Objective To investigate the prevalence of obstructive sleep apnea-hypopnea syndrome(OSAHS)combined with metabolic syndrome(MS),and analyze the related factors affecting OSAHS combined with MS.Methods Totally 290 patients with OSAHS hospitalized in the First Affiliated Hospital of Baotou Medical College and diagnosed as OSAHS were collected from August 2020 to October 2022.According to whether the patients were complicated with MS,they were divided into OSAHS combined with MS group and simple OSAHS group.According to apnea hypopnea index(AHI),the patients of OSAHS combined with MS group were divided into three subgroups:mild group,moderate group and severe group.The general condition,biochemical indicators and sleep parameters of patients were recorded,and the relevant factors affecting OSAHS with MS were determined by logistic regression analysis.Results(1)Among the 290 patients with OSAHS,the incidence of MS was 51.7%,male patients were more than female patients,and the peak of OSASH with MS was between 50 and 59 years old.(2)body mass index(BMI),systolic blood pressure,hypertension history,diabetes history,AHI,fasting blood glucose(FBG),triglyceride(TG),high density lipoprotein-cholesterol(HDL-C),uric acid(UA)were statistically different between the two groups(P<0.05);Logistic regression analysis showed that BMI,FBG,TG,HDL-C,UA,history of hypertension and history of diabetes were independent risk factors for OSAHS with MS(P<0.05).(3)There were statistically significant differences in gender,age,BMI,AHI,TG,HDL-C and UA among the three groups of OSAHS with MS with different severity(P<0.05).Logistic regression analysis showed that BMI,TG and HDL-C were independent risk factors affecting OSAHS with MS with different severity(P<0.05).Conclusion(1)The inpatients with OSAHS have a high incidence of MS.(2)OSAHS combined with MS is related to BMI,blood pressure,blood glucose,blood lipid,blood uric acid level and other factors.(3)Overweight and dyslipidemia play an important role in the process of inducing disease aggravation.

Patients with severe trauma require an extremely timely treatment and transfusion plays an irreplaceable role in the emergency treatment of such patients. An increasing number of evidence-based medicinal evidences and clinical practices suggest that patients with severe traumatic bleeding benefit from early transfusion of low-titer group O whole blood or hemostatic resuscitation with red blood cells, plasma and platelet of a balanced ratio. However, the current domestic mode of blood supply cannot fully meet the requirements of timely and effective blood transfusion for emergency treatment of patients with severe trauma in clinical practice. In order to solve the key problems in blood supply and blood transfusion strategies for emergency treatment of severe trauma, Branch of Clinical Transfusion Medicine of Chinese Medical Association, Group for Trauma Emergency Care and Multiple Injuries of Trauma Branch of Chinese Medical Association, Young Scholar Group of Disaster Medicine Branch of Chinese Medical Association organized domestic experts of blood transfusion medicine and trauma treatment to jointly formulate Chinese expert consensus on blood support mode and blood transfusion strategies for emergency treatment of severe trauma patients ( version 2024). Based on the evidence-based medical evidence and Delphi method of expert consultation and voting, 10 recommendations were put forward from two aspects of blood support mode and transfusion strategies, aiming to provide a reference for transfusion resuscitation in the emergency treatment of severe trauma and further improve the success rate of treatment of patients with severe trauma.

