Biomedical subjects
Publications and source records attributed to K Sano.
Eosinophilic cystitis (EC) is rather an uncommon disease in childhood. A case of EC in a 5-year-old boy, in which open biopsy was needed for final diagnosis, is reported. After diagnosis, he was treated with pemirolast potassium followed-up with eosinophil cationic protein (ECP) in serum and urine. Eosinophil cationic protein is an appropriate marker of EC.
BACKGROUND: We have previously reported that animals recovering from uranyl acetate (UA)-induced acute renal failure (ARF) were resistant to subsequent insult. Recent evidence suggests that apoptosis participates in tubular damage. We investigated the role of apoptosis in UA-induced ARF and attenuation of ARF in acquired resistance to UA in rats. METHODS: ARF was induced by an intravenous injection of UA (5 mg/kg) in rats. Rats of group 1 were injected with UA and followed for 28 days. Group 2 rats were injected with a second dose of UA (5 mg/kg) 14 days after the first injection and were followed for 14 days. All rats received an intraperitoneal injection of bromodeoxyuridine (BrdU) one hour before sacrifice. Using kidneys, histologic examination and immunohistochemical detection of proliferating cell nuclear antigen (PCNA), BrdU, Bcl-2, and Bax were performed. To detect apoptosis, electron microscopy, analysis of DNA fragmentation, and the TUNEL methods were adopted. RESULTS: UA increased the number of damaged renal tubules and serum creatinine, which peaked at 5 days in group 1, but both returned to baseline values by 14 days. Apoptosis was confirmed by electron microscopy and the "ladder" pattern of DNA fragments on gel electrophoresis. The number of apoptotic tubular cells evaluated by the TUNEL method showed two peaks at days 5 and 14 in group 1. The second peak of TUNEL-positive cells was preceded by an increased number of BrdU-positive nuclei, PCNA-positive nuclei, and total number of tubular epithelial cells. Renal damage after the second UA injection was markedly reduced. The peak number of apoptotic cells in group 2 was significantly less than that in group 1. CONCLUSIONS: Two peak levels of apoptotic cells occurred in UA-induced ARF. The first peak might play a role in UA-induced tubular damage, while the second one might represent the removal of excess regenerating cells during the recovery phase. Modulation of apoptotic cell death might be involved in the acquired resistance to rechallenge injury by UA.
BACKGROUND: In living related liver transplantation (LRLT), reconstruction of the hepatic vein (HV) by end-to-end anastomosis has been reported to be associated with acute or late outflow block. METHODS: We reviewed 42 patients who underwent LRLT from January 1996 to September 1998. RESULTS: In 7 (27%) of the 26 donor grafts obtained from left lateral segmentectomy or extended lateral segmentectomy and in 9 (56%) of the 16 grafts obtained from left lobectomy, venoplasty was required. In the remaining 26 grafts, 1-orifice left HV was obtained. In addition to the division of the duct of Arantius, the left inferior phrenic vein was divided routinely in 16 patients, which contributed to reducing the venoplasty rate from 46% to 25% (P =.1704). In all 42 patients, HV was reconstructed successfully by end-to-end anastomosis. The median ratio of the diameter of the recipient's HV to that of the graft's HV was 1.2 (range, 0.8-2.1). The grafts were fixed to the abdominal wall by using the falciform and round ligaments at a site where Doppler ultrasound showed sufficient flow in the respective vessels. Three patients developed late-onset HV obstruction and required balloon dilatation either by means of a venous route or a transhepatic route: 1 patient received a new liver on the 232nd postoperative day, 1 patient died of sepsis without outflow block, and the last patient is doing well. CONCLUSIONS: In LRLT, the division of the duct of Arantius and the left inferior phrenic vein followed by extensive clamping of the common trunk contributed to obtaining a 1-orifice HV. This facilitates anastomosis of the HVs of the grafts to the recipients' HVs, and fixation of the grafts by using the falciform and round ligaments prevents rotation of the grafts and subsequent acute outflow block.
