妊娠期顽固性肾绞痛的腔内处理

目的探讨腔内诊治妊娠期肾积水合并顽固性肾绞痛的安全性和有效性。 方法回顾性分析2017年3月至2018年9月我院收治的78例妊娠期肾积水合并顽固性肾绞痛患者的病例资料。根据顽固性肾绞痛持续时间将患者分为A组（6 h以内16例）,B组（6～12 h 53例）和C组（12 h以上9例）。 结果58例术中发现输尿管结石,16例（27.6%）术前彩超未见输尿管结石,行输尿管镜碎石取石和留置输尿管双J管。输尿管结石清除率87.9%（51/58）。20例未发现输尿管结石但合并肾盂结石患者,术中留置输尿管双J管。9例（11.5%）有先兆流产表现,其中A组1例（6.25%）,B组4例（7.55%）,C组4例（44.4%）。C组先兆流产的发生率高于A和B组（P<0.05）。1例（6.25%）患者出现尿源性脓毒血症,抗感染等对症处理后痊愈。所有患者均成功通过围产期并生产健康婴儿。 结论对于妊娠期肾积水合并顽固性肾绞痛的患者,早期输尿管镜腔内处理是有效安全的诊断和治疗手段,可降低孕妇和胎儿的风险。     

The life story of the pancreatic B cell

Summary Most research on the pancreatic B cell has so far focussed on the regulation and molecular biology of insulin biosynthesis and release. The present review draws attention to some additional areas of islet research which have become accessible to investigation by recent methodological progress and which may advance our understanding of the role of the B cell in diabetes. There is now evidence to suggest that B cells arise from a pool of undifferentiated precursor cells in the fetal and newborn pancreas. These cells may contribute to islet growth and, if inappropriately stimulated, also to early islet hyperplasia. In the postnatal state, B-cell function is finely tuned by a complex set of incoming signals, one of which is the nutrient supply provided by the blood. Recent studies indicate that a disproportionately high fraction of pancreatic blood is diverted to the islets and that the islet blood flow is increased by glucose. An acute stimulus to insulin release may thus be accompanied by a process which enhances the distribution of the hormone to the target cells. Long-term adjustments of B-cell function are made by changes in B-cell number and total mass. Adaptive growth responses to an increased insulin demand occur in a number of hereditary diabetic syndromes in animals, but in some of these there is an inherited restriction on the capacity for B-cell proliferation leading to further deterioration of the glucose tolerance. Some evidence suggests that a similar mechanism may operate also in human non-insulin-dependent diabetes. A critical appraisal of this hypothesis requires, however, that human B cells should be tested for their growth characteristics. Studies of B-cell proliferation in experimental animals have shown that the B cell passes through the cell cycle at a relatively high rate but that the fraction of proliferating cells is low. Regulation of growth of the total B-cell mass seems to take place by changes in the number of B cells passing through the cell cycle rather than by changes in the rate of the cycle. The number of proliferating B cells also shows a marked decrease with age. It is at present uncertain to what extent these regulatory mechanisms apply also to the human B cell but it can be anticipated that further technical developments will elucidate this problem.The Claude Bernard Lecture 1983 of the European Association for The Study of Diabetes     

Ectopic pancreas: Usual and unusual features

Nine patients with ectopic pancreas in the stomach (8 patients) and duodenum (1 patient) were studied both radiographically and endoscopically. Correct diagnosis was made by radiography in six cases and by endoscopy in seven cases. Masses radiographically larger than 3 cm in diameter were seen in three patients. The incorrect radiographic diagnoses were related to the presence of a large mass in one patient and to the complications of severe bleeding and gastric outlet obstruction in the other two. Endoscopy and radiography are complementary modalities in the diagnosis of ectopic pancreas.     

