Biomedical subjects

H Kitamura

Publications and source records attributed to H Kitamura.

At least 289 records · Page 16Linked to original sources

PubMed1996

[Unilateral and synchronous occurrence of renal cell carcinoma and ureteral tumor: a case report].

An 81-year-old woman was admitted to our hospital with left flank pain. Excretory urography revealed left hydronephrosis. Abdominal computed tomography (CT) revealed a large heterogenous tumor in the upper pole and marked hydronephrosis and hydroureter in the lower portion of the left kidney. Left total nephroureterectomy was performed under the diagnosis of renal pelvic and ureter tumor. The pathological diagnosis was of renal cell carcinoma (spindle type, grade 3) in the kidney and transitional cell carcinoma (grade 2) in the ureter. Postoperative chemotherapy was not given. Convalescence was uneventful and fifteen months after the operation she is alive with no recurrence or metastasis.

Aged↗

PubMed1996

Retinopathy in diabetic (KKA gamma) mice: diabetic microvascular changes to the retina in KKA gamma mice revealed by light and electron microscopy.

Pericytic changes in the retinal vessels of diabetic (KKA gamma) and control (C57BL) mice were studied by light and electron microscopy. An improved histochemical technique for alkaline phosphatase was used in the light microscopic study. In the control mice, a continuous pathway was identified extending from the retinal arterioles, via the superficial and deep retinal capillaries, to the retinal venules. The deep retinal capillaries formed networks and were localized within the deeper retinal layers; the retinal arterioles, superficial capillaries, and venules were present in the nerve fiber layer. Examination of KKA gamma mice, aged 16 to 28 weeks, revealed engorgement of the arterioles, hypertrophy of the pericytes (which contained numerous actin filaments) within the superficial retinal capillaries, and narrowing of the deep retinal capillaries. These microvascular changes indicate retinal hyperperfusion, local hypertension of the superficial retinal capillaries, adaptive hyperfunctional changes in the pericytes of these capillaries, and ischemia of the deep retinal capillaries. The pericytic changes observed in the diabetic capillaries contrasted sharply with previous reports; an explanation for this variance is suggested.

Alkaline Phosphatase↗

PubMed1995

Trypsinogen expression in human ovarian carcinomas.

Increased secretion of matrix metalloproteinases and serine proteinases is well known to be associated with cancer invasion and metastasis. We aimed to elucidate the implication of trypsin, a serine proteinase and a representative digestive enzyme in invasion and metastasis of human carcinomas. Northern blot, RT-PCR and Western blot analyses and immunohistochemical studies were performed to detect and analyze trypsinogen expression in 5 ovarian carcinoma cell lines and 10 human ovarian carcinoma tissues using a DNA probe for trypsinogen I, and monoclonal and polyclonal antibodies to human trypsin I. Among the 5 ovarian carcinoma cell lines, only the MCAS (mucinous cystadenocarcinoma) cell line showed a high level of trypsinogen production and mRNA expression by Western and Northern blot analyses, respectively. However, Southern blot analysis of RT-PCR products could detect considerable levels of trypsinogen mRNA in all ovarian cancer cell lines. In Northern analysis of ovarian cancer tissues, all advanced cancer samples showed trypsinogen gene expression. Serous cystadenocarcinomas exhibited particularly high levels of gene expression. Immunohistochemical staining also detected trypsin in ovarian carcinoma tissues. In contrast, normal ovaries and tumors with low malignant potential did not show trypsinogen expression. Our results demonstrate the extra-pancreatic production and distribution of trypsinogen in human ovarian carcinomas.

Adenocarcinoma↗

PubMed1995

Cementum-impregnated gelatine membrane: its effect on periodontal tissue regeneration.

This study was designed to evaluate the ability of cementum-impregnated gelatine membranes (CGM) to stimulate regeneration of periodontal ligament following surgery. Three monkeys with no periodontal disease were used. Following flap elevation, recession type defects were created on the buccal side of maxillary lateral incisors and second premolars, and roots were subsequently planed. Experimental sites received CGM at approximately 2-3 mm below the cementoenamel junction while control sites received gelatine membrane (GM) free of cementum. Wounds were allowed to heal for 3 weeks, during which time daily plaque control measures were maintained. Tissues prepared from sacrificed animals revealed that experimental specimens exhibited formation of new cementum, new bone, and periodontal ligament. Control specimens exhibited connective tissue adhesion without either new cementum or significant new bone formation. Histometric analysis showed that the average vertical growth of cementum (NC) and bone (NB) at experimental sites were 3.48 +/- 0.29 and 0.64 +/- 0.43 mm, respectively. At the control sites the corresponding results were NC = 0.09 +/- 0.03 and NB = 0.06 +/- 0.28. It was concluded that placement of CGM resulted in significantly greater postsurgical cementum and bone formation than that of GM alone.