Objective : By observing the changes of interleukin-22 ( IL-22) ，signal transduction and transcriptional activator 3 (STAT3) ，fasting blood glucose ( FBG) and fasting insulin ( FINS) of rats under the circumstance of chronic intermittent hypoxia and reoxygenation，to explore the role of IL-22 / STAT3 pathway in insulin resistance in- duced by chronic intermittent hypoxia． Methods : 4 SD rats were randomly divided into control group (NC group) and intermittent hypoxia group ( CIH group) ，with 12 rats in each group．NC group was placed in normoxia environment for 12 weeks，while CIH group was first given intermittent hypoxia for 8 weeks and then resumed normoxia feeding until 12 weeks．FBG，FINS，IL-22 and p-STAT3 / STAT3 levels were measured at baseline，week 8 and week 12 in both groups，and insulin resistance index (HOMA-IR) was calculated．The differences between the two groups were compared. Results : ① There was no significant difference of the observation indexes between the two groups at baseline (P＞0. 05) ．At 8 weeks，the levels of FBG，FINS and HOMA-IR in CIH group were higher than those in NC group (P＜0. 05) ，and the levels of IL-22 were lower than those in NC group (P ＜0. 05) ．p-STAT3 / STAT3 showed a decreasing trend，but not statistically significant．At 4 weeks of reoxygenation，there were no significant differences in FBG，FINS，HOMA-IR and IL-22 levels between the two groups (P ＞0. 05 ) ．p-STAT3 / STAT3 in CIH group was significantly higher than that in NC group ( P ＜0. 05 ) . ② Spearman rank correlation analysis showed that HOMA-IR was negatively correlated with IL-22 and p-STAT3 / STAT3 ( all P ＜0. 05) ． Conclusion Chronic intermittent hypoxia can inhibit the expression of IL-22 / STAT3 signaling pathway，IL-22 / STAT3 signaling pathway may mediate insulin resistance induced by chronic intermittent hypoxia.

Objective : To investigate the role of endoplasmic reticulum stress in hepatic insulin resistance induced by intermittent hypoxia in rats． Methods : Twenty-four SD rats were randomly divided into control group ( NC group) and intermittent hypoxia group ( CIH group) ．The NC group was placed in a normoxia environment for 12 weeks，and the CIH group was given intermittent hypoxia for 8 weeks，and then returned to normoxia until the 12th week．In both groups，fasting blood glucose (FBG) ，fasting insulin (FINS) ，and liver inositol-requiring enzyme- 1 α(IRE1 α) ，X-box binding protein 1s(XBP1s) ，forkhead box transcription factor O1 (FoxO1) ，activating transcription factor-6(ATF6) ，cAMP-response element binding protein( CREB) ，CREB-regulated transcription coacti- vator-2( CRTC2) ，double-stranded RNA-dependent protein kinase-like ER kinase ( PERK) ，eukaryotic initiation factor 2 α(eIF2 α) ，protein kinase B ( AKT) ，phosphoenolpyruvate carboxykinase ( PEPCK) ，glucose-6-phosphat- ase( G6Pase) mRNA were measured at baseline，week 8，and week 12 . Results : There was no significant differ- ence in each observation index between the two groups at baseline ; at 8 weeks，the levels of FBG，FINS and the mRNA levels of IRE1α , XBP1s，ATF6，PERK，eIF2 α , PEPCK and G6Pase in the CIH group were higher than those in the NC group (P＜0. 05) ，while the mRNA levels of CREB，CRTC2 and AKT were lower than those in the NC group (P＜0. 05) ; at 12 weeks，there was no significant difference in each observation index between the two groups．Pearson correlation analysis showed(8th week of intermittent hypoxia group) : homeostasis model as- sessment-insulin resistance(HOMA-IR) was positively correlated with FoxO1，CREB，CRTC2 and PERK，eIF2 α mRNA levels (r = 0. 172，0. 595，0. 183，0. 702，0. 608 ; P＜0. 05) while it was negatively correlated with IRE1α , XBP1s，ATF6，AKT mRNA levels (r = －0. 422 ，－0. 327 ，－0. 309 ，－0. 399 ; P＜0. 05) ． Conclusion Intermittent hypoxia can lead to insulin resistance，and endoplasmic reticulum stress may mediate this effect.

