The condition of patients with severe traumatic brain injury (sTBI) complicated by corona virus 2019 disease (COVID-19) is complex. sTBI can significantly increase the probability of COVID-19 developing into severe or critical stage, while COVID-19 can also increase the surgical risk of sTBI and the severity of postoperative lung lesions. There are many contradictions in the treatment process, which brings difficulties to the clinical treatment of such patients. Up to now, there are few clinical studies and therapeutic norms relevant to sTBI complicated by COVID-19. In order to standardize the clinical treatment of such patients, Critical Care Medicine Branch of China International Exchange and Promotive Association for Medical and Healthcare and Editorial Board of Chinese Journal of Trauma organized relevant experts to formulate the Chinese expert consensus on clinical treatment of adult patients with severe traumatic brain injury complicated by corona virus infection 2019 ( version 2023) based on the joint prevention and control mechanism scheme of the State Council and domestic and foreign literatures on sTBI and COVID-19 in the past 3 years of the international epidemic. Fifteen recommendations focused on emergency treatment, emergency surgery and comprehensive management were put forward to provide a guidance for the diagnosis and treatment of sTBI complicated by COVID-19.

Objective:To explore the role of long non-coding RNA (LncRNA) AC000061.1 involved in the pathogenesis of nonobstructive azoospermia (NOA) by regulating the CFTR gene expression. Methods:Bioinformatics analysis was conducted with the use of gene microarray to screen the differentially expressed LncRNAs and corresponding mRNAs in the testicular tissue of patients in three groups including obstructive azoospermia (OA) group ( n=50), NOA group ( n=50), and control group ( n=50). The expression of apoptosis-related gene Bcl-2 in the testicular tissue of patients in these three groups was detected by qRT-PCR and Western blotting. Additionally, qRT-PCR was performed to determine the expression of LncRNA AC000061.1 and CFTR mRNA in the testicular tissue, serum, and seminal plasma of patients in the three groups, and enzyme-linked immunosorbent assay (ELISA) was conducted to detect the CFTR protein level in the serum and seminal plasma. LncRNA AC000061.1 overexpression (H-LncRNA group) and silencing vectors (Si-LncRNA group) and empty vectors were constructed and transfected into the testicular cancer cell line NTERA-2. Subsequently, the expression of LncRNA AC000061.1 and CFTR mRNA was determined by qRT-PCR, and CFTR protein expression was measured by Western blotting assay. Cell proliferation was assessed using CCK-8 and cell apoptosis was evaluated by flow cytometry and TUNEL. Results:Microarray analysis and qRT-PCR showed that the expression of LncRNA AC006100.1 and CFTR decreased in NOA group compared with control group ( P=0.033 and P=0.042). But there was no difference in the expression of LncRNA AC000061.1 between OA group and control group, while CFTR in OA group was lowly expressed compared with that in control group ( P=0.039). Bcl-2 expression was sequentially upregulated in OA and NOA groups relative to normal control group ( P=0.031 and P=0.008). No significant difference was noted in the serum levels of LncRNA AC000061.1 and CFTR mRNA and protein among the three groups ( P>0.05). The results also showed sequentially decreased levels of LncRNA AC000061.1 and CFTR mRNA and protein in seminal plasma in NOA and OA groups when compared with control group ( P=0.002, P=0.038 and P=0.006, P=0.026) and a positive correlation of LncRNA AC000061.1 expression with CFTR mRNA expression ( r=0.169, P=0.039). LncRNA AC000061.1 and CFTR mRNA and protein expression decreased in Si-LncRNA group ( P=0.005, P=0.003), but significantly increased in H-LncRNA group ( P=0.002, P=0.009). Furthermore, cell proliferation was significantly repressed while apoptosis rate was elevated in Si-LncRNA group ( P=0.003 and P=0.001). On the contrary, enhanced cell proliferation and inhibited apoptosis were observed in H-LncRNA group ( P=0.017 and P=0.017). Conclusion:LncRNA AC00006.1 in the testicular tissue of NOA patients induced abnormal cell proliferation and apoptosis via mediating CFTR gene expression, thereby participating in the pathogenesis of NOA.

