Research advances in myocardial injury caused by COVID-19.

Coronavirus disease 2019 (COVID-19) caused a large-scale infection in China at the end of 2019. The virus, named severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has the characteristics of strong transmission capacity, diverse clinical manifestations, long incubation period, strong infection in incubation period, etc. With the increase of the number of cases and the continuous improvement of clinical data, we found that patients with COVID-19 have myocardial injury besides typical respiratory system manifestations. According to published data, we summarized the clinical manifestations of myocardial injury in COVID-19 patients, and discussed the probable injury mechanism, treatment methods and future research directions.

Efficacy of continuous positive airway pressure treatment in treating obstructive sleep apnea hypopnea syndrome associated with carotid arteriosclerosis.

Sleep apnea negatively impacts patients' ability to oxygenate the bloodstream during sleep and has far-reaching, deleterious effects. The present study sought to assess the correlation between obstructive sleep apnea hypopnea syndrome (OSAHS), carotid atherosclerosis, and blood pressure variability (BPV), and to evaluate the therapeutic effects of continuous positive airway pressure (CPAP). Patients with OSAHS were classified as mild, moderate, or severe according to their condition and compared with healthy control participants. CPAP treatment was used to treat patients with OSAHS for 6 months. Prior to CPAP treatment, the apnea-hypopnea index (AHI), lowest blood oxygen saturation (LSaO2), carotid intima media thickness (IMT), and plasma levels of endothelin-1 (ET-1), nitric oxide (NO), and tumor necrosis factor-α (TNF-α) were measured in all participants, along with the low frequency components of BPV (BPV LF). The results demonstrated that carotid IMT, AHI, plasma ET-1, and plasma TNF-α were significantly higher in patients with OSAHS than those in the control group (P<0.05); whereas LSaO2 and plasma NO levels were significantly higher in the control group (P<0.05). The degree to which these indices differed was associated with the severity of OSAHS. Furthermore, the carotid IMT of patients with OSAHS was significantly correlated with AHI (P=0.037), plasma ET-1 (P=0.001), plasma NO (P<0.001), BPV LF before retiring (P<0.001). Following CPAP treatment, the observation indices of patients with moderate or severe OSAHS improved significantly (P<0.01). These results support the use of CPAP to improve the significant vascular endothelial dysfunction, increased inflammatory response, and high blood pressure variability correlated with carotid atherosclerosis observed in patients with OSAHS.

Suppression of EGFR-STAT3 signaling inhibits tumorigenesis in a lung cancer cell line.

Overactive epidermal growth factor receptor (EGFR) signaling often underlies the rapid expansion of cancerous tissue. EGFR signaling is mediated by transcription factor signal transducer and activator of transcription 3, or STAT3. This study sought to investigate the effects of altered EGFR/STAT3 signal transduction on lung cancer cells in vitro. Lung cancer cells from the cell line A549 were divided into test and control groups. Test group cells were treated with an EGFR monoclonal antibody, Nimotuzumab, while control cells received no treatment. EGFR and STAT3 protein expression, cell apoptosis rate, cell proliferation, cell invasion, and cell division were analyzed and compared. Compared to cells in the control group, lung cancer cells treated with Nimotuzumab showed slowed proliferation rates, accelerated apoptosis, decreased invasion, and arrested cell division (P < 0.05). In conclusion, altered EGFR/STAT3 signaling results in significant changes in the biology of lung cancer cells.

Effects of the recombinant allergen rDer f 2 on neuro-endocrino-immune network in asthmatic mice.

Severe and life-threatening side effects can occur in patients receiving allergen-specific immunotherapy (SIT), and recombinant allergens made from cDNA have been used in clinical trials for ten years and appear promising for SIT. The aim of this study is to explore the effects of the recombinant allergen Der f 2 (the group 2 allergen from Dermatophagoides farinae) on the neuro-endocrino-immune network in asthmatic mice. Twenty-eight mice were divided into four groups - A, B, C and D. To induce asthma, a crude extract of D. farinae was injected intraperitoneally into the mice in groups B, C and D. Later, the crude extract or recombinant allergen rDer f 2 was given to groups C and D, respectively. Normal saline was given to groups A and B. Serum corticotropin-releasing hormone (CRH), adrenocorticotropic hormone (ACTH), corticosterone (CORT), interleukin 4 (IL-4), and interferon γ (IFN-γ) were detected by immunoassay and the pathological change of lung tissue was observed by hematoxylin and eosin (HE) staining. Serum CRH, ACTH, CORT, and IFN-γ were highest in healthy group A but lowest in asthma group B. Treatment with the crude extract or recombinant allergen rDer f 2 significantly attenuated this response in asthmatic mice, but there was no difference between the two treatments (p > 0.05). Serum IL-4 was elevated in asthma group B but lowest in healthy group A. Treatment with the crude extract or recombinant allergen rDer f 2 significantly attenuated this response in asthmatic mice, but there was no significant difference between the two treatments (p > 0.05). However, lung pathology as measured histologically (Underwood Score) showed that rDer f 2-treatment was significantly better than crude extract treatment (p < 0.05). In brief, recombinant allergen Der f 2 can strengthen the function of hypothalamus-pituitary-adrenal (HPA) axis, affect the balance of Th1 and Th2 cytokines, and reduce pulmonary inflammation in asthmatic mice.

