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The association between traditional Chinese medicine (TCM) treatment intensity (TI) and the clinical therapeutic outcomes of patients with mild to moderate COVID-19 symptoms has not been fully understood. A retrospective cohort study was undertaken to assess the therapeutic effect of traditional Chinese medicine (TCM) on patients with mild COVID-19. Between April and May 2022, a total of 6,120 confirmed COVID-19 cases were enrolled from temporary hospitals in Shanghai City. Patients receiving TCM treatment were identified through their daily prescriptions. The nonlinearity and cutoff point of this relationship were determined using a restricted cubic spline model. The study included 6,120 mild COVID-19 cases with a median (range) age of 43.0 (2.0, 75.0) years,a median (range) hospitalization duration of 9.7 (4.1, 22.5) days, a median (range) of taking TCM of 2.0 (0.0, 15.0) days, and the median (range) negative conversion time of SARS-CoV-2 nucleic acid was 6.67 (95% confidence interval [ CI]: 4.1, 22.5) days, with 1854 women (30.3%) among the participants. The restricted cubic spline model revealed significant nonlinear association between TCMTI and the negative nucleic acid conversion time, and the statistical test results of all three parameters were statistically significant. The cutoff value of TCMTI is 0.65. The high TCMTI group showed a significant reduction in the median negative conversion time of SARS-CoV-2 nucleic acid (hazard ratio [ HR]=1.769 [95% CI: 1.575, 1.986]) and a decrease in hospitalization duration (coefficient=-0.146, PPTrial Registration: The trial was prospectively registered on Chinese Clinical Trial Registry (ChiCTR, ChiCTR2200063151, [http://www.chictr.org.cn/](http://www.chictr.org.cn/) ).

The immunoregulation of platelets and platelet–monocyte aggregates (PMAs) is increasingly recognized, but it roles in tuberculosis (TB) remain to be elucidated. In this study, we found that CD14+CD41+ PMAs were increased in peripheral blood of patients with active TB. CD14+CD41+ PMAs highly expressed triggering receptors expressed on myeloid cells (TREMs)-like transcript-1 (TLT-1), P-selectin (CD62P), and CD40L. Our in vitro study found that platelets from patients with active TB aggregate with monocytes to induce IL-1β and IL-6 production by monocytes. Importantly, we identified that TLT-1 was required for formation of PMAs. The potential TLT-1 ligand was expressed and increased on CD14+ monocytes of patients with TB determined by using TLT-1 fusion protein (TLT-1 Fc). Blocking of ligand–TLT-1 interaction with TLT-1 Fc reduced PMA formation and IL-1β and IL-6 production by monocytes. Further results demonstrated that PMAs induced IL-10 production by B cells (B10) dependent on IL-1β, IL-6, and CD40L signals in a coculture system. Moreover, TLT-1 Fc treatment suppressed B10 polarization via blocking PMA formation. Taking all of these data together, we elucidated that TLT-1 promoted PMA-mediated B10 polarization through enhancing IL-1β, IL-6, and CD40L origin from PMAs, which may provide potential targeting strategies for TB disease treatment.

T cell–interacting activating receptor on myeloid cells 1 (TARM-1) is a novel leukocyte receptor expressed in neutrophils and macrophages. It plays an important role in proinflammatory response in acute bacterial infection, but its immunomodulatory effects on chronic Mycobacterium tuberculosis infections remain unclear. TARM-1 expression was significantly upregulated on CD14high monocytes from patients with active pulmonary tuberculosis (TB) as compared that on cells from patients with latent TB or from healthy control subjects. Small interfering RNA knockdown of TARM-1 reduced expression levels of proinflammatory cytokines IL-12, IL-18, IL-1β, and IL-8 in M. tuberculosis–infected macrophages, as well as that of HLA-DR and costimulatory molecules CD83, CD86, and CD40. Moreover, TARM-1 enhanced phagocytosis and intracellular killing of M. tuberculosis through upregulating reactive oxygen species. In an in vitro monocyte and T cell coculture system, blockade of TARM-1 activity by TARM-1 blocking peptide suppressed CD4+ T cell activation and proliferation. Finally, administration of TARM-1 blocking peptide in a mouse model of M. tuberculosis infection increased bacterial load and lung pathology, which was associated with decreased macrophage activation and IFN-γ production by T cell. Taken together, these results, to our knowledge, demonstrate a novel immune protective role of TARM-1 in M. tuberculosis infection and provide a potential therapeutic target for TB disease.

