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4% versus 25.0% and 41.0% versus 0%, respectively. The median postrelapse survival was 24.9 versus 13.5months, respectively. Pulmonary metastasectomy was independently associated with improved survival (hazard ratio, 0.185; 95% confidence interval, 0.103-0.330; P<.001). These results were confirmed by multiple propensity score analyses. Further stratified analysis revealed that the survival advantage associated with metastasectomy was not significant in patients with metastases involving ≥3 lung lobes and patients with very high pretreatment serum alkaline phosphatase (more than twice the upper limit).

Pulmonary metastasectomy is associated with improved survival in patients with recurrent osteosarcoma.

Pulmonary metastasectomy is associated with improved survival in patients with recurrent osteosarcoma.

To report outcomes in a pilot study of autologous mitochondrial transplantation (MT) in pediatric patients requiring postcardiotomy extracorporeal membrane oxygenation (ECMO) for severe refractory cardiogenic shock after ischemia-reperfusion injury (IRI).

A single-center retrospective study of patients requiring ECMO for postcardiotomy cardiogenic shock following IRI between May 2002 and December 2018 was performed. Postcardiotomy IRI was defined as coronary artery compromise followed by successful revascularization. Patients undergoing revascularization and subsequent MT were compared with those undergoing revascularization alone (Control).

Twenty-four patients were included (MT, n=10; Control, n=14). Markers of systemic inflammatory response and organ function measured 1day before and 7days following revascularization did not differ between groups. Successful separation from ECMO-defined as freedom from ECMO reinstitution within 1week after initial separation-was possible for 8 patients in the MT grourol group (hazard ratio, 4.6; 95% confidence interval, 1.0 to 20.9; P = .04) CONCLUSIONS In this pilot study, MT was associated with successful separation from ECMO and enhanced ventricular strain in patients requiring postcardiotomy ECMO for severe refractory cardiogenic shock after IRI.

The presence of olfactory dysfunction or “loss of smell” has been reported as an atypical symptom in patients with coronavirus disease 2019 (COVID-19). We performed a systematic review and meta-analysis of the available literature to evaluate the prevalence of “loss of smell” in COVID-19 as well as its utility for prognosticating the disease severity.

An exhaustive search of the PubMed/Medline, Embase, Web of Science, Cochrane Library, LitCovid NIH, and WHO COVID-19 database was conducted through August 6

, 2020. All studies reporting the prevalence of “loss of smell” (anosmia and/or hyposmia/microsmia) in laboratory-confirmed COVID-19 patients were included. Pooled prevalence for cases (positive COVID-19 through reverse transcriptase (RT-PCR) and/or serology IgG/IgM) and controls (negative RT-PCR and/or serology) was compared, and the odds ratio (OR), 95% confidence interval (CI) and the p-value were calculated. A p-value of <0.05 was considered statistically significant.

A total of 51 studies with 11074 confirmed COVID-19 patients were included. Of these, 21 studies used a control group with 3425 patients. Olprinone supplier The symptom of “loss of smell” (OR 14.7, CI 8.9-24.3) was significantly higher in the COVID-19 group when compared to the control group. Seven studies comparing severe COVID-19 patients with- and without “loss of smell” demonstrated favorable prognosis for patients with “loss of smell” (OR 0.36, CI 0.27-0.48).

Olfactory dysfunction or “loss of smell” is a prevalent symptom in COVID-19 patients. Moreover, COVID-19 patients with “loss of smell” appear to have a milder course of the disease.

Olfactory dysfunction or “loss of smell” is a prevalent symptom in COVID-19 patients. Moreover, COVID-19 patients with “loss of smell” appear to have a milder course of the disease.The Covid-19 pandemic struck physicians at a time of unprecedented dissatisfaction and burnout, providing a stress test whose lessons might guide structural changes in healthcare. While selflessly rescuing patients from death, many doctors were exposed to unacceptable risk, with little protection for themselves, and, by extension, for their families and patients. This essay examines the basis and limits of duty to treat in a time of crisis and explores how these experiences could leave doctors morally stressed and even compromised. We question whether a physician-patient relationship that treats patients’ safety and well-being as separate from their doctors’ personal and professional values, needs, and dignity is the best way to deliver care. Such questions predated coronavirus but were brought to the forefront because of the epidemic. As physicians process their experiences, we hope to begin a deeper moral and social conversation that might help us be better prepared for future crises.Klotho long recognized for its role in anti-aging, is potentially implicated in the pathogenesis of rheumatoid arthritis, systemic lupus erythematosus, and systemic sclerosis. Aging of the immune system coincides with the inability of the body to recognize self-antigens, which often leads to autoimmune responses. The role of Klotho in these autoimmune diseases should be of high interest; however, few articles have been published exploring the role of Klotho in the pathogenesis, organ involvement, or clinical manifestation of rheumatoid arthritis, systemic lupus erythematosus, and systemic sclerosis. Herein, we discuss information gathered from peer-reviewed publications to describe the emerging role of Kl in these select rheumatologic autoimmune diseases.Chronic exposure to UVR is known to disrupt tissue homeostasis, accelerate the onset of age-related phenotypes, and increase the risk for skin cancer-a phenomenon defined as photoaging. In this paper, we review the current knowledge on how UV exposure causes cells to prematurely enter cellular senescence. We describe the mechanisms contributing to the accumulation of senescent cells in the skin and how the persistence of cellular senescence can promote impaired regenerative capacity, chronic inflammation, and tumorigenesis associated with photoaging. We conclude by highlighting the potential of senolytic drugs in delaying the onset and progression of age-associated phenotypes in the skin.