Cloning, expression, and analysis of a cDNA coding for the Dermatophagoides farinae group 21 (Der f 21) allergen.

Domestic mite species like Dermatophagoides farinae induce allergies in people worldwide. Here, the cDNA coding for group 21 allergen of Dermatophagoides farinae (Hughes; Acari: Pyroglyphidae) from China was cloned, sequenced, and expressed in E. coli to aid in the development of diagnostic and treatment options for domestic mite hypersensitivity. First, the Der f 21 cDNA fragment was synthesized by RT-PCR; the confirmed full-length sequence comprised 411 nucleotides. The cDNA was ligated to the vector pCold-TF to construct an expression plasmid, pCold-TF-Der f 21. pCold-Tf-Der f 21 was transformed into E. coli BL21 cells, and its expression was induced by IPTG treatment. SDS-PAGE showed a specific band at the predicted molecular weight of Der f 21, demonstrating its successful expression. The recombinant fusion protein was obtained and its structure and molecular weight were confirmed by MALDI-TOF/TOF. Bioinformatics analysis revealed that the protein contained a signal peptide of 17 amino acids. The molecular weight of the mature Der f 21 allergen was approximately 14.16 kDa with a theoretical pI of 4.87. Its predicted secondary structure comprises a-helix (84.03%), extension chain (1.68%), and random coil (14.29%). The successful cloning of Der f 21 and a basic bioinformatics analysis of the protein provide a foundation for further study of this allergen in diagnosis and treatment of domestic mite hypersensitivity.

HMGB1 and RAGE levels in induced sputum correlate with asthma severity and neutrophil percentage.

Previous work indicated that high mobility group box-1 (HMGB1) protein may be involved in neutrophilic asthma. Here, we sought to investigate the correlation between HMGB1 and one of its receptors, receptor for advanced glycosylation end products (RAGE), with the severity of bronchial asthma. Compared to the control group (30 healthy individuals), patients in the asthma group (n=72) exhibited a higher percentage of neutrophils and higher HMGB1 and RAGE levels in induced sputum samples (P<0.05). Concurrently, FEV(1)% was significantly lower in the asthma group (P<0.05). Further, compared to mild and moderate asthma, in patients with severe asthma ACQ scores, the percentage of neutrophils, and HMGB1 levels were significantly higher, while FEV(1)% was significantly lower (P<0.05). The percentage of neutrophils and HMGB1 and RAGE levels were lower after treatment than before treatment (P<0.05). Finally, negative correlations were observed between HMGB1 or RAGE levels and FEV(1)% (r=-0.777 and r=-0.291, P<0.05), and positive correlations were detected between HMGB1 or RAGE levels and percentage of neutrophils (r=0.803 and r=0.326, P<0.05). Additionally, positive correlations were observed between HMGB1 and RAGE levels within the asthma group (r=0.306, P<0.05). Therefore, HMGB1 protein levels correlate with the severity of asthma, and HMGB1 may contribute to the inflammatory process of asthma.

[The effect of positive pressure ventilation combined with diaphragm pacing on respiratory mechanics in patients with respiratory failure].

OBJECTIVE: To observe the effects of combining positive pressure ventilation with diaphragm pacing on respiratory mechanics in patients with respiratory failure. METHODS: Twenty patients with central respiratory failure were studied with cohorts. The effects on respiratory mechanics were respectively observed in patients in control group, in whom ventilation by positive pressure only, and patients in experimental group in whom ventilation was instituted by combining positive pressure ventilation with diaphragm pacing. RESULTS: Compared with control group, mean airway pressure (Paw, cm H(2)O, 1 cm H(2)O= 0.098 kPa) and plateau pressure (Pplat, cm H(2)O) were significantly decreased in experimental group (Paw: 6.1±1.3 vs. 7.3±1.8; Pplat: 10.4±2.5 vs. 12.1±2.6, both P<0.05), while the negative value of peak esophageal pressure (P(PEAK ES) , cm H(2)O), the negative value of the difference between peak and basic esophageal pressure (dP(ES), cm H(2)O), transpulmonary pressure at end of inspiration hold (Ptp plat, cm H(2)O ), static compliance (Cst, ml/cm H(2)O) were significantly increased in experimental group (P(PEAK ES): -8.3± 1.9 vs. -3.2±1.4; dP(ES) : -11.2±2.6 vs. -8.2±2.2; Ptp plat: 23.6±3.8 vs. 15.6±3.1; Cst: 52.7±8.2 vs. 48.3±7.2, all P<0.05). No differences were found in airway resistance (Raw, cm H(2)O×L(-1) ×s(-1) ) and lung resistance (R(L), cm H(2)O×L(-1) ×s(-1) ) between experimental group and control group (Raw: 2.1±0.5 vs. 2.3±0.4; R(L): 2.9±0.6 vs. 3.1±0.5, both P>0.05). Work of breath by patient (WOBp, J/L) was significantly increased and work of breath by ventilator (WOBv, J/L) was significantly decreased in experimental group compared with control group (WOBp: 0.18±0.03 vs. 0; WOBv: 0.31±0.07 vs. 0.53±0.11, both P<0.05). CONCLUSION: Compared with positive pressure ventilation , positive pressure ventilation combined with diaphragm pacing can decrease the Paw, increase intrathoracic negative pressure, transpulmonary pressure, and Cst, and decrease WOBv, while there is no effect on Raw and R(L).