Multiple Origins and Genomic Basis of Complex Traits in Sighthounds.

Sighthounds, a distinctive group of hounds comprising numerous breeds, have their origins rooted in ancient artificial selection of dogs. In this study, we performed genome sequencing for 123 sighthounds, including one breed from Africa, six breeds from Europe, two breeds from Russia, and four breeds and 12 village dogs from the Middle East. We gathered public genome data of five sighthounds and 98 other dogs as well as 31 gray wolves to pinpoint the origin and genes influencing the morphology of the sighthound genome. Population genomic analysis suggested that sighthounds originated from native dogs independently and were comprehensively admixed among breeds, supporting the multiple origins hypothesis of sighthounds. An additional 67 published ancient wolf genomes were added for gene flow detection. Results showed dramatic admixture of ancient wolves in African sighthounds, even more than with modern wolves. Whole-genome scan analysis identified 17 positively selected genes (PSGs) in the African population, 27 PSGs in the European population, and 54 PSGs in the Middle Eastern population. None of the PSGs overlapped in the three populations. Pooled PSGs of the three populations were significantly enriched in "regulation of release of sequestered calcium ion into cytosol" (gene ontology: 0051279), which is related to blood circulation and heart contraction. In addition, ESR1, JAK2, ADRB1, PRKCE, and CAMK2D were under positive selection in all three selected groups. This suggests that different PSGs in the same pathway contributed to the similar phenotype of sighthounds. We identified an ESR1 mutation (chr1: g.42,177,149 T > C) in the transcription factor (TF) binding site of Stat5a and a JAK2 mutation (chr1: g.93,277,007 T > A) in the TF binding site of Sox5. Functional experiments confirmed that the ESR1 and JAK2 mutation reduced their expression. Our results provide new insights into the domestication history and genomic basis of sighthounds.

Genetic and cultural adaptations underlie the establishment of dairy pastoralism in the Tibetan Plateau.

BACKGROUND: Domestication and introduction of dairy animals facilitated the permanent human occupation of the Tibetan Plateau. Yet the history of dairy pastoralism in the Tibetan Plateau remains poorly understood. Little is known how Tibetans adapted to milk and dairy products. RESULTS: We integrated archeological evidence and genetic analysis to show the picture that the dairy ruminants, together with dogs, were introduced from West Eurasia into the Tibetan Plateau since ~ 3600 years ago. The genetic admixture between the exotic and indigenous dogs enriched the candidate lactase persistence (LP) allele 10974A > G of West Eurasian origin in Tibetan dogs. In vitro experiments demonstrate that - 13838G > A functions as a LP allele in Tibetans. Unlike multiple LP alleles presenting selective signatures in West Eurasians and South Asians, the de novo origin of Tibetan-specific LP allele - 13838G > A with low frequency (~ 6-7%) and absence of selection corresponds - 13910C > T in pastoralists across eastern Eurasia steppe. CONCLUSIONS: Results depict a novel scenario of genetic and cultural adaptations to diet and expand current understanding of the establishment of dairy pastoralism in the Tibetan Plateau.

[Effect and mechanism of Bovis Calculus on ulcerative colitis by inhibiting IL-17/IL-17RA/Act1 signaling pathway].

