Association between muscle strength and depressive symptoms among Chinese female college freshmen: a cross-sectional study.

BACKGROUND: Increased physical activity level is related to lower risk of depressive symptoms, and there is an inverse association between muscle strength and risk of depressive symptoms among the elderly. Although there is evidence of an inverse association between muscle strength and depressive symptoms, the relationship between these variables in a younger population is still unknown. This study aimed to examine the association between handgrip strength, a representative indicator of skeletal muscle strength, and the risk of depressive symptoms among Chinese female college freshmen. METHODS: A cross-sectional study was conducted among 867 participants aged between 16 and 23 years. Handgrip strength was measured with a handheld digital Smedley dynamometer, and handgrip strength relative to body weight (kg/kg) was calculated and was classified into tertiles as follows: low (0.32-0.50), medium (0.51-0.58), and high (0.59-0.94). Depressive symptoms were evaluated using the 20-item Zung self-rating depression scale (SDS), and three cutoff points were used to indicate different depression levels. RESULTS: We found that 10.7% of participants were classified as having severe depressive symptoms using an SDS score of 50 as the cutoff point. After adjusting for potential confounders, the adjusted odds ratios and 95% confidence intervals (CIs) for moderate-to-severe depressive symptoms across tertiles of the relative handgrip strength were 1.00 (reference) for tertile 1, 0.614 (0.353, 1.069) for tertile 2, and 0.537 (0.292, 0.988) for tertile 3 (P for trend = 0.041). The significant associations remained when other cutoff points (SDS scores: 48 or 45) were used. Interactions between handgrip strength and potential confounders for depressive symptoms in the final models were not significant. CONCLUSIONS: Our findings indicate that handgrip strength is inversely and independently related to the risk of depressive symptoms among Chinese female college freshmen. The present findings can help develop an effective intervention strategy against depression. Further intervention studies are needed to explore the mechanisms underlying the effects of handgrip strength on depressive symptoms.

An age-structured model for coupling within-host and between-host dynamics in environmentally-driven infectious diseases.

In this paper, an age-structured epidemic model for coupling within-host and between-host dynamics in environmentally-driven infectious diseases is investigated. The model is described by a mixed system of ordinary and partial differential equations which is constituted by the within-host virus infectious fast time ordinary system and the between-host disease transmission slow time age-structured system. The isolated fast system has been investigated in previous literatures, and the main results are introduced. For the isolated slow system, the basic reproduction number R b0, the positivity and ultimate boundedness of solutions are obtained, the existence of equilibria, the local stability of equilibria, and the global stability of disease-free equilibrium are established. We see that when R b0 ≤ 1 the system only has the disease-free equilibrium which is globally asymptotically stable, and when R b0 > 1 the system has a unique endemic equilibrium which is local asymptotically stable. With regard to the coupled slow system, the basic reproduction number Rb , the positivity and boundedness of solutions and the existence of equilibria are firstly obtained. Particularly, the coupled slow system can exist two positive equilibria when Rb  < 1 and a unique endemic equilibrium when Rb  > 1. When Rb  < 1 the disease-free equilibrium is local asymptotically stable, and when Rb  > 1 and an additional condition is satisfied the unique endemic equilibrium is local asymptotically stable. When there exist two positive equilibria, under an additional condition the local asymptotic stability of a positive equilibrium and the instability of other positive equilibrium also are established. The numerical examples show that the additional condition may be removed. The research shows that the coupled slow age-structured system has more complex dynamical behavior than the corresponding isolated slow system.

Involvement of DHX9/YB-1 complex induced alternative splicing of Krüppel-like factor 5 mRNA in phenotypic transformation of vascular smooth muscle cells.

