[Fat emulsion tolerance in preterm infants of different gestational ages in the early stage after birth].

OBJECTIVE: To investigate the fat emulsion tolerance in preterm infants of different gestational ages in the early stage after birth. METHODS: A total of 98 preterm infants were enrolled and divided into extremely preterm infant group (n=17), early preterm infant group (n=48), and moderate-to-late preterm infant group (n=33). According to the dose of fat emulsion, they were further divided into low- and high-dose subgroups. The umbilical cord blood and dried blood filter papers within 3 days after birth were collected. Tandem mass spectrometry was used to measure the content of short-, medium-, and long-chain acylcarnitines. RESULTS: The extremely preterm infant and early preterm infant groups had a significantly lower content of long-chain acylcarnitines in the umbilical cord blood and dried blood filter papers within 3 days after birth than the moderate-to-late preterm infant group (P<0.05), and the content was positively correlated with gestational age (P<0.01). On the second day after birth, the low-dose fat emulsion subgroup had a significantly higher content of short-, medium-, and long-chain acylcarnitines than the high-dose fat emulsion subgroup among the extremely preterm infants (P<0.05). In the early preterm infant and moderate-to-late preterm infant groups, there were no significant differences in the content of short-, medium-, and long-chain acylcarnitines between the low- and high-dose fat emulsion subgroups within 3 days after birth. CONCLUSIONS: Compared with moderate-to-late preterm infants, extremely preterm infants and early preterm infants have a lower capacity to metabolize long-chain fatty acids within 3 days after birth. Early preterm infants and moderate-to-late preterm infants may tolerate high-dose fat emulsion in the early stage after birth, but extremely preterm infants may have an insufficient capacity to metabolize high-dose fat emulsion.

[Association of chemokines and their receptors genes polymorphisms with risk of myocardial infarction].

OBJECTIVE: To assess the association of variations in chemokines (CCL5, CCL2), chemokine receptor (CCR5 and CCR2) genes with susceptibility to myocardial infarction (MI) through a case-control study. METHODS: Genotypes of patients with MI (n = 634) were compared with those of controls (n = 601). Genetic polymorphisms of CCL5 rs2107538 (-403G > A), CCL2 rs1024611 (-2518A > G), CCR5 rs333 ( δ 32 ins or del) and CCR2 rs1799864 (190G > A) of 1235 individuals were determined with polymerase chain reaction and restriction fragment length polymorphism (PCR-RFLP). Particular genotypes were confirmed with DNA sequencing. RESULTS: No subject was found to carry the CCR5 - δ 32 allele. No association was found between CCL2 rs1024611 and CCR2 rs1799864 polymorphisms and MI. For CCL5 rs2107538 polymorphism, the A allele has occurred at a higher frequency in MI patients than controls, and its AA genotype has been associated with a significantly increased risk of MI independent of conventional risk factors (OR = 3.346, 95%CI = 1.938-5.775, P < 0.01, AA vs. GG). Further analysis indicated that MI patients had significantly more A-403 - A-2518 haplotype (CCL5 -403G > A and CCL2 -2518A > G, 21.8% vs. 26.6%, OR = 1.229, 95%CI = 1.012-1.493, P = 0.038) and AA or AA genotype (CCL5 -403G > A - CCL2 -2518A > G, 5.0% vs. 12.1%, OR = 3.245, 95%CI = 1.780-5.914, P < 0.01). CONCLUSION: Although our data dose not support an association between CCL2 rs1024611, CCR2 rs1799864 and CCR5 rs333 polymorphisms and MI, genetic variation in CCL5 gene may still be a useful marker for assessing susceptibility to MI in ethnic Han Chinese population.

[Association of haptoglobin 1/2 polymorphism with coronary heart disease in Chinese].

OBJECTIVE: To assess the association of haptoglobin (HP)1/2 polymorphism with coronary heart disease (CHD) in Chinese Hans. METHODS: One hundred and eighty-nine CHD patients and 242 healthy controls confirmed with angiography were recruited. Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method was utilized to genotype the HP1 and HP2 alleles and genotype frequencies in cases and controls were compared. RESULTS: The frequency of HP2-2 genotype was significantly higher in CHDs than in controls (0.54 vs.0.35, P = 0.000). The HP2-2 genotype significantly increased the risk for CHD in univariable analysis (OR = 2.166, 95%CI: 1.467-3.196). Multifactor Logistic regression analysis indicated that HP2-2 genotype is an independent risk factor to CHD (P = 0.002; OR = 2.101, 95%CI: 1.311-3.367). Similarly, the HP2 allele frequency in the CHD group was significantly higher than that in the control subjects (0.74 vs.0.61, P = 0.000). CONCLUSION: The HP2-2 genotype is associated with CHD in Chinese. HP2-2 genotype may be an independent risk factor to CHD, and HP2 allele may be a genetic susceptibility factor to CHD in Chinese.

[Association of thrombospondin-1 gene N700S polymorphism with coronary artery disease].

