Successful haemostasis of a ruptured liver tumour using flaps of gallbladder serosa and the falciform ligament.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to Y Kuroda.
Explore the source record for details and available documents.
OBJECTIVE: To examine the changes in the number of T cells and macrophages in the mucosal lamina propria in the presence or absence of bile in the gastrointestinal tract. DESIGN: Clinical study. SETTING: University hospital, Japan. SUBJECTS: 6 patients with obstructive jaundice who had external biliary drainage (drainage group) and 6 patients with no signs of obstructive jaundice (control group). INTERVENTIONS: Gastrointestinal specimens were taken at the time of operation. MAIN OUTCOME MEASURES: The number of CD4+ T cells, CD8+ T cells and CD68+ macrophages in the lamina propria mucosae in each group measured immunohistochemically. RESULTS: The numbers of CD8 T cells and CD68+ macrophages in the lamina propria of the patients treated by external drainage were significantly less than in the control group (p < 0.01). However, there was no difference in the number of CD4+ T cells between the groups (p = 0.45). CONCLUSIONS: In the absence of bile, mucosal immune function fails as a result of reduced numbers of CD8+ T cells and macrophages.
BACKGROUND: When stem-cell grafts are infused into the venous circulation and stem/progenitor cells egress from BM, pulmonary capillary beds are the first microcirculation site that they encounter. This provides the potential for circulating progenitor cells to be trapped in the pulmonary circulation. METHODS: We compared the number of progenitor cells [CD34(+) cells, colony-forming unit-granulocyte-macrophage (CFU-GM), CD34(+) CD41(+) cells and CFU-megakaryocyte (CFU-meg)] and their expression of cell-adhesion molecules (CAM) in samples taken simultaneously from radial arteries and central veins of 21 patients following PBSC mobilization. RESULTS: The mean (+/- SD) frequency of progenitor cells in the radial arteries was reduced to 79% +/- 25% for CD34(+) cells, 73% +/- 27% for CFU-GM, 77% +/- 25% for CD34(+) CD41(+) cells and 70% +/- 29% for CFU-meg of the number in the central veins. This suggests that some progenitor cells might be trapped in the lung. No association between progenitor-cell expression of CAM and pulmonary trapping was observed. DISCUSSION: Our data demonstrate pulmonary trapping of PBSC during mobilization, suggesting a potential inhibitory effect on PBSC harvest and medullary trafficking following graft infusion. However, the impact associated with pulmonary PBSC trapping may be negligible in the clinical setting if sufficient cells are infused.
We analyzed response, side effects, and local control rates of a multimodal treatment consisting of intraarterial infusion chemotherapy (IAIC) and radiotherapy with or without surgery for patients with locally advanced or recurred breast cancer. Thirty-three patients, clinically diagnosed as stage IIB in 1, IIIA in 2, IIIB in 12, IV in 18, were treated from 1991 to 1998. Twenty-five were primary and eight were recurrent cases after surgery. IAIC started as initial treatment up to three times maximum. In most cases, doxorubicin 50 mg, cisplatin 50 mg, and mitomycin 10 mg were infused in the subclavian and/or internal mammary artery. After IAIC, patients in primary cases underwent radical mastectomy or breast conservation surgery, after radiotherapy at a total dose of 50 Gy/25 fractions/5 weeks with a boost of 10 Gy. In recurrent cases, a full dose of radiotherapy was delivered. Clinical objective and complete response rates were 78% and 9% after IAIC. Despite a high rate of residual positive margin (67%) or clinically residual carcinoma, local recurrence developed only in 2 patients (6%) and local control rates at 5 years were calculated as 89%. Bone marrow suppression was frequent, and skin vesiculation (15%) and ulceration (9%) were experienced after IAIC. Skin ulcer (6%), brachial plexus neuropathy (3%), and radiation pneumonitis (3%) occurred as late toxicity. IAIC was effective as an induction treatment and radiotherapy played a role of local control for patients with locally advanced or recurrent breast cancer.
A 39-year-old woman came to us complaining of severe anemia (hemoglobin: 2.3 g/dl) and a painful right breast that was entirely occupied by an ulcerative, foul-smelling tumor approximately 20 cm in maximum dimension. The tumor, which was determined to be mucinous adenocarcinoma at biopsy, had invaded the chest wall with multiple lung metastases (T4cN2M1 stage IV). After a blood transfusion, the patient received the following multimodal treatment: concurrent chemoradiotherapy (50 Gy), intraarterial infusion chemotherapy consisting of doxorubicin 50 mg, mitomycin-C 10 mg, and cisplatin 50 mg, and skin graft surgery. After intraarterial infusion chemotherapy, the fungating tumor disappeared. The patient experienced a relapse of right pleural effusion 2 years later and received multimodal treatment. Now, March 30, 2000, the patient is doing well without local recurrence, 8 years after her first admission. The combination of intraarterial infusion chemotherapy and radiotherapy plays a role in successful treatment of extensive local disease of the breast.