Phenotypic transformation of vascular smooth muscle cells is a key phenomenon in the development of aortic dissection disease. However, the molecular mechanisms underlying this phenomenon have not been fully understood. We used ß-BAPN combined with ANG II treatment to establish a disease model of acute aortic dissection (AAD) in mice. We first examined the gene expression profile of aortic tissue in mice with AAD using a gene chip, followed by confirmation of DExH-box helicase 9 (DHX9) expression using RT-PCR, Western blot, and immunofluorescence analysis. We further developed vascular smooth muscle cell-specific DHX9 conditional knockout mice and conducted differential and functional analysis of gene expression and alternative splicing in mouse vascular smooth muscle cells. Finally, we examined the involvement of DHX9 in Krüppel-like factor 5 (KLF5) mRNA alternative splicing. Our study reported a significant decrease in the expression of DHX9 in the vascular smooth muscle cells (VSMCs) of mice with AAD. The smooth muscle cell-specific knockout of DHX9 exacerbated the development of AAD and altered the transcriptional level expression of many smooth muscle cell phenotype-related genes. Finally, we reported that DHX9 may induce alternative splicing of KLF5 mRNA by bridging YB-1. These results together suggested a new pathogenic mechanism underlying the development of AAD, and future research of this mechanism may help identify effective therapeutic intervention for AAD.

Energy Consumption, Carbon Emissions and Global Warming Potential of Wolfberry Production in Jingtai Oasis, Gansu Province, China.

During the last decade, China's agro-food production has increased rapidly and been accompanied by the challenge of increasing greenhouse gas (GHG) emissions and other environmental pollutants from fertilizers, pesticides, and intensive energy use. Understanding the energy use and environmental impacts of crop production will help identify environmentally damaging hotspots of agro-production, allowing environmental impacts to be assessed and crop management strategies optimized. Conventional farming has been widely employed in wolfberry (Lycium barbarum) cultivation in China, which is an important cash tree crop not only for the rural economy but also from an ecological standpoint. Energy use and global warming potential (GWP) were investigated in a wolfberry production system in the Yellow River irrigated Jingtai region of Gansu. In total, 52 household farms were randomly selected to conduct the investigation using questionnaires. Total energy input and output were 321,800.73 and 166,888.80 MJ ha-1, respectively, in the production system. The highest share of energy inputs was found to be electricity consumption for lifting irrigation water, accounting for 68.52%, followed by chemical fertilizer application (11.37%). Energy use efficiency was 0.52 when considering both fruit and pruned wood. Nonrenewable energy use (88.52%) was far larger than the renewable energy input. The share of GWP of different inputs were 64.52% electricity, 27.72% nitrogen (N) fertilizer, 5.07% phosphate, 2.32% diesel, and 0.37% potassium, respectively. The highest share was related to electricity consumption for irrigation, followed by N fertilizer use. Total GWP in the wolfberry planting system was 26,018.64 kg CO2 eq ha-1 and the share of CO2, N2O, and CH4 were 99.47%, 0.48%, and negligible respectively with CO2 being dominant. Pathways for reducing energy use and GHG emission mitigation include: conversion to low carbon farming to establish a sustainable and cleaner production system with options of raising water use efficiency by adopting a seasonal gradient water pricing system and advanced irrigation techniques; reducing synthetic fertilizer use; and policy support: smallholder farmland transfer (concentration) for scale production, credit (small- and low-interest credit) and tax breaks.

Zinc finger protein ZBTB20 promotes Toll-like receptor-triggered innate immune responses by repressing IκBα gene transcription.

Toll-like receptor (TLR) signaling is critical in innate response against invading pathogens. However, the molecular mechanisms for full activation of TLR-triggered innate immunity need to be fully elucidated. The broad complex tramtrack bric-a-brac/poxvirus and zinc finger (BTB/POZ) family is a class of transcription factors involved in many biological processes. However, few BTB/POZ proteins were reported to function in innate immune response. Zinc finger and BTB domain-containing 20 (ZBTB20), a member of BTB/POZ family, functions in neurogenesis and represses α-fetoprotein gene transcription in liver. However, the immunological functions of ZBTB20 remain unknown. Here, we found that myeloid cell-specific ZBTB20 KO mice were resistant to endotoxin shock and Escherichia coli-caused sepsis. ZBTB20 deficiency attenuated TLR-triggered production of proinflammatory cytokines and type I IFN in macrophages, which attributed to higher abundance of IκBα protein and impaired activity of NF-κB. Furthermore, ChIP and next generation high-throughput DNA sequencing assay showed that ZBTB20 specifically bound to IκBα gene promoter (+1 to +60 region) after TLR activation. ZBTB20 could inhibit IκBα gene transcription, govern IκBα protein expression, and then promote NF-κB activation. Therefore, transcriptional repressor ZBTB20 is needed to promote full activation of TLR signaling and TLR-triggered innate immune response by selectively suppressing the suppressor IκBα gene transcription.

