The importance of fecal nucleic acid detection in patients with coronavirus disease (COVID-19): A systematic review and meta-analysis.

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.

Pilot study of the Mini Nutritional Assessment on predicting outcomes in older adults with type 2 diabetes.

AIM: To date, few studies have focused on the nutritional status of elderly hospitalized patients with diabetes. Our aims were to explore the prevalence of malnutrition among elderly diabetes patients admitted to the hospital, and to explore the relationships between malnutrition and geriatric syndromes, diabetic complications, and clinical outcomes. METHODS: A prospective, observational study including diabetes patients aged ≥65 years was carried out in a central hospital in Western China. Nutritional status was assessed using the Mini Nutritional Assessment incorporated into a comprehensive geriatric assessment. Follow up was carried out for ≤2.8 years. RESULTS: Of 302 participants, the prevalence of malnutrition, risk of malnutrition, and normal nutrition was 18.5%, 33.1% and 48.3%, respectively. In multivariate analysis, incontinence (odds ratio [OR] 3.17, 95% confidence interval [CI] 1.08-9.36), diabetic microvascular complications (OR 2.22, 95% CI 1.06-4.61) and activities of daily living (ADL) dependence (OR 11.6, 95% CI 5.10-26.5) were independently associated with malnutrition. Malnourished patients had longer hospital stays (P = 0.003) and higher mortality rates (P < 0.001) than patients either at risk of malnutrition or with a normal nutritional status. Multivariate analysis also showed that malnutrition was independently associated with an increased risk of death (OR 2.86, 95% CI 1.30-6.28). CONCLUSIONS: The present study showed a high prevalence of malnutrition among elderly diabetes patients hospitalized for geriatric care. Considering the negative impact of malnutrition on hospital stay and mortality, adequate nutritional care should be emphasized for each elderly patient with diabetes, regardless of body mass index. Geriatr Gerontol Int 2017; 17: 2485-2492.

Glial-derived neurotrophic factor reduces inflammation and improves delayed colonic transit in rat models of dextran sulfate sodium-induced colitis.

BACKGROUND: Intestinal inflammation is well known to cause gut dysmotility through the effects on the enteric nervous system. Glial-derived neurotrophic factor (GDNF) has been demonstrated to have anti-inflammatory effects and neuronal protective actions. The aim of this study was to investigate whether the GDNF could improve inflammation-induced gut dysmotility. METHODS: Recombinant adenoviral vectors encoding GDNF (Ad-GDNF) were administered intracolonically in experimental colitis induced by dextran sulfate sodium (DSS). The disease activity index (DAI) and histological score were measured. Colonic transit was measured by using phenol red and assessed with the geometric center. PGP 9.5 immunostaining was used to examine the number and distribution of enteric neurons. The expression of tumor necrosis factor-α (TNF-α), interleukin-1ß (IL-1ß), and myeloperoxidase (MPO) activity were measured by ELISA assay. The expression of Akt, caspase-3, bcl-2 and PGP 9.5 was analyzed by western blot assay. RESULTS: A significant neuronal cell loss and a significant delay in colonic transit accompanied with the neuronal loss following inflammation were observed. GDNF prevented partially the loss of enteric neurons and ameliorated significantly experimental colitis and delayed colonic transit by, at least in part, down-regulation of TNF-α and IL-1ß expression, decrease of infiltration of leukocytes, and inhibition of neuronal cell apoptosis. CONCLUSIONS: GDNF reduces inflammation and improves delayed colonic transit in DSS-induced colitis. GDNF may be a useful therapeutic agent for the treatment of gut dysmotility in patients with UC.

Curcumin ameliorates dextran sulfate sodium-induced experimental colitis by blocking STAT3 signaling pathway.

BACKGROUND AND AIMS: Although a series of studies have shown that curcumin can exert anti-inflammatory effects in colitis by inhibiting NF-κB activation, whether these anti-inflammatory effects of curcumin are also attributed to its ability to inhibiting STAT3 pathway has never been tested in experimental colitis to date. The purpose of the study was to investigate whether curcumin could exert its therapeutic effects in experimental colitis by inhibiting STAT3 pathway. MATERIALS AND METHODS: Curcumin was administered in experimental colitis induced by dextran sulfate sodium (DSS). The disease activity index (DAI) and histological score were observed. The phospho-STAT3 was assessed by western blot analysis. The DNA-binding activity of STAT3 dimers was evaluated by electrophoretic mobility shift assay (EMSA). The expression of tumor necrosis factor (TNF)-α and interleukin (IL)-1ß was measured by enzyme-linked immunosorbent assay. Myeloperoxidase (MPO) activity was determined by using MPO assay kit. RESULTS: A significant improvement was observed in DAI and histological score in mice with curcumin, and the increases in phospho-STAT3 activity, DNA-binding activity of STAT3 dimers, MPO activity, IL-1ß, and TNF-α expression in mice with DSS-induced colitis were significantly reduced following treatment with curcumin. CONCLUSION: Curcumin exerts beneficial effects in experimental colitis by the suppression of STAT3 pathway, which may therefore provide a better understanding of the mechanism of action for curcumin in treating colitis.

Effect of adenovirus-mediated PTEN gene on ulcerative colitis-associated colorectal cancer.

PURPOSE: This study investigated the expression pattern of PTEN and its effect on carcinogenesis of ulcerative colitis-associated colorectal cancer, leading to insights into the underlying molecular mechanism. METHODS: We established a mouse model of ulcerative colitis-associated colorectal cancer by treating the animals with azoxymethane (AOM) and dextran sulphate sodium (DSS), and investigated the inflammation-dysplasia-carcinoma sequence. Expression patterns of PTEN, p-Akt and Ki-67 were shown by immunohistochemistry; western blotting techniques were used to detect protein expression of PTEN, p-Akt and caspase 3; TUNEL assay was used to measure apoptosis in colon epithelial cells; and colorimetric analysis was able to determine MPO activity in colon tissues. RESULTS: During the inflammation-dysplasia-carcinoma sequence, PTEN expression gradually decreased, while p-Akt expression increased; PTEN and p-Akt levels were negatively correlated. Compared to the AOM-DSS and Ad-0 groups, Ad-PTEN mice had longer colons, fewer tumours (P < 0.01) and smaller tumour sizes (P < 0.05). After injecting Ad-PTEN, expression of p-Akt, Ki-67 and MPO activity decreased dramatically, whereas PTEN increased. The TUNEL assay showed increased apoptotic cells and caspase 3 expression in the Ad-PTEN group. CONCLUSION: PTEN plays an important role in the inflammation-dysplasia-carcinoma sequence and may be a new molecular target in preventing and treating ulcerative colitis-associated colorectal cancer.