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Biomedical subjects

H Maeda

Publications and source records attributed to H Maeda.

At least 235 records · Page 13Linked to original sources

[A case of bladder hemangioma showing bladder tamponade during late pregnancy].

We report a case of bladder hemangioma manifesting bladder tamponade during pregnancy. A 25-year-old woman at 36 weeks of gestation was admitted with a two-week history of gross hematuria and clot retention. Blood hemoglobin concentration was 6.3 g/dl. After blood transfusion and Caesarian section, cystoscopy was performed. Bleeding was noticed from a strawberry-like tumor 5 mm in diameter near the right ureteral orifice, which was easily resected endoscopically. Histopathological diagnosis was cavernous hemangioma of the urinary bladder. This is the first report of a case of bladder hemangioma during pregnancy.

Adult↗

Impact of interventional therapy for benign prostatic hyperplasia on quality of life and sexual function: a prospective study.

PURPOSE: Treatment for benign prostatic hyperplasia (BPH), including minimally invasive therapy, can impair the quality of life. We prospectively determined the impact of 4 different interventional therapies on quality of life and sexual function. MATERIALS AND METHODS: A total of 173 patients were prospectively evaluated between February 1995 and August 1997. Treatment modalities consisted of standard transurethral resection of the prostate in 55 cases, transurethral microwave thermotherapy in 34, interstitial laser coagulation of the prostate in 42 and transurethral needle ablation in 42. Disease specific quality of life was assessed using the International Prostate Symptom Score quality of life assessment index and BPH impact index. In addition, a self-reporting questionnaire was completed before and 3 months after treatment to determine the impact on sexual function. RESULTS: All 4 treatment groups showed significant improvement in the symptom score, International Prostate Symptom Score quality of life assessment score and BPH impact index score. Satisfaction with treatment was highest in patients treated with transurethral resection or laser coagulation. A mild to moderate decrease in erectile function was noted in 26.5%, 18.2%, 18.4% and 20.0% of the transurethral resection, microwave thermotherapy, laser coagulation and needle ablation groups, respectively, but there was no significant difference of mean pretreatment and posttreatment erectile function or libido scores in any group. Ejaculation loss or severe decrease in ejaculate volume was reported by 48.6%, 28.1%, 21.6% and 24.3% of the patients, respectively. Interestingly, 20 of the 44 patients (45. 5%) with loss of ejaculation or severe decrease in ejaculate reported deterioration of the sex life, while only 2 (3.6%) of the 56 without any change in ejaculate volume reported such deterioration. The association of ejaculatory dysfunction with an adverse impact on sexual activity was highly significant (p <0.0001). CONCLUSIONS: Significant improvement in quality of life could be achieved with the present assessed interventional therapies. There was no significant change in sexual desire or erectile function with these therapies. Posttreatment sexual dysfunction appears to be mainly related to impaired ejaculatory function. Urologists should provide proper counseling regarding the possibility of this complication even in patients receiving minimally invasive treatment.

Aged↗

[A case of Wegener's granulomatosis with pachymeningitis].

A 62-year-old woman who had been receiving corticosteroid therapy for pachymeningitis since 1997 was admitted to our hospital when an abnormal shadow was noticed in her chest radiograph. In bronchial and nasal mucosal biopsies, the findings of a necrotic granulomatous lesion and vasculitis were compatible with Wegener's granulomatosis, although this is rarely seen with pachymeningitis. After further corticosteroid therapy together with cyclophosphamide treatment, the size of the thoracic X-ray shadow decreased. Methicillin-resistant Staphylococcus aureus (MRSA) was cultured from the sputum and the nasal fluid, and may have contributed to the advance of the disease in the airway. This case will require continuing careful observation.

Female↗

Vitamin D receptor gene polymorphism and calcium metabolism in sarcoidosis patients.

BACKGROUND: Hypercalcemia has been recognized as an important complication of sarcoidosis, caused by overproduction of the active form of vitamin D, 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) at sites of granulomatous reactions. Polymorphism of the vitamin D receptor (VDR) gene has recently been shown to be related to bone mineral density, and also associated with hyperparathyroidism and risk of granulomatous disease. In light of the possible impact on hypercalcemia of sarcoidosis, an investigation of calcium metabolism and polymorphism of the VDR gene in sarcoidosis patients was carried out. METHODS: Genotypes were determined using the polymerase chain reaction and restriction fragment length polymorphism. Maximum calcium, 1,25(OH)2D3, and intact PTH levels were also determined. RESULTS: Depressed PTH levels were found in sarcoidosis patients, especially in those with the bb genotype, but there was no difference in 1,25(OH)2D3 levels among the VDR genotypes, and this polymorphism also had no association with onset of hypercalcemia. CONCLUSION: From these results, we speculate that although the VDR gene polymorphism may affect the serum PTH level, it is not a risk factor for hypercalcemia in sarcoidosis.

