Treatment of warfarin-induced hair loss with ubidecarenone.
Explore the source record for details and available documents.
Alopecia↗
Biomedical subjects
K Fujii
Publications and source records attributed to K Fujii.
Orally active and long-term acting insulin-mimetic vanadyl complex:bis(picolinato)oxovanadium (IV).
The blood glucose level of rats with streptozotocin (STZ)-induced diabetes has been found to be normalized by administration of vanadyl or vanadate complexes. During our investigations on the development of anti-diabetic vanadyl complexes with various types of coordination mode such as V-O, V-N and V-S, we found that a new bis(picolinato)oxovanadium (IV) complex (VPA) has a strong insulin-mimetic effects as evaluated by an in vitro experiments, in which the inhibition of free fatty acid release in isolated rat adipocytes treated with epinephrine was observed to be similar to that of insulin. VPA was also effective for normalizing the blood glucose level of STZ-induced diabetic rats when given intraperitoneally or orally. The serum glucose level was maintained in the normal range for about 30 days with body weight gain after the end of oral administration of VPA for 14 days. VPA was confirmed to be an orally active and long-term acting insulin-mimetic vanadyl complex to treat insulin-dependent diabetes mellitus (IDDM) in rats.
Adipocytes↗
Use of a guanidine extract of demineralized bone in the treatment of osteochondral defects of articular cartilage.
In order to evaluate the ability of a guanidine extract of demineralized bone to repair osteochondral defects in articular cartilage, plugs made of this extract were implanted into defects in rabbit knees. The repair tissue was examined macroscopically, histologically, and immunohistochemically at 4, 8, 12, and 30 weeks. Controls (defects that were left empty) showed no cartilage formation. Four weeks after implantation of a guanidine extract plug, histological examination showed a nonhomogeneous metachromatically stained region extending from the surface of the repair tissue down to cancellous bone. This region also was labeled by an anti-type-II collagen antibody, indicating that cartilage-like tissue had been induced. At 8 weeks, the newly formed cartilage in the subchondral and cancellous bone had been partially replaced by bone. At 12 weeks, the thickness of the newly formed cartilage layer had decreased, and most of the newly formed cartilage in the subchondral and cancellous bone had been replaced by bone. In addition, a tidemark was observed. At 30 weeks, the repair tissue was a mixture of cartilage and fibrocartilage, and there was severe degeneration of the cartilage surrounding the repaired defects. These findings indicate that osteochondral defects of articular cartilage can be partially repaired by the implantation of a guanidine extract and that the newly formed cartilage-like tissue is not permanent.
Animals↗
Epidermal growth factor enhancement of HSC-1 human cutaneous squamous carcinoma cell adhesion and migration on type I collagen involves selective up-regulation of alpha 2 beta 1 integrin expression.
Some human neoplasms show aberrant expression or overexpression of epidermal growth factor (EGF) receptor, and the degree of the receptor expression is correlated with the malignant phenotype in certain epithelial tumors including squamous carcinoma cells. Since phenotypic transformation of cells could involve quantitative and qualitative alteration of integrin function, the effects of EGF on cell-matrix interactions were studied using HSC-1 cells, a human squamous carcinoma cell line showing EGF receptor overexpression. The EGF-treated HSC-1 cells interacted with matrix proteins differently from the untreated cells, as shown by cell adhesion and phagokinetic track assays. Among fibronectin, laminin, fibrinogen, and type I collagen, fibronectin was the most efficient substratum to promote untreated HSC-1 cell adhesion and migration. Pretreatment of the cells with 50 ng/ml EGF for 18 h selectively increased the number of spread cells and the size of the individual cell migration area on type I collagen by 250 and 400%, respectively. The same pretreatment diminished cell adhesion and migration on other substrata so that the EGF treatment converted type I collagen as the most efficient substratum for cell adhesion and migration of the HSC-1 cells. ELISA and immunoprecipitation studies showed that EGF up-regulated the expression of alpha 2 beta 1 integrin collagen receptor in a time- and dose-dependent manner by stimulating biosynthesis of alpha 2 subunit, but did not up-regulate those of the alpha 3 beta 1, alpha 5 beta 1, or alpha v beta 3 integrins. These results suggest that EGF preferentially enhances HSC-1 cell interaction with type I collagen, leading to the enhanced cellular migratory activity on the substratum, as a result of selective up-regulation of alpha 2 beta 1 integrin expression.