Animals↗

PubMed1995

Tumor suppressor gene p53 mutations in human prostate cancer.

The genetic background underlying the growth and development of human prostatic cancer is not yet clear. Here we searched for possible mutations in the entire coding region of tumor suppressor gene p53 in primary human prostatic carcinomas, using polymerase chain reaction and single-strand conformational polymorphism analysis of RNA. We found p53 gene mutations in 4 of 21 cases (19%). DNA sequencing of the polymerase chain reaction products revealed missense point mutations that resulted in amino acid changes in exon 5 or 3 in three cases and single base deletions in exon 7 in two cases. One case contained both a missense point mutation and a single base deletion. Three of these four cases were pathologically diagnosed as poorly differentiated adenocarcinomas, and three of the four cases were clinically localized to stage C or D. None of seven noncancerous prostate tissues nor three well-differentiated adenocarcinoma tissues showed any mutations. The present results suggest that p53 gene mutation is involved in the late progression steps of human prostate carcinogenesis.

Adenocarcinoma↗

PubMed1995

Retinoblastoma gene mutations in primary human prostate cancer.

Structural alterations in the entire coding regions (exons 1 to 27) of the retinoblastoma (RB) gene in primary human prostate cancers were investigated, using polymerase chain reaction and single strand conformational polymorphism analysis of RNA. Of 25 samples obtained from patients, four (16.4%) were found to have RB alterations. DNA sequencing of the PCR products revealed point mutations resulting in single amino-acid substitutions of exons 6 and 19 in two cases, and base deletions of exons 8 and 17 in two cases. Two of four cases with RB mutations were moderately differentiated localized tumors and other two with RB mutations were poorly differentiated tumors with metastases. Our results suggest that RB gene mutation is involved in progression steps of prostate carcinogenesis.

Adenocarcinoma↗

PubMed1995

Changes in glycoconjugates revealed by lectin staining and stage-specific embryonic antigen-1 immunostaining in hamster submandibular glands during the postnatal period.

Lectin binding and stage-specific embryonic antigen-1 (SSEA-1) immunoreactivity were studied in the developing submandibular glands of young Syrian golden hamsters (Mesocricetus auratus) from postnatal day 1 (the day of birth) to day 28. The submandibular glands were fixed in a solution containing 6% mercuric chloride, 1% sodium acetate, and 0.1% glutaraldehyde (HgCl2-G) or 4% paraformaldehyde (4P), and embedded in paraffin. Sections from HgCl2-G fixation were stained with three lectin-peroxidase conjugates: peanut agglutinin (PNA), Ulex europeus I agglutinin (UEA I), and wheat germ agglutinin (WGA). Sections from the 4P-fixed tissues were immunostained with monoclonal antibodies against SSEA-1, sialyl SSEA-1 and fucosyl SSEA-1. On the day of birth, the terminal unit of the submandibular gland was composed of fetal type secretory cells and proacinar cells. The secretory cells were PNA, UEA I, and WGA positive. The number of secretory terminal tubule cells decreased rapidly, and lectin-positive secretory cells were replaced by adult secretory cells that did not show PNA or UEA I stainings but were weakly positive for WGA. Fetal secretory cells were positively immunostained for SSEA-1 and sialyl SSEA-1, and immature ductal cells were stained for fucosyl SSEA-1. The positive stainings disappeared with regression of the fetal epithelial cells. Hence, modulation of glycoconjugate expression in the submandibular glands, which reflects changes in secretory cells from the fetal type to adult type during postnatal development, is revealed by lectin staining and immunostaining for SSEA-1 and related antigens.

Animals↗

PubMed1995

Endothelial regeneration during the repair process following Habu-snake venom induced glomerular injury.

