Background: Previous studies on coronavirus disease 2019 have focused on populations with normal immunity, but lack data on immunocompromised populations. Objective: To evaluate the clinical features and outcomes of COVID-19 pneumonia in kidney transplant recipients. Design, setting, and participants: A total of 10 renal transplant recipients with laboratory-confirmed COVID-19 pneumonia were enrolled in this retrospective study. In addition, 10 of their family members diagnosed with COVID-19 pneumonia were included in the control group. Intervention: Immunosuppressant reduction and low-dose methylprednisolone therapy. Outcome measurements and statistical analysis: The clinical outcomes (the severity of pneumonia, recovery rate, time of virus shedding, and length of illness) were compared with the control group by statistical analysis. Results and limitations: The clinical symptomatic, laboratory, and radiological characteristics of COVID-19 pneumonia in the renal transplant recipients were similar to those of severe COVID-19 pneumonia in the general population. The severity of COVID-19 pneumonia was greater in the transplant recipients than in the control group (five severe/three critical cases vs one severe case). Five patients developed transient renal allograft damage. After a longer time of virus shedding (28.4 AE 9.3 vs 12.2 AE 4.6 d in the control group) and a longer course of illness (35.3 AE 8.3 vs 18.8 AE 10.5 d in the control group), nine of the 10 transplant patients recovered successfully after treatment. One patient developed acute renal graft failure and died of progressive respiratory failure. Conclusions: Kidney transplant recipients had more severe COVID-19 pneumonia than the general population, but most of them recovered after a prolonged clinical course and virus shedding. Findings from this small group of cases may have important implications for the treatment of COVID-19 pneumonia in immunosuppressed populations. Patient summary: Immunosuppressed transplant recipients with coronavirus disease 2019 infection had more severe pneumonia, but most of them still achieved a good prognosis after appropriate treatment.

To the Editor, Coronavirus disease 2019 (COVID-19), caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is a disease characterized by pneumonia. The main clinical presentations are fever, dry cough, and fatigue, but in addition to respiratory symptoms, a minority of patients may present only with muscle soreness, gastrointestinal symptoms, or dispiritedness in the early stages. 1 According to limited pathological autopsy results, in addition to lung involvement, the heart, liver, kidneys, spleen, hilar lymph nodes, bone marrow, and even brain tissues are also affected in patients with COVID-19. 2 Herein, we report a case of a patient diagnosed with COVID-19 who manifested with neurological symptoms.

The Mediator complex functions as a control center, orchestrating diverse signaling, gene activities, and biological processes. However, how Mediator subunits determine distinct cell fates remains to be fully elucidated. Here, we show that Mediator MED23 controls the cell fate preference that directs differentiation into smooth muscle cells (SMCs) or adipocytes. Med23 deficiency facilitates SMC differentiation but represses adipocyte differentiation from the multipotent mesenchymal stem cells. Gene profiling revealed that the presence or absence of Med23 oppositely regulates two sets of genes: the RhoA/MAL targeted cytoskeleton/SMC genes and the Ras/ELK1 targeted growth/ adipogenic genes. Mechanistically, MED23 favors ELK1-SRF binding to SMC gene promoters for repression, whereas the lack of MED23 favors MAL-SRF binding to SMC gene promoters for activation. Remarkably, the effect of MED23 on SMC differentiation can be recapitulated in zebrafish embryogenesis. Collectively, our data demonstrate the dual, opposing roles for MED23 in regulating the cytoskeleton/SMC and growth/adipogenic gene programs, suggesting its ''Ying-Yang'' function in directing adipogenesis versus SMC differentiation.[Keywords: Mediator complex; MED23; MAL; ELK1; smooth muscle cell; adipocyte; differentiation] Supplemental material is available for this article. Received March 26, 2012; revised version accepted August 13, 2012. Cell fate determination in metazoans is precisely controlled by sophisticated spatiotemporal patterns of RNA polymerase II (Pol II)-mediated transcription in response to various intracellular and extracellular signals. Genetic or environmental alterations that perturb the regulation of transcription can alter cell fate specifications, leading to a variety of developmental defects. Control over lineagespecific transcriptional programs has generally been attributed to the specific DNA-binding transcription factors. To ensure precise transcriptional control of cell fate determination and development, the master transcription factors are subjected to further regulatory control. Eukaryotes have evolved elaborate transcriptional machinery consisting of multiple cofactors/cofactor complexes to modulate the basal transcriptional apparatus. Two recent studies demonstrated that the cofactors control the cell fate by modulating the distinct transcription factors. First, TAZ coactivates Runx2-dependent 7 Present address: Department of Cardiovascular and Thoracic Surgery, Affiliated Hospital of Xuzhou Medical College, Xuzhou 221002, China. 8 Corresponding author E-mail gwang22@sibs.ac.cn Article published online ahead of print. Article and publication date are online at http://www.genesdev.org/cgi