Clinical characteristics of 82 death cases with COVID-19

BackgroundA recently developing pneumonia caused by SARS-CoV-2 was originated in Wuhan, China, and has quickly spread across the world. We reported the clinical characteristics of 82 death cases with COVID-19 in a single center. MethodsClinical data on 82 death cases laboratory-confirmed as SARS-CoV-2 infection were obtained from a Wuhan local hospitals electronic medical records according to previously designed standardized data collection forms. ResultsAll patients were local residents of Wuhan, and the great proportion of them were diagnosed as severe illness when admitted. Most of the death cases were male (65.9%). More than half of dead patients were older than 60 years (80.5%) and the median age was 72.5 years. The bulk of death cases had comorbidity (76.8%), including hypertension (56.1%), heart disease (20.7%), diabetes (18.3%), cerebrovascular disease (12.2%), and cancer (7.3%). Respiratory failure remained the leading cause of death (69.5%), following by sepsis syndrome/MOF (28.0%), cardiac failure (14.6%), hemorrhage (6.1%), and renal failure (3.7%). Furthermore, respiratory, cardiac, hemorrhage, hepatic, and renal damage were found in 100%, 89%, 80.5%, 78.0%, and 31.7% of patients, respectively. On the admission, lymphopenia (89.2%), neutrophilia (74.3%), and thrombocytopenia (24.3%) were usually observed. Most patients had a high neutrophil-to-lymphocyte ratio of >5 (94.5%), high systemic immune-inflammation index of >500 (89.2%), increased C-reactive protein level (100%), lactate dehydrogenase (93.2%), and D-dimer (97.1%). A high level of IL-6 (>10 pg/ml) was observed in all detected patients. Median time from initial symptom to death was 15 days (IQR 11-20), and a significant association between aspartate aminotransferase (p=0.002), alanine aminotransferase (p=0.037) and time from initial symptom to death were interestingly observed. ConclusionOlder males with comorbidities are more likely to develop severe disease, even die from SARS-CoV-2 infection. Respiratory failure is the main cause of COVID-19, but either virus itself or cytokine release storm mediated damage to other organ including cardiac, renal, hepatic, and hemorrhage should be taken seriously as well. FundingNo founding. Research in contextO_ST_ABSEvidence before this studyC_ST_ABSAs the seventh member of enveloped RNA coronavirus, severe acute respiratory syndrome coronavirus (SARS-CoV)-2 causes a cluster of severe respiratory disease which is similar to another two fatal coronavirus infection caused by SARS-CoV and Middle Eastern respiratory syndrome coronavirus (MERS-CoV). Through searching PubMed and the China National knowledge infrastructure databases up to February 20, 2020, no published article focusing on hospitalized dead patients was identified. Added value of this studyWe conducted a single-center investigation involving 82 hospitalized death patients with COVID-19 and focused on their epidemiological and clinical characteristics. 66 of 82 (80.5%) of patients were older than 60 years and the median age was 72.5 years. The bulk of death cases had comorbidity (76.8%). Respiratory failure remained the leading cause of death, following by sepsis syndrome/MOF, cardiac failure, hemorrhage, and renal failure. Most patients had a high neutrophil-to-lymphocyte ratio, high systemic immune-inflammation index, and increased levels of proinflammatory cytokines. Implications of all the available evidenceSARS-CoV-2 causes a cluster of severe respiratory illness which is similar to another two fatal coronavirus infection caused by SARS-CoV and MERS-CoV. Death is more likely to occur in older male patients with comorbidity. Infected patients might develop acute respiratory distress and respiratory failure which was the leading cause of death, but damages of other organs and systems, including cardiac, hemorrhage, hepatic, and renal also contribute to the death. These damages might be attributable to indirect cytokines storm initiated by immune system and direct attack from SARS-CoV-2 itself.