BACKGROUND: Accumulating evidence suggests that mitochondrial rather than sarcolemmal adenosine triphosphate-sensitive K+ (K(ATP)) channels may have an important role in the protection of myocardium during ischemia. Because both lidocaine and mexiletine are frequently used antiarrhythmic drugs during myocardial ischemia, it is important to investigate whether they affect mitochondrial K(ATP) channel activities. METHODS: Male Wistar rats were anesthetized with ether. Single, quiescent ventricular myocytes were dispersed enzymatically. The authors measured flavoprotein fluorescence to evaluate mitochondrial redox state. Lidocaine or mexiletine was applied after administration of diazoxide (25 microM), a selective mitochondrial K(ATP) channel opener. The redox signal was normalized to the baseline flavoprotein fluorescence obtained during exposure to 2,4-dinitrophenol, a protonophore that uncouples respiration from ATP synthesis and collapses the mitochondrial potential. RESULTS: Diazoxide-induced oxidation of flavoproteins and the redox changes were inhibited by 5-hydroxydecanoic acid, a selective mitochondrial K(ATP) channel blocker, suggesting that flavoprotein fluorescence can be used as an index of mitochondrial oxidation mediated by mitochondrial K(ATP) channels. Lidocaine (10(-3) to 10 mM) and mexiletine (10(-3) to 10 mM) reduced oxidation of the mitochondrial matrix in a dose-dependent manner with an EC50 of 98+/-63 microM for lidocaine and 107+/-89 microM for mexiletine. CONCLUSIONS: Both lidocaine and mexiletine reduced flavoprotein fluorescence induced by diazoxide in rat ventricular myocytes, indicating that these antiarrhythmic drugs may produce impairment of mitochondrial oxidation mediated by mitochondrial K(ATP) channels.
OBJECTIVE: To measure cerebrospinal fluid and plasma concentrations of nitrate and nitrite as indicators of nitric oxide production in adults after subarachnoid hemorrhage (SAH). DESIGN: A prospective, clinical study. SETTING: Multidisciplinary intensive care unit. PATIENTS: Nine patients (three males and six females, aged 29-64 yrs) with aneurysm-induced SAH were studied. Glasgow Coma Scale score on admission ranged from 9 to 15. Ruptured aneurysms were clipped within 72 hrs of ictus, and then conventional hypervolemic, hemodilution, and induced hypertension methods were applied. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Nitrate and nitrite concentrations of patients were examined sequentially by a capillary zone electrophoresis every day for 13 days. As a control group, cerebrospinal fluid was sampled from patients (n = 9, six males and three females, aged 30-60 yrs) without neurologic disorders who underwent spinal taps for spinal anesthesia, and plasma from healthy human volunteers (n = 43, 21 males and 22 females, aged 23-49 yrs). There were no significant differences over time in cerebrospinal fluid nitrate concentrations after SAH. Concentrations of cerebrospinal fluid nitrate after SAH were increased compared with control values. Plasma nitrate concentration was decreased compared with control values, but the value on day 14 was increased significantly (p < .05) compared with those during days 2-11. Plasma and cerebrospinal fluid nitrite concentrations after SAH were similar to those in control subjects. Similar concentrations of nitric oxide metabolite in plasma and cerebrospinal fluid were observed between the patients with and without symptomatic vasospasm. CONCLUSION: The increase of cerebrospinal fluid nitrate after SAH may attribute to the endogenous nitric oxide production in the injured brain.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
INTRODUCTION: Recently, results of the clinical application of the two-layer method have shown the morphologic quality of the human pancreas grafts after reperfusion to be excellent, although ischemia-reperfusion injury is related to early graft loss in pancreas transplantation. However, some reports have indicated that heat shock proteins (HSPs) have important functions in response to the stress-related events. AIM: To examine whether the two-layer method reduced ischemia-reperfusion injury in a canine pancreas autotransplantation model by investigating the expression of HSPs. METHODOLOGY: There were three experimental groups in which dogs received segmental autografts after preservation by the two-layer method using University of Wisconsin solution (UW) (group 1), simple storage in UW (group 2) for 24 hours, or no preservation (group 3). RESULTS: In group 1, pancreatic tissue perfusions were high, and pancreatic exocrine functions were well preserved after 1, 2, and 4 hours of reperfusion with low incidence of graft pancreatitis or vessel thrombosis compared with that in group 2. Moreover, ATP rapidly recovered, and HSP 60 was strongly enhanced after reperfusion in group 1. On the other hand, ATP recovery and the enhancement of HSP 60 were weak after reperfusion in group 2. CONCLUSION: The two-layer method reduced ischemia-reperfusion injury compared with UW simple storage in canine pancreas autotransplantation with a strong expression of HSP 60.
