Volatile organic compounds (VOCs) are a type of organic compounds that exist in the form of vapor in the air at room temperature, and are common pollutants in industrial production and living environments. The health hazards caused by exposure to VOCs are gradually gaining recognition and social attention. At present, the research on the harm of VOCs to human health mainly involves the respiratory system, cardiovascular system and nervous system. However, in recent years, people have realized that VOCs can induce glucose metabolism disorder through insulin resistance, oxidative stress and oxidative damage, inflammatory reaction and liver damage, leading to increased blood sugar and increased potential risk of diabetes, and even increased the risk of complications of diabetes. This review summarizes the epidemiology and related mechanisms of VOCs, diabetes and its complications, providing a reference for effective prevention and control of VOC induced diabetes.

Volatile organic compounds (VOCs) are a type of organic compounds that exist in the form of vapor in the air at room temperature, and are common pollutants in industrial production and living environments. The health hazards caused by exposure to VOCs are gradually gaining recognition and social attention. At present, the research on the harm of VOCs to human health mainly involves the respiratory system, cardiovascular system and nervous system. However, in recent years, people have realized that VOCs can induce glucose metabolism disorder through insulin resistance, oxidative stress and oxidative damage, inflammatory reaction and liver damage, leading to increased blood sugar and increased potential risk of diabetes, and even increased the risk of complications of diabetes. This review summarizes the epidemiology and related mechanisms of VOCs, diabetes and its complications, providing a reference for effective prevention and control of VOC induced diabetes.

Objective To investigate the effects of different doses of chronic nicotine exposure on the pathology of Alzhei-mer's disease(AD),to clarify the effects of nicotine on cognitive function and related pathology in AD model mice,and to pro-vide laboratory evidence for clinical prevention and intervention of AD.Methods Nine-month-old triple-transgenic(3 × Tg)mice(APPswe,PS1M146V,and Tau P301L transgenes)were treated with low(5％,50 μg/mL),medium(10％,100 μg/mL)and high(20％,200 μg/mL)doses of nicotine for 3 months.Western blot,immunofluorescence and qPCR were used to detect amyloid be-ta(Aβ)pathology,Tau phosphorylation,synaptic damage and neuroinflammation in different groups of mice.Microglia was co-stained with Aβ to show the phagocytosis of plaques.Behavioral test was used to detect the cognitive learning ability of experi-mental mice.Results Administration of high dosage of nicotine over the course of three consecutive months resulted in an aug-mentation in Aβ plaques,while the utilization of low dosage of nicotine for an equivalent period yields a mitigating influence on Aβ accumulation and effectively alleviated synaptic impairments within the hippocampus.Moreover,chronic exposure of high nicotine exacerbated both microglial activation and neuroinflammation,along with astrogliosis in the brains of 3 X Tg mice,whereas the administration of low dosage of nicotine exhibited no discernible impact.Chronic exposure to different doses of nico-tine had no significant effect on Tau phosphorylation and cognitive behaviors in mice.Conclusion Chronic exposure to low dose nicotine alleviates Aβ accumulation and brain synaptic damage in AD model mice.Chronic exposure to high dose nicotine aggra-vates Aβ deposition and neuroinflammation.

【Objective】 To understand the prevalence of retinopathy (ROP) in preterm infants with gestational age ≤34 weeks in the First Affiliated Hospital of Xinjiang Medical University, and to analyze the associated risk factors, so as to provide a basis for early screening of high-risk premature infants. 【Methods】 A retrospective analysis was conducted on the relevant case data of hospitalized premature infants with gestational age ≤34 weeks in neonatal intensive care unit (NICU) of the First Affiliated Hospital of Xinjiang Medical University from June 2015 to June 2020. Infants were divided into ROP group and non-ROP group based on the results of fundus screening. Relevant data were collected to analyze the relevant risk factors for ROP in premature infants. 【Result】 A total of 1 738 premature infants with gestational age ≤34 weeks were included, with 292 cases (16.8%) in ROP group and 1 446 cases in non-ROP group. Logistic regression analysis revealed that bronchopulmonary dysplasia(BPD) (OR=3.379, 95%CI:1.835 - 6.221), anemia (OR=7.388, 95%CI: 4.262 - 12.806), receiving blood transfusion treatment (OR=2.129, 95%CI: 1.278 - 3.547), oxygen requirement time >7 days (OR=3.429, 95%CI: 2.309 - 5.094), and the fraction of inspired oxygen greater than 40% (OR=2.541, 95%CI: 1.540 - 4.193) were independent risk factors for the occurrence of ROP. Among these patients, 167 eyes (103 patients) received treatment of ROP, including 108 eyes treated with intraocular injection of Rizumab, 35 eyes treated with fundus laser, and 24 eyes treated with combination of both. All patients had acceptable outcomes during the follow-up. 【Conclusions】 Premature infants with anemia, BPD, receiving blood transfusion treatment, oxygen requirement time >7 days, and the fraction of inspired oxygen >40% are at high risk of developing ROP. Standardized fundus screening and timely treatment measures are essential to reduce the risk of visual impairment in premature infants.