Multi-drug resistant tuberculosis (MDR-TB) is a critical global public health problem.Sputum cultures and lung images show a strong association with treatment outcomes, serving as a multi-dimensional approach to identify MDR-TB patients with poor outcomes.The results imply that funds and policy investments should be increased by early monitoring of MDR-TB patients, especially regarding imaging and sputum bacterium. By informing physicians on changes to the therapeutic schedule, treatment outcomes can be improved.

Background. CD147/basigin (Bsg), a transmembrane glycoprotein, activates matrix metalloproteinases and promotes inflammation. Objective. The aim of this study is to explore the clinical significance of CD147 in the pathogenesis of inflammatory bowel disease (IBD). Results. In addition to monocytes, the clinical analysis showed that there is no significance obtained in leucocyte, neutrophil, eosinophil, basophil, and erythrocyte between IBD and controls. Immunohistochemistry analysis showed that CD147 was increased in intestinal tissue of patients with active IBD compared to that in the control group. What is more, CD147 is involved in intestinal barrier function and intestinal inflammation, which was attributed to the fact that it has an influence on MCT4 expression, a regulator of intestinal barrier function and intestinal inflammation, in HT-29 and CaCO2 cells. Most importantly, serum level of CD147 content is higher in active IBD than that in inactive IBD or healthy control, which could be a biomarker of IBD. Conclusion. The data suggested that increased CD147 level could be a biomarker of IBD in children.

Mucosal associated invariant T (MAIT) cells play a critical role in Helicobacter pylori (H. pylori)-induced gastritis by promoting mucosal inflammation and aggravating mucosal injuries (1, 2). However, the underlying mechanism and key molecules involved are still uncertain. Here we identified OX40, a co-stimulatory molecule mainly expressed on T cells, as a critical regulator to promote proliferation and IL-9 production by MAIT cells and facilitate mucosal inflammation in H. pylori-positive gastritis patients. Serum examination revealed an increased level of IL-9 in gastritis patients. Meanwhile, OX40 expression was increased in mucosal MAIT cells, and its ligand OX40L was also up-regulated in mucosal dendritic cells (DCs) of gastritis patients, compared with healthy controls. Further results demonstrated that activation of the OX40/OX40L pathway promoted IL-9 production by MAIT cells, and MAIT cells displayed a highly-activated phenotype after the cross-linking of OX40 and OX40L. Moreover, the level of IL-9 produced by MAIT cells was positively correlated with inflammatory indexes in the gastric mucosa, suggesting the potential role of IL-9-producing MAIT cells in mucosal inflammation. Taken together, we elucidated that OX40/OX40L axis promoted mucosal MAIT cell proliferation and IL-9 production in H. pylori-induced gastritis, which may provide potential targeting strategies for gastritis treatment.

