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Biomedical subjects

B Ji

Publications and source records attributed to B Ji.

At least 19 recordsLinked to original sources

Effect of cold blood cardioplegia enriched with potassium-magnesium aspartate during coronary artery bypass grafting.

AIM: The aim of this investigation is to evaluate the effect of enriched with potassium-magnesium aspartate cold-blood cardioplegia on early reperfusion injury and postoperative arrhythmias in patients with ischemic heart disease undergoing coronary artery bypass grafting (CABG), using measurements of cardiac troponin I (CTnI), hemodynamic indexes and clinical parameters. METHODS: Forty patients with three-vessel coronary artery disease (CAD) and stable angina, receiving first-time elective CABG, were randomly divided into 2 groups: patients in control group (C group n=20) received routine institutional cold blood cardioplegia (4 degrees C) concentration of Mg2+4 mmol/L, Ca2+1.2 mmol/L and K+ 24mmol/L during myocardial arrest. Patients in P group (n=20) received modified cold blood cardioplegia enriched with potassium-magnesium aspartate and maintained concentration of Mg2+10 mmol/L, Ca2+1.2 mmol/L and K+20mmol/L in the final blood cardioplegia solution. Clinical outcomes were observed during operation and postoperatively. Serial venous blood samples for CTnI were obtained before induction, after cardiopulmonary bypass (CPB), and postoperative 6, 24, and 72 hours. Hemodynamic indexes were obtained before and after bypass by the radial catheter and Swan-Ganz catheter. RESULTS: In both groups, there were no differences regarding preoperative parameters. There were no cardiac related deaths in either group. The time required to achieve cardioplegic arrest after cardioplegia administration was significantly shorter in P group (47.5+/-16.3 s) than in C group (62.5+/-17.6 s) (P<0.01). The number of patients showing a return to spontaneous rhythm after clamp off was significantly greater in P group (n=20, 100%) than in C group (n=14, 70%) (P<0.01). Eight patients in C group had atrial fibrillation (AF) compared with two patients in P group (P<0.05) in the early of postoperative period. The level of CTnI increased 6 hours and 12 hours postoperatively, and there was a significant difference between groups (P<0.05). P group also shortened the time of postoperative mechanical ventilation (P<0.05) after surgery. CONCLUSIONS: Cold blood cardioplegia enriched with potassium-magnesium aspartate is beneficial on reducing reperfusion injury.

Aged↗

A possible mechanism of naproxen-induced lipid peroxidation in rat liver microsomes.

Previous papers from our laboratory report that naproxen and salicylic acid induced lipid peroxidation in rat liver microsomes, however, the mechanism is still unclear. In the present paper, ferrous iron release, nicotinamide-adenine dinucleotide phosphate reduced form (NADPH) oxidation and hydrogen peroxide (H2O2) formation have been measured to find out which mechanisms are involved in naproxen- and salicylic acid-induced lipid peroxidation. While the increase of ferrous iron release was observed with high concentrations of naproxen, salicylic acid did not stimulate ferrous iron release. Neither of these drugs stimulated NADPH oxidation and H2O2 formation. However hexobarbital and perfluorohexane, known as uncouplers of cytochrome P450, stimulated microsomal NADPH oxidation, O2 consumption, H2O2 formation and water (H2O) formation involving four-electron oxidase reaction. These results suggest that ferrous iron release contributes to naproxen-induced microsomal lipid peroxidation and that naproxen and salicylic acid are not uncouplers of cytochrome P450. Apparently H2O2 does not play an important role in naproxen- and salicylic acid-induced microsomal lipid peroxidation.

Animals↗

Human pancreatic acinar cells lack functional responses to cholecystokinin and gastrin.

BACKGROUND & AIMS: Pancreatic acinar cells from various species express cholecystokinin (CCK) A, CCK-B, or a combination of these CCK receptor subtypes. The presence and functional roles of CCK receptors on human acinar cells remain unclear. METHODS: Acini isolated from human pancreas were treated with CCK receptor agonists, CCK-8 and gastrin, and an agonist for m3 muscarinic acetylcholine receptors (m3 AchR), carbachol. Functional parameters measured included intracellular [Ca(2+)], amylase secretion, and ERK phosphorylation. Binding studies were performed using (125)I-CCK-8. Expression of messenger RNAs (mRNAs) was determined using real-time quantitative reverse-transcription polymerase chain reaction (RT-PCR) and localized by in situ hybridization. RESULTS: Human acini did not respond to CCK agonists. In contrast, they responded to carbachol with robust increases in each of the functional parameters. Moreover, the cells responded to CCK agonists after adenoviral-mediated gene transfer of CCK-A or CCK-B receptors. A low level of specific and a high level of nonspecific binding of (125)I-CCK-8 were observed. Quantitative RT-PCR indicated that the message levels for CCK-A receptors were approximately 30-fold lower than those of CCK-B receptors, which were approximately 10-fold lower than those of m3 Ach receptors. In situ hybridization indicated the presence of m3 Ach receptor and insulin mRNA but not CCK-A or CCK-B receptor mRNAs in adult human pancreas. CONCLUSIONS: These data indicate that human pancreatic acinar cells do not respond to CCK receptor agonists in terms of expected functional parameters and show that this is due to an insufficient level of receptor expression.