This study aimed to elucidate the effect and underlying mechanism of Bovis Calculus in the treatment of ulcerative colitis(UC) through network pharmacological prediction and animal experimental verification. Databases such as BATMAN-TCM were used to mine the potential targets of Bovis Calculus against UC, and the pathway enrichment analysis was conducted. Seventy healthy C57BL/6J mice were randomly divided into a blank group, a model group, a solvent model(2% polysorbate 80) group, a salazosulfapyridine(SASP, 0.40 g·kg~(-1)) group, and high-, medium-, and low-dose Bovis Calculus Sativus(BCS, 0.20, 0.10, and 0.05 g·kg~(-1)) groups according to the body weight. The UC model was established in mice by drinking 3% dextran sulfate sodium(DSS) solution for 7 days. The mice in the groups with drug intervention received corresponding drugs for 3 days before modeling by gavage, and continued to take drugs for 7 days while modeling(continuous administration for 10 days). During the experiment, the body weight of mice was observed, and the disease activity index(DAI) score was recorded. After 7 days of modeling, the colon length was mea-sured, and the pathological changes in colon tissues were observed by hematoxylin-eosin(HE) staining. The levels of tumor necrosis factor-α(TNF-α), interleukin-1ß(IL-1ß), interleukin-6(IL-6), and interleukin-17(IL-17) in colon tissues of mice were detected by enzyme-linked immunosorbent assay(ELISA). The mRNA expression of IL-17, IL-17RA, Act1, TRAF2, TRAF5, TNF-α, IL-6, IL-1ß, CXCL1, CXCL2, and CXCL10 was evaluated by real-time polymerase chain reaction(RT-PCR). The protein expression of IL-17, IL-17RA, Act1, p-p38 MAPK, and p-ERK1/2 was investigated by Western blot. The results of network pharmacological prediction showed that Bovis Calculus might play a therapeutic role through the IL-17 signaling pathway and the TNF signaling pathway. As revealed by the results of animal experiments, on the 10th day of drug administration, compared with the solvent model group, all the BCS groups showed significantly increased body weight, decreased DAI score, increased colon length, improved pathological damage of colon mucosa, and significantly inhibited expression of TNF-α,IL-6,IL-1ß, and IL-17 in colon tissues. The high-dose BCS(0.20 g·kg~(-1)) could significantly reduce the mRNA expression levels of IL-17, Act1, TRAF2, TRAF5, TNF-α, IL-6, IL-1ß, CXCL1, and CXCL2 in colon tissues of UC model mice, tend to down-regulate mRNA expression levels of IL-17RA and CXCL10, significantly inhibit the protein expression of IL-17RA,Act1,and p-ERK1/2, and tend to decrease the protein expression of IL-17 and p-p38 MAPK. This study, for the first time from the whole-organ-tissue-molecular level, reveals that BCS may reduce the expression of pro-inflammatory cytokines and chemokines by inhibiting the IL-17/IL-17RA/Act1 signaling pathway, thereby improving the inflammatory injury of colon tissues in DSS-induced UC mice and exerting the effect of clearing heat and removing toxins.

[The role and molecular mechanism of miR-494 in disease development and progression].

MicroRNA-494 (miR-494) is a small non-coding RNA located in chromosome 14q32.31 and regulates post-transcriptional gene expression by promoting the degradation of its target mRNAs via binding to the 3' untranslated regions (3'UTR). It has been reported that miR-494 plays an important role in the occurrence, development and prognosis of various diseases. Several signaling pathways modulated by miR-494 including the PTEN/PI3K/AKT, nuclear factor κ-B (NF-κB), mitogen-activated protein kinase (MAPK), transforming growth factor-ß (TGF-ß)/SMAD, and Wnt/ß-catenin are associated with physiological regulation and pathological process in many diseases. The stably expression of miR-494 in the blood stream suggests its potential as a biological marker for disease diagnosis, treatment, and prognosis. Based on recent research, we summarize the role and molecular mechanism of miR-494 in disease development and progression. We also discuss its potential as a marker for clinical diagnosis and prognosis of various diseases.

First case of COVID-19 complicated with fulminant myocarditis: a case report and insights.

BACKGROUND: Coronavirus disease 2019 (COVID-19) has been demonstrated to be the cause of pneumonia. Nevertheless, it has not been reported as the cause of acute myocarditis or fulminant myocarditis. CASE PRESENTATION: A 63-year-old male was admitted with pneumonia and cardiac symptoms. He was genetically confirmed as having COVID-19 according to sputum testing on the day of admission. He also had elevated troponin I (Trop I) level (up to 11.37 g/L) and diffuse myocardial dyskinesia along with a decreased left ventricular ejection fraction (LVEF) on echocardiography. The highest level of interleukin-6 was 272.40 pg/ml. Bedside chest radiographs showed typical ground-glass changes indicative of viral pneumonia. Laboratory test results for viruses that cause myocarditis were all negative. The patient conformed to the diagnostic criteria of the Chinese expert consensus statement for fulminant myocarditis. After receiving antiviral therapy and mechanical life support, Trop I was reduced to 0.10 g/L, and interleukin-6 was reduced to 7.63 pg/mL. Moreover, the LVEF of the patient gradually recovered to 68%. The patient died of aggravation of secondary infection on the 33rd day of hospitalization. CONCLUSION: COVID-19 patients may develop severe cardiac complications such as myocarditis and heart failure. This is the first report of COVID-19 complicated with fulminant myocarditis. The mechanism of cardiac pathology caused by COVID-19 needs further study.