Background The coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) has led to a significant number of mortalities worldwide. COVID-19 poses a serious threat to human life. The clinical manifestations of COVID-19 are diverse and severe and 20% of infected patients are reported to be in a critical condition. A loss in lung function and pulmonary fibrosis are the main manifestations of patients with the severe form of the disease. The lung function is affected, even after recovery, thereby greatly affecting the psychology and well-being of patients, and significantly reducing their quality of life. Methods Participants must meet the following simultaneous inclusion criteria: over 18 years of age, should have recovered from severe or critical COVID-19 cases, should exhibit pulmonary fibrosis after recovery, and should exhibit Qi-Yin deficiency syndrome as indicated in the system of traditional Chinese medicine (TCM). The eligible candidates will be randomized into treatment or control groups. The treatment group will receive modern medicine (pirfenidone) plus TCM whereas the control group will be administered modern medicine plus TCM placebo. The lung function index will be continuously surveyed and recorded. By comparing the treatment effect between the two groups, the study intend to explore whether TCM can improve the effectiveness of modern medicine in patients with pulmonary fibrosis arising as a sequelae after SARS-CoV-2 infection. Discussion Pulmonary fibrosis is one of fatal sequelae for some severe or critical COVID-19 cases, some studies reveal that pirfenidone lead to a delay in the decline of forced expiratory vital capacity, thereby reducing the mortality partly. Additionally, although TCM has been proven to be efficacious in treating pulmonary fibrosis, its role in treating pulmonary fibrosis related COVID-19 has not been explored. Hence, a multicenter, parallel-group, randomized controlled, interventional, prospective clinical trial has been designed and will be conducted to determine if a new comprehensive treatment for pulmonary fibrosis related to COVID-19 is feasible and if it can improve the quality of life of patients. Trial registration: This multicenter, parallel-group, randomized controlled, interventional, prospective trial was registered at the Chinese Clinical Trial Registry (ChiCTR2000033284) on 26th May 2020 (prospective registered).

CD103 is considered as a surface marker for the resident immune cells. However, little is known about the intrinsic function of CD103 in infection and inflammation. In this study, we found that CD103 was highly expressed in CD4+T cells of the gastric mucosa from patients with H. pylori-positive gastritis. Mucosal resident CD103+CD4+T cells exhibited an increase in the CD45RO+CCR7− effector memory phenotype and high expression of the chemokine receptors CXCR3 and CCR9 compared with those in CD103−CD4+T cells. An In vitro coculture study demonstrated that H. pylori-specific antigen CagA/VacA-primed dendritic cells (DCs) induced proliferation and IFN-γ, TNF as well as IL-17 production by CD103+CD4+T cells from patients with H. pylori-positive gastritis, while blocking CD103 with a neutralizing antibody reduced proliferation and IFN-γ, TNF, and IL-17 production by CD103+CD4+T cells cocultured with DCs. Moreover, immunoprecipitation revealed that CD103 interacted with TCR α/β and CD3ζ, and activation of CD103 enhanced the phosphorylation of ZAP70 induced by the TCR signal. Finally, increased T-bet and Blimp1 levels were also observed in CD103+CD4+T cells, and activating CD103 increased T-bet and Blimp1 expression in CD4+T cells. Our results explored the intrinsic function of CD103 in gastric T cells from patients with H. pylori-positive gastritis, which may provide a therapeutic target for the treatment of gastritis.

The local immune response plays an important role in the pathogenesis of colorectal carcinoma. Patients with colorectal polyps are at increased risk of colorectal cancer. However, the immunoregulation of early-stage colorectal polyps remain unknown. In the study, 202 biopsy samples from 80 pediatric patients with colorectal polyps and from 42 normal controls were collected. We found that the number of CD4

Fatigue crack damage in the epoxy asphalt concrete pavement of long-span steel bridge deck is still one of the most severe problems even though the fatigue endurance performance has been studied for a long time. In this study, it aimed at exploring the mechanism why the fatigue damage of the epoxy asphalt concrete occurred, as well as finding out the reason why fatigue test results in laboratory were different from those in practical engineering application. A finite element mechanics method was first applied to analyze the maximum strain value of the epoxy asphalt concrete pavement at different load positions, then fatigue performance of the epoxy asphalt concrete was investigated using a four-point bending fatigue testing method, and finally a three-parameter fatigue equation model, which was demonstrated to be feasible and rational, was utilized to determine fatigue endurance limit for the first time. The fatigue damage of the epoxy asphalt concrete occurred in a short time once the strain level with driving load was larger than fatigue endurance limit. In contrast, the fatigue damage did not appear in a long time if the strain level was less than the fatigue endurance limit. It is suggested that the fatigue endurance limit be adopted as a control parameter in the design phase of epoxy asphalt concrete pavement. These findings advance previous design specifications in the world, and could help extending service life of epoxy asphalt concrete pavement of long-span steel bridge deck. Keywords: Long-span steel bridge deck, Epoxy asphalt concrete pavement, Fatigue damage, Fatigue endurance limit, Three-parameter model, Finite element mechanics method

