Objective To investigate the role pituitary adenylate cyclase activating polypeptide (PACAP) in the growth modulation of PACAP of human pancreas carcinoma cells and determine whether sphingomyolin (SM) may act as a second messenger involved in the postreceptor signal transduction. Methods Human pancreas carcinoma cell strains, JF305, HS766T and ASPC 1 cells were cultivated, reproduced and then treated with PACAP 1 38 (10 -12 -10 -6 M). The amounts of proliferated carcinoma cells were estiimated with Mosmann's method (MTT). The concentrations of intracellular SM in cells were determined with thin layer chromotograph. Intracellular adenosine monophosphate and Ca 2+ levels were detected by radioimmunoassay and Fura 2/AM respectively. Results It was found that three kind of human pancreatic cancer cells were proliferated and the intracellular levels of SM, cAMP and cytosolic Ca 2+ were increased by treating PACAP 1 38 . The effect of PACAP 1 38 in JF305, HS766T and ASPC 1 could be inhibited by Somatostatin. Conclusion PACAP 1 38 may play a role in the proliferation of human pancreatic cancer cells. The postreceptorsignal transduction of PACAP may be mediated by both adenosine cyclinase and Calcium calmodin pathways. SM may be a second messenger involved in this process.

Objective To investigate the role pituitary adenylate cyclase-activating polypeptide (PACAP) in the growth modulation of PACAP of human pancreas carcinoma cells and determine whether sphingomyolin (SM) may act as a second messenger involved in the postreceptor signal transduction. Methods Human pancreas carcinoma cell strains, JF305, HS766T and ASPC-1 cells were cultivated, reproduced and then treated with PACAP1-38 (10- 12 - 10- 6 M). The amounts of proliferated carcinoma cells were estiimated with Mosmann's method (MTT). The concentrations of intracellular SM in cells were determined with thin layer chromotograph. Intracellular adenosine monophosphate and Ca2 + levels were detected by radioimmunoassay and Fura-2/AM respectively. ResultsIt was found that three kind of human pancreatic cancer cells were proliferated and the intracellular levels of SM, cAMP and cytosolic Ca2+ were increased by treating PACAP1-38. The effect of PACAP1-38 in JF305, HS766T and ASPC-1 could be inhibited by Somatostatin.ConclusionPACAP1-38 may play a role in the proliferation of human pancreatic cancer cells. The postreceptorsignal transduction of PACAP may be mediated by both adenosine cyclinase and Calcium-calmodin pathways. SM may be a second messenger involved in this process.

ObjectiveTo observe the growth inhibition of somatostatin (SS) on human pancreas carcinoma cell strains HS766T and its mechanism.MethodsHS766T cells cultured in DMEM medium containing 10% FCS were treated with SS.Proliferation and viability of cell was measured by the Mosmann′s method (MTT). Intracellular adenosine monophosphate levels was detected by radioimmunoassay. Intracellular Ca 2+ level were measured using a F-2000 flurorescence spectrophotometer.ResultsSS inhibited the proliferation of HS766T in a concentration dependent manner (P

Objective:Our purpose was to investigate the growth regulation and postreceptor signal transduction of somatostatin (SS) on human colon cancer cell line. Methods:Low differentiated clone A cells of human carcinoma were treated with different concentrations of SS and the growth status was observed. Intracellular 1,4,5-trisphosphate (IP3) and cyclic adenosine monophosphate (cAMP) were extracted, then the concentrations of them were measured by liquid scintillation technique and gamma scintillation counter.Intracellular free calcium concentration was detected by loading Fura-2 and fluorescental technique. Protein kinase C (PKC) was extracted from cytosol and membrane, then the activity of both parts was determined with TaKai method. Results:The clone A cell growth was inhibited greatly by different concentrations of SS (10-10 to 10-5　mol/L) and it is related to the doses of SS.Somatortatin could largely inhibit the production of intracellular IP3, ［Ca2+］i, and cAMP, and decrease the activity of PKC. Conclusion:The growth of Clone A cell can be inhibited by SS. The inhibition may be mediated by phosphate inositol pathway, so intracellular IP3, ［Ca2+］i decreased, or inhibited the cell growth by inhibiting the activity of PKC.On the other hand, the cell proliferation may be inhibited by adenosine cyclase pathway, that is decreasing intracellular cAMP ,inhibiting cAMP-depending protein kinase.

Objective: To study the protective effect of enteral nutrition with Salvia miltiorrhiza on injuries multiple organs in rabbits. Method: Forty-four rabbits were randomly divided into four groups: Normal control group (N) 8 rabbits, Endotoxin group (LPS), Enteral nutrition group (LPS+EN) and Enteral nutrition with Salvia miltiorrhiza group (LPS+DS),each 12 rabbits. Three days before given endotoxin, LPS+DS group was fed enteral nutrition fluid with Sallvia miltiorrhiza 80 ml/kg bw (15g salvia per 100 ml fluid) and LPS+ EN group was fed enteral nutrition only.N group was fed the same quantity of normal saline. At the end of 10 d, the rabbits were killed and serum SOD, MDA, endotoxin and intestinal mucus SIgA contents were determined. Small intestine, liver, lung, kidney and heart were taken for pathological examination. Results: Serum MDA of LPS+DS group was much lower than LPS group, endotoxin level also lower , but intestinal SIgA content higher LPS group . The pathological examination showed that the intestinal villi were shortend, injured , and necrotic in LPS group; liver was hemorrhagic at portal area with cytoplasmic vacuolization, lung and kidney were also injuried pathologically. These pathological features were comparatively mild in LPS+EN group and much better in LPS+ DS group. Conclusion: Enteral nutrition with Salvia miltiorrhiza may reduce the oxidative damages of multiple organs induced by endotoxin as shown by increased SIgA of small intestine, maintenance of intestinal mucosa integrity and alleviation of pathological changes of multiply organs in rabbits.

