To investigate the early epidemic of COVID-19, a total of 176 confirmed COVID-19 cases in Shiyan city, Hubei province, China were surveyed. Our data indicated that the rate of emergence of early confirmed COVID-19 cases in Hubei province outside Wuhan was dependent on migration population, and the second-generation of patients were family clusters originating from Wuhan travelers. Epidemiological investigation indicated that the reproductive number (R 0) under containment strategies was 1.81, and asymptomatic SARS-CoV-2 carriers were contagious with a transmission rate of 10.7%. Among the 176 patients, 53 were admitted to the Renmin Hospital of Hubei University of Medicine. The clinical characteristics of these 53 patients were collected and compared based on a positive RT-PCR test and presence of pneumonia. Clinical data showed that 47.2% (25/53) of COVID-19 patients were co-infected with Mycoplasma pneumoniae, and COVID-19 patients coinfected with M. pneumoniae had a higher percentage of monocytes (P < 0.0044) and a lower neutrophils percentage (P < 0.0264). Therefore, it is important to assess the transmissibility of infected asymptomatic individuals for SARS-CoV-2 transmission; moreover, clinicians should be alert to the high incidence of co-infection with M. pneumoniae in COVID-19 patients.
BackgroundSulfadoxine–pyrimethamine (SP) is recommended for intermittent preventive treatment of malaria in Africa. However, increasing SP resistance (SPR) affects the therapeutic efficacy of the SP. As molecular markers, Pfdhfr (dihydrofolate reductase) and Pfdhps (dihydropteroate synthase) genes are widely used for SPR surveillance. This study aimed to assess the prevalence of Pfdhfr and Pfdhps genes mutations and haplotypes in Plasmodium falciparum isolates collected from Bioko Island, Equatorial Guinea (EG).MethodsIn total, 180 samples were collected in 2013–2014. The single nucleotide polymorphisms (SNPs) of the Pfdhfr and Pfdhps genes were identified with nested PCR and Sanger sequencing. The genotypes and linkage disequilibrium (LD) tests were also analysed.ResultsSequences of Pfdhfr and Pfdhps genes were obtained from 92.78% (167/180) and 87.78% (158/180) of the samples, respectively. For Pfdhfr, 97.60% (163/167), 87.43% (146/167) and 97.01% (162/167) of the samples carried N51I, C59R and S108N mutant alleles, respectively. The prevalence of the Pfdhps S436A, A437G, K540E, A581G, and A613S mutations were observed in 20.25% (32/158), 90.51% (143/158), 5.06% (8/158), 0.63% (1/158), and 3.16% (5/158) of the samples, respectively. In total, 3 unique haplotypes at the Pfdhfr locus and 8 haplotypes at the Pfdhps locus were identified. A triple mutation (CIRNI) in Pfdhfr was the most prevalent haplotype (86.83%), and a single mutant haplotype (SGKAA; 62.66%) was predominant in Pfdhps. A total of 130 isolates with 12 unique haplotypes were found in the Pfdhfr and Pfdhps combined haplotypes, 65.38% (85/130) of them carried quadruple allele combinations (CIRNI-SGKAA), whereas only one isolate (0.77%, 1/130) was found to carry the wild-type (CNCSI-SAKAA). For LD analysis, the Pfdhfr N51I was significantly associated with the Pfdhps A437G (P < 0.05).ConclusionBioko Island possesses a high prevalence of the Pfdhfr triple mutation (CIRNI) and Pfdhps single mutation (SGKAA), which will undermine the pharmaceutical effect of SP for malaria treatment strategies. To avoid an increase in SPR, continuous molecular monitoring and additional control efforts are urgently needed in Bioko Island, Equatorial Guinea.
