factors linked to the regulation of heterochromatin nucleation and the distal spreading of gene silencing. We find that mechanisms underlying gene silencing distal to a nucleation site differ by chromatin context. For example, Clr6 histone deacetylase complexes containing the Fkh2 transcription factor are specifically required for heterochromatin spreading at constitutive sites. Fkh2 recruits Clr6 to nucleation-distal chromatin sites in such contexts. In addition, we find that a number of chromatin remodeling complexes antagonize nucleation-distal gene silencing. Our results separate the regulation of heterochromatic gene silencing at nucleation versus distal sites and show that it is controlled by context-dependent mechanisms. The results of our genetic analysis constitute a broad community resource that will support further analysis of the mechanisms underlying the spread of epigenetic silencing along chromatin.

Background Recent serological investigations imply waning immune responses following SARS-CoV-2 vaccination, but prior infection may impact the breadth and duration of vaccine immune responses. Methods Using longitudinally collected blood samples from the COMMUNITY study, we determined binding (WHO BAU/ml) and neutralizing antibody titers against ten SARS-CoV-2 variants over seven months following BNT162b2 in healthcare workers with (n=111) and without (n=298) confirmed prior SARS-CoV-2 infection. A smaller group with (n=47) and without (n=61) confirmed prior SARS-CoV-2 infection receiving ChAdOx1 ncov-19 was followed for three months. Results Vaccination (BNT162b2 and ChAdOx1 ncov-19) following SARS-CoV-2 infection resulted in higher wild-type BAU/ml geometric mean titers (GMTs) at all sampling time points when compared to SARS-CoV-2 naive vaccinees (all p

BackgroundSARS-CoV-2 variants, such as Alpha, Beta, Gamma and Delta, are raising concern about the efficiency of neutralizing antibodies (NAb) induced by wild-type infection or vaccines based on the wild-type spike.MethodsWe determined IgG and NAb against SARS-CoV-2 variants one year following mild wild-type infection (n=104) and two-dose regimens with BNT162b2 (BNT/BNT) (n=67), ChAdOx1 (ChAd/ChAd) (n=82), or heterologous ChAdOx1 followed by BNT162b2 (ChAd/BNT) (n=116).FindingsWild type spike IgG and NAb remained detectable in 80% (83/104) of unvaccinated participants one year post mild infection. The neutralizing capacity was similar against wild type (reference), Alpha (0.95 (0.92-0.98) and Delta 1.03 (0.95-1.11) but significantly reduced against Beta (0.54 (0.48-0.60)) and Gamma 0.51 (0.44-0.61). Similarly, BNT/BNT and ChAd/ChAd elicited sustained capacity against Alpha and Delta (1.01 (0.78-1.31) and 0.85 (0.64-1.14)) and (0.96 (0.84-1.09) and 0.82 (0.61-1.10) respectively), with reduced capacity against Beta (0.67 (0.50-0.88) and 0.53 (0.40-0.71)) and Gamma (0.12 (0.06-0.27) and 0.54 (0.37-0.80)). A similar trend was found following ChAd/BNT (0.74 (0.66-0.83) and 0.70 (0.50-0.97) against Alpha and Delta and 0.29 (0.20-0.42) and 0.13 (0.08-0.20) against Beta and Gamma).InterpretationPersistent neutralization of the wide-spread Alpha and Delta variants one year after wild-type infection may aid vaccine policy makers in low-resource settings when prioritizing vaccine supply. The reduced capacity of neutralizing Beta and Gamma strains, but not the Alpha and Delta strains following both infection and three different vaccine regimens argues for caution against Beta and Gamma-exclusive mutations in the efforts to optimize next generation SARS-CoV-2 vaccines.FundingA full list of funding bodies that contributed to this study can be found in the Acknowledgements section

Background Recent reports demonstrate robust serological responses to a single dose of messenger RNA (mRNA) vaccines in individuals previously infected with SARS-CoV-2. Data on immune responses following a single-dose adenovirus-vectored vaccine expressing the SARS-CoV-2 spike protein (ChAdOx1 nCoV-19) in individuals with previous SARS-CoV-2 infection are however limited, and current guidelines recommend a two-dose regimen regardless of preexisting immunity. Methods We compared RBD-specific IgG and RBD-ACE2 blocking antibodies against SARS-CoV-2 wild type and variants of concern following two doses of the mRNA vaccine BNT162b2 in SARS-CoV-2 naive healthcare workers (n=65) and a single dose of the adenovector vaccine ChAdOx1 nCoV-19 in 82 healthcare workers more than (n=45) and less than (n=37) 11 months post mild SARS-CoV-2 infection at time of vaccination. Findings The post-vaccine levels of RBD-specific IgG and neutralizing antibodies against the SARS-CoV-2 wild type and variants of concern including Delta lineage 1.617.2 were similar or higher in participants receiving a single dose of ChAdOx1 nCoV-19 vaccine post SARS-CoV-2 infection (both more than and less than 11 months post infection) compared to SARS-CoV-2 naive participants who received two doses of BNT162b2 vaccine. Interpretation Our data support that a single dose ChAdOx1 nCoV-19 vaccine that is administered up to at least 11 months post SARS-CoV-2 infection serves as an effective immune booster. This provides a possible rationale for a single-dose vaccine regimen. Funding A full list of funding bodies that contributed to this study can be found in the Acknowledgements section

