CCK receptor belongs to G-protein-coupled receptor (GPCR) superfamily.Polymorphism of CCK receptors can alter drug affinity and/or biological efficacy, and its genetic differences in amino acid sequences can induce ligand-independent signaling, which in turn can lead to disease. With growing efforts in the field of pharmacogenomics, it is anticipated that polymorphism-induced alterations in drug and/or receptor function will be a focus of increasing concern in the future drug-development project. Study of CCK receptor polymorphism may reveal some universal rules in GPCR superfamily. In this review, the alterations of receptor function and/or drug efficacy resulted from polymorphism in CCK receptors will be discussed in the viewpoint of molecular biology and pharmacogenomics, and some strategies in development of receptor-specific drugs will be put forward.

Multinolular and intrahepatic recurrent HCC can originate from intrahepatic metastasis and multiple origins,and their colnal origin is closely related to the clinical diagnosis and treatment.To designate suitable therapeutic strategies according to their colnal origin is a new challenge needs to be tackled urgently.This paper reviews recent progress in the clinicopathological features,molecular diagnosis and clinical outcomes of multiple origin HCC.

Objective To investigate the role of Stat1 in pathological process of nerve cells apoptosis induced by diffuse axonal injury (DAI) on rats. MethodsThe DAI model was established by using an injury model adapted from Marmarou et al. in 1994. All animals were divided into three groups, including control group, mock group and test group sacrificed on 6, 12, 24, 48, 72, 120 and 240 hours post injury (hpi). The paraffin-embedded sections of brain tissue were processed for HE staining and Bielschowsky’s silver method. Cell apoptosis was examined by flow cytometry and the expression of bax and bcl-2 were analyzed by RT-PCR. And Phospho-Ser727 Stat1 expression was examined by immunohistochemistry in different brain regions. ResultsThere was no brain contusion within HE staining, however, waving and enlargement of axons were observed within Bielschowsky’s silver method. The apoptotic rate of brain cells as well as PCR products ratio of bax to bcl-2 was highest at 24 hpi and decreased with time. An up-regulation of Phospho-Ser727 Stat1 at 6 hpi was discernible, and then reached the top at 24 hpi in cortex, cerebellum, brain stem and corpus callosum, and at 12 hpi in hippocampus. This increase was associated with the nerve cells apoptosis, r=0.921. In addition, the Phospho-Ser727 Stat1 positive cells were neurons and glial cells assessed from morphous. ConclusionsOur data indicate that Stat1 may contribute to the apoptosis of DAI on rats. In addition, the expression of Phospho-Ser727 Stat1 in glial cells suggested that glial cells may play an important role in the pathogenic mechanism of DAI.

Objective To investigate the contents of cAMP and cGMP in the central nervous system in morphine dependent and withdrawal rats.Methods A physical morphine dependent model in rats was established by subcutaneous injection of morphine in gradually increasing doses.The cAMP and cGMP contents in the brain regions were determined by radioimmunoassay.Results Compared with control group,morphine dependence could significantly decrease the cGMP content or profoundly increase the cAMP content and the cAMP/cGMP ratio in rat striatum,diencephalons,midbrain,pons and hippocampus,but these changes described above were not detected in cerebellum.Compared with morphine dependent group,naloxone induced withdrawal could significantly decrease the cGMP contents or increase the cAMP contents and the cAMP/cGMP ratio in striatum and hippocampus,but these changes described above were not observed in the other regions.Conclusion The changes of the cAMP and cGMP contents may be one of the important molecular mechanisms leading to morphine dependence and abstinence.

Recent studies show that cholecystokinin, a brain-gut peptide, also locates in lung tissues in many animals. Cholecystokinin in lung tissues participates in the modulation of the tone of the tracheae and the pulmonary vessels. It also regulates the breathing pattern as a nerve transmitter in the respiratory center. This paper discusses the location and the biological role of cholecystokinin in lung tissues and focuses on its part during lung diseases.

Animals ; Arrhythmias, Cardiac ; etiology ; therapy ; Captopril ; therapeutic use ; Disease Models, Animal ; Electric Stimulation Therapy ; methods ; Myocardial Ischemia ; physiopathology ; therapy ; Rabbits ; Ventricular Fibrillation

Aim To observe the influence of CCK-8 on expression of MMPs/TIMP-1 in TNF-α-induced rat fibroblast-like synovial cell line RSC-364.Methods The secretion levels of MMP-1, MMP-3, MMP-9 and TIMP-1 were determined using ELISA;MMP-3 and MMP-9 mRNA expressions were detected by RT-PCR.Results MMP-3 and MMP-9 could not be examined in RSC-364 incubated with CCK-8 and unstimulated RSC-364, which was able to product a little MMP-1, TIMP-1 and express even less MMP-3,-9 mRNA.CCK-8 inhibited the increase in MMP-1, MMP-3, MMP-9 secretion and MMP-3,-9 mRNA expression in TNF-α-induced RSC-364.TIMP-1 production was also increased in TNF-α-induced RSC-364.CCK-8 had no effect on TIMP-1 production in TNF-α-induced RSC-364, but was able to reduce the ratios of MMP-1, MMP-3, MMP-9 to TIMP-1.Conclusion The inhibitory effect of CCK-8 on MMPs activity may be related to the decrease of MMPs mRNA expression, MMPs secretion and the ratios of MMPs to TIMP-1 in TNF-α-induced RSC-364, which indicates that CCK-8 might be a possible regulator in the pathogenesis of rheumatoid arthritis.

Aim To investigate the hippocampal neuronal injury induced by ?-amyloid peptide ( A?) in rats and the candidate contribution of JNK signal transduction pathway to A? toxicity. Methods Rats were bilaterally injected with A?1 -40 into hippocampi CA1 area. The pathological changes,survival and apoptosis,and ultrastructure of hippocampal neurons,as well as p-JNK positive cells were observed by HE staining,Nissl staining,TUNEL staining,immunohistochemistry and transmission electron microscopy,respectively. Results Thepyramidal cells in hippocampus arranged loosely with decreased cell number. The gliacytes significantly proliferated. Significant apoptotic features were observed in CA1 ultrastructure. TUNEL-positive cells and p-JNK-positive cells significantly increased ( P

0.05).But PMA increased and SC-3088 decreased cAMP content and PKA activity in LPS-stimulated rat PIMs(P

Objective To describe the pathogenic and serological test results of the plague in China from 2001 to 2009, and human and animal plague distribution. Methods Through access to information of the plague surveillance report in China from 2002 to 2010, national plague pathogenic and serological test results and the epidemic situation were analyzed from 2001 to 2009. Results From 2001 to 2009, 2966 strains of Yersinia pestis were isolated in the seven provinces which were Guizhou, Guangxi, Yunnan, Qinghai, Tibet, Gansu and Inner Mongolia. Of these, 1 138 000 animals were detected by bacteriological method, 1998 strains of Yersinia pestis were isolated;379 227 groups of intermediary animals were detected, 927 strains of Yersinia pestis were isolated;41 strains of Yersinia pestis were isolated from human body. Animal serums of 1 169 702 were detected by indirect hemagglutination assay(IHA), of these 3177 animal serums were positive, 168 human serums were positive;53 323 animal samples were detected by reverse indirect hemagglutination assay(RIHA), of these 500 were positive. There were outbreak or epidemic of plague in 9 types of plague foci, 2925 strains of Yersinia pestis were isolated. Two animals and 6 fleas were judged as new reservoir and new vector. There were 23 counties of 6 provinces were judged as plague new natural foci counties. Conclusions The plague epidemic in China is still serious between 2001 and 2009. There are nine types of foci in the active state.