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We report a case of intrahepatic cholangiocarcinoma and portal hypertension developing in a liver with biliary microhamartomas (von Meyenburg's complex).The patient was a 55-year-old man who had a past medical history of diffuse multiple liver abscesses. During follow-up examination, a hypovascular nodule measuring 2.1 cm in diameter was incidentally found in segment 8 of the liver. Surgical resection was performed based on a suspected diagnosis of hepatocellular carcinoma. A gastrofiberscopy examination detected characteristic findings of portal hypertensive gastropathy. During the laparotomy, multiple tiny cystic lesions were observed in a diffuse pattern across the liver surface. The liver parenchyma was slightly fibrotic and haemorrhagic. A histopathological examination revealed intrahepatic cholangiocarcinoma with vascular invasions in von Meyenburg's complex. Multiple biliary adenomas were also observed among the biliary microhamartomas adjacent to the main tumour, suggesting that the malignant transformation of the biliary adenomas might have been responsible for the development of the intrahepatic cholangiocarcinoma. The histopathologic examination also revealed sinusoidal dilation and abnormal spacing of the portal tracts and central veins as evidence of portal hypertension.

Carbon dioxide (CO2) insufflation is expected to be safe and effective in endoscopic submucosal dissection (ESD) as well as in other endoscopic procedures. The present study aimed to clarify the usefulness and safety of CO2 insufflation in gastric ESD.A total of 102 consecutive patients were randomly assigned to CO2 insufflation (CO2 group, n = 54) or air insufflation (Air group, n = 48). Abdominal pain and distension were chronologically recorded on a 100-mm visual analog scale (VAS). The volume of residual gas in the digestive tract was measured by computed tomography performed immediately after ESD.Abdominal pain on a 100-mm VAS in the CO2 vs. Air group was 4 vs. 3 immediately after ESD, 4 vs. 4 one hour after the procedure, 3 vs. 3 three hours after the procedure, and 1 vs. 4 the next morning, showing no difference between the groups. In addition, there was no difference in abdominal distension on the 100-mm VAS over the time course of the study. The volume of residual gas in the digestive tract in the CO2 group was significantly smaller than that in the Air group (643 mL vs. 1037 mL, P0.001). The dose of sedative drugs did not differ between the groups. Neither the incidences of complications nor clinical courses differed between the groups.Compared with air insufflation, CO2 insufflation during gastric ESD significantly reduced the volume of residual gas in the digestive tract but not the VAS score of abdominal pain and distension.

Arthropathy in dogs induced by ofloxacin, a quinolone antimicrobial agent, was pathophysiologically investigated. In the in vivo studies, ofloxacin was administered orally once or twice at 20 mg/kg/day to male juvenile (3-month-old, n = 3) or adult (36-month-old, n = 2) dogs, and the humeral and femoral heads were examined pathologically. Unlike adult dogs, fluid-filled vesicles were macroscopically observed on the articular surfaces of one juvenile dog 24 hours after a single treatment with ofloxacin. These lesions were seen in all juvenile dogs by twice dosing. Microscopically, fissures or cavity formations in the middle zone of the articular cartilage were noted only in juvenile dogs. Furthermore, the cartilage matrix from the abnormal area to the articular surface showed a decreased safranin-O staining intensity, suggesting proteoglycan depletion. Ultrastructurally, chondrocytes in the middle zone of juvenile dogs displayed dilatation of the cisternae in the rough endoplasmic reticulum as an initial hallmark. In the in vitro studies, chondrocytes isolated from the articular cartilage of naive juvenile dogs were exposed to ofloxacin at 6.3–100 μg/ml for 24 hours. Although no changes were noted in the deoxyribonucleic acid synthesis, protein synthesis, or proteoglycan release at concentrations of up to 100 μg/ml, the proteoglycan synthesis was evidently decreased in a dose-dependent manner from 12.5 μg/ml. The results obtained suggest that the inhibitory action of ofloxacin on proteoglycan syntheses in the chondrocytes may largely contribute to the early morphologic features in the articular cartilage of the juvenile dog.

In order to obtain the standard treatment results of medically inoperable non-small cell lung cancer (NSCLC) in Stage I in the post-CT scan era, a retrospective analysis of patients who were treated by radical radiotherapy was performed.149 cases treated between 1980 and 1989 were accumulated from ten large hospitals in Japan. All patients received a total dose of 55-75 Gy (mean 64.7 Gy) with conventional fractionation. For evaluation of treatment results, complete response (CR) rate, median survival period and long-termed survival rates were used.The median survival of the all cases was 27.2 months and the actuarial 3- and 5-year survival rates were 34.2% and 22.2%, respectively. CR was obtained in 57 cases (38%). The CR rate was strongly correlated with the long-term survival (5-year survival rate in CR group: 35.1% compared with PR + NC group: 14.1% (P0.0001)). The size of tumor was also of prognostic importance. In 116 patients who died within 5 years after treatment, 66 patients (57%) died of local tumor regrowth.Although the medically inoperable NSCLC patients in Stage I should be offered curative radiation therapy, development of some new steps to increase the CR rate and local control rate is urgently needed.

Congenital lipoid adrenal hyperplasia results in severe impairment of steroid biosynthesis in the adrenal glands and gonads that is manifested both in utero and postnatally. We recently found mutations in the gene for the steroidogenic acute regulatory protein in four patients with this syndrome, but it was not clear whether all patients have such mutations or why there is substantial clinical variation in these patients.We directly sequenced the gene for steroidogenic acute regulatory protein in 15 patients with congenital lipoid adrenal hyperplasia from 10 countries. Identified mutations were confirmed and recreated in expression vectors, transfected into cultured cells, and assayed for the presence and activity of steroidogenic acute regulatory protein.Fifteen different mutations in the gene for steroidogenic acute regulatory protein were found in 14 patients; the mutation Gln258Stop was found in 80 percent of affected alleles from Japanese and Korean patients, and the mutation Arg182Leu was found in 78 percent of affected alleles from Palestinian patients. We developed diagnostic tests for these and eight other mutations. Thirteen of the 15 mutations were in exons 5, 6, or 7, and all rendered the steroidogenic acute regulatory protein inactive in functional assays. Some mutants with amino acid replacements were capable of normal mitochondrial processing, indicating that the activity of steroidogenic acute regulatory protein is not associated with its translocation into mitochondria. Steroidogenic cells lacking the protein retained low levels of steroidogenesis. This explains the secretion of some steroid hormones by the ovaries after puberty before affected cells accumulate large amounts of cholesterol esters.The congenital lipoid adrenal hyperplasia phenotype is the result of two separate events, an initial genetic loss of steroidogenesis that is dependent on steroidogenic acute regulatory protein and a subsequent loss of steroidogenesis that is independent of the protein due to cellular damage from accumulated cholesterol esters.