Gastrins↗

Glutathione S-transferase genotypes and stomach cancer in a population-based case-control study in Warsaw, Poland.

Glutathione S-transferases are important in the detoxification of a wide range of human carcinogens. Previous studies have shown inconsistent associations between the GSTT1 and GSTM1 null genotypes and stomach cancer risk. We investigated the relationship between these and related genotypes and stomach cancer risk in a population-based case-control study in Warsaw, Poland, where stomach cancer incidence and mortality rates are among the highest in Europe. DNA from blood samples was available for 304 stomach cancer patients and 427 control subjects. We observed a 1.48-fold increased risk for stomach cancer (95% confidence interval 0.97-2.25) in patients with the GSTT1 null genotype but no evidence of increased risk associated with the GSTM1, GSTM3 or GSTP1 genotypes. Furthermore, the stomach cancer risk associated with the GSTT1 null genotype varied by age at diagnosis, with odds ratios of 3.85, 1.91, 1.78 and 0.59 for those diagnosed at ages less than 50, 50-59, 60-69 and 70 years or older, respectively (P trend = 0.01). This was due to a shift in the GSTT1 genotype distribution across age groups among stomach cancer patients only. These results suggest that the GSTT1 null genotype may be associated with increased risk of stomach cancer.

Adult↗

Efficacies of clarithromycin regimens against Mycobacterium xenopi in mice.

Mice were infected intravenously with 3.5 x 10(7) CFU of Mycobacterium xenopi and treated with various clarithromycin-containing regimens or left untreated for 4 weeks. All nine of the clarithromycin-containing regimens reduced the CFU counts to the levels below the pretreatment values, indicating that these regimens had a bactericidal effect on M. xenopi in mice. The rifampin-isoniazid-ethambutol regimen was significantly less bactericidal than clarithromycin alone or clarithromycin-containing combined regimens.

Animals↗

Effectiveness of once-weekly rifapentine and moxifloxacin regimens against Mycobacterium tuberculosis in mice.

Mice infected with 1.6 x 10(7) CFU of Mycobacterium tuberculosis were treated 14 days later for 6 months with a regimen of once-weekly 10 mg of rifapentine and 75 mg of isoniazid per kg of body weight supplemented with either 150 mg of streptomycin per kg or 100 mg of moxifloxacin per kg during either both the 2-week daily initial and once-weekly continuation phases or only in the daily 2-week initial phase. On completion of treatment, all lung cultures were negative, except for three mice, each with a single colony: two whose rifapentine-isoniazid regimen was supplemented with streptomycin during the whole course of therapy and one whose rifapentine-isoniazid regimen had no initial daily phase, but was supplemented with streptomycin and moxifloxacin during the whole course of therapy. After 3 months of follow-up, positive lung cultures were obtained from 61 and 56% of mice supplemented with streptomycin during either the full course of therapy or only the daily 2-week initial phase, respectively, and 15 and 50% of mice supplemented with moxifloxacin during either the full course of therapy or only the daily 2-week initial phase, respectively. These results suggest that moxifloxacin has sterilizing activity against M. tuberculosis.

Animals↗

CCK independently activates intracellular trypsinogen and NF-kappaB in rat pancreatic acinar cells.

In the cholecystokinin (CCK) hyperstimulation model of acute pancreatitis, two early intracellular events, activation of trypsinogen and activation of nuclear factor-kappaB (NF-kappaB), are thought to be important in the development of the disease. In this study, the relationship between these two events was investigated. NF-kappaB activity was monitored by using a DNA binding assay and mob-1 chemokine gene expression. Intracellular trypsin activity was measured by using a fluorogenic substrate. Protease inhibitors including FUT-175, Pefabloc, and E-64d prevented CCK stimulation of intracellular trypsinogen and NF-kappaB activation. Likewise, the NF-kappaB inhibitors pyrrolidine dithiocarbamate and N-acetyl-L-cysteine inhibited CCK stimulation of NF-kappaB and intracellular trypsinogen activation. These results suggested a possible codependency of these two events. However, CCK stimulated NF-kappaB activation in Chinese hamster ovary-CCK(A) cells, which do not express trypsinogen, indicating that trypsin is not necessary for CCK activation of NF-kappaB. Furthermore, adenovirus-mediated expression in acinar cells of active p65 subunits to stimulate NF-kappaB, or of inhibitory kappaB-alpha molecules to inhibit NF-kappaB, did not affect either basal or CCK-mediated trypsinogen activation. Thus trypsinogen and NF-kappaB activation are independent events stimulated by CCK.