In this study, the kinetics of glomerular endothelial cells during the repair process following glomerular injury was investigated in a model of mesangial proliferative glomerulonephritis induced by Habu-snake venom (HSV) in rats. Intravenous injection of HSV led to a cystic ballooning type lesion at day 1. Subsequently a marked segmental proliferative lesion was observed in the cystic areas at day 5. Thereafter cellularity decreased and reconstruction of the glomerular tuft was gradually observed with time. The histological structure of the glomeruli had almost returned to normal 21 days following HSV injection. After prominent depletion at day 1, the number of endothelial cells increased rapidly and reached a plateau at day 7, not significantly different from that of the control group. Morphologically endothelial cell elongation from the vascular pole into the cystic lesion was seen together with premature capillary formation in the proliferative lesion. Accompanying the reduction of mesangial expansion, the endothelial cells gradually formed definite capillary lumens. We conclude that the mesangial proliferative glomerulonephritis induced by HSV recovers to its original structural state and that the migration and proliferation of endothelial cells with accompanying capillary formation are essential for the repair process, in addition to mesangial cell proliferation.

Animals↗

PubMed1995

Nicorandil suppressed myocardial purine metabolism during exercise in patients with angina pectoris.

To elucidate the effect of Nicorandil on myocardial energy metabolism and myocardial sympathetic activity, we administered Nicorandil orally to eight patients with angina pectoris prior to exercise testing. Arterial and coronary sinus levels of lactate, ammonia, hypoxanthine (HX), adrenaline and noradrenaline were measured during exercise in order to determine the irrespective myocardial extraction ratios (MER). Compared to placebo, Nicorandil increased the time to development of significant ST depression (322 vs 390 s) while decreasing the maximum amplitude of ST depression (0.244 vs 0.216 mV). Heart rate, systolic blood pressure, and the rate pressure product during exercise were not significantly affected. The MER of lactate, measured during exercise, was significantly higher after Nicorandil than placebo (13.6 vs 27.9). Similarly, the MERs of ammonia and HX were significantly higher after Nicorandil (-46.0 vs 7.4% and -47.0 vs 9.9% respectively). Nicorandil, had no apparent effect on myocardial sympathetic activity as the MERs of adrenaline and noradrenaline were essentially unaffected. We conclude that Nicorandil decreased myocardial ischaemia and suppressed myocardial accelerated purine metabolism (a marker of cellular energy metabolism) during exercise in patients with angina pectoris. This effect appears not to be related to myocardial sympathetic activity.

Administration, Oral↗

PubMed1995

Hamster pulmonary endocrine cells with neural cell adhesion molecule (NCAM) immunostaining.

Pulmonary endocrine cells of Syrian golden hamster were stained for neural cell adhesion molecule (NCAM) with indirect fluorescent immunostaining and observed with a confocal laser scanning microscope equipped with an argon laser. Sections 100 microns thick of hamster lung fixed with phosphate-buffered 4% paraformaldehyde were prepared. The sections were incubated with rat monoclonal antibody against NCAM, followed by fluorescence-labeled antibody against rat immunoglobulin. Some were doubly immunostained for NCAM and one of the following endocrine markers: neuron-specific enolase, calcitonin gene-related peptide and serotonin. Expression of NCAM in the hamster airway epithelium was seen in cell nests resembling neuroepithelial bodies (NEBs). NCAM immunostaining was positive at the lateral cell borders between the cells composing the nest, but negative at the border with the adjacent, presumably non-endocrine cells. Double immunostaining confirmed that the grouped cells with NCAM immunoreactivity were of an endocrine nature, but that single endocrine cells did not show NCAM immunoreactivity. An electron microscopic study with NCAM immunostaining confirmed the light microscopic study. These suggest that NCAM expression could be important for the morphogenesis of NEBs. A confocal laser microscope was used to make three-dimensional images of NEBs after NCAM immunostaining and the spatial interaction between NEBs and the surrounding microenvironment was studied.

Animals↗

PubMed1995

Alkaline phosphatase reactivity in rabbit airway epithelium: a potentially useful marker for airway basal cells.

The purpose of this study was to investigate alkaline phosphatase (ALPase) reactivity in rabbit airway epithelial cells. Acetone-fixed, methyl benzoate and xylene-cleared (AMeX-treated) paraffin sections of trachea, bronchus, and lung tissue were stained by an azo dye coupling method for ALPase and examined by light microscopy. Electron histochemical staining was also performed in order to study the sensitivity and specificity of reactivity in each cell type. ALPase reactivity at the light microscopic level was observed exclusively in tracheo-bronchial basal cells, and not in bronchiolar basal cells. By electron microscopy, ALPase reactivity was noted in 97.9% of basal cells in the trachea, 97.0% of basal cells in the bronchus, and 94.5% of basal cells and 15.4% of Clara cells in the bronchiole. This was also true for dispersed tracheal epithelial cells. Reactivity was rarely observed in ciliated cells, non-goblet-type secretory cells, and undetermined cells. The reactivity was heat-labile, levamisole-sensitive, and of a non-specific type. These findings indicate that basal cells of rabbit trachea and bonchus have fairly high specificity for ALPase of a non-specific isozyme (92.2% and 95.6%, respectively). Therefore, ALPase is considered to be a useful marker for these cells.

