Background:Throughout China, during the recent epidemic in Hubei province, frontline medical staff have been responsible for tracing contacts of patients infected with coronavirus disease 2019 . This study aimed to investigate the psychological impact and coping strategies of frontline medical staff in Hunan province, adjacent to Hubei province, during the COVID-19 outbreak between January and March 2020. Material/Methods:A cross-sectional observational study included doctors, nurses, and other hospital staff throughout Hunan province between January and March 2020. The study questionnaire included five sections and 67 questions (scores, 0 -3). The chi-squared χ² test was used to compare the responses between professional groups, age-groups, and gender. Results:Study questionnaires were completed by 534 frontline medical staff. The responses showed that they believed they had a social and professional obligation to continue working long hours. Medical staff were anxious regarding their safety and the safety of their families and reported psychological effects from reports of mortality from COVID-19 infection. The availability of strict infection control guidelines, specialized equipment, recognition of their efforts by hospital management and the government, and reduction in reported cases of COVID-19 provided psychological benefit. Conclusions:The COVID-19 outbreak in Hubei resulted in increased stress for medical staff in adjacent Hunan province. Continued acknowledgment of the medical staff by hospital management and the government, provision of infection control guidelines, specialized equipment and facilities for the management of COVID-19 infection should be recognized as factors that may encourage medical staff to work during future epidemics.

Successful engraftment of organ transplants has traditionally relied on preventing the activation of recipient (host) T cells. Once T-cell activation has occurred, however, stalling the rejection process becomes increasingly difficult, leading to graft failure. Here we demonstrate that graft-infiltrating, recipient (host) dendritic cells (DCs) play a key role in driving the rejection of transplanted organs by activated (effector) T cells. We show that donor DCs that accompany heart or kidney grafts are rapidly replaced by recipient DCs. The DCs originate from non-classical monocytes and form stable, cognate interactions with effector T cells in the graft. Eliminating recipient DCs reduces the proliferation and survival of graft-infiltrating T cells and abrogates ongoing rejection or rejection mediated by transferred effector T cells. Therefore, host DCs that infiltrate transplanted organs sustain the alloimmune response after T-cell activation has already occurred. Targeting these cells provides a means for preventing or treating rejection.

In mid-December 2019, a novel atypical pneumonia broke out in Wuhan, Hubei Province, China and was caused by a newly identified coronavirus, initially termed 2019 Novel Coronavirus and subsequently severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). As of 19 May 2020, a total of 4,731,458 individuals were reported as infected with SARS-CoV-2 among 213 countries, areas or territories with recorded cases, and the overall case-fatality rate was 6.6% (316,169 deaths among 4,731,458 recorded cases), according to the World Health Organization. Studies have shown that SARS-CoV-2 is notably similar to (severe acute respiratory syndrome coronavirus) SARS-CoV that emerged in 2002–2003 and Middle East respiratory syndrome coronavirus (MERS-CoV) that spread during 2012, and these viruses all contributed to global pandemics. The ability of SARS-CoV-2 to rapidly spread a pneumonia-like disease from Hubei Province, China, throughout the world has provoked widespread concern. The main symptoms of coronavirus disease 2019 (COVID-19) include fever, cough, myalgia, fatigue and lower respiratory signs. At present, nucleic acid tests are widely recommended as the optimal method for detecting SARS-CoV-2. However, obstacles remain, including the global shortage of testing kits and the presentation of false negatives. Experts suggest that almost everyone in China is susceptible to SARS-CoV-2 infection, and to date, there are no effective treatments. In light of the references published, this review demonstrates the biological features, spread, diagnosis and treatment of SARS-CoV-2 as a whole and aims to analyse the similarities and differences among SARS-CoV-2, SARS-CoV and MERS-CoV to provide new ideas and suggestions for prevention, diagnosis and clinical treatment.

Although fibrosis is a common pathological feature of most end-stage organ diseases, its pathogenesis remains unclear. There is growing evidence that mitochondrial dysfunction contributes to the development and progression of fibrosis. The heart, liver, kidney and lung are highly oxygen-consuming organs that are sensitive to mitochondrial dysfunction. Moreover, the fibrotic process of skin and islet is closely related to mitochondrial dysfunction as well. This review summarized emerging mechanisms related to mitochondrial dysfunction in different fibrotic organs and tissues above. First, it highlighted the important elucidation of mitochondria morphological changes, mitochondrial membrane potential and structural damage, mitochondrial DNA (mtDNA) damage and reactive oxidative species (ROS) production, etc. Second, it introduced the abnormality of mitophagy and mitochondrial transfer also contributed to the fibrotic process. Therefore, with gaining the increasing knowledge of mitochondrial structure, function, and origin, we could kindle a new era for the diagnostic and therapeutic strategies of many fibrotic diseases based on mitochondrial dysfunction. Facts • Fibrosis is the major pathophysiologic basis and ultimate pathway for most parenchymatous organ injury. How to prevent or slow down fibrosis through targeting mitochondria?

