ObjectiveNonalcoholic Wernicke’s encephalopathy (WE) is a devastating neuropsychiatric syndrome caused by thiamine deficiency. Although many case reports on WE have been published, more studies are required to guide the diagnosis and treatment of nonalcoholic WE.MethodsWe retrospectively studied patients who were diagnosed with WE in our hospital. Data on demographics, possible causes, phenomenology, and diagnostic and treatment delays were abstracted from medical records by chart reviews.ResultsSeventeen patients were diagnosed with nonalcoholic WE. Nonalcoholic WE had many causes, such as gastrointestinal surgery, gastrointestinal tract diseases, vomiting, and psychiatric diseases. Most patients presented with abnormal mental symptoms, including those in a coma.ConclusionIn summary, we recommend using operational criteria to diagnose and treat nonalcoholic WE as early as possible to avoid misdiagnosis and treatment delays. Nonalcoholic WE remains a clinical diagnosis, and certain examinations are helpful for this diagnosis, such as measuring serum thiamine concentrations. We should focus on patients who present with abnormal mental symptoms, even those in a coma, and administer parenteral thiamine before any carbohydrate to reduce the high frequency of residual morbidity.

PDT with FOB offers the advantages of a high rate of first-time success, a low complication rate and short-procedure duration. Thus, FOB-PDT is a better option in critically ill patients.

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This systematic review and meta-analysis was performed to evaluate the efficacy of using a helmet for oxygen therapy in critically ill patients with respiratory failure. Methods: The Cochrane Library, Embase, and PubMed databases were searched for all randomized controlled trials (RCTs) examining the efficacy of a helmet versus standard oxygen therapy or a mask in critically ill patients with respiratory failure. The quality of all included studies was evaluated by the method recommended by The Cochrane Collaboration. The systematic review and meta-analysis was conducted using Review Manager software, version 5.3 (Nordic Cochrane Centre, The Cochrane Collaboration, Copenhagen, Denmark). Results: Ten RCTs involving 708 patients were included in the present meta-analysis. The results of the meta-analysis showed that the oxygenation index, partial pressure of carbon dioxide, and complications were not significantly different between the helmet group and the standard oxygen therapy or mask group. The incidence of intubation and the mortality rate were significantly lower in the helmet group than in the standard oxygen therapy or mask group. Conclusion: Delivering oxygen via a helmet can decrease the incidence of required intubation and improve the mortality rate, resulting in beneficial outcomes in critically ill patients with respiratory failure.

Intestinal barrier dysfunction often occurs in various acute or chronic pathological conditions and has been identified as an important clinical problem. Herein, we explored the biological role and molecular mechanism of Polo‐like kinase 1 (PLK1) and differentiation antagonizing non‐protein coding RNA (DANCR) in intestinal barrier dysfunction caused by sepsis. RT‐qPCR analysis was used to examine PLK1, miR‐1306‐5p, and DANCR expression in NCM460 cells after LPS treatment. TUNEL assay and Western blot analysis were performed to explore PLK1 function in cell apoptosis and intestinal barrier in vitro. Hematoxylin and eosin staining, Western blot analysis, and TUNEL assay were used to investigate DANCR function in the intestinal barrier and cell apoptosis in vivo. The interaction between miR‐1306‐5p and PLK1 (or DANCR) was validated by luciferase reporter assay. As a result, PLK1 overexpression decreased cell apoptosis and promoted intestinal barrier function. Moreover, DANCR was validated as a sponge of miR‐1306‐5p to target PLK1. In addition, we found that DANCR overexpression decreased intestinal mucosal permeability and colon mucosa epithelial cell apoptosis in vivo. Conclusively, DANCR improved intestinal barrier dysfunction and alleviated epithelial injury by targeting the miR‐1306‐5p/PLK1 axis in sepsis.