Acetylcysteine↗

[Effects of grazing and cultivating on emission of nitrous oxide, carbon dioxide and uptake of methane from grasslands].

Measurement of N2O, CO2 and CH4 with the optimized closed chamber/GC technique in the typical grassland, which were influenced by human activities, grazing and cultivating first time in situ were carried out in Inner Mongolia of P. R. China from 1998 to 1999. It was found that wheat cropping can increase N2O production 3 times than the native, and changed a CO2 sink of Inner Mongolia Steppe to a significant source, increased efflux CO2(C) average 14.3 mg.(m2.h)-1 from Jun. to Dec. in 1998. CH4 uptake was highly increased if there was grazing lightly. There were no effects of wheat cropping on CH4 uptake and no significant results of grazing on N2O emission. Soil moisture and temperature were the key factors, other than human activities, which affect the patterns of seasonal variation of N2O and CO2 emission and CH4 uptake. Highly inter-annual variations, which resulted from the annual precipitation, of the exchange fluxes and seasonal variation patterns of N2O and CO2 emission and CH4 uptake there were. It was a fact that N2O and CO2 emission from the soils was inversely related to CH4 uptake.

Animal Husbandry↗

[Study on the association of pathologic myopia with HLA-DQB1 gene].

OBJECTIVE: To investigate the association of pathologic myopia (PM) with HLA-DQB1 alleles in order to study the pathogenesis of PM. METHODS: The genome DNA of 66 patients with PM was extracted from the blood. The second exon of the HLA-DQB1 gene was amplified by polymerase chain reaction (PCR), and individual PCR products were digested by allele specific restriction enzymes of Hae III, BssH II, Apa I, BsaH I, Hae II, Hpa II, Rsa I, Bsp 1286 I for typing. Genotype was determined by restriction fragment length polymorphism (RFLP) pattern. The frequency of 16 alleles of HLA-DQB1 was detected and compared with that of the healthy control. RESULTS: The frequencies of HLA-DQB1 * 0301 and * 0303 were significantly higher in the patients with PM (P < 0.0001), while that of HLA-DQB1 * 0601 and * 0602 were significantly lower (P < 0.0001) than that of the control group. CONCLUSION: HLA-DQB1 * 0301, * 0303 alleles are susceptible alleles, and possibly they are the pathogenic genes, * 0601, * 0602 are resistant alleles, and may be they possess the protective property.

Adolescent↗

Species differences between rat and mouse CCKA receptors determine the divergent acinar cell response to the cholecystokinin analog JMV-180.

The cholecystokinin (CCK) analog JMV-180 acts as a partial agonist in rats and a full agonist in mice. Whether this functional variability is due to species differences in CCK receptor structure or to alterations in the cellular environment is unknown. To address this question, an adenoviral construct encoding the rat CCK(A) receptor (AdCCK(A)R) was used to express the rat receptor in acini from CCK(A) receptor-deficient mice (CCK(A)R -/-). Infection of CCK(A)R -/- acini in vitro with pAdCCK(A)R led to a time-dependent increase in (125)I-CCK(8) binding. The affinity for JMV-180 of the adenovirally transferred rat and the endogenous mouse CCK(A) receptors was not different. In native mouse acini, JMV-180 acted as a full agonist (both stimulation and inhibition of amylase release). In contrast, in mouse acini expressing pAdCCK(A)R JMV-180 acted as a partial agonist (only stimulation of amylase release). In addition, the pattern of protein synthesis induced by JMV-180 in CCK(A)R -/- mouse acini infected with AdCCK(A)R resembled the pattern observed in wild-type rats (lack of inhibition) rather than the respective pattern in wild-type mice (inhibition). These data suggest that species differences in the CCK(A) receptor of rats and mice account for the observed divergence in the acinar cell response to JMV-180.

Adenoviridae↗

Bactericidal activities of HMR 3647, moxifloxacin, and rifapentine against Mycobacterium leprae in mice.