Fibroblast growth factor 10 protects neuron against oxygen-glucose deprivation injury through inducing heme oxygenase-1.

Fibroblast growth factors (FGFs) are a family of structurally related heparin-binding proteins with diverse biological functions. FGFs participate in mitogenesis, angiogenesis, cell proliferation, development, differentiation and cell migration. Here, we investigated the potential effect of FGF10, a member of FGFs, on neuron survival in oxygen-glucose deprivation (OGD) model. In primary cultured mouse cortical neurons upon OGD, FGF10 treatment (100 and 1000 ng/ml) attenuated the decrease of cell viability and rescued the LDH release. Tuj-1 immunocytochemistry assay showed that FGF10 promoted neuronal survival. Apoptosis assay with Annexin V+PI by flow cytometry demonstrated that FGF10 treatment reduced apoptotic cell proportion. Moreover, immunoblotting showed that FGF10 alleviated the cleaved caspase-3 upregulation caused by OGD. FGF10 treatment also depressed the OGD-induced increase of caspase-3, -8 and -9 activities. At last, we found FGF10 triggered heme oxygenase-1 (HO-1) protein expression rather than hypoxia-inducible factor-1 (HIF-1), AMP-activated protein kinase (AMPK) signaling and extracellular signal-regulated kinases 1/2 (ERK1/2) signaling. Knockdown of HO-1 by siRNA partly abolished the neuroprotection of FGF10 in OGD model. In summary, our observations provide the first evidence for the neuroprotective function of FGF10 against ischemic neuronal injury and suggest that FGF10 may be a promising agent for treatment of ischemic stroke.

Protein tyrosine phosphatase with proline-glutamine-serine-threonine-rich motifs negatively regulates TLR-triggered innate responses by selectively inhibiting IκB kinase ß/NF-κB activation.

TLRs are essential for sensing the invading pathogens and initiating protective immune responses. However, aberrant activation of TLR-triggered inflammatory innate responses leads to the inflammatory disorders and autoimmune diseases. The molecular mechanisms that fine-tune TLR responses remain to be fully elucidated. Protein tyrosine phosphatase with proline-glutamine-serine-threonine-rich motifs (PTP-PEST) has been shown to be important in cell adhesion, migration, and also T cell and B cell activation. However, the roles of PTP-PEST in TLR-triggered immune response remain unclear. In this study, we report that PTP-PEST expression was upregulated in macrophages by TLR ligands. PTP-PEST inhibited TNF-α, IL-6, and IFN-ß production in macrophages triggered by TLR3, TLR4, and TLR9. Overexpression of catalytically inactive mutants of PTP-PEST abolished the inhibitory effects, indicating that PTP-PEST inhibits TLR response in a phosphatase-dependent manner. Accordingly, PTP-PEST knockdown increased TLR3, -4, and -9-triggered proinflammatory cytokine and type I IFN production. PTP-PEST selectively inhibited TLR-induced NF-κB activation, whereas it had no substantial effect on MAPK and IFN regulatory factor 3 activation. Moreover, PTP-PEST directly interacted with IκB kinase ß (IKKß) then inhibited IKKß phosphorylation at Ser(177/181) and Tyr(188/199), and subsequently suppressed IKKß activation and kinase activity as well as downstream NF-κB activation, resulting in suppression of the TLR-triggered innate immune response. Thus, PTP-PEST functions as a feedback-negative regulator of TLR-triggered innate immune responses by selectively impairing IKKß/NF-κB activation.

Carbon benefits of wolfberry plantation on secondary saline land in Jingtai oasis, Gansu--A case study on application of the CBP model.