The purpose of the present study was to evaluate long-term results of chemoradiotherapy for clinical T1b-2N0M0 esophageal cancer and to compare outcomes for operable and inoperable patients. Patients with stage I esophageal cancer (Union for International Cancer Control [UICC] 2009), excluding patients with cT1a esophageal cancer, were studied. All patients had histologically proven squamous cell carcinoma. Operable patients received cisplatin and 5-fluorouracil with concurrent radiotherapy of 60 Gy including a 2-week break. Inoperable patients received nedaplatin and 5-fluorouracil with concurrent radiotherapy of 60-70 Gy without a pause. End-points were overall survival rate (OS), cause-specific survival rate (CSS), progression-free survival rate (PFS), and locoregional control rate (LC). Thirty-seven operable patients and 30 medically inoperable patients were enrolled. There was a significant difference in only age between the operable group and inoperable group (P = 0.04). The median observation period was 67.9 months. In all patients, 5-year OS, CSS, PFS, and LC were 77.9%, 91.5%, 66.9%, and 80.8%, respectively. Comparison of the operable group and inoperable group showed that there was a significant difference in OS (5-year, 85.5% vs. 68.7%, P = 0.04), but there was no difference in CSS, PFS, or LC. Grade 3 or more late toxicity according to Common Terminology Criteria for Adverse Events v 3.0 was found in seven patients. Even in medically inoperable patients with stage I esophageal cancer, LC of more than 80% can be achieved with chemoradiotherapy. However, OS in medically inoperable patients is significantly worse than that in operable patients.

Background and aims : Mediastinal emphysema sometimes develops following esophageal endoscopic submucosal dissection (ESD) without perforation because the esophagus has no serosa. Carbon dioxide (CO 2 ) insufflation during esophageal ESD may reduce the incidence of mediastinal emphysema. The aim of the present study was to compare the incidence and severity of post-ESD mediastinal emphysema in patients receiving CO 2 insufflation vs. standard air insufflation during esophageal ESD. Patients and methods : A total of 27 patients who had undergone esophageal ESD with insufflation of CO 2 between July 2009 and March 2010 were enrolled in this study (CO 2 group). Another 105 patients who had undergone esophageal ESD with air insufflation between March 2004 and May 2009 were included as historical controls (air group). Multi-detector row computed tomography (MDCT) was carried out immediately after ESD. A conventional chest radiograph was taken the next day. Mediastinal emphysema findings on MDCT and radiography were compared between the groups. Results : Mediastinal emphysema detected by chest radiography was 0 % in the CO 2 group vs. 6.6 % in the air group (n.s.). Mediastinal emphysema on MDCT was significantly less frequent in the CO 2 group compared with the air group (30 % vs. 63 %; P = 0.002). The severity of mediastinal emphysema also tended to be lower in the CO 2 group. Conclusions : Whereas mediastinal emphysema detected by radiography is not so common, MDCT immediately after ESD revealed a certain prevalence of post-ESD mediastinal emphysema. Insufflation of CO 2 rather than air during esophageal ESD significantly reduced postprocedural mediastinal emphysema. CO 2 can be considered as insufflating gas for esophageal ESD.

The CNS inflammatory reaction occurring after aneurysmal subarachnoid hemorrhage (SAH) involves the upregulation of numerous cytokines and prostaglandins. Cyclooxygenase (COX) inhibition is a well-established pharmacological anti-inflammatory agent. Previous studies have shown marked increases in COX-2 expression in neurons, astrocytes, microglia, and endothelial cells following brain injury. COX-2 inhibition has been shown to be beneficial following various types of brain injury. This experiment investigates the role of COX-2 activity in early brain injury following SAH. CD-1 mice were subjected to an endovascular perforation model of SAH or SHAM surgery. Following experimental SAH animals were treated with the specific COX-2 inhibitor, NS398, in dosages of either 10 or 30 mg/kg. Neurological performance and brain edema were evaluated 24 and 72 h after SAH. NS398 at 30 mg/kg significantly reduced SAH-induced neurological deterioration. NS 398 at 30 mg/kg resulted in a trend toward the reduction of SAH-induced cerebral edema. Treatment had no effect on mortality. This experiment provides preliminary evidence that COX-2 inhibition is an effective pharmacological intervention for the prevention of brain edema and the preservation of neurological function following SAH.

IgE levels in faecal extracts (Copro-IgE levels) were investigated in food allergy (FA) patients before and after the challenge test administration of food allergens. IgE levels were measured by time-resolved fluoroimmunometric assay. In addition, the effects of administration of oral sodium cromoglycate (SCG) on the Copro-IgE levels were studied. Copro-IgE levels in patients with FA, who were placed on an elimination diet, did not differ from those of healthy children. After a challenge test immediate symptoms of urticaria and wheezing were observed in all FA patients. Copro-IgE levels in each patient increased markedly within 24 h of the challenge test. Moreover, FA patients treated orally with SCG showed neither the increase in Copro-IgE levels nor any remarkable symptoms after the challenge. Our results suggest that the increased Copro-IgE levels may be a specific consequence of the local immune response to food allergen stimulation in the gut mucosa.

This report describes our retrospective evaluation of CT features of the acute phase in 34 cases of ruptured cerebral aneurysms of the posterior cranial fossa. The results are as follows. 1. Examination of cisternal haematoma distribution revealed that SAH had extended to the supra- and infratentorial cisterns in 28 cases (82%). There were only 6 cases (18%) in which SAH was confined to the posterior cranial fossa only but even when there was subarachnoid haematoma in both the supra- and infratentorial cisterns, thick haematomas were seen at the periphery of the brain stem. In cases of vertebral artery-posterior inferior cerebellar artery aneurysms (VA-PICA AN), haematomas in the ambient cistern were thicker on the aneurysm side. In addition, in cases of basilar artery-bifurcation (BA-Bifurcation AN) and basilar artery-superior cerebelli artery aneurysms (BA-SCA AN), there were many thick, high-density haematomas in the interpeduncular cistern. 2. The rate of intracerebral haemorrhage was extremely low (1 patient). 3. The rate of intraventricular haemorrhage was high, and these haemorrhages demonstrated a reflux pattern. 4. The rate of hydrocephalus was high (76.5%) in comparison with that noted in association with SAH due to the rupture of anterior circulation aneurysms.

We investigated surgical complications and prognosis of bronchoplasty and bronchoplasty with pulmonary angioplasty (broncho-angioplasty) for lung cancer. Between October 2000 and October 2007, 37 bronchoplastic procedures were done in 572 patients who underwent lung resections for lung cancer. Eleven (29.7%) bronchoplasties were done with pulmonary angioplasty. There was no operative mortality and 1 hospital mortality (2.7%) causing by myocardial infarction. Six of 11 postoperative complications were bronchial complications and 2 additional lung resections were needed. The 5-year survival for all patients was 55.2% and for bronchoplasty was 57.8%. Though the 5-year survival of broncho-angioplasty was not able to calculate at present, the 3-year survival of which was 72.9%. There was no death of patients with adenocarcinoma after introduction of pre-operative assessment by FDG-PET for lymph node metastasis. These data suggest that bronchoplasty and broncho-angioplasty are safe operative procedures and could provide acceptable intermediate survivals with modern multimodality diagnostic and therapeutic tools.

