Endoscopic band ligation for postpolypectomy gastric bleeding

We report a case of a patient in whom endoscopic band ligation was achieved for postpolypectomy gastric bleeding. A 76‐year‐old man visited our hospital because of anemia. Endoscopy revealed a gastric polyp, approximately 12 mm in diameter, on the lesser curvature in the distal gastric body. The polyp was considered to be the source of chronic anemia and was therefore removed by using standard careful snare‐cautery polypectomy technique. Four days later, follow‐up endoscopy was performed to evaluate the postpolypectomy site, and an active bleeding postpolypectomy ulcer was identified. Initial attempts to achieve hemostasis with ethanol injection were unsuccessful. Immediate hemostasis was obtained with a subsequent endoscopic band ligation device. There has been no recurrent bleeding. Endoscopic band ligation might be a good treatment modality for the treatment of a postpolypectomy gastric bleeding lesion.     

A mild case of nesidioblastosis with diagnostic and therapeutic difficulty

A female infant with nesidioblastosis who showed mild clinical symptoms is reported. In this patient, insulin levels and insulin to glucose ratios (IRI/G) were often normal. Regular milk feedings supplemented with continuous glucose infusion (0.7-2 mg/kg per min) or oral glucose feedings (4.5 mg/kg per min) prevented hypoglycemia. As leucine-sensitivity was diagnosed at 2 months of age, she was started on diazoxide. This was, however, ineffective, and adverse effects appeared. Subtotal pancreatectomy (95%) was therefore attempted at 5 months of age, and persistent normoglycemia as well as normal growth and development followed up to 3 years after the operation. The pancreas showed characteristic signs of nesidioblastosis. The above clinical observation suggests that a patient with nesidioblastosis whose blood glucose level is easily controllable may develop an unexpected episode of hypoglycemia in the presence of a leucine sensitivity. In such a patient, diazoxide or, when it is of no avail, surgical intervention should promptly be instituted to prevent possible neurologic sequelae induced by hypoglycemia.     

Kabuki make-up syndrome associated with West syndrome

A Japanese boy with Kabuki make-up syndrome associated with West syndrome is reported. He developed periodic tonic spasms at 6 months of age while his electro-encephalogram also revealed hypsarrhythmia. Although only a few previously reported cases of Kabuki make-up syndrome have been associated with epilepsy, it is likely that epileptic seizures are another primary feature of Kabuki make-up syndrome.     

Lignocaine–induced convulsion does not induce c–fos protein (c–Fos) in rat hippocampus

Recent studies have shown that proto–oncogene c–fos mRNA is induced in the central nervous system by a variety of stimuli including generalised convulsions. In this study, the expression of c–fos protein (c–Fos) following lignocaine–induced convulsions was examined and compared with that following convulsions induced by non–anesthetic convulsants, such as pentylenetetrazol, kainic acid and electroconvulsive shocks, in rat brain.
Administration of 120 mg kg^-1 lignocaine by the intraperitoneal route induced generalised convulsions in all rats examined within 10 min. C–Fos was markedly induced in the piriform cortex and amygdala, and slightly induced in the neocortex and thalamus, while no c–Fos expression was observed in the hippocampus. In contrast, c–Fos expression following generalised convulsions induced by non–anaesthetic convulsants was very marked in the hippocampal region, piriform cortex and amygdala, and extended to the thalamus and neocortex.
These results contradict those of previously reported local cerebral metabolic studies using 2–deoxyglucose as a metabolic marker, and suggest that lignocaine–induced convulsions, unlike those induced by non–anaesthetic convulsants, may not cause severe sequelae (plastic changes) in the hippocampus.     

