Objective To determine the relationships between serum leptin levels and maternal weights in late pregnancy and cord blood leptin levels to birth weights, C peptide, insulin and insulin like growth factor (IGF II). Methods Fifty normal pregnant women at 37～38 weeks and their newborns were studied, and 29 non pregnant women were set as control. Venous blood was taken from women and from the cord at delivery. Blood leptin and cord blood C peptide, insulin, and IGF II were measured by radio immunoassay. Results The average leptin level in maternal sera was (13.62?3.68)?g/L, significantly higher than that in the control (6.60?3.04)?g/L and that in cord blood (8.05?4.61)?g/L. Maternal leptin levels were significantly correlated with maternal weights and body mass index (BMI. r =0.33, 0.35, P 0.05). Cord blood leptin levels were significantly correlated with birth weights and BMI ( r =0.54, 0.49, P 0.05). Significant difference of the cord leptin levels was not seen between the males and females. The cord blood C peptide was (0.86?0.35) ?g/L, insulin (8.49?4.76) mU/L and IGF Ⅱ(0.218?0.076) ?g/L. Cord leptin levels were correlated with C peptide levels ( r =0.37, P 0.05). Conclusions Maternal leptin levels in late pregnancy were significantly higher than those in normal non pregnant women and positively correlated with maternal weights and BMI. Cord blood leptin levels were positively correlated with birth weights and BMI of the newborns. The leptin levels of cord blood were correlated with those of C peptide but not insulin and IGF II.

Objective:To investigate the effect of cPLA 2(cytosolic PLA 2, 85-kD PLA 2) on the signaling pathways of IL-1?、IL-6 release in LPS induced Hela cells.Methods:①LPS stimulated Hela cells were exposed to the complex of cPLA 2 initiation site-directed antisense oligonucleotide and liposome in the indicated doses and time, and then,analyzed the changes of cPLA 2 both in mRNA and in protein by RT-PCR and Western blot.②At the same time, the supernatants were collected to detect the level of IL-1? and IL-6 under radioimmunoassay(RIA).Results:①The transfection led to a dose-dependent decrease in cPLA 2 protein, while the change of mRNA is not notable.②The levels of IL-1?、IL-6 in the transfected cells were reduced following the repression of cPLA 2 compared with that of LPS added only.Conclusion:cPLA 2 probably plays an important role in the signaling mechanisms on IL-1?、IL-6 release in LPS-induced Hela cell. [

AIM: To detect the effect of sepsis on hepatic,renal functions and corresponding enzymes in intestine of mice,and to explore the role of leptin in acute inflammation.METHODS: A mice model of sepsis was made by cecum ligation and perforation,and 96-well spectrophotometry was used to detecte the levels of alanine aminotransferase(ALT),uric acid(UA) and activities of myeloperoxidase(MPO),glutathin-S-transferase(GST),xanthine oxidase(XOD),superoxide dismutase(SOD) in serum and intestinal homogenized fluids,respectively.Hematoxylin-eosin staining was used simultaneously to check the histopathologic changes of intestine.RESULTS: Compared with sham group(330.12 ?mol/L?94.15 ?mol/L),serum UA level(521.92 ?mol/L?91.86 ?mol/L) at 6 h after sepsis was significantly higher.12 h after sepsis,both serum ALT(83.55 U/L?40.44 U/L) and UA(474.03 ?mol/L?75.22 ?mol/L) were significantly higher than those in sham group(66.23 U/L?16.80 U/L and 320.95 ?mol/L?99.14 ?mol/L,respectively).12 h after leptin injection(0.1 mg/kg,ip) or indomethacin injection(2 mg/kg,ip),the serum ALT and UA levels significantly decreased(vs sepsis group,P

Objective To investigate the relationship between baseline serum uric acid and the severity of coronary artery disease ( CAD ) in the first-degree relatives or non-first-degree relatives of men with type 2 diabetes. Methods Three hundred and eighty-one men with negative coronary angiography for the first time were divided into diabetes and non-diabetes groups and followed-up for 5 years. The primary outcome was acute coronary syndrome suspected during subsequent 5 years, and the coronary angiography was conducted simultaneously. The severity of CAD was assessed by the coronary stenosis index ( CSI) and the number of coronary lesion vessels. Results In normal blood glucose group, serum uric acid was higher in the first-degree relatives of diabetics compared with non-first-degree relatives(P<0. 01), along with higher morbidity of CAD, CSI, and coronary lesion vessels (all P<0.01). Correlation analysis showed that CSI(r=0. 250, P=0. 041) and coronary lesion vessels(r=0. 252, P=0. 040) in non-diabetics group were associated with baseline levels of serum uric acid. Conclusion The elevation of serum uric acid was closely related to subsequent CAD, especially in first-degree relatives of male with type 2 diabetes, which could be used as an early indicator for CAD prediction.