The local immune response plays an important role in the pathogenesis of colorectal carcinoma. Patients with colorectal polyps are at increased risk of colorectal cancer. However, the immunoregulation of early-stage colorectal polyps remain unknown. In the study, 202 biopsy samples from 80 pediatric patients with colorectal polyps and from 42 normal controls were collected. We found that the number of CD4+, CD8+T cells and CD19+B cells were reduced, whereas CD68+macrophages (Mϕ) were increased in colorectal polyps compared to the distal normal tissue from the same patients and the tissue from healthy donors. The frequency of Mϕwas negatively correlated with the number of CD4+ and CD8+T cells but not CD19+B cells in colorectal polyps. We further identified that CD163 was highly expressed on Mϕϕ from colorectal polyps compared to those from normal controls. Furthermore, real-time PCR revealed that TGF-β, but not IL-10 and IL-4, was increased in colorectal polyps. Immunofluorescence and flow cytometry showed that TGF-β was predominantly produced by CD163+Mϕ. In vitro experiments demonstrated that the supernatant from cultured polyps induced CD163 expression and TGF-β production in blood-derived Mϕ. A co-culture experiment revealed that purified Mϕ from colorectal polyps suppressed T cell proliferation. Based on these results, we hypothesized that abundant CD163+Mϕ may promote the progression of colorectal polyps by inhibiting the local T cell response through TGF-β production.

Background Blastocystis is a widespread zoonotic protozoan of mammalian species, especially in HIV/AIDS individuals. The aim of this study was to analyze the prevalence and risk factors related with Blastocystis infection among HIV/AIDS patients in Southwest China. Methods The cross-sectional study was performed in 311 HIV/AIDS cases in Tengchong City, Yunnan Province from July 2016 to March 2017. For each subject, stool specimen was collected to detect the Blastocystis, and the blood sample was used to detect HIV virus load and CD4+ T cell count, in addition, structured questionnaire was used to collect the basic information and risk factors. Findings The result showed that the detection rate of Blastocystis was 3.86% (95% CI: 2.22–6.62) among HIV/AIDS patients. Both raising animal (OR = 12.93, 95% CI: 1.54–108.36) and drinking un-boiled water (OR = 8.17, 95% CI: 1.76–37.90) were risk factors for Blastocystis infection in HIV/AIDS individuals. In addition, the interaction of CD4+ T cell count and HIV virus load was also contribution to Blastocystis infection (P = 0.007). Conclusions A high prevalence of Blastocystis infection was found in HIV/AIDS patients in Tengchong. Poor hygienic habits, the interaction of HIV virus load and CD4+ T cell count were identified as main risk factors for infection. These results will help us to develop efficient control strategies to intervene with and prevent the occurrence of Blastocystis among HIV-infected individuals.

Objective Inflammatory bowel disease (IBD) is a disorder intestinal inflammation and impaired barrier function, associated with increased epithelial expression of monocarboxylate transporter 4 (MCT4). However, the specific non‐metabolic function and clinical relevance of MCT4 in IBD remain to be fully elucidated. Methods Lentivirus‐mediated overexpression of MCT4 was used to assess the role of MCT4 in transcriptionally regulating ZO‐1 and IL‐6 expression by luciferase assays, WB and ChIP. IP was used to analyse the effect of MCT4 on the interaction NF‐κB‐CBP or CREB‐CBP, and these MCT4‐mediated effects were confirmed in vivo assay. Results We showed that ectopic expression of MCT4 inhibited ZO‐1 expression, while increased pro‐inflammatory factors expression, leading to destroy intestinal epithelial barrier function in vitro and in vivo. Mechanistically, MCT4 contributed NF‐κB p65 nuclear translocation and increased the binding of NF‐κB p65 to the promoter of IL‐6, which is attributed to MCT4 enhanced NF‐κB‐CBP interaction and dissolved CREB‐CBP complex, resulting in reduction of CREB activity and CREB‐mediated ZO‐1 expression. In addition, treatment of experimental colitis with MCT4 inhibitor α‐cyano‐4‐hydroxycinnamate (CHC) ameliorated mucosal intestinal barrier function, which was due to attenuation of pro‐inflammation factors expression and enhancement of ZO‐1 expression. Conclusion These findings suggested a novel role of MCT4 in controlling development of IBD and provided evidence for potential targets of IBD.

