Background: Among discharged COVID-19 patients, the health-related quality of life is poor, and patients suffer from significant physical and psychological impairment. This study was designed to investigate the effects of Liuzijue exercise on the rehabilitation of COVID-19 patients. Methods: Thirty three eligible patients with COVID-19 were enrolled in the study after discharge. All the participants practiced Liuzijue exercise once per day for 20 minutes over 4 weeks. Data were collected at baseline and the end of the intervention. Primary outcomes involved functional capacity and secondary outcomes involved quality of life. Results: The maximal inspiratory pressure (MIP), peak inspiratory flow (PIF), and diaphragm movement in deep breathing (DM-DB) of patients increased significantly after 4 weeks of intervention. The dyspnea was also alleviated and exercise capacity was significantly improved. In terms of quality of life, physical functioning and role-physical scores were significantly increased. Moreover, Liuzijue could significantly alleviate the depression and anxiety status of the patients. Conclusion: Liuzijue exercise is a viable alternative home exercise program that produced better functional capacity and quality of life in discharged patients with COVID-19. These findings also showed the necessity of rehabilitation intervention for cured COVID-19 patients.

The results from the published studies on the relationship between GSTM1/GSTT1 null genotypes and renal cell carcinoma (RCC) risk are still conflicting. This meta-analysis was performed to evaluate the relationship between GSTM1/GSTT1 null genotypes and RCC susceptibility. Association studies were identified from the databases of PubMed, Embase, Cochrane Library, and CBM-disc (China Biological Medicine Database) on 1 February 2012, and eligible investigations from 1950 to 2012 were synthesized using meta-analysis method. Results were expressed as odds ratios (ORs) for dichotomous data, and 95% confidence intervals (CIs) were also calculated. Six studies were identified for the analysis of association between polymorphic deletion of GSTM1/GSTT1 and RCC risk. There was no association between GSTM1/GSTT1 null genotype and RCC susceptibility (GSTM1: N = 6, p-heterogeneity = 0.07, OR = 1.07, 95% CI: 0.85-1.35, p = 0.57; GSTT1: N = 6, p-heterogeneity < 0.00001, OR = 0.98, 95% CI: 0.58-1.65, p = 0.94). Interestingly, null genotype of GSTT1 was associated with RCC risk in Caucasians and Asians (Caucasians: N = 4, p-heterogeneity = 0.38, OR = 0.76, 95% CI: 0.61-0.95, p = 0.01; Asians: N = 1, OR = 2.39, 95% CI: 1.63-3.51, p < 0.00001). For the GSTM1-GSTT1 interaction analysis, the dual null genotype of GSTM1/GSTT1 was not significantly associated with RCC susceptibility (N = 4, p-heterogeneity = 0.006, OR = 1.17, 95% CI: 0.98-1.39, p = 0.09). However, the dual null genotype of GSTM1-GSTT1 was associated with RCC risk in Asians (N = 1, OR = 2.06, 95% CI: 1.36-3.13, p = 0.007). In conclusion, our study results suggest that GSTT1 null genotype is associated with the RCC susceptibility in Caucasians and Asians, and the dual null genotype of GSTM1-GSTT1 is associated with RCC risk in Asians. However, more genetic epidemiological investigations are required to further explore this relationship.

