Pooled data from 2352 hospitalized coronavirus disease 2019 (COVID‐19) patients with viral RNA in feces across 46 studies were analyzed and the pooled prevalence of fecal RNA was 46.8% (95% confidence interval [CI]: 0.383–0.554). The pooled analysis showed that the occurrence of total gastrointestinal (GI) symptoms was 28.5% (95% CI: 0.125–0.44) in COVID‐19 patients with fecal RNA, that of both respiratory and GI symptoms was 21.9% (95% CI: 0.09–0.346), that of only GI symptoms was 19.8% (95% CI: 0.107–0.288), and that of only respiratory symptoms was 50.5%（95% CI: 0.267–0.744). The pooled data showed no significant difference in positive fecal RNA between severe and nonsevere cases (odds ratio = 2.009, p = 0.079, 95% CI: 0.922–4.378). During hospital admission, after samples from the respiratory system tested negative for viral RNA, 55.4% (95% CI: 0.418–0.669) of the patients with positive fecal RNA had persistent shedding of fecal RNA and pooled results from the other 4 studies including 848 discharged patients with nucleic acid‐negative stool samples indicated that the occurrence of repositive stool swabs was 18.1% (95% CI: 0.028–0.335), that of repositive respiratory swabs was 22.8% (95% CI: 0.003–0.452), that of both repositive stool and respiratory swabs was 19.1% (95% CI: 0.019–0.363), and that of only repositive stool swabs was 9.6% (95% CI: 0.010–0.203). The digestive tract may be an important organ involved in COVID‐19 infection and in the excretion of the virus. Because of the potential risk of fecal–oral transmission, giving emphasis on stool swab tests can help increase the detection rate of asymptomatic carriers and reduce missed diagnoses.

Diabetic neuropathy can damage systemic nervous system, including alteration of enteric nervous system and subsequent gastrointestinal dysfunction. The effect of diabetes on enteric glia cell (EGC) is not clear. We investigated the effect of diabetes and hyperglycemia on EGC, and the role of microRNA375 in modulating EGC survival in vivo and in vitro. Streptozotocin-induced diabetic mice were intraperitoneally injected with microRNA375 inhibitor or its negative control. EGC was transfected with microRNA375 inhibitor or its mimic. Diabetes mice with gastrointestinal dysfunction showed increased apoptosis of EGC (no difference in cell numbers) and gene expression of micorRNA375 in the myenteric plexus. Hyperglycemia triggered apoptosis of EGC in vitro with decreased expression of Pdk1 and p-Akt, but increased expression of micorRNA375. MicorRNA375 mimic induced apoptosis of EGC in vitro with repressed Pdk1and p-Akt. MicorRNA375 inhibitor could both prevent hyperglycemia-induced apoptosis of EGC in vitro and diabetes-induced gastrointestinal dysfunction in vivo. Our results suggest that diabetes-induced gastrointestinal dysfunction is related to increased apoptosis of EGC in the myenteric plexus. Hyperglycemia can increase the expression of microRNA375 and damage EGC survival through PI3K/Akt pathway. MicroRNA375 specific inhibition can prevent hyperglycemia induced EGC damage and diabetes-induced gastrointestinal dysfunction.

BackgroundCommon variants of multiple genes played a crucial role in osteonecrosis of the femoral head (ONFH) onset which was proved by many previous reports. We hypothesized that polymorphisms in NOS3, ABCB1 and IL23R were related to individual differences in alcohol sensitivity and the development of alcohol-induced ONFH.MethodsIn this case-control study, we evaluated 8 SNPs in three genes in the Chinese Han population including 355 male cases and 355 healthy male controls. These SNPs were genotyped by Sequenom MassARRAY RS1000. To identify their relationship with alcohol-induced ONFH susceptibility using χ2 test and genetic model analysis.ResultsWe found an association with alcohol-induced ONFH susceptibility for 4 SNPs (rs743506, rs3918184, rs13233308 and rs6693831) in three genes after adjusted by age. The genotype “G/A” of rs743506 in NOS3 gene acts as a risk factor in genotype (P = 0.003), dominant (P = 0.048), recessive (P = 0.005) and additive model(P = 0.006); The genotype “T/C” of rs3918184 in NOS3 gene acts as a risk factor in genotype (P = 0.012) and recessive model (P = 0.009); The genotype “T/C” of rs13233308 in ABCB1 gene acts as a risk factor in genotype (P = 0.038) and additive model(P = 0.041); The genotype “T/C” of rs6693831 in IL23R gene acts as a protective factor in genotype model (P = 0.046).ConclusionsThis study provides evidence for three alcohol-induced ONFH susceptibility genes (NOS3, ABCB1 and IL23R) in Chinese males and polymorphisms of them may be associated with alcohol-induced ONFH risk.

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