Evaluation of the source and count of urinary erythrocytes in healthy individuals using an automated urinary flowcytometer.
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Biomedical subjects
Publications and source records attributed to K Kumano.
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Interleukin-12 (IL-12) is a key cytokine that promotes Th1-type cell-mediated immunity and inhibits Th2-type responses. We have previously shown that antigen-induced eosinophil recruitment into the airways of sensitized mice is mediated by Th2-type CD4+ T cells that produce IL-5. Therefore, to determine whether IL-12 regulates antigen-induced eosinophil recruitment into the airways, we studied the effect of recombinant murine IL-12 on antigen-induced eosinophil infiltration into the tracheas of sensitized mice, and also the effect of IL-12 on IL-5 and interferon-gamma (IFN-gamma) levels in bronchoalveolar lavage fluid (BALF) from the mice. The intraperitoneal administration of recombinant IL-12 (rIL-12) inhibited antigen-induced eosinophil infiltration into the mouse trachea in a dose-dependent manner. The administration of rIL-12 suppressed IL-5 levels but enhanced IFN-gamma levels in the BALF of the mice after antigen inhalation. The administration of rIL-12 also decreased in vitro antigen-induced IL-4 and IL-5 production, but not IFN-gamma production, in spleen cells of the mice. Furthermore, pretreatment with anti-IFN-gamma monoclonal antibody prevented the IL-12 inhibition of antigen-induced eosinophil infiltration into the tracheas of the mice. These results indicate that IL-12 downregulates antigen-induced eosinophil recruitment into the airways by inhibiting IL-5 production in sensitized animals.
BACKGROUND: Although the lesions of Bowen's disease often show conspiciously irregular configurations, there have been no studies performed to elucidate what these clinical features imply. Of 90 patients with Bowen's disease, 34 (group 1) had such irregular lesions with patches of normal-appearing interlesional skin. Their clinical backgrounds were compared with those of 56 patients without irregular lesions (group 2). Specimens of lesional, interlesional, and perilesional skin from 17 patients in group 1 were examined to evaluate the histopathologic evidences of regression. OBSERVATIONS: The lesions of group 1 patients were more commonly located on the trunk, larger in size, and of longer duration than those of group 2 patients. The specimens of lesional skin from the 17 group 1 patients revealed amyloid deposition (12 patients), melanophages (three patients), increased vascularity (15 patients), and inflammatory cell infiltrates (17 patients). The interlesional skin also exhibited amyloid deposition (12 patients), melanophages (six patients), increased vascularity (15 patients), dermal fibrosis (16 patients), inflammatory cell infiltrates (15 patients), and epidermal atrophy (eight patients). The perilesional skin showed no amyloid depositions, melanophages, or increased vascularity. CONCLUSION: These histopathologic findings in normal-appearing interlesional skin may represent partial spontaneous regression of Bowen's disease.
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Assessment was made of the contribution of lymphatic and nonlymphatic fluid absorption to net fluid loss from the peritoneal cavity. Diaphragmatic, visceral, and parietal pathways in lymphatics and nonlymphatics were examined using a rat model with adhesion of the diaphragm to the liver, evisceration, these two procedures in combination, and without treatment. In each of these cases, six rats were used, each dialyzed for 180 min with Krebs-Ringer solution. The peritoneal net fluid absorption rate (PNFAR) was determined based on the disappearance of 125I-bovine serum albumin (BSA) from the peritoneal cavity and the lymphatic absorption rate (LAR), was based on the appearance of this albumin in the blood. Seventy-eight percent of net fluid loss occurred via the nonlymphatic pathway, primarily through parietal and visceral absorption; and the remaining 22% through the lymphatics, the main pathway being the subdiaphragmatic lymphatics. Nonlymphatic fluid absorption would thus appear to be a major route of fluid loss from the peritoneal cavity in rat peritoneal dialysis.
