PurposeNight shift is associated with adverse physical and psychological health outcomes such as poor sleep quality and depressive symptoms. We aimed to compare sleep quality as well as depressive symptoms in nurses working night shifts to those working day shifts only and explore the association between sleep quality and depressive symptoms among nurses.Patients and methodsEight hundred sixty-five nurses were enrolled in the current study. Sleep quality and depressive symptoms among nurses were evaluated by the Pittsburgh Sleep Quality Index (PSQI) and Hospital Anxiety and Depressive Disorders Rating Scale (HADS), respectively.ResultsPSQI and HADS scores were both significantly higher in the nurses working night shifts (P<0.05) than in those working day shifts only. Besides, there was a positive correlation between PSQI and HADS scores. Binary logistic regression showed that night shift and poor sleep quality were independent risk factors of depressive symptoms among nurses.ConclusionHigher rates of depression among Chinese nurses working night shifts may be associated with poor sleep quality induced by night shift.

BackgroundBaicalin has been reported to have anti-fibrosis effect; however, its mechanism still remains to be elucidated. Adenosine A2a receptor (A2aR) is a novel inflammation regulator, and transforming growth factor-β1 (TGF-β1)-induced extracellular signal regulated kinase1/2 (ERK1/2) signaling pathway plays an important role in idiopathic pulmonary fibrosis (IPF). This study was to explore the relationship of A2aR and TGF-β1-induced ERK1/2 in bleomycin (BLM)-induced pulmonary fibrosis in mice, and to investigate whether A2aR mediate the anti-fibrosis effect of Baicalin on BLM-induced pulmonary fibrosis.MethodsThe A2aR−/− and A2aR+/+ mice were respectively divided into three groups: control group, model group, baicalin group. Pulmonary fibrosis was induced in mice of model groups by intratracheal instillation of bleomycin, and baicalin was administered in mice of baicalin groups daily for 28 days. Histopathological and ultrastructural changes of lung tissues were evaluated. Lung coefficient and the levels of hydroxyproline (HYP) in lung tissues were measured at the same time. The levels of serum TGF-β1 were measured by ELISA. The expression of TGF-β1, ERK1/2, p-ERK1/2 and A2aR were detected by western blot and immunohistochemical staining techniques.ResultsSevere lung fibrosis was observed in the bleomycin-treated mice on day 28. The histopathological findings and collagen content of lung tissues were much severer/higher in A2aR−/− mice than in A2aR+/+ mice. We also showed that TGF-β1 and p-ERK1/2 were upregulated in bleomycin-treated mice and expressed higher in A2aR−/− mice compared to A2aR+/+ mice. Besides, bleomycin-treated A2aR+/+ mice had increased A2aR level in lungs. However, long-term treatment with baicalin in A2aR−/− and A2aR+/+ mice significantly ameliorated the histopathological changes in lungs. Moreover, Increased TGF-β1 and p-ERK1/2 expressions in bleomycin-treated A2aR−/− and A2aR+/+ mice were obviously diminished by baicalin. The baicalin-treated A2aR−/− mice had severer lung fibrosis and higher expressions of TGF-β1 and p-ERK1/2 than A2aR+/+ mice. Baicalin has also upregulated the expression of A2aR in A2aR+/+ mice.ConclusionsGenetic inactivation of A2aR exacerbated the pathological processes of bleomycin-induced pulmonary fibrosis. Together, baicalin could inhibit BLM-induced pulmonary fibrosis by upregulating A2aR, suggesting A2aR as a therapeutic target of baicalin for the treatment of pulmonary fibrosis.

