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Objective To provide a basis for further optimizing the diagnosis and treatment strategies of severe and critical corona virus disease 2019 (COVID-19) by investigating and analyzing the epidemiological and clinical characteristics of the death cases. Methods The epidemiological and clinical characteristics of 47 death cases obtained from Huoshenshan Hospital in Whuhan, Hubei Province were retrospectively analyzed. Results All the patients developed initial symptoms in Wuhan. The time from onset to admission was (12.60±5.60) days. Most of them were male (68.09%) with non-nosocomial infection (91.49%), advanced age (>60 years, 89.36%). Over half of the cases (51.06%) reported a history of contact with suspected or confirmed patients, and comorbidity of chronic diseases (70.21%). Multiple organ dysfunction syndrome (MODS) occurred in 29 cases (61.70%) with heart failure (51.06%) and renal failure (36.17%). The main clinical symptoms included fever, fatigue, dyspnea and cough. At admission,most cases were severe (55.32%) or critical (42.55%), and the in-hospital survival was longer for the severe than for the critical (P=0.02). 76.59% of the patients received invasive mechanical ventilation, and they had a longer in-hospital survival than those with non-invasive mechanical ventilation (P

Sulfur dioxide (SO2) is naturally synthesized by glutamate-oxaloacetate transaminase (GOT) from l-cysteine in mammalian cells. We aim to investigate the role of SO2 in inflammation in acute lung injury (ALI) following limb ischemia/reperfusion (I/R). Male Wistar rats were subjected to limb I/R and were injected with saline, GOT inhibitor hydroxamate (HDX, 0.47 mmol/kg), or the SO2 donor Na2SO3/NaHSO3 (0.54 mmol/kg/0.18 mmol/kg). Compared with the sham operation, the plasma SO2 levels were significantly decreased by limb I/R treatment. In addition, SO2 concentration and GOT activity in the lung tissue were also reduced in ALI. The occurrence of ALI following limb I/R can be prevented by Na2SO3/NaHSO3 treatment, whereas it can be significantly aggravated by HDX. The plasma IL-1β, IL-6, and IL-10 levels were consistent with myeloperoxidase activity and inflammation in lung tissue. In conclusion, our data suggest that downregulation of endogenous SO2 production might be involved in pathogenesis of ALI following limb I/R in rats. © 2013 Wiley Periodicals, Inc. J BiochemMol Toxicol 27:389-397, 2013; View this article online at wileyonlinelibrary.com. DOI 10.1002/jbt.21492

The optimal surgical treatment for displaced proximal humeral fractures continues to be controversial. One of the new treatment options is the minimally invasive intramedullary nail. The purpose of this study was to evaluate the functional outcome of using the TRIGEN proximal humeral nail (PHN) for the treatment of displaced proximal humeral fractures in elderly patients. From January 2004 to December 2008, 64 elderly patients (age > 60 years old) with displaced proximal humeral fractures were treated using TRIGEN PHN. A complete 12-month postoperative follow-up was available for 54 patients. The study cohort included two-part (29 shoulders), three-part (22 shoulders), and four-part (3 shoulders) Neer classification fracture types. The Constant-Murley score was used to assess functional outcome. Radiological outcomes were evaluated, and all complications were recorded. All fractures were united. The Constant-Murley score data indicated that the patients experienced improvement from 6 to 12 months postoperatively. The mean absolute Constant-Murley score on the injured side increased from 71.2 ± 11.2 points at 6 months to 82.4 ± 16.4 points at 12 months (P = 0.01). The mean neck-shaft angle 1 year after surgery was 125° ± 8.1° (95°–140°). Secondary complications were minimal and observed in only 6 of 54 patients. In conclusion, the TRIGEN intramedullary humeral nail is effective for the treatment of proximal humeral fractures.