The largest global source of anthropogenic CO2 emissions comes from the burning of fossil fuel and approximately 30% of total net emissions come from land use and land use change. Forestation and reforestation are regarded worldwide as effective options of sequestering carbon to mitigate climate change with relatively low costs compared with industrial greenhouse gas (GHG) emission reduction efforts. Cash trees with a steady augmentation in size are recognized as a multiple-beneficial solution to climate change in China. The reporting of C changes and GHG emissions for sustainable land management (SLM) practices such as afforestation is required for a variety of reasons, such as devising land management options and making policy. The Carbon Benefit Project (CBP) Simple Assessment Tool was employed to estimate changes in soil organic carbon (SOC) stocks and GHG emissions for wolfberry (Lycium barbarum L.) planting on secondary salinized land over a 10 year period (2004-2014) in the Jingtai oasis in Gansu with salinized barren land as baseline scenario. Results show that wolfberry plantation, an intensively managed ecosystem, served as a carbon sink with a large potential for climate change mitigation, a restorative practice for saline land and income stream generator for farmers in soil salinized regions in Gansu province. However, an increase in wolfberry production, driven by economic demands, would bring environmental pressures associated with the use of N fertilizer and irrigation. With an understanding of all of the components of an ecosystem and their interconnections using the Drivers-Pressures-State-Impact-Response (DPSIR) framework there comes a need for strategies to respond to them such as capacity building, judicious irrigation and institutional strengthening. Cost benefit analysis (CBA) suggests that wolfberry cultivation was economically profitable and socially beneficial and thus well-accepted locally in the context of carbon sequestration. This study has important implications for Gansu as it helps to understand the role cash trees can play in carbon emission reductions. Such information is necessary in devising management options for sustainable land management (SLM).

Immune responsive gene 1 (IRG1) promotes endotoxin tolerance by increasing A20 expression in macrophages through reactive oxygen species.

Sepsis-associated immunosuppression (SAIS) is regarded as one of main causes for the death of septic patients at the late stage because of the decreased innate immunity with a more opportunistic infection. LPS-tolerized macrophages, which are re-challenged by LPS after prior exposure to LPS, are regarded as the common model of hypo-responsiveness for SAIS. However, the molecular mechanisms of endotoxin tolerance and SAIS remain to be fully elucidated. In addition, negative regulation of the Toll-like receptor (TLR)-triggered innate inflammatory response needs further investigation. Here we show that expression of immune responsive gene 1 (IRG1) was highly up-regulated in the peripheral blood mononuclear cells of septic patients and in LPS-tolerized mouse macrophages. IRG1 significantly suppressed TLR-triggered production of proinflammatory cytokines TNF-α, IL-6, and IFN-ß in LPS-tolerized macrophages, with the elevated expression of reactive oxygen species (ROS) and A20. Moreover, ROS enhanced A20 expression by increasing the H3K4me3 modification of histone on the A20 promoter domain, and supplement of the ROS abrogated the IRG1 knockdown function in breaking endotoxin tolerance by increasing A20 expression. Our results demonstrate that inducible IRG1 promotes endotoxin tolerance by increasing A20 expression through ROS, indicating a new molecular mechanism regulating hypoinflammation of sepsis and endotoxin tolerance.

A Content Analysis of Online Messages about Sugar-Sweetened Beverages.

Media campaigns can reduce or promote the consumption of sugar-sweetened beverages (SSBs). Brief, US-based English-language online messages were gathered from searchable media platforms, a process that yielded 112 anti-SSB videos and 29 pro-SSB commercials. Using a combination of inductive and deductive methods, a content analysis of those messages was conducted to identify their properties. They were coded for the direction (pro vs. anti), target of the advocacy (e.g., consumption vs. policy), actor demographics (gender, age, and ethnicity), persuasive theme (e.g., excessive sugar, nurturing), and message sensation value. Anti-SSB appeals primarily targeted individual-level consumption behavior. They utilized six persuasive themes and often included more than one theme in a single message. Pro-SSB messages used feel-good themes and utilized only one theme per message. The proportions of adults, adolescents, and children differed by the direction of the advocacy. Black, Hispanic, and Asian actors were under-represented in the anti-SSB sample relative to Whites. Pro-SSB appeals were slightly higher than anti-SSB appeals in message sensation value (p = 0.09). The findings illuminate the message features that characterize the universe of brief anti-SSB appeals available online, highlight messaging disparities, and reveal the absence of certain common, effective persuasive themes.

miR-328-5p functions as a critical negative regulator in early endothelial inflammation and advanced atherosclerosis.