Objective To investigate the effects of different doses of chronic nicotine exposure on the pathology of Alzhei-mer's disease(AD),to clarify the effects of nicotine on cognitive function and related pathology in AD model mice,and to pro-vide laboratory evidence for clinical prevention and intervention of AD.Methods Nine-month-old triple-transgenic(3 × Tg)mice(APPswe,PS1M146V,and Tau P301L transgenes)were treated with low(5％,50 μg/mL),medium(10％,100 μg/mL)and high(20％,200 μg/mL)doses of nicotine for 3 months.Western blot,immunofluorescence and qPCR were used to detect amyloid be-ta(Aβ)pathology,Tau phosphorylation,synaptic damage and neuroinflammation in different groups of mice.Microglia was co-stained with Aβ to show the phagocytosis of plaques.Behavioral test was used to detect the cognitive learning ability of experi-mental mice.Results Administration of high dosage of nicotine over the course of three consecutive months resulted in an aug-mentation in Aβ plaques,while the utilization of low dosage of nicotine for an equivalent period yields a mitigating influence on Aβ accumulation and effectively alleviated synaptic impairments within the hippocampus.Moreover,chronic exposure of high nicotine exacerbated both microglial activation and neuroinflammation,along with astrogliosis in the brains of 3 X Tg mice,whereas the administration of low dosage of nicotine exhibited no discernible impact.Chronic exposure to different doses of nico-tine had no significant effect on Tau phosphorylation and cognitive behaviors in mice.Conclusion Chronic exposure to low dose nicotine alleviates Aβ accumulation and brain synaptic damage in AD model mice.Chronic exposure to high dose nicotine aggra-vates Aβ deposition and neuroinflammation.

Laparoscopic renal pedicle lymphatic disconnection is the most effective method for treating chyluria that has failed to respond to conservative management. Chylous hemothorax is a rare clinical occurrence resulting from the anatomic abnormality. This paper reported a case, who was admitted with painless gross hematuria for 1 month and was diagnosed with left chylous hematuria. Laparoscopic left renal pedicle lymphatic disconnection was performed, and bilateral chylous hemothorax occurred after the operation. After conservative treatment such as bilateral closed thoracic drainage and blood transfusion support, the patient recovered well. After 2 months of follow-up, there was no obvious effusion in the bilateral thoracic cavity, and the chylous test of urine fluid was negative.

Objective:To construct a diabetic foot classification prediction model based on radiomics features of fundus photographs.Methods:A total of 2 035 fundus photographs of patients with type 2 diabetes diagnosed at Nanfang Hospital between December 2011 and December 2018 were retrospectively collected [282 photographs from patients with diabetic foot(DF), and 1 753 from patients with diabetes mellitus(DM)]. All fundus photographs were randomly divided into a training set(1 424 photos) and a test set(611 photos) using a computer generated random number at 7∶3. After pre-processing the fundus photographs, a total of 4 128 texture features based on the gray matrix were extracted by the Radiomic toolkit, and 11 339 other features were extracted using the ToolboxDESC toolkit. The LASSO algorithm was used to select the 30 features most relevant to DF, and then the Bootstrap + 0.632 self-sampling method was used to further select the 7 best combinations. Logistic regression analysis was used to obtain the regression coefficients and establish the final diabetic foot classification prediction model. ROC curve was drawn, and AUC, sensitivity, specificity, and accuracy of the training and test sets were calculated to verify its prediction performance. Results:We screened 7 fundus radiomics markers for diabetic foot patients, and based on this established a DF/DM classification prediction model. The AUC, sensitivity, specificity, and accuracy of the model were 0.958 6, 0.984 0, 0.920 0, and 0.928 0 in the training set, and 0.927 1, 0.988 9, 0.881 0, and 0.896 9 in the test set, respectively.Conclusion:In this study, seven DF fundus markers were screened using radiomics technology. Based on this, a highly accurate and easy-to-use DF/DM classification model was constructed. This technology has the potential to increase the efficiency of DF screening programs.

