Determination of risk factors for predicting the onset of symptoms in asymptomatic COVID-19 infected patients.

Background: The number of asymptomatic infected patients with coronavirus disease 2019 (COVID-2019) is rampaging around the world but limited information aimed on risk factors of asymptomatic infections. The purpose of this study is to investigate the risk factors of symptoms onset and clinical features in asymptomatic COVID-19 infected patients. Methods: A retrospective study was performed in 70 asymptomatic COVID-2019 infected patients confirmed by nucleic acid tests in Hunan province, China between 28 January 2020 and 18 February, 2020. The epidemiological, clinical features and laboratory data were reviewed and analyzed. Presence or absence at the onset of symptoms was taken as the outcome. A Cox regression model was performed to evaluate the potential predictors of the onset of symptoms. Results: The study included 36 males and 34 females with a mean age of 33.24±20.40 years (range, 0.5-84 years). There were 22 asymptomatic carriers developed symptoms during hospitalization isolated observation, and diagnosed as confirmed cases, while 48 cases remained asymptomatic throughout the course of disease. Of 70 asymptomatic patients, 14 (14/70, 20%) had underlying diseases, 3 (3/70, 4.3%) had drinking history, and 11 (11/70, 15.7%) had smoking history. 22 patients developed symptoms onset of fever (4/22, 18.2%), cough (13/22, 59.1%), chest discomfort (2/22, 9.1%), fatigue (1/22, 4.5%), pharyngalgia (1/22, 4.5%) during hospitalization; only one (1/22, 4.5%) patient developed signs of both cough and pharyngalgia. Abnormalities on chest CT were detected among 35 of the 69 patients (50.7%) after admission, except for one pregnant woman had not been examined. 4 (4/70, 5.7%) and 8 (8/70, 11.4%) cases showed leucopenia and lymphopenia. With the effective antiviral treatment, all the 70 asymptomatic infections had been discharged, none cases developed severe pneumonia, admission to intensive care unit, or died. The mean time from nucleic acid positive to negative was 13.2±6.84 days. Cox regression analysis showed that smoking history (P=0.028, hazard ratio=4.49, 95% CI 1.18-17.08) and existence of pulmonary disease (P=0.038, hazard ratio=7.09, 95% CI 1.12-44.90) were risk factors of the onset of symptoms in asymptomatic carries. Conclusion: The initially asymptomatic patients can develop mild symptoms and have a good prognosis. History of smoking and pulmonary disease was prone to illness onset in asymptomatic patients, and it is necessary to be highly vigilant to those patients.

Up-regulation of TNF-alpha in neurons of dorsal root ganglia and spinal cord during coronary artery occlusion in rats.

Knowledge about the physiologic and pathophysiologic roles of tumor necrosis factor-alpha (TNF-alpha) in acute myocardial ischemia/infarction is still very limited. Evidence implies that TNF-alpha is involved in neural activity including nociception in peripheral and central nervous system. Current study was designed to examine the association of change in TNF-alpha and its mRNA in upper thoracic dorsal root ganglia and spinal cord (T1-T5) during acute myocardial ischemia/infarction induced by coronary artery occlusion (CAO) in rats. The experiment was performed using immunohistochemistry, enzyme immunoassay, in situ hybridization and real time reverse transcription-polymerase chain reaction techniques. At 0.5h, 1h, 3h and 6h of acute myocardial ischemia/infarction, TNF-alpha was mainly up-regulated in a sub-population of small and medium neurons and satellite cells in the dorsal root ganglia (DRG) and spinal neurons, mainly in laminae I, II and V, VI of the spinal dorsal horn of upper thoracic segments. The up-regulation of TNF-alpha mRNA was observed at 30min of CAO, which was statistically significant, compared with the control and the sham surgery groups (P<0.01). The TNF-alpha mRNA was located in the satellite cells and afferent neurons of the DRG and spinal neurons, located mainly in laminae II-VI. The findings indicate an association of up-regulation of TNF-alpha in DRG and spinal cord with acute myocardial ischemia/infarction, suggesting that TNF-alpha may be associated with the nociception initiated by acute myocardial ischemia/infarction, while the pathophysiological role needs to be studied.

[Effects of epidurally administration of morphine at thoracic level on expression of tumor necrosis factor-alpha in the lungs in acute myocardial ischemia in rats].

