The mediating role of sleep quality in the relationship between dispositional mindfulness and fatigue in Chinese nurses during the COVID-19 pandemic.

BACKGROUND: During the COVID-19 epidemic in China, clinical nurses are at an elevated risk of suffering fatigue. This research sought to investigate the correlation between dispositional mindfulness and fatigue among nurses, as well as the potential mediation role of sleep quality in this relationship. METHODS: This online cross-sectional survey was performed from August to September 2022 to collect data from 2143 Chinese nurses after the re-emergence of COVID-19. The significance of the mediation effect was determined through a bootstrap approach with SPSS PROCESS macro. RESULTS: Higher levels of dispositional mindfulness were significantly negatively related to fatigue (r = -0.518, P < 0.001) and sleep disturbance (r = -0.344, P < 0.001). Besides, insufficient sleep was associated with fatigue (r = 0.547, P < 0.001). Analyses of mediation revealed that sleep quality mediated the correlation of dispositional mindfulness to fatigue (ß = -0.137, 95% Confidence Interval = [-0.156, -0.120]). CONCLUSIONS: In the post-COVID-19 pandemic era, Chinese nurses' dispositional awareness was related to the reduction of fatigue, which was mediated by sleep quality. Intervention strategies and measures should be adapted to improve dispositional mindfulness and sleep quality to reduce fatigue in nurses during the pandemic.

Predictive Ability of Systemic Inflammation Response Index for the Risk of Pneumonia in Patients with Acute Ischemic Stroke.

INTRODUCTION: 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). PATIENTS AND METHODS: 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. RESULTS: 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], p < 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 p < 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, p < 0.001). The RCS model showed an increasing trend of the SAP risk with the increase of SIRI. CONCLUSION: 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.

Geriatric Nutritional Risk Index is related to the risk of stroke-associated pneumonia.

BACKGROUND: Stroke-associated pneumonia (SAP) occurs frequently after a stroke. Geriatric Nutritional Risk Index (GNRI) is a valuable indicator of elderly individuals' nutritional status. This research was designed to obtain insight into the link between GNRI and SAP. METHODS: Patients with acute ischemic stroke (AIS) were categorized into the SAP and non-SAP groups. GNRI scores were divided into four layers: Q1, GNRI < 82; Q2, 82≤ GNRI < 92; Q3, 92≤ GNRI ≤98; Q4, GNRI > 98. To identify the independent risk and protective factors of developing SAP, logistic regression analyses were conducted. Additionally, we utilized the restricted cubic spline (RCS) analysis to test the effect of GNRI on the SAP risk. RESULTS: The SAP group showed lower GNRI scores than the non-SAP group (96.88 ± 9.36 vs. 100.88 ± 8.25, p  <  0.001). According to the logistic regression model, the Q1 and Q2 layers showed a higher risk of SAP than the Q3 layer, while the Q4 layer showed a lower SAP risk (all p < 0.05). Besides, the RCS model found that the risk of SAP dropped dramatically as GNRI scores increased, which got stable when the GNRI score was more significant than 100. CONCLUSION: Lower GNRI scores were linked to a higher prevalence of SAP. In clinical practice, GNRI showed predictive value for SAP, which could be helpful in early SAP intervention and therapy.

Lactic Dehydrogenase to Albumin Ratio Is Associated With the Risk of Stroke-Associated Pneumonia in Patients With Acute Ischemic Stroke.

Background: Stroke-associated pneumonia (SAP) is one of the common complications of stroke patients. Higher lactic dehydrogenase (LDH) and lower albumin levels were associated with SAP, but the contribution of the LDH to albumin ratio (LAR) to the risk of SAP in acute ischemic stroke (AIS) patients remained unclear. Methods: A total of 3173 AIS patients were included in this study, divided into SAP (n = 417) and non-SAP groups (n = 2756). Characteristics were compared between these two groups. The receiver operating characteristic curves (ROC) were used to evaluate the discrimination ability of the LAR, LDH, and albumin levels in predicting SAP. Logistic regression analysis was furtherly adopted to estimate the association between LAR and SAP. We also used the restricted cubic spline (RCS) to clarify the relationship between LAR and the risk of SAP. Results: LAR in the SAP group was significantly higher than that of the non-SAP group (8.75 ± 4.58 vs. 6.10 ± 2.55, P < 0.001). According to the results of ROC, LAR had the highest prognostic accuracy compared to LDH and albumin (P < 0.05). Besides, the logistic regression model showed that higher LAR (LAR > 6.75) were more vulnerable to SAP (OR, 2.80; 95% CI, 2.18-3.59, P < 0.001), controlling the confounders. The RCS model showed that there was a non-linear relationship between LAR and the risk of SAP. Conclusion: High LAR was associated with an increased risk of SAP in patients with AIS. LAR may be a potential predictor for the incidence of SAP. Appropriate prevention measures were needed in patients with high LAR (LAR > 6.75).