To determine the optimal conditions for the immobilization of cells in a cell capture enzyme immunoassay (CC-EIA), the most suitable diluent, and the optimal pH, temperature and period of incubation were examined using WI-38, a human embryonic lung fibroblast cell line. For the evaluation, we devised a simple Giemsa assay method, in which immobilized cells on a microplate were stained with Giemsa solution, the stained dye was eluted with ethanol after washing the plate, and the optimal density (O.D.) was measured at wavelength 620 nm. The optimal conditions for the immobilization were determined to be treatment with 5% formalin in phosphate-buffered saline (PBS) (pH 7.2) for 15 minutes at room temperature, which were confirmed to be suitable for the measurement of cell associated collagen by CC-EIA. Additionally, we found that the simple Giemsa staining method was also useful for evaluating the number of immobilized cells on the microplate after CC-EIA.
We encountered a 53-year-old man associated with acute renal failure caused by Waldenström's macroglobulinemia and type I cryoglobulinemia. Treatment with prednisolone and cyclophosphamide induced a rapid recovery from acute renal failure. Renal histology revealed endocapillary proliferation and lobular formation with scattered subendothelial, amorphous and periodic acid-Schiff (PAS)-positive materials in the glomerular capillaries which were positive for IgM on immunofluorescence study. Although the exact mechanism for pathophysiology of acute renal failure remains unknown, treatment with prednisolone and cyclophosphamide could induce a rapid recovery from acute renal failure accompanied by Waldenström's macroglobulinemia and type I cryoglobulinemia.
Vertebrate skeletal muscle alpha-tropomyosin polymerizes in a head-to-tail manner and binds cooperatively to actin. It has been postulated that the cooperative actin binding is governed by the strength of the head-to-tail interaction. In order to know the relationship between the head-to-tail affinity and actin binding, we studied the properties of tropomyosin variants with single residue substitutions at serine-283, the penultimate residue at the carboxyl terminus that is involved in the head-to-tail interaction. It has been shown that the phosphorylation of serine-283 strengthens the head-to-tail interaction. Viscometry was employed to compare the head-to-tail affinity of tropomyosin variants. Variant S283E showed higher viscosity whereas variant S283K showed lower viscosity compared with the wild type non-phosphorylated alpha-tropomyosin. The results confirm the idea that the interaction is sensitive to the ionic properties of residue 283. The strength of the head-to-tail interaction was assessed directly by sedimentation equilibrium using two pairs of tropomyosin variants designed so that only dimeric interactions were allowed within each pair. From one pair of variants with serine-283, the association constant was determined to be 2.6 x 10(4) M(-1) (SD =1.0 x 10(4)), whereas for the second pair with glutamate-283, the affinity was 3.9 x 10(4) M(-1) (SD =1.6 x 10(4)), slightly stronger than the former, consistent with the results of viscometry. The results indicate that the head-to-tail association is weak as previously implicated from light scattering measurements. Cosedimentation was employed to measure the cooperative actin binding of tropomyosin variants. Although previous results indicated the phosphorylation has no significant influence on the actin affinity, variant S283E shows a lower affinity compared with the control. Variants S283K and S283A show even lower affinities to actin, although these species bind to actin more cooperatively than does variant S283E. The results indicate that the affinity of the head-to-tail interaction between adjacent tropomyosin molecules is weak, and is substantially influenced by an extra charge at residue 283. On the other hand, the interaction with actin, the affinity and the cooperativity in actin binding, is dependent on amino acid residues at 283 and is not simply correlated with the strength of the head-to-tail interaction between Tm molecules in solution.
