穴位坦线配合中药治疗银屑病疗效观察

０　引言　银屑病是一原因不明的常见皮肤病,临床以慢性、复发性,表面覆盖有多层的银白色鳞屑,境界清楚的红斑、丘疹为特征．３ａ来我们采用穴拉埋线配合自拟中药验方治疗银屑病４６例,取得较好疗效．１　对象和方法１．１　对象　本组４６（男２１,女２５）例,年龄...     

Ras gene activation in human small intestinal tumors

Expression of the ras oncoprotein in thirteen human small intestinal tumors was investigated employing an immunohistochemical technique. The level of ras p21 was analysed using the monoclonal antibody Y13-259 and the biotin-streptavidin-peroxidace-DAB technique. Nine out of thirteen tumors including one hyperplastic - metaplastic polyp, one adenomatous and papillary polyp of the duodenum, one adenomatous polyp, one leiomyoma, one carcinoid, one lymphoma, one angiosarcoma of the jejunum, one leiomyosarcoma and one metastatic adenocarcinoma of the colon, were found to 'press the ras p21 oncoprotein at elevated levels, as compared to adjacent normal tissue. Whereas in one Brunner's gland adenoma of the duodenum, one neurilemoma, one adenocarcinoma of the small intestine and one metastatic adenocarcinoma of the colon expression of ras p21 was not elevated. The detection of H-ras mutations in codon 12 and K-ras mutations in codons 12 and 13 was also examined using the polymerase chain reaction technique. Four out of the thirteen small intestinal tumors examined possessed mutations of the H-ras gene in codon 12. These included the following, tumors: one Brunner's gland adenoma of the duodenum, one lymphoma, one leiomyo-sarcoma and one metastatic adenocarcinoma of the colon. This is the first demonstration of ras mutations in small intestinal tumors. None of the tumors had mutations in K-ras codons 12 or 13 (Gly-->Asp) It is suggested that the ras p21 oncoprotein may be involved in the pathogenesis and H-ras mutations and be a molecular genetic marker in small intestinal tumors.     

Automated sequencing detects all mutations in Northern Irish patients with phenylketonuria and mild hyperphenylalaninaemia

In the first phase of the Northern Ireland PKU Study, we used automated sequencing to identify the spectrum of mutations in a random group of 32 unrelated phenylketonuria (PKU) families. We also investigated 7 Northern Irish patients with mild hyperphenylalaninaemia not requiring dietary intervention (MHP, previously referred to as non-PKU HPA). Disease-causing mutations were identified on all 78 investigated chromosomes. We found 23 different mutations, including 20 missense, 1 nonsense and 2 splice site mutations. All mutations were located within exons or at intronexon boundaries of the phenylalanine hydroxylase gene. Seven mutations occurred at CpG sites, confirming these sites as mutation hot-spots in PKU. Mutations R408W and I65T are the two commonest PKU mutations in the Northern Irish population. Two mutations (T380M and V245A) can be characterized as MHP mutations; they are quasi dominant markers for MHP since they cause mild hyperphenylalaninaemia even when occurring in conjunction with the most severe PKU mutations. The results have proven valuable for the development of a routine PKU mutation analysis system in Northern Ireland.     

Complementary role of helical CT cholangiography to MR cholangiography in the evaluation of biliary function and kinetics

To explore the potential role of computed tomographic cholangiography (CTC) in relation to magnetic resonance cholangiography (MRC) in cases in which knowledge of biliary kinetics and functional information are important for therapeutic decisions, 31 patients (14 men and 17 women) underwent MRC followed by CTC. We examined nine post-cholecystectomy cases with right upper quadrant abdominal pain, six cases with a previous biliary-enteric anastomosis and clinical evidence of cholangitis, eight biliary strictures with pain or symptoms of cholangitis, four cases with strong clinical evidence of sclerosing cholangitis, three cases with suspected post-laparoscopic cholecystectomy bile leakage, and one case with chronic pancreatitis and a common bile duct stent associated with cholangitis. In relation to MRC, CTC provided additional biliary functional information as follows: abnormal biliary drainage through the ampulla in 7/9 cholecystectomy cases, impaired drainage in 3/6 biliary-enteric anastomoses, and complete obstruction in 2/8 biliary strictures. CTC diagnosed early sclerosing cholangitis in 4/4 cases and confirmed suspected bile leakage in 1/3 post-laparoscopic cholecystectomy patients, and the patency of the biliary stent in the patient with chronic pancreatitis. Thus, CTC provides clinically important information about the function and kinetics of bile and complements findings obtained by MRC.     

The course of traumatic pancreatitis in a patient with pancreas divisum: a case report

Background  

The peculiar anatomy of pancreatic ducts in pancreas divisum (PD) may interfere with the development of acute chronic pancreatitis. In the presented case, PD influenced the evolution of lesions after pancreatic trauma.     