Self-reported confidence in patient safety competencies among Chinese nursing students: a multi-site cross-sectional survey.

BACKGROUND: Nursing interns are an important backup force for nursing professionals, so efforts to strengthen their patient safety (PS) competencies are a major priority. To do so requires assessing the strengths and weaknesses of Chinese nursing students' PS competence and identifying the influencing factors. METHODS: This was a multi-site, cross-sectional, web-based study that was carried out between September 2018 and January 2019. A national online survey was completed by 732 Chinese undergraduate nursing students. Our primary outcome factor was the Health Professional Education in Patient Safety Survey score. We also collected socio-demographic and clinical practice-related characteristics as independent variables. Multiple stepwise linear regression was performed to identify predictors of PS competence. RESULTS: Chinese undergraduate nursing students were fairly confident in their clinical safety skills but less confident in what they learned about sociocultural or context-dependent aspects of PS and speaking up about PS, including effective communication and understanding human and environmental factors. Less than half of the students felt that they could approach someone engaging in unsafe practice and were reluctant to voice concern about adverse events. We observed significant differences in PS competence between students from different regions, across different PS learning styles (self-study and classroom theoretical study), with different self-assessed PS competence levels, and with experiences of adverse events (p < 0.05). These factors accounted for almost 15% of the total variance in PS competence scores (adjusted R2 = 0.15, p = 0.00). CONCLUSIONS: The results of this study provide a better understanding of PS competence among final-year nursing students in China. Our findings may help nursing educators or healthcare organizations to cultivate and improve PS competence by establishing documented policies or by improving the efficacy of intervention.

Response of genes involved in lipid metabolism in rat epididymal white adipose tissue to different fasting conditions after long-term fructose consumption.

There has been much concern regarding the dietary fructose contributes to the development of metabolic syndrome. High-fructose diet changes the expression of genes involved in lipid metabolism. Levels of a number of hepatic lipogenic enzymes are increased by a high-carbohydrate diet in fasted-refed model rats/mice. Both the white adipose tissue (WAT) and the liver play a key role in the maintenance of nutrient homeostasis. Here, the aim of this study was to analyze the expression of key genes related to lipid metabolism in epididymal WAT (eWAT) in response to different fasting condition after long-term chronic fructose consumption. Rats were fed standard chow supplemented with 10% w/v fructose solution for 5 weeks, and killed after chow-fasting and fructose withdrawal (fasting) or chow-fasting and continued fructose (fructose alone) for 14 h. Blood parameters and the expression of genes involved in fatty acid synthesis (ChREBP, SREBP-1c, FAS, SCD1), triglyceride biosynthesis (DGAT-1, DGAT-2) and lipid mobilization (ATGL, HSL) in eWAT were analyzed. In addition, mRNA levels of PPAR-γ, CD36 and LPL were also detected. As expected, fructose alone increased the mRNA expression of FAS, SCD1, and correspondingly decreased ATGL and HSL mRNA levels. However, ChREBP, DGAT-2, ATGL and HSL mRNA levels restored near to normal while FAS and SCD1 tend to basic level under fasting condition. The mRNA expression of SREBP-1c, PPAR-γ and LPL did not changed at any situations but CD36 mRNA decreased remarkably in fructose alone group. In conclusion, these findings demonstrate that genes involved in lipid metabolism in rat eWAT are varied in response to different fasting conditions after long-term fructose consumption.

Long-term fructose consumption prolongs hepatic stearoyl-CoA desaturase 1 activity independent of upstream regulation in rats.