The effect of night shift on sleep quality and depressive symptoms among Chinese nurses.

PURPOSE: Night 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 METHODS: Eight 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. RESULTS: PSQI 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. CONCLUSION: Higher rates of depression among Chinese nurses working night shifts may be associated with poor sleep quality induced by night shift.

Asiatic acid prevents the development of interstitial lung disease in a hypochlorous acid-induced mouse model of scleroderma.

Interstitial lung disease is the most common complication of systemic sclerosis (SSc) and is associated with a high rate of mortality. Due to the complex pathogenesis of SSc, the therapies currently available remain limited. In the present study, the effect of asiatic acid (AA) on SSc-associated pulmonary fibrosis (PF) and its association with the transforming growth factor-ß1 (TGF-ß1)/Smad2/3 signaling pathway were evaluated. A hypochlorous acid (HOCl)-induced model of SSc was used to evaluate the therapeutic effect of AA on PF in SSc, where AA was administered to SSc mice by gavage. PF was alleviated in the AA-treated SSc mice groups when examined under light microscopy. In addition, there was a decrease in histopathological progression and collagen in the lungs. AA significantly reduced expression of type I collagen in the lungs of mice with SSc. It also significantly suppressed α-smooth muscle actin expression, which attenuated the conversion of fibroblasts into muscle fibroblasts. These AA-associated antifibrosis and anti-immune effects were mediated through the significant downregulation of advanced oxidation protein product, E-selectin, and anti-DNA topoisomerase-1 autoantibody levels in the serum. Furthermore, the expression levels of TGF-ß1 and the phosphorylated-Smad2/3/Smad2/3 ratios in AA-treated SSc mice were similar to the control. The presence of pulmonary inflammation and fibrosis was confirmed in the HOCl-induced SSc mice and the results demonstrated that selective inhibition of reactive oxygen species prevented PF. By focusing on the classical TGF-ß1/Smad2/3 signaling pathway, a mechanism of action of AA was identified to be associated with the inhibition of Smad2/3 activation through negative regulation of Smad2/3 phosphorylation.

Baicalin attenuates bleomycin-induced pulmonary fibrosis via adenosine A2a receptor related TGF-ß1-induced ERK1/2 signaling pathway.

BACKGROUND: Baicalin 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-ß1 (TGF-ß1)-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-ß1-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. METHODS: The 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-ß1 were measured by ELISA. The expression of TGF-ß1, ERK1/2, p-ERK1/2 and A2aR were detected by western blot and immunohistochemical staining techniques. RESULTS: Severe 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-ß1 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-ß1 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-ß1 and p-ERK1/2 than A2aR+/+ mice. Baicalin has also upregulated the expression of A2aR in A2aR+/+ mice. CONCLUSIONS: Genetic 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.

Identification of a Novel NLRP12 Nonsense Mutation (Trp408X) in the Extremely Rare Disease FCAS by Exome Sequencing.

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.

Pleural effusion as the initial clinical presentation in disseminated cryptococcosis and fungaemia: an unusual manifestation and a literature review.

BACKGROUND: Cryptococcus 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 PRESENTATION: We 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. CONCLUSION: Pleural 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.

Anti-Inflammatory Effects of Monoammonium Glycyrrhizinate on Lipopolysaccharide-Induced Acute Lung Injury in Mice through Regulating Nuclear Factor-Kappa B Signaling Pathway.

The present study aimed to investigate the therapeutic effect of monoammonium glycyrrhizinate (MAG) on lipopolysaccharide- (LPS-) induced acute lung injury (ALI) in mice and possible mechanism. Acute lung injury was induced in BALB/c mice by intratracheal instillation of LPS, and MAG was injected intraperitoneally 1 h prior to LPS administration. After ALI, the histopathology of lungs, lung wet/dry weight ratio, protein concentration, and inflammatory cells in the bronchoalveolar lavage fluid (BALF) were determined. The levels of tumor necrosis factor-α (TNF-α) and interleukin-1ß (IL-1ß) in the BALF were measured by ELISA. The activation of NF-κB p65 and IκB-α of lung homogenate was detected by Western blot. Pretreatment with MAG attenuated lung histopathological damage induced by LPS and decreased lung wet/dry weight ratio and the concentrations of protein in BALF. At the same time, MAG reduced the number of inflammatory cells in lung and inhibited the production of TNF-α and IL-1ß in BALF. Furthermore, we demonstrated that MAG suppressed activation of NF-κB signaling pathway induced by LPS in lung. The results suggested that the therapeutic mechanism of MAG on ALI may be attributed to the inhibition of NF-κB signaling pathway. Monoammonium glycyrrhizinate may be a potential therapeutic reagent for ALI.