OBJECTIVE: To investigate the expression of tumor necrosis factor-alpha (TNF-alpha) in lungs following coronary artery occlusion (CAO) and the effect of morphine pretreatment via epidural administration on its expression in the rats. METHODS: Eighteen adult healthy male Sprague-Dawley (SD) rats were randomly divided into sham operation group (S group), CAO group and morphine pretreatment group (M group), with 6 in each group. In S group the left anterior descending branch of coronary artery was not occluded. In CAO group the left anterior descending branch of coronary artery was occluded. In M group the rats were pre-treated with morphine 60 microg/kg by epidural injection 15 minutes before CAO. The right lung was harvested 3 hours after CAO. The expression of TNF-alpha in lungs was assessed with immuno- histochemistry and enzyme linked immunosorbent assay (ELISA). RESULTS: The immunohistochemistry results showed, compared with S group (8.68+/-0.29,1.609+/-0.050), the positive unit and average light density of TNF-alpha in CAO group (24.55+/-6.25, 1.844+/-0.027) and M group (11.60+/-1.21,1.733+/-0.027) were higher significantly, while they were lower significantly in M group compared with CAO group (all P<0.01). ELISA results showed the level of TNF-alpha in the lung was significantly higher in CAO group [(221.58+/-5.23) ng/L] and M group [(103.45+/-4.56) ng/L] than that in S group [(47.14+/-1.36) ng/L], while it was significantly lower in M group compared with CAO group (all P<0.01). CONCLUSION: Acute myocardial ischemia could cause up-regulation of TNF-alpha in lungs, which is likely to be mediated by neural mechanisms. Opioid and its receptors in spinal cord might be involved in modulation of inflammatory reaction in the lung after acute coronary ischemia.

[Observation on therapeutic effect of chronic fatigue syndrome treated with coiling dragon needling and moving cupping on back].

OBJECTIVE: To compare the differences of therapeutic effect of chronic fatigue syndrome treated with the combined therapy of coiling dragon needling and cupping on back and the western medicine therapy with Prednisone. METHODS: Seventy-two cases were randomly divided into an acupuncture and cupping group (37 cases) and a Prednisone group (35 cases). In acupuncture and cupping group, Jiaji (EX-B 2) points of T1--L5 were applied with coiling dragon needling (once a day), combined with moving cupping on back (once every two days); in Prednisone group, Prednisone tablets were orally taken for 10 mg at 8:00 am. Seven days made one course, and 2 courses were carried on totally. FS-14 scale and BELL's chronic fatigue syndrome integral table were applied to evaluate the fatigue degree of patients before and after treatment, and the therapeutic effects of both groups were compared. RESULTS: After one course of treatment, the BELL's scores of both groups were obviously improved (both P < 0.01), but there was no significant difference between groups (P > 0.05); after two courses of treatment, the BELL's score in acupuncture and cupping group improved more obviously than that in Prednisone group, and the total effective rate of 91.9% (34/37) in acupuncture and cupping group was superior to that of 71.4% (25/35) in Prednisone group (P < 0.05). CONCLUSION: The therapeutic effect of chronic fatigue syndrome treated with coiling dragon needling and moving cupping on back is positive, superior to that of Prednisone with oral administration.

Up-regulation of substance P in the lungs during acute myocardial ischemia and infarction in rats.

OBJECTIVE: Previous studies indicate that disturbance of respiratory functions during acute myocardial ischemia and infarction was not always parallel with decline of cardiac functions, indicating that some non-hemodynamic mechanism might be underlying the changes in the lungs. METHODS: The current study was designed to investigate the changes in the expression of substance P and its mRNA in the lungs and dorsal root ganglia using assays of immunohistochemistry, enzyme immunoassay, in situ hybridization and real-time quantitative reverse transcription-polymerase chain reaction, with a rodent model of acute myocardial infarction induced by permanent coronary artery occlusion, without and with epidural anesthesia in the upper thoracic segments of the spinal cord. RESULTS: Marked up-regulation of substance P in the lungs and the dorsal root ganglia of upper thoracic segments (T1-T5) was detected at 15, 30, 60, 180 and 360 min of coronary artery occlusion. The peptide was observed in the alveolar epithelium, mainly in type II pneumocytes, epithelium of bronchiole and the vascular walls. The preprotachykinin mRNA was mainly observed in the dendrites of nerve cells in the alveolar wall, the bronchiole and the pulmonary vessels and the basal lamina of the bronchiole. Pre-treatment of the animals with epidural local anesthetic could completely abolish the up-regulation of SP in the lungs and the dorsal root ganglia. CONCLUSIONS: The findings may suggest the involvement of substance P in the pathology of cross-talk between the heart and lungs in acute myocardial ischemia and infarction. Neural mechanism may be involved in the up-regulation of substance P in the lungs.