Dietary fructose is considered a risk factor for metabolic disorders, such as fatty liver disease. However, the mechanism underlying the effects of fructose is not well characterized. We investigated the hepatic expression of key regulatory genes related to lipid metabolism following fructose feeding under well-defined conditions. Rats were fed standard chow supplemented with 10% w/v fructose solution for 5 weeks, and killed after chow-fasting and fructose withdrawal (fasting) or chow-fasting and continued fructose (fructose alone) for 14 h. Hepatic deposition of triglycerides was found in rats from both groups. As expected, fructose alone increased mRNA levels of lipogenesis-related genes and correspondingly decreased mRNA levels of lipid oxidative genes in the liver. Interesting, hepatic levels of stearoyl-CoA desaturase (SCD)1 mRNA remained elevated under fructose withdrawn conditions, although expression levels of other genes, including two key transcription factors (carbohydrate response element binding protein (ChREBP) and sterol regulatory element-binding protein (SREBP)-1c) fell to normal levels, indicating that long-term fructose intake increased SCD1 activity, independent of upstream regulatory genes, such as ChREBP and SREBP-1c. In conclusion, SCD1 overexpression in fatty liver disease is not affected by fasting after long-term fructose consumption in rats. Regulation of SCD1 plays an important role in fructose-induced hepatic steatosis.

Postpolypectomy syndrome without abdominal pain led to sepsis/septic shock and gastrointestinal bleeding: A case report.

BACKGROUND: Postpolypectomy syndrome (PPS) is a rare postoperative complication of colonic polypectomy. It presents with abdominal pain and fever accompanied by coagulopathy and elevated inflammatory markers. Its prognosis is usually good, and it only requires outpatient treatment or observation in a general ward. However, it can be life-threatening. CASE SUMMARY: The patient was a 58-year-old man who underwent two colonic polypectomies, each resulting in life-threatening sepsis, septic shock, and coagulopathy. Each of the notable manifestations was a rapid drop in blood pressure, an increase in heart rate, loss of consciousness, and heavy sweating, accompanied by shortness of breath and decreased oxygen in the finger pulse. Based on the criteria of organ dysfunction due to infection, we diagnosed him with sepsis. The patient also experienced severe gastrointestinal bleeding after the second operation. Curiously, he did not complain of any abdominal pain throughout the course of the illness. He had significantly elevated concentrations of inflammatory markers and coagulopathy. Except for the absence of abdominal pain, his fever, significant coagulopathy, and elevated inflammatory marker concentrations were all consistent with PPS. Abdominal computed tomography and superior mesenteric artery computed tomography angiography showed no free air or vascular damage. Thus, the diagnosis of colon perforation was not considered. The final blood culture results indicated Moraxella osloensis. The patient was transferred to the intensive care unit and quickly improved after fluid resuscitation, antibiotic treatment, oxygen therapy, and blood transfusion. CONCLUSION: PPS may induce dysregulation of the systemic inflammatory response, which can lead to sepsis or septic shock, even in the absence of abdominal pain.

Remote regulation of rs80245547 and rs72673891 mediated by transcription factors C-Jun and CREB1 affect GSTCD expression.

Chronic obstructive pulmonary disease (COPD), the third leading cause of death worldwide, is influenced by genetic factors. The genetic signal rs10516526 in the glutathione S-transferase C-terminal domain containing (GSTCD) gene is a highly significant and reproducible signal associated with lung function and COPD on chromosome 4q24. In this study, comprehensive bioinformatics analyses and experimental verifications were detailly implemented to explore the regulation mechanism of rs10516526 and GSTCD in COPD. The results suggested that low expression of GSTCD was associated with COPD (p = 0.010). And C-Jun and CREB1 transcription factors were found to be essential for the regulation of GSTCD by rs80245547 and rs72673891. Moreover, rs80245547T and rs72673891G had a stronger binding ability to these transcription factors, which may promote the allele-specific long-range enhancer-promoter interactions on GSTCD, thus making COPD less susceptible. Our study provides a new insight into the relationship between rs10516526, GSTCD, and COPD.

Cell atlas of CCl 4-induced progressive liver fibrosis reveals stage-specific responses.

