A study on differences about the influencing factors of depressive symptoms between medical staff and residents during 2022 city-wide temporary static management period to fighting against COVID-19 pandemic in Shanghai.

Objectives: Our study aimed to identify the latent class of depressive symptoms in the Shanghai population during the city-wide temporary static management period and compare differences in the factors influencing depressive symptoms between medical staff and residents. Methods: An online cross-sectional survey was conducted with 840 participants using questionnaires, including Patient Health Questionnaire-9 (PHQ-9), Generalized Anxiety Disorder-7 (GAD-7), Pittsburgh Sleep Quality Index (PSQI), and self-compiled questionnaire (demographic characteristics and internet usage time). Latent class analysis (LCA) was performed based on participants' depressive symptoms. The latent class subgroups were compared using the chi-square test and t-test. Logistic regression was used in our study to analyze the factors influencing depressive symptoms within the medical staff group and residents group and then compare their differences. Results: Two distinct subgroups were identified based on the LCA: the group with low-depressive symptoms and the group with high-depressive symptoms. There were significant differences between the two groups (P < 0.05) on age, education level, marital status, internet usage time, identity characteristics (medical staff or residents), family income level, living style, overall quality of sleep, and anxiety levels. Furthermore, logistic regression analysis results showed that compared with the residents group, the participants in the group of medical staff with "increasing internet usage time" and the "daytime dysfunction" would have nearly two times the possibility of getting serious depressive symptoms. Conclusions: There are differences in the factors influencing depression symptoms between medical staff and residents during the 2022 city-wide temporary static management period to fighting against the COVID-19 pandemic in Shanghai. We should pay special attention to those with increasing internet usage time and daytime dysfunction in medical staff working in a special environment such as the COVID-19 pandemic.

A study on differences about the influencing factors of depressive symptoms between medical staff and residents during 2022 city-wide temporary static management period to fighting against COVID-19 pandemic in Shanghai

Objectives Our study aimed to identify the latent class of depressive symptoms in the Shanghai population during the city-wide temporary static management period and compare differences in the factors influencing depressive symptoms between medical staff and residents. Methods An online cross-sectional survey was conducted with 840 participants using questionnaires, including Patient Health Questionnaire-9 (PHQ-9), Generalized Anxiety Disorder-7 (GAD-7), Pittsburgh Sleep Quality Index (PSQI), and self-compiled questionnaire (demographic characteristics and internet usage time). Latent class analysis (LCA) was performed based on participants' depressive symptoms. The latent class subgroups were compared using the chi-square test and t-test. Logistic regression was used in our study to analyze the factors influencing depressive symptoms within the medical staff group and residents group and then compare their differences. Results Two distinct subgroups were identified based on the LCA: the group with low-depressive symptoms and the group with high-depressive symptoms. There were significant differences between the two groups (P < 0.05) on age, education level, marital status, internet usage time, identity characteristics (medical staff or residents), family income level, living style, overall quality of sleep, and anxiety levels. Furthermore, logistic regression analysis results showed that compared with the residents group, the participants in the group of medical staff with "increasing internet usage time” and the "daytime dysfunction” would have nearly two times the possibility of getting serious depressive symptoms. Conclusions There are differences in the factors influencing depression symptoms between medical staff and residents during the 2022 city-wide temporary static management period to fighting against the COVID-19 pandemic in Shanghai. We should pay special attention to those with increasing internet usage time and daytime dysfunction in medical staff working in a special environment such as the COVID-19 pandemic.

Multiple Death Pathways of Neutrophils Regulate Alveolar Macrophage Proliferation.

Alveolar macrophage (AM) proliferation and self-renewal play an important role in the lung tissue microenvironment. However, the impact of immune cells, especially the neutrophils, on AM homeostasis or function is not well characterized. In this study, we induced in vivo migration of neutrophils into bronchoalveolar lavage (BAL) fluid and lung using CXCL1, and then co-cultured these with AMs in vitro. Neutrophils in the BAL (BAL-neutrophils), rather than neutrophils of bone marrow (BM-neutrophils), were found to inhibit AM proliferation. Analysis of publicly available data showed high heterogeneity of lung neutrophils with distinct molecular signatures of BM- and blood-neutrophils. Unexpectedly, BAL-neutrophils from influenza virus PR8-infected mice (PR8-neutrophils) did not inhibit the proliferation of AMs. Bulk RNA sequencing further revealed that co-culture of AMs with PR8-neutrophils induced IFN-α and -γ responses and inflammatory response, and AMs co-cultured with BAL-neutrophils showed higher expression of metabolism- and ROS-associated genes; in addition, BAL-neutrophils from PR8-infected mice modulated AM polarization and phagocytosis. BAL-neutrophil-mediated suppression of AM proliferation was abrogated by a combination of inhibitors of different neutrophil death pathways. Collectively, our findings suggest that multiple cell death pathways of neutrophils regulate the proliferation of AMs. Targeting neutrophil death may represent a potential therapeutic strategy for improving AM homeostasis during respiratory diseases.