Tumor necrosis factor alpha induces endothelial galactosyl transferase activity and verocytotoxin receptors. Role of specific tumor necrosis factor receptors and protein kinase C

Infections with verocytotoxin (VT) producing Escherichia coli have been strongly implicated in the epidemic form of hemolytic uremic syndrome (HUS). Endothelial damage plays a central role in the pathogenesis of HUS. In vitro studies have shown that VT can damage endothelial cells after interaction with its cellular receptor globotriaosylceramide (GbOse3cer). Cytokines, such as tumor necrosis factor alpha (TNF alpha) and interleukin-1 (IL-1) can potentiate the toxic effect of VT by inducing a protein-synthesis dependent increase in VT receptors on endothelial cells. In this study, the mechanisms underlying the increase in endothelial VT receptors induced by TNF alpha were studied in more detail. To investigate which proteins were involved in this induction, endothelial cells were incubated with and without TNF alpha in the presence of 14C-galactose or 14C-glucose. Thin-layer chromatography (TLC) analysis of the glycolipid extracts of these cells demonstrated a markedly enhanced incorporation of 14C-galactose in GbOse3cer and other galactose-containing glycolipids, suggesting that TNF alpha enhanced galactosyl-transferase activity. To examine the role of the two recently cloned TNF-receptors (TNFR-p75 and TNFR-p55) in the TNF alpha-induced increase in GbOse3cer in human endothelial cells, cells were incubated with TNF alpha, the TNFR-p55 selective R32W-S86T- TNF alpha-mutant, or the TNFR-p75 selective D143N-A145R-TNF alpha- mutant. The effect of TNF alpha activation, determined by binding- experiments with 125I-VT-1, could be largely, but not completely mimicked by R32W-S86T-TNF alpha. Although incubation of cells with D143N-A145R-TNF alpha did not show an increase in VT-1 binding, the monoclonal antibody utr-1, which prevents binding to TNFR-p75, decreased the TNF alpha-induced VT-1 binding. Activation of protein kinase C (PKC) by phorbol ester increases the expression of VT-1 receptors; this effect was prevented by the PKC inhibitor Ro31-8220 and by homologous desensitization by pretreatment with phorbol ester. In contrast, the presence of the protein kinase inhibitor Ro31-8220 or desensitization of PKC activity reduced the TNF alpha-induced increase in VT-1 receptors maximally by 50% and 24%, respectively. Comparable reductions in overall protein synthesis and the synthesis of E-selectin and plasminogen activator inhibitor-1 (PAI-1) were observed. This suggests an effect on general protein synthesis rather than a specific effect of PKC in the signal transduction pathway, by which TNF alpha induces VT-1 receptors. Our results indicate that TNF alpha can increase the VT-1 receptors on endothelial cells by inducing galactosyl- transferase activity, that this action of TNF alpha mainly occurs via the TNFR-p55; and that PKC activation increases expression of VT-1 receptors by a separate mechanism that acts additively to the TNF alpha- induced increase in VT-1 receptors.     

Homozygous deletions of the p16 tumor-suppressor gene are associated with lymphoid transformation of chronic myeloid leukemia

The p16 gene, also referred to as MTS1, INK4, CDK4I, or CDKN2, at chromosome 9p21 has recently been described as a tumor suppressor that may be involved in a wide range of tumors. We have used a semiquantitative multiplex polymerase chain reaction assay to search for deletions of the p16 gene in 34 patients with chronic myeloid leukemia in blast crisis (CML BC), 19 patients with acute lymphoblastic leukemia (ALL), and 25 patients with acute myeloid leukemia (AML). Homozygous deletions of p16 exons were found in 5 of 10 (50%) patients with CML in lymphoid BC and in 5 (26%) ALL patients, but in only 1 (2%) case with AML. No deletions were found in CML BC of nonlymphoid phenotype. Comparison of chronic phase DNA or remission DNA with acute leukemia DNA in 5 individuals showed that the p16 deletions were acquired and not inherited, directly implicating these lesions in the pathogenesis of the disease. We conclude that functional elimination of the p16 gene, or a closely mapping gene, is involved in a significant number of patients with CML in lymphoid transformation.     

Epidemiologic study of asymptomatic men screened by maximal treadmill testing for latent coronary artery disease

A group of 1,390 asymptomatic men screened for latent coronary artery disease by maximal treadmill testing and double Master two-step test were followed up for a mean of 6.3 years. Angina, sudden death or acute myocardial infarction was used as the end point for coronary heart disease. There were differences in testing sensitivity and specificity among age and subject groups, but maximal treadmill testing out-performed the double Master test as a screening technique. Maximal treadmill testing demonstrated a 60.9 percent sensitivity, 92 percent specificity and a 20 percent probability that coronary artery disease would develop in a subject with an abnormal response. A risk ratio of 14.3 was obtained and demonstrated that maximal treadmill testing was a valuable screening technique for latent coronary artery disease. However, limitations of the sensitivity and specificity of the functional S-T segment response were apparent. The abnormal S-T segment response to exercise testing did not absolutely predict the future presentation of coronary artery disease, and a normal response to maximal treadmill testing did not rule out this possibility. Because premature ventricular contractions demonstrated a very low sensitivity, predictive value and risk ratio they were not a practical indicator of increased risk for latent coronary artery disease except when associated with an abnormal S-T segment response.