Choledochal cyst associated with duodenal obstruction

The association between congenital duodenal obstruction and concomitant choledochal cyst has not been reported, although duodenal obstruction is known to be associated with many other anomalies. The authors describe 2 patients with choledochal cyst with duodenal obstruction. In 1 patient, a diverticulum type of choledochal cyst was found within an annular pancreas. Cyst excision, choledochojejunostomy, and side-to-side duodeno-duodenostomy were performed. The other patient showed separated duodenal atresia and other multiple anomalies including imperforate anus. A choledochal cyst was noted at the time of duodeno-duodenostomy and sigmoid colostomy. Cyst-enterostomy was performed at the age of 8 months, but the patient died of multiple anomalies. Intraoperative cholangiography indicated an anomalous pancreatobiliary ductal junction (APBDJ). In both patients the bile in the cyst contained high levels of amylase, suggesting the presence of an APBDJ. An APBDJ is considered to play an etiologic role in the development of the choledochal cysts associated with duodenal obstruction.     

Vascular endothelial growth factor receptor-1 regulates postnatal angiogenesis through inhibition of the excessive activation of Akt

Vascular endothelial growth factor (VEGF) binds both VEGF receptor-1 (VEGFR-1) and VEGF receptor-2 (VEGFR-2). Activation of VEGFR-2 is thought to play a major role in the regulation of endothelial function by VEGF. Recently, specific ligands for VEGFR-1 have been reported to have beneficial effects when used to treat ischemic diseases. However, the role of VEGFR-1 in angiogenesis is not fully understood. In this study, we showed that VEGFR-1 performs "fine tuning" of VEGF signaling to induce neovascularization. We examined the effects of retroviral vectors expressing a small interference RNA that targeted either the VEGFR-1 gene or the VEGFR-2 gene. Deletion of either VEGFR-1 or VEGFR-2 reduced the ability of endothelial cells to form capillaries. Deletion of VEGFR-1 markedly reduced endothelial cell proliferation and induced premature senescence of endothelial cells. In contrast, deletion of VEGFR-2 significantly impaired endothelial cell survival. When VEGFR-1 expression was blocked, VEGF constitutively activated Akt signals and thus induced endothelial cell senescence via a p53-dependent pathway. VEGFR-1(+/-) mice exhibited an increase of endothelial Akt activity and showed an impaired neovascularization in response to ischemia, and this impairment was ameliorated in VEGFR-1(+/-) Akt1(+/-) mice. These results suggest that VEGFR-1 plays a critical role in the maintenance of endothelial integrity by modulating the VEGF/Akt signaling pathway.     

Hemangioma located just above the left main coronary artery, in a subject who had cardiac arrest due to ventricular fibrillation, led to a diagnosis of Brugada syndrome

We report the case of a 38-year-old Asian man with a pericardial hemangioma on the left main coronary artery. The patient presented initially at our hospital after cardiopulmonary resuscitation following an episode of ventricular fibrillation (VF). Because of spontaneous coved-type ST segment elevation on the higher intercostal space V1 to V2 in a 12-lead electrocardiogram, documented VF in the absence of structural heart disease, and a family history of sudden death, he was diagnosed with Brugada syndrome. Transesophageal echocardiography showed a smooth-surfaced mass with well-demarcated borders, directly above the left main coronary artery. Computed tomography confirmed the presence of the mass, which showed no enhancement at early phase, but did demonstrate homogenous enhancement at delay phase by contrast material. There were no findings from either the nuclear medicine or the tumor marker investigations which indicated that the mass located just above the main coronary arteries was malignant. Therefore, taken together, these findings suggested that the tumor might be a pericardial hemangioma. The relationship between the location of the hemangioma just above the left main coronary artery and the occurrence of VF was not clear, i.e. whether the presence of the hemangioma caused the stimulation of the left main coronary artery and as a result, led to the spasm of the left main coronary artery and the occurrence of VF. Furthermore, as the tumor did not extend into any of the adjacent structures, such as the coronary arteries or the right ventricular outflow tract, surgical resection was not performed; instead, the patient received a dual chamber implantable cardioverter-defibrillator.     