The pharmacological manipulation by vasodilators of peritoneal solutes and fluid kinetics was investigated. Rats were dialyzed for 240 minutes with 30 mL 4.25% glucose dialysate containing dextran 70. An angiotensin-converting enzyme inhibitor (captopril), three calcium channel blockers (nicardipine, diltiazem, and verapamil), and an +/-blocker (maxisylite) were administered intraperitoneally at various concentrations. Membrane permeability to urea, glucose, and protein, actual net ultrafiltration rate (UFR), transcapillary ultrafiltration rate (TCUFR), and peritoneal net fluid absorption rate (PNFAR) were measured. All three vasodilators caused a decrease in blood pressure, which, except for moxisylite, was associated with a decrease in net UFR. Captopril and the three calcium antagonists increased PNFAR dose dependently. Captopril increased membrane permeability to small and large molecular solutes, with a consequent decrease in TCUFR. Nicardipine and verapamil increased permeability to urea and glucose but not to protein. Only the latter decreased TCUFR. Diltiazem caused no change in permeability. In conclusion, various vasodilators administered intraperitoneally affect peritoneal solute and fluid transport differently. This should, perhaps, be taken into consideration when working with continuous ambulatory peritoneal dialysis (CAPD) patients to whom antihypertensive drugs are administered in large doses.
Assessment was made on the serum protein binding of clarithromycin (CAM), a representative oral macrolide, using sera from healthy subjects (HS) and patients with chronic renal failure (CRF) applying equilibrium dialysis in vitro. The protein binding of CAM was 81.9 +/- 1.9%, 85.9 +/- 3.6%, 82.9 +/- 3.3% and 86.8 +/- 3.3% for sera from HS, from patients in conservative treatment (ND), from those receiving hemodialysis (HD) and from those with continuous ambulatory peritoneal dialysis (CAPD), respectively. There was no significant difference among these values. The protein binding of CAM was 82.9 +/- 3.3% and 68.8 +/- 3.5% for sera before and after HD, respectively. There was significant difference between these values. In the study of the protein binding in patients on HD at an albumin concentration of 0.5 mM, the protein binding of CAM for sera was found to be significantly decreased following HD as compared to that prior to HD. The addition of palmitic acid (PA), a common NEFA, to pooled sera from HS, the protein binding of CAM showed no change. These findings suggest that changes in the protein binding of CAM with HD have been possibly caused by an increase in a drug binding inhibiter other than NEFA (PA) or by an allosteric effect on the albumin binding capacity. At therapy using CAM, the possibility of enhanced pharmacological effects and increased adverse reactions of CAM due to decreased protein binding in patients on HD should be considered.
To evaluate reduction methods using two of the several types of Cotrel-Dubousset instrumentation (CDI), 39 patients with low-grade (Meyerding grades I and II [12]) lumbar spondylolisthesis were followed clinically and radiologically for a minimum of 6 months. Our surgical methods were classified into three types as follow: reduction by 2-level assembly using double-threaded screws (type I); reduction by single-level assembly using the double-threaded screws (type II); and reduction by single-level assembly using tulip screws (type III). We found that satisfactory reduction could be achieved by single-level assembly using either the double-threaded or tulip screw without resection of disc material or the posterior leverage method. We found that the tulip screw was superior in obtaining stable reduction. We discuss the mechanism of reducing spondylolisthesis in comparison with that of previously reported methods.
BACKGROUND: Intracerebral hematoma from ruptured aneurysms is one of the unfavorable factors for outcome in patients with subarachnoid hemorrhage. In this study, the clinical characteristics of intracerebral hematoma in patients with ruptured aneurysms were examined. METHODS: The subjects were 512 patients who had been admitted by day 3 after aneurysmal rupture without episodes of rebleeding before the initial computed tomography (CT) scan. They were divided into two groups according to the findings of initial CT; groups 1 and 2 comprised patients with and without intracerebral hematoma, respectively. RESULTS: Of the 512 patients, intracerebral hematoma was observed in 98 (19%). The incidence of intracerebral hematoma was higher in patients with distal anterior cerebral and middle cerebral artery aneurysms, compared with those at other sites (both, p < 0.01). Interhemispheric, callosal, and temporal lobe/sylvian hematomas were observed more frequently in patients with anterior communicating, distal anterior cerebral, and middle cerebral artery aneurysms, respectively, than in those with aneurysms at other sites. The incidence of rebleeding was 22% in group 1 and 14% in group 2 (p < 0.05). Clinical grades on admission were higher and outcome at 6 months after onset was less favorable in group 1 than in group 2 (both, p < 0.01). The larger the intracerebral hematoma, the higher was the clinical grade and the less favorable the outcome. However, when comparing management and surgical outcome under the same clinical grades, there was no significant difference between the two groups. CONCLUSIONS: There was a close correlation between the site of hematoma and that of the ruptured aneurysm. Poor outcome in patients with intracerebral hematoma seems to be related to severity of clinical grade on admission.