Chronic liver injury leads to progressive liver fibrosis and ultimately cirrhosis, a major cause of morbidity and mortality worldwide. However, there are currently no effective anti-fibrotic therapies available, especially for late-stage patients, which is partly attributed to the major knowledge gap regarding liver cell heterogeneity and cell-specific responses in different fibrosis stages. To reveal the multicellular networks regulating mammalian liver fibrosis from mild to severe phenotypes, we generated a single-nucleus transcriptomic atlas encompassing 49 919 nuclei corresponding to all main liver cell types at different stages of murine carbon tetrachloride (CCl 4)-induced progressive liver fibrosis. Integrative analysis distinguished the sequential responses to injury of hepatocytes, hepatic stellate cells and endothelial cells. Moreover, we reconstructed cell-cell interactions and gene regulatory networks implicated in these processes. These integrative analyses uncovered previously overlooked aspects of hepatocyte proliferation exhaustion and disrupted pericentral metabolic functions, dysfunction for clearance by apoptosis of activated hepatic stellate cells, accumulation of pro-fibrotic signals, and the switch from an anti-angiogenic to a pro-angiogenic program during CCl 4-induced progressive liver fibrosis. Our dataset thus constitutes a useful resource for understanding the molecular basis of progressive liver fibrosis using a relevant animal model.

Swimming Suppresses Cognitive Decline of HFD-Induced Obese Mice through Reversing Hippocampal Inflammation, Insulin Resistance, and BDNF Level.

Obesity is an important public health problem nowadays. Long-term obesity can trigger a series of chronic diseases and impair the learning and memory function of the brain. Current studies show that scientific exercise can effectively improve learning and memory capacity, which also can provide benefits for obese people. However, the underlying mechanisms for the improvement of cognitive capacity under the status of obesity still need to be further explored. In the present study, the obesity-induced cognition-declined model was established using 4-week-old mice continuously fed with a high-fat diet (HFD) for 12 weeks, and then the model mice were subjected to an 8-week swimming intervention and corresponding evaluation of relevant indicators, including cognitive capacity, inflammation, insulin signal pathway, brain-derived neurotrophic factor (BNDF), and apoptosis, for exploring potential regulatory mechanisms. Compared with the mice fed with regular diets, the obese mice revealed the impairment of cognitive capacity; in contrast, swimming intervention ameliorated the decline in cognitive capacity of obese mice by reducing inflammatory factors, inhibiting the JNK/IRS-1/PI3K/Akt signal pathway, and activating the PGC-1α/BDNF signal pathway, thereby suppressing the apoptosis of neurons. Therefore, swimming may be an important interventional strategy to compensate for obesity-induced cognitive impairment.

miR-21 Exerts Anti-proliferative and Pro-apoptotic Effects in LPS-induced WI-38 Cells via Directly Targeting TIMP3.

Idiopathic pulmonary fibrosis (IPF) is a progressive lung disease, which was caused by a complex interplay of inflammatory responses and chronic damage. miR-21 is increased in patients with IPF, but its function in the embryonic lung-derived diploid fibroblasts cells subjected to LPS is elusive. miRNA expression profile was obtained from GEO database and target genes of miRNAs were forecasted by TargetScan. To mimic the LPS-induced injury, different concentrations of LPS were applied to treat WI-38 cells. Functional in vitro experiments were conducted to examine the role of miR-21 and TIMP3. Luciferase report assay was performed to verify the relationship between miR-21 and TIMP3. qRT-PCR, western blotting, and ELISA were conducted to detect the levels of the related miRNAs, proteins, and inflammatory factors. miR-21 presented higher levels in interstitial pneumonia patients and LPS-induced WI-38 cells. Overexpression of miR-21 was negatively correlated with the proliferative capability of LPS-treated WI-38 cells. miR-21 directly targets TIMP3. TIMP3 restored the suppressive impact of miR-21 mimic on the proliferation, while TIMP3 alleviated the promoting impact of miR-21 mimic on the apoptosis of WI-38 cells treated by LPS. miR-21 inhibited Bcl-2 but increased Bax, cleaved caspase-3, and cleaved caspase-9. Besides, miR-21 elevated the levels of IL-6 and IL-ß but reduced the IL-10, which were weakened by TIMP3. Totally, miR-21 aggravated the LPS-induced lung injury and modulated inflammatory responses by targeting TIMP3.

Development of septic shock and prognostic assessment in critically ill patients with coronavirus disease outside Wuhan, China.