Adult↗

[A proposal of essentials for forensic pathological diagnosis of sudden infant death syndrome (SIDS)].

There are many sudden unexpected infant death cases which are easily diagnosed as sudden infant death syndrome (SIDS) both with or without autopsy in Japan. A SIDS diagnosis may provide a cover for accidental or criminal death. SIDS should not be a convenient diagnostic box that shelters the cases of unexpected infant death which lack the necessary antemortem information to make the correct diagnosis. The authors consider that SIDS should be diagnosed according to the direction of the international definition of SIDS, and propose the following essentials for a forensic pathological diagnosis. 1) A thorough autopsy should be performed based on precise autopsy protocol, including not only histological observation, but also, if necessary, toxicological, bacteriological, viral and/or biochemical examinations. 2) The forensic pathologist should be provided with pertinent information regarding antemortem health status, past clinical history, social circumstances, death scene investigation, etc. In order to collect more precise information, the authors recommend using a questionnaire such as the example in this report to record information from the deceased's guardians. 3) Suspicion of accidental death or infanticide should be completely ruled out. SIDS should be diagnosed only after these three essentials have been satisfied. When there is even a slight suspicion of accidental death or infanticide, or when the forensic pathologist can not obtain pertinent information about the deceased, the causes and classification of the death should be diagnosed as unspecified or undetermined. That is, the causes and classification of the death are undetermined as to whether it is a natural or unnatural death. Furthermore, several warning flags indicating a possible SIDS diagnosis were proposed: a case found dead in a supine position, the existence of a foreign body in the respiratory tract or mild infectious findings. The authors also emphasize the physician's responsibility to report a case found dead or dying of unnatural or clinically unexplained causes to the police. This is the crucial first step in getting an accurate diagnosis of SIDS.

Autopsy↗

Protective effect of S-nitrosylated alpha(1)-protease inhibitor on hepatic ischemia-reperfusion injury.

S-Nitrosylated compounds (nitrosothiols; RS-NOs) function as nitric oxide (NO) reservoirs and preserve the antioxidant activities of NO. We found remarkable cytoprotection by an S-nitrosylated protease inhibitor from human plasma, S-nitroso-alpha(1)-protease inhibitor (S-NO-alpha(1)-PI) that possesses a completely nitrosylated SH group, in hepatic ischemia-reperfusion injuries in rats. Liver ischemia was induced in rats by occluding both the portal vein and hepatic artery for 30 min and was followed by reperfusion. S-NO-alpha(1)-PI and control compounds such as native alpha(1)-PI, an NO synthase (NOS) inhibitor, and standard RS-NOs were given via the portal vein just after reperfusion was initiated. Liver injury was evaluated by measuring the extracellular release of liver enzymes (aspartate aminotransferase, alanine aminotransferase, and lactate dehydrogenase). Infiltration of neutrophils and induction of apoptosis and heme oxygenase-1 (HO-1) in the liver were also examined. Maximal liver injury occurred at 3 h after reperfusion and then decreased gradually. Not only did S-NO-alpha(1)-PI treatment (0.1 micromol; 5.3 mg/rat) greatly reduce elevation of liver enzymes in plasma, as well as neutrophil accumulation and apoptotic change in liver, it also improved the impaired hepatic blood flow as assessed by laser Doppler flowmetry and potentiated the induction of HO-1 in the liver. Although native alpha(1)-PI moderately reduced liver injury, low molecular weight RS-NOs such as S-nitrosoglutathione and S-nitroso-N-acetyl penicillamine produced no obvious protective effect. An NOS inhibitor exacerbated the hepatic ischemia-reperfusion injuries. These results suggest that S-NO-alpha(1)-PI exerts a potent cytoprotective effect on ischemia-reperfusion liver injury by maintaining tissue blood flow, inducing HO-1, and suppressing neutrophil-induced liver damage and apoptosis.

Animals↗

Wounding dynamics in distorted bitemarks: two case reports.

An essential factor involved in distortion of bitemarks on the skin is the dynamics of biting related to the location on the body. This study describes the comparison between the identification of bitemarks left on different regions of the victims' bodies in two homicide cases. The findings indicated that a stepwise dynamic comparison of serial adjacent marks with a part of the dentition in consideration of movement of the jaws and distortion of the skin was useful in identifying matching points. The identification process indicated possible wounding dynamics of biting.