To discuss the influence of intensive insulin therapy on insulin resistance of patients with severe burn or trauma.Sixty patients with severe burn or trauma hospitalized in the Third People's Hospital of Chongqing or Southwest Hospital of the Third Military Medical University from January 2010 to December 2011 were randomly divided into intensive insulin therapy group (IT, treated with intensive insulin therapy to control the blood glucose to the level of 6.0-8.0 mmol/L) and control group (C, treated with routine therapy) according to the paired grouping method, with 30 patients in each group. Before treatment and on post treatment day (PTD) 1, 3, 7, 10, 14, the levels of fasting blood glucose and fasting plasma insulin were determined. Insulin resistance index and β-cell function index were calculated using homeostasis model assessment. Data were processed with t test, analysis of variance, and LSD test.On PTD 1, 3, 7, 10, levels of fasting blood glucose in group IT [(6.8 ± 1.4), (6.7 ± 1.3), (5.8 ± 1.9), (5.4 ± 1.6) mmol/L] were significantly lower than those of group C [(14.8 ± 4.9), (12.7 ± 3.7), (7.7 ± 1.9), (6.6 ± 1.3) mmol/L, with t values respectively 12.453, 11.386, 5.563, 4.731, P0.05 or P0.01]. On PTD 3, 7, levels of fasting insulin in group IT [(14 ± 5), (10 ± 3) mU/L] were significantly lower than those of group C [(16 ± 4), (13 ± 4) mU/L, with t values respectively 4.212, 4.364, P values below 0.05]. Levels of fasting blood glucose and fasting insulin in the two groups at each time point were statistically significantly different from those before treatment (with P values below 0.01), except for the level of fasting blood glucose on PTD 3. On PTD 1, 3, 7, 10, levels of insulin resistance index in group IT (1.60 ± 0.80, 1.46 ± 0.70, 0.96 ± 0.21, 0.90 ± 0.23) were significantly lower than those in group C (2.15 ± 1.35, 2.21 ± 1.21, 1.50 ± 0.95, 1.17 ± 0.66, with t values respectively 8.316, 10.607, 7.825, 5.217, P0.05 or P0.01). Levels of insulin resistance index of patients in the two groups at each time point after treatment were significantly lower than those before treatment (with P values below 0.01). On PTD 1, 3, 7, levels of β-cell function index in group IT (4.6 ± 2.9, 4.5 ± 3.3, 4.5 ± 3.6) were significantly higher than those in group C (3.4 ± 2.5, 3.6 ± 2.2, 4.2 ± 2.5, with t values respectively 8.243, 7.914, 4.338, P0.05 or P0.01). Levels of β-cell function index in group C on PTD 1 and 3 were significantly lower than that before therapy (with P values below 0.05).Intensive insulin therapy can alleviate insulin resistance of patients with severe burn or trauma.

Sulfur dioxide (SO2) is naturally synthesized by glutamate-oxaloacetate transaminase (GOT) from L-cysteine in mammalian cells. We aim to investigate the role of SO2 in inflammation in acute lung injury (ALI) following limb ischemia/reperfusion (I/R). Male Wistar rats were subjected to limb I/R and were injected with saline, GOT inhibitor hydroxamate (HDX, 0.47 mmol/kg), or the SO2 donor Na2 SO3 /NaHSO3 (0.54 mmol/kg/0.18 mmol/kg). Compared with the sham operation, the plasma SO2 levels were significantly decreased by limb I/R treatment. In addition, SO2 concentration and GOT activity in the lung tissue were also reduced in ALI. The occurrence of ALI following limb I/R can be prevented by Na2 SO3 /NaHSO3 treatment, whereas it can be significantly aggravated by HDX. The plasma IL-1β, IL-6, and IL-10 levels were consistent with myeloperoxidase activity and inflammation in lung tissue. In conclusion, our data suggest that downregulation of endogenous SO2 production might be involved in pathogenesis of ALI following limb I/R in rats.

Nogo, also known as Reticulon-4, is a protein that is specific to the central nervous system (CNS), and has been identified as an inhibitor of neurite outgrowth. Nogo-A is the largest member of the Nogo family and is responsible for inhibition of CNS regeneration. The structural information and biological functions of Nogo family members are reviewed in this study. The Nogo-66 receptor (NgR), a membrane protein which binds to Nogo, may play an important role in signal transduction for several myelin-associated inhibitors. The discovery of the Nogo family and the NgR provides an opportunity to develop interventions to promote axonal regeneration in the CNS after brain injury. Basic and clinical research of Nogo has increased our understanding of the mechanisms underlying spinal cord injury, multiple sclerosis, and neuroregenerative diseases. Understanding the biological functions of Nogo family members may open up a new avenue for the development of therapeutic agents. The anatomical and biological plastic changes are reviewed in animal models of injuries in the adult CNS. The role of Nogo A in neuroregeneration, and the mechanisms underlying functional recovery after CNS injury, are also detailed in this review.

Spinal cord injury (SCI) remains a formidable challenge in the clinic. In the current study, we examined the effects of the TLX gene on the proliferation and neuronal differentiation of dermal multipotent stem cells (DMSCs) in vitro and the potential of these cells to improve SCI in rats in vivo. DMSCs were stably transfected with TLX-expressing plasmid (TLX/DMSCs). Cell proliferation was examined using the MTT assay, and neuronal differentiation was characterized by morphological observation combined with immunocytochemical/immunofluorescent staining. The in vivo functions of these cells were evaluated by transplantation into rats with SCI, followed by analysis of hindlimb locomotion and post-mortem histology. Compared to parental DMSCs, TLX/DMSCs showed enhanced proliferation and preferential differentiation into NF200-positive neurons in contrast to GFAP-positive astrocytes. When the undifferentiated cells were transplanted into rats with SCI injury, TLX/DMSCs led to significant improvement in locomotor recovery and healing of SCI, as evidenced by reduction in scar tissues and cavities, increase in continuous nerve fibers/axons and enrichment of NF200-positive neurons on the histological level. In conclusion, TLX promotes the proliferation and neuronal differentiation of DMSCs and thus, may serve as a promising therapy for SCI in the clinic.