Background Central obesity is a risk factor for metabolic syndrome. Subjects with central obesity have a higher risk of developing type 2 diabetes and cardiovascular disease. Many conditions affect the prevalence of central obesity, including energy expenditure, aging, proinflammatory conditions, and hormonal, genetic, and ethnic differences. Polymorphism of the APM1 gene, encoding the protein adiponectin, is closely related to metabolic syndrome. Adiponectin influences fatty acid oxidation and glucose intake in muscle. Therefore, variation in the APM1 gene is associated with diabetes and obesity. Purpose The aim of the present study was to investigate the correlation of the single-nucleotide polymorphism (SNP) of the APM1 SNP rs2241766 with body mass index (BMI) and lipid profiles in Indonesian (Bandung) subjects. Patients and methods Genotyping of the APM1 gene was performed using the Amplification Refractory Mutation System. Whole blood and serum of 54 subjects with central obesity (waist circumference [WC] ≥90 cm) and 53 healthy subjects (WC

This review describes the authors' experiences in offering gender-affirming primary care and hormonal care using an evidence-based, interprofessional, and multidisciplinary approach. The authors offer references for best practices set forth by organizations and thought leaders in transgender health and describe the key processes they developed to respectfully deliver affirming care to transgender and nonbinary patients.

The number of mental disorders has been increasing but has yet to receive sufficient attention. In particular, healthcare students and professionals tend to have high stress burden. Finding the root cause of psychological distress is important to formulate a method for early detection and prevention. The association of brain-derived neurotrophic factor val66met polymorphism to neuropsychiatric disorders has been widely studied. To study the interplay between brain-derived neurotrophic factor val66met polymorphism and sociodemographic factors in the pathogenesis of psychological distress among Indonesian Pharmacy students. Level of psychological distress and sociodemographic profiling was collected by using the Kessler Psychological Distress Scale and sociodemographic questionnaires, respectively. Genotyping was performed using polymerase chain reaction-amplified refractory mutation system. Pearson's chi square and binomial logistic tests were used to evaluate the correlation. This study recruited 148 participants. The psychological distress levels of the participants were well (27.03%), mild (37.16%), moderate (25.00%), and severe (10.81%). Genotypic distributions were AA (25.67%), GA (50.68%), and GG (23.65%). No statistical significance between genotype and psychological distress was found in the study (P = .076). The sociodemographic factors also showed non significance, except for the source of tuition fee among women students (P = .049). Psychological distress is not affected by genotypic and sociodemographic factors. Further confirmatory research with larger and broader populations is required.

Pro-angiogenic neutrophils (PAN) form a small subset of circulating neutrophils expressing CD49d+ VEGFR1hi CXCR4hi, which play a crucial role in the revascularization of transplanted islets. To determine the role of PANs in re-establishing tissue perfusion following a large ischemic event we used the mouse model for peripheral artery disease, the hindlimb ischemia (HLI) model. We found that numbers of PANs in the affected gastrocnemius muscle increased ≈4 times 3h following ischemia induction and reached its peak 2 days following ischemia onset. Similarly, in patients undergoing surgery where peripheral perfusion is transiently clamped, numbers of circulating PANs increase ≈3 times 30 min post-HLI. In healthy mice, PANs are found in high frequency in the spleen (spleen: 9,8% of total neutrophils, blood: 0,78%). Splenectomy prior to induction of HLI reduced recruitment of PANs to the ischemic muscle, which demonstrates that the spleen acts as a reservoir for PANs. Furthermore, HLI downregulated the CXCR4-ligand CXCL12α in the splenic red pulp. This was prevented by chemically induced sympathectomy, resulting in increased retention of PANs in spleen, reduced PAN accumulation in the ischemic muscle and reduced blood flow recovery. Therefore, we propose that the downregulation of CXCL12α controlled by sympathetic nerve signaling pathways drives retention of PANs in the spleen, thereby regulating their release in response to HLI. In summary, we identified that the spleen contains a peripheral pool of PANs and emphasize the pivotal role of the neuro-immune axis in the recruitment of PANs to the site of ischemia. These discoveries open new avenues for drug development to limit damage and accelerate healing following ischemic events. This study was supported by the Swedish Research Council, Knut and Alice Wallenberg foundation, The Swedish Cancer Society, and O. E. and Edla Johansson’s foundation.

