Choledochal duct cyst: resection with physiologic reconstruction.

BACKGROUND. The accepted surgical treatment of choledochal duct cyst is complete excision and enteric drainage through an intestinal conduit. Peptic ulceration and fat malabsorption have been reported after Roux-en-Y reconstruction. Such long-term complications may be avoided by a technique that simulates normal physiology. METHODS. Twenty-one patients have undergone resection of a choledochal duct cyst in the past 12 1/2 years. The pathologic duct is resected to the level of normal mucosa. A short segment of jejunum with a intussusception valve (1.5 to 2 cm) is interposed between the common hepatic duct and the duodenum. The medical records and all radiographs of each patient were reviewed. Eighteen children were reexamined or the parents were contacted by phone. RESULTS. Twenty of 21 patients recovered without major perioperative complications. Twelve of them are well and have no symptoms at 3 to 12+ years (mean, 6 years) after operation. Four children are currently well 6 to 19 months after operation. Three children were well when lost to follow-up. Two patients have radiographic evidence of incompetence of the interposition valve. One of these, who initially underwent operation at 9 months of age, was reexplored at 10 months and at 10 years for a stricture at the hepaticojejunal anastomosis. The other, a 7-year-old girl who was admitted with jaundice and pancreatitis, has had episodic abdominal pain for 7 years after operation but is well. CONCLUSIONS. The valved jejunal interposition hepaticoduodenostomy offers superior biliary reconstruction after excision of a choledochal duct cyst. Normal physiology is simulated, with bile draining directly into the duodenum. A short conduit prevents stasis, and biliary reflux is minimized with the addition of an intussusception valve.     

The onset of ablation of the evoked adductor pollicis muscle twitch in children: a clinical perspective

The time to loss of the adductor pollicis muscle response to ulnar nerve stimulation at 1 Hz (twitch) after succinylcholine, 1.5 mg.kg-1 intravenously (IV), or vecuronium, 0.1 mg.kg-1 (IV), administration was assessed visually in 134 children, age 2-13 yr, during clinically determined, deep halothane, enflurane and isoflurane anaesthesia. The overall time to twitch ablation and duration of succinylcholine's action is in agreement with published times obtained under controlled experimental conditions; the onset time following vecuronium is comparable to those observed during a similar anaesthetic background measured under controlled experimental conditions. Twitch ablation after succinylcholine was achieved in half the time needed following vecuronium regardless of anaesthetic agent. Succinylcholine's and vecuronium's onset time as well as succinylcholine's duration is adequately assessed by the outlined, simple clinical means. The choice of inhalation agent does not affect the time to visible twitch ablation in a clinically relevant manner; nor does it make an appreciable difference, in clinical terms, in succinylcholine's duration of action.     

Advances in understanding cell interactions in tissue resorption. Relevance to the pathogenesis of periodontal diseases and a new hypothesis

Much of the connective tissue degradation that takes place in periodontal diseases is mediated by proteolytic enzymes. Previous studies have focused on the action of proteinases released by invading polymorphonuclear neutrophils and macrophages, and bacterial enzymes. In view of recent work establishing that resident connective tissue cells can be induced by cytokines to bring about the destruction of their own matrix, we propose a new hypothesis. In this we envisage that a critical step is the interaction of bacterial antigens with inflammatory cells, resulting in the production of a cytokine, interleukin-1. Our interpretation of in vitro evidence is that the loss of connective tissue attachment and bone matrix resorption in periodontal diseases is mediated by metalloproteinases such as collagenase and stromelysin released by cells of the periodontium. Such proteolytic destruction can be induced by interleukin-1, whose production may not be dependent on a specific microbial flora but may be triggered by a number of organisms. It is now clear that interleukin-1 has multiple actions on both immune and non-immune cells; these include the induction of lymphocyte differentiation and proliferation and the stimulation of bone and cartilage resorption, and prostaglandin and metalloproteinase synthesis by connective tissues. It seems likely that further knowledge about the production and function of this cytokine will have an increasing impact in many diseases that involve resorption, particularly since interleukin-1-like molecules can be produced by cell types other than monocytes/macrophages, including keratinocytes and fibroblasts.     