Long noncoding RNAs (lncRNAs) play a crucial role in several malignances, involving nasopharyngeal carcinoma (NPC), a heterogeneous disease. This study investigated mechanism of serine/arginine repetitive matrix protein 2‐alternative splicing (SRRM2‐AS) in NPC cell proliferation, differentiation, and angiogenesis. Initially, differentially expressed lncRNAs were screened out via microarray analysis. Vascular endothelial growth factor (VEGF) protein positive rate and microvessel density (MVD) were determined in NPC and adjacent tissues. NPC CNE‐2 cells were treated with a series of vector and small interfering RNA to explore the effect of SRRM2‐AS in NPC. The target relationship between myosin light chain kinase (MYLK) and SRRM2‐AS was verified. Levels of SRRM2‐AS, MYLK, cGMP, PKG, VEGF, PCNA, Ki‐67, B‐cell lymphoma‐2 (Bcl‐2), Bcl‐2‐associated X protein (Bax), and Caspase 3 were determined after transfection. Finally, the effect of SRRM2‐AS on cell proliferation, colony formation, angiogenesis, cell cycle, and apoptosis in NPC was evaluated. SRRM2‐AS was highly expressed and MYLK was poorly expressed in NPC tissues. VEGF protein positive rate and MVD were elevated in NPC tissues. MYLK was confirmed to be a target gene of SRRM2‐AS. Silencing of SRRM2‐AS elevated levels of MYLK, cGMP, PKG, Bax, and Caspase 3, but decreased levels of VEGF, PCNA, Ki‐67, and Bcl‐2. Especially, silencing of SRRM2‐AS suppressed cell proliferation, colony formation and angiogenesis, blocked cell cycle, and enhanced cell apoptosis in NPC. Our results suggested that silencing of SRRM2‐AS protected against angiogenesis of NPC cells by upregulating MYLK and activating the cGMP‐PKG signaling pathway, which provides a new target for NPC treatment.

The present study investigated the preventive effects of microRNA (miR)‑146a against severe burn‑induced remote acute lung injury (ALI) in rats and the underlying mechanism. The surface area of the skin was immersed in 100˚C water for 5‑10 sec on the dorsal surface. The expression level of miR‑146a was significantly downregulated in rats with burn‑induced ALI. Downregulation of miR‑146a increased inflammation, and inducible nitric oxide synthase (iNOS) and cyclooxygenase‑2 (COX‑2) expression in a model of ALI in vitro via the promotion of the Toll‑like receptor (TLR)4/nuclear factor (NF)‑κB signaling pathway. In addition, the overexpression of miR‑146a reduced inflammation, and iNOS and COX‑2 protein expression in the model of ALI in vitro via the suppression of the TLR4/NF‑κB signaling pathway. A TLR4 inhibitor reduced the function of anti‑miR‑146a on inflammation in the model of ALI. Collectively, the results of the present study demonstrated the preventive effects of miR‑146a against severe burn‑induced remote ALI in rats through the anti‑inflammatory‑regulated TLR4/NF‑κB signaling pathway.

Long non-coding RNAs (lncRNAs) are associated with the healing of burn wounds in the dermis. The present study aimed to probe the role and regulatory network of the lncRNA TPT1 antisense RNA 1 (TPT1-AS1) in human dermal fibroblasts (HDFs) following thermal injury. A model of thermally injured cells was constructed with HDFs. The levels of TPT1-AS1, microRNA (miR)-324-5p and cyclin-dependent kinase (CDK)16 were determined through reverse transcription-quantitative PCR. Cell viability, cell cycle distribution, cell apoptosis rate and extracellular matrix (ECM) synthesis were assessed with a series of in vitro gain-of-function experiments and MTT, flow cytometry and western blot analyses. The binding ability of miR-324-5p and TPT1-AS1 (or the 3' untranslated region of CDK16) was identified via bioinformatics analysis and luciferase reporter assay. It was found that TPT1-AS1 and CDK16 were downregulated, but miR-324-5p was upregulated, in the HDFs after thermal injury. TPT1-AS1 elevation induced cell viability and ECM synthesis but attenuated cell cycle arrest at the G 0 /G 1 stage and decreased the cell apoptosis rate of thermally injured HDFs. In addition, TPT1-AS1 sponged miR-324-5p to modulate CDK16 expression. Moreover, silencing CDK16 weakened the impacts of TPT1-AS1 upregulation on cell function and ECM synthesis in heat-treated HDFs. In summary, TPT1-AS1 relieved cell injury and induced ECM synthesis by sponging miR-324-5p and targeting CDK16 in the HDFs after thermal injury, implying a protective role for TPT1-AS1 in the burn wound healing process.