The signal axis GATA2-EDN1-AGT induced hypertension from obstructive sleep apnea-hypopnea syndrome with the clinical and animal study

Hypertension occurred in 50% obstructive sleep apnea-hypopnea syndrome (OSAHS) patients meanwhile OSAHS occurred in 30% hypertension patients. The present study aimed to explore the molecular mechanism of GATA2-EDN1-AGT induced hypertension in the development of obstructive sleep apnea-hypopnea syndrome. OSAHS patients (56 cases: 36 cases of male, 20 cases of female, 42~60 years old) were divided into two groups (case group: patients with hypertension monitored by 24 h ambulatory blood pressure and polysomnography; control group: patients without hypertension). Wistar rats were used to establish the OSAHS model (narrow pharyngeal cavity). PaO2 and PaCO2 of patients and rats were measured by an automatic blood gas analyzer. The profile of total protein in the OSAHS group and normal group was evaluated. Protein-protein-interaction (PPI) was carried out to show all matter proteins related. The levels of EDN-1, AGTII and atrial natriuretic peptide (ANP) in blood samples of patients and rats were analyzed by enzyme-linked immunosorbent assay (ELISA). The expression of GATA2, EDN1, endothelin-converting enzyme 1 (ECE-1) and AGTⅡ was measured. The results showed that SaO2 and AHI were positively associated with systolic pressure (P<0.05) in OSAHS patients. There was no correlation among other indexes (P>0.05). It was also observed that GATA2 had a strong relationship with AGTⅡ and EDN1. The results of ELISA presented that the levels of EDN1, AGTⅡ and ANP in the OSAHS group of human and animal models were significantly increased (P<0.05). The results of immunochemistry showed that the expression of GATA2 and AGTⅡ in the vascular of OSAHS group was upregulated manifestly (P<0.05). It was concluded that OSAHS can induce AHI, which increases hypertension via the GATA2-EDN1-AGT Ⅱ axis.

Expression Profile Analysis and Image Observation of miRNA in Serum of Patients with Obstructive Sleep Apnea-Hypopnea Syndrome

The expression profile and image observation of miRNA in serum of patients with obstructive sleep apnea-hypopnea syndrome were investigated. Bioinformatics methods were used to explore the molecular mechanism of obstructive sleep apnea-hypopnea syndrome (OSAHS)-related hypertension and explore the differentially expressed core miRNAs and regulatory factors, providing a theoretical basis for seeking molecular targets for clinical diagnosis and treatment. The miRNA datasets of patients with OSAHS and those with hypertension were downloaded from the public database to obtain differentially expressed miRNAs and explore the biological processes and pathways involved in the target genes. The core miRNAs and competitive endogenous RNA (ceRNA) transcription factors (TFs) were obtained by database mining and Cytoscape network analysis. The results showed that 2,579 differentially expressed miRNAs were obtained from the GSE112093 dataset. Seven upregulated miRNAs (hsa-miR-7107-5p, hsa-miR-7110-5p, hsa-miR-595, hsa-miR-1268b, hsa-miR-3064-5p, hsa-miR-68565p, and hsa-miR-1180-3p) and one downregulated miRNA (hsa-miR-22-3p) were obtained from the GSE112093 dataset. It is proved that hsa-miR-22-3p, hsa-miR-595, hsa-miR-6856-5pKcnq1ot1, neat1, Tsix, ERG, kdm2b, and Runx1 may be involved in the pathogenesis of OSAHS-related hypertension, which provided a theoretical basis for the mechanism research and clinical treatment of OSAHS.

Edaravone mitigates cognitive impairment and hippocampal injury in juvenile rats with obstructive sleep apnea hypopnea syndrome via regulation of cAMP/PKACREB pathway

Purpose: To investigate the influence of edaravone on cognitive impairment and hippocampal injury in juvenile rats with obstructive sleep apnea hypopnea syndrome (OSAHS), and the mechanism involved.Methods: Fifty-four young Wistar rats were randomly selected into control, intermittent hypoxia and edaravone groups. The contents of the antioxidants CAT, Mn-SOD, Cu/Zn SOD and oxidative stress products malondialdehyde (MDA) in hippocampus were assayed and compared. The expressions of brain-derived neurotrophic factor (BDNF), Bcl-2, CREB, p-CREB and PKAc were determined.Results: The times taken to cross the target quadrant and the platform; levels of CAT and Mn-SOD, as well as protein levels of BNDF, Bcl-2, p-CREB and PKAc were markedly lower in intermittent hypoxia group than in controls; and MDA contents, 8-OHdG and protein hydroxyl were markedly higher in intermittent hypoxic rats group than in controls. Time taken to cross the platform and quadrant; activities of CAT and Mn-SOD, and protein concentrations of BDNF, Bcl-2, p-CREB and PKAc were markedly higher in the edaravone-treated rats than in intermittent hypoxia rats.Conclusion: Edaravone significantly mitigated cognitive damage and hippocampal lesions in OSAHS rats via a mechanism related to alleviation of oxidative stress and up-regulation of the expressions of p-CREB and its downstream proteins BDNF and Bcl-2. This finding provides a theoretical basis for research and development of new drugs against OSAHS.

