Diabetic microvascular disease is a severe complication of diabetes mellitus (DM).There are many hypoth-esis for its mechanisms.This overview aimed at effect of C-peptide,coagulant factors,platelet and D-dimer in dia-betic microvascular disease,and provided evidence for its prevention and treatment in clinic.

Female ; Humans ; Leukemia, Myeloid, Acute ; complications ; etiology ; Middle Aged ; Myelodysplastic Syndromes ; complications ; etiology ; Uterine Cervical Neoplasms ; complications ; drug therapy ; radiotherapy

Objective To investigate the effect of dexmedetomidine on the cerebral injury in patients undergoing cardiac valve replacement under cardiopulmonary bypass (CPB).Methods Forty ASA Ⅱ or Ⅲ patients of both sexes,aged 43-64 yr,scheduled for elective cardiac valve replacement,were randomly divided into 2 groups (n =20 each):control group (group C) and dexmedetomidine group (group D).Dexmedetomidine 0.6 μg/kg was injected intravenously over 15 min before induction of anesthesia,followed by infusion at 0.2μg· kg-1 · h-1 until the end of operation in group D.While the equal volume of normal saline was given in group C.Blood samples were obtained from the radial artery and jugular bulb for blood gas analysis before CPB,immediatelv after declamping of the ascending aorta,at the end of CPB and at 6 h after operation (T1-4).The arteriovenous blood O2 difference (Da-jvO2) and cerebral O2 extraction rate (CERO2) were calculated.The plasma concentrations of S-100β and neuron-specific enolase (NSE) in the blood samples obtained from the jugular bulb were measured at T1-4 and 24 h after operation.Results Compared with group C,the jugular venous oxygen saturation was significantly increased and Da-jvO2 and CERO were decreased at T2,3,and the plasma concentrations of S100β and NSE were decreased at T2-4 in group D (P ＜ 0.05).Conclusion Dexmedetomidine can decrease the cerebral O2 metabolic rate and reduce the cerebral injury in patients undergoing cardiac valve replacement under CPB.

Objective To investigate the effects of penehyclidine hydrochloride combined with ulinastatin on lung injury in patients undergoing cardiac valve replacement with cardiopulmonary bypass(CPB).Methods Sixty ASA Ⅱ or Ⅲ patients of both sexes,aged 33-64,weighing 47-81 kg,NYHA class Ⅱ or Ⅲ ,scheduled for cardiac valve replacement,were randomly divided into 4 groups(n = 15 each): control group(group C),ulinastatin group(group U),penehyclidine hydrochloride group(group P)and penehyclidine hydrochloride + ulinastatin group(group PU).Group U,P and PU received iv injection of ulinastatin 20 000 U/kg,penehyclidine hydrochloride 0.05 mg/kg and ulinastatin 20 000 U/kg + penehyclidine hydrochloride 0.05 mg/kg 30 min after the end of CPB,respectively,while group C received equal volume of normal saline.Then PEEP was increased to 8 cm H2O in all groups.Blood samples were taken at 30 min,3 and 6 h after the end of CPB and 12 and 24 h after operation for determination of PaO2 and serum concentrations of TNF-α,IL-6,IL-8 and IL-10.Airway peak pressure and airway plateau pressure were recorded at the corresponding time points.Oxygen index(OI)and pulmonary compliance(CL)were calculated.Lung injury was scored at 6 h after the end of CPB and 12 and 24 h after operation.Results OI and CL were significantly increased and lung injury score was significantly decreased in group U,P and PU compared with group C(P ＜ 0.05 or 0.01),and in group PU compared with group U and P (P ＜ 0.05).Serum concentrations of TNF-α,IL-6 and IL-8 were significantly lower and the serum IL-10 concentration was significantly higher in group U,P and PU than in group C(P ＜ 0.05 or 0.01),and in group PU than in group U and P(P ＜ 0.05).There was no significant difference in the indices mentioned above between group U and P(P ＞ 0.05).Conclusion Penehyclidine hydrochloride combined with ulinastatin can attenuate lung injury by inhibiting inflammatory response in patients undergoing cardiac valve replacement with CPB.

China ; Clinical Laboratory Techniques ; Laboratories ; statistics & numerical data ; Occupational Health ; Quality Control

OBJECTIVETo explore the effect of Shengjiang Xiexin Decoction (SXD) on the intestinal mucosal and functional cells of rats after irinotecan (CPT-11) chemotherapy.