13-cis-retinoic acid (NSC 122758) in the treatment of children with metastatic neuroblastoma unresponsive to conventional chemotherapy: Report from the childrens cancer study group

The Childrens Cancer Study Group evaluated daily oral 13-cis-retinoic acid to determine its therapeutic efficacy in 28 children with advanced neuroblastoma refractory to conventional therapy. Cheilitis and fissured lips were the most common side effects; however, fewer than 50% of the patients experienced any toxicity. Two of twenty-two evaluable children demonstrated positive response to therapy. In one case, a child received the drug for 11 months. Seventeen patients demonstrated progressive disease within 28 days of the start of treatment. Three other patients with stable disease, or removed from study at day 28, were considered nonresponsive. Our data demonstrate that, when given as a single daily oral dose of 100 mg/m², 13-cis-retinoic acid does not have significant activity in children with advanced neuroblastoma. © 1992 Wiley-Liss, Inc.     

Disturbed myelinogenesis and recovery in hyperphenylalaninemia in rats: An immunohistochemical study

Chronic hyperphenylalaninemia (HPA) in rats has been used as an experimental model of the human inborn error of metabolism phenylketonuria (PKU). Impaired brain development in PKU and HPA is reflected in reduced myelin formation. We have used immunohistochemistry, with antibodies to cell-specific antigenic markers, to investigate the cellular basis of the hypomyelination in the corpus callosum and cerebral cortex of rats made hyperphenylalaninemic from Postnatal Days 3-17. The rats were then allowed to recover until Day 59. No effects were seen on the number and differentiation pattern of ganglioside GD3-expressing glial progenitors. Myelin basic protein and 2'3'-cyclic nucleotide 3'-phosphohydrolase (CNP) immunostaining demonstrated a reduction in myelin formation in the corpus callosum and subcortical white matter at 12 and 17 days postnatal. However, numbers of CNP+ oligodendrocytes appeared normal throughout development. No reactive astrogliosis was seen at any stage. The intensity of axonal neurofilament immunostaining was reduced in the corpus callosum at 17 days. In layers II and III of the cortical gray matter there was an increase in the cell packing density and a concomitant decrease in cell body size. Myelination in the corpus callosum was rapid during the recovery period with no difference noted at Day 59. Axonal neurofilament staining also returned to normal in the corpus callosum. However, recovery became increasingly incomplete away from the corpus callosum into the cortical gray matter. Our data suggest a primary effect of HPA on axonal maturation with hypomyelination consequential upon this.     

Heroin-Induces Differential Protein Expression by Normal Human Astrocytes (NHA)

Heroin use is postulated to act as a cofactor in the neuropathogenesis of human immunodeficiency virus (HIV-1) infection. Astrocytes, integral components of the CNS, are reported to be susceptible to HIV-1 infection. Upon activation, astrocytes release a number of immunoregulatory products or modulate the expression of a number of proteins that foster the immunopathogenesis of HIV-1 infection. However, the role of heroin on HIV-1 infectivity and the expression of the proteome of normal human astrocytes (NHA) have not been elucidated. We hypothesize that heroin modulates the expression of a number of proteins by NHA that foster the neuoropathogenesis of HIV-1 infection. We utilized LTR amplification and the p24 antigen assay to quantitate the effect of heroin on HIV-1 infectivity while difference gel electrophoresis (DIGE) combined with protein identification through high performance liquid chromatography-tandem mass spectrometry (HPLC-MS/MS) to analyze the effects of heroin on the proteomic profile of NHA. Results demonstrate that heroin potentiates HIV-1 replication in NHA. Furthermore, heroin significantly increased protein expression levels for protein kinase C (PKC), reticulocalbin 1 precursor, reticulocalbin 1, tyrosine 3-monooxgenase/tryptophan 5-monooxgenase activation protein, chloride intracellular channel 1, cathepsin D preproprotein, galectin 1 and myosin light chain alkali. Heroin also significantly decreased protein expression for proliferating cell nuclear antigen, proteasome beta 6 subunit, tropomyosin 3, laminin receptor 1, tubulin alpha 6, vimentin, EF hand domain family member D2, Tumor protein D54 (hD54), ATP synthase, H+ transporting, mitochondrial F1 complex and ribosomal protein S14. Identification of unique, heroin-induced proteins may help to develop novel markers for diagnostic, preventative and therapeutic targeting in heroin using subjects.