Autoregressive integrated moving average (ARIMA) model was used to predict the monthly reported severe cases of hand-foot-mouth disease(HFMD) in China to provide a reference for prevention and control of HFMD and the application of ARIMA in of ARIMA in HFMD and other infectious diseases. On the basis of time series supplied by the monthly reported severe cases of the national HFMD from 2010 ~ 2015, ARIMA model was established with the actual cases of HFMD from January to September 2016 as the validated data and with the comparison of ARIMA model based on the data from 2010-2014- The models based on the 2010~2014 and 2010~2015 data of monthly reported severe cases of HFMD in China are ARIMA(1,1,0,) (2, 1,0)(12),ARIMA(0,1,1,) (2,1,0)(12) respectively. The comparison of two models shows that the average of the relative error decreases with the accumulated data and does not do the same with the shorter time of predication. Different time series may have different ARIMA models as for the same infectious diseases. It is needed to be further verified that the more data are accumulated, the more shorter time of predication is, the more-smaller the average of the relative error is.

Background: Inflammatory bowel disease(IBD) is characterized by intestinal inflammation and impaired barrier function, associated with increased epithelial expression of monocarboxylate Transporter 4 (MCT4). Methods: we performed qPCR, IF, WB and utilized luciferase, and ChIP to analyze MCT4 on NF-κB and CREB activity and DNA binding in IECs. IP was used to analyze the effect of MCT4 on the interaction NF-κB-CBP or CREBCBP. In vivo assay were detected by IF, WB and to analyze the role and mechanism of MCT4 in IBD. Findings: Functional studies further showed that ectopic expression of MCT4 disrupted tight junction protein 1(ZO-1) expression and increased pro-inflammatory factors expression, leading to destroy intestinal epithelial barrier function in vitro and in vivo. Mechanistically, one hand, MCT4 led to nuclear translocation of p65 and increased the binding of NF-κB p65 to the promoter of IL-6, on the other hand, MCT4 suppressed cAMP-response element binding protein (CREB) activity and reduced CREBmediated ZO-1 expression. these effect were attributed to MCT4 contributed to NF-κB-CBP interaction, while dissolved CREB-CBP complex. Treatment of experimental colitis with MCT4 inhibitor by α-cyano-4- hydroxycinnamate (CHC) significantly ameliorated mucosal intestinal barrier function in vivo, which was attributed to attenuation of proinflammation factors expression and enhancement of ZO-1 expression. Interpretation: These findings suggested a novel MCT4 role in controlling development of IBD, which could serve as a new therapeutic target of IBD. Funding Statement: This work was supported by National Natural Science Foundation of China (No.81770552, No.81860101), Natural Science Foundation of Guangdong (No.2017A030313838, No.2018A0303130175), Medical Science and Technology Foundation of Guangdong (No.A2018395), Science and Technology plan program of Guangzhou (No.201804010148), General program of Guangzhou Health and plan commission (No.805150202068), Postdoctoral Research Funding of Guangzhou Women and Children’s Medical Center (NO.5001-3001075), Funding of Guangzhou Institute of Pediatrics/Guangzhou Women and Children’s Medical Center (NO.IP-2016-005, NO.IP2018-009). Declaration of Interests: The authors declared that they have no competing interests. Ethics Approval Statement: Human study: Based on the declaration of Helsinki as reflected in a prior approval by the institution’s human research committee, this study was conducted in a cohort of 54 patients with inflammatory bowel disease (IBD) and 16 healthy control in Guangzhou Women and Children’s Medical Center from 2016 to 2018 approved by the Medical Ethical Review Board(2017030602). Animal study: All animal experiments were approved by the Guangzhou Women and Children’s Medical Center animal care and use committee.