BACKGROUND: The study aims to illustrate the clinical characteristics and development of septic shock in intensive care unit (ICU) patients confirmed with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, and to perform a comprehensive analysis of the association between septic shock and clinical outcomes in critically ill patients with coronavirus disease (COVID-19). METHODS: Patients confirmed with SARS-CoV-2 infection, who were admitted to the ICU of the Third People's Hospital of Shenzhen from January 1 to February 7, 2020, were enrolled. Clinical characteristics and outcomes were compared between patients with and without septic shock. RESULTS: In this study, 35 critically ill patients with COVID-19 were included. Among them, the median age was 64 years (interquartile range [IQR] 59-67 years), and 10 (28.4%) patients were female. The median ICU length of stay was 16 days (IQR 8-23 days). Three (8.6%) patients died during hospitalization. Nine (25.7%) patients developed septic shock in the ICU, and these patients had a significantly higher incidence of organ dysfunction and a worse prognosis than patients without septic shock. CONCLUSIONS: Septic shock is associated with a poor outcome in critically ill COVID-19 patients and is one of the hallmarks of the severity of patients receiving ICU care. A dysregulated immune response, uncontrolled inflammation, and coagulation disorders are strongly associated with the development and progression of COVID-19-related septic shock.

Validated tool for early prediction of intensive care unit admission in COVID-19 patients.

BACKGROUND: The novel coronavirus disease 2019 (COVID-19) pandemic is a global threat caused by the severe acute respiratory syndrome coronavirus-2. AIM: To develop and validate a risk stratification tool for the early prediction of intensive care unit (ICU) admission among COVID-19 patients at hospital admission. METHODS: The training cohort included COVID-19 patients admitted to the Wuhan Third Hospital. We selected 13 of 65 baseline laboratory results to assess ICU admission risk, which were used to develop a risk prediction model with the random forest (RF) algorithm. A nomogram for the logistic regression model was built based on six selected variables. The predicted models were carefully calibrated, and the predictive performance was evaluated and compared with two previously published models. RESULTS: There were 681 and 296 patients in the training and validation cohorts, respectively. The patients in the training cohort were older than those in the validation cohort (median age: 63.0 vs 49.0 years, P < 0.001), and the percentages of male gender were similar (49.6% vs 49.3%, P = 0.958). The top predictors selected in the RF model were neutrophil-to-lymphocyte ratio, age, lactate dehydrogenase, C-reactive protein, creatinine, D-dimer, albumin, procalcitonin, glucose, platelet, total bilirubin, lactate and creatine kinase. The accuracy, sensitivity and specificity for the RF model were 91%, 88% and 93%, respectively, higher than those for the logistic regression model. The area under the receiver operating characteristic curve of our model was much better than those of two other published methods (0.90 vs 0.82 and 0.75). Model A underestimated risk of ICU admission in patients with a predicted risk less than 30%, whereas the RF risk score demonstrated excellent ability to categorize patients into different risk strata. Our predictive model provided a larger standardized net benefit across the major high-risk range compared with model A. CONCLUSION: Our model can identify ICU admission risk in COVID-19 patients at admission, who can then receive prompt care, thus improving medical resource allocation.

Clinical diagnosis of severe COVID-19: A derivation and validation of a prediction rule.