Bactericidal activities of HMR 3647 (HMR), moxifloxacin (MXFX), and rifapentine (RPT) against Mycobacterium leprae, measured by the proportional bactericidal technique in the mouse footpad system, were compared with those of the established antileprosy drugs clarithromycin (CLARI), ofloxacin (OFLO), and rifampin (RMP). Administered in five daily doses of 100 mg/kg of body weight, HMR appeared slightly more bactericidal than CLARI. In a single dose, MXFX at 150 mg/kg was more active than the same dose of OFLO and displayed exactly the same level of activity as RMP at 10 mg/kg; the combination MXFX-minocycline (MINO) (MM) was more bactericidal than the combination OFLO-MINO (OM); RPT at 10 mg/kg was more bactericidal than the same dose of RMP and even more active than the combination RMP-OFLO-MINO (ROM); the combination RPT-MXFX-MINO (PMM) killed 99.9% of viable M. leprae and was slightly more bactericidal than RPT alone, indicating that the combination PMM showed an additive effect against M. leprae.

Animals↗

Antituberculosis activity of once-weekly rifapentine-containing regimens in mice. Long-term effectiveness with 6- and 8-month treatment regimens.

The effectiveness of various once-weekly 10 mg/kg rifapentine (P)- containing regimens for treatment of tuberculosis was assessed in mice infected intravenously with 4.3 x 10(6) colony-forming units (cfu) of Mycobacterium tuberculosis H37Rv, and treated 14 d later with various combinations of rifampin (R), P, isoniazid (H), pyrazinamide (Z), ethambutol (E), or streptomycin (S). Control mice treated daily with either 2-mo HRZ + 4-mo HR or 2-mo HRZ + 6-mo HE were rendered spleen and lung culture-negative at 6 mo and 8 mo, respectively. Treatment failure with emergence of R-resistant bacilli occurred in all mice given once-weekly monotherapy with P for 6 mo. Once-weekly PH treatment was successful at 6 mo when it was preceded by a 2-mo daily phase with HRZ. When the initial daily phase was reduced to 2 wk, once-weekly PH-containing treatment was successful, at 6 mo, only if it was supplemented with S during the initial daily and the once-weekly phases, and at 8 mo if it was supplemented with daily H during the once-weekly phase. Without these supplements, once-weekly treatment failed in some mice with selection of R-resistant or H-resistant mutants.

Animals↗

Combination of rifapentine-moxifloxacin-minocycline (PMM) for the treatment of leprosy.

To further the development of a multidrug regimen for treatment of leprosy that is suitable for monthly administration and fully supervisable, the bactericidal activities against Mycobacterium leprae of HMR 3647 (HMR), moxifloxacin (MXFX) and rifapentine (RPT) were measured by the proportional bactericide technique in the mouse footpad system, and compared with those of the established antileprosy drugs clarithromycin (CLARI), ofloxacin (OFLO) and rifampicin (RMP). Administered in five daily doses of 100 mg per kg body weight, HMR appeared slightly more bactericidal than CLARI, but the difference did not attain statistical significance. Administered as single doses, MXFX in a dosage of 150 mg per kg was more active than OFLO in the same dosage, and displayed the same level of activity as RMP in a dosage of 10 mg per kg; the combination MXFX-minocycline (MINO) (MM) was more bactericidal than the combination OFLO-MINO (OM); RPT in a dosage of 10 mg per kg was more bactericidal than RMP administered in the same dosage, and even more active than the combination RMP-OFLO-MINO (ROM); the combination RPT-MXFX-MINO (PMM) killed 99.9% of viable M. leprae, and was slightly more bactericidal than was RPT alone, indicating that the combination PMM showed an additive effect against M. leprae. These promising results justify a clinical trial among lepromatous patients, in which MM is being compared with OM, and PMM with ROM, in terms of efficacy and tolerance.

Animals↗

[The relationship among proinsulin and true insulin to coronary artery disease].

OBJECTIVE: Whether proinsulin (PI) and true insulin (TI) are independently related to coronary artery disease (CAD). METHODS: 54 patients with CAD diagnosed by coronary angiography and/or intravascular ultrasound, 37 patients without CAD by coronary angiography and/or intravascular ultrasound and 23 healthy volunteers. All subjects had oral glucose tolerance test after an overnight 14 h fast. PI and TI concentrations were detected at different phases by BA-ELISA in which PI cross -reactivity is less than 0.1%. RESULTS: Fasting and post-glucose loading PI and TI levels in both CAD and non-CAD groups significantly increased when compared with the control group (P < 0.05), after adjustment for age, body mass index and waist hip ratio, all statistically significant associations weakened or disappeared among three groups; but there was no significant difference of all the above variables between CAD group and non-CAD group (P > 0.05). CONCLUSION: PI and TI, whether fasting or post-glucose loading, may not be independently related to CAD.

Adult↗