Variation analysis of β3-adrenergic receptor and melanocortin-4 receptor genes in childhood obesity

BACKGROUND: Decreased energy expenditure and increased food intake are principal causes for obesity. In the present study, genotypes of beta(3)-adrenergic receptor (beta(3)AR) and of melanocortin-4 receptor (MC4R), both of which are believed to have a close link to the cause of obesity, were analyzed and compared with phenotypes of childhood obesity. METHODS: Thirty-five obese children with moderate to severe obesity were enrolled. Direct sequencing of the MC4R coding region and pinpoint-polymerase chain reaction were used to detect genomic variation in the beta(3)AR gene using peripheral blood-derived DNA. RESULTS: Allele frequency of Trp64Arg variation in the beta(3)AR gene in the obese subjects was 0.16, which is comparable with that in the healthy general population in eastern Asia. Comparison of phenotypical characteristics did not show a significant difference between Trp/Trp and Trp/Arg subjects. It was notable that body height SD was significantly higher in the Trp/Trp than the Trp/Arg subjects (0.93 +/- 1.0 SD vs 0.07 +/- 1.3 SD, P= 0.03). Annual weight gains were far beyond a hypothetical fat gain in an Arg64 heterozygote with decreased energy consumption, suggesting increased food intake in childhood obesity. There was, however, no variation in the MC4R gene despite thorough sequencing of the entire coding region. CONCLUSIONS: The Trp64Arg variation in the beta(3)AR gene has no relationship to the degree or the incidence of childhood obesity. The majority of childhood obesity can be characterized as tall stature, more rapid weight gain than that expected by decreased energy expenditure. Further investigation is necessary in regard to the increased food intake as a major cause of childhood obesity.     

HtrA2 is up-regulated in the rat testis after experimental cryptorchidism

AIM: The aim of the present study was to elucidate the role of high temperature requirement A2 (HtrA2) in germ cell loss in the heat-stressed testis. METHODS: We examined the expression of HtrA2, caspase-9 activity and proteolytic activity of HtrA2 in the rat testis, and their in vivo responses to experimental cryptorchid treatment. RESULTS: Northern analysis revealed the expression of HtrA2 mRNA peaked at days 1 and 7 after cryptorchid treatment. While expression of HtrA2 mRNA was seen in the spermatogonium, spermatocytes and some spermatids in normal adult rat testis, experimental cryptorchidism treatment resulted in a marked increase in its signal intensity in spermatocytes and some spermatids, and the layers of spermatogonium and early primary spermatocytes became negative at days 1 and 7 after the treatment. However, the spermatogonium, Sertoli cells and interstitial cells appeared to have strong intensities at days 14, 28 and 56 after the treatment. Western analysis revealed the expression of HtrA2 protein peaked at day 2 coinciding with the increase of positive spermatogonium, the appearance of protein-positive interstitial cells, and day 28 coinciding with the reappearance of protein-positive interstitial cells. Caspase-9 activity peaked at day 2 and HtrA2 proteolytic activity peaked at day 28. Consequently, the first peak of HtrA2 mRNA expression was followed by the peak of caspase-9 activity and the second peak was followed by the peak of proteolytic activity; however, the second peak of mRNA expression had considerable chronological difference from that of the protein. CONCLUSION: These findings suggest the probabilities that the heat stress results in germ cell death by a caspase-independent manner with the elevation of HtrA2 proteolytic activity, as well as a caspase-dependent manner with the elevation of caspase-9 activity.     

Chemokine receptor CCR6 as a prognostic factor after hepatic resection for hepatocellular carcinoma

Background and Aims: Chemokines and their receptors have recently been shown to have major roles in cancer metastasis. The aim of this study was to determine whether the interaction between chemokine receptor 6 (CCR6) and its ligand, macrophage inflammatory protein‐3 alpha (MIP‐3α), correlates with metastasis of hepatocellular carcinoma (HCC). Methods: To observe the reaction of CCR6 expressed cancer cells to MIP‐3α stimulation, chemotactic and actin polymerization assays for both CCR6 high cells (HepG2) and CCR6 low cells (MCF‐7) were performed. CCR6 mRNA levels in tumor specimens from 30 HCC patients were quantified by real‐time polymerase chain reaction. Patients were classified into two groups, high (≥ 20 copies; n = 10) CCR6 and low (<20 copies; n = 20) CCR6 on the basis of CCR6 expression, and the groups were compared with respect to clinicopathological features. Results: When HepG2 cells (CCR6 high) were stimulated with MIP‐3α, they migrated in a dose‐dependent manner, and formation of pseudopodia was observed. These phenomena were not observed in the CCR6 low cells. The incidence of intrahepatic metastasis was higher in the high CCR6 expression group than in the low CCR6 expression group (P < 0.05). Disease‐free survival was significantly poorer in the high CCR6 expression group than in the low CCR6 expression group (P < 0.05). Conclusions: It was indicated that CCR6 might be associated with intrahepatic metastasis of HCC and might be able to become one of the prognostic factor after hepatic resection for HCC.     