Objective To evaluate the imaging diagnosis of anomalous origin of coronary artery from the pulmonary artery(ACAPA).Methods A total of 11 cases with ACAPA were included in the present study.Chest films,echocardiography,cardioangiography,and electron beam computed tomography (EBCT) were employed as diagnostic modalities.Macroscopic anatomy at operation was referred. Results Ten cases were classified as anomalous origin of left coronary artery from the pulmonary artery(ALCAPA) and 1 case as anomalous origin of right coronary artery from the pulmonary artery(ARCAPA).They could not be diagnosed by chest films,but could be diagnosed by echocardiography in 3 cases,by EBCT in 1 case,and by cardioangiography in all cases.In ALCAPA,cardioangiography showed that the left coronary arteries arising from the posterior sinus or posterior wall of the pulmonary artery were perfused retrogradely via the collaterals from the dilated right coronary artery.In ARCAPA,the right coronary artery originated from the right sinus of the pulmonary artery.Gross anatomy at operation showed that the sites of the anomalous origins were the same as that of cardioangiography.Ischemic fibrosis of the anterior papillary muscles,mitral valve annulus enlargement,and prolapse of mitral valve,which led to mitral valve insufficiency,were found in 3 cases.Conclusion Chest film has limitation in the diagnosis and echocardiography should be further improved.Cardioangiography remains the “gold standard” of the preoperative diagnosis.

OBJECTIVE: To explore the genetic basis for a pedigree affected with X-linked mental retardation. METHODS: The proband was subjected to chromosomal karyotyping, FMR1 mutation testing and copy number variation analysis with a single nucleotide polymorphism microarray (SNP array). His family members were subjected to multiplex ligation-dependent probe amplification (MLPA) assaying. Expression of genes within the repeated region were analyzed. RESULTS: The proband had a normal chromosomal karyotype and normal number of CGG repeats within the FMR1 gene. SNP array identified a 370 kb duplication in Xq28 (ChrX: 153 027 633-153 398 515), which encompassed 14 genes including MECP2. The patient was diagnosed as Lubs X-linked mental retardation syndrome (MRXSL). MLPA confirmed the presence of copy number variation, its co-segregation with the disease, in addition with the carrier status of females. Genes from the duplicated region showed higher levels of expression (1.79 to 5.38 folds) within peripheral blood nucleated cells of the proband. CONCLUSION The patients were diagnosed with MRXSL. The expression of affected genes was up-regulated due to the duplication. Genetic counseling and prenatal diagnosis may be provided based on the results.
DNA Copy Number Variations ; Female ; Fragile X Mental Retardation Protein ; Humans ; Mental Retardation, X-Linked ; Methyl-CpG-Binding Protein 2 ; Pedigree ; Pregnancy

Objective:To summarize and elucidate the impact of ambient air pollution on biological aging among middle-aged and older adults.Methods:"Air pollution""Biological age""Epigenetic age""Biological aging"and"Epigenetic aging", as well as specific names of air pollutants and biological age were used as search keywords. This study searched the databases of PubMed and Web of Science for eligible English articles and CNKI, CQVIP, Wanfang, CBM, CSTP and other Chinese databases for eligible Chinese articles from inception until June 30, 2023. The language was limited to Chinese and English.Results:Among the 14 included articles, five studies investigated the impact of air pollution on DNA methylation age using different algorithms, while six studies explored the relationship between air pollutants and telomere length. Six studies focused on frailty as an outcome, and an additional study revealed the relationship between fine particulate matter (PM 2.5) and its components with composite indicator age (KDM age). The results indicated that, although different forms of biological ages were susceptible to different ambient air pollutants at different degrees, previous studies had consistently found that the increased levels of PM 2.5 and one of its major components, black carbon (BC), could significantly accelerate the biological aging of middle-aged and older adults. Similar trends were observed with nitrogen oxides (NO x) and ozone (O 3) but with relatively limited evidence. Conclusion:Major air pollutants could accelerate the biological aging of middle-aged and older adults.

Objective:To summarize and elucidate the impact of ambient air pollution on biological aging among middle-aged and older adults.Methods:"Air pollution""Biological age""Epigenetic age""Biological aging"and"Epigenetic aging", as well as specific names of air pollutants and biological age were used as search keywords. This study searched the databases of PubMed and Web of Science for eligible English articles and CNKI, CQVIP, Wanfang, CBM, CSTP and other Chinese databases for eligible Chinese articles from inception until June 30, 2023. The language was limited to Chinese and English.Results:Among the 14 included articles, five studies investigated the impact of air pollution on DNA methylation age using different algorithms, while six studies explored the relationship between air pollutants and telomere length. Six studies focused on frailty as an outcome, and an additional study revealed the relationship between fine particulate matter (PM 2.5) and its components with composite indicator age (KDM age). The results indicated that, although different forms of biological ages were susceptible to different ambient air pollutants at different degrees, previous studies had consistently found that the increased levels of PM 2.5 and one of its major components, black carbon (BC), could significantly accelerate the biological aging of middle-aged and older adults. Similar trends were observed with nitrogen oxides (NO x) and ozone (O 3) but with relatively limited evidence. Conclusion:Major air pollutants could accelerate the biological aging of middle-aged and older adults.