BackgroundCryptococcus neoformans infection usually presents as chronic meningitis and is increasingly being recognized in immunocompromised patients. Presentation with pleural effusion is rare in cryptococcal disease; in fact, only 4 cases of pleural effusion as the initial clinical presentation in cryptococcosis have been reported in English-language literature to date. We report the first case of pleural effusion as the initial clinical presentation in a renal transplant recipient who was initially misdiagnosed with tuberculous pleuritis but who then developed fungaemia and disseminated cryptococcosis. The examination of this rare manifestation and the accompanying literature review will contribute to increased recognition of the disease and a reduction in misdiagnoses.Case presentationWe describe a 63-year-old male renal transplant recipient on an immunosuppressive regimen who was admitted for left pleural effusion and fever. Cytological examinations and pleural fluid culture were nonspecific and negative. Thoracoscopy only found chronic, nonspecific inflammation with fibrosis in the pleura. After empirical anti-tuberculous therapy, the patient developed an elevated temperature, a severe headache and vomiting and fainted in the ward. Cryptococci were specifically found in the cerebrospinal fluid following lumbar puncture. Blood cultures were twice positive for C. neoformans one week later. He was transferred to the respiratory intensive care unit (RICU) immediately and was placed on non-invasive ventilation for respiratory failure for 2 days. He developed meningoencephalitis and fungaemia with C. neoformans during hospitalization. He was given amphotericin B liposome combined with 5-flucytosine and voriconazole for first 11 days, then amphotericin B liposome combined with 5-flucytosine sustained to 8 weeks, after that changed to fluconazole for maintenance. His condition improved after antifungal treatment, non-invasive ventilation and other support. Further pathological consultation and periodic acid-Schiff staining revealed Cryptococcus organisms in pleural sections, providing reliable evidence for cryptococcal pleuritis.ConclusionPleural effusion is an unusual manifestation of cryptococcosis. Cryptococcal infection must be considered in the case of patients on immunosuppressives, especially solid-organ transplant recipients, who present with pleural effusion, even if pleural fluid culture is negative. Close communication between the pathologist and the clinician, multiple special biopsy section stains and careful review are important and may contribute to decreasing misdiagnosis.

Familial cold autoinflammatory syndrome (FCAS) is an extremely rare autosomal dominant inherited disease. Although there are four genes that have been linked with FCAS, its molecular diagnosis has been challenging in a relatively large proportion of cases. In this study, we aimed to investigate the genetic defect of a recruited FCAS family using exome sequencing followed by in-depth bioinformatics analysis. As a result, a novel heterozygous stop-gain mutation (Trp408X) in NLRP12 was identified in autosomal dominant inherited FCAS with clinical features of recurrent fever and skin urticaria due to cold conditions. When combined with previous studies, all of the reported mutations were found to have occurred in a highly conserved region in the NACHT domain coding sequence in NLRP12 exon 3, suggesting that a screening strategy for FCAS should focus on this area of the gene. In conclusion, this study demonstrates the importance of exome sequencing for clinical diagnosis of genetic disorders and provides molecular insight into FCAS treatment and diagnosis.

<b><i>Introduction:</i></b> Several studies have examined the crucial role of inflammatory indexes such as the ratio of monocyte and lymphocyte (MLR), systemic-immune-inflammation-index, and the ratio of neutrophil and lymphocyte (NLR) in stroke-associated pneumonia (SAP). However, the function of the systemic inflammation response index (SIRI) in SAP is not known. This study investigated whether SIRI at admission could predict the incidence of SAP in patients with acute ischemic stroke (AIS). <b><i>Patients and Methods:</i></b> 2,802 AIS patients collected from 2013 to 2021 were divided into the SAP and non-SAP groups. The predictive performance of SIRI in SAP was evaluated by the receiver operating characteristic curve. Multivariate regression analysis and the restricted cubic spline (RCS) were performed to explore the relationship between SIRI and SAP risk. <b><i>Results:</i></b> The SIRI at admission in SAP patients was significantly higher than that in non-SAP patients (median [IQR]: 3.75 [2.05, 6.99] vs. 1.51 [0.94, 2.62], <i>p</i> &#x3c; 0.001). SIRI had a predictive ability for predicting the incidence of SAP with area under the curve of 0.757, better than NLR and MLR (both <i>p</i> &#x3c; 0.05). SIRI ≥2.74 was an independent risk factor for the incidence of SAP (odds ratio: 5.82, 95% confidence interval: 4.54, 7.49, <i>p</i> &#x3c; 0.001). The RCS model showed an increasing trend of the SAP risk with the increase of SIRI. <b><i>Conclusion:</i></b> SIRI showed a good predictive value for SAP. In clinical practice, AIS patients with high SIRI levels (SIRI ≥2.74) should be aware of the risk of SAP.