We studied whether delivering postoperative analgesia, using a patient-controlled epidural analgesia (PCEA) device was effective and safe in elderly patients. We enrolled 40 patients aged65 years (elderly group) and 40 patients aged 20-64 years (young group) scheduled for elective major abdominal surgery. PCEA infusion was started following completion of surgery. Mean (SD) fentanyl consumption (10.7 (3.7) compared with 10.5 (2.7) microg.kg(-1), p = 0.76) and number of times patients pressed the bolus switch (32 (36) compared with 44 (38), p = 0.16) during the first 24 h postoperatively were similar in the two groups. Pain scores, which were similar in both groups at rest, were significantly lower in the elderly on coughing (at 24 h, p0.05). In addition, average pain scores were similar at the time of PCEA bolus demands in the two groups. Elderly and young adult patients therefore required similar amounts of patient-controlled epidural fentanyl to produce satisfactory pain relief.

Aspirin prevents the production of thromboxane A2 (TXA2) by irreversibly inhibiting platelet cyclooxygenase, exhibiting antiplatelet actions. This agent has been reported to prevent relapse in patients with ischemic heart disease or cerebral infarction via this action mechanism. However, there are individual differences in this action, and aspirin is not effective in some patients, which is referred to as 'aspirin resistance'. In this study, we analyzed laboratory aspirin resistance by platelet aggregation in 110 healthy adult Japanese males using 24 single-nucleotide polymorphisms (SNPs) of nine genes involved in platelet aggregation/hemorrhage. Among SNPs involved in platelet aggregation, aspirin was less effective for 924T homozygote of a TXA2 receptor, 924T>C, and 1018C homozygote of a platelet membrane glycoprotein GPIbalpha, 1018C>T, suggesting that 924T and 1018C alleles are involved in aspirin resistance.

This study was carried out to clarify the efficacy of magnetic resonance cholangiopancreatography (MRCP) in the diagnosis of biliary tract diseases, Three hundred and eleven patients who underwent MRCP and ERCP during the period from January 1999 to December 1999 at our institution were included in the study. Two gastroenterologists who were blinded to results of direct cholangiography and final diagnoses interpreted MRCP images prospectively. The biliary duct was visualized by MRCP and ERCP in 99.4% and 89.5% of the cases, respectively. The sensitivity, specificity, and accuracy of MRCP in the diagnosis of choledocholithiasis were 95%, 97%, and 97%, respectively. MRCP depicted the presence of strictures with a sensitivity, specificity, and accuracy of 97%, 96%, and 96%, respectively. There were three false-positive cases because of artifacts from arterial compression, The accuracy of MRCP and ERCP in differentiation of benign strictures from malignant ones was 85% and 96%, respectively. Based on these results, it is concluded that MRCP has high capability in visualization of the biliary tree, and in detection of stones and strictures, To avoid over and under-diagnosis, awareness of some pitfalls inherent in, MRCP is important. We suggest that MRCP should be recommended for patients with suspicion of biliary tract diseases in the initial stage of making diagnosis.

Multiseptate gallbladder is an extremely rare congenital anomaly. We report three cases of this clinical entity. The third patient, a 70-year-old male who was asymptomatic with this condition, also had a gallbladder carcinoma. The three surgically removed gallbladders had multiple thin septa with a honeycomb appearance. Histologically, the septa contained a muscular layer that was continuous with the gallbladder wall. Furthermore, in the third patient, mucinous cystadenoma with focal carcinomatous change in the epithelium was observed. To our knowledge, this is the first description of a multiseptate gallbladder with carcinoma.

To correlate retinal functional changes with structural changes in P23H rhodopsin transgenic rats as a model of autosomal dominant retinitis pigmentosa.P23H heterozygote (lines 1 and 3) and Sprague-Dawley control rats were studied at 4 to 29 weeks by retinal histology, electroretinogram (ERG), and a-wave transduction modeling.Both line 1 (faster degeneration) and line 3 (slower degeneration) showed progressive rod outer segment (ROS) shortening and outer nuclear layer (ONL) cell loss with age. ERG b-wave maximum amplitude (Vb(max)) decreased with age, but b-wave threshold remained constant within each line despite progressive ONL thinning and ROS shortening. The only exception was in line 1 at 29 weeks, which showed a slight threshold change relative to earlier ages. Va(max) and a-wave threshold changed more rapidly and were more sensitive than the b-wave in reflecting histologic degeneration. Va(max) was linearly proportional to the product of (ROS x ONL) across a two log unit range of data combined from both lines. The photopic b-wave was normal for both lines until the ONL thinned beyond 50%. Phototransduction sensitivity was normal for both lines, and dark-adaptation recovery after bleaching rhodopsin was normal.The P23H transgenic rat has a slow rod degeneration with initially normal cone function, consistent with clinical findings of P23H patients. However, the normal bleach recovery and the normal phototransduction sensitivity in this rat model are different from human P23H disease. a-Wave measures were more sensitive than the b-wave for tracking changes. b-Wave threshold was inexplicably poor for tracking degeneration. Although line 1 degenerated faster than line 3, the functional-structural correlates were the same. The tight linear relationship between saturated a-wave amplitude and the product of (ROS x ONL) indicates that the density of cGMP-gated channels per unit ROS plasma membrane area remains constant over a wide range of degenerations.

This report describes two cases of Philadelphia chromosome-negative (Ph(-)) non-Hodgkin's lymphomas (NHLs) recognized in patients with chronic phase Ph-positive (Ph(+)) chronic myelogenous leukemia (CML). Lymph node biopsy of patient 1 was initially diagnosed as diffuse large B cell non-Hodgkin's lymphoma (NHL, T cell rich variant), but at relapse showed immunoblastic features with a marked decrease of admixed lymphocyte components. Patient 2 presented with thickened parietal pleura which revealed a CD30-positive anaplastic large cell lymphoma showing null cell phenotype and genotype with abundant admixed neutrophils and lymphocytes. At the time of lymphoma diagnosis, the patients had CML for 33 and 10 months, respectively. DNA obtained from bone marrow cells at the time of lymphoma diagnosis showed BCR/ABL gene rearrangements by both Southern blot analysis and reverse transcription polymerase chain reaction (RT-PCR), but lacked both immunoglobulin and T cell receptor gene rearrangements. BCR gene rearrangement and BCR/ABL fusion gene were also identified in lymph node and pleural biopsies by Southern blot and RT-PCR analysis, respectively. However, both biopsy specimens also contained reactive lymphocytes and neutrophils, and no fusion signals between BCR and ABL genes were identified in the hyperdiploid lymphoma cells of either case by fluorescence in situ hybridization (FISH). These data suggest the lymphoma cells in both cases were not genetically associated with BCR/ABL. Therefore, these cases were not diagnosed as an extramedullary localized blast crisis in CML, but as Ph(-) NHLs. This represents the first definitive demonstration of peripheral B cell lymphoma occurring by a separate genetic pathway, lacking BCR/ABL, in patients with Ph(+) CML. A review of the literature identified two different subtypes of malignant lymphomas arising in patients with an antecedent or concurrent diagnosis of CML. The most common are T cell lymphomas displaying an immature thymic phenotype, while peripheral B cell lymphomas are more rare. Our study shows, however, that 'Ph(+) NHL' occurring in CML or acute lymphocytic leukemia (ALL) may represent an unrelated neoplasm, even if standard cytogenetic analysis reveals a Ph(+) chromosome, and that FISH is required to confirm whether a localized lymphoid neoplasm is either a true extramedullary localized blast crisis or genetically distinct neoplasm. Leukemia(2000) 14, 169-182.