In patients with subarachnoid hemorrhage (SAH), the effect of clot removal on cerebral vasospasm is still in dispute. The purpose of this study is to investigate whether rapid spontaneous diminution of subarachnoid blood alleviates vasospasm. We analyzed the effect of diminution of SAH on vasospasm in 36 patients with SAH grades III-IV who were operated on by the same surgeon by day 6 after SAH. The diminution of subarachnoid blood became more apparent with shorter interval between hemorrhage and initial computed tomography (CT) scan, with increasing patient age, and with higher SAH grades. The incidences of angiographic vasospasm grades III-IV, permanent symptomatic vasospasm, and low-density area on CT scans decreased with the increase in the degree of diminution of subarachnoid blood. Permanent symptomatic vasospasm and low-density area on CT scans were found in 5 of 9 patients with no diminution, whereas they occurred only in 5 of 27 patients with diminution (p < .05). We concluded that spontaneous diminution of subarachnoid blood in the acute stage after SAH seems to reduce the severity of vasospasm.
Ultrafiltration failure has been one of the major causes of drop out from CAPD treatment. The present study was designed to develop an ultrafiltration failure model in the rat and to assess whether various agents could prevent a decrease in ultrafiltration capacity in this rat model. Peritoneal hyperpermeability was induced by repeated intraperitoneal injection of 15 ml of 4.25% dextrose dialysate for 7 days. Some of the rats received agents, such as phosphatidylcholine, chondroitin sulfate, siliac acid, heparan sulfate, keratan sulfate, sodium sulfate, sodium phosphate, and heparin sodium, simultaneously administered with 4.25 % dextrose dialysate for the same duration. Ultrafiltration volume, D4/D0 ratio of glucose and peritoneal net fluid absorption were evaluated by 4-hour dwelling of 30 ml of 2.5% dextrose dialysate. Sodium phosphate and heparan sulfate prevented peritoneal hyperpermeability due to repeated injection of hypertonic dialysate. Sodium phosphate, sodium sulfate, heparin and heparan sulfate suppressed peritoneal net fluid absorption, resulting in an increase in ultrafiltration. These findings may be applicable to CAPD patients with ultrafiltration loss.
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In neurologic examination of patients with a suspected compressive lesion at the thoracic region, the dermatomic level of sensory disturbance is the only index indicating the anatomic level of a lesion. Because spinal cord tumors usually are solitary compressive lesions, the relationship between the anatomic and dermatomic levels is conveniently examined. We examined the relationship between the highest dermatomic level of sensory disturbance and the anatomic level, axial location, and type of spinal cord tumors in the thoracic region in 19 patients (8 men and 11 women aged 27-78 years; 11 neurinomas, 7 meningiomas, 1 neurofibroma). The distribution of sensory disturbance was evaluated with 3-g Frey hair and 1-g pin-prick examinations. The dermatomic distribution of sensory disturbance was diagnosed according to the dermatome chart of Keegan and Garrett. The anatomic level and axial location of the tumor were highly related to the sensory disturbance. Eight of 12 tumors in which the dermatomic level of sensory disturbance was within one vertebral segment of the anatomic level were situated in the middle or lower thoracic region (T6-T10). All five tumors in which the dermatomic level was two or more vertebral segments away from the anatomic level were situated at the conus medullaris (T12) or upper thoracic region (T1-T5); the highest level of sensory disturbance was from 4 to 11 segments below the anatomic level of the tumor. In two patients with no sensory disturbance, the tumor was in the upper thoracic region (T5) and compressed the spinal cord from the dorsal side. When a spinal cord tumor at the thoracic region is suspected, imaging examinations should be performed sufficiently cranially.
A microbiological assay method for measurement of T-3761 and its stability in body fluids were investigated. The paper disc method proved suitable for this assay using Escherichia coli Kp as a test organism and commercially available heart infusion agar as a test medium. When using the paper disc method, lower detection limit of T-3761 was approximately 0.05 microgram/ml and 0.1 microgram/ml for 1/15M phosphate buffer (pH 7.0) and human serum, respectively. T-3761 in human serum and urine was stable under freezing -20 degrees C for at least 28 days.