OBJECTIVE: To explore the change of orexin-A expression in hepatic reperfusion and their association with liver injury, and to find out the role of orexin-A in traumatic stress responses. METHODS: A 70% hepatic reperfusion model of rats was established, setting groups of sham-operation and injury ones with different reperfusion time. A self-produced radioimmunoassay and relevant kits were used to detect the protein level of orexin-A in the plasma and the hypothalamus, serum glucose, total anti-oxidation capacity and alanine transaminase, HE staining and immunohistochemistry were used to investigate the pathological variation and protein expression of orexin-A in the liver, while RT-PCR was applied to observe mRNA expression of orexin-A in the hypothalamus and the liver. RESULTS: Both the shape of standard curve and metrical results of the self-produced orexin-A radioimmunoassay were good. Protein levels of orexin-A in the plasma and the hypothalamus in each reperfusion group showed no significant change. Serum glucose and total anti-oxidation capacity increased significantly at the later phase of injury. There was significant and positive linear correlation between the plasma orexin-A and serum glucose and total anti-oxidation capacity; serum alanine transaminase in each reperfusion group was significantly higher, and liver damage was significantly alleviated at the later phase of the injury. Different extents of variation were observed in protein expression of orexin-A in the liver and its mRNA expression in the hypothalamus and the liver. CONCLUSION Orexin-A undergoes significant changes during hepatic reperfusion, indicating that orexin-A participates in the modulation of hepatic reperfusion-induced liver injury and internal disorders.
Animals ; Hypothalamus ; metabolism ; Intracellular Signaling Peptides and Proteins ; genetics ; metabolism ; Liver ; blood supply ; metabolism ; Male ; Neuropeptides ; genetics ; metabolism ; Orexins ; RNA, Messenger ; genetics ; metabolism ; Radioimmunoassay ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury ; metabolism

OBJECTIVE: To investigate relationship between anti-endothelial cell antibody(AECA) and response to dexamethasone in sudden hearing loss(SHL). METHOD: Forty-eight SHL patients and thirty normal controls with SHL were recruited in present study. AECA was detected by ELISA in serum of all normal controls and SHL patients as well as pure-tone average was examined by electronic audiometry during treatment in SHL patients. Both AECA-positive and -negative subjects received 10 mg/d venous dexamethasone for 5 days followed by gradual tapering of dose of 5 mg/d for another 5-day. Then pure-tone average was reexamined. Differences in hearing recovery between AECA-positive and -negative subjects and relationship between AECA level and hearing recovery were analyzed. RESULT: The prevalence of AECA detection was 68.75% (33 of 48 patients) in SHL patients, with significant difference compared with control subjects with 23.33% (7 of 30 controls) (P<0.01). After treatment, rates of response to dexamethasone in AECA-positive and -negative SHL patients were 81.8% (27 of 33 patients) and 33.3% (5 of 15 patients), respectively. Meanwhile, there was a significant difference in cure, excellent recovery, partly recovery and invalid between AECA-positive and -negative groups [21.2% (7/33), 33.3% (11/33), 27.3% (9/33) and 18.2% (6/33) versus 0, 13.3% (2/15), 20.0% (3/15) and 66.7% (10/15), P<0.01]. Except 5 subjects with AECA level more than 263 microg/L, hearing recovery was correlated to pretreatment AECA level (r=0.8084, P<0.01). CONCLUSION In sudden HL patients treated with dexamethasone, AECA might represent a serological marker of prognosis.
Adolescent ; Adult ; Aged ; Audiometry, Pure-Tone ; Autoantibodies ; blood ; Case-Control Studies ; Child ; Dexamethasone ; therapeutic use ; Female ; Hearing Loss, Sudden ; blood ; drug therapy ; Humans ; Male ; Middle Aged ; Prognosis ; Young Adult

The effects of black rice anthocyanidins (BRACs) on retinal damage induced by photochemical stress are not well known. In the present study, Sprague-Dawley rats were fed AIN-93M for 1 week, after which 80 rats were randomly divided into two groups and treated with (n = 40) or without BRACs (n = 40) for 15 days, respectively. After treatment, both groups were exposed to fluorescent light (3,000 +/- 200 lux; 25degrees C), and the protective effect of dietary BRACs were evaluated afterwards. Our results showed that dietary BRACs effectively prevented retinal photochemical damage and inhibited the retinal cells apoptosis induced by fluorescent light (p < 0.05). Moreover, dietary BRACs inhibited expression of AP-1 (c-fos/c-jun subunits), up-regulated NF-kappaB (p65) expression and phosphorylation of IkappaB-alpha, and decreased Caspase-1 expression (p < 0.05). These results suggest that BRACs improve retinal damage produced by photochemical stress in rats via AP-1/NF-kappaB/Caspase-1 apoptotic mechanisms.
Animal Feed/analysis ; Animals ; Anthocyanins/administration & dosage/*pharmacology ; Antioxidants/administration & dosage/*physiology ; Blotting, Western ; Caspase 1/*genetics/metabolism ; Diet ; Dietary Supplements/analysis ; I-kappa B Proteins/genetics/metabolism ; NF-kappa B/*genetics/metabolism ; Neoplasm Proteins/genetics/metabolism ; Nucleocytoplasmic Transport Proteins/genetics/metabolism ; Oryza sativa/chemistry ; Proto-Oncogene Proteins c-fos/genetics/metabolism ; Proto-Oncogene Proteins c-jun/genetics/metabolism ; Rats ; Rats, Sprague-Dawley ; Real-Time Polymerase Chain Reaction ; Retinal Diseases/etiology/*prevention & control ; Signal Transduction/*drug effects/radiation effects ; Transcription Factor AP-1/*genetics/metabolism

