Fukuoka igaku zasshi = Hukuoka acta medica最新文献

Chronic inflammation in the myocardium is involved in the development of left ventricular (LV)remodeling and failure after myocardial infarction (MI). Invariant natural killer T (iNKT) cells havebeen shown to produce inflammatory cytokines and orchestrate tissue inflammation. However, noprevious studies have determined the pathophysiological role of iNKT cells in post-MI LV remodeling.We thus examined whether the activation of iNKT cells might affect the development of LVremodeling and failure. After creation of MI, mice received the injection of either a-galactosylceramide(aGC), the activator of iNKT cells, or phosphate-buffered saline 1 and 4 days after surgery, andwere followed during 28 days. Survival rate was significantly higher in MI +aGC than MI + PBS. LVcavity dilatation and dysfunction were significantly attenuated inMI +aGC, despite comparable infarctsize, accompanied by a decrease in myocyte hypertrophy, interstitial fibrosis, and apoptosis. Theinfiltration of iNKT cells were increased during early phase in noninfarcted LV from MI and aGCfurther enhanced them. It also enhanced LV interleukin (IL)-10 gene expression at 7 days, whichpersisted until 28 days. AntiIL-10 receptor antibody abrogated these protective effects of aGC on MIremodeling. The administration of aGC into iNKT cell-deficient Ja18(-/-) mice had no such effects,suggesting that aGC was a specific activator of iNKT cells. iNKT cells play a protective role againstpost-MI LV remodeling and failure through the enhanced expression of cardioprotective cytokinessuch as IL-10.

Pattern formation of vascular structure has been extensively studied in vascular biology. Classicallythe pattern formation process falls into three categories-vasculogenesis, angiogenesis and remodeling.Mathematical modeling study of these phenomena has been done byrelatively independent ofexperimental works by applied mathematicians, and not well understood by experimental biologists. Inthis review I provide intuitive explanations of proposed theoretical models and recent advance inmodelling study of vascular development.

Recent advances reveal that mitochondria are not limited to functioning only as the cellularpowerhouse and in apoptosis, but that they act as central hubs for multiple signal transductions.Studies over the last decade indicate that mitochondria in vertebrates are involved in the front line ofhost defense, especially against RNA viruses. Mitochondrial-mediated antiviral innate immunitydepends on activation of the retinoic acid-inducible gene I (RIG-I)-like receptors signal transductionpathway, and the mitochondrial surface acts as a platform for the assembly of signaling molecules,including mitochondrial antiviral signaling (MAVS) during the process. Some viral encoded proteinstarget to the mitochondria post-infection, however, thereby evading the cellular immune response.Here we review specific interactions between mitochondria and viral proteins and discuss theirphysiologic effects on the host cells.

We here describe a case of solitary basaloid follicular hamartoma (BFH) : the case developing incompany with senile lentigo on the nose. BFH is a relatively rare benign follicular neoplasm ofundetermined etiology. Histologically, the specimen consisted of small-sized squamoid or basaloid cellsand follicular germ-like cells in the periphery of the tumor nests. There were no infundibular cysts.BFH should be differentiated from infundibulocystic basal cell carcinoma (BCC), which consists ofsquamoid or basaloid cells in company with infundibular cysts, tumor of follicular infundibulum ortrichoepithelioma. We analyzed the immunohistochemical findings of the case in comparison withthose of BCC and trichoepithelioma. An immunohistochemical examination revealed 1) that Bcl-2 andCD10 was preferentially expressed in the outermost cells in the tumor nests consisting of folliculargerm-like cells, 2) that most of the tumor cells, especially germ-like cells, were strongly positive forBer-EP4, and 3) that peritumoral stroma was positive for CD34. The immunohistochemical findings ofour cases supported that BFH should be differentiated from BCC, a common malignant neoplasm.

The causative agent of hepatic encephalopathy (HE) has not been identified with certainty. Therecovery of consciousness in patients with acute liver failure (ALF) who underwent livertransplantation (LT) is sometimes drastic ; therefore, we thought that the causative agents of HEwould change markedly peri-operatively in these patients. We examined the biomarkers includingnew agents in the serum of patients using the ProteinChip® System 4000 (Ciphergen Biosystems,Yokohama, JAPAN). Sixteen samples were obtained from four patients with ALF who underwent living donor LT(LDLT) at four time points ; pre-operative, one post-operative day (1POD), 3POD, and 7POD. We usedthree chips made by the Biomek2000 robot. All duplicated samples were assayed and analyzed usingthe CiphergenExpressTM data manager. We divided the peri-operative changes in the intensity ofidentified peaks into seven patterns. The number of peaks whose intensity shows significant changesperi-operatively reached 755. Of course, it is difficult to determine each structure in all 755 peaks ; therefore, we should narrowdown the candidates for causative agents of HE in further studies. Our own results suggest that manydifficulties lie ahead in determining the causative agent of HE.

We experienced a case of the cardiopulmonary arrest due to subglottic stenosis developed on thesecond day after lung cancer surgery. Case : A 73-year-old female who was diagnosed with primarylung cancer was referred to our department for surgery. The second day after left lungsegmentectomy, she showed respiratory discomfort symptoms and exhibited hoarseness and stridor,which were revealed as the subglottic stenosis by bronchoscopy. During the emergency airwaymanagement, she went into cardiopulmonary arrest. We performed cardiopulmonary resuscitationand simultaneous urgent tracheotomy.

Esophageal motility disorders (EMD) is characterized by impaired coordinated esophageal motilityfunction with symptoms including dysphasia, heartburn or noncardiac chest pain. Since EMDs isfunctional disorders, it is usually difficult to make a diagnosis by conventional examinations includingendoscopy and esophagography. Recently developed high-resolution manometry allows us to evaluateesophageal motility function precisely and to make a differential diagnosis of EMDs, together withChicago Classification (CC) version 3.0 (CC ver3.0). In this article, we reviewed diagnosis of EMDsbased on CC ver3.0 and current treatment strategy for EMDs.