Adult↗

[The Endotoxin 10,000 Reference Standard of the National Institute of Health Sciences (the Japanese Pharmacopoeia Endotoxin 10,000 Reference Standard) (Control 0001)].

To establish the fourth lot (Control 0001) of the Endotoxin 10,000 Reference Standard of the National Institute of Health Sciences (the Japanese Pharmacopoeia Endotoxin 10,000 Reference Standard), a candidate standard (CS) was prepared and then evaluated. The potency of the CS was assayed against USP Endotoxin Reference Standard (Lot G-1) and defined as containing approximately 20,000 endotoxin units (EU) per vial by a collaborative study in which 5 laboratories participated. Based on the results, the CS was authorized to be the fourth lot of the Endotoxin 10,000 Reference Standard containing 20,000 EU per vial.

Endotoxins↗

Nitrosothiol formation catalyzed by ceruloplasmin. Implication for cytoprotective mechanism in vivo.

Ceruloplasmin (CP) is a major multicopper-containing plasma protein that is not only involved in iron metabolism through its ferroxidase activity but also functions as an antioxidant. However, physiological substrates for CP have not been fully identified nor has the role of CP been fully understood. The reaction of nitric oxide (NO) with CP was investigated in view of nitrosothiol (RS-NO) formation. First, formation of heavy metal- or CP-catalyzed RS-NO was examined with physiologically relevant concentrations of NO and various thiol compounds (RSH) such as glutathione (GSH). Among the various heavy metal ions and copper-containing enzymes and proteins examined, only copper ion (Cu(2+)) and CP showed potent RS-NO (S-nitrosoglutathione)-producing activity. Also, RS-NO-forming catalytic activity was evident for CP added exogenously to RAW264 cells expressing inducible NO synthase in culture, but this was not the case for copper ion. Similarly, CP produced endogenously by HepG2 cells showed potent RS-NO-forming activity in the cell culture. One-electron oxidation of NO appears to be operative for RS-NO production via electron transfer from type 1 copper to a cluster of types 2 and 3 copper in CP. Neurological disorders are associated with aceruloplasminemia; besides RS-NO, S-nitrosoglutathione particularly has been shown to have neuroprotective effect against oxidative stress induced by iron overload. Thus, we suggest that CP plays an important catalytic role in RS-NO formation, which may contribute to its potent antioxidant and cytoprotective activities in vivo in mammalian biological systems.

Animals↗

Osteoclast-derived zinc finger (OCZF) protein with POZ domain, a possible transcriptional repressor, is involved in osteoclastogenesis.

The differentiation of osteoclasts is regulated by transcription factors expressed in cells of osteoclast lineage. We isolated here a potential transcription factor from a cDNA library of an enriched population of preosteoclasts and osteoclasts. The cDNA encodes a protein with N-terminal POZ domain and C-terminal Krüppel-like zinc fingers. We designate this protein as osteoclast-derived zinc finger (OCZF). OCZF was found to be rat homologue of mouse leukemia/lymphoma-related factor (LRF). Northern blot and in situ hybridization analysis showed OCZF mRNA at a high level in osteoclasts and kidney cells. OCZF had a nuclear targeting sequence and was localized in the nucleus of transfected cells. In addition, OCZF specifically bound to the guanine-rich consensus sequences of Egr-1 and c-Krox. Transient transfection assays indicate that OCZF can repress transcription activity like other POZ domain proteins. Furthermore, antisense but not sense phosphorothioate oligodeoxynucleotides (ODNs) for OCZF cDNA suppressed the formation of osteoclast-like multinucleated cells (MNCs) in bone marrow culture, whereas the same ODNs did not significantly affect the formation of macrophage polykaryons and mononuclear preosteoclast-like cells (POCs). These results suggest that OCZF is a unique transcription factor that plays an important role in the late stage of osteoclastogenesis.

Amino Acid Sequence↗

Free radical generation from heterocyclic amines by cytochrome b5 reductase in the presence of NADH.

We previously reported findings that NADPH/cytochrome P450 reductase can generate superoxide anion radical (O2*-) from heterocyclic amines (HCA) and from many anticancer agents in vitro. Here we present more evidence in which O2*- is generated when recombinant human cytochrome b5 reductase (rh-Cytb5Rd) was incubated with HCAs such as IQ and MeIQ in the presence of NADH in vitro. This indicates that free radical generation by rh-Cytb5Rd in the presence of HCA may add new insight into the damage of DNA in addition to the previously known mechanism: interaction of activated HCA-intermediates to form DNA adduct.

Cytochrome Reductases↗

Simultaneous assay of prostaglandins and thromboxane in the cerebrospinal fluid by gas chromatography-mass spectrometry-selected ion monitoring.