ObjectiveTo investigate the potential mechanism of serum N-glycan alterations in patients with hepatitis B virus (HBV)-related hepatocellular carcinoma (HCC) by measuring serum N-glycan profile and comparing glycosyltransferase gene expression between HCC tissue and adjacent tissue. MethodsThe samples of HCC tissue, adjacent tissue, and normal liver tissue were collected from 34 patients with HBV-related HCC who were admitted to Chinese PLA General Hospital, and serum samples were also collected. Among these 34 patients, 8 were randomly selected and their serum samples were established as HCC experimental group, and the serum samples of 20 healthy adults were established as control group. DNA sequencer-aided fluorophore-assisted carbohydrate electrophoresis was used to analyze serum N-glycan profile in the HCC experimental group and the control group. Quantitative real-time PCR was used to measure the mRNA expression of 8 glycosyltransferase genes (FUT3, FUT4, FUT6, FUT7, FUT8, Gn-TIII, Gn-TIVa, and Gn-TV) in the HCC tissue and adjacent tissue of 34 patients with HBV-related HCC, and Western blot was used to measure the expression of corresponding proteins. The independent samples t-test was used for comparison of continuous data between two groups. ResultsCompared with the control group, the HCC experimental group had a significant increase in the abundance of N-glycan peak9 (NA3Fb) in serum(t=-2.514,P＜0.05). There were significant differences in the mRNA expression of FUT8, Gn-TIVa, and Gn-TV between HCC tissue and adjacent tissue, and the mRNA and protein expression levels of FUT8 and Gn-TV in HCC tissue were significantly higher than those in adjacent tissue (FUT8 mRNA: 1.50±0.34 vs 0.65±0.11, t=-2.354，P=0.022; Gn-TV mRNA: 3.57±0.64 vs 1.33±016, t=-3.384,P=0001; FUT8 protein: 0.70±0.11 vs 0.083±0.017, t=9.555,P=0.001; Gn-TV protein: 1.33±0.19 vs 0.60±0.15, t=5.097,P=0.007). The mRNA expression level of Gn-TIVa in HCC tissue was significantly higher than that in adjacent tissue (2.90±0.47 vs 1.68±0.19, t=-2.403,P=0.019), but there was no significant difference in the protein expression level of Gn-TIVa between HCC tissue and adjacent tissue (052±0.24 vs 0.24±0.11,t=1.833, P=0.141). The changes of glycosyltransferase gene expression in HCC tissue were consistent with the alteration of serum N-glycan profile. ConclusionSerum N-glycan alterations in patients with HBV-related HCC may be closely associated with the upregulated expression of the glycosyltransferase genes FUT8, Gn-TIVa, and Gn-TV in HCC tissue.

Objective To investigate the expression of c-Myc in gastric mucosa associated lymphoid tissue (MALT) lymphoma and its implications on prognosis.Methods The clinical data of 79 patients hospitalized in our hospital from 2009 to 2015 were retrospectively analyzed.In these patients,38 patients were low-grade MALT lymphoma,20 patients were high-grade MALT lymphoma,21 patients were diffused large B cell lymphoma (DLBCL).Real-time PCR was used to detect the levels of c-Myc expression in gastric MALT tissues and pair-matched adjacent normal tissues.The relationship between the expression of c-Myc and prognosis of patients was evaluated combing with the clinical data.Results Compared with the normal tissues,the expression levels of c-Myc protein were 15.7％ (6/38),25％ (5/20) and 28.5％ (6/21)in patients with low-grade MALT lymphoma,high-grade MALT lymphoma,and DLBCL.The relative expression levels of cMyc mRNA were gradually elevated in low-grade MALT lymphoma,high-grade MALT lymphoma and DLBCL.The tumor size and depth of invasion can influence the expression level of c-Myc.Survival analysis found that the overall survival rates and relapse-free survival rates were lower in patients with c-Myc positive expression than those of patients with negative expression (P ＜ 0.05).Conclusion C-Myc plays a key role in the malignant transformation of gastric MALT lymphoma.