METHODSTotally 24 healthy Sprague-Dawley (SD) male rats were divided into three groups, the normal control group, the CPT-11 group, the SXD combined CPT-11 group according to random digit table, 8 in each group. CPT-11 was injected at the daily dose of 150 mg/kg to rats in the CPT-11 group and the SXD combined CPT-11 group from the caudal vein on the 4th day, once daily for 2 successive days to duplicate delayed diarrhea model. Equal volume of normal saline was injected to rats in the normal control group from the caudal vein. SXD at 2 g/mL (10 g/kg body weight) was administered to rats in the SXD combined CPT-11 group by gastrogavage for 9 successive days. Deionized water was administered to rats in the CPT-11 group and the normal control group. Diarrhea was observed at 48, 60, 72, 84, 96, and 108 h to calculate the incidence rate of diarrhea. Meanwhile, scoring for diarrhea was performed by referring methods of Akinobu Kurita. Rats were killed on day 10, ileum, cecum, and colon tissues were collected and fixed in 10% formalin solution. HE staining was performed. Intestinal mucosa injuries were graded under light microscope according to the criterion of Chiu's score. The expressions of goblet cells and Paneth cells were observed by PAS stain. Enteroendocrine cells were observed by immunohistochemical CgA staining. Positive cells were counted and cumulative optical density (IOD) analyzed by Image-Pro-Plus 6.0.

RESULTSNo diarrhea occurred in rats of the normal control group at each time point. The incidence rate of diarrhea was 75.0% (6/8) at 48 h, 100.0% (8/8) at 60 h, 100.0% (8/8) at 72 h, 87.5% (7/8) at 84 h, 75.0% (6/8) at 96 h, and 75.0% (6/8) at 108 h in the CPT-11 group. The incidence rate of diarrhea was 25.0% (2/8) at 48 h, 50.0% (4/8) at 60 h, 12.5% (1/8) at 72 h, 0.0% (0/8) at 84 h in the SXD combined CPT-11 group. Compared with the same group at 60 h, scores for diarrhea at 48, 84, 96, and 108 h obviously decreased in the CPT-11 group, and scores for diarrhea at 48, 72, 84, 96, and 108 h obviously decreased in the SXD combined CPT-11 group (P < 0.05, P < 0.01). Compared with the same group at 72 h, scores for diarrhea at 84, 96, and 108 h obviously decreased in the CPT-11 group (P < 0.05, P < 0.01). Compared with the normal control group, scores for diarrhea increased in the CPT-11 group at each time point (P < 0.01); grading of ileum, cecum, and colon mucosal tissues increased (P < 0.05, P < 0.01); expressions of ileum and cecum mucosal epithelial goblet cells obviously decreased (P < 0.05); the number and expressions of ileum and cecum mucosal epithelial Paneth cells increased (P < 0.01). Expressions of ilium endocrine cells increased, while those of cecum and colon endocrine cells decreased in the CPT-11 group (P < 0.01). Compared with the CPT-11 group, scores for diarrhea were obviously lowered (P < 0.05, P < 0.01), grading of ileum, and cecum mucosal tissues decreased (P < 0.05, P < 0.01); expressions of ileum, cecum, and colon mucosal epithelial goblet cells obviously increased (P < 0.05, P < 0.01); the number and expressions of ileum cecum mucosal epithelial Paneth cells increased (P < 0.05); expressions of cecum and colon endocrine cells increased (P < 0.05, P < 0.01) in the SXD combined CPT-11 group.

CONCLUSIONSXD played roles in preventing and treating CPT-11 induced delayed diarrhea by improving CPT-11 chemotherapy induced apoptosis and necrosis of intestinal mucosal and functional cells.

Animals ; Apoptosis ; Camptothecin ; adverse effects ; analogs & derivatives ; Colon ; Diarrhea ; Drug Therapy ; Drugs, Chinese Herbal ; pharmacology ; therapeutic use ; Ileum ; Intestinal Mucosa ; drug effects ; Male ; Rats ; Rats, Sprague-Dawley ; Wound Healing ; drug effects

BACKGROUND: Exhaled nitric oxide (eNO) is one of the airway condensate derived markers, reflecting mainly airway inflammation in asthma and other lung diseases. The changes of eNO levels as pathophysiology of neonatal hypoxemic respiratory failure (HRF) in early postnatal life have not been thoroughly studied. The present study was to establish a method for measuring eNO concentrations in neonates with or without HRF. METHODS: Twenty-two newborn infants with HRF and 26 non-NRF controls were included within the first 24 hours of postnatal life. Their eNO levels were detected with a rapid-response chemiluminescence analyzer daily during the first week of their postnatal life, and lung mechanics and gas exchange efficiency were monitored at the same time, such as pulse oxygen saturation (SpO2), inspired fraction of oxygen (FiO2) and other parameters. RESULTS: During the first two days of postnatal life, eNO values of HRF neonates were significantly higher than those of the control neonates (day 1, 7.9±3.2 vs. 5.8±1.8 parts per billion [ppb], P<0.05; day 2, 8.8±3.2 vs. 6.0±2.4 ppb, P<0.05), but there were no significant differences in the following days. With SpO2/FiO2 increasing, difference of eNO values between the HRF and non-HRF neonates became narrowed, but there was still a two-fold difference of eNO/[SpO2/(FiO2×100)] on days 5-7. CONCLUSION: We established a method for measuring eNO and found difference in neonates with or without HRF, which diminished with prolonged postnatal days, reflecting pathophysiological characteristics of HRF.