Current SARS-CoV-2 serological assays generate discrepant results, and the longitudinal characteristics of antibodies targeting various antigens after asymptomatic to mild COVID-19 are yet to be established. This longitudinal cohort study including 1965 healthcare workers, of which 381 participants exhibited antibodies against the SARS-CoV-2 spike antigen at study inclusion, reveal that these antibodies remain detectable in most participants, 96%, at least four months post infection, despite having had no or mild symptoms. Virus neutralization capacity was confirmed by microneutralization assay in 91% of study participants at least four months post infection. Contrary to antibodies targeting the spike protein, antibodies against the nucleocapsid protein were only detected in 80% of previously anti-nucleocapsid IgG positive healthcare workers. Both anti-spike and anti-nucleocapsid IgG levels were significantly higher in previously hospitalized COVID-19 patients four months post infection than in healthcare workers four months post infection (p=2*10−23 and 2*10−13 respectively). Although the magnitude of humoral response was associated with disease severity, our findings support a durable and functional humoral response after SARS-CoV-2 infection even after no or mild symptoms. We further demonstrate differences in antibody kinetics depending on the antigen, arguing against the use of the nucleocapsid protein as target antigen in population-based SARS-CoV-2 serological surveys.

BackgroundSARS-CoV-2 may pose an occupational health risk to health care workers, but the prevalence of infections in this population is unknown. We examined the seroprevalence of SARS-CoV-2 antibodies among health care workers at a large acute care hospital in Stockholm, Sweden. We determined correlations between seroprevalence, self-reported symptoms and occupational exposure to SARS-CoV-2.Methods and findingsAll employees at Danderyd Hospital (n=4375) were invited to participate in a cross-sectional study. 2149 employees from all hospital departments were enrolled in the study between April 14th and May 8th 2020. Study participants completed a questionnaire consisting of symptoms compatible with SARS-CoV-2 infection since January 2020 and occupational exposure to patients infected with SARS-CoV-2. IgG antibodies against SARS-CoV-2 were analyzed using a multiplex assay evaluated to have 99.4% sensitivity and 99.1% specificity. The over-all seroprevalence among 2149 participants was 19.1% (n=410). There was no difference in age or sex between seropositive and seronegative participants. The symptoms with the strongest correlation to seroprevalence were anosmia and ageusia, with odds ratios of 28.4 (p=2.02*10^-120) and 19.2 (p=1.67*10^-99) respectively. Seroprevalence was strongly associated with patient-related work (OR 2.9, p=4.24*10^-8), covid-19 patient contact (OR 1.43, p=0.003), and occupation as assisting nurse (OR 3.67, p=2.16*10^-9).ConclusionThese results demonstrate that anosmia and ageusia should be included in screening guidance and in the recommendations of self-isolation to reduce further spread of SARS-CoV-2. The results furthermore imply an occupational health risk for SARS-CoV-2 infection among hospital workers. Continued measures are warranted to assure healthcare worker safety and reduce transmission from health care settings to the community during the covid-19 outbreak.

Background The number of mental disorders has been increasing but has yet to receive sufficient attention. Healthcare students and professionals tend to have high stress burden. Finding the root cause of psychological distress is important to formulate a method for early detection. The association of BDNF val66met polymorphism to neuropsychiatric disorders has been widely studied. The aim of this study was to interplay between BDNF val66met polymorphism and sociodemographic factors in the pathogenesis of psychological distress among Indonesian students. Methods Level of psychological distress and sociodemographic profiling was assessed using the Kessler Psychological Distress Scale (K10) and sociodemographic questionnaires, respectively. Genotyping was performed using polymerase chain reaction-amplified refractory mutation system. Pearson’s chi square and binomial logistic tests were used to evaluate the correlation. Results This study recruited 148 participants. The psychological distress levels of the participants were well (27.03%), mild (37.16%), moderate (25.00%), and severe (10.81%). Genotypic distributions were AA (25.67%), GA (50.68%), and GG (23.65%). No statistical significance was found in the study (p > 0.05). Conclusion Psychological distress is not affected by genotypic and environmental factors. Further confirmatory research with larger and broader populations is required.