AIM: To investigate the effect of CP466722, an inhibitor of ataxia telangiectasia mutated protein (ATM), on the proliferation and apoptosis of human hepatocellular carcinoma HepG2 cells.METHODS: The cell viability was detected by MTT assay.The cell growth inhibition was measured by colony formation assay.The effect of CP466722 on the cell cycle distribution of the HepG2 cells was examined by flow cytometry.The cell apoptosis was analyzed by TUNEL staining.The protein expression was examined by Western blotting.RESULTS: CP466722 inhibited the cell viability and cell proliferation in a dose-dependent manner.In CP466722-treated HepG2 cells, the cell cycle was arrested in G2/M phase, and the protein levels of phosphorylated cell division cycle protein 2 (p-Cdc2), cell division cycle protein 25C (Cdc25C) and phosphorylated Cdc25C (p-Cdc25C) were inhibited, whereas the protein expression of p27 was up-regulated.CP466722 triggered the apoptosis of HepG2 cells through cleavages of caspase-3 and poly (ADP-ribose) polymerase (PARP).In addition, CP466722 increased the phosphorylation of p38 mitogen-activated protein kinase (p38 MAPK) and suppressed the expression of β-catenin and survivin in the HepG2 cells.CONCLUSION: CP466722 inhibits the proliferation and induces the apoptosis of HepG2 cells, which may be related to activating p38 MAPK and inhibiting the expression of β-catenin and survivin.

Objective To investigate the prevalence, etiology, rehabilitation demands and service condition of hearing disorders based on the whole population in Jilin Province, China. Methods Using the probability proportion to size (PPS) sampling, 9246 (93.3%) out of 9909 residents sampled form 36 counties were targeted for investigation from August, 2014 to January, 2015, followed the WHO Ear and Hearing Disorders Survey Protocol. The hearing loss and disability were classified as WHO recommended and Classification and Grading Criteria of Disability (GB/T 26341-2010). Results The standardized prevalence of hearing loss and disability was 16.41%and 4.78%, re-spectively. Age, sex, residence, occupation and marriage status, education level and household income were significantly associated with hearing loss prevalence, while nationality was not. The main etiologies included non-infectious disease (47.33%), ear disease (14.17%), un-known causation (13.89%), and noise (8.59%). Among all people with hearing loss, those who accepted intervention service accounted for 11.02%. Among all people with hearing disability, those who used hearing aids accounted for 5.58%, and 0.67%used artificial cochlea. Con-clusion Demographics and socioeconomic factors are significantly associated with the prevalence of hearing loss. The main etiology con-tains non-infectious disease, ear disease and noise. Both the rate of service utilization among people with hearing loss and the rate of adopt-ing hearing aids among people with hearing disability are low. It is needed to do more in prevention and rehabilitation of hearing impairment.

Acupuncture Points ; Acupuncture Therapy ; Humans ; Male ; Meniere Disease ; therapy ; Middle Aged ; Treatment Outcome

Objective:To explore the influence on inflammation cytokines for anti-IL-1βand TNF-αIgY intranasal treatment in guinea pigs with allergic rhinitis.Methods:The allergic rhinitis model in guinea pigs was established using ovalbumin(OVA).Hartley guinea pigs were randomly divided into the control group(group C,n=17),the allergic rhinitis model group(group M,n=27),the 0.1%anti-IL-1βand TNF-αIgY treatment group(group Z1,n=21)and the fluticasone propionate treatment group(group Z2,n=21). At 2 h,4 h and 8 h after the last treatment,blood was got by heart puncture,as well as nose was lavaged using 0.9% saline and the nasal lavage fluid( NLF) was collected.The level of cytokines was examined using ELISA kits.Results: In the peripheral blood, the levels of IL-1β,IL-5,IL-9,IL-13,IL-18,IL-33 and TGF-β1 from 2 h to 8 h;TNF-αand OVA-specific IgE from 2 h to 4 h;and IL-22 from 4 h to 8 h were significantly decreased in the 0.1%anti-IL-1βand TNF-αIgY treatment group compared with the allergic rhinitis model group(P<0.05).In the NLF,the levels of IL-1β,IL-5,IL-9,IL-13,IL-22,IL-33,TNF-α,TGF-β1 and OVA-specific IgE from 2 h to 8 h;and IL-18 at 2 h were significantly decreased in the 0.1% anti-IL-1βand TNF-αIgY treatment group compared with the allergic rhinitis model group ( P<0.05 ) .Conclusion: Anti-IL-1βand TNF-αIgY intranasal treatment can significantly reduce inflammation cytokine levels in allergic rhinitis guinea pigs.