We describe two patients with primary cardiac malignant lymphoma involving the right atrium and superior vena cava, resulting in intractable right cardiac failure and superior vena cava syndrome. Patients were diagnosed by surgical myocardial biopsy and were treated with combination chemotherapy for non-Hodgkin's lymphoma. Each attained a marked response, and hence avoided sudden death from tricuspid atresia. Both have remained alive for more than 21 and 34 months, respectively, and continue intermittent combination chemotherapy.

The purpose of this study was to compare the effect of premixed 5% dextrose in Ringer's acetate solution and premixed lidocaine with propofpl on the reduction of pain during injection of propofol in adult patients. We conducted a prospective, randomized, double-blinded trial. Ninety-six patients were randomly allocated to one of three groups according to the agents added to 1% propofol 20 ml; Group C, normal saline 2 ml, Group L, 2% lidocaine 2 ml, and Group A, 5% dextrose in Ringer's acetate solution 2 ml. The pain on injection was rated as none, mild, moderate, or severe. Seventy percent of patients in the C group experienced pain, while 33% and 25% of patients experienced pain in the A group and the L group, respectively. Forty-two percent of patients in the C group complained moderate to severe pain but only one patient in both A group and L group. In conclusion, 5% dextrose in Ringer's acetate solution premixed with 200 mg propofol significantly reduces incidence and severity of pain associated with propofol injection and is easier to use than premixed lidocaine.

Gallbladder carcinoma limited to the mucosa (pT1a) or muscularis proper (pT1b) with no lymph node metastasis (stage I) is defined as early carcinoma of the gallbladder. Eleven patients with early carcinoma of the gallbladder, treated by either simple or extended cholecystectomy (cholecystectomy plus wedge resection of the gallbladder bed of the liver and lymphadenectomy), were reviewed to determine the diagnostic capability and to clarify the rational resectional procedure for this stage of the disease. A definitive pre-operative diagnosis was made in only 2 patients with pT1b tumors. Most of the remaining 9 patients were diagnosed incidentally after cholecystectomy for polyps or stones. Among 7 patients with pT1a tumors, 5 underwent simple cholecystectomy and 2 underwent extended cholecystectomy. All 7 patients survived with a recurrence-free condition for 5 years or more following the operation. Two patients with pT1b tumors, however, died of a local recurrence or bile duct carcinoma following simple cholecystectomy. Two patients with pT1b tumors who were correctly diagnosed before the operation and underwent extended cholecystectomy survived without recurrence. It is concluded that patients with pT1a tumors can be successfully treated by simple cholecystectomy, while patients with pT1b tumors require extended cholecystectomy.

Systemic administration of melatonin can increase retinal light damage in the rat. The role of retinal melatonin receptors in modulating light-damage susceptibility was investigated by intravitreally injecting the melatonin receptor antagonist luzindole into rats.Nine Sprague-Dawley albino rats 8 to 9 weeks of age were kept in 50 lux cyclic light for at least 7 days before receiving an intravitreal injection of 1 microl 1 mM luzindole in one eye and 1 microl vehicle in the other eye. The injection was given just before the beginning of the normal 12-hour dark phase. At the end of this dark period, animals were exposed to constant light of 2500 lux for 48 hours. Animals were returned to dim cyclic light for 7 days, and dark-adapted electroretinograms (ERGs) were then recorded from the two eyes simultaneously. The eyes were processed for retinal morphology. Photoreceptor nuclei were counted in the outer nuclear layer (ONL), and the thickness of the ONL and that of the rod outer-segment plus inner-segment layer were measured at several points along sections through the vertical meridian. Two age-matched control rats were maintained in dim cyclic light but received no injections.Luzindole-treated eyes had ERG b-wave thresholds of 2.7 +/- 0.5 (mean +/- SEM) log candela (cd)/m2 lower than the fellow eyes injected with vehicle (P0.001), and the maximum b-wave amplitude was 1.0 +/- 0.2 log microV greater in luzindole-treated eyes (P0.001). Thresholds of the scotopic threshold response were 0.5 +/- 0.1 log cd/m2 lower than those in vehicle-injected eyes (P0.05). Luzindole-treated eyes on average had twice as many photoreceptor cells remaining (P0.005). In some areas, several rows of photoreceptor nuclei and outer segments remained in the luzindole-treated eye, whereas the fellow control eye showed cells only occasionally and no outer segments.Eyes pretreated with the melatonin receptor competitive antagonist luzindole before the dark phase preceding constant light exposure were substantially protected from light damage to the retinal photoreceptors. These results implicate the intraocular melatonin-dopamine system in the regulation of light-damage susceptibility.

We studied the reproducibility of multifocal electroretinography by repeated measurements in normal subjects. We also analyzed the amplitude and implicit time of the waves. Nine healthy eyes including myopic cases (-4.1 D on average) of 9 normal males, aged 19 to 42 years, were the objects of study. We used a (Visual Evoked Response Imaging System III (VERIS III), by TOMEY Corp.) for multifocal electroretinography. Each eye was examined 4 times on different days. The stimulus elements consisted of 103 hexagons. The net recording time was 4 minutes. We used the coefficient of variation (standard deviation/average) of 4 measurements of response density as index of reproducibility. Poor fixation and blinking were important factors that affected the reproducibility. In all the 9 eyes, reproducibility of multifocal electroretinography, expressed as average of the coefficient of variation of all regions, was 22% on average. In 6 eyes with good fixation and without blinking, the reproducibility was 15% on average. In 6 eyes with good reproducibility, we analyzed three parameters of the focal response waves: all traces, quadrants and rings, as well as the amplitude and latency of the waves. These data served as controls. Our studies showed that the response density correlated closely with the amplitude and not with the latency in normal subjects.

We studied relationships between maximal walking distance (WDmax) and frequency of both outing enumerated by the aim of each outing as well as by each outing per se in patients receiving home oxygen therapy (n = 109). The results were compared with those from members of a seniors' club (n = 434). A questionnaire was used to obtain WDmax, defined as the distance a subject could walk without rest on level ground. In the questionnaire, WDmax was classified into five groups including 50 m (the distance between two electric posts), 500 m, 1 km, 1.5 km and more than 1.5 km. Since few patients could walk 1.5 km or more, they were included into the "can walk 1 km or more group". Outing frequency was measured using a 4-week diary which showed eight aims of outings including shopping, seeing a doctor, visiting friends or relatives, doing a hobby practicing something, participating in a seniors' club and neighborhood meetings or events, traveling, work and others. The subjects checked the diary each time they went out. True outing frequency was defined as the number of outings. If a subject left home to shop and visited a friend on the way home, the outing frequency enumerated by aims was two, while the true outing frequency was one. The mean and SE (1/4 weeks/one subject) of true outing frequency for patients (21.4 +/- 2.2) was significantly less than that of seniors' club members (45.6 +/- 1.4). Even in patients with a WDmax of 1 km or more, the frequency of travel was significantly lower than in seniors' club members. Although outing frequencies for shopping, seeing friends or relatives, doing a hobby and work were not significantly different between the two groups at a WDmax of 1 km or more, the outing frequency for work of patients was significantly lower at a WDmax of 500 m, and outing frequencies for the remaining three aims became significantly lower at a WDmax of 50 m. We demonstrated that in patients receiving home oxygen therapy, outing frequency was limited. A new modality is necessary to increase the outing frequency and to improve the quality of life for these patients.