Blood Transcriptomes of SARS-CoV-2-Infected Kidney Transplant Recipients Associated with Immune Insufficiency Proportionate to Severity.

BACKGROUND: Among patients with COVID-19, kidney transplant recipients (KTRs) have poor outcomes compared with non-KTRs. To provide insight into management of immunosuppression during acute illness, we studied immune signatures from the peripheral blood during and after COVID-19 infection from a multicenter KTR cohort. METHODS: We ascertained clinical data by chart review. A single sample of blood was collected for transcriptome analysis. Total RNA was poly-A selected and RNA was sequenced to evaluate transcriptome changes. We also measured cytokines and chemokines of serum samples collected during acute infection. RESULTS: A total of 64 patients with COVID-19 in KTRs were enrolled, including 31 with acute COVID-19 (<4 weeks from diagnosis) and 33 with post-acute COVID-19 (>4 weeks postdiagnosis). In the blood transcriptome of acute cases, we identified genes in positive or negative association with COVID-19 severity scores. Functional enrichment analyses showed upregulation of neutrophil and innate immune pathways but downregulation of T cell and adaptive immune activation pathways. This finding was independent of lymphocyte count, despite reduced immunosuppressant use in most KTRs. Compared with acute cases, post-acute cases showed "normalization" of these enriched pathways after 4 weeks, suggesting recovery of adaptive immune system activation despite reinstitution of immunosuppression. Analysis of the non-KTR cohort with COVID-19 showed significant overlap with KTRs in these functions. Serum inflammatory cytokines followed an opposite trend (i.e., increased with disease severity), indicating that blood lymphocytes are not the primary source. CONCLUSIONS: The blood transcriptome of KTRs affected by COVID-19 shows decreases in T cell and adaptive immune activation pathways during acute disease that, despite reduced immunosuppressant use, associate with severity. These pathways show recovery after acute illness.

Molecular Analysis of the Kidney From a Patient With COVID-19-Associated Collapsing Glomerulopathy.

Recent case reports suggest that coronavirus disease 2019 (COVID-19) is associated with collapsing glomerulopathy in African Americans with apolipoprotein L1 gene (APOL1) risk alleles; however, it is unclear whether disease pathogenesis is similar to HIV-associated nephropathy. RNA sequencing analysis of a kidney biopsy specimen from a patient with COVID-19-associated collapsing glomerulopathy and APOL1 risk alleles (G1/G1) revealed similar levels of APOL1 and angiotensin-converting enzyme 2 (ACE2) messenger RNA transcripts as compared with 12 control kidney samples downloaded from the GTEx (Genotype-Tissue Expression) Portal. Whole-genome sequencing of the COVID-19-associated collapsing glomerulopathy kidney sample identified 4 indel gene variants, 3 of which are of unknown significance with respect to chronic kidney disease and/or focal segmental glomerulosclerosis. Molecular profiling of the kidney demonstrated activation of COVID-19-associated cell injury pathways such as inflammation and coagulation. Evidence for direct severe acute respiratory syndrome coronavirus 2 infection of kidney cells was lacking, which is consistent with the findings of several recent studies. Interestingly, immunostaining of kidney biopsy sections revealed increased expression of phospho-STAT3 (signal transducer and activator of transcription 3) in both COVID-19-associated collapsing glomerulopathy and HIV-associated nephropathy as compared with control kidney tissue. Importantly, interleukin 6-induced activation of STAT3 may be a targetable mechanism driving COVID-19-associated acute kidney injury.

Reversed-engineered human alveolar lung-on-a-chip model.

Here, we present a physiologically relevant model of the human pulmonary alveoli. This alveolar lung-on-a-chip platform is composed of a three-dimensional porous hydrogel made of gelatin methacryloyl with an inverse opal structure, bonded to a compartmentalized polydimethylsiloxane chip. The inverse opal hydrogel structure features well-defined, interconnected pores with high similarity to human alveolar sacs. By populating the sacs with primary human alveolar epithelial cells, functional epithelial monolayers are readily formed. Cyclic strain is integrated into the device to allow biomimetic breathing events of the alveolar lung, which, in addition, makes it possible to investigate pathological effects such as those incurred by cigarette smoking and severe acute respiratory syndrome coronavirus 2 pseudoviral infection. Our study demonstrates a unique method for reconstitution of the functional human pulmonary alveoli in vitro, which is anticipated to pave the way for investigating relevant physiological and pathological events in the human distal lung.