Molecular epidemiologic study of Clostridium difficile infections in university hospitals: Results of a nationwide study in Japan

We conducted a nationwide molecular epidemiological study of Clostridium difficile infection (CDI) in Japan investigated the correlation between the presence of binary toxin genes and CDI severity. This is the first report on molecular epidemiological analyses for CDI in multiple university hospitals in Japan, to our knowledge. We examined 124,484 hospitalized patients in 25 national and public university hospitals in Japan between December 2013 and March 2014, investigating antimicrobial susceptibilities and toxin-related genes for C. difficile isolates from stools. Epidemiological genetic typing was performed by PCR-ribotyping and repetitive sequence-based (rep)-PCR to examine the genetic similarities. The results detected toxin A-positive, toxin B-positive, binary toxin-negative (A⁺B⁺CDT^?) detected from 135 isolates (80.8%) and toxin A-negative, toxin B-positive, binary toxin-negative (A^??B⁺CDT^?) in 23 (13.8%). Toxin A-positive, toxin B-positive, and binary toxin-positive (A⁺B⁺CDT⁺) were seen in 9 isolates (5.4%). Vancomycin (n = 81, 37.7%) or metronidazole (n = 88, 40.9%) therapies were undertaken in analyzed cases. Ribotypes detected from isolates were 017/subgroup 1, 070, 078, 126, 176, 449, 475/subgroup 1, 499, 451, 566 and newtypes. Rep-PCR classified 167 isolates into 28 cluster groups including 2–15 isolates. In addition, 2 pairs of strains isolated from different institutions belonged to the same clusters. Seven out of 9 (77.8%) of the patients with binary toxin producing strains had “mild to moderate” outcome in evaluated symptoms. In conclusion, we found that binary toxin did not show regional specificity and had no relevance to severity of CDI.     

Pulmonary lymphomatoid granulomatosis radiologically mimicking interstitial pneumonia]

We report a rare case of pulmonary lymphomatoid granulomatosis radiologically mimicking interstitial pneumonia. A 57-year-old man was admitted to our hospital because of chest bilateral reticular shadow with sustained cough and breathlessness for 10 years. Chest CT scans showed multiple ground-glass opacities, traction bronchiectasis and cystic change in both lungs, in addition to hilar and mediastinal lymphadenopathy. A histopathologically diagnosis of pulmonary lymphomatoid granulomatosis (angiocentric immunoproliferative lesion, grade 1) was made by thoracoscopic lung biopsy. In this case, serological and immunohistochemical analyses did not show Epstein-Barr virus infection. No clinical or radiological deterioration has been observed thereafter despite no medication.     

Vascular relaxing mechanism of denopamine in isolated canine coronary,femoral, mesenteric,and renal arteries

Summary We investigated the mechanism of vascular relaxation produced by denopamine (deno), an oral positive inotropic agent that has selective ₁-adrenergic action. Deno concentration-dependently (0.1 µM–30 µM) relaxed ring segments of canine femoral, mesenteric, and renal arteries which were partially precontracted with 1 µm phenylephrine or norepinephrine, but did not relax those precontracted with 5 µM prostaglandin F₂ or 40 mM K⁺. The relaxation was not significantly inhibited by pretreatment with 10 µM propranolol or metoprolol. Deno produced a parallel rightward shift in concentration-response curves to phenylephrine in femoral and renal arteries. The Schild plot yielded linear regressions of slopes of 1.301 ± 0.106 and 0.823 ± 0.122, respectively, which were not significantly different from unity. The pA₂ values of Deno against phenylephrine in femoral and renal arteries were 5.41 ± 0.03 and 5.76 ± 0.06, respectively.On the other hand, Deno concentration-dependently (10 nM–10 µM) relaxed ring segments of canine coronary arteries which were partially precontracted with 5 µM prostaglandin F₂. The relaxation was significantly inhibited by pretreatment with 10 µM metoprolol.In conclusion, vascular smooth muscle relaxation by Deno was mediated through ₁-adrenergic action in canine coronary arteries and through the blocking effect of -adrenoceptors in canine femoral, mesenteric, and renal arteries.