One-stage laparoscopic-assisted resection of gastrojejunocolic fistula after gastrojejunostomy for duodenal ulcer: a case report

<p>Abstract</p> <p>Introduction</p> <p>Gastrojejunocolic fistula is a rare condition after gastrojejunostomy. It was thought to be a late complication related to stomal ulcers as a result of inadequate gastrectomy or incomplete vagotomy. We report a case of gastrojejunocolic fistula after gastrojejunostomy for peptic ulcer treated with one-stage laparoscopic resection.</p> <p>Case presentation</p> <p>A 41-year-old Japanese man complained of diarrhea for 10 months, as well as severe weight loss and weakness. After admission, we immediately started intravenous hyperalimentation. On performing colonoscopy and barium swallow, gastrojejunocolic fistula was observed close to the gastrojejunostomy site leading to the transverse colon. After our patient's nutritional status had improved, one-stage surgical intervention was performed laparoscopically. After the operation, our patient recovered uneventfully and his body weight increased by 5 kg within three months.</p> <p>Conclusions</p> <p>Modern management of gastrojejunocolic fistula is a one-stage resection because of the possibility of early recovery from malnutrition using parenteral nutritional methods. Today, laparoscopic one-stage en bloc resection may be feasible for patients with gastrojejunocolic fistula due to the development of laparoscopic instruments and procedures. We describe the first case of gastrojejunocolic fistula treated laparoscopically by one-stage resection and review the literature.</p

Elevated α-synuclein mRNA levels in individual UV-laser-microdissected dopaminergic substantia nigra neurons in idiopathic Parkinson's disease

The presynaptic protein α-synuclein is involved in several neurodegenerative diseases, including Parkinson's disease (PD). In rare familial forms of PD, causal mutations (PARK1) as well as multiplications (PARK4) of the α-synuclein gene have been identified. In sporadic, idiopathic PD, abnormal accumulation and deposition of α-synuclein might also cause degeneration of dopaminergic midbrain neurons, the clinically most relevant neuronal population in PD. Thus, cell-specific quantification of α-synuclein expression-levels in dopaminergic neurons from idiopathic PD patients in comparison to controls would provide essential information about contributions of α-synuclein to the etiology of PD. However, a number of previous studies addressing this question at the tissue-level yielded varying results regarding α-synuclein expression. To increase specificity, we developed a cell-specific approach for mRNA quantification that also took into account the important issue of variable RNA integrities of the individual human postmortem brain samples. We demonstrate that PCR –amplicon size can confound quantitative gene-expression analysis, in particular of partly degraded RNA. By combining optimized UV-laser microdissection- and quantitative RT–PCR-techniques with suitable PCR assays, we detected significantly elevated α-synuclein mRNA levels in individual, surviving neuromelanin- and tyrosine hydroxylase-positive substantia nigra dopaminergic neurons from idiopathic PD brains compared to controls. These results strengthen the pathophysiologic role of transcriptional dysregulation of the α-synuclein gene in sporadic PD