Antimalarial drug resistance developed in has become a problem for malaria control. Evaluation of drug resistance is the first step for effective malaria control. In this study, we investigated the gene mutations of using blood samples from returned Chinese migrant workers in order to identify drug resistance-associated molecular markers. These workers returned from Africa and Southeast Asia (SEA) during 2011 to 2016. Polymorphisms in ,, and genes and the haplotype patterns of Pfcrt and Pfmdr1 were analyzed. The results showed the presence of four haplotypes of Pfcrt codons 72 to 76, including CVMNK (wild type),VMN and CV (mutation types), and CV M N K (mixed type), with 50.57%, 1.14%, 25.00%, and 23.30% prevalence, respectively. For Pfmdr1, N86 (22.28%) and Y184 (60.01%) were the main prevalent mutations (mutations are underlined). The prevalence of mutation at position 550, 561, 575, and 589 of K13-propeller were 1.09%, 0.54%, 0.54%, and 0.54%, respectively. These data suggested that Pfcrt, Pfmdr1, and K13-propeller polymorphisms are potential markers to assess drug resistance of in China, Africa, and SEA.
AIM:To explore the mechanism of action of gypenosides (GPs) on type 2 diabetes mellitus and non-alcoholic fatty liver disease (T2DM-NAFLD) in rats. METHODS:Sixty rats were randomly divided into a healthy group, an untreated disease model group and GP-treatment groups. The study involved the evaluation of biochemical parameters, including serum aspartate transaminase (AST), alanine transferase (ALT), blood glucose (BG), triglycerides (TG) and total cholesterol (TC). Additionally, the protective effect of the treatments were confirmed histopathologically and the expression of TNF-α and NF-κB in the rat liver was analyzed using immunohistochemistry. The expression of proliferatoractivated receptor gamma (PPARγ) and cytochrome P450 (CYP450) 1A1 mRNA was determined by quantitative RT-PCR. RESULTS:GP treatments at oral doses of 200, 400, and 800 mg/kg per day significantly decreased the levels of serum AST and ALT (P < 0.05, P < 0.01), especially at the dose of 800 mg/kg per day. To a similar extent, GP at 800 mg/kg per day reduced the levels of BG (4.19 ± 0.47, P < 0.01), TG (80.08 ± 10.05, P < 0.01), TC (134.38 ± 16.39, P < 0.01) and serum insulin (42.01 ± 5.04, P < 0.01). The expression of TNF-α and NF-κB measured by immunohistochemistry was significantly reduced by GPs in a dose-dependent manner, and the expression of PPARγ and CYP4501A1 mRNA, as measured using quantitative real-time PCR, were significantly down-regulated by GPs. Moreover, GPs decreased the infiltration of liver fats and reversed the histopathological changes in a dosedependent manner. CONCLUSION:This study suggests that GPs have a protective effect against T2DM-NAFLD by down-regulating the expression of TNF-α and NF-κB proteins, and PPARγ and CYP4501A1 mRNAs. Core tip: Gypenosides (GPs) are one of the most pharmacologically active components in G. pentaphyllum . Basic Study ORIGINAL ARTICLEHe Q et al . Mechanism of action of GPs on T2DM-NAFLD Intervention with GPs significantly decreased the levels of aspartate aminotransferase, alanine aminotransferase, blood glucose, insulin, triglycerides and total cholesterol in type 2 diabetes mellitus and non-alcoholic fatty liver disease (T2DM-NAFLD) model rats, down-regulated the expression of TNF-α, NF-κB, rabbit anti-proliferator activated receptory (PPARγ) and rabbit anti-cytochrome P4501A1 (CYP1A1) mRNA, decreased the infiltration of liver fats and reversed the histopathological changes in a dose-dependent manner. These findings suggest that GPs have a protective effect against T2DM-NAFLD by downregulating the expression of TNF-α and NF-κB proteins, and PPARγ and CYP4501A1 mRNAs.He Q, Li JK, Li F, Li RG, Zhan GQ, Li G, Du WX, Tan HB. Mechanism of action of gypenosides on type 2 diabetes and non-alcoholic fatty liver disease in rats.
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