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The outcome associated with COVID-19 Widespread in Workplace Accidents within South korea.
Fungal endocarditis (FE) is a rare but fatal disease. The incidence of infective endocarditis (IE) in hemodialysis patients with catheters is thought to be obviously higher than that in the general population. We reported a case of IE caused by Aspergillus flavus (A. flavus) in a 36-year-old woman on hemodialysis. Because the blood cultures were persistently negative, so we used mNGS (Metagenomic next generation sequencing) for early clinical diagnosis. After treatment with voriconazole, the patient's condition improved rapidly. She continued oral voriconazole treatment 1 year after discharge and is in good condition. The diagnosis and treatment strategies of FE in hemodialysis patients were discussed.The chronic obstructive pulmonary disease (COPD) emphysematous phenotype is characterized by destruction of lung tissue structure. Patients with this phenotype usually present with typical emphysema-like changes on chest computed Tomography CT, experience higher mortality and poorer prognosis, and are insensitive to routine pharmacological COPD therapy. However, the pathogenesis for the COPD emphysematous phenotype remains unclear, resulting in diagnostic and therapeutic challenges. The imbalance between injury and defense mechanisms is essential in the progression of many pulmonary diseases. Thus, in this review, we focus on the pathogenesis of the COPD emphysematous phenotype and discuss the pathophysiological processes involved in disease progression, from the perspective of injury and defense imbalance.Ferroptosis is a newly discovered type of regulated cell death that is different from apoptosis, necrosis and autophagy. Ferroptosis is characterized by iron-dependent lipid peroxidation, which induces cell death. Iron, lipid and amino acid metabolism is associated with ferroptosis. Ferroptosis is involved in the pathological development of various diseases, such as neurological diseases and cancer. Recent studies have shown that ferroptosis is also closely related to acute lung injury (ALI)/ acute respiratory distress syndrome (ARDS), suggesting that it can be a novel therapeutic target. This article mainly introduces the metabolic mechanism related to ferroptosis and discusses its role in ALI/ARDS to provide new ideas for the treatment of these diseases.Extramedullary multiple myeloma (EMM) is an aggressive sub-entity of multiple myeloma (MM). Despite an excellent improvement in survival for most patients with MM over recent decades, the overall survival (OS) of patients with EMM was usually not longer than 3 years. Standard treatment for patients with EMM has not been established, and their management is particularly challenging. We presented a heavily pretreated young patient with relapsed EMM and refractoriness to a proteasome inhibitor (PI; bortezomib), a next-generation PI (ixazomib), immunomodulatory drugs (IMiDs; lenalidomide), autologous hematopoietic stem cell transplantation (ASCT), and monoclonal antibody (directed against CD38 daratumumab) and indicated that myeloablative haploidentical hematopoietic stem cell transplantation (haploidentical-HSCT) as a salvage treatment of relapse after a chimeric antigen receptor (CAR)-T cell therapy that targeted B-cell maturation antigen (BCMA) (NCT04650724) is feasible. Taken together of the contemporary literature, the promising results on the effect of anti-BCMA CAR-T cell therapy and allogeneic HSCT might present a proof-of-principle for patients with EMM, and therefore, patients with the disease need to be included in future studies.The ocular surface microbiome is an essential factor that maintains ocular surface homeostasis. Since the ocular surface is continuously exposed to the external environment, its microbiome, tears, and local immunity are vital for maintaining normal conditions. Additionally, this microbiome helps prevent pathogen colonization, which commonly leads to opportunistic infection. The abnormal ocular surface microbiome has previously been reported in several conditions, including dry eyes, allergy, blepharitis, graft-versus-host disease (GVHD), and Stevens-Johnson syndrome (SJS). Several approaches were applied to identify the ocular microbiome, including conventional culture techniques and molecular sequencing techniques. By using 16s rRNA sequencing, alterations in the type, proportion, and composition of bacterial communities, described by alpha (α)-and beta (β)-diversity, were observed in SJS patients compared to the healthy group. Conventional culture techniques indicated a higher number of positive bacterial cultures in the SJS group, with a predominance of gram-positive cocci and gram-positive bacilli. Besides, there are increased variations and multiple detections of bacterial genera. Taken together, SJS causes structural changes in the ocular surface and significantly affects its microbiome. Further studies into the area of temporal relationship, metagenomics, proteomics, and metabolomics analysis of the microbiome will lead to a better understanding of this disease. Finally, the treatment using prebiotics and probiotics to re-establish the normal ocular ecosystem and bring back a healthy ocular surface await confirmation.Atopic dermatitis (AD) is among the most frequent inflammatory skin diseases in humans, affecting up to 20% of children and 10% of adults in higher income countries. Chronic pruritus is a disease-defining symptom of AD, representing the most burdensome symptom for patients. Severe chronic pruritus causes significant sleep disturbances and impaired quality of life, as well as increased anxiety, depression and suicidal behavior. Until recently, skin care, topical corticosteroids, and calcineurin-inhibitors were primarily used to treat mild