Probiotics are commensal or nonpathogenic microbes that confer beneficial effects on the host through several mechanisms such as competitive exclusion, antibacterial effects, and modulation of immune responses. Some probiotics have been found to regulate immune responses via immune regulatory mechanisms. T regulatory (Treg) cells, T helper cell balances, dendritic cells, macrophages, B cells, and natural killer (NK) cells can be considered as the most determinant dysregulated mediators in immunomodulatory status. Recently, fecal microbiota transplantation (FMT) has been defined as the transfer of distal gut microbial communities from a healthy individual to a patient’s intestinal tract to cure some immune disorders (mainly inflammatory bowel diseases). The aim of this review was followed through the recent literature survey on immunomodulatory effects and mechanisms of probiotics and FMT and also efficacy and safety of probiotics and FMT in clinical trials and applications.

Organ transplantation is a life-saving strategy for patients with end-stage organ failure. Over the past few decades, organ transplantation has achieved an excellent success in short-term survival but only a marginal improvement in long-term graft outcomes. The pathophysiology of graft loss is multifactorial and remains incompletely defined. However, emerging evidence suggests macrophages as crucial mediators of acute and chronic allograft immunopathology. In this process, macrophage-mediated mobilization of first-line defenses, particularly phagocytosis and the release of acute inflammatory mediators, is important, but macrophages also launch adaptive alloimmune reactions against grafts through antigen processing and presentation, as well as providing costimulation. Additionally, crosstalk with other immune cells and graft endothelial cells causes tissue damage or fibrosis in transplanted organs, contributing to graft loss or tolerance resistance. However, some macrophages function as regulatory cells that are capable of suppressing allogeneic T cells, inhibiting DC maturation, inducing the differentiation of Tregs, and subsequently promoting transplant tolerance. This functional diversity of macrophages in organ transplantation is consistent with their heterogeneity. Although our knowledge of the detrimental or beneficial effects of macrophages on transplants has exponentially increased, the exact mechanisms controlling macrophage functions are not yet completely understood. Here, we review recent advances in our understanding of the multifaceted nature of macrophages, focusing on their evolving roles in organ transplantation and the mechanisms involved in their activation and function in allograft transplantation. We also discuss potential therapeutic options and opportunities to target macrophage to improve the outcomes of transplant recipients.

H2 has shown anti-inflammatory and antioxidant ability in many clinical trials, and its application is recommended in the latest Chinese novel coronavirus pneumonia (NCP) treatment guidelines. Clinical experiments have revealed the surprising finding that H2 gas may protect the lungs and extrapulmonary organs from pathological stimuli in NCP patients. The potential mechanisms underlying the action of H2 gas are not clear. H2 gas may regulate the anti-inflammatory and antioxidant activity, mitochondrial energy metabolism, endoplasmic reticulum stress, the immune system, and cell death (apoptosis, autophagy, pyroptosis, ferroptosis, and circadian clock, among others) and has therapeutic potential for many systemic diseases. This paper reviews the basic research and the latest clinical applications of H2 gas in multiorgan system diseases to establish strategies for the clinical treatment for various diseases.

Respiratory diseases are one of the most common pediatric diseases in clinical practice. Their pathogenesis, diagnosis, and treatment are thus worthy of further investigation. The nuclear factor erythroid 2-related factor 2/heme oxygenase 1 (Nrf2/HO-1) signaling axis is a multiple organ protection chain that protects against oxidative stress injury. This signaling axis regulates anti-inflammation and antioxidation by regulating calcium ions, mitochondrial oxidative stress, autophagy, ferroptosis, pyroptosis, apoptosis, alkaliptosis, and clockophagy. This review presents an overview of the role of the Nrf2/HO-1 signaling axis in the pathogenesis of pediatric respiratory diseases and the latest research progress on this subject. Overall, the Nrf2/HO-1 signaling axis has an important clinical value in pediatric respiratory diseases, and its protective effect needs further exploration.