To evaluate the effect of chemotherapy of 5-fluorouracil (5-FU) in human biliary tract carcinoma, we studied 5-FU sensitivity, thymidylate synthase (TS) content, and dihydropyrimidine dehydrogenase (DPD) activity in 4 human biliary tract carcinoma cell lines compared to 12 various digestive carcinoma cell lines of human organs in vitro. 5-FU sensitivity in the cell lines was analyzed by MTT assay. TS content was analyzed by the [6-(3)H]FdUMP binding assay method, and DPD activity was analyzed by thin-layer chromatography (TLC). 5-FU IC(50) values of biliary tract carcinoma cell lines were significantly higher than those of the carcinoma cell lines of the other digestive organs: 97, 45, 119, and 194 times the concentration of the other digestive, pancreas, colon, and gastric carcinoma cell lines, respectively. TS content of biliary tract carcinoma cell lines was also significantly greater than that of the carcinoma cell lines of the other organs. No difference in DPD activity, however, was recognized between the carcinoma cell lines of each organ. TS content in the cell lines significantly correlated with 5-FU sensitivity, but DPD activity did not. Therefore, in the present study, TS expression was concluded to influence the high resistance to 5-FU of biliary tract carcinoma in comparison with the carcinomas of the other digestive organs.
The Ile-Phe-Met (IFM) motif located in the Ill-IV linker of voltage-gated sodium channels has been identified as a major component of the fast inactivation gate. If Gln was substituted for Phe, the role in the gate was disrupted completely. If Ile was replaced by Gln inactivation became slightly incomplete and if the Thr, which is adjacent to the IFM motif (-IFMT-), was replaced by Met, inactivation became much more incomplete than in the I/Q mutation, but not as vigorous as in the F/Q mutation. Previously, we studied the structures of the inactivation gate-related peptide (K1480-K1496 in rat brain type-IIA, MP-3A) and its F1489/Q substituted one (MP-4A) in SDS micelles and found that the conformational change of the IFM hydrophobic cluster due to the F/Q substitution may be a reason for disrupting the gate. In this study, in order to obtain supporting evidence for this view and also to further knowledge of the effect of I/Q and T/M mutations on the structure of the IFM cluster, we studied the structures of 11488Q [MP(rb)-3QFMT] and T1491M [MP(rb)-31FMM] substituted peptides. The fragment peptide K1477-K1493 [MP(hh)-3A] and its T1488M substituted peptide [MP(hh)-3IFMM] in the human heart sodium channel were also studied. It was found that the backbone structures around the IMF motif of MP-3A, MP(hh)-3A and MP(rb)-3QFMT resemble one another in such a manner that the residues Ile(Gln) and Thr are brought so close together that they form a unique type of lid to occlude the pore. In contrast, the residues between Ile and M1491 of MP(rb)-3IFMM or M1488 of MP(hh)-3IFMM were fairly far apart from each other. We conclude that Thr plays an important role in forming a structure of the IFM hydrophobic cluster for inactivation.
BACKGROUND: Neuroendocrine cell (NEC) carcinoma is occasionally accompanied by adenocarcinoma but the relationship between these two morphologically distinct tumours is unclear. Two hypotheses have arisen regarding the mechanism for the association of adenocarcinoma and NEC carcinoma. One is that both are derived from a common multipotential epithelial stem cell. The second hypothesis is that adenocarcinoma and NEC carcinoma arise from a multipotential epithelial stem cell and a primitive NEC, respectively. AIMS: To elucidate the relationship between the two histologically distinct tumours, adenocarcinoma of the stomach and NEC carcinoma of the duodenum. PATIENT/METHODS: We present a case in which the tumour extended across the pyloric ring, the gastric portion of which revealed adenocarcinoma while the duodenal portion showed argyrophil NEC carcinoma. The two histologically distinct lesions of the tumour were examined by immunohistochemistry and genetic analysis of p53. RESULTS: The gastric region was negative for chromogranin A staining but positive for carcinoembryonic antigen (CEA) staining. In contrast, the duodenal region was positive for chromogranin A but negative for CEA. All tumour regions showed a point mutation in p53 gene at exon 7 (GGC (glycine)-->GTC (valine) at codon 245). The distal portion of the duodenal tumour showed an additional point mutation in p53 gene at exon 5 (GCC (alanine)-->GTC (valine) at codon 129). CONCLUSIONS: The two histologically distinct tumours, adenocarcinoma of the stomach and NEC carcinoma of the duodenum, appear to be derived from a common epithelial cell.