Effect of FK506 on expression of hepatocyte growth factor in murine spinal cord following peripheral nerve injury / 华中科技大学学报（医学）（英德文版）

This study is to investigate the effect of FK506 on expression of hepatocyte growth factor (HGF) in rats' spinal cord following peripheral nerve injury and to elucidate the mechanisms for neuroprotective property of FK506. Fifty male rats were randomly divided into normal group, injury group and treatment group. Models of peripheral nerve injury were established by bilateral transection of sciatic nerve 0.5 cm distal to piriform muscle. Then the treatment group received subcutaneous injection of FK506 (1 mg/kg) at the back of neck, while the injury group was given 0.9% saline. The L(4-6) spinal cords were harvested at various time points after the surgery. Western blotting and immunofluorescent staining were used to detect the level and position of HGF in spinal cord. Immunofluorescent staining showed that HGF-positive neurons were located in anterior horn, intermediate zone and posterior horn of gray matter in normal spinal cord. Western blotting revealed that there was no significant difference in the expressions of HGF between the injury group and the normal group, while the expression of HGF was significantly higher in the treatment group than in the injury group 7 and 14 days after surgery. It is suggested that peripheral nerve injury does not result in up-regulation of the expression of HGF in spinal cord, while FK506 may induce high expression of endogenous HGF after injury thereby protecting neurons and promoting axonal outgrowth.

Differentiation of mesenchymal stem cells into nucleus pulposus cells in vitro / 华中科技大学学报（医学）（英德文版）

To find a new source of seed cells for constructing tissue-engineered intervertebral disc, nucleus pulposus (NP) cells and mesenchymal stem cells (MSCs) were isolated from New Zealand white rabbits. The nucleus pulposus cells population was fluorescence-laelled and co-cultured with MSCs with or without direct contact. Morphological changes were observed every 12 h. Semi-quantitative reverse transcriptase-polymerase chain reaction was performed to assess the expression levels of Sox-9, aggreacan and type II collagen every 24 h after the co-culture. MSCs treated with direct contact rounded up and presented a ring-like appearance. The expression of marker genes was significantly increased when cells were co-cultured with direct contact for 24 h. No significant change was found after coculture without direct contact. Co-culture of NP cells and MSCs with direct contact is a reliable method for generating large amount of NP cells used for cell-based tissue engineering therapy.

Effect of tacrolimus on expression of hepatocyte growth factor in rat spinal cord following peripheral nerve injury / 中国矫形外科杂志

[Objective]To explore the effect of tacrolimus on expression of hepatocyte growth factor(HGF)in rat spinal cord following peripheral nerve injury.[Method]Fifty male rats were randomly divided into normal group,injury group and treatment group.Models of peripheral nerve injury were established by transection of bilateral sciatic nerve at 0.5 cm distal to piriform muscle.Then treatment group received subcutaneous injection of tacrolimus(1 mg/kg)at the back of the neck,while injury group received 0.9 % saline.The L4~6 spinal cords were harvested at various time points after surgery.Western blotting and immunofluorescence staining were used to detect the level and position of HGF in the spinal cord.[Result]HGF-positive neurons were located in anterior horn,intermediate zone and posterior horn of gray matter in normal spinal cord.There was no significant difference in the expressions of HGF between injury group and normal group,while the expression of HGF was significantly higher in treatment group than that in injury group at 7 and 14 days after surgery.[Conclusion]Peripheral nerve injury does not up-regulate the expression of HGF in spinal cord,while tacrolimus can induce high expression of endogenous HGF after injury to protect neurons and promote axonal outgrowth.

Long term effects of end-to-end suture on repairing acute closed Achilles tendon ruptures / 解放军医学杂志

Objective To retrospectively evaluate the clinical effects of end-to-end suture in repairing acute closed Achilles tendon ruptures.Methods Twenty-eight consecutive patients(20 males and 8 females,aged from 19 to 48 years with a mean of 36.5) with acute closed Achilles tendon rupture admitted from Nov.2000 to Jun.2006 were involved in present study.All patients were produced to have complete Achilles tendon rupture by MRI,and they received surgical procedure within 4 days after injury.An incision of 1cm long was made medial to the tendon,sparing the lesser saphenous vein and sural nerve.The tendon stumps were minimally debrided and end-to-end sutured using the Kessler or Bunnell techniques.The patients were followed-up for 12 to 36 months(mean 20 months),the therapeutic effects were evaluated by Arner-Lindholm scoring system,and postoperative complications were documented during the follow-up period.Results Of the 28 patients,19 got excellent therapeutic effect and 9 got good as evaluated by Arner-Lindholm scoring system,the satisfactory rate was 100%.All the patients regained normal gait,and rehabilitative training was initiated 3 months after operation.The postoperative complications included superficial wound infection in one case and skin edge necrosis in one case,resulting in a 7.1% incidence of complication.No peripheral nerve injury or Achilles tendon re-rupture occurred during the follow-up period.Conclusions An excellent therapeutic effect and minimal postoperative complication may be expected with end-to-end suture for repairing acute closed Achilles tendon rupture.