Carcinoma, Hepatocellular ; complications ; Hemangioma ; complications ; diagnosis ; immunology ; pathology ; Hepatitis B, Chronic ; complications ; Hepatocytes ; cytology ; pathology ; Humans ; Liver Cirrhosis ; complications ; Liver Neoplasms ; complications ; Male ; Middle Aged ; Platelet Endothelial Cell Adhesion Molecule-1 ; immunology ; Spleen ; immunology ; pathology ; Tomography, X-Ray Computed

Objective To determine the effect of iron deficiency on hemoglobin A2(HbA2) expression in patients with β-thalassemia.Methods The participants were recruited from the out-patient clinics of the Pediatrics Department and Obstetrics Department of Affiliated Hospital of Guilin Medical College and from some β-thalassemia major families.Blood samples from the participants were used for blood smear tests and hemoglobin electrophoresis and to analyze serum ferritin (SF),3 alpha-globin gene deletions,and 17 beta-globin point mutations.Results Of the 408 individuals,304 were assigned to group A (normal controls),26 to group B (iron deficiency),56 to group C (β-thalassemia),and 22 to group D (β-thalassemia combined with iron deficiency). The results for the comparison of the mean HbA2 values among pairs of groups were as follows: group A vs group B,q=5.074 7,P<0.05; group A vs group C,q=37.650 8,P<0.05; group A vs group D,q=16.043 0,P<0.05;group C vs group D,q=7.682 9,P<0.05; Group B vs group D,q=15.806 6,P<0.05. There were no significant correlation between SF and HbA2 in all 4 groups.Conclusions Iron deficiency decreased the HbA2 level in both controls and individuals with β-thalassemia. HbA2 levels decreased significantly in individuals with both β-thalassemia and iron deficiency as compared with β-thalassemia group alone. However,they remained significantly higher than both the control and iron-deficient groups. Therefore,the elevation of HbA2 could be used to diagnose β-thalassemia reliably even in the presence of iron deficiency.

Animals ; Aspartame ; pharmacology ; Carbon Tetrachloride ; administration & dosage ; Disease Models, Animal ; Ethanol ; administration & dosage ; chemistry ; Liver ; pathology ; ultrastructure ; Liver Cirrhosis, Experimental ; chemically induced ; pathology ; Male ; Plant Oils ; administration & dosage ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Sweetening Agents ; pharmacology

To investigate the influence of sulfur dioxide (SO₂) on lipopolysaccharide (LPS)-induced acute lung injury (ALI), we examined the influence of exogenous SO₂ on pulmonary tissue inflammatory response. A rat model of ALI induced by intravenous (IV) injection of LPS was developed. Male Sprague-Dawley (SD) rats were divided into four groups randomly: control group, LPS group, LPS plus SO₂ group (IV injection of 0.5 mL Na₂SO₃/NaHSO₃ 10 min before LPS administration) and SO₂ group (only given Na₂SO₃/NaHSO₃). Animals were sacrificed 6 h after agent administration. Lung weight/body weight ratio (LW/BW) was measured and calculated. Morphological changes of lung tissues were observed. The number of polymorphonuclear neutrophil (PMN) in the bronchoalveolar lavage fluid (BALF), intercellular adhesion factor-1 (ICAM-1) expression in the lung tissue and IL-1, IL-6 and IL-10 levels in the serum were tested. The results showed that, compared to control rats, the LPS-treated rats had severe injuries of lung tissues and an increased LW/BW, increased index of quantitative assessment (IQA) score, increased PMN number in the BALF, increased ICAM-1 expression in the lung tissue and increased IL-1, IL-6 and IL-10 levels in the serum 6 h after LPS injection. Administration of the SO₂ donor, Na₂SO/₃NaHSO₃, into LPS-treated rats reduced the LW/BW, PMN number and ICAM-1 expression, and alleviated the degree of ALI (measured by the IQA score). In addition, Na₂SO₃/NaHSO₃ decreased IL-1 and IL-6 levels, but increased IL-10 level in the serum. There were no significant differences in the above indexes between SO₂-treated rats and control rats. These results suggest that exogenous SO₂ could inhibit the pulmonary tissue inflammatory response in rats with LPS-induced ALI.
Acute Lung Injury ; chemically induced ; drug therapy ; Animals ; Bronchoalveolar Lavage Fluid ; cytology ; Inflammation ; drug therapy ; metabolism ; Intercellular Adhesion Molecule-1 ; metabolism ; Interleukin-1 ; blood ; Interleukin-10 ; blood ; Interleukin-6 ; blood ; Lipopolysaccharides ; adverse effects ; Lung ; pathology ; Male ; Neutrophils ; cytology ; Rats ; Rats, Sprague-Dawley ; Sulfur Dioxide ; pharmacology

The animal model of acute lung injury (ALI) caused by intravenous injection of lipopolysaccharides (LPS) and cultured human peripheral blood polymorphonuclear neutrophil (PMN) were used to study the effects of sodium hydrosulfide (NaHS), hydrogen sulfide (H2S) donor, on LPS-induced PMN accumulation, microvascular permeability and PMN apoptosis. Control group, NaHS group, LPS group and LPS + NaHS group were established both in in vivo and in vitro studies. Microvascular permeability, PMN accumulation in lung and apoptosis of PMN were detected. The results showed that: (1) In in vivo study, PMN accumulation in lung, the protein content in bronchoalveolar lavage fluid (BALF) and the Evans blue dye in lung tissue of LPS group were markedly higher than those of both sham operation group and LPS + NaHS group (P<0.05, P<0.01); (2) In in vitro study, the apoptotic rates of PMN in LPS group and NaHS group were significantly higher than that in control group (P<0.01), while compared with LPS group, LPS + NaHS group showed significantly higher apoptotic rate (P<0.01). These results suggest that NaHS attenuates LPS-induced microvascular permeability and alleviates ALI. PMN apoptosis induced by NaHS is possibly one of the potential mechanisms underlying the decrease of PMN accumulation in lung tissue.
Acute Lung Injury ; chemically induced ; immunology ; pathology ; Animals ; Apoptosis ; Disease Models, Animal ; Humans ; Hydrogen Sulfide ; pharmacology ; Lipopolysaccharides ; adverse effects ; Lung ; pathology ; Neutrophils ; immunology ; Rats ; Sulfides ; pharmacology

OBJECTIVETo study the genetic association of apolipoprotein (apo) E and apoCI gene polymorphisms with coronary heart disease (CHD) in China.

METHODSapoE genotypes were identified by multiplex amplification refractory mutation system (multi-ARMS) and the apoCI promoter polymorphisms were detected by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) in 186 cases with CHD (age: 65.0 +/- 10.5 years) and 350 controls (age: 63.6 +/- 8.3 years). The haplotype frequencies were estimated.

RESULTSThe frequencies of apoE E4/3 genotype (26.9%) and epsilon4 (14.5%) in CHD group were significantly higher than that in the control group (12.6%, 7.0%), P <0.05. The significant difference was also found for the apoCI locus and the CHD group showed higher rate of both for the H2 allele and genotypes, carrying this allele. Estimation of the haplotype frequencies indicated that the association between the apoE-CI haplotype and CHD was significantly strong. The apoE-epsilon4/apoCI-H2 was estimated to be responsible for 9.86% of CHD.

CONCLUSIONWhen the subjects carrying both epsilon4 and H2 alleles, they would have higher risk of suffering from CHD than controls.

Adult ; Aged ; Aged, 80 and over ; Alleles ; Apolipoproteins C ; genetics ; Apolipoproteins E ; genetics ; China ; epidemiology ; Coronary Disease ; blood ; epidemiology ; genetics ; Female ; Genotype ; Haplotypes ; Humans ; Male ; Middle Aged ; Polymerase Chain Reaction ; Polymorphism, Restriction Fragment Length ; Risk Factors

Translational medicine is a new research system for rapid translation from basic research achievement to clinical treatment. This article summarized the research progress in the field of translational medicine in the recent months, and carried out an inventory of the frontier from important journals (such as Nature, Science, J Clin Invest, Nat Genet, Cell, Eur Heart J) in order to provide references for scientists and doctors, and promote the translation from basic medicine to clinical diagnosis and treatment.

In the context of internationalization of education,the military graduate education concepts and models also come to change,and opportunities and challenges coexist.In this article,the challenges and problems of army medical college graduate education were mentioned and analyzed,and the exploration and attempt of graduate education in the process of international were summarized.

Objective To explore the effect of ox-LDL,MCP-1,CD68 on the survival of arteriovenous fistula in radial arteries of uremic patients.Methods Segments of radial arteries were obtained from 23 uremic subjects (29～68 years old) in the initial operation of arteriovenous fistula prior to hemodialysis.The deposit of ox-LDL and the expression of MCP-1,CD68 on the vascular wall were measured by immunohistochemistry.The survival time of arteriovenous fistula was followed by survival analysis.Results COX regression revealed that each of these risk factors,ox-LDL,MCP-1, CD68,played an important role in the survival time of arteriovenous fistula when they entered the model independently.The hazard ratios were 1.008 (P=0.008,95% CI:1.002064～1.014104), 1.007(P=0.O00,95%CI:1.003853～1.010966),and 1.098496 (P=0.000,95%CI:1.047909～1.151526)respectively.When all the three factors entered the COX regression model,the whole model was still founded.MCP-1 and CD68 still played important roles in the survival of arteriovenous fistula.The hazard ratios were 1.006(P=0.025) and 1.113(P=0.001) respectively.With the hazard ratio of 0.997,ox-LDL did not reach the statistic significance (P=0.414).Conclusions The more deposit of ox-LDL and the more expression of MCP-1,CD68 on the vascular wall,the more shortened survival time of arteriovenous fistula.Particularly,the inflammation is the independent risk factor for the prognosis of arteriovenous fistula in uremic patients.

AIM To prepare bergenin nanostructured lipid carriers,and to investigate their in vivo pharmacokinetics.METHODS The nanostructured lipid carriers were prepared by melting method.With solid lipid type,liquid lipid type,solid-liquid lipid ratio,lipid-drug ratio and poloxamer 188 concentration as influecing factors,encapsulation efficiency,drug loading and particle size as evaluation indices,the formulation was optimized by single factor test,after which the in vitro drug release was investigated,the stability was determined,and crystalline form analysis was performed.Eighteen rats were randomly assigned into three groups and given intragastric administration of the 0.5%CMC-Na suspensions of bergenin,physical mixture and bergenin solid dispersions(60 mg/kg),respectively,after which blood collection was made at 0.25,0.5,1,2,3,4,5,6,8,10,12 h,HPLC was adopted in the plasma concentration determination of bergenin,and main pharmacokinetic parameters were calculated.RESULTS The optimal formulation was determined to be glyceryl behenate as solid lipid,oleic acid as liquid lipid,4 ∶ 1 for solid-liquid lipid ratio,10 ∶ 1 as lipid-drug ratio 2.0%for poloxamer 188 concentration,the average concentration,drug loading,particle size and Zeta potential were(84.16±1.57)%,(7.73±0.27)%and(215.53±18.04)nm and-(37.56±2.03)mV,respectively.The nanostructured lipid carriers demonstrated the accumulative release rate of less than 50%within 240 min in simulated gastric fluid,which was 71.04%within 36 h in simulated intestinal fluid,along with good stability within 12 h in the latter.Bergenin existed in the nanostructured lipid carriers in an amorphous state.Compared with raw medicine and physical mixture,the nanostructured lipid carriers displayed prolonged tmax and t1/2(P<0.01),and increased Cmax,AUC0-t,AUC0-∞(P<0.01),whose relative bioavailability was enhanced to 6.08 times as compared with that of raw medicine.CONCLUSION Nanostructured lipid carriers can improve the stability and oral bioavailability of bergenin.