Objective:To investigate the effect of smart air cell mattresses on sleep quality.Methods:Twenty healthy young people were enrolled as subjects, and each subject underwent a four-night polysomnographic monitoring experiment, including two nights each on a smart air cell mattress and a general mattress. The differences in sleep quality were compared by self-assessment of sleep quality, objective sleep indicators, and electroencephalogram (EEG) spectral analysis.Results:In the comparison between the smart air cell mattress and the general mattress, the differences in self-assessment of sleep quality and objective sleep indicators were not statistically significant (all P > 0.05), but the smart air cell mattress had a slight overall advantage. The relative power of EEG in the low-frequency band and the relative power of EEG in the high-frequency band were higher in the subjects with the smart air cell mattress. Conclusions:For the healthy young population, the smart air cell mattress can positively influence sleep quality to some extent, and the change in EEG relative power indicates an increase in sleep depth.

Objective: To investigate the expression and clinical significance of circDLGAP4 from peripheral blood in coronary heart disease (CAD). Methods: The relative expression level of circDLGAP4 in peripheral blood leukocytes (PBLs) from 142 CAD patients and 169 healthy controls were detected by real-time PCR. Logistic regression, Spearman correlation and multivariate regression analysis were used to investigate the correlation of circDLGAP4 with CAD. THP-1 macrophages were treated with oxidized low density lipoprotein (ox-LDL) to construct an atherosclerotic foam cell model. The levels of circDLGAP4 mRNA were detected at different time points. Results: The mRNA expression of circDLGAP4 in PBLs of CAD patients was significantly decreased compared with controls (P=0.019). With increased unit (2 -ΔCt ) of circDLGAP4 expression, the risk of CAD occurrence reduced by 41.6% (adjusted OR=0.584, 95% CI: 0.394-0.866, P=0.007). The expression of circDLGAP4 was negatively correlated with T2DM history (β=-0.182，P=0.030). The level of circDLGAP4 in ox-LDL-treated THP-1 macrophages was decreased in a time-dependent manner. Conclusion The expression of circDLGAP4 was significantly decreased in PBLs of CAD patients and THP-1 macrophages-derived foam cells, and might be a protective factor in the pathophysiology of CAD.

Objective: To explore the relationship between HCM pathogenic gene mutations and clinical phenotypes by analyzing the prenatal diagnosis and genetic characteristics of a pregnant woman from a family with hypertrophic cardiomyopathy (HCM). Methods: The clinical data of the proband and her family members was collected. The DNA was extracted from the peripheral blood, amniotic fluid cells and cultured amniotic fluid cells of proband. Next generation sequencing (NGS) was utilized for screening pathogenetic loci of the proband. The suspected mutation sequences of HCM pathogenic candidate genes MYH7 and MYBPC3 were directly sequenced after PCR. Pathogenicity prediction of amniotic fluid cells was performed by using genetic data and bioinformatics software, such as Mutation taster, PolyPhen-2 and ANTHEPROT. Results: The sequencing results showed that heterozygous mutations of MYH7 c.1988G＞A (p.Arg663His) and MYBPC3 c.151G＞A (p.Ala51Thr) were found in the proband. The phenotype of her father was normal, and no abnormal mutations were detectable. Her mother also showed normal phenotype but carried MYBPC3 c.151G＞A heterozygous mutation. Only MYH7 c.1988G＞A heterozygous mutation was found in the fetus and no abnormal variation of MYBPC3 was showed. The prediction of mutation effect and analysis of protein structure and function revealed that the two missense mutations could affect the hydrophobicity and antigenicity of the protein. The genetic data demonstrated MYH7 c.1988G＞A was defined as a pathogenic mutation. Conclusion MYH7 c.1988G＞A should be a newly generated pathogenic mutation in the proband, or caused by reproductive chimerism of her parents. MYBPC3 c.151G＞A mutation may promote the occurrence of HCM. Although the fetus only carries MYH7 c.1988G＞A, her phenotype may still display as HCM.