Antigens, CD↗
Cell surface proteolysis by serine proteinases enhances RGD-sensitive melanoma cell adhesion on fibrinogen and vitronectin.
Tumor cells avidly secrete various proteinases, and cascades of proteolytic activation occur around the cells. Therefore, cell surface receptors of tumor cells are under the constant influence of proteinases. In this study, the effects of serine proteinases on integrin-medicated cell-matrix interactions were studied in C32TG and Mewo human melanoma cells. These melanoma cells were pretreated with proteinases and their adhesive properties on various substrata were evaluated by cell adhesion assays. Paradoxically, appropriate cell surface proteolysis enhanced the RGD-sensitive cell adhesion on fibrinogen and vitronectin, but not the RGD-insensitive adhesion on type I collagen or laminin. Pretreatment of these cells with 0.1 to 1 microM of trypsin, chymotrypsin, or plasmin for 30 min at 37 degrees C increased the number of spread cells on fibrinogen and vitronectin by 200-300%. The enhancement of cell spreading was not accompanied by up-regulation of the relevant RGD-sensitive integrin expression. Analysis of the cell surface receptor by GRGDSPK-Sepharose affinity chromatography showed that trypsin treatment did not up-regulate alpha v beta 3 integrin, an RGD-sensitive receptor for fibrinogen and vitronectin in the melanoma cells, nor the induced appearance of novel receptors. Treatment of cells with 100 nM proteinases increased cell binding of both monoclonal and polyclonal antibodies against alpha v beta 3 integrin subunits by 70%, but not that of monoclonal antibody against alpha 2, alpha 3, or alpha 6 subunit, indicating that cell surface proteolysis exposed more alpha v beta 3 integrin on the cell surface. These results suggest that exposure of alpha v beta 3 integrin is a part of the mechanisms underlying the serine proteinase-induced enhancement of melanoma cell adhesion on fibrinogen and vitronectin.
Amino Acid Sequence↗
Immunohistochemical analysis of nm23 gene product in human gallbladder carcinomas.
The expression of nm23, the product of a candidate suppressor gene for tumour metastasis, was examined immunohistochemically in human gallbladder carcinomas and compared with clinicopathological features. Seventy-eight (72%) of 107 carcinomas expressed nm23 protein regardless of histological type, while non-neoplastic mucosa occasionally showed very weak immunoreactivity to nm23. No obvious correlation was observed between nm23 protein expression and depth of tumour invasion or tumour stage. The expression of nm23 protein was detected in 60% and 74% of the cases with and without lymph node metastasis, respectively, indicating no relationship to metastatic ability. Fifty-eight percent of the cases showed reduction of nm23 immunoreactivity in tumour cells invading the stroma at the border of tumour cell nests compared with cells at the centre of the tumour. Only 7% of the cases showed increased nm23 expression in tumour cells at the border. These results suggest that in gallbladder carcinoma decreased expression of nm23 may not have implications for metastasis but may play a part in local invasion.
Carcinoma↗
"Rebound" phenomenon of hepatitis C viremia after interferon therapy in "relapsed" patients with chronic hepatitis C.
The correlation between serum hepatitis C virus (HCV)-RNA and aminotransferase levels following completion of interferon therapy was evaluated in eight relapsed patients with chronic hepatitis C. Both HCV-RNA and aminotransferase levels were significantly increased in the relapsed patients 1 month after completion of therapy, compared to pretreatment values, despite aminotransferase levels being normal and HCV-RNA being undetectable by reverse transcription polymerase chain reaction assay at the end of therapy. The serum levels of HCV-RNA and aminotransferase were significantly elevated 1 and 2 months post-treatment. They then decreased to pretreatment values 3-5 months after the completion of therapy. Thus, in relapsed patients after the completion of therapy, the changes in HCV-RNA levels preceded the elevation in aminotransferase levels. These findings suggest a correlation between serum HCV-RNA levels and aminotransferase levels in relapsed patients with chronic hepatitis C after the completion of interferon therapy.
Adult↗
Venous tumor thrombosis and cavernous transformation of the portal vein in a patient with gastric carcinoma.