Early proatherogenic inflammation constitutes a significant risk factor for atherogenesis development. Despite this, the precise molecular mechanisms driving this pathological progression largely remain elusive. Our study unveils a pivotal role for the microRNA miR-328-5p in dampening endothelial inflammation by modulating the stability of JUNB (JunB proto-oncogene). Perturbation of miR-328-5p levels results in heightened monocyte adhesion to endothelial cells and enhanced transendothelial migration, while its overexpression mitigates these inflammatory processes. Furthermore, miR-328-5p hinders macrophage polarization toward the pro-inflammatory M1 phenotype, and exerts a negative influence on atherosclerotic plaque formation in vivo. By pinpointing JUNB as a direct miR-328-5p target, our research underscores the potential of miR-328-5p as a therapeutic target for inflammatory atherosclerosis. Reintroduction of JUNB effectively counteracts the anti-atherosclerotic effects of miR-328-5p, highlighting the promise of pharmacological miR-328-5p targeting in managing inflammatory atherosclerosis.

Ste20-Like Kinase TAOK1 Positively Regulates Antiviral Responses by Controlling the TBK1-IRF3 Signaling Axis.

The cytosolic viral nucleic acid-sensing pathways converge on the protein kinase TANK-binding kinase 1 (TBK1) and the transcription factor interferon (IFN)-regulatory factor 3 (IRF3) to induce type I IFN production and antiviral immune responses. However, the mechanism that triggers the binding of TBK1 and IRF3 after virus infection remains not fully understood. Here, we identified that thousand and one kinase 1 (TAOK1), a Ste20-like kinase, positively regulated virus-induced antiviral immune responses by controlling the TBK1-IRF3 signaling axis. Virus invasion downregulated the expression of TAOK1. TAOK1 deficiency resulted in decreased nucleic acid-mediated type I IFN production and increased susceptibility to virus infection. TAOK1 was constitutively associated with TBK1 independently of the mitochondrial antiviral signaling protein MAVS. TAOK1 promoted IRF3 activation by enhancing TBK1-IRF3 complex formation. TAOK1 enhanced virus-induced type I IFN production in a kinase activity-dependent manner. Viral infection induced TAOK1 to bind with dynein instead of microtubule-associated protein 4 (MAP4), leading to the trafficking of TBK1 to the perinuclear region to bind IRF3. Thus, the depolymerization of microtubule impaired virus-mediated IRF3 activation. Our results revealed that TAOK1 functioned as a new interaction partner and regulated antiviral signaling via trafficking TBK1 along microtubules to bind IRF3. These findings provided novel insights into the function of TAOK1 in the antiviral innate immune response and its related clinical significance.

Gelsevirine is a novel STING-specific inhibitor and mitigates STING-related inflammation in sepsis.

Background: Stimulation of IFN genes (STING) is central to the production of interferon and proinflammatory cytokines in response to microbial DNA or self-DNA in the cytosol. The detrimental role of the activation of STING during sepsis has been well documented. Methods: Here, we found that gelsevirine (GS) potently inhibit interferon and inflammatory cytokine induction in macrophages exposed to STING agonists (2'3'-cGAMP, IFN stimulatory DNA (ISD), and poly(dA:dT)). I n silico docking analysis and surface plasmon resonance binding study showed that GS bonds with high affinity to the cyclic dinucleotide (CDN)-binding pocket of STING. Biotin pull-down assay also confirmed that GS competitively bonded to STING protein. Furthermore, GS inhibited 2'3'-cGAMP-induced STING dimerization and subsequent activation. In addition, GS induced K48-linked STING ubiquitination and degradation, which was likely through upregulating and recruiting TRIM21. In mice exposed to cecal ligation and puncture (CLP)-induced sepsis, post-operative administration of GS significantly extended the survival period and mitigated acute organ damage. Results: Overall, GS inhibited STING signaling by competitively binding to the CDN-binding pocket to lock STING in an inactive open conformation, while also promoting K48-linked STING ubiquitination and degradation. Conclusions: Our findings identify a novel STING-specific inhibitor that could be applied in the treatment of sepsis.

