[Necrosis of cancer and pronase].
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Biomedical subjects
Publications and source records attributed to S Miyazaki.
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The purpose of this study was to elucidate the function of the sphincter of Oddi (SO) in patients with juxtapapillary duodenal diverticula (JDDs). The SO function was evaluated by intraoperative biliary manometry in three groups of patients. Group 1 consisted of nine patients with JDDs and a dilated common bile duct (CBD) (diameter > 10 mm). Group 2 consisted of six patients with JDDs and a normal-sized CBD (diameter < 10 mm). Group 3 consisted of 26 patients without JDDs and with normal-sized CBDs. In the absence of a duodenal pressure load, the patients in group 1 demonstrated a lower baseline SO pressure and lower resistance of the biliary outflow than patients in group 3. They also demonstrated a lower baseline SO pressure and shorter decay time (which represented terminal biliary ductal resistance) than patients in group 2. In the presence of a duodenal pressure load of 300 mm H2O, the patients in group 1 demonstrated a lower incidence of phasic SO contractions, a higher baseline SO pressure, and a higher resistance of the biliary outflow than group 2 and group 3 patients. The decay time in group 1 and group 2 patients was higher than that of group 3 patients. Based on these findings, we conclude that the SO function in patients with JDDs is impaired owing in part to long-standing compression of the terminal biliary ductal system by a distended JDD associated with a rise in intraduodenal pressure in daily life.
We report the midterm results of percutaneous transluminal coronary balloon angioplasty (PCBA) for localized stenosis (LS) caused by Kawasaki disease (KD). Two 2-year-olds, a girl and a boy, underwent PCBA for severe LS of the left anterior descending artery caused by KD. After 4 years, there was no ischemia and no significant restenosis in the target vessels. PCBA provided a good result for early appearing LS caused by KD in two small infants. The 5-years-old boy was the youngest patient to undergo percutaneous transluminal coronary rotablator. Although the postprocedure result was very effective, 1 year later asymptomatic occlusion occurred.
In Japan, the results of histopathologic analyses on esophageal carcinomas have shown that almost all of them are squamous epithelial cancers. The abnormal epithelium that is difficult to differentiate by endoscopy can be easily visualized by chromoendoscopy with the use of iodine staining. Since the establishment of endoscopic mucosal resection (EMR), it has been used increasingly to treat mucosal cancers. It is necessary to diagnose accurately the depth of invasion of mucosal cancer when it is to be treated by EMR. In this article, we explain our routine techniques to visualize and interpret the lesions that are candidates for EMR. It is of great benefit to detect lesions at their early stage, which leads to the most desirable endoscopic treatment.
Golden hamster oocytes show repetitive Ca2+ transients at fertilization: a propagating Ca2+ rise from the sperm attachment site in the first 2-3 responses and synchronous Ca2+ rise in the entire egg in the succeeding responses. Cyclic Ca2+ rises are produced in unfertilized eggs by an injection of GTP gamma S or continuous injection of inositol 1,4,5-trisphosphate (InsP3). Both InsP3-induced Ca2+ release (IICR) and Ca(2+)-induced Ca2+ release (CICR) are observed in hamster eggs, associated with a refractory period of 1-2 min after a Ca2+ release. In addition, external Ca2+ is a prerequisite for maintaining the repeated Ca2+ transients. The conditions that are expected to alter Ca2+ influx affect the frequency of Ca2+ transients with little effect on each response. The fertilizing sperm causes an increase in Ca2+ permeability of the egg plasma membrane and an increase in Ca2+ sensitivity of CICR. Feedback inhibition through protein kinase C is observed in G-protein-mediated Ca2+ transients but this inhibition seems to operate rather tonically. A model of Ca2+ oscillation is proposed: basically a second messenger-controlled oscillator model. InsP3 as the rigger of Ca2+ release is continuously supplied while an elevated basal [Ca2+]i level due to Ca2+ influx provides a favourable condition for IICR and CICR as well as for recharging the Ca2+ pools ready to release Ca2+ again.
The pathophysiologic results of respiratory disturbances caused by adenoid-tonsillar hypertrophy are reported. In each case, we monitored intraesophageal pressure to accurately assess respiratory effort, and recorded a sleep diary to detect disorganized sleep habits and disturbed sleeping-waking rhythms. We noticed that great respiratory effort existed not only during light sleep, but was also continuously observed during deep sleep despite the total disappearance of obstructive apneas. Furthermore, upper airway obstruction caused by adenoid-tonsillar hypertrophy and hypoxemia during sleep in the rapid eye movement stage were found to be closely related to the sudden infant death syndrome. A sleep diary recording sleep habits and regularity of night sleep seems to provide reliable indicators for the determination of surgical intervention.