BACKGROUND: The widespread coronavirus disease 2019 (COVID-19) has led to high morbidity and mortality. Therefore, early risk identification of critically ill patients remains crucial. AIM: To develop predictive rules at the time of admission to identify COVID-19 patients who might require intensive care unit (ICU) care. METHODS: This retrospective study included a total of 361 patients with confirmed COVID-19 by reverse transcription-polymerase chain reaction between January 19, 2020, and March 14, 2020 in Shenzhen Third People's Hospital. Multivariate logistic regression was applied to develop the predictive model. The performance of the predictive model was externally validated and evaluated based on a dataset involving 126 patients from the Wuhan Asia General Hospital between December 2019 and March 2020, by area under the receiver operating curve (AUROC), goodness-of-fit and the performance matrix including the sensitivity, specificity, and precision. A nomogram was also used to visualize the model. RESULTS: Among the patients in the derivation and validation datasets, 38 and 9 participants (10.5% and 2.54%, respectively) developed severe COVID-19, respectively. In univariate analysis, 21 parameters such as age, sex (male), smoker, body mass index (BMI), time from onset to admission (> 5 d), asthenia, dry cough, expectoration, shortness of breath, asthenia, and Rox index < 18 (pulse oxygen saturation, SpO2)/(FiO2 × respiratory rate, RR) showed positive correlations with severe COVID-19. In multivariate logistic regression analysis, only six parameters including BMI [odds ratio (OR) 3.939; 95% confidence interval (CI): 1.409-11.015; P = 0.009], time from onset to admission (≥ 5 d) (OR 7.107; 95%CI: 1.449-34.849; P = 0.016), fever (OR 6.794; 95%CI: 1.401-32.951; P = 0.017), Charlson index (OR 2.917; 95%CI: 1.279-6.654; P = 0.011), PaO2/FiO2 ratio (OR 17.570; 95%CI: 1.117-276.383; P = 0.041), and neutrophil/lymphocyte ratio (OR 3.574; 95%CI: 1.048-12.191; P = 0.042) were found to be independent predictors of COVID-19. These factors were found to be significant risk factors for severe patients confirmed with COVID-19. The AUROC was 0.941 (95%CI: 0.901-0.981) and 0.936 (95%CI: 0.886-0.987) in both datasets. The calibration properties were good. CONCLUSION: The proposed predictive model had great potential in severity prediction of COVID-19 in the ICU. It assisted the ICU clinicians in making timely decisions for the target population.

[Eighteen cases of 2009 influenza A H1N1 associated with respiratory failure in adults].

OBJECTIVE: To investigate the clinical feature, treatment and outcome of respiratory failure in patients with 2009 influenza A H1N1 infection in critically ill adults. METHODS: A prospective observational study of 18 patients with respiratory failure suffering from 2009 influenza A H1N1 infection admitted between November 22, 2009 and January 16, 2010. Their clinical data were analyzed. RESULTS: Respiratory failure occurred in 18 patients with confirmed (n=9) or probable (n=9) 2009 influenza A H1N1. Among the 18 patients 8 patients were male, 10 patients were female (7 were pregnant or postpartum). Eight patients had pre-existing medical conditions. Twelve patients were between 20 and 40 years of age, the mean age was 37.1 years. Three were obese with body mass index over 30 kg/m (2). The 28-day mortality was 33.3% (6/18) with 1 additional late death. The median duration from the onset of the illness to hospital admission was 4.1 days (1-5 days) and from the onset to first dose of oseltamivir was 5.5 days (2-12 days), from onset to mechanical ventilation initiation was 6.8 days (4-12 days). Seventeen patients had primary viral pneumonia and 1 patient had an asthma exacerbation and 3 patients experienced multiple organ dysfunction syndrome (MODS). Twelve patients received corticosteroids, 10 patients required vasopressors. All patients were mechanically ventilated, 1 patient underwent extracorporeal membrane oxygenation (ECMO). Patients who died had higher acute physiology and chronic health evaluation II score compared to survivors (29.2 + or - 7.3 vs. 18.6 + or - 6.4, P=0.02). All deceased patients received high-level ventilation settings [peak inspiratory pressure > or = 35 cm H(2)O (1 cm H(2)O=0.098 kPa) and positive end-expiratory pressure > or = 18 cm H(2)O] within the first 7 days of ventilation, and the hypoxemia [oxygenation index < or = 60 mm Hg (1 mm Hg=0.133 kPa)] lasted 24 hours. In contrast only 1 among survivors did (9.1% vs. 100.0%, P<0.01). Compared with survivors, acute kidney injury and barotrauma occurred more frequently in non-survivors (42.9% vs. 27.3%, 28.6% vs. 9.1%, both P<0.05). Whereas all deceased patients received vasopressors, only 4 survivors required vasopressor support (100.0% vs. 36.4%, P<0.05). CONCLUSION: Severe acute respiratory distress syndrome is the most common manifestation in critically ill patients with 2009 influenza A H1N1 infection in adult. Failure to obtain satisfactory oxygenation with high-level ventilation settings within the first 7-days, onset of acute kidney injury and barotrauma, and continuous need for vasopressors portend a poor prognosis.