We examined family APGAR scores in patients on home oxygen therapy (n = 101) and their main caregivers (n = 91), and compared them with those obtained from members of a seniors' club who were not on home oxygen therapy themselves, nor had any family members on home oxygen therapy. Furthermore, the relationship between the main caregivers recognition of the patients' mental state and the patients' CESD score was examined. Family APGAR scores for the main caregivers were significantly lower than those of the patients (p0.002), or the seniors' club members (p0.004). Since most the main caregivers were women, we compared family APGAR scores of the female main caregivers and the age-matched female members of the seniors' club, revealing that the satisfaction of the female main caregivers with the "adaptation" component of the APGAR score (the component dealing with support given when something troublesome happens), was significantly lower than that of the members of the seniors' club (p0.0001). The CESD of the patients whom the main caregivers recognized as depressed was significantly higher. Thus, we concluded that satisfaction of the main caregivers with family function who were family members was low, and that the role of the main caregivers is important in alleviating the depression of patients on home oxygen therapy.

We described an autopsy case of a ruptured aneurysmal subarachnoid hemorrhage treated with endovascular embolization by interlocking detachable coils. An 85-year-old male presented with sudden onset of severe subarachnoid hemorrhage. Cerebral angiogram revealed a right internal carotid-posterior communicating artery aneurysm. Post-operative angiogram revealed complete obliteration of the aneurysm, except for its orifice. Following the embolization of the aneurysm, tissue plasminogen activator was intrathecally perfused for anti-vasospasm treatment. Follow-up angiogram showed stable obliteration of the aneurysm, and no particular findings of cerebral vasospasm. The patient had been recovering without any neurological deficits, but died from pneumonia on the 25th day after the embolization. Autopsy findings revealed the disappearance of the subarachnoid hemorrhage, and no visible finding of cerebral infarction or edema. The inner lumen of the aneurysm was occupied by a mixture of the coils and the clots. The surface of the embolized coils was directly observed through the orifice of the aneurysm without any membranous substance from the inner lumen of the internal carotid artery. This pathological finding is different from the previously reported animal models in which the surface of the embolized coils was covered with endothelial membrane 2 weeks after embolization. Further examinations are required to clarify the pathogenesis of the endothelial regrowth.

We report a case of large cystic acoustic neurinoma. A 52-year-old male was admitted to hospital with a history of progressive dysphagia, gait disturbance and diplopia for 2 months. On admission, neurological examinations revealed Bruns' type nystagmus to the left side, hypesthesia in the distribution of the second and third divisions of the left trigeminal nerve, and partial paresis of cranial nerves IX, X, and XII on the left side, and truncal ataxia. A pure-tone threshold audiogram indicated the presence of 32 dB hearing loss in the left ear. Speech discrimination was 80%. Caloric vestibular responses were absent on the left side. Skull radiographs with polytomographs of the internal auditory canal (IAC) were normal. Bony changes in the IAC were not found by high-resolution bone-window computed tomography (CT) scan. A plain CT scan revealed a large low-attenuated cystic mass in the left cerebellopontine angle (CPA), which was associated with displacement of the fourth ventricle. An enhanced CT scan demonstrated a thin rim-enhancement in the cyst wall. Magnetic resonance imaging (MRI) scans disclosed a large rim-enhanced cystic mass extending superiorly into the tentorial incisura and inferiorly into the foramen magnum. At surgery via a left suboccipital approach, a large cystic mass was found at the left CPA arising from the VIIIth nerve, and compressing the Vth, VIth, VIIth and lower cranial nerves. The cyst was filled with a xanthochromic fluid and was firmly attached to the internal auditory meatus (IAM). However no tumor extension into the IAM was confirmed. The tumor was excised completely. The postoperative course was uneventful, except for impairment of the VIIth and VIIIth nerves. At 6 months after the first operation, the facial nerve had improved up to grade III (Hause-Brackmann stage). Histological examinations revealed a typical benign acoustic neurinoma with predominant representation of Antoni B tissues. The cyst wall contained numerous abnormal sinusoid and telangiectasia-like vessels which showed occasional thromboses. The vessel walls displayed endothelial proliferations and were frequently hyalinized. Hemosiderin deposits and hemosiderin-containing phagocytes were also found near these vessels. Myxoid degeneration and necrosis were evident in vast areas. These degenerative changes appeared to be the principal causes of the large cystic formation. 16 cases including our case have been reported. The broad characteristics of the clinical symptoms and radiological findings of these tumors are discussed.

We report a rare case of a giant thrombosed fusiform aneurysm at the branch of left middle cerebral artery presenting with intramural hemorrhage of the aneurysm. A twenty-year-old man with familial and past history of migraine presented sudden temporalgia on August 13, 1995. Computed tomography (CT) scan on the day of the first attack revealed a well delineated high density area at the left Sylvian fissure, 2.5cm in diameter. Angiogram showed avascular area corresponding to the lesion, but no visualization of the aneurysm. On October 18, this patient presented sudden temporalgia again. CT scan on the day of the second attack indicated new intramural hemorrhage and surgery was performed on October 31. No evidence of subarachnoid hemorrhage was shown during the operation, and the lesion was proven to be a thrombosed fusiform aneurysm at the branch of the middle cerebral artery. The parent artery was clipped at both proximal and distal sides of the aneurysm, and the aneurysm was totally removed with success. Histological finding further supported the idea that the attacks mentioned were due to intramural hemorrhage of the thrombosed aneurysm. Postoperative course was uneventful and the patient was discharged without any neurological deficit. Intramural hemorrhage of a giant fusiform aneurysm is relatively rare, only reported in several autopsy cases. Furthermore, we failed to discover any comparable cases of giant fusiform aneurysm presenting symptoms directly caused by intramural hemorrhage of the aneurysm.

We report a case of 53-year-old man with acute myelogenous leukemia (M2) showing a karyotype of t(7;11) (p15;p15), del(10) (q11;q12), who was complicated with perforation of a duodenal ulcer during the antileukemic chemotherapy using behenoyl ara-C, daunorubicin, 6-mercaptopurine and prednisolone. As his bone marrow still showed high cell density and leukemic proliferation at the time of intestinal perforation, the therapeutic regimen was changed to a combination of behenoyl are-C and mitoxantrone, and daily rhG-CSF was concurrently administered for the purpose of early establishment of bone marrow hypoplasia. On the 8th day after the therapeutic regimen had been changed, his bone marrow became nearly aplastic, and complete remission was obtained on the 24th day. This case may indicate that the concurrent administration of cell-cycle specific antileukemic drugs and rhG-CSF is available for AML patients with emergent need of leukemic cell reduction.

The intestinal walls of the irradiated pelvic tumor cases of 20 patients were studied. CT manifestations of the irradiated intestinal wall were examined at the early vascular phase (examined 40 seconds after the injection of contrast medium by helical scan) and at the delayed equilibrium phase (examined 4 to 5 minutes after the injection of contrast medium by rapid sequence scan). Two characteristics were identified: intestinal wall thickening and a three-layered pattern. The former was better depicted on equilibrium phase, whereas the latter was clearer on early vascular phase. Differences in visualization of the wall thickening on vascular phase and delayed phase were statistically significant. The three-layered pattern was considered to suggest severe inflammatory edematous change of the intestinal wall. Early enhancement of the mucosal and muscular-serosal layers with less enhancement of the submucosal layer, and homogeneous distribution of the contrast medium to the interstitium on delayed phase were considered to be the reason.