IRG1 prevents excessive inflammatory responses and cardiac dysfunction after myocardial injury.

Acute myocardial infarction (MI) and chemotherapeutic drug administration can induce myocardial damage and cardiomyocyte cell death, and trigger the release of damage-associated molecular patterns (DAMPs) that initiate the aseptic inflammatory response. The moderate inflammatory response is beneficial for repairing damaged myocardium, while an excessive inflammatory response exacerbates myocardial injury, promotes scar formation, and results in a poor prognosis of cardiac diseases. Immune responsive gene 1 (IRG1) is specifically highly expressed in activated macrophages and mediates the production of tricarboxylic acid (TCA) cycle metabolite itaconate. However, the role of IRG1 in the inflammation and myocardial injury of cardiac stress-related diseases remains unknown. Here, we found that IRG1 knockout mice exhibited increased cardiac tissue inflammation and infarct size, aggravated myocardial fibrosis, and impaired cardiac function after MI and in vivo doxorubicin (Dox) administration. Mechanically, IRG1 deficiency enhanced the production of IL-6 and IL-1ß by suppressing the nuclear factor red lineage 2-related factor 2 (NRF2) and activating transcription factor 3 (ATF3) pathway in cardiac macrophages. Importantly, 4-octyl itaconate (4-OI), a cell-permeable derivative of itaconate, reversed the inhibited expression of NRF2 and ATF3 caused by IRG1 deficiency. Moreover, in vivo 4-OI administration inhibited the cardiac inflammation and fibrosis, and prevented adverse ventricle remodeling in IRG1 knockout mice with MI or Dox-induced myocardial injury. Our study uncovers the critical protective role of IRG1 in suppressing inflammation and preventing cardiac dysfunction under ischemic or toxic injury conditions, providing a potential target for the treatment of myocardial injury.

Black-Phosphorus-Nanosheet-Reinforced Coating of Implants for Sequential Biofilm Ablation and Bone Fracture Healing Acceleration.

Incurable implant-related infection may cause catastrophic consequences due to the existence of a biofilm that resists the infiltration of host immune cells and antibiotics. Innovative approaches inspired by nanomedicine, e.g., engineering innovative multifunctional bionic coating systems on the surface of implants, are becoming increasingly attractive. Herein, 2D black phosphorus nanosheets (BPs) were loaded onto a hydroxyapatite (HA)-coated metal implant to construct a BPs@HA composite coating. With its photothermal conversion effect and in situ biomineralization, the BPs@HA coating shows excellent performances in ablating the bacterial biofilm and accelerating fracture healing, which were verified through both in vitro and in vivo studies. Moreover, differentially expressed genes of bone formation and bone mesenchymal stem cells (BMSCs) regulated by the BPs@HA coating were identified using absolute quantitative transcriptome sequencing followed by the screening of gene differential expressions. A functional enrichment analysis reveals that the expression of core markers related to BMSC differentiation and bone formation could be effectively regulated by BPs through a metabolism-related pathway. This work not only illustrates the great potential in clinical application of the BPs@HA composite coating to eliminate bacteria and accelerate bone fracture healing but also contributes to an understanding of the underlying molecular mechanism of osteogenesis physiological function regulation based on an analysis of absolute quantitative transcriptome sequencing.

Comparing COVID-19 and the 1918-19 influenza pandemics in the United Kingdom.

We compared the COVID-19 and 1918-19 influenza pandemics in the United Kingdom. We found that the ongoing COVID-19 wave of infection matched the major wave of the 1918-19 influenza pandemic surprisingly well, with both reaching similar magnitudes (in terms of estimated weekly new infections) and spending the same duration with over five cases per 1000 inhabitants over the previous two months. We also discussed the similarities in epidemiological characteristics between these two pandemics.

Dynamic variations of the COVID-19 disease at different quarantine strategies in Wuhan and mainland China.