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Intracytoplasmic sperm injection (ICSI) into mammalian eggs induces repetitive rises in intracellular Ca2+ concentration ([Ca2+]i) which are the pivotal signal in fertilization. Spatiotemporal aspects of [Ca2+]i rises following ICSI into the periphery of mouse eggs were investigated with high-speed confocal microscopy. The first Ca2+ response was generated 25-30 min after ICSI, when [Ca2+]i increased slowly and reached a certain level. The [Ca2+]i rise occurred synchronously over the ooplasm, attained the peak in 40-70 s, and lasted for 5-7 min. Succeeding Ca2+ responses occurred at intervals of 20-30 min, associated with the faster rate of [Ca2+]i rise and the shorter duration as Ca2+ oscillations progressed. The [Ca2+]i rises took the form of a wave that started from an arbitrary cortical region, but not from the vicinity of the injected sperm head. The Ca2+ wave became more pronounced and propagated across the egg faster in the later Ca2+ responses. An artifactual [Ca2+]i rise was inevitably produced during the ICSI procedure. The larger artifact affected the subsequent first Ca2+ response, resulting in the faster [Ca2+]i rise (time to peak, 10-20 s), slight spatial heterogeneity of [Ca2+]i rise in the ooplasm (but not a wave) and the shorter duration (3-4 min). The artifact slightly affected the amplitude of the second Ca2+ response, but little affected the later Ca2+ responses. It is suggested that the factor(s) that leaked out of the injected spermatozoon diffuses to a wide area and sensitizes Ca2+ channels of the endoplasmic reticulum to induce Ca2+ release synchronously over the ooplasm. The enhanced sensitization leads to propagating Ca2+ release initiated from the cortex that is more sensitive to the sperm factor.
The FLT3 gene encodes a tyrosine kinase receptor that regulates proliferation and differentiation of hematopoietic cells. Recently, the internal duplication of FLT3 has been observed in hematological malignancies, suggesting the involvement of these mutations in leukemogenesis. The authors analyzed the expression of FLT3 mRNA and the incidence of its internal tandem duplication in normal hematopoietic and blood samples by reverse transcription-polymerase chain reaction (RT-PCR). Mononuclear cells (MNCs) in cord blood and bone marrow highly expressed FLT3 mRNA, whereas MNCs and polymorphonuclear cells (PMNs) in peripheral blood showed low or undetectable levels of FLT3. When the ratio of FLT3/beta-actin PCR products was calculated, the level of FLT3 mRNA expression was significantly higher in cord blood MNCs (n = 42) than that in peripheral MNCs (n = 14) or PMNs (n = 10). Although several PCR bands with different sizes were observed, no internal tandem duplication of FLT3 was detected in these normal blood samples. These findings indicate that the expression of FLT3 is lineage specific and consistently decreases during hematopoietic differentiation. The internal duplication of FLT3 is restricted in hematological malignancies and may occur at a specific stage in leukemogenesis.
A total of 62 patients with standard-risk acute lymphoblastic leukemia received three-drug induction consisting of vincristine, prednisolone, and L-asparaginase (l-Asp) followed by consolidation therapy with intermediate-dose methotrexate (MTX), intrathecal MTX, and 18 Gy of cranial irradiation. Maintenance therapy consisting of 6 drugs including daunorubicin (DNR, 450 mg/m2 in total) was continued for 3 years. Patients were randomized and half of them received weekly l-Asp during maintenance therapy as a late intensification. Complete remission (CR) was achieved in 61/62 (98.4%), and 11 of 61 patients relapsed. At 10 years, the event-free survival (EFS) was 80.6 +/- 5.0% and overall survival was 88.7 +/- 4.0%; median follow-up time was 9.3 years. The 10-year EFS of patients with additional l-Asp (84.8 +/- 6.2%) was superior to that without l-Asp (75.9 +/- 7.9%), although it was not statistically significant. No patients who received a full dose of DNR and maintained CR developed heart failure, although the shortening fraction decreased from 41.0% at diagnosis to 35.2% (median). The protocol AL841 provided good long-term disease control without severe late cardiac dysfunction.