Severe obesity in a patient on long-term treatment of chronic myeloid leukemia with imatinib: Body composition, associated disorders and outcome

Chronic Myeloid Leukemia (CML) is a highly curable malignancy with tyrosine kinase inhibitors (TKI) as target therapy. As treatment is usually prolonged, there is a need to improve our knowledge about the impact of comorbidities in this context. Severe obesity is among the common comorbidities in these patients. We present the case of a patient with morbid obesity and associated sleep apnea hypopnea syndrome who was succesfully treated during 14 years with imatinib, a cornerstone TKI for this disease. Visceral fat area was extremely elevated in this patient. Keywords: chronic myeloid leukemia; obesity; imatinib; sleep apnea hypopnea syndrome. Abbreviations: CML: Chronic Myeloid Leukemia; BMI: Body Mass Index; TKI: Tyrosine Kinase Inhibitors.

STOP-Bang as a predictor of obstructive sleep apnea-hypopnea syndrome in outpatients

The STOP-Bang has been promoted as a valuable tool for identifying obstructive sleep apnea-hypopnea syndrome (OSAHS) in medical and surgical patients. However, its performance in Colombian samples is unknown. The objective of this study was to determine the clinimetric performance of the STOP-Bang index versus the study of polysomnography in patients from Santa Marta, Colombia. An accuracy study of diagnostic tests with a test-based approach was designed. Seven hundred sixty-two adults referred for polysomnography to evaluate OSAHS were included in the research. They were aged between 18 and 94 years old (mean=47.2, SD=13.4), 63.3% were men, and 46.5% were classified as obese. The STOP-Bang performance was compared against the best reference criterion, the hypopnea/apnea index determined by polysomnography. The diagnosis of OSAHS was confirmed in 461 (60.5%) and corroborated in 301 (39.5%). The area under the curve was 0.70 (95%CI 0.66-0.74), and the best cut-off point was 4, with a sensitivity of 79.2%, a specificity of 53.5%, the positive predictive value of 72.2%, the negative predictive value of 62.6%, positive likelihood ratio was 1.70, negative likelihood ratio was 0.39; OR=4.08 (CI95% 2.99-5.56) and Cohen's kappa of 0.33. As conclusions, performance indicators show that STOP-Bang...

An Exploratory Study on the Treatment of Obstructive Apnea-Hypopnea Syndrome by Nasal Cavity Expansion

Background. Respiratory disorder is a disease with a very high incidence, in which obstructive apnea-hypopnea syndrome is the most harmful. It has become a common and frequently occurring disease, which seriously influences the health of the affected population. The pathogenesis of obstructive sleep apnea/hypopnea syndrome (OSAHS) is numerous. With the continuous research on OSAHS disease, it has been found that one of its main pathogeneses is caused by the anatomical characteristics of upper airway obstruction induced during sleep. The narrowing and collapse of any plane can affect the ventilation of the upper respiratory tract. In recent years, with the deepening of research, the importance of the upper respiratory tract obstruction as a source of the disease has attracted increasing attention. Nasal stenosis can cause increased nasal resistance, increased pharyngeal inhalation negative pressure, soft palate collapse, and narrow pharyngeal cavity, resulting in open mouth breathing, which can be the initiating factor of the upper airway obstruction. With the development and popularization of nasal endoscopy technology, domestic and foreign scholars have reported more on the treatment of rhinogenic OSAHS with nasal cavity expansion, but they are different. There is still more controversy; the main controversy centered on the effective rate of surgical treatment and the improvement of objective indicators. Therefore, this study performed individualized nasal cavity expansion for patients with OSAHS who are mainly rhinogenic, from subjective symptoms, objective indicators, and effective rate of surgery. Methods and Patients. Conduct research and analysis to provide references for the clinical treatment of such patients. For patients with the obstructive apnea-hypopnea syndrome with nasal congestion, individualized nasal cavity expansion was performed to study the clinical effect of nasal cavity expansion in the treatment of OSAHS. This article mainly screens cases through big data and selects a large hospital in China to perform individualized nasal cavity expansion surgery to treat 43 adult OSAHS patients with nasal congestion. Results. There are uploaded sleep monitoring, nasal reflex, nasal resistance, and nasal symptoms before and after surgery. Conclusion. Spirometer examination records, along with apnea-hypopnea index and minimum arterial blood oxygen saturation, the minimum cross-sectional area of the nasal cavity, nasal cavity volume, nasal airway resistance, total nasal respiratory volume, and other information. Also we fill in the nasal obstruction symptom assessment scale, sleepiness scale, and study and analyze the surgical effect of nasal cavity expansion.