to moderate AD, while phototherapy and immunosuppressive agents such as corticosteroids, cyclosporine, and methotrexate were used to treat patients with moderate to severe AD. The potential short- and long-term adverse events associated with these treatments or their insufficient therapeutic efficacy limited their use in controlling pruritus and eczema in AD patients over longer periods of time. As our understanding of AD pathophysiology has improved and new systemic and topical treatments have appeared on the market, targeting specific cytokines, receptors, or their intracellular signaling, a new era in atopic dermatitis and pruritus therapy has begun. This review highlights new developments in AD treatment, placing a specific focus on their anti-pruritic effects.The coronavirus disease 2019 (COVID-19) pandemic has caused considerable socio-economic burden, which fueled the development of treatment strategies and vaccines at an unprecedented speed. However, our knowledge on disease recovery is sparse and concerns about long-term pulmonary impairments are increasing. Causing a broad spectrum of symptoms, COVID-19 can manifest as acute respiratory distress syndrome (ARDS) in the most severely affected patients. Notably, pulmonary infection with Severe Acute Respiratory Syndrome coronavirus 2 (SARS-CoV-2), the causing agent of COVID-19, induces diffuse alveolar damage (DAD) followed by fibrotic remodeling and persistent reduced oxygenation in some patients. It is currently not known whether tissue scaring fully resolves or progresses to interstitial pulmonary fibrosis. The most aggressive form of pulmonary fibrosis is idiopathic pulmonary fibrosis (IPF). IPF is a fatal disease that progressively destroys alveolar architecture by uncontrolled fibroblast proliferation and ARS-CoV-2 infection in multicellular systems that recapitulate tissue regeneration and fibrotic remodeling. Current evidence for SARS-CoV-2 mediated pulmonary fibrosis and a selection of classical and novel lung models will be discussed in this review.Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causative virus of the coronavirus disease 2019 (COVID-19), has been identified in China in late December 2019. SARS-CoV-2 is an enveloped, positive-sense, single-stranded RNA betacoronavirus of the Coronaviridae family. Coronaviruses have genetic proofreading mechanism that corrects copying mistakes and thus SARS-CoV-2 genetic diversity is extremely low. Despite lower mutation rate of the virus, researchers have detected a total of 12,706 mutations in the SARS-CoV-2 genome, the majority of which were single nucleotide polymorphisms. Sequencing data revealed that the SARS-CoV-2 accumulates two-single nucleotide mutations per month in its genome. SC144 Recently, an amino acid aspartate (D) to glycine (G) (D614G) mutation due to an adenine to guanine nucleotide change at position 23,403 at the 614th amino-acid position of the spike protein in the original reference genotype has been identified. The SARS-CoV-2 viruses that carry the spike protein D614G mutation have become dominant variant around the world. The D614G mutation has been found to be associated with 3 other mutations in the spike protein. Clinical and pseudovirus experimental studies have demonstrated that the spike protein D614G mutation alters the virus phenotype. However, the impact of the mutation on the rate of transmission between people, disease severity and the vaccine and therapeutic development remains unclear. Three variants of SARS-CoV-2 have recently been identified. They are B.1.1.7 (UK) variant, B.1.351 (N501Y.V2, South African) variant and B.1.1.28 (Brazilian) variant. Epidemiological data suggest that they have a higher transmissibility than the original variant. There are reports that some vaccines are less efficacious against the B.1.351 variant. This review article discusses the effects of novel mutations in the SARS-CoV-2 genome on transmission, clinical outcomes and vaccine development.Backgrounds Recently, the association between sarcopenia and various musculoskeletal disorders, such as lumbar spine stenosis and fibromyalgia, has been highlighted. However, the relationship between sarcopenia and rotator cuff tendon diseases has rarely been investigated. This study aimed to evaluate whether sarcopenia was associated with shoulder pain and to determine whether rotator cuff tendons differed in echotexture between the sarcopenic and non-sarcopenic populations. Methods The thickness and echogenicity ratio of the tendon vs. the overlying muscle (ERTM) or subcutaneous tissue (ERTT) were measured using high-resolution ultrasonography in 56 sarcopenic patients and 56 sex- and age- matched controls. The association between ultrasound measurements of the rotator cuff tendon complex and sarcopenia was investigated using the generalized estimating equation (GEE). Results The sarcopenic group had an increased prevalence of shoulder pain. Based on the GEE analysis, sarcopenia was significantly associated with an increase in supraspinatus tendon thickness (β coefficient = 0.447, p less then 0.001) and a decrease in the ERTM for the biceps long head and rotator cuff tendons. A negative trend of association was observed between sarcopenia and ERTT in the supraspinatus tendons (β coefficient = -0.097, p = 0.070). Nevertheless, sarcopenia was not associated with an increased risk of rotator cuff tendon tears. Conclusions Patients with sarcopenia have a higher risk of shoulder pain. A consistent tendinopathic change develops in the supraspinatus tendons in sarcopenic patients. However, sarcopenia is less likely to be associated with serious rotator cuff pathology, such as tendon tears. Prospective cohort studies are warranted to explore the causal relationship between sarcopenia and shoulder disorders.
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