OBJECTIVE: The surgical outcome of idiopathic tarsal tunnel syndrome (TTS) is reported to be worse than that attributable to ganglion, tarsal coalition, or tumour, and therefore further development in the surgical treatment for idiopathic TTS is considered to be necessary. Here the efficacy of neurovascular decompression for patients with idiopathic TTS is evaluated. METHODS: Twelve feet from nine patients with idiopathic TTS were treated. The patients were aged 52-78 years (mean 64.6 years), and all of them complained of pain or dysaesthesia of the sole of the foot. The posterior tibial nerve was freed from the attached arteriovenous complex (posterior tibial artery and veins). The dissected nerve had a flattened appearance in all of the patients, suggesting nerve compression by the adjacent arteriovenous complex and superficially by the flexor retinaculum. A graft of fat was inserted as both a cushion and an antiadhesive between the vessels and the nerve to achieve neurovascular decompression. RESULTS: Patients on whom neurovascular decompression was performed had resolution or lessening of symptoms in their feet. Neither wound infection nor recurrence of symptoms was found during the follow up period (mean 26.8 months). CONCLUSION: Neurovascular compression syndrome plays a part in idiopathic TTS, and adding neurovascular decompression to resection of the flexor retinaculum is effective.
Tissue-nonspecific alkaline phosphatase (TNAP) is essential for bone matrix mineralization, but the central mechanism for TNAP action remains undefined. We observed that ATP-dependent (45)Ca precipitation was decreased in calvarial osteoblast matrix vesicle (MV) fractions from TNAP-/- mice, a model of infantile hypophosphatasia. Because TNAP hydrolyzes the mineralization inhibitor inorganic pyrophosphate (PP(i)), we assessed phosphodiesterase nucleotide pyrophosphatase (PDNP/NTPPPH) activity, which hydrolyzes ATP to generate PP(i). Plasma cell membrane glycoprotein-1 (PC-1), but not the isozyme B10 (also called PDNP3) colocalized with TNAP in osteoblast MV fractions and pericellular matrix. PC-1 but not B10 increased MV fraction PP(i) and inhibited (45)Ca precipitation by MVs. TNAP directly antagonized inhibition by PC-1 of MV-mediated (45)Ca precipitation. Furthermore, the PP(i) content of MV fractions was greater in cultured TNAP-/- than TNAP+/+ calvarial osteoblasts. Paradoxically, transfection with wild-type TNAP significantly increased osteoblast MV fraction NTPPPH. Specific activity of NTPPPH also was twofold greater in MV fractions of osteoblasts from TNAP+/+ mice relative to TNAP-/- mice. Thus TNAP attenuates PC-1/NTPPPH-induced PP(i) generation that would otherwise inhibit MV-mediated mineralization. TNAP also paradoxically regulates PC-1 expression and NTPPPH activity in osteoblasts.
The characteristic features of bronchial asthma, including airway eosinophilia and elevated immunoglobulin (Ig)E levels, are known to be orchestrated by T-helper (Th) 2 cells. Oligodeoxynucleotides containing CpG motifs (CpG) have recently been highlighted as an immunomodulator that biases toward a Th1-dominant phenotype. However, CpG may incur nonspecific Th1 activation and toxic effects. In this study we report a novel inhibition of Th2 cells by transmucosal inoculation of antigen and CpG. Intratracheal instillation of CpG inhibited airway eosinophilia and Th2 cytokine production in antigen-sensitized mice. The inhibition was observed when CpG was given at the same time or in advance of antigen challenge. Notably, concomitant administration of CpG and antigen (as opposed to either one alone) was essential for the inhibitory effects. The antigen dose could be minimized to avoid a harmful boost of eosinophilia. CpG had few effects on systemic anti-ovalbumin IgE responses. These results demonstrate that a synergism between transmucosally administered allergen and CpG inhibits Th2 cells in parallel with an improvement in airway eosinophilia and hyperresponsiveness without impeding systemic immune responses. Our data imply that inhalation of a minimal amount of allergen plus CpG could be a novel desensitization therapy for patients with bronchial asthma.
The 2-thio- or 2-selenoglycosides of N-acetylneuraminic acid methyl ester were transformed by successive treatment with dimethyl(methylthio)sulfonium triflate (DMTST) and 1,8-diazabicyclo[5.4.0]-7-undecene (DBU) to give the corresponding methyl 2-deoxy-2,3-didehydroneuraminates in excellent yields. Their acids and their analogues are sialidase inhibitors of pharmaceutical interest.
