Rupture of the Right Hepatic Artery After Left Lobectomy of the Liver in Patients with Bile Duct Carcinoma

Transcatheter arterial embolization (TAE) has been reported as the treatment of choice for rupture of the visceral artery. We experienced two clinical cases of rupture of the right hepatic artery after left lobectomy of the liver for radical resection of the bile duct carcinoma. In the first case, TAE was performed on the right hepatic artery twice under a condition of hemorrhagic shock. Consequently, hepatic ischemia developed into complete infarction of the remnant liver tissue in spite of control of bleeding from the rupture site. In the second case, TAE was successfully accomplished because of the patient\u27s good general condition and sufficient collaterals to the remnant liver. Bile leakage from the hepaticojejunostomy was observed early in the postoperative course, and episodes of intermittent flow of blood through the abdominal drain were experienced in both cases. Injury to the exposed arterial wall by leaking bile after lymph-node dissection was considered to be a possible contributive factor of rupture. TAE following initial diagnostic arteriography should be performed at an early stage when there are several episodes of intraabdominal bleeding. However, hypovolemic shock from massive hemorrhage and poor arterial collaterals due to the primary surgical procedure unfavorably affected the prognosis of a patient undergoing TAE

Clique-based data mining for related genes in a biomedical database

<p>Abstract</p> <p>Background</p> <p>Progress in the life sciences cannot be made without integrating biomedical knowledge on numerous genes in order to help formulate hypotheses on the genetic mechanisms behind various biological phenomena, including diseases. There is thus a strong need for a way to automatically and comprehensively search from biomedical databases for related genes, such as genes in the same families and genes encoding components of the same pathways. Here we address the extraction of related genes by searching for densely-connected subgraphs, which are modeled as cliques, in a biomedical relational graph.</p> <p>Results</p> <p>We constructed a graph whose nodes were gene or disease pages, and edges were the hyperlink connections between those pages in the Online Mendelian Inheritance in Man (OMIM) database. We obtained over 20,000 sets of related genes (called 'gene modules') by enumerating cliques computationally. The modules included genes in the same family, genes for proteins that form a complex, and genes for components of the same signaling pathway. The results of experiments using 'metabolic syndrome'-related gene modules show that the gene modules can be used to get a coherent holistic picture helpful for interpreting relations among genes.</p> <p>Conclusion</p> <p>We presented a data mining approach extracting related genes by enumerating cliques. The extracted gene sets provide a holistic picture useful for comprehending complex disease mechanisms.</p

Slitrk2 deficiency causes hyperactivity with altered vestibular function and serotonergic dysregulation

SLITRK2 encodes a transmembrane protein that modulates neurite outgrowth and synaptic activities and is implicated in bipolar disorder. Here, we addressed its physiological roles in mice. In the brain, the Slitrk2 protein was strongly detected in the hippocampus, vestibulocerebellum, and precerebellar nuclei—the vestibular-cerebellar-brainstem neural network including pontine gray and tegmental reticular nucleus. Slitrk2 knockout (KO) mice exhibited increased locomotor activity in novel environments, antidepressant-like behaviors, enhanced vestibular function, and increased plasticity at mossy fiber–CA3 synapses with reduced sensitivity to serotonin. A serotonin metabolite was increased in the hippocampus and amygdala, and serotonergic neurons in the raphe nuclei were decreased in Slitrk2 KO mice. When KO mice were treated with methylphenidate, lithium, or fluoxetine, the mood stabilizer lithium showed a genotype-dependent effect. Taken together, Slitrk2 deficiency causes aberrant neural network activity, synaptic integrity, vestibular function, and serotonergic function, providing molecular-neurophysiological insight into the brain dysregulation in bipolar disorders