Alkaline Phosphatase↗

PubMed1995

Covalently-bound human C4b dimers consisting of C4B isotype show higher hemolytic activity than those of C4A in the C3-bypass complement pathway.

The ability to form a covalent dimer of human C4b was investigated with purified isotypes C4A and C4B, and antibody-sensitized liposomes supplemented with C1. In this system, no C4A or C4B formed a complex with the antibody or C1. Whereas both C4A and C4B isotypes formed dimers to a similar extent, C4B formed an ester-linked dimer and C4A an amide-linked dimer. Both of these dimers served as a subunit for the C3-bypass pathway C5 convertase, since liposomes bearing Ab, C1 and a dimer of C4A or C4B, allowed the formation of C5 convertase by the addition of C2. The degree of complement-mediated liposome lysis however, was observed to be 2-3 times higher in the C4B-bearing particles than in those bearing C4A. These results indicate that the second C4b-binding site on the first C4b is different between C4A and C4B, and that in the C3-bypass pathway, C4B has a higher degree of hemolytic activity than C4A, as in the conventional classical complement pathway.

Biopolymers↗

PubMed1995

The endocrine pancreas of spontaneously diabetic db/db mice: microangiopathy as revealed by transmission electron microscopy.

Abnormalities in ultrastructures of islet capillaries were detected in db/db mice, with the visual inspection and morphometry of electron micrographs. The observed changes are: (1) capillary scarcity; (2) increase in the mean and diversity of capillary size; (3) pericapillary edema and fibrosis; (4) hypertrophy of the pericyte and abundance therein of actin-like microfilaments; and (5) luminal irregularity. Changes (2), (3) and (4) are conceived to indicate hyperperfusion, capillary hypertension and secondary vascular response. In particular, such pericyte changes were found to be shared by other organs whose capillaries are susceptible to diabetic complications.

Animals↗

PubMed1995

Roles of hematocrit and fibrinogen in red cell aggregation determined by ultrasonic scattering properties.

Parameters of the power spectrum of backscattered echoes were applied to quantitatively evaluate red cell aggregation in vitro. Human red cell suspensions were circulated in a closed loop of tubing, and ultrasonic, radiofrequency, echo-signal data were obtained using a 10-MHz transducer. Data acquisition was performed at 30-s to 1-min intervals for 5 min after flow stoppage. Two parameters of the normalized power spectrum of the echo signals, spectral slope and Y-intercept, were computed, and estimates of two scattering properties, the scatterer size and acoustic concentration were calculated from these parameters using equations based on scattering theory. Size and acoustic concentration were observed as they changed over time after the stoppage of flow. The key findings were that hematocrit affected the rate of cell aggregation while fibrinogen controlled aggregate size and acoustic concentration.

Adult↗

PubMed1995

Identification of the antithrombin III Kyoto mutation by restriction fragment length polymorphism analysis.

Clarification of the molecular biologic abnormality underlying antithrombin III (AT III) deficiency is important to a complete understanding of the coagulation system. We have reported previously the deficiency of AT III Kyoto in which there has been a single substitution of thymine for guanine at codon 406 of exon VI. This results in the amino acid substitution of methionine for arginine. The nucleotide substitution at codon 406 in the mutant allele eliminates a Hae III restriction site. Accordingly, Hae III restriction analysis of the PCR fragments in this family could segregate the deficient members from the normal members, enabling the detection of the existence of Hae III restriction fragment length polymorphism of the PCR product (PCR-RFLP). Moreover, we confirmed by direct DNA sequencing with the polymerase chain reaction that the tested deficient members in an AT III Kyoto family inherit the same type of mutation in their genes. In conclusion, Hae III PCR-RFLP can be a useful method for screening of this mutant gene in the family.

Adult↗

PubMed1995

Determining the acuteness and stability of deep venous thrombosis by ultrasonic tissue characterization.