Food allergies, as a type of adverse immune-mediated reactions to ingested food proteins, have become a serious public health issue that harms children and adults health, with increasing incidence year by year. However, without effective therapy for food allergies, doctors-have mostly advised to avoid allergens and provided symptomatic treatment. According to the findings of many studies, allergic diseases are correlated with intestinal barrier function injury, as evidenced by the significant increase in the intestinal permeability among patients with food allergies. In this paper, recent studies on correlations between food allergies and intestinal barrier functions, intestinal barrier function injury mechanisms of allergic foods and food allergy intervention strategies based on intestinal barrier functions were summarized to provide reference for laboratory researches and clinical treatment of food allergic diseases.
Animals ; Food Hypersensitivity ; immunology ; therapy ; Humans ; Intestines ; immunology

Objective To investigate the effects of chronic high glucose on α-cells glucagon releasing in relation to insulin resistance induced by high glucose. Methods TC1-6 cells, an α-cell line, were incubated separately in DMEM containing high (25.0 mmol/L), medium (11.1 mmol/L) and low (5.5 mmol/L) concentrations of glucose for 1 to 5 days. The secretion and gene expression of glueagon were measured. When TC1-6 cells had been cultured for 5 days, three different concentrations of insulin were added for 6 h and then glucagon secretion was detected. Western blot was used for 1 and 3 days to confirm the effect of high glucose on phosphorylation of Akt in TC1-6 cells. Results (1) Exposure of TC1-6 cells to 11.1 and 25.0 mmol/L glucose resulted in a slight increase of glucagon secretion compared with those incubated with 5.5 mmol/L. However, after 5 days in media containing 25.0 mmol/L glucose, glucagan secretion was significantly increased as compared to cells treated with low glucose [(136.80±10.94 vs 78.62±4.72 ) ng/106 cells, P<0.05]; moreover, in TC1-6 cell cultured with high glucose glucagon mRNA expression was increased significantly. (2) 10-7 mol/L insulin reduced significantly glucagon secretion of TC1-6 ceils exposed to low glucose [(21.59±1.30 vs 55.12±3.86) ng/106 cells], but just scarcely inhibited glucagon secretion of cells incubated with high glucose [(106.58±8.53 vs 117.18±10.55) ng/106 cells]. When insulin concentration was increased to 10-5 mol/L, glucagon secretion of TC1-6 cells in high glucose was also reduced [(46.55±3.72 vs 118.61±10.68 )ng/106 cells]. (3) After treated with 10-5 mol/L insulin for 2h, the levels of Akt phosphorylation in both groups of TC1-6 cells were increased by 180% and 70%, while the level in high glucose group was significantly lower than that in low glucose group. In the presence of phosphoinositide 3 kinase inhibitor, the levels of Akt phosphorylation were both lowered, but the inhibition in low glucose group was more significant than in high glucose group. Conclusion High glucose induces hypersecretion of glucagon, which may be due to the a-cell insulin resistance.

AIM:To analyze the correlation between serum angiotensin-converting enzyme 2 (ACE2) levels and different stages of coronary heart disease (CHD), and to explore the change of serum ACE2 level during the development of CHD.METHODS:The control group included 85 non-CHD samples, and 174 CHD samples were divided into light stenosis (ls-CHD, stenosis degree <50%) group, moderate stenosis (ms-CHD, stenosis degree 50%~75%) group and severe stenosis (ss-CHD, stenosis degree ≥75%) group.The ACE2 level in each serum sample was detected by ELISA.The relationship between the ACE2 level and the development of coronary heart disease was explored by statistical analysis of serum ACE2 levels in different stages of CHD.RESULTS:The serum ACE2 levels in ls-CHD group, ms-CHD group and ss-CHD group were all higher than that in control group.The more severe the coronary artery stenosis existed, the higher the ACE2 level was observed.The serum ACE2 level in the males was higher than that in the females.In a single sex, the serum ACE2 levels in ls-CHD group, ms-CHD group and ss-CHD group were higher than that in control group with significant differences.Regression analysis found that sex, diabetes and CHD were associated with the serum ACE2 levels.Among them, sex and CHD were the independent factors to affect serum ACE2 levels.CONCLUSION:The serum ACE2 level of males was higher than that of females.Compared with the non-CHD samples, the serum ACE2 level of CHD patients was higher than that of the non-CHD samples.During the development of coronary heart disease, the serum ACE2 level increased constantly.