Objective:The aMAP score is a hepatocellular carcinoma (HCC) risk prediction model based on an international cooperative cohort, which can be applied to various liver diseases. The aim of this study is to use the aMAP score to stratify the risk of HCC in patients with chronic liver disease (combined or non-combined metabolic diseases) admitted to People's Hospital of Yudu County, Ganzhou City, Jiangxi Province, in order to guide personalized HCC screening.Methods:The demographic information, laboratory test results (platelets, albumin, and total bilirubin) and combined disease information of patients with chronic liver disease who were admitted to People's Hospital of Yudu from January 2016 to December 2020 were collected, and the aMAP score was calculated to stratify HCC risk in this population.Results:A total of 3629 cases with chronic liver disease were included in the analysis, including 3 452 (95.1%) cases with hepatitis B virus (HBV) infection, 177 (4.9%) cases with fatty liver, and 22 (0.6%) cases with HBV infection and fatty liver. There were 2 679 (73.8%) male and the median age was 44 (35, 54). In the overall population, low, medium and high risk of HCC accounted for 52.6%, 29.0%, and 18.4% respectively. In the HBV-infected population, the proportion of high risk of HCC was significantly higher than that of fatty liver (18.9% vs. 9.6%, P = 0.001). The proportion of chronic liver disease patients with combined hypertension or diabetes was significantly higher than that of those with non-combined metabolic diseases (combined hypertension: 32.3% vs. 17.9%, P < 0.001; combined diabetes: 36.5% vs. 18.1%, P < 0.001). Moreover, the proportion of high-risk population with two metabolic diseases was significantly higher than that with one and no metabolic diseases (40.9% vs. 31.8% vs. 17.7%, P < 0.001). Conclusion:The aMAP score can be used as a simple tool for HCC screening and management of chronic liver disease in primary hospitals, and it is helpful to improve the personalized follow-up management system of chronic liver disease population. Chronic liver disease patients with metabolic diseases have a higher risk of HCC, and people with high risk of HCC should be given special priority in follow-up visits, so as to improve the rate of HCC early diagnosis and reduce the mortality rate.

Objective:To investigate the clinical characteristics and prognosis of patients with RUNX1-RUNX1T1 fusion gene-positive acute myeloid leukemia (AML) with ASXL2 gene mutation.Methods:The clinical data of 145 newly diagnosed RUNX1-RUNX1T1 fusion gene-positive AML patients treated at the Second Hospital Center of Shanxi Medical University from October 2010 to March 2021 were retrospectively analyzed. Sanger sequencing was used to detect the gene mutation. According to the presence or absence of ASXL2 gene mutation, the patients were divided into mutation group and non-mutation group. The clinical characteristics, gene mutations and prognosis were compared among the two groups.Results:Among 145 AML patients with positive RUNX1-RUNX1T1 fusion gene, we identified recurrent mutations of c-kit, ASXL2, N/KRAS, FLT3, ASXL1, TET2, NPM1 and DNMT3A genes, with mutation rates of 40.7% (59/145), 20.7% (30/145), 15.9% (23/145), 12.4% (18/145), 11.7% (17/145), 11.0% (16/145), 5.5% (8/145), and 2.1% (3/145), respectively. A total of 18 mutation sites were detected in 30 patients with ASXL2 gene mutations including 5 point mutations and 13 frameshift mutations, which mainly occured in the exons 12 and 13. Lactate dehydrogenase (LDH) at initial diagnosis of 30 AML patients with ASXL2 mutation was lower than that of those with ASXL2 non-mutation ( Z = 2.34, P = 0.020), while prothrombin time (PT) of AML patients with ASXL2 mutation was longer than that of those with ASXL2 non-mutation ( Z = 1.99, P = 0.047). A total of 21 (21/30, 70%) patients simultaneously had other gene mutations. The incidence of RAS mutations in patients with ASXL2 mutation was higher than that those with ASXL2 non-mutation, and the difference was statistically significant [30.0% (9/30) vs. 12.1% (14/115), χ2 = 4.41, P = 0.036]. There were no statistically significant differences in complete remission rate [86.7% (26/30) vs. 74.8% (86/115)] and recurrence rate [43.3% (13/30) vs.31.3% (36/115)] of patients with ASXL2 mutation and ASXL2 non-mutation ( χ2 = 0.39, P = 0.534; χ2 = 0.54, P = 0.432). The median overall survival (OS) time was 26 months (1-135 months) and 30 months (1-120 months), respectively in patients with ASXL2 mutation and ASXL2 non-mutation; the median disease-free survival (DFS) time was 14 months (0-60 months) and 13 months (0-94 months), respectively in patients with ASXL2 mutation and ASXL2 non-mutation; and the differences in OS and DFS were not statistically significant of both groups ( χ2 = 0.05, P = 0.822; χ2 = 0.34, P = 0.562). Compared with ASXL1 mutant patients, cases with ASXL2 mutation had higher OS and DFS rates, and the differences were statistically significant ( P = 0.003, P = 0.007). The differences in OS and DFS between patients with ASXL2 mutations and those with positive mutations of c-kit, RAS, FLT3, TET2, NPM1, DNMT3A were not statistically significant (all P > 0.05). Conclusions:RUNX1-RUNX1T1 positive AML patients with ASXL2 mutation tend to have low LDH and high PT, and often coexist with RAS mutations, and their prognosis is better than that in patients with ASXL1 positive mutation.

