Search PubMed⌕ Search

Biomedical subjects

M Kamada

Publications and source records attributed to M Kamada.

At least 199 records · Page 11Linked to original sources

Clinico-pathological analysis of foal diseases from 237 autopsy cases.

To elucidate the current status of foal diseases in Japan, clinico-pathological analysis was conducted on 237 foal autopsy cases. As a result, bacterial infection was identified as an important cause of foal death. Most of the bacteria isolated from these cases were ubiquitous, opportunistic, environmental organisms, known to be non-pathogenic to mature animals. Most of cases with bacterial infection were diagnosed as having hypogammaglobulinemia, i.e., failure of passive transfer. In addition, the mean weight of thymuses in foals affected by bacterial infection tended to be lower than that of foals without infection. These findings suggest that the common cause of foal diseases were mainly due to the opportunistic bacterial infections associated with the weakened immune function, serving as precursor to or promotor of infection.

Animals↗

Observation of tissue prokallikrein activation by some serine proteases, arginine esterases in rat submandibular gland.

Two serine proteases, arginine esterases (esterases I and II) which showed the activity of tissue prokallikrein activation were identified in rat submandibular gland. These enzymes were separated from the homogenate of rat submandibular gland by two successive DEAE-cellulose chromatographies and were further purified and characterized. Esterases I and II were found to be identical with tonin and esterase B-like enzyme, respectively. Both enzymes activated rat urinary prokallikrein at near neutral pH. Esterase B-like enzyme activated rat urinary prokallikrein better than tonin.

Amino Acid Sequence↗

The cerebral circulation in cases of carotid cavernous fistula. Findings of single photon emission computed tomography.

Ten patients with carotid cavernous fistula (CCF) were reviewed. Single photon emission computed tomography (SPECT) for regional cerebral blood flow (rCBF) study was performed in six patients with fast flow shunt. Five of these six patients with fast flow shunt angiographically demonstrated cortical venous drainage, and two of these patients suffered intracerebral hemorrhage. The rCBF decreased in the region demonstrating the cortical venous drainage in five patients, and in one patient the angiography demonstrated arterial steal and the rCBF decreased in a part of the ipsilateral cerebral hemisphere. SPECT proved to be useful in assessing the cerebral circulation in cases of CCF.

Adult↗

An enormous shunt between the portal and hepatic veins associated with multiple coronary artery fistulas.

A 9-year-old boy with a rare combination of multiple coronary artery fistulas and congenital shunt between the portal and hepatic veins (portal-systemic shunt) is presented. The most likely pathogenesis for the portal-systemic shunt in this case was persistence of the ductus venosus as a bypass tract of the portal vein. This shunt is considered as one cause of cardiomegaly and dilatation of the hepatic vein in this case, and careful follow-up is mandatory because this shunt could induce portal-systemic encephalopathy. There are a few reports of an anomalous portal venous connection to the hepatic vein as a result of abnormal portal embryogenesis. We experienced a unique case of congenital portal-systemic shunt associated with coronary artery fistulas. The present paper reports angiographic findings in this case and the etiological importance of the congenital portal-systemic shunt.

Cardiomyopathies↗

Generation of a different type of beta-kallikrein from porcine pancreatic alpha-kallikrein by the action of chymotrypsin--observation of proteolytic processing occurring around "kallikrein autolysis loop" region.

The generation of a different type of beta-kallikrein, designated C beta-kallikrein, from alpha-kallikrein by chymotryptic action was ascertained by the following observations: 1) When alpha-kallikrein was incubated with chymotrypsin, an increase of esterolytic activity of kallikrein was observed. 2) In sodium dodecyl sulfate polyacrylamide gel electrophoresis, C beta-kallikrein was found to be different from the beta-kallikrein obtained from alpha-kallikrein by tryptic digestion, and was designated T beta-kallikrein. 3) N-Terminal amino acid sequence analyses of internal light and heavy chains of C beta-kallikrein indicated that N-termini of the light and the heavy chains were isoleucine and lysine, respectively, and that the heavy chain had most of the "kallikrein autolysis loop" sequence in its N-terminal end. In the case of T beta-kallikrein, N-termini of the light and the heavy chains were isoleucine and alanine, respectively, and the light chain retained the "kallikrein autolysis loop" region in its C-terminal end. These observations demonstrated that C beta-kallikrein was different from the beta-kallikrein prepared from autolyzed pancreas, A beta-kallikrein, which had lost the "kallikrein autolysis loop" sequence. Structural differences of the above four kallikreins (alpha-, T beta-, C beta-, and A beta-) result in somewhat different enzyme properties. The kinetic constants for the hydrolysis of synthetic substrates (N alpha-benzoyl-L-arginine ethyl ester and N alpha-tosyl-L-arginine methyl ester) of these kallikreins differed from each other, and inhibitory profiles against alpha 1-antitrypsin were also different.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Sequence↗

Isolation of Clostridium perfringens from foals.

Clostridium perfingens was isolated from four of 29 healthy foals and from all twelve foals with gastrointestinal diseases. The range of viable counts of C. perfringens in the faeces was 10(1)-10(5)/g and in the intestinal specimens 10(1)-10(7)/g. Of 41 isolates of C. perfringens, 37 were considered to be type A. Enterotoxin of the organism was demonstrated in the intestinal contents of five of eight foals with enteric diseases. These findings suggested that C. perfringens is a likely pathogen of foal intestinal diseases.

Animals↗

Characterization of N-linked oligosaccharides of human urinary kallikrein molecules.

The micro-heterogeneity due to varied N-linked oligosaccharides of both active- and pro-types of human urinary kallikrein (HUK) in normal subjects and some patients were investigated by the methods of serial lectin affinity chromatography and crossed affino-immunoelectrophoresis. In the case of both types of normal HUK, the species carrying tri- and/or tetra-antennary oligosaccharide(s), corefucosylated bi-antennary oligosaccharide(s), and bi-antennary oligosaccharides containing outer galactose residues and an N-acetylglucosamine residue linked beta 1,4 to a beta-linked mannose residue (bisecting N-acetylglucosamine residue) amounted to approximately 36, 33 and 17% of the total of each type of HUK, respectively