Objective Viral encephalitis is an infectious disease severely affecting human health.It is caused by a wide variety of viral pathogens,including herpes viruses,flaviviruses,enteroviruses,and other viruses.The laboratory diagnosis of viral encephalitis is a worldwide challenge.Recently,high-throughput sequencing technology has provided new tools for diagnosing central nervous system infections.Thus,In this study,we established a multipathogen detection platform for viral encephalitis based on amplicon sequencing. Methods We designed nine pairs of specific polymerase chain reaction(PCR)primers for the 12 viruses by reviewing the relevant literature.The detection ability of the primers was verified by software simulation and the detection of known positive samples.Amplicon sequencing was used to validate the samples,and consistency was compared with Sanger sequencing. Results The results showed that the target sequences of various pathogens were obtained at a coverage depth level greater than 20×,and the sequence lengths were consistent with the sizes of the predicted amplicons.The sequences were verified using the National Center for Biotechnology Information BLAST,and all results were consistent with the results of Sanger sequencing. Conclusion Amplicon-based high-throughput sequencing technology is feasible as a supplementary method for the pathogenic detection of viral encephalitis.It is also a useful tool for the high-volume screening of clinical samples.

The chemical constituents of Helleborus thibetanus were isolated and purified by silica gel column chromatography, Sephadex LH-20 gel column chromatography, and semi-preparative RP-HPLC, and the structures of all compounds were identified by modern spectrographic technology(MS, NMR). The MTT method was used to measure the cytotoxicity of compounds 1-8. Twelve compounds were isolated from the roots and rhizomes of H. thibetanus and were identified as(25R)-22β,25-expoxy-26-[(O-β-D-glucopyranosyl)oxy]-1β,3β-dihydroxyfurosta-5-en(1), β-sitosterol myristate(2), β-sitosterol lactate(3), β-sitosterol 3-O-β-D-glucopyrannoside(4), 4,6,8-trihydroxy-3,4-dihydronaphthalen-1(2H)-one(5), 1,3,5-trimethoxybenzene(6), 7,8-dimethylbenzo pteridine-2,4(1H,3H)-dione(7), 1H-indole-3-carboxylic acid(8), p-hydroxy cinnamic acid(9), lauric acid(10), n-butyl α-L-arabinofuranoside(11) and methyl-α-D-fructofuranoside(12), respectively. Among them, compound 1 is a new compound and named thibetanoside L; compounds 2, 5-8, 11 are first isolated from the family Ranunculaceae; compound 12 is isolated from the genus Helleborus for the first time. The results of MTT assay showed that the IC_(50) values of compounds 1-8 against HepG2 and HCT116 cells were greater than 100 μmol·L~(-1).
Helleborus/chemistry* ; Molecular Structure ; Plant Roots/chemistry* ; Rhizome/chemistry* ; Magnetic Resonance Spectroscopy

OBJECTIVES: To investigate the risk factors for neonatal asphyxia in Hubei Enshi Tujia and Miao Autonomous Prefecture and establish a nomogram model for predicting the risk of neonatal asphyxia. METHODS: A retrospective study was conducted with 613 cases of neonatal asphyxia treated in 20 cooperative hospitals in Enshi Tujia and Miao Autonomous Prefecture from January to December 2019 as the asphyxia group, and 988 randomly selected non-asphyxia neonates born and admitted to the neonatology department of these hospitals during the same period as the control group. Univariate and multivariate analyses were used to identify risk factors for neonatal asphyxia. R software (4.2.2) was used to establish a nomogram model. Receiver operator characteristic curve, calibration curve, and decision curve analysis were used to assess the discrimination, calibration, and clinical usefulness of the model for predicting the risk of neonatal asphyxia, respectively. RESULTS: Multivariate logistic regression analysis showed that minority (Tujia), male sex, premature birth, congenital malformations, abnormal fetal position, intrauterine distress, maternal occupation as a farmer, education level below high school, fewer than 9 prenatal check-ups, threatened abortion, abnormal umbilical cord, abnormal amniotic fluid, placenta previa, abruptio placentae, emergency caesarean section, and assisted delivery were independent risk factors for neonatal asphyxia (P<0.05). The area under the curve of the model for predicting the risk of neonatal asphyxia based on these risk factors was 0.748 (95%CI: 0.723-0.772). The calibration curve indicated high accuracy of the model for predicting the risk of neonatal asphyxia. The decision curve analysis showed that the model could provide a higher net benefit for neonates at risk of asphyxia. CONCLUSIONS The risk factors for neonatal asphyxia in Hubei Enshi Tujia and Miao Autonomous Prefecture are multifactorial, and the nomogram model based on these factors has good value in predicting the risk of neonatal asphyxia, which can help clinicians identify neonates at high risk of asphyxia early, and reduce the incidence of neonatal asphyxia.
Infant, Newborn ; Humans ; Male ; Pregnancy ; Female ; Nomograms ; Retrospective Studies ; Cesarean Section ; Risk Factors ; Asphyxia Neonatorum/etiology*

