Transjugular intrahepatic portosystemic shunts (TIPS) in children

The transjugular intrahepatic portosystemic shunt procedure is an accepted treatment for adults with complications of portal hypertension. We performed a retrospective review of all pediatric TIPS placements performed at the University of California, San Francisco between 1990 and 1996. Twelve procedures were attempted in nine children, with a mean age (+/- SD) of 9.4 +/- 3.9 years (range, 5 to 15 years) and a mean weight of 31 +/- 18 kg (range, 16 to 70 kg). The indications for TIPS placement were portal hypertension complicated by chronic variceal hemorrhage not controlled with sclerotherapy (n = 7) and hypersplenism with thrombocytopenia (n = 2). TIPS placement was successfully completed initially in seven of nine (78%) patients. Unfavorable vascular anatomy was the cause of failure in two cases. The seven patients who underwent successful TIPS placement were followed up for an average of 136 days (range, 1 to 800 days); two still have patent shunts, three underwent liver transplantation, one had a splenorenal shunt after stenosis, and one died of underlying liver disease. Variceal bleeding was controlled in four of five patients who successfully underwent TIPS placement. Shunt occlusion occurred in four patients; patency was restored by transjugular shunt revision in three, and a splenorenal shunt was performed in one.     

Animal models of bacterial gastritis: the role of host, bacterial species and duration of infection on severity of gastritis

Gastric bacteria from cheetahs with gastritis were used to inoculate specific-pathogen free kittens and conventional mice. Helicobacter sp. and Gastrospirillum sp. colonized kittens, while only Gastrospirillum sp. colonized mice. In kittens, both bacterial species induced mild lymphofolliclar gastritis which did not change over the course of the 11 months observation period. In mice, Gastrospirillum sp. induced lymphoplasmacytic and follicular gastritis which increased in severity over 6 months and persisted for the 12 month observation period. Gastric ulcers and gastric mucosal hypertrophy were present in chronically infected mice. These results indicate that host but not bacterial factors influence the severity of gastritis, and that in mice, bacterial gastritis increases in severity with time and may lead to gastric ulceration in some individuals.     

Deposition of thin film silicon using the pulsed PECVD and HWCVD techniques

We report on the use of pulsed plasma-enhanced chemical vapor deposition (P-PECVD) technique and show that “state-of-the-art” amorphous silicon (a-Si:H) materials and solar cells can be produced at a deposition rate of up to 15 Å/s using a modulation frequency in the range 1–100 kHz. The approach has also been developed to deposit materials and devices onto large area, 30 cm×40 cm, substrates with thickness uniformity (<5%), and gas utilization rate (>25%). We have developed a new “hot wire” chemical vapor deposition (HWCVD) method and report that our new filament material, graphite, has so far shown no appreciable degradation even after deposition of 500 μm of amorphous silicon. We report that this technique can produce “state-of-the-art” a-Si:H and that a solar cell of p/i/n configuration exhibited an initial efficiency approaching 9%. The use of microcrystalline silicon (μc-Si) materials to produce low-cost stable solar cells is gaining considerable attention. We show that both of these techniques can produce thin film μc-Si, dependent on process conditions, with 1 1 1 and/or 2 2 0 orientations and with a grain size of approx. 500 A. Inclusion of these types of materials into a solar cell configuration will be discussed.     

Chronic pain in the lives of older women

We investigated the effect of chlorpromazine (CPZ) in a murine model of T-cell-dependent liver injury caused by concanavalin A (ConA). CPZ (3 and 10 mg/kg) treatment 1 h before ConA injection prevented liver injury. CPZ (3, 10 mg/kg) administered 1 h after a ConA injection was also hepatoprotective, whereas cyclosporin (CsA, 100 mg/kg) was active only when given before ConA. Under either condition, CsA but not CPZ prevented concurrent increases in splenic ornithine decarboxylase (ODC) activity, a putative index of T-cell proliferation/differentiation. CPZ down-regulated tumor necrosis factor-alpha (TNF-alpha) and up-regulated IL-10 in mice that then received ConA, whereas delayed administration of CPZ had no effect. These results suggest that CPZ prevented liver injury without affecting the proliferation/differentiation of T-cells. The dissociation of hepatoprotection by CPZ from cytokine modulation indicates that this drug intervenes in the adherence of T-cells or the death of hepatocytes in the ConA-model.     

Genetic mapping of a major susceptibility locus for juvenile myoclonic epilepsy on chromosome 15q

The epilepsies are a group of disorders characterised by recurrent seizures caused by episodes of abnormal neuronal hyperexcitability involving the brain. Up to 60 million people are affected worldwide and genetic factors may contribute to the aetiology in up to 40% of patients. The most common human genetic epilepsies display a complex pattern of inheritance. These are categorised as idiopathic in the absence of detectable structural or metabolic abnormalities. Juvenile myoclonic epilepsy (JME) is a distinctive and common variety of familial idiopathic generalised epilepsy (IGE) with a prevalence of 0.5-1.0 per 1000 and a ratio of sibling risk to population prevalence (lambda(s)) of 42. The molecular genetic basis of these familial idiopathic epilepsies is entirely unknown, but a mutation in the gene CHRNA4, encoding the alpha4 subunit of the neuronal nicotinic acetylcholine receptor (nAChR), was recently identified in a rare Mendelian variety of idiopathic epilepsy. Chromosomal regions harbouring genes for nAChR subunits were therefore tested for linkage to the JME trait in 34 pedigrees. Significant evidence for linkage with heterogeneity was found to polymorphic loci encompassing the region in which the gene encoding the alpha7 subunit of nAChR (CHRNA7) maps on chromosome 15q14 (HLOD = 4.4 at alpha = 0.65; Z(all) = 2.94, P = 0.0005). This major locus contributes to genetic susceptibility to JME in a majority of the families studied.