Prognostic Factors of Survival in a Randomized Phase III Trial (MPACT) of Weekly nab‐Paclitaxel Plus Gemcitabine Versus Gemcitabine Alone in Patients With Metastatic Pancreatic Cancer

Background.

nab-Paclitaxel in combination with gemcitabine has emerged as a new treatment option for patients with metastatic pancreatic cancer (MPC), based on superiority over gemcitabine demonstrated in the phase III MPACT trial. Previously, Karnofsky performance status (KPS) score and the presence of liver metastases were shown to be predictive of survival with nab-paclitaxel plus gemcitabine treatment. This analysis sought to further explore the relationship between clinical characteristics and survival in the MPACT trial and to identify potential predictors of overall survival and progression-free survival in patients with MPC.

Materials and Methods.

Cox regression models adjusted for stratification factors and a stepwise multivariate analysis of prespecified baseline prognostic factors were performed.

Results.

Treatment effect was significantly associated with survival, with a similar magnitude of reduction in risk of death compared with the previously reported primary analysis. Treatment effect consistently favored nab-paclitaxel plus gemcitabine across the majority of the prespecified factors. In addition to KPS score and presence of liver metastases, age and number of metastatic sites were independent prognostic factors of overall and progression-free survival. Baseline carbohydrate antigen 19-9 was not found to be an independent prognostic factor of survival in this analysis.

Conclusion.

The results of this analysis confirm broad utility of nab-paclitaxel plus gemcitabine for the treatment of MPC. In addition, these findings suggest that KPS score, presence of liver metastases, age, and number of metastatic sites are important predictors of survival that may be useful when making treatment decisions and designing future clinical trials.     

Gemcitabine resistant pancreatic cancer cell lines acquire an invasive phenotype with collateral hypersensitivity to histone deacetylase inhibitors

Gemcitabine based treatment is currently a standard first line treatment for patients with advanced pancreatic cancer, however overall survival remains poor, and few options are available for patients that fail gemcitabine based therapy. To identify potential molecular targets in gemcitabine refractory pancreatic cancer, we developed a series of gemcitabine resistant (GR) cell lines. Initial drug exposure selected for an early resistant phenotype that was independent of drug metabolic pathways. Prolonged drug selection pressure after 16 weeks, led to an induction of cytidine deaminase (CDA) and enhanced drug detoxification. Cross resistance profiles demonstrate approximately 100-fold cross resistance to the pyrimidine nucleoside cytarabine, but no resistance to the same in class agents, azacytidine and decitabine. GR cell lines demonstrated a dose dependent collateral hypersensitivity to class I and II histone deacetylase (HDAC) inhibitors and decreased expression of 3 different global heterochromatin marks, as detected by H4K20me3, H3K9me3 and H3K27me3. Cell morphology of the drug resistant cell lines demonstrated a fibroblastic type appearance with loss of cell-cell junctions and an altered microarray expression pattern, using Gene Ontology (GO) annotation, consistent with progression to an invasive phenotype. Of particular note, the gemcitabine resistant cell lines displayed up to a 15 fold increase in invasive potential that directly correlates with the level of gemcitabine resistance. These findings suggest a mechanistic relationship between chemoresistance and metastatic potential in pancreatic carcinoma and provide evidence for molecular pathways that may be exploited to develop therapeutic strategies for refractory pancreatic cancer.     

胰腺癌患者血清CA242定量测定及其意义

目的 探讨定量测定胰腺癌患者血清CA242的临床意义。方法 链亲和素-生物素双抗体夹心ELISA法定量测定83例健康人、28例胰腺癌、16例胰腺炎及68例其它肿瘤患者的血清CA242,并比较其在不同疾病间的差异。结果 血清CA242含量（U/ml）在83例正常人为7.34±5.09;28例胰腺癌为112.85±56.54;16例胰腺炎为8.91±4.58;68例其它肿瘤为23.10±39.89。该法测定胰腺癌患者血清CA242的灵敏度为85.7％,特异性为92.2％,阳性预示值为64.9％,阴性预示值为97.5％。结论血清CA242的定量测定是诊断胰腺癌的敏感而又特异的指标。