One-month oral toxicity of (S)-10-[(S)-(8-amino-6-azaspiro[3,4] octan-6-yl)]-9-fluoro-2,3-dihydro-3-methyl-7-oxo-7H-pyrido[1,2,3-de] [1,4]benzoxazine-6-carboxylic acid hemihydrate (CAS 151390-79-3, DV-7751a) a new quinolone antibacterial agent was investigated in Sprague-Dawley rats at doses of 12.5, 50, 200 and 800 mg/kg/d and in cynomolgus monkeys at 10, 30 and 100 mg/kg/d. Rats receiving 200 mg/ kg showed abnormal urine crystals, enhanced deposition of lipid in hepatocytes and exacerbation of osteochondrotic lesions in the femoral condyle. In addition, dosing at 800 mg/kg induced decrease in body weight gain and increased levels of serum alkaline phosphatase (ALP), cholinesterase, leucine aminopeptidase and total cholesterol. Monkeys receiving 100 mg/kg showed abnormal urine crystals and increases in serum glutamic oxaloacetic transaminase, glutamic pyruvic transaminase and ALP levels. The non-toxic doses of DV-7751a in rats and monkeys were 50 and 30 mg/kg, respectively, under the present experimental conditions.

We report a case of intraorbital conjunctival cyst following a penetrating orbitocranial injury. The patient was a 28-year-old male who was hospitalized with exophthalmos, retrobulbar pain and upper gaze disturbance of his left eye. When he was 4 years old, a thin iron rod had penetrated intracranially through the inner angle of his left orbit. He was hospitalized and treated conservatively for about two weeks. The left eye ball was intact and visual acuity was normal, although bloody fluid had continuously flowed out from the left inner angle of the conjunctival wound for a few days. He had been febrile to 39 degrees C and complained of headache for one week. Subsequentry, the symptoms gradually improved through conservative therapy. When he was a junior high school student, he noticed exophthalmos of his left eye. However, he had never been examined closely, until he was 28 years old. We suspect that he had suffered from meningitis caused by the penetrating orbitocranial injury, and had fortunately improved under the conservative therapy. On admission to our hospital, a craniogram showed fracture of the left orbital roof, and coronal and three-dimensional computed tomography (CT) scans clearly demonstrated the orbital fracture. CT revealed a cystic mass in the retrobulbar space, and a porencephalic cyst in the medial basal frontal lobe. On magnetic resonance imaging (MRI) scans, both cysts were of low intensity on T1-weighted imaging, and of high intensity on T2-weighted images. Coronal and sagittal MRI scans showed that the two cysts were connected with each other through the fracture in the orbital roof. We diagnosed therefore that the orbital cyst was a herniated porencephalic cyst of the frontal lobe. Surgery was performed by a transcranial approach. The porencephalic cyst adhered to the fractured lesion of the frontal base but did not extend into the orbita. The intraorbital cyst was totally removed by opening the orbital roof including the fractured lesion. The cyst contained milky fluid. Postoperatively, the exophthalmos, retrobulbar pain and upper gaze disturbance showed gradual improvement. On histological examination, the cyst was found to be lined by non-keratinized stratified squamous epithelium and was diagnosed as a conjunctival cyst. This case was considered to be one of traumatic conjunctival cysts caused by a penetrating orbitocranial injury. Orbital conjunctival cysts have been reported to comprise about 10% of orbital epidermoid and dermoid cysts. Of these cysts, traumatic conjunctival cysts are rare, and only a few cases have been described. The etiology and therapy of orbital conjunctival cysts are discussed.

A therapeutic trial of interleukin-3 (IL-3) was carried out in four patients with aplastic anemia refractory to the prior therapies. Daily subcutaneous doses of 2.5, 5.0 or 7.5 micrograms/kg was given for 7 or 14 days. In a patient who had co- and immediate boost-administration of granulocyte colony-stimulating factor (G-CSF) and/or erythropoietin (Epo) and another who had sequential administration of G-CSF and Epo two weeks after IL-3, definite hematological response was obtained during the course after IL-3. In one patient, moderate to severe side effects consisting of facial edema, conjunctival bleeding, chills and fever, were observed after two days' administration of IL-3. Co- or sequential administration of other hemopoietic factor(s) may be essential in IL-3 therapy for aplastic anemia.

We present here an interesting case of multiple dural arteriovenous shunts (dAVS) in different locations at the same time. There have been very few reports on multiple dAVS. A 63-year-old man was admitted with a sudden onset of headache and vomiting. CT scan showed a typical subarachnoid hemorrhage (Fisher Group 3). Cerebral angiogram (6 vessel study) revealed two dural arteriovenous shunts at the same time. One was located on the anterior fossa fed by the anterior ethmoidal artery, and the other was located on the posterior fossa near the marginal sinus fed by the left ascending pharyngeal and occipital arteries. At first, transarterial embolization was performed for dAVS located on the posterior fossa. Radical operation was performed for both anterior and posterior fossa dAVS. Both dAVS had disappeared on postoperative angiograms.

We reported a very rare case of an epidural hematoma soon after nose blowing. A 22-year-old male visited our hospital complaining of severe headache and nausea soon after he blew his nose. Thirteen years ago, he had a ventriculo-peritoneal (V-P) shunt operation for a pineal region tumor which had not recurred after irradiation. His left auditory tube had been patent. He hit his head about 3 months ago. On his arrival, his consciousness was almost clear but we observed slight right hemiparesis. Computed tomography of his head obtained on the first day showed the air in the hematoma in the left parietal epidural space which penetrated his petrosal bone from the mastoid air cells. Removal of his epidural hematoma was performed the next day and there was no abnormality of his parietal bone, dura and meningeal arteries. We supposed that nose blowing was what triggered his epidural hematoma. From pressure of nose blowing, the air of his nasopharyngeal space passed through his patent auditory tube into the tympanic cavity, and entered into the epidural space penetrating a microfracture or dissociation in the petrosal bone. In addition to this, V-P shunt system and the looser adhesion of dura to the skull in the young promoted entrance of air. Associated with formation of epidural hematoma in this case were four factors, "patency of auditory tube", "defect or microfracture of petrosal bone", "V-P shunt", "younger age" and triggered by nose blowing.

Muramyl dipeptide-Lys(L18) given by daily subcutaneous injection for 14 days induced arthritis in male Lewis, Fischer and nude rats, to a lesser degree in the last two than in the first strain. On the other hand, a single intradermal administration of Freund's complete adjuvant induced arthritis in Lewis and Fischer but not nude rats. Cyclosporin A (CsA) co-administered for 14 days markedly exacerbated the muramyl dipeptide-Lys(L18) induced arthritis (MIA) in rats of all three strains, but completely blocked the development of the adjuvant induced arthritis (AIA) in Lewis rats. Furthermore, AIA was transferred to recipient Lewis rats through spleen cells obtained from the donors with AIA, whereas MIA was not. Antibodies against type II collagen and DNA were not detected in sera from MIA or AIA rats. These data show a clear difference between MIA and AIA in the pattern of development of arthritis and suggest that delayed hypersensitivity reactions may be involved in the pathogenetic mechanisms of AIA, but not in MIA.