BACKGROUND: The Coronavirus Disease 2019 (COVID-19) firstly announced in Wuhan of Hubei province, China is rapidly spreading to all the other 31 provinces of China and to more than 140 countries. Quarantine strategies play the key role on the disease controlling and public health in the world with this pandemic of the COVID-19 defined by the World Health Organization. METHODS: In this study, a SEIRQ epidemic model was developed to explore the dynamic changes of COVID-19 in Wuhan and mainland China, from January 27, 2020 to March 5, 2020. Moreover, to investigate the effects of the quarantine strategies, two perspectives are employed from the different quarantine magnitudes and quarantine time points. RESULTS: The major results suggest that the COVID-19 variations are well captured by the epidemic model with very high accuracy in the cumulative confirmed cases, confirmed cases, cumulative recovered cases and cumulative death cases. The quarantine magnitudes in the susceptible individuals play larger roles on the disease control than the impacts of the quarantines of the exposed individuals and infectious individuals. For the quarantine time points, it shows that the early quarantine strategy is significantly important for the disease controlling. The time delayed quarantining will seriously increase the COVID-19 disease patients and prolongs the days of the disease extinction. CONCLUSIONS: Our model can simulate and predict the COVID-19 variations and the quarantine strategies are important for the disease controlling, especially at the early period of the disease outbreak. These conclusions provide important scientific information for the government policymaker in the disease control strategies.

MaxEnt Modeling of Dermacentor marginatus (Acari: Ixodidae) Distribution in Xinjiang, China.

Dermacentor marginatus Sulkzer is a common tick species found in the Xinjiang Uygur Autonomous Region (XUAR) of China, and is a vector for a variety of pathogens. To determine the potential distribution of this tick species in Xinjiang, a metadata containing 84 D. marginatus presence records combined with four localities from field collection were used for MaxEnt modeling to predict potential distribution of this tick species. Identification of tick samples showed 756 of 988 (76%) were D. marginatus. MaxEnt modeling results indicated that the potential distribution of this tick species was mainly confined to northern XUAR. Highly suitable areas included west side of Altay mountain, west rim of Junggar basin, and Yili River valley in the study area. The model showed an AUC value of 0.838 ± 0.063 (SD), based on 10-fold cross-validation. Although tick presence records used for modeling were limited, this is the first regional tick distribution model for D. marginatus in Xinjiang. The model will be helpful in assessing the risk of tick-borne diseases to human and animals in the region.

Glutamine-induced heat shock protein protects against renal ischaemia-reperfusion injury in rats.

AIM: To find out if a single dose of glutamine can relieve acute renal ischaemia-reperfusion injury in rats, to explore the role of heat shock protein in this process. METHODS: Forty-eight Sprague-Dawley rats were assigned to four groups: saline as control group; glutamine group; quercetin (heat shock protein inhibitor) plus glutamine group; and quercetin plus saline group. The renal ischaemia-reperfusion rat model was established 1 h after drug administration. Serum creatinine (CR) and blood urea nitrogen (BUN) were analyzed. The kidneys were harvested to evaluate the degree of renal injuries. Heat shock protein expression was detected by immunohistochemistry and western blot. Cell apoptosis was detected by terminal deoxynucleotidyl transferase dUTP nick end labelling (TUNEL) assay and apoptosis index was calculated. RESULTS: Statistical data from CR, BUN, haematoxylin-eosin (HE) dyeing and TUNEL assay results showed that ischaemia-reperfusion injury and cell apoptosis in the glutamine group were significantly milder than those in control group (P < 0.05), while ischaemia-reperfusion injury and cell apoptosis in the quercetin plus glutamine group and quercetin plus saline group were more severe than those in the control group (P < 0.05). Statistical data from immunohistochemistry and western blot results showed that heat shock protein expression was enhanced in the glutamine group compared with that in the control group (P < 0.01), while it was weaker in the quercetin plus glutamine group and quercetin plus saline group than that in the control group (P < 0.01). CONCLUSION: Our experiment suggested that a single dose of glutamine could relieve renal ischaemia-reperfusion injury in rats in 24 h, and its mechanism may be associated with enhanced heat shock protein expression. This finding may provide a new alternative for protecting against clinical renal ischaemia-reperfusion injury.