The enzyme phytase dephosphorylates phytin (inositol hexaphosphate), a major phosphate reserve in plants. We found that a large number of yeast species secreted a phytase. Several species were identified as high phytase producers. The yeast enzymes had an optimal activity at pH 4-5 and generally a very high optimal temperature, ranging from 60 degrees C to 80 degrees C.
We performed positron emission tomography (PET) with 18 fluorine-fluoro-2-deoxy-D-glucose (FDG) on 55 patients with tumours involving the musculoskeletal system in order to evaluate its role in operative planning. The standardised uptake value (SUV) of FDG was calculated and, to distinguish malignancies from benign lesions, the cases were divided into high (> or =1.9) and low (< 1.9) SUV groups. The sensitivity of PET for correctly diagnosing malignancy was 100% with a specificity of 76.9% and an overall accuracy of 83.0%. The mean SUV for metastatic lesions was twice that for primary sarcomas (p < 0.0015). Our results suggest that the SUV may be useful in differentiating malignant tumours from benign lesions. However, some of the latter, such as schwannomas, had high SUVs so that biopsy or wide resection was selected as the first operation. Thus, some other quantitative analysis may be required for preoperative planning in cases of high-SUV neurogenic benign tumours. The reverse transcription-polymerase chain reaction revealed that the RNA message of a key enzyme in glucose metabolism, phosphohexose isomerase (PHI)/autocrine motility factor, was augmented in only high FDG-uptake lesions, suggesting that a high expression of the PHI message may be associated with accumulation of FDG in musculoskeletal tumours.
The mechanism of radiation-induced diffuse brain injury was investigated using a model of delayed myelination in the irradiated neonatal rat brain in which the number of oligodendrocytes decreases without associated necrosis of the cerebral white matter. Immunohistochemical analysis using antibody against the large myelin-associated glycoprotein, a specific marker of oligodendrocytes at an early stage of development, showed that the number of the oligodendrocytes associated with myelination decreased in the irradiated hemisphere 1 day after irradiation and remained low until 5 days after irradiation. In situ terminal deoxynucleotidyl transferase-mediated nick end-labeling assay revealed that apoptosis mainly occurred in the cerebral white matter of the irradiated hemisphere. Three hours after irradiation, apoptotic cells were found in the subcortical white matter and the periventricular white matter. Six hours after irradiation, apoptotic cells were found in the internal capsule, and the numbers of apoptotic cells in the periventricular white matter and subcortical white matter increased. One day after irradiation, the number of apoptotic cells in the periventricular white matter decreased. Three days after irradiation, apoptotic cells were not observed in the cerebral white matter. These results suggest that the oligodendrocytes associated with myelination may be damaged via radiation-induced apoptosis, and depletion of the oligodendrocytes may cause delay of myelination.
We present a case of benign angiomyxoid tumor arising in the inguinal region of a 27-year-old man. The tumor was a gelatinous mass completely encapsulated by a thin fibrous capsule with no hemorrhage or necrosis. Histologically, a proliferation of spindle cells as well as occasional pleomorphic cells was observed within the myxofibrous stroma, intermingled with abundant capillary-sized blood vessels. Immunohistochemical staining of the tumor demonstrated spindle, oval, and pleomorphic cells equally positive for vimentin, desmin, and CD34, but not for alpha-smooth muscle actin. Based on these histologic and immunophenotypic features, we conclude that this angiomyxoid tumor of the male inguinal region is indistinguishable from the female angiomyofibroblastoma of the pelvic and perineal regions.