Under the current national comprehensive promotion and deployment of “building territorial spatial planning system and supervise its implementation” background, power network planning and construction must be based on the “multi-plan integration”, in line with the requirements of territorial spatial planning. This paper puts forward the construction scheme of the “early stage of power network auxiliary decision-making tool basing on multi-plan integration”. This tool is based on GIS technology to realize the intelligence, visualization and refinement of substation site and network path selection, which can solve the problem that at present, the grid planning is not coordinated, and inconsistent with other planning, and help improve the efficiency of power network planning and construction.

Group A rotavirus (RVA) is one of the leading cause of acute diarrhea worldwide, the RVA-related disease burden and the genotypes of RVA is important reference to introduce RVA variance to national immunisation programmes, 1,121 diarrhea cases and 319 healthy controls were recruited from four sentinel hospital outpatient from July 2014 to June 2015. The prevalence of RVA was 244 (21.8%) in gastroenteritis cases and in 12 (3.8%) in healthy controls across all age group (OR = 7.12, 95%CI = 3.93-12.89); the detection rate of RVA in diarrhea patients under 5 years was more higher than in diarrhea cases over 5 years (26.1%, 222/850; 8.1%, 22/271, respectively, P = 0.000). Of 244 RVA strains isolated from acute diarrhea cases, G9 (66.4%) was predominant G genotype, followed by G3 (18.7%), G1 (8.9%), and G1G3 (3.8%); P[8] was the overwhelming prevalence P genotype, followed by P[4] (4.7%); G9P[8] (54.9%) was most common G and P Combination, followed by G3P[8] (17.6%) and G1[8] (8.6%). The conclusion of the study was important to provide reference for introducing the RVA vaccine to prevent and control RVA-associated disease burden. J. Med. Virol. 89:71-78, 2017. © 2016 Wiley Periodicals, Inc.

Background Bacterial diarrhea is one of the most common causes for medical consultations, mortality and morbidity in the world. Diarrheagenic Escherichia coli (DEC) and non-typhoidal Salmonella (NTS) are major intestinal pathogens in developing countries, and the indiscriminate use of antibiotics has greatly contributed to resistant strains. Hence, the aim of the present study is to identify the antimicrobial resistance patterns and the molecular characteristics of DEC and NTS in southwest, China. Methods 1121 diarrheal patients and 319 non-diarrheal subjects across all age groups were recruited from four sentinel hospitals from June 2014 to July 2015 in Kunming City, Yunnan Province. Each stool specimen was collected to detect DEC and NTS with standard microbiological and molecular methods. Antimicrobial resistance testing was performed with the Kirby-Bauer disk diffusion method, and the standards for antimicrobial susceptibility testing complied with the Clinical and Laboratory Standards Institute (CLSI). Molecular characterization of strains was carried out using pulsed-field gel electrophoresis (PFGE). A structured questionnaire was used to record basic epidemiological data (e.g. sex, age, residence, season, etc.). Data were analyzed using Chi-square or Fisher’s exact test. Results DEC was detected in 127 (11.33%) diarrhea cases and 9 (2.82%) non-diarrheal cases (χ2 = 20.69, P

Background Acute diarrhea is one of the most serious problems in global public health that causes considerable morbidity and mortality worldwide. Human caliciviruses (HuCV) including norovirus (NoV, genogroup GI and GII) and sapovirus (SaV), is a leading cause of acute sporadic diarrhea in individuals across all age groups. However, few studies had been conducted clarifying the characteristics of HuCV in diarrhea cases across all age groups in China. Our study was aimed at assessing the HuCV-related diarrhea burden and NoV genotypes distribution in southwest China. Methods The study was conducted in four hospitals in Kunming city, Yunnan province, from June 2014 to July 2015. Stool specimens were collected from 1,121 diarrhea cases and 319 healthy controls in outpatient departments. Reverse transcription polymerase chain reaction (RT-PCR) was used to detect NoV (GI, GII) and SaV. Sequencing was applied to confirm the three viral infections and phylogenetic analysis was performed to determine their genotypes. A structured questionnaire was used to record the demographic information and clinical symptoms of subjects. Results HuCV was detected at an 11.0 % infection rate in 1,121 diarrhea cases and at 3.4 % rate in 319 non-diarrhea subjects (p