Symptomatic and optimal supportive care of critical COVID-19: A case report and literature review.

BACKGROUND: Coronavirus disease 2019 (COVID-19) severity is classified as asymptomatic, mild, moderate, severe, and critical. Mild cases account for a large percentage of cases in the epidemic and typically exhibit a favorable prognosis. However, a 49%-67% mortality is noted in critical cases. No COVID-19-specific drug has been reported to date, and symptomatic and optimal supportive care, including oxygenation, anti-coinfection treatments, and ventilation, represent the mainstay of treatment for this disease, especially in critical patients. CASE SUMMARY: In the above-mentioned context, we share our experience with the treatment of one critical COVID-19 case and review the relevant literature. CONCLUSION: Timely tracheal intubation, reasonable mechanical ventilation support, appropriate anti-infection treatment, and early anticoagulation and immunity support are key factors in the successful treatment of this case.

[Evaluation of pre-harvest sprouting resistance of wheat varieties from different ecological regions.] / 不同生态区小麦品种的穗发芽抗性评价.

The pre-harvest sprouting (PHS) resistance of 137 wheat varieties from different regions was evaluated and the relative germination index (RGI) was calculated. The relationships between PHS and grain quality traits, amylase activity and related gene expression level of these varieties were analyzed. The results showed that wheat varieties from the middle and lower reaches of Yangtze River Valley winter wheat region had the lowest RGI value and the highest ratio of resistant pre-harvest sprouting wheat varieties, followed by the varieties from the upper reach of Yangtze River Valley winter wheat region and from the Yellow and Huai River Valley. Red-grain wheat had lower RGI than white-grain wheat. RGI was positively correlated with seed length, seed width, and spikelet number, but not correlated with other grain traits (panicle type, ear color, ear length, and spikelet density, grain per spike and 1000-grain weight). RGI was negatively associated with the test weight, dough development time, and flour yield, but not with other quality indices (protein content, wet gluten content, water absorption, stability time, sedimentation, extension area, extensibility and max resistance). Amylase activity of different varieties increased with seed imbibition time. RGI was positively associated with α-amylase activity after germinating for 24-72 hours. The cluster analysis results of resistant varieties were consistent with the PHS resistance evaluation after 48 hours. RGI was positively associated with the related gene expression with seed imbibition time.

Coronavirus disease 2019 (COVID-19) associated coagulopathy and its impact on outcomes in Shenzhen, China: A retrospective cohort study.

BACKGROUND: Early detection of suspected critical patients infected with coronavirus disease 2019 (COVID-19) is very important for the treatment of patients. This study aimed to investigate the role of COVID-19 associated coagulopathy (CAC) to preview and triage. METHODS AND RESULTS: A cohort study was designed from government designated COVID-19 treatment center. CAC was defined as International Society on Thrombosis and Haemostasis (ISTH) score ≥2. Data from 117 patients COVID-19 were reviewed on admission. The primary and secondary outcomes were admission to Intensive Care Unit (ICU), the use of mechanical ventilation, vital organ dysfunction, discharges of days 14, 21 and 28 from admission and hospital mortality. Among them, admission to ICU was increased progressively from 16.1% in patients with non-CAC to 42.6% in patients with CAC (P < 0.01). Likely, invasive ventilation and noninvasive ventilation were increased from 1.8%, 21.4% in patients with non-CAC to 21.3%, 52.5% in patients with CAC, respectively (P < 0.01). The incidences of acute hepatic injury and acute respiratory distress syndrome in non-CAC and CAC were 28.6% vs. 62.3%, 8.9% vs. 27.9%, respectively (P < 0.01). The discharges of days 14, 21 and 28 from admission were more in non-CAC than those of CAC (P < 0.05). Multiple logistic regression results showed that ISTH score ≥2 was obviously associated with the admission to ICU (OR 4.07, 95% CI 1.47-11.25 P = 0.007) and the use of mechanical ventilation (OR 5.54, 95% CI 2.01-15.28 P = 0.001) in patients with COVID-19. CONCLUSION: All results show ISTH score ≥2 is an important indicator to preview and triage for COVID-19 patients.