Intravenous glycerol therapy should not be used in patients with unrecognized fructose-1,6-bisphosphatase deficiency

BACKGROUND: In Asian countries, glycerol solution that contains fructose (5%) is often used for management of brain edema. However, glycerol and fructose may cause severe hypoglycemia and metabolic acidosis in patients with fructose-1,6-bisphosphatase (FBPase) deficiency, even under stable conditions. The aim of the present study was to determine whether glycerol solution was used for brain edema during acute metabolic decompensation of hypoglycemia and metabolic acidosis in patients with unrecognized FBPase deficiency in Japan and to examine a long-term prognosis of the patients who had this kind of severe metabolic decompensation with or without glycerol therapy. METHODS: A retrospective study of 20 children with FBPase deficiency was conducted, based on their medical records. RESULTS: Six of the 20 children were given glycerol solution for the presence or possibility of brain edema during acute metabolic decompensation of hypoglycemia and metabolic acidosis; two of the six patients administered with glycerol were given dialysis. In four patients treated with glycerol alone without dialysis, two had no brain edema before glycerol administration but it developed later after the administration. These four patients treated with glycerol alone died or developed severe neurological complications. Fourteen patients who were not treated with glycerol solution had no brain edema and showed good prognosis. CONCLUSIONS: Glycerol solution, which contains fructose in Asian countries including Japan, should not be used as an osmotic agent for treatment of brain edema in patients who have hypoglycemia and retention-type metabolic acidosis, until FBPase deficiency is ruled out by measuring blood concentration of lactate.     

三羟基异黄酮对日本比目鱼(牙鲆)性腺分化的影响

[目的] 研究5,7,4’-三羟基异黄酮(genistein,GEN)对日本比目鱼(牙鲆)生殖腺性分化的作用,并在基因表达上探索其分子机制。[方法]运用日本比目鱼随饲养水温决定其性别的生物学特性,在鱼卵孵化后第30天到第100天性分化敏感期内,在27 ℃水温下饲养,会使幼鱼分化成雄性。同时,分别给予幼鱼投食GEN 10和100 μg/g饲料进行喂养染毒,直到第100天(青年期)和第300天(成年期),分别对各组比目鱼样本做病理组织切片,判断其性别和雌雄比例,并通过原位杂交和RT-PCR分析,探索它们的作用机制。[结果] GEN对27 ℃水温饲养下的比目鱼幼鱼有雌性化诱导作用,两组成年比目鱼雌性分别有不同的百分比:10 μg/g组为46.7%,100 μg/g组为96.7%,其诱导效应呈现一定剂量依赖性;比目鱼幼鱼出生后第100天时原位杂交实验显示,P450芳香化酶的mRNA在各组的雌鱼卵巢中有明显表达,但在雄鱼精巢中未见表达;而MIS(苗勒氏管抑制物质)的mRNA在各组的雌鱼卵巢中不表达,而在雄鱼精巢中能见到非常明显的表达。RT-PCR实验显示,在雌鱼卵巢中P450芳香化酶的mRNA表达被诱导,而MIS基因表达被抑制,进一步证实了原位杂交的结果。[结论] GEN对日本比目鱼的生殖腺性分化有雌性化诱导作用,其分子机制很可能是通过诱导P450芳香化酶基因表达和抑制MIS的基因表达从而发挥雌激素样干扰作用的。