Group A rotavirus (RVA) is one of the leading cause of acute diarrhea worldwide, the RVA-related disease burden and the genotypes of RVA is important reference to introduce RVA variance to national immunisation programmes, 1,121 diarrhea cases and 319 healthy controls were recruited from four sentinel hospital outpatient from July 2014 to June 2015. The prevalence of RVA was 244 (21.8%) in gastroenteritis cases and in 12 (3.8%) in healthy controls across all age group (OR = 7.12, 95%CI = 3.93-12.89); the detection rate of RVA in diarrhea patients under 5 years was more higher than in diarrhea cases over 5 years (26.1%, 222/850; 8.1%, 22/271, respectively, P = 0.000). Of 244 RVA strains isolated from acute diarrhea cases, G9 (66.4%) was predominant G genotype, followed by G3 (18.7%), G1 (8.9%), and G1G3 (3.8%); P[8] was the overwhelming prevalence P genotype, followed by P[4] (4.7%); G9P[8] (54.9%) was most common G and P Combination, followed by G3P[8] (17.6%) and G1[8] (8.6%). The conclusion of the study was important to provide reference for introducing the RVA vaccine to prevent and control RVA-associated disease burden. J. Med. Virol. 89:71-78, 2017. © 2016 Wiley Periodicals, Inc.

Background Acute diarrhea is a global health problem, resulting in high morbidity and mortality in children. It has been suggested that enteric pathogen co-infections play an important role in gastroenteritis, but most research efforts have only focused on a small range of species belonging to a few pathogen groups. This study aimed to assess the impact of co-infections with a broad range of enteric pathogens on children aged below five years who suffer from acute diarrhea in southwest China. Method A total of 1020 subjects (850 diarrhea cases and 170 healthy controls) were selected from four sentinel hospitals in Kunming, Yunnan province, southwest China, from June 2014 to July 2015. Stool specimens were collected to detect five virus (rotavirus group A, RVA; norovirus, NoV; Sapovirus, SaV; astrovirus, As; and adenovirus, Ad), seven bacterial (diarrheagenic Escherichia coli, DEC; non-typhoidal Salmonella, NTS; Shigella spp.; Vibrio cholera; Vibrio parahaemolyticus; Aeromonas spp.; and Plesiomonas spp.), and three protozoan (Cryptosporidium spp., Giardia lamblia, and Blastocystis hominis, B. hominis) species using standard microbiologic and molecular methods. Data were analyzed using the partial least square regression technique and chi-square test. Results At least one enteric pathogen was detected in 46.7 % (n = 397) of acute gastroenteritis cases and 13.5 % (n = 23) of healthy controls (χ2 = 64.4, P

Background Acute diarrhea is one of the major public health problems worldwide. Most of studies on acute diarrhea have been made on infants aged below 5 years and few efforts have been made to identify the etiological agents of acute diarrhea in people over five, especially in China. Methods 271 diarrhea cases and 149 healthy controls over 5 years were recruited from four participating hospitals between June 2014 and July 2015. Each stool specimen was collected to detect a series of enteric pathogens, involving five viruses (Rotavirus group A, RVA; Norovirus, NoV; Sapovirus, SaV; Astrovirus, As; and Adenovirus, Ad), seven bacteria (diarrheagenic Escherichia coli, DEC; non-typhoidal Salmonella, NTS; Shigella spp.; Vibrio cholera; Vibrio parahaemolyticus; Aeromonas spp.; and Plesiomonas spp.) and three protozoa (Cryptosporidium spp., Giardia lamblia, G. lamblia, and Blastocystis hominis, B. hominis). Standard microbiological and molecular methods were applied to detect these pathogens. Data was analyzed using Chi square, Fisher-exact tests and logistic regressions. Results The prevalence of at least one enteric pathogen was detected in 29.2% (79/271) acute diarrhea cases and in 12.1% (18/149) in healthy controls (p