PURPOSE: The intent of the study was to determine whether ultrasonic tissue characterization (UTC) could indicate acuteness and stability of deep venous thrombosis (DVT) of the lower extremities. METHODS: Thrombi presenting as filling defects on color Doppler imaging in the common or superficial femoral or popliteal veins in 50 extremities in 45 patients with DVT were studied. Acute DVT was less than 4 days duration, and chronic DVT was greater than 21 days duration. UTC analysis of parameters from the normalized power spectrum of backscattered ultrasound signals from venous filling defects was performed. This spectrum approaches a straight line, and its basic parameters, slope, and Y-intercept are related to scatterer size, concentration, and the square of the scatterer-to-medium acoustic impedances. Ten of the DVT extremities were reexamined at 1 week to assess UTC changes that would indicate thrombus instability. RESULTS: Acute DVT (19 of the 50 extremities) could be distinguished from chronic DVT, mainly on the basis of significantly higher intercept values for the acute group, which were 11.6 relative decibels (dBr) higher than those of the chronic DVT group. Discriminant linear analysis of the two parameters indicated a sensitivity of 94.7% and specificity of 90.3% in correctly diagnosing acute DVT. In a small sample of 10 extremities reexamined at 1 week, acute DVT extremities showed a mean 9.4 dBr decrease in intercept values with no significant change in slope. CONCLUSIONS: UTC distinguished clinically defined acute from chronic DVT. In a small series of extremities, UTC revealed significant instability of acute thrombi in a selected patient population.

Acute Disease↗

PubMed1995

Apoptosis in the repair process of experimental proliferative glomerulonephritis.

The recovery from the proliferative glomerulonephritis (GN) with reduction of hypercellularity is known in various experimental and human GN. To elucidate the participation of apoptosis in GN, we studied the experimental Thy-1.1 GN for six weeks. Apoptosis was recognized by both light and electron microscopy, and the biochemical expression of apoptosis was morphologically confirmed by in situ end-labeling method of fragmented DNA, using terminal deoxy-transferase. Mesangioproliferative GN was induced by a single administration of anti-Thy-1.1 monoclonal antibody in a rat. Mesangial cell proliferation started early in the process and the number of glomerular cells peaked from day 7 to day 10. Subsequently, the degree of proliferative lesion diminished with obvious reconstruction of the capillary structure, as well as decrease in the number of glomerular cells. During this period, proliferated mesangial cells returned to their original level of cellularity and apoptosis apparently increased in number among the glomeruli. Apoptosis was significantly noted from day 7 to week 4 and was in its maximum at day 10 to week 2. Following this period, by week 6 most of the glomeruli reverted to their original structure. The number of infiltrated neutrophils and macrophages in the glomeruli slowly decreased during the course of the disease, and a few apoptosis were also observed. It is concluded that proliferated glomerular cells regress by apoptosis in the repairing process of GN. Apoptosis plays an essential role in the recovery to the original glomerular structure in GN.

Animals↗

PubMed1995

Roles of prostaglandins D2 and E2 in interleukin-1-induced activation of norepinephrine turnover in the brain and peripheral organs of rats.

Possible roles of prostaglandins (PGs) in interleukin-1 (IL-1)-induced activation of noradrenergic neurons were examined by assessing norepinephrine (NE) turnover in the brain and peripheral organs of rats. An intraperitoneal injection of human recombinant IL-1 beta accelerated NE turnover in the hypothalamus, spleen, lung, diaphragm, and pancreas. A similar increase in NE turnover was also observed after intracerebroventricular injection of corticotropin-releasing hormone (CRH). Pretreatment with indomethacin (cyclooxygenase inhibitor) abolished the IL-1-induced, but not the CRH-induced, increase in hypothalamic and splenic NE turnover. To elucidate which eicosanoid-cyclooxygenase product(s) is responsible for accelerating NE turnover, PGD2, PGE2, PGF2 alpha, U-46619 (stable thromboxane A2 analogue), or carbacyclin (stable prostacyclin analogue) was administered intracerebroventricularly. Among them, PGE2 was the only eicosanoid effective in increasing NE turnover in spleen, whereas PGD2 was effective in the hypothalamus. The stimulative effect of PGD2 was abolished by pretreatment with intracerebroventricular injection of a CRH antiserum. These results suggest that the action of IL-1 is mediated through PGD2 production to activate the noradrenergic neurons in the hypothalamus, and through PGE2 production to increase sympathetic nerve activity in spleen.

Animals↗