A case of extensive extra- and intrahepatic portal tumor thrombosis, with no metastatic foci in liver parenchyma, secondary to advanced gastric carcinoma in a 69-year-old man is reported. The portal tumor thrombosis was characterized by enlargement of the thrombosed segment of the vein, decreased density mass without intraluminal enhancement of the involved vein, nonvisualization of the portal venous branch in the involved lobe, and the so-called cavernous transformation of the portal vein. The surgically resected gastric specimen showed Borrmann type 3 advanced papillary adenocarcinoma. The portal tumor thrombus is presumed to have arisen from vascular invasion in the primary foci of gastric carcinoma, and then to have permeated the portal vein without invasion of liver parenchyma.
Adenocarcinoma, Papillary↗
Isolation and characterization of a cDNA that encodes maize glutamate dehydrogenase.
A full-length cDNA clone, pMGDH1, encoding maize NADH-glutamate dehydrogenase (NADH-GDH) was isolated from a maize root cDNA library. The identity of the cDNA was established by the coincidence of the structure of the purified protein with that inferred from the nucleotide sequence of the cDNA. pMGDH1 had a cDNA insert of 1,638 bp and the open reading frame encoded 411 amino acid residues. The deduced amino acid sequence was similar to putative partial sequences of GDHs from higher plants and to the sequences of GDHs from organisms as diverse as mammals and bacteria. The NH2-terminal sequence deduced from the open reading frame had a typical structure that is associated with the import of proteins into the mitochondrial matrix. The cDNA hybridized to an RNA of about 1.6 kb. This transcript was more abundant in roots than in leaves and was localized in the bundle sheath cells in leaf tissues. Analysis of genomic DNA by Southern hybridization suggested the existence of gene(s) for another NADH-GDH subunit(s).
Amino Acid Sequence↗
Mechanism of action of antimycobacterial activity of the new benzoxazinorifamycin KRM-1648.
The mechanism of antimicrobial activity of KRM-1648 (KRM), a new rifamycin derivative with potent antimycobacterial activity, was studied. Both KRM and rifampin (RMP) inhibited RNA polymerases from Escherichia coli and Mycobacterium avium at low concentrations: the 50% inhibitory concentrations (IC50s) of KRM and RMP for E. coli RNA polymerase were 0.13 and 0.10 micrograms/ml, respectively, while the IC50s for M. avium RNA polymerase were 0.20 and 0.07 microgram/ml. Both KRM and RMP exerted weak inhibitory activity against Mycobacterium fortuitum RNA polymerase, rabbit thymus RNA polymerases, E. coli DNA polymerase I, and two types of reverse transcriptases. Uptake of 14C-KRM by M. avium reached 18,000 dpm/mg (dry weight) 1.5 h after incubation, while uptake by E. coli cells was slight. KRM was much more effective in inhibiting uptake of 14C-uracil than was RMP (IC50 of KRM, 0.04 microgram/ml; IC50 of RMP, 0.12 microgram/ml). These findings suggest, first, that the potent antimycobacterial activity of KRM is due to inhibition of bacterial RNA polymerase and, second, that the activity of KRM against target organisms depends on target cell wall permeability.
Antibiotics, Antitubercular↗
Can transcranial Doppler really detect reduced cerebral perfusion states?
BACKGROUND AND PURPOSE: This study was designed to determine whether transcranial Doppler ultrasonography (TCD) may detect reduced perfusion states of the brain in patients with hypertension or diabetes mellitus with suspected cerebral atherosclerosis and arteriolosclerosis. METHODS: We determined blood flow velocity with TCD in the middle cerebral artery and cerebrovascular vasodilator responses to carbon dioxide in 22 patients with or without carotid artery occlusive disease and minor stroke; we compared the results with the measurements of cerebral blood flow and oxygen metabolism by positron emission tomography (PET). RESULTS: Blood flow velocity measured by TCD correlated with ipsilateral cerebral blood flow measured by PET in frontal, temporal, and striatal regions and throughout the entire hemisphere (P < .05 to P < .005). Relative changes in blood flow velocity and calculated cerebrovascular resistance tested by carbon dioxide inhalation both correlated closely with regional mean transit time (calculated as the ratio of cerebral blood volume divided by cerebral blood flow) in frontal, striatal, temporal, parietal, and occipital regions and also in the entire hemisphere (P < .05 to P < .0001). TCD variables did not correlate with hemispheric measurements of oxygen metabolism by PET. CONCLUSIONS: Although TCD is not useful in assessing impairments of cerebral metabolism, it is useful for detecting abnormalities of cerebral hemodynamics among patients with risk factors for cerebrovascular disease.