Explore the source record for details and available documents.
Autosomal recessive juvenile parkinsonism (AR-JP) is characterised by homogenous clinical features and selective degeneration of nigral neurons. Recent progress in molecular genetic analyses of AR-JP has led to the identification of a novel ubiquitin-like protein, parkin, whose precise function still remains to be elucidated. Two unrelated Japanese families had levodopa unresponsive parkinsonism complicated with cerebellar and pyramidal tract dysfunction. Genetic analysis of the parkin gene and mRNA in both families disclosed identical mutations with large deletions extending from exons 3 to 4. These results suggest that the parkin protein possesses an important function not only in the substantia nigra but also in extranigral neurons of the CNS and that the phenotype of multiple system dysfunction can also be a complication in patients with AR-JP due to variations in sites of or changes in functions by parkin mutation.
The present study, which aimed to determine the predictors of distal embolization and restenosis after stenting for vein graft disease, retrospectively analyzed 51 consecutive patients who underwent stent implantation for diseased saphenous vein grafts. Follow-up angiography was performed 6 months after the procedure and the clinical and angiographic variables were analyzed by multivariate logistic regression to determine the predictors of distal embolization and restenosis. Initial clinical success was achieved in 49 patients, 44 of whom underwent follow-up angiography and were enrolled in the retrospective analysis. Distal embolization occurred in 6 grafts (13.6%). Multivariate analysis showed that the lesion length and the total cholesterol level were independent predictors of distal embolization. Angiographic restenosis occurred in 13 (26.5%) of 49 lesions. The minimum luminal diameter and the percent diameter stenosis after stenting were associated with the occurrence of restenosis. Multivariate analysis of lesions located in the graft body identified graft age as an independent predictor of restenosis. Distal embolization can occur after vein graft stenting, especially in patients with hypercholesterolemia and diffuse stenosis. The post-stenting minimum luminal diameter and the percent diameter stenosis are predictors of restenosis. In particular, graft age is associated with the restenosis of graft body lesions.
A 59-year-old man who had received chronic hemodialysis developed left occipital pain and hypoglossal nerve palsy. He was diagnosed as having skull base metastasis from renal cell carcinoma related to acquired cystic kidney. Retrospective analysis revealed the patient had had elevated serum C-reactive protein and alkaline phosphatase levels before the symptoms appeared. Radiotherapy to the skull base relieved the pain. Finally he died with generalized metastases. Serum interleukin-6 levels measured during admission had been elevated, and interleukin-6 mRNA was detected in the autopsy specimen of renal cell carcinoma. Interleukin-6 might be involved in the etiology of paraneoplastic signs.
We examined the effects of temperature on excitatory synaptic transmission and the recurrent inhibitory loop in CA1 neurons in guinea pig hippocampal slices. Increasing the temperature of the perfusing medium from 30 to 49 degrees C resulted in attenuation of both the amplitude of the synaptically evoked CA1 population spikes and the paired-pulse inhibition (PPI) of the spikes. A bath application of 2 microM picrotoxin, a gamma-aminobutyric acid receptor antagonist, did not affect the amplitude of the CA1 population spikes, but it significantly reduced PPI during the early heating phase (30-32 degrees C). In contrast, the application of 1 mM theophylline or 50 microM 8-phenyltheophylline, a selective adenosine A1 receptor antagonist, resulted in significant augmentation of the PPI during the early phase of hyperthermia (30-34 degrees C) and a significant increase in the amplitude of the CA1 population spikes at higher temperatures (34-43 degrees C). These results suggest that increased activation of adenosine A1 receptors in response to a temperature increase depresses not only excitatory synaptic responses, but also the strength of the inhibitory circuit in CA1 neurons. Furthermore, hyperexcitability of CA1 pyramidal neurons was seen in the middle of the heating range (34-38 degrees C), excitatory responses still being present, but the strength of the inhibitory circuit significantly reduced.