The expression of an auto-antibody in patients with edematous acute pancreatitis and its possible clinical significance was investiaged. Eighteen cases of acute pancreatitis were chosen as experimental group and 25 subjects served as control group. Venous blood samples were taken in both groups at 4 time points: at the day of admission, the 2nd, 4th and 7th day of hospitalization. By using indirect immuno-fluorescence tests the expression of auto-antibody in the samples was semiquantitatively detected. Other biochemical indexes, such as serum amylase, urine amylase, were determined simultaneously. As well, the clinical signs or symptoms were mornitored. It was found that the expression of the auto-antibody was gradually enhanced with the development of acute pancreatitis. The inceased positive expression of auto-antibody showed a correlationship with the improvement of biochemical indexes (r=0.951) and clinical manifestations (r=0.996). There was significant difference between experimental and control groups (P<0.05). During the recovery period of acute pancreatitis, gradually increased auto-antibody expression was detectable. This antibody is against the interstitial structure of the pancreas.
The relationship between 3 polymorphisms sites [interleulin-4 (IL-4), IL-4 receptor (IL-4R) α chain and activation-induced cytidine deaminase (AICDA)] and adult allergic asthma in China was studied. By using case-control method, DNA and clinical data were obtained from allergic asthmatic patients and compared with those in the control subjects. The subjects were genotyped for the IL-4 C-589T promoter polymorphism, the IL-4R α chain Q576R and the AICDA C8408T by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method. The results showed that the IL-4 C-589T was not associated with adult allergic asthma in China. However, the IL-4R α chain 576R/R and AICDA 8408T/T frequency was significantly increased in allergic asthma group as compared with that in the control group [odd ratio (OR)=3.797 and 9.127, respectively;P<0.01)] and was correlated with the increased plasma total IgE. These data suggested that the IL-4R α chain 576R/R and AICDA 8408T/T genotypes confer genetic susceptibility to adult allergic asthma in China.
In order to investigate the relationship between the expression of cyclin A and drug resistance in adult patients with acute leukemia (AL), the mRNA expression of cyclin A, mdr1, Top IIα, bcl-2 was detected in 64 adult patients with AL and 20 normal controls by semi-reverse transcription polymerse chain reaction (semi-RT-PCR). It was found that the cyclin A and Top IIα mRNA expression levels in drug resistant group were significantly lower than in sensitive group (P<0.01). Under the same experimental condition no cyclin A mRNA expression was detectable in all normal controls. The mdr1 and bcl-2 mRNA expression levels in resistant group were significantly higher than in sensitive group (P<0.01). cyclin A and Top IIα gene expression levels were closely correlated (r3=+0.794,P=0.000,n=64) in all AL patients, but cyclin A was not correlated with mdr1 and bcl-2 gene expression levels. In drug resistant group there was a negative correlation between the gene expression levels of cyclin A and mdr1 (r3=−0.337,P=0.029). The 10 AL patients with positive lower expression of both cyclin A and Top IIα were all resistant to drugs. Logistic regression of Binary analysis showed the correlation between the lower expression of cyclin A and drug resistance. It was concluded that lower expression of cyclin A gene might be an unfavorable prognostic factor for patients with AL, and detection of both cyclin A and Top IIα gene expression would predict drug resistance in AL patients.
In this study, the effect of prophylactic anti-inflammation on the development of smoke-induced emphysema was investigated. Young male guinea-pigs aged 1.5–2 months (weighing 198.3±26.9 g) were randomly divided into 4 groups: group A (cigarette smoke exposure only), group B (cigarette smoke exposure plus pentoxifylline-rich (PTX, 10 mg/d) forage feeding), group C (cigarette smoke exposure plus intermittent cortical steroid injection (Triamcinolone acetonide, 3 mg, im, every three weeks) and control group (group D: animals with sham smoke exposure, raised under the same conditions). Animals in group A, B and C were exposed to smoke of cigarettes for 1 to 1.5 h twice a day, 5 days a week. All animals were killed at the 16th week and followed by morphometrical analysis of the midsagittal sectioned lung slices. Smoke exposure of 16 weeks resulted in visible emphysematous development in Group A but not in Group B and C. It was evidenced by the indicator of air-space size, mean linear intercept (Lm): 120.6±16.0 μm in Group a: 89.8±9.2 μm in Group B and 102.4±17.7 μm in Group C. The average Lm in either group B or group C was shorter than that in Group A (ANOVA and Newman-Keuls test, F=8.80,P=0.0002) but comparable to that (94.8±13.2 μm) in group D (P>0.05). It is concluded that long-term prophylactic anti-inflammation inhibits pulmonary emphysema induced by cigarette smoking in the guinea pigs.