To examine the involvement of lymphocytes in the development of MDP-Lys(L18)-induced arthritis (MIA) in rats and the exacerbation of MIA by cyclosporin A (CsA), we analysed the spleen lymphocyte subset using monoclonal antibodies and flow cytometry during the development of arthritis and compared the results with those found in adjuvant-induced arthritis (AIA). Subcutaneous injection of MDP-Lys(L18) 4 mg/kg to male Lewis rats for 14 days caused very slight and quite clear increases in tarsal joint thickness on days 8 and 15, respectively. This increase was significantly enhanced by co-administration of CsA 10 mg/kg on both of these days. Adjuvant intracutaneously injected once increased the thickness only on day 15, and this was completely inhibited by CsA. The populations of CD4+ and CD8+ cells were increased and decreased, respectively, increasing the CD4+/CD8+ ratio, from day 8 in MIA. CsA enhanced the MDP-Lys(L18)-induced changes in these populations and caused additional decreases in the number of CD5+ cells. Only the CD4+ cell population was increased on day 15 in AIA, and this increase was inhibited by CsA. These results suggest that the spleen lymphocyte subsets in MIA have a different role from those in AIA, and that the contribution of enhancement of the subset changes to the exacerbating effect of CsA on MIA.

We report a case of hypereosinophilia which was associated with the onset of anginal attacks. A 64-year-old man progressed to end-stage renal failure due to diabetic nephropathy, and was treated with continuous ambulatory peritoneal dialysis (CAPD). He had no past history of angina pectoris nor hypereosinophilia. Three weeks after the initiation of CAPD, the eosinophil count in peripheral blood increased (up to 4093/mm3). Two weeks later, he suffered from an anterior chest pain attack, and angina pectoris was diagnosed. As a result of treatment with isosorbide dinitrate and prednisolone, hypereosinophilia disappeared rapidly and repeated episodes of anginal attacks also disappeared. After an interval of 3 months, however, hypereosinophilia (up to 15190/mm3) and anginal attacks recurred. He underwent coronary angiography, in which no stenotic change was observed. The administration of prednisolone was effective in the treatment of these episodes. Although a close relationship between hypereosinophilia and anginal attack has been reported, it has not been known in CAPD patients as described here. Attention should be paid to these relationships in CAPD patients, because hypereosinophilia is frequently observed in maintenance peritoneal dialysis patients.

A retrospective evaluation was performed to determine whether accelerated hyperfractionation (AHF) improves the survival rate of patients with malignant gliomas. One hundred and seven patients with malignant gliomas, including glioblastoma multiforme, who had received radical radiotherapy were evaluated. Of the patients, 36 were treated by conventional fractionation (CF), and 71 by AHF. The treatment results of the two regimens were compared with regard to survival rate after therapy. Treatment by AHF was conducted at 10-15 F/W (1.5 Gy/F); the mean total dose was 61 Gy over an average of 27 days. Treatment by CF was conducted at 5 F/week (1.8-2 Gy/F); the mean total dose was 59 Gy over 51 days. Multivariate analysis using Cox's proportional hazard model revealed that AHF significantly increased survival rate. Besides pointing to the selection of the AHF method as a treatment regimen, multivariate analysis showed the following factors to be indicators of favorable prognosis: a histopathological diagnosis other than glioblastoma multiforme, age below 40 years, and supratentorial location of the tumor.

Single oral dose toxicity of nefiracetam (N-(2,6-dimethylphenyl)-2-(2-oxo- 1-pyrrolidinyl) acetamide, DM-9384, CAS 77191-36-7), a new cognition-enhancing agent, was examined in ddY mice, SD rats and beagle dogs. The LD50 values of nefiracetam were 2005 mg/kg for male mice and 1940 mg/kg for female mice, 1182 mg/kg for male rats and 1408 mg/kg for female rats and more than 500 mg/kg for beagle dogs. Common toxic signs in all species were a decrease in locomotor activity, lying on the side or back and loss of righting reflex, considered to be caused by depression of the central nervous system. Pathologically, no remarkable change associated with nefiracetam administration was observed in any species. In addition, toxicities of the decomposition product (D-2) and by-products (Bis, 3-Me and 4-Me) of nefiracetam were examined by oral administration, and of the metabolites (M-3 and M-11) by intravenous injection in male ddY mice. LD50 values of the 3-Me and 4-Me forms were 1399 and 1534 mg/kg, respectively. Clinical signs in mice treated with these by-products were similar to those caused by nefiracetam. The other compounds induced no toxic signs or death up to the highest dose (2000 mg/kg) used.

The 13-week oral toxicity of nefiracetam (N-(2,6-dimethylphenyl)-2-(2-oxo- 1-pyrrolidinyl) acetamide, DM-9384, CAS 77191-36-7), a new cognition-enhancing agent, was investigated in Beagle dogs of both sexes. No change was observed in the 20 mg/kg group. Hypospermatogenesis and slightly increased deposition of hemosiderin in the spleen were seen in male dogs treated with 60 mg/kg or more. Dosing at 180 mg/kg induced a decrease in food consumption, increases in urinary volume and urinary protein, and renal papillary necrosis in both male and female dogs. The non-toxic dose was 20 mg/kg under these experimental conditions.

A clinical study was performed on 38 patients with renal pelvic and ureteral cancers who were treated in our hospital between 1977 and 1992. Nine patients (23.7%) had lymph node metastasis. The risk factors of lymph node metastasis were high grade, high stage and class IV or V or urine cytology. None of the patients with G1 or under pT1 had lymph node metastasis. The 5-year survival rate of the patients without [lymph node metastasis was 76.7% and that of the patients with lymph node metastasis was 11.1%. Although 6 of the 9 patients with G1 or G2 and under pT1 did not have adjuvant therapy, none of them died of the cancer. We concluded that lymph node metastasis in renal pelvic and ureteral cancers was the most important prognostic factor and that regional lymphadenectomy might be useful for the decision of adjuvant therapy.

A patient with adult-onset Still's disease who presented with myelodysplastic syndrome (MDS) after a course of 6 years is reported. To our knowledge, this is the first such reported case. The patient died of acute myelocytic leukemia. The possibility that cyclosporine contributed to the onset of MDS is discussed.

We performed surgical treatment in 22 cases of torsion of the spermatic cord during the past sixteen years. Orchiopexy was performed in 9 cases, but in 13 cases orchiectomy was unavoidable. For five patients the visit to a doctor was too late. In five other cases a mistaken diagnosis was made by local medical doctors. Improvement of the success rate of orchiopexy requires that adolescents, their families and teachers should learn to recognize this disease, and doctors of other departments should recognize it as acute scrotum.