Objective:To explore the characteristics of sleep disorders in patients with Parkinson's disease (PD) and its correlation with homocysteine.Methods:Totally 75 PD patients hospitalized in the department of neurology from January 2017 to June 2021 were selected and divided into sleep disorder group ( n=39) and non-sleep disorder group ( n=36)according to polysomnography, Parkinson's disease sleep scale(PDSS) and Epworth sleepiness scale(ESS). The basic clinical data, hematological examination results, scale evaluation data and polysomnography monitoring data of the above patients were collected during hospitalization to analyze the sleep characteristics of patients with Parkinson's disease and its correlation with homocysteine.SPSS 26.0 statistical analysis software was used for t test, Mann-Whitney U test, Pearson analysis, Spearman analysis and multivariate Logistic analysis. Results:The sleep efficiency (56.82±19.07)%, N2 phase ratio(48.67±17.70)%, N3 phase ratio(9.20%(19.00%)) and the leg movement micro-arousal index(0(1.20)) in the sleep disorder group were lower than those in the non-sleep disorder group (sleep efficiency (82.15±5.55)%, N2 phase ratio(57.02±2.80)%, N3 phase ratio(20.01%(3.93%)), the leg movement micro-arousal index(1.15(1.80)). The differences were statistically significant ( t/ Z=-6.087, -2.905, -3.773, -3.683, all P<0.05). The proportion of AHI (0.90(14.60)), N1 stage (19.50%(15.70%)), and periodic limb index (0(24.80)) in sleep disorder group were higher than those in non-sleep disorder group (AHI (0.60(0.30)), N1 stage (12.15%(3.15%)), and periodic limb index (0(0)). The difference was statistically significant ( Z=2.154, 5.250, 3.559, all P<0.05). The homocysteine (15.80(3.90) μmol/L), NMSS-insomnia correlation score (3.00(5.00)), MDS-UPDRS-Ⅰ(7.00 (10.00)), MDS-UPDRS-Ⅲ (23.00 (16.00)) in the sleep disorder group were higher than those in the non-sleep disorder group (homocysteine (14.10 (4.20)μmol/L), NMSS-insomnia correlation score (0(1.00)), MDS-UPDRS-Ⅰ(3.00 (2.00)), MDS-UPDRS-Ⅲ (17.00 (4.00)), and the differences were statistically significant( Z=2.557, 4.487, 2.952, 2.180, all P<0.05). The NMSS-olfactory correlation scores (2.00(4.00)) and PDSS (99.00 (40.00)) were lower than those in the non-sleep disorder group (NMSS-olfactory correlation scores (4.50 (7.00)) and PDSS (122.00 (28.00)), and the differences were statistically significant ( Z=2.450, 4.126, both P<0.05). Hcy was positively correlated with sleep disorder in PD patients ( r=0.297, P<0.05). Binariate logistic regression analysis showed that elevated homocysteine level might be a risk factor for sleep disorder in PD patients ( β=0.193, OR=1.213, 95% CI=1.029-1.430). Conclusion:Parkinson's disease patients with sleep disorder have the characteristics of sleep structure disorder, often accompanied by more serious motor disorders, and the olfactory function impairment is relatively mild. Elevated homocysteine levels may be a risk factor for sleep disorder in Parkinson's disease.