Recently, the mechanism of longevity in females was proposed to be associated with female hormones. This study examined the effect of aging and sex on vascular endothelial function, and the relationship between female hormone level and endothelial function by ischemic reactive hyperemic response in the forearm using plethysmography. The study population consisted of 246 healthy subjects aged from 20 to 76 years (119 males, 127 females) and 20 healthy females aged 85 years and older (85 to 103 years; mean age 94 years) without distinct cardiovascular disease, hypertension, diabetes mellitus, renal disease, liver dysfunction or anemia. Levels of the female hormones, estradiol and estriol, were measured in females aged more than 85 years. The duration of reactive hyperemia decreased with aging, but the difference between males and females was not significant at any age. In females, the duration was markedly decreased from 110 +/- 36 sec in the fifties to 81 +/- 29 sec in the sixties or older (p < 0.05). Excess flow also showed similar changes to the duration of reactive hyperemia. The duration of reactive hyperemia and excess flow in females aged 85 years and older were similar to those in the fifties, but was significantly longer than those in females 60 years or older. The concentrations of estradiol (44.9 +/- 27.1 pg/ml) and estriol (22.1 +/- 13.4 pg/ml) in females aged 85 years were higher than in the sixties. There was a positive correlation between the duration of reactive hyperemia and the concentration of estradiol (r = 0.56, p < 0.01) or estriol (r = 0.57, p < 0.01). In summary, vascular endothelial function was impaired gradually with aging, but preservation of the function in healthy, very old females was closely associated with levels of female hormone.
A 45-year-old woman was referred to our hospital because of hyperthyroidism complicated by atrial fibrillation and heart failure. Laboratory data revealed pancytopenia, with a white blood cell count of 2,600/microliter, red blood cell count of 330 x 10(4)/microliter, and platelet count of 6.2 x 10(4)/microliter. The patient had normal transaminase levels, but tests for hepaplastin and cholinesterase showed values of 34% and 1.4 U/ml, respectively, indicating liver dysfunction. There was also decreased excretion of indocyanine green. After initiation of treatment with 30 mg thiamazole and 20 mg propranolol daily, the patient's thyroid function normalized and the other abnormal laboratory findings such as pancytopenia and liver dysfunction also disappeared. Pancytopenia is a rare complication of hyperthyroidism. In this case, various laboratory abnormalities were normalized by antithyroid therapy alone, indicating that the hyperthyroidism itself was closely related to the pathogenesis of pancytopenia and liver dysfunction.
Anti-mitochondrial antibody(AMA) has been reported to be detectable in approximately 85% of patients with primary biliary cirrhosis(PBC). Therefore, a test for AMA is acceptable to be essential for diagnosing PBC. However, the positive rate in Japanese general population has not yet been determined. We tested sera from 1,145 corporate workers who took an annual health check and evaluated the liver of AMA-positive subjects. An indirect immunofluorescence method was used for screening AMA. ELISA and immunoblotting method were used for detecting anti-M2 in AMA-positive cases. AMA was detected in 5 of 1,145(0.44%) corporate workers. AMA positive rate was higher in females than in males(0.91% and 0%, respectively) and the AMA-positive people are all females over age 40. All of the AMA-positive sera are also positive for Anti-M2. Liver biopsy was performed in two AMA-positive cases and the histology was compatible with PBC in both cases.
INTRODUCTION: We evaluated the effect of combination therapy with thromboxane A2 synthesis inhibitor and leukotriene receptor antagonist in a patient with exercise-induced asthma using krypton-81 m ventilation scintigraphy. CLINICAL PICTURE: In a patient with exercise-induced asthma, we found exercise-induced abnormalities of respiratory function test and ventilation scintigraphy, and increases in plasma concentrations of thromboxane B2 and leukotriene C4 with exercise. TREATMENT: A thromboxane A2 synthesis inhibitor (ozagrel) and a leukotriene receptor antagonist (pranlukast) were prescribed. OUTCOME: After treatment for 2 weeks, abnormalities of respiratory function test and ventilation scintigraphy improved. CONCLUSIONS: The combination therapy with ozagrel and pranlukast might be useful for the relief of symptoms in patients with exercise-induced asthma, and krypton-81 m ventilation scintigraphy could be a useful tool for visible evaluation of treatment.