Adult↗
Alterations in the mitral flow velocity pattern induced by acute myocardial infarction. Doppler findings before and after infarction.
Several studies have demonstrated that myocardial infarction (MI) is likely to alter left ventricular diastolic function. However, it is unclear whether MI per se alters Doppler transmitral flow velocity patterns (TMF) clinically. To investigate how myocardial infarction alters TMF clinically, we assessed serial changes in TMF in 13 patients whose TMF patterns were recorded at a mean of 7 months before and after MI in relation to the size of MI. From TMF, early and atrial filling flow velocities (E and A (m/s), respectively), and the E/A ratio, were measured. From simultaneously recorded two-dimensional echocardiograms, left ventricular dimensions and wall motion score (WMS: sum of 17 segmental scores (dys/akinesis = 3 to normal = 0)) were determined. The patients were divided into two subsets based on the values for WMS in the convalescent stage; 8 patients had small MI (WMS < or = 10) and 5 patients had large MI (WMS > 10). In patients with small MI, although E and the E/A ratio decreased at day-1 compared with pre-MI values (pre-MI vs day-1, E; 0.54 +/- 0.12 vs 0.39 +/- 0.15, p < 0.05, E/A ratio 0.91 +/- 0.23 vs 0.68 +/- 0.14, p < 0.05), these values increased to levels similar to those observed at pre-MI in the convalescent stage. There were no changes in left ventricular dimensions between pre-MI and in the convalescent period. In patients with large MI, the changes in the TMF patterns varied among patients after MI. In 3 patients with WMS < or = 25, E and E/A ratio were decreased in the convalescent stage, compared with pre-MI values. In 2 patients with WMS > 25, TMF patterns showed 'pseudonormalization' (E/A ratio > 1.0) throughout the follow-up period, with a progressive increase in left ventricular dimension. Thus, MI per se does not always produce clear changes in the Doppler TMF pattern in clinical settings, and the size of the MI seems to be a determinant of the TMF pattern after MI.
Adult↗
Cerebral blood flow and brain function in hypertension.
In mild hypertensive patients, regional cerebral blood flow, measured by positron emission tomography, was reduced in the frontal cortex and basal ganglia compared with normotensive patients. In moderate to severe hypertensive patients, cerebral oxygen metabolism was diminished, although the patients were neurologically intact. In elderly hypertensives, white matter vascular lesions on brain imaging were more frequent and cognitive function was impaired, compared with age-matched normotensives. In nontreated spontaneously hypertensive rats (SHR), local cerebral blood flow was decreased in the cortex and thalamus, compared with normotensive rats (NTR). Spatial memory and learning in maze tests were more impaired in aged SHR than in old NTR or young SHR. This impairment was related to decreased cerebral glucose utilization in the medial septal nucleus, hippocampus, and other regions of the brain. Reduced cerebral blood flow, increased media thickness of the cerebral arteries and impaired cognitive function in SHR were improved by long-term antihypertensive treatment. In humans as well as animals, long-standing hypertension per se leads to reductions in cerebral blood flow, metabolism, and cognitive function, each of which possibly may be improved by controlling hypertension with long-term antihypertensive treatment.
Animals↗
Inhibitory effects of corticoids on reductive halothane dehalogenation.