Author(s): Greenstein, RA; Ng, Henry; Barrales, Ramon; Tan, Catherine; Braun, Sigurd; Al-Sady, Bassem | Abstract: ABSTRACT Heterochromatin spreading, the expansion of gene-silencing structures from DNA-encoded nucleation sites, occurs in distinct settings. Spreading re-establishes gene-poor constitutive heterochromatin every cell cycle, but also invades gene-rich euchromatin de novo to steer cell fate decisions. How chromatin context, i.e. euchromatic, heterochromatic, or different nucleator types, influences the determinants of this process remains poorly understood. By screening a nuclear function gene deletion library in fission yeast using a previously established heterochromatin spreading sensor system, we identified regulators that positively or negatively alter the propensity of a nucleation site to spread heterochromatin. We find that different chromatin contexts are dependent on unique sets of genes for the regulation of heterochromatin spreading. Further, we find that spreading in constitutive heterochromatin requires Clr6 histone deacetylase complexes containing the Fkh2 transcription factor, while the Clr3 deacetylase is globally required for silencing. Fkh2 acts by recruiting Clr6 to nucleation-distal chromatin sites. Our results segregate the pathways that control lateral heterochromatin spreading from those that instruct DNA-directed assembly in nucleation.

Introduction: Poor subjective sleep quality in undergraduate students has not been widely studied in Bandung city, Indonesia. Poor sleep quality has been related to a number of risk factors for poor health outcomes. Objective: To analyze the association between psychological distress and subjective sleep quality. Methods: A cross sectional survey was done in one of the universities of Bandung city, Indonesia. Data were collected from 290 undergraduate students selected through consecutive sampling. Pittsburg Sleep Quality Index (PSQI) and Kessler-10 questionnaire were administered. Results: The prevalence of psychological distress was well (43.1%), mild (28.6%), moderate (20.7%), and severe (7.6%). The overall sleep quality was poor and good in 84.5% and 15.5% of the students. There was a significant association between psychological distress and poor sleep quality (p=0.006). The multivariate analysis suggested that psychological distress was a predictor of poor sleep quality (OR 1.991; 95% CI, 1.311−3.026). Conclusion: There is a need for an awareness of the college resources to help manage the stress levels of students through effective coping strategy-related study habits.

Steady multi-hole pressure probes are used extensively in turbomachinery research. While various sources of error are known, this paper demonstrates that fluctuations in probe incidence can be particularly damaging for accuracy. A simple, quasi-steady model of five-hole-probe response explains why angle fluctuations can cause large errors in the indicated total and static pressure. The model explains why measurements in a shedding wake over-estimated loss by 40%. Simulated traverses behind rotors show similar behavior: fluctuating incidence causes efficiency to be under-estimated by over 1% in some cases. The model can correct five-hole-probe errors using an estimate of unsteady flow angles. This approach reduces errors by an order of magnitude and can be used to post-correct existing test data.

Background Central obesity is a risk factor for metabolic syndrome. Subjects with central obesity have a higher risk of developing type 2 diabetes and cardiovascular disease. Many conditions affect the prevalence of central obesity, including energy expenditure, aging, proinflammatory conditions, and hormonal, genetic, and ethnic differences. Polymorphism of the APM1 gene, encoding the protein adiponectin, is closely related to metabolic syndrome. Adiponectin influences fatty acid oxidation and glucose intake in muscle. Therefore, variation in the APM1 gene is associated with diabetes and obesity. Purpose The aim of the present study was to investigate the correlation of the single-nucleotide polymorphism (SNP) of the APM1 SNP rs2241766 with body mass index (BMI) and lipid profiles in Indonesian (Bandung) subjects. Patients and methods Genotyping of the APM1 gene was performed using the Amplification Refractory Mutation System. Whole blood and serum of 54 subjects with central obesity (waist circumference [WC] ≥90 cm) and 53 healthy subjects (WC

SummaryMany metazoan genes express alternative long 3′ UTR isoforms in the nervous system, but their functions remain largely unclear. In Drosophila melanogaster, the Dscam1 gene generates short and long (Dscam1-L) 3′ UTR isoforms due to alternative polyadenylation (APA). Here, we found that the RNA-binding protein Embryonic Lethal Abnormal Visual System (Elav) impacts Dscam1 biogenesis at two levels, including regulation of long 3′ UTR biogenesis and skipping of an upstream exon (exon 19). MinION long-read sequencing confirmed the connectivity of this alternative splicing event to the long 3′ UTR. Knockdown or CRISPR deletion of Dscam1-L impaired axon growth in Drosophila. The Dscam1 long 3′ UTR was found to be required for correct Elav-mediated skipping of exon 19. Elav thus co-regulates APA and alternative splicing to generate specific Dscam1 transcripts that are essential for neural development. This coupling of APA to alternative splicing might represent a new class of regulated RNA processing. Graphical AbstractHighlightsElav regulates Dscam1 long 3′ UTR (Dscam1-L) biogenesisLong-read sequencing reveals connectivity of long 3′ UTR to skipping of upstream exon 19Loss of Dscam1-L impairs axon outgrowthDscam1 long 3′ UTR is required for correct splicing of exon 19