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ObjectiveReceptor for advanced glycation end products (AGEs; RAGE) binds to both AGEs and amyloid-beta peptides. RAGE is involved in chronic complications of type 2 diabetes and Alzheimer’s disease. We aimed to investigate the roles of RAGE, AGEs and the Gly82Ser polymorphism of RAGE in mild cognitive impairment (MCI) among type 2 diabetes patients.MethodsOf the 167 hospitalized type 2 diabetes patients recruited, 82 satisfied the diagnostic criteria for MCI, and 85 matched control individuals were classified as non-MCI. Demographic data were collected, and the soluble RAGE (sRAGE) concentrations, serum AGE-peptide (AGE-P) levels, RAGE Gly82Ser genotype and neuropsychological test results were examined.ResultsThe MCI group exhibited a decreased sRAGE level (0.87±0.35 vs. 1.05±0.52 ng/ml, p<0.01) and an increased serum AGE-P level (3.54±1.27 vs. 2.71±1.18 U/ml, p<0.01) compared with the control group. Logistic regression analysis indicated that each unit reduction in the sRAGE concentration increased the MCI risk by 54% (OR 0.46[95% CI 0.22–0.96], p = 0.04) and that each unit increase in the AGE-P level increased the MCI risk by 72% in the type 2 diabetes patients (OR 1.72[95% CI 1.31–2.28], p<0.01). The serum sRAGE level was negatively correlated with the score on the trail making test-B (TMT-B) (r = -0.344, p = 0.002), which indicates early cognitive deficits related to diabetes. Moreover, the AGE-P level was positively correlated with multiple cognitive domains (all p<0.05). No significant differences in the neuropsychological test results or serum RAGE concentrations between the different RAGE genotypes or in the RAGE genotype frequencies between the MCI and control groups were identified (all p>0.05).ConclusionsThe RAGE pathway partially mediates AGE-induced MCI in diabetic patients. The serum AGE-P level may serve as a serum biomarker of MCI in these individuals, and sRAGE represents a predictor and even a potential intervention target of early cognitive decline in type 2 diabetes patients.Trial registrationAdvanced Glycation End Products Induced Cognitive Impairment in Diabetes: BDNF Signal Meditated Hippocampal Neurogenesis ChiCTR-OCC-15006060

Coronavirus disease 2019 (COVID-19) is a predominantly respiratory infectious disease caused by novel coronavirus infection (SARS-CoV-2), respiratory failure is the main clinical manifestation and the leading cause of death. Even though it can meet the acute respiratory distress syndrome (ARDS) Berlin definition, only some clinical features of COVID-19 are consistent with typical ARDS, and which has its own peculiar phenotypes. When compared with typical ARDS, in addition to the typical diffuse alveolar injury, COVID-19 has unique pathological and pathophysiological features, such as endothelial injury, extensive microthrombus, and pulmonary capillary hyperplasia. The clinical features of patients with respiratory failure caused by COVID-19 are heterogeneous and can be generally divided into two phenotypes: progressive respiratory distress and unique “silent hypoxemia”. The “H-type” characteristics of reduced lung volume, decreased lung compliance, and unmatched ventilator-perfusion ratio. While some patients may have close to normal lung compliance, that is “L-type”. Identifying the exact phenotype in whom are suffered with COVID-19 is crucial to guide clinicians to adopt appropriate treatment strategies. This review discussed the similarities and differences in the pathogenesis, pathophysiology, clinical features and treatment strategies of COVID-19 induced acute respiratory failure and typical ARDS.

This study aims to explore the predictive noninvasive biomarker for obstructive coronary artery disease (CAD). By using the data set GSE90074, weighted gene co‐expression network analysis (WGCNA), and protein–protein interactive network, construction of differentially expressed genes in peripheral blood mononuclear cells was conducted to identify the most significant gene clusters associated with obstructive CAD. Univariate and multivariate stepwise logistic regression analyses and receiver operating characteristic analysis were used to predicate the diagnostic accuracy of biomarker candidates in the detection of obstructive CAD. Furthermore, functional prediction of candidate gene biomarkers was further confirmed in ST‐segment elevation myocardial infarction (STEMI) patients or stable CAD patients by using the datasets of GSE62646 and GSE59867. We found that the blue module discriminated by WGCNA contained 13 hub‐genes that could be independent risk factors for obstructive CAD (P < .05). Among these 13 hub‐genes, a four‐gene signature including neutrophil cytosol factor 2 (NCF2, P = .025), myosin‐If (MYO1F, P = .001), sphingosine‐1‐phosphate receptor 4 (S1PR4, P = .015), and ficolin‐1 (FCN1, P = .012) alone or combined with two risk factors (male sex and hyperlipidemia) may represent potential diagnostic biomarkers in obstructive CAD. Furthermore, the messenger RNA levels of NCF2, MYO1F, S1PR4, and FCN1 were higher in STEMI patients than that in stable CAD patients, although S1PR4 showed no statistical difference (P > .05). This four‐gene signature could also act as a prognostic biomarker to discriminate STEMI patients from stable CAD patients. These findings suggest a four‐gene signature (NCF2, MYO1F, S1PR4, and FCN1) alone or combined with two risk factors (male sex and hyperlipidemia) as a promising prognostic biomarker in the diagnosis of STEMI. Well‐designed cohort studies should be implemented to warrant the diagnostic value of these genes in clinical purpose.

Here, we aimed to retrospectively analyze the clinical characteristics of 27 patients with severe pneumonia caused by Chlamydia psittaci between January 2019 and April 2021 in southwest China. To this end, we collected data on the exposure history, clinical symptoms, laboratory examination, imaging characteristics, evolution, etiology, treatment, and outcomes to suggest a better diagnosis and prevention system. Our results showed that a metagenomic next-generation sequencing test could provide early diagnosis. All patients were sensitive to quinolones and tetracyclines, and the recovery rate was relatively high. Overall, all patients were in critical condition with moderate to severe acute respiratory distress syndrome and shock. In conclusion, early diagnosis of pneumonia caused by C. psittaci depends on effective molecular testing, and most patients recover after treatment.