The effects of corticoids, hydrocortisone, methylprednisolone, betamethasone and dexamethasone, on the reductive metabolism of halothane to produce chloro-difluoroethylene (CDE) and chlorotrifluoroethane (CTE) in the liver microsomes of guinea-pig were examined. The substrate differential spectrum for methylprednisolone showed a peak at 412 nm and trough at 395 nm, typical modified type II. The other corticoids showed a similar spectral change. The corticoids had no effect on NADPH-cytochrome P450 reductase. All of these corticoids inhibited the reductive dehalogenation of halothane. The concentrations of hydrocortisone, methylprednisolone, betamethasone and dexamethasone causing 50% inhibition of CDE formation from halothane were 5.1 +/- 0.7 mg/ml, 3.1 +/- 1.2 mg/ml, 2.3 +/- 0.4 mg/ml and 2.4 +/- 0.6 mg/ml, respectively, with no significant differences except for hydrocortisone. The concentrations of hydrocortisone, methylprednisolone, betamethasone and dexamethasone causing 50% inhibition of CTE formation from halothane were 4.9 +/- 0.5 mg/ml, 3.1 +/- 1.0 mg/ml, 2.4 +/- 0.3 mg/ml and 28.0 +/- 9.1 mg/ml, respectively, with no significant differences except for dexamethasone. Our results showed that corticoids inhibit halothane metabolism.
Adrenal Cortex Hormones↗
Autopsy findings of Addison's disease caused by systemic cytomegalovirus infection in a patient with acquired immunodeficiency syndrome.
We previously reported a case of Addison's disease associated with acquired immunodeficiency syndrome (AIDS) (Endocr J, 41:13, 1994). A 46-year-old man with hemophilia B and AIDS was diagnosed as Addison's disease. The positive cytomegalovirus (CMV) antigen in urine suggested that CMV adrenalitis may have caused the adrenal insufficiency. Despite treatment with ganciclovir, the patient died one year later. Autopsy findings revealed that the typical inclusions of CMV were seen in the lung, adrenal glands (both cortex and medulla) and small intestine. Here, we describe the subsequent clinical course and postmortem findings of this case.
AIDS-Related Opportunistic Infections↗
[Clinical evaluation of positive- and negative-stranded HCV-RNAs in liver in relation to IFN therapy].
Explore the source record for details and available documents.
Adult↗
[MR imaging of thyroid masses].
Magnetic resonance (MR) imaging was performed in 35 patients with histologically proved thyroid masses. Gadopentetate dimeglumine was used in 25 of these cases. The thyroid tumors were analyzed by MR imaging as to shape, margin, pseudocapsulation, homogeneity, and enhanced pattern. Gd-DTPA was helpful in identifying pseudocapsules and showing the extent of the tumor. Papillary carcinoma tended to display unclear margins, heterogeneous intensity, and inhomogeneously enhanced patterns. In follicular adenoma, the tumor margin was smooth and pseudocapsules were clearly detected. Follicular adenoma was enhanced homogeneously, but it was difficult to distinguish follicular adenoma from follicular carcinoma by MR imaging. Adenomatous goiter was delineated as multiple nodules with smooth margins, but without pseudocapsules. These nodules were enhanced in various ways after Gd-DTPA administration.
Female↗
New approach for detection of amplification in cancer DNA using restriction landmark genomic scanning.
We developed a new approach for detecting the gene amplification of cancer DNAs with restriction landmark genomic scanning (RLGS). In cancer research, much effort has been made to find the amplified loci of cancer DNAs, because many lines of evidence indicate association between oncogene amplification and carcinogenesis. Conventionally, such gene amplification has been detected by using Southern hybridization with DNA probes. However, only the information of one locus can be obtained by one hybridization procedure, and analysis of many loci throughout the genome is too laborious and time consuming, even if only several candidate genes are investigated. On the other hand, the "in-gel renaturation method" was reported as another alternative for detection of amplified regions. However, even though this method is much improved, it is difficult to detect less than 7-fold amplification, which is often higher than the amplification of many cancer cases. To overcome these limitations and, in addition, to locate the amplified DNA two dimensionally, we applied RLGS for analysis of DNA amplification in cancer tissues, such as breast cancer (infiltrative tubuloadenocarcinoma), neuroblastoma, meningioma (endotheliomatous meningioma), and thyroid cancer (papillary adenocarcinoma). In some cases of breast cancer, several amplified spots located on the same amplicon were detected. In thyroid cancer, in which no amplification has yet been reported, low-grade amplification was also detected. In this report, we demonstrated that RLGS allows us to screen 2000-3000 restriction landmarks distributed on the genome simultaneously, and even low-grade amplification could be detected effectively. Thus, RLGS has proven to be a very useful method in detecting DNA amplification.
Breast Neoplasms↗