A method of simultaneous analysis of prostaglandins (PGs) and thromboxane (TX) B2 in cerebrospinal fluid (CSF) with GC-MS-SIM was established. Deuterated PGs and TXB2 were used as internal standards: tetra-deuterated PGE2 (d4-PGE2) for PGE2, PGE1 and PGD2; d5-PGF2alpha for PGF2alpha and 9alpha,11beta-PGF2 and 8-epi PGF2alpha; d4-TXB2 for TXB2; and d4-6-keto PGF1alpha for 6-keto PGF1alpha. The PGs and TXB2 were derivatized to the methyl ester of the methoxim dimethyisopropylsilyl (DMiPSi) ether form or the methyl ester of the DMiPSi ether form with simultaneous preparation. Samples were extracted with octadecyl silica gel and purified in two steps with silisic acid gel chromatography between derivatization steps. The calibration curve of each PG and TXB2 was linear from 10 pg to 10 ng with the isotope dilution method. The levels of the seven types of PG and of TXB2 were assayed simultaneously in the cerebrospinal fluid (CSF) from patients with aseptic meningitis. The CSF pattern of the PG and TXB2 concentrations in mumps meningitis differed from those in other types of aseptic meningitis and in disease controls.

Calibration↗

Combined effects of both bacteria and gastric juice on pneumonia in mice.

The effects of a combined inoculation of gastric juice and Streptococcus pneumoniae on the lungs of mice was investigated. Survival rates of mice inoculated with bacteria alone, gastric juice alone, and both bacteria and gastric juice were compared over 18 days. Xanthine oxidase (XO) activities in the lung tissues of mice inoculated with bacteria and gastric juice were measured and injected with a free radical scavenger, pyran-superoxide dismutase (pyran-SOD). A high mortality rate was observed in mice inoculated with both gastric juice and Streptococcus pneumoniae (81%). Mice inoculated with either Streptococcus pneumoniae or gastric juice showed a separate mortality rate of up to 10% during 18 days after inoculation. XO activity in the lung tissue of the mice inoculated with both gastric juice and bacteria was higher than in mice inoculated with either of them separately. The high mortality rate in the group inoculated with both two agents was reduced to 25% by the administration of pyran-SOD. XO activity raised by Streptococcus pneumoniae and gastric juice was significantly reduced by pyran-SOD. Thus, we suggest an important role in the combined effects of gastric juice and bacteria on pneumonia.

Animals↗

Activation of telomerase is induced by a natural antigen in allergen-specific memory T lymphocytes in bronchial asthma.

The function of the immune system is known to be dependent on the cellular differentiation and clonal expansion of allergen-specific lymphocytes. Telomerase, a ribonucleoprotein enzyme, is believed to be essential for the indefinite proliferation of human cells. To clarify whether telomerase is involved in the pathogenesis of immune diseases as well as of malignancies, we investigated the upregulation of telomerase activity in allergen-specific T lymphocytes. Upregulation of telomerase in allergen-sensitized lymphocytes was induced not only by artificial mitogenic stimulations but also by the natural antigen, house dust mite, which causes allergic diseases. Moreover, the upregulation of telomerase activity in memory T cells activated during allergen-specific immune responses might be associated with the enduring allergen-specific atopic propensity in asthmatics.

Adolescent↗

A predominant apoptotic death pathway of neuronal PC12 cells induced by activated microglia is displaced by a non-apoptotic death pathway following blockage of caspase-3-dependent cascade.

Activated microglia have been implicated in the regulation of neuronal cell death. However, the biochemical mechanism for neuronal death triggered by activated microglia is still unclear. When treated with activated microglia, neuronal PC12 cells undergo apoptosis accompanied by caspase-3-like protease activation and DNA fragmentation. Apoptotic bodies formed were subsequently phagocytosed by neighboring activated microglia. Pretreatment of the cells with the caspase-3-like protease inhibitor N-acetyl-Asp-Glu-Val-Asp-aldehyde did not reverse this cell death. Although Bcl-2 overexpression in the cells caused the inhibition of caspase-3-like protease activity and DNA fragmentation and the effective interference of apoptosis induced by deprivation of trophic factors, it could not suppress the activated microglia-induced neuronal death. At the electron microscopic level, degenerating cells with high levels of Bcl-2 were characterized by slightly condensed chromatins forming irregular-shaped masses, severely disintegrated perikarya, and marked vacuolation. Various protease inhibitors tested did not inhibit this cell death, whereas the radical oxygen species scavenger N-acetyl-L-cysteine significantly suppressed this death. Altogether, our study provides an alternative death pathway for the activated microglia-induced neuronal death by blockage of the caspase-3 protease cascade.

Acetylcysteine↗