Objective:To explore the role of long non-coding RNA (LncRNA) AC000061.1 involved in the pathogenesis of nonobstructive azoospermia (NOA) by regulating the CFTR gene expression. Methods:Bioinformatics analysis was conducted with the use of gene microarray to screen the differentially expressed LncRNAs and corresponding mRNAs in the testicular tissue of patients in three groups including obstructive azoospermia (OA) group ( n=50), NOA group ( n=50), and control group ( n=50). The expression of apoptosis-related gene Bcl-2 in the testicular tissue of patients in these three groups was detected by qRT-PCR and Western blotting. Additionally, qRT-PCR was performed to determine the expression of LncRNA AC000061.1 and CFTR mRNA in the testicular tissue, serum, and seminal plasma of patients in the three groups, and enzyme-linked immunosorbent assay (ELISA) was conducted to detect the CFTR protein level in the serum and seminal plasma. LncRNA AC000061.1 overexpression (H-LncRNA group) and silencing vectors (Si-LncRNA group) and empty vectors were constructed and transfected into the testicular cancer cell line NTERA-2. Subsequently, the expression of LncRNA AC000061.1 and CFTR mRNA was determined by qRT-PCR, and CFTR protein expression was measured by Western blotting assay. Cell proliferation was assessed using CCK-8 and cell apoptosis was evaluated by flow cytometry and TUNEL. Results:Microarray analysis and qRT-PCR showed that the expression of LncRNA AC006100.1 and CFTR decreased in NOA group compared with control group ( P=0.033 and P=0.042). But there was no difference in the expression of LncRNA AC000061.1 between OA group and control group, while CFTR in OA group was lowly expressed compared with that in control group ( P=0.039). Bcl-2 expression was sequentially upregulated in OA and NOA groups relative to normal control group ( P=0.031 and P=0.008). No significant difference was noted in the serum levels of LncRNA AC000061.1 and CFTR mRNA and protein among the three groups ( P>0.05). The results also showed sequentially decreased levels of LncRNA AC000061.1 and CFTR mRNA and protein in seminal plasma in NOA and OA groups when compared with control group ( P=0.002, P=0.038 and P=0.006, P=0.026) and a positive correlation of LncRNA AC000061.1 expression with CFTR mRNA expression ( r=0.169, P=0.039). LncRNA AC000061.1 and CFTR mRNA and protein expression decreased in Si-LncRNA group ( P=0.005, P=0.003), but significantly increased in H-LncRNA group ( P=0.002, P=0.009). Furthermore, cell proliferation was significantly repressed while apoptosis rate was elevated in Si-LncRNA group ( P=0.003 and P=0.001). On the contrary, enhanced cell proliferation and inhibited apoptosis were observed in H-LncRNA group ( P=0.017 and P=0.017). Conclusion:LncRNA AC00006.1 in the testicular tissue of NOA patients induced abnormal cell proliferation and apoptosis via mediating CFTR gene expression, thereby participating in the pathogenesis of NOA.

OBJECTIVE: Evaluation of different repair mechanism and influencing factors for Prognosis of tympanic membrane perforations. METHOD: One hundred and twelve female patients of tympanic membrane perforations were randomly divided into two groups: control group (natural repair group) and treatment group (gelatin sponge patch bonded repair group). The perforation healing were dynamically observed in two groups by endoscope. RESULT: The result show that low, medium and high perforations healing rates were 100.00%, 90.48%, 93.33%. The healing time of low, medium and high was (9.0 +/- 2.8) d, (13.0 +/- 2.6) d, (22.0 +/- 4.7) d, the epithelial layer reverse growth in 5 cases. The result show that low, medium and high perforations healing rates were 91.67%, 95.24%, 84.62%. The healing time of low, medium and high was (11.0 +/- 3.7) d, (24.0 +/- 3.8) d, (36.0 +/- 2.1) d, 2 cases were undergone surgeries. CONCLUSION There are differences in repair mechanism between natural repair and patch bonded repair patch bonded repair can promote granulation hyperplasia, it can help recovering and lessening the patient's conductive hearing loss and occasional tinnitus. granulation hyperplasia and the healing time is closely related. The epithelial layer reverse growth may affect the healing of tympanic membrane perforation.
Adult ; Female ; Humans ; Middle Aged ; Tympanic Membrane Perforation ; etiology ; therapy ; Wound Healing ; Young Adult

Objective To discuss wound edge characteristics at different clinical periods and in-tervention of traumatic perforation of tympanic membrane. Methods A total of 494 patients wth trau-matic perforation of tympanic membrane were treated and grouped based on treatment time and size of per-foration. Group A (n = 154, within 12 hours after injury) were treated by residual tympanic membrane repair and gelfoam. Group B (n =149, 12 hours after injury) were treated by simple gelfoam. Group C (n = 116) and Group D (n =75) were treated by conventional therapy. The wound healing of peroration was observed after one month. Results Of all, there were 419 patients with maximum perforation diameter > 2.5 mm within five hours after injury, of which 349 patients (83.3%) were with residual tympanic membrane valgus of perforation rim, 29 (6.9%) with involution of perforation rim and 41 (9.8%) with complete loss of tympanic membrane. Of 75 patients with maximum perforation diameter <2.5 ram, residual valgus of perforation rim was found in 18 (24.0%) and tympanic membrane wrinkle near wound edge in the other patients. Under endoscopic repair of crimp tympanic membrane, maximum perforation diameter was reduced for (6.5±2.5)mm in 143 patients at 6th hour, (6.0±1.5)mm in 11at 7-11 hours, (2.0±1.5) mm in 27 at 13-24 hours, (1.5±1.0) mm in 59 at 25.5-48 hours, (1.0±0.5) mm in 49 at 51-73 hours and 0 mm in 14 at 75-192 hours. The follow up lasted for one month, which showed that healing rate of perforation in groups A, B, C and D were 85.3%, 71.2%, 59.2% and 81.4%, respectively. Healing time span was (10±4) days, (19±4) days, (25±2) days and (16±2) days, respectively. Conclusions Traumatic perforation of tympanic membrane is not com-plete tympanal deletion but residual tympanic membrane valgus of perforation rim,involution and tympanicmembrane crushing, which shows insignificant change with time. In time repair of residual tympanic membrane 12 hours(especially 6 hours) after injury may reduce the largest diameter of perforation and re-markably shorten the healing time of perforation.