OBJECTIVE: To investigate the association of thrombospondin-1 (TSP- 1) gene A8831G (N700S) polymorphism with coronary artery disease (CAD). METHODS: This study was conducted with a case-control design including 178 patients with CAD (55 AMI) and 158 healthy subjects. The TSP-1 N700S polymorphism was determined by polymerase chain reaction and restriction fragment length polymorphism analysis. RESULTS: No significant difference of the AG genotype in CAD group and control group (1.7% compared with 0.6%, P=0.375) was detected. None of the homozygotes was detected for the G allele. The prevalence of the G allele was not significantly different between CAD group and controls (0.8% compared with 0.3%, P=0.376). No significant difference of the AG genotype in AMI group and control group (3.6% compared with 0.6%, P=0.104). The prevalence of G allele was not significantly different between AMI patients and controls (1.8% compared with 0.3%, P=0.364). CONCLUSION: There are TSP-1 N700S polymorphisms in Chinese Zhejiang Han people, but the TSP-1 N700S variant shows a much lower prevalence compared with Western populations and may be not a potential risk for CAD and AMI.

Alternaria yunnanensis sp. nov., a New Alternaria Species Causing Foliage Spot of Rubber Tree in China.

A new species of Alternaria causing leaf spots on the rubber tree (Hevea brasiliensis) in Yunnan, China, was isolated, examined, and illustrated. Morphologically, it belongs to the section Porri of Alternaria, which produces relatively large conidia and a simple or branched, filamentous long beak. It is, however, characterized by conidiophores gradually enlarging near the apex into a clavate conidiogenous cell and long ellipsoid to obclavate, smooth-walled conidia with a long filamentous beak. Molecular phylogenetic analyses based on ITS rDNA, GAPDH, and TEF1-alpha sequences demonstrate that the phytopathogen falls in the clade of the section Porri, being most closely related to A. sidae, A. sennae, A. deseriticola, A. cyamopsidis, A. rostellata, A. nitrimali, A. crassa, and A. thunbergiae.

[Polymorphism of angiotensin converting enzyme in Han populations and its relevance to the severity of coronary atherosclerosis].

OBJECTIVE: To explore the polymorphism angiotensin converting enzyme (ACE) in Han populations and its relevance to the severity of coronary atherosclerosis. METHODS: The ACE genotype distribution was detected in 169 patients [aged (62.0 +/-9.9) years] with coronary artery disease (CAD) confirmed with angiography and in 168 normal controls [aged (61.0 +/-7.7) years]. The severity of coronary lesions in the patients was assessed by the number of major coronary arteries with more than 50% luminal obstructions and by the Gensini coronary score. Associations of the severity of coronary artery lesions with the ACE I/D polymorphism in the patients were analyzed. RESULT: The frequencies of the ACE genotype in the CAD patients were 0.296 for DD, 0.391 for ID, and 0.314 for II genotypes, while in the normal controls the genotype distribution was in Hardy-Weinberg equilibrium (DD, 0.161; ID, 0.512; II, 0.327); a significantly excess of the DD genotype in CAD patients was found (P<0.01). No associations were observed between the ACE polymorphism and the number of significantly stenosed coronary arteries. CONCLUSION: The ACE gene polymorphism is a significant predictor for CAD in the Han population but is not a marker for the severity of coronary atherosclerosis.

[Study on differentially expressed gene of the liver of treble fatty metabolism genes mutant mice using cDNA microarray].

OBJECTIVE: To study the gene expression profile of liver of young apoE(-/-)/LDLR(-/-)/Lepr(db/db) treble genes mutant mice and disclose its relationship to hyperlipidemia and the following atherosclerotic lesion. METHODS: The gene expression profile was investigated using cDNA microarray technique; the plasma total cholesterol(TC) and triglyceride(TG) levels were analyzed by COD-PAP and GPO-PAP method. And morphological observations of the aorta were made. RESULTS: Among the 4000 target genes, 92 genes were up-regulated and 105 genes were down-regulated in the treble genes mutants, compared with wild type control. Among the differentially expressed lipid metabolism related genes, cholesterol synthesis gene coding for farnesyl diphosphate farnesyl transferase was down-regulated, while triglyceride metabolism gene e.g. pancreatic lipase related protein 1 gene (Pnliprp1) was up-regulated. Expression profile of carbohydrate, cell skeleton and immune related genes were also altered. On the other hand, in the plasma from the treble genes mutant mice at 5 weeks of age, hyperlipidemia was found to be combined with atheroslerotic lesion. All these biochemical and pathological changes were aggravated following aging. CONCLUSION: The data suggested that the multiple genes mutations, especially those involved in lipid metabolism, were contributing to the alteration of liver gene expression profile that might lead to hyperlipidemia and atherosclerotic lesion in the young apoE(-/-)/LDLR(-/-)/Lepr(db/db) mutants.