Intrathoracic lymphadenopathy in eosinophilic pneumonia is very rare and few cases have been confirmed histologically. This is the first case of eosinophilic pneumonia with mediastinoscopic lymph node biopsy reported in Japan. The case is a 42-year-old man who was admitted to our hospital complaining of cough, general fatigue and dyspnea of one month's duration. Chest X-ray demonstrated bilateral hilar and mediastinal lymph node enlargement with interlobar pleural thickening and infiltrative shadows in right lower lung field. Computed tomography revealed infiltrative shadows at right S4, S5, S8 and S9 and S10 segments and #2, #3, #5, #6 lymph node enlargement. Biopsy of the lymph node via mediastinoscopy demonstrated that the architecture was preserved, sinusoids were filled with histiocytes and eosinophils, and lymphoid follicles were compressed. Immunohistochemical technique using monoclonal antibody EG2 which reacts with the secreted form of Eosinophilic Cationic Protein (ECP), demonstrated that eosinophils infiltrating the mediastinal lymph nodes were activated. The pathogenesis of mediastinal lymphadenopathy in eosinophilic pneumonia remains to be determined, but our case suggests that mediastinal lymph nodes may play a role in eosinophilic pneumonia.

A 59-year-old male patient presented in 1991 with left-sided hemiplegia and hemihypesthesia and left homonymous hemianopsia, which had developed for the preceding 12 months. The cerebrospinal fluid (CSF) level of protein was mildly elevated, oligoclonal IgG band was initially negative, but finally positive and myelin basic protein was absent. Magnetic resonance imaging and X-ray computed tomography (CT) of the brain revealed a unilateral demarcated lesion extending around the posterior horn and triagular part of the right lateral ventricle, apparently capped by remarkably gadolinium enhancement at its front, which had no mass effect, and several small isolated plaques were also observed in other areas of the brain. All lesions appeared as high intensity areas on T2 weighted images and hypodense areas on CT. The JC virus hemagglutination-inhibition antibody titers were 1:32 in serum and 1:8 in CSF; the antibody titer ratio and index both suggested an intrathecal antibody production. Pathological examination of brain biopsy specimen taken from the large lesion demonstrated profound demyelination with preservation of axons, a large number of macrophages and spotted perivascular lymphocyte cuffings. Based on this experience, we discussed the features in this case which differentiated it from multiple sclerosis, leukodystrophy and typical progressive multifocal leukoencephalopathy (PML). Diffuse-disseminated sclerosis or transitional sclerosis was most likely so far as the clinical picture, imaging and histology were concerned. However, we implicated the possible involvement of JC virus infection to the etio-pathogenesis of the demyelinating lesions in view of the intrathecal JC virus antibody production in CSF observed in this case.(ABSTRACT TRUNCATED AT 250 WORDS)

For the elucidation of the mechanism of membrane stabilization by vitamin E, the effects of alpha-tocopherol and its model compounds on either retinol-induced hemolysis of rabbit erythrocytes or the permeability and fluidity of liposomal membranes have been studied. Retinol-induced rabbit erythrocyte hemolysis has been found not to be caused by the oxidative disruption of erythrocyte membrane lipids initiated by retinol oxidation, but rather to arise from physical damage of the membrane micelle induced by penetration of retinol molecules. In suppressing hemolysis, alpha-tocopherol was more effective than other naturally occurring tocopherols. alpha-Tocopheryl acetate, nicotinate, and 6-deoxy-alpha-tocopherol were more effective than alpha-tocopherol itself. The inhibitory effects of alpha-tocopherol model compounds having side chains with at least two isoprene units or a long straight chain instead of the isoprenoid side chain were similar to those of alpha-tocopherol. These data suggest that for protection of membranes against retinol-induced damage, the hydroxyl group of alpha-tocopherol is not critical, but rather the chroman ring, three methyl groups on the aromatic ring, and the long side chain are necessary. To verify the mechanism of the inhibitory effect on hemolysis, not only the effect of vitamin E and its model compounds on the membrane permeability and fluidity, but also the mobility of alpha-tocopherol molecule in membranes has been investigated using bilayer liposomes as the model membranes. Addition of alpha-tocopherol to membranes produced a greater decrease in the permeability and fluidity of rat liver phosphatidylcholine liposomes compared with egg yolk phosphatidylcholine liposomes. In dipalmitoylphosphatidylcholine liposomes, however, alpha-tocopherol was less effective, that is, the more unsaturated the lipids, the more they interact with alpha-tocopherol. 2,2,5,7,8-Pentamethyl-6-chromanol with no isoprenoid side chain and phytol without the chromanol moiety had no effect. The measurement of 13C NMR relaxation times revealed that the mobility of methyl groups on the aromatic ring of alpha-tocopherol in membranes is significantly restricted. In contrast, the methyl groups at positions 4'a and 8'a on the isoprenoid side chain have high degrees of motional freedom in the lipid core of membranes. Furthermore, it was found that alpha-tocopherol in membranes interacts with chromate ions added as potassium chromate outside the membranes, resulting in an increase in membrane fluidity. These results are compatible with those of the inhibitory effect on retinol-induced erythrocyte hemolysis. On the basis of the results obtained here, a possible mechanism for membrane stabilization by vitamin E is proposed.

We report two cases of mucinous adenocarcinoma of the prostate. A 56-year-old man underwent subcapsular prostatectomy under the diagnosis of benign prostatic hyperplasia in 1968, and was found to have mucinous adenocarcinoma of the prostate, which proved to be prostatic acid phosphatase (PAP) and prostate specific antigen (PSA) positive, and carcinoembryonic antigen (CEA) negative by immunohistochemical staining. Subsequently he received 70 Gy of irradiation to the prostate, but died in 1976, when serum PAP was elevated. Autopsy revealed metastases to the liver, lungs, bone, peritoneum, spleen, pancreas, lymph nodes, and no primary gastrointestinal adenocarcinoma. The other case was a 57-year-old man, who underwent transurethral resection (TUR) for papillary tumor located just lateral to the verumontanum in 1982. The tumor was misdiagnosed as adenomatous polyp, and was PSA and PAP negative, and CEA positive. After 3 TURs of the recurrent tumor on the prostatic urethra, he underwent prostatourethrectomy, pelvic lymphadenectomy, and cystostomy for radical cure in 1985. The specimen proved to be mucinous adenocarcinoma of the prostate. He suffered recurrence of the tumor in the retrovesical space in 1987, and died in 1990. Autopsy revealed no evidence of metastasis except the local recurrence and no primary gastrointestinal adenocarcinoma.

This experimental report evaluates the histopathological effects of a new embolization method using estrogen-alcohol (E-A) and polyvinyl acetate solution (PVac) as tested on 21 mongrel dogs. Three other animals treated with normal saline served as controls. All agents were introduced through an isolated cortical artery. Estrogen-alcohol induced immediate occlusion of small vessels (less than 20 microns), and then progressive obstruction of larger ones (200-300 microns) within several days. Animals treated with PVac showed vascular obliteration (greater than 100 microns) and moderate chronic fibrosis. The effects of embolization using E-A followed by PVac were found to have the combined advantages of both materials, showing diffuse occlusion of the vascular network with less tissue reaction. Hyalinization of embolized vessels with extensive fibrosis occurred afterward. For 6 weeks there was no evidence of recanalization or foreign body giant cell reaction. This study shows that E-A and PVac are capable of producing vascular occlusions with only mild tissue reaction. Because they are easily controllable and have no adverse effects, they may be suitable for intravascular application in the central nervous system.