This study aimed to investigate the neurotoxicity induced by trichloroacetic acid (TCA) and the possible protective mechanisms of boron (B). Mouse BV2 cells were treated with TCA (0, 0.39, 0.78, 1.56, 3.12, 6.25, or 12.5 mmol/L) and B (0, 7.8, 15.6, 31.25, 62.5, 125, 500, or 1,000 mmol/L) for 3 h and 24 h, respectively. Then, reactive oxygen species, and supernatant proinflammatory cytokine and protein levels were analyzed after 24 h of combined exposure. Beyond the dose-dependent decrease in the cellular viability, it clearly increased after B supplementation ( P < 0.05). Moreover, B decreased oxidative damage, and significantly down-regulated IL-6 levels and up-regulated TNF-β production ( P < 0.05). B also decreased apoptosis via the p53 pathway. The present findings indicated that TCA may induce oxidative damage, whereas B mitigates these adverse effects by decreasing cell apoptosis.
Animals ; Apoptosis ; Boron/toxicity* ; Mice ; Oxidative Stress ; Reactive Oxygen Species/metabolism* ; Trichloroacetic Acid/toxicity* ; Tumor Suppressor Protein p53/metabolism*

Objective: To our knowledge, no definitive conclusion has been reached regarding the relationship between glucocorticoids and hypertension. Here, we aimed to explore the characteristics of glucocorticoids in participants with dysglycemia and hypertension, and to analyze their association with blood pressure indicators. Methods: The participants of this study were from the Henan Rural Cohort study. A total of 1,688 patients 18-79 years of age were included in the matched case control study after application of the inclusion and exclusion criteria. Statistical methods were used to analyze the association between glucocorticoids and various indices of blood pressure, through approaches such as logistic regression analysis, trend tests, linear regression, and restricted cubic regression. Results: The study population consisted of 552 patients with dysglycemia and hypertension (32.7%). The patients with co-morbidities had higher levels of serum cortisol ( Conclusions Serum deoxycortisol was positively correlated with systolic blood pressure, pulse pressure, mean arterial pressure, mean blood pressure, and mean proportional arterial pressure. Glucocorticoids (deoxycortisol and cortisol) increase the risk of hypertension in people with dysglycemia, particularly in those with T2DM.
Adult ; Aged ; Aged, 80 and over ; Blood Pressure ; Case-Control Studies ; China/epidemiology* ; Cohort Studies ; Female ; Glucocorticoids/blood* ; Glycemic Load ; Humans ; Hydrocortisone/blood* ; Hypertension/etiology* ; Male ; Middle Aged ; Prevalence ; Risk Factors ; Rural Population ; Young Adult

Adult ; Aged ; China ; epidemiology ; Cholestanetriol 26-Monooxygenase ; genetics ; Cytochrome P450 Family 2 ; genetics ; Female ; Humans ; Male ; Middle Aged ; Polymorphism, Genetic ; Rural Population ; statistics & numerical data ; Vitamin D ; blood ; Vitamin D Deficiency ; epidemiology

Objective To explore the effect of the combination of carnitine palmityl transferase 1( CPT1) inhibitor etomoxir and chemotherapy drug cisplatin on lung cancer cell line A549 proliferation and migration of lung cancer. Methods CCK8 was applied to investigate the effect of the combination of etomoxir and cisplatin on A549 survival. Transwell test was used to detect migration of lung cancer cell line A549 treated with the combination of etomoxir and cisplatin. Apoptosis of A549 was detected by annexin V/PI. A549 transplanted mice were used to test therapeu-tic effect of etomoxir combined with cisplatin. Results Tumor cells proliferation and migration were inhibited by the combination of etomoxir and cisplatin. Apoptosis of tumor cells was enhanced by the combination of etomoxir. After the treatment of the combination of etomoxir and cisplatin, tumor growth of mouse was inhibited. Conclusions The combination of etomoxir and cisplatin can decrease tumor cells survival and induce tumor cells apoptosis, and then inhibit tumor growth in mouse lung cancer model.

Aged ; Biliary Tract Diseases ; surgery ; China ; Humans

Phosphoglycerate mutase 1 (PGAM1) is upregulated in many cancer types and involved in cell proliferation, migration, invasion, and apoptosis. However, the relationship between PGAM1 and prostate cancer is poorly understood. The present study investigated the changes in PGAM1 expression in prostate cancer tissues compared with normal prostate tissues and examined the cellular function of PGAM1 and its relationship with clinicopathological variables. Immunohistochemistry and Western blotting revealed that PGAM1 expression was upregulated in prostate cancer tissues and cell lines. PGAM1 expression was associated with Gleason score (P = 0.01) and T-stage (P = 0.009). Knockdown of PGAM1 by siRNA in PC-3 and 22Rv1 prostate cancer cell lines inhibited cell proliferation, migration, and invasion and enhanced cancer cell apoptosis. In a nude mouse xenograft model, PGAM1 knockdown markedly suppressed tumor growth. Deletion of PGAM1 resulted in decreased expression of Bcl-2, enhanced expression of Bax, caspases-3 and inhibition of MMP-2 and MMP-9 expression. Our results indicate that PGAM1 may play an important role in prostate cancer progression and aggressiveness, and that it might be a valuable marker of poor prognosis and a potential therapeutic target for prostate cancer.
Animals ; Apoptosis/genetics* ; Caspase 3/metabolism* ; Cell Line, Tumor ; Cell Movement/genetics* ; Cell Proliferation/genetics* ; Gene Deletion ; Gene Knockdown Techniques ; Humans ; Male ; Matrix Metalloproteinase 2/metabolism* ; Matrix Metalloproteinase 9/metabolism* ; Mice ; Mice, Nude ; Neoplasm Invasiveness/genetics* ; Neoplasm Transplantation ; PC-3 Cells ; Phosphoglycerate Mutase/genetics* ; Prostatic Neoplasms/pathology* ; Proto-Oncogene Proteins c-bcl-2/metabolism* ; RNA, Small Interfering ; Transplantation, Heterologous ; bcl-2-Associated X Protein/metabolism*

Objective: To investigate the relationship between menopausal status at different FPG levels and the risk of new onset of impaired fasting glucose (IFG) and type 2 diabetes mellitus (T2DM). Methods: Female subjects were selected from the females who joined in the epidemiological survey between May and September in 2009 in six counties of Guanlin Village and Xushe Village in Yixing City in Jiangsu Province by cluster sampling method. Subjects with diabetes at baseline or pre-menopause with age above 65 years old or surgical menopause were excluded. Finally there were 2 084 eligible subjects included in this study. According to FPG at baseline, subjects were categorized into two groups as normal FPG group (FPG<5.6 mmol/L) and IFG group (5.6≤FPG≤6.9 mmol/L). Follow-up study was conducted from May in 2014 to January in 2016. Cox regression model was used to investigate the association between menopausal factors and IFG and T2DM among groups based on FPG. Results: The average age of subjects at baseline was 58.08 (51.74-65.82) years old, and the number of post-menopausal women was 1 631 (78.3%). The number of subjects in normal FPG group was 1 569 (75.3%), and in IFG group was 515 (24.7%). There were 104 subjects with new onset T2DM among which 34 subjects from normal FPG group and 70 subjects from IFG group. And there were 199 subjects with new onset IFG in normal FPG group. Among subjects with normal FPG, the incidence density of IFG in post-menopausal women (2 752/100 000 person-years) was statistically higher than that in premenopausal women (1 670/100 000 person-years) (P<0.001). After age and BMI adjusted, post-menopausal women had a higher risk of having IFG in normal FPG subjects with hazard ratio (HR) at 2.60 (P<0.001). Among subjects with normal FPG, the risk of new onset IFG decreased in post-menopausal women with menopause age increasing after age and BMI adjusted, with HR at 0.96 (P=0.046). No statistical association was found between menopausal factors and risk of T2DM either in the overall subjects or in the subgroups(P>0.05). Conclusion Menopause can increase the risk of IFG incidence in subjects with normal FPG. The incidence of IFG decreases with the menopause age increasing.