[Association of angiotensinogen gene M235T variant with hypertrophic cardiomyopathy].

OBJECTIVE: To evaluate the influence of the angiotensinogen(AGT) gene M235T variant on the prevalence and severity of hypertrophic cardiomyopathy(HCM). METHODS: The authors conducted a case-control study on 152 subjects, including 72 HCM patients and 80 normal controls. Polymerase chain reaction(PCR) combined with restriction fragment length polymorphism(RFLP) was used to detect the M235T variant of AGT gene. Interventricular septum thickness, left ventricular posterior wall thickness and apical wall thickness were measured by means of M-mode echocardiography under two-dimensional guidance in the parasternal long-axis plane and apical two- and four-chamber views. RESULTS: (1) The genotype distributions of AGT gene in both groups were in agreement with Hardy-Weinberg equilibrium. (2) The genotype distributions of the M235T variant differed significantly in HCM patients and controls(chi-square=6.090 P<0.05). The frequencies of TT genotype and T235 allele in HCM patients were higher than did the patients in controls(TT genotype 0.63 vs 0.45 OR=2.037 95%CI 1.064-7.899 P<0.05 T235 allele 0.78 vs 0.64 OR=1.990 95%CI 1.197-3.308 P<0.01). (3)The patients with the TT genotype had significantly greater mean left ventricular maximal wall thickness than did the patients with the MM and MT genotypes [(19.1+/-4.8) mm vs(15.3+/-2.6)mm and(16.2+/-5.1)mm F=4.261 P<0.05]. CONCLUSION: The variant M235T of the AGT gene is significantly associated with HCM in this population. The genotype TT or allele T might be a genetic risk factor for the development and extent of hypertrophy in HCM patients.

[Association of angiotensinogen gene M235T variant with essential hypertension].

OBJECTIVE: To investigate the association of the AGT gene M235T variant with essential hypertension in Han population of Zhejiang Province. METHODS: The study included 230 subjects: 116 hypertensive patients and 114 normotensive controls. Polymerase chain reaction (PCR) combined with restrictive fragment length polymorphism (RFLP) was used to detect the M235T variant of angiotensinogen (AGT) gene. Blood pressure, body height and weight, fasting blood glucose and serum lipid were measured in all subjects. RESULTS: (1)The systolic blood pressure and diastolic blood pressure of hypertensive group were significantly higher than those of control group, while no significant difference was observed with regard to age, gender, body mass index, blood glucose, or lipid profile. (2)The genotype distribution of AGT gene in both groups was in agreement with Hardy-Weinberg equilibrium. (3)The genotype distribution of the M235T variant differed significantly in hypertensives and controls (chi(2)=6.966,P<0.05). The frequencies of genotype TT and T235 allele in hypertensives were higher than those in controls (TT genotype: 0.47 compared with 0.33, chi(2)=5.36,P<0.05; T235 allele: 0.71 compared with 0.60, chi(2)=6.179, P<0.05). CONCLUSION: The molecular variant M235T of the AGT gene is significantly associated with essential hypertension in this population. The genotype TT or allele T235 might be a genetic risk factor for hypertension.

[Simvastatin induced apoptosis and its effect on apoptosis-related gene expression in rat vascular smooth muscle cell]

OBJECTIVE: To observe the influence of simvastatin on the apoptosis of vascular smooth muscle cells (VSMC) and its effects on the expression of apoptosis-related genes. METHODS: The presence of apoptosis was detected by electron microscope and flow cytometry assessment of PI/Annexin V stain; The protein levels of Bax, Bel-2 and activation of caspase-3 were examined using Western blot technique. RESULTS: After treatment with 30 &mgr;mol/L simvastatin for 24 h, apoptosis were identified with electron microscope in VSMC and flow cytometry showed that rate of apoptosis in simvastatin group (35.5+/-5.8)% was singificantly higher than that in control group (15.1+/-5.0)%. Western blot analyses revealed that the apoptosis process was associated with upregulation of Bax protein and activation of caspase-3, but not with Bel-2 expression. CONCLUSION: Simvastatin can induce apoptosis in VSMC in associated with induction of bax and activation of caspase-3.

In situ measurements of the solubilities of salt-water systems by a fiber sensor.

A novel fiber sensor for measuring solid solubilities of salt-water systems in situ is described. The sensor consists of a diode laser as light source, three couplers, two sensing fiber ends with protective cladding, and two photodetectors. The measurement principle is based on relative Fresnel reflective intensity. This method enabled us to observe in situ transitional process of the equilibration of a solid-liquid system with a small quantity of specimens. By the relatively simple technique, fast determination of the solid solubility is possible. We applied this method to measure a temperature dependence of the solubility of potassium chloride in water in situ and compared with the previous data obtained by other techniques. The measured result has the long-term standard deviation of the concentration of 0.1%, and agrees with the data obtained by the classical method within the error of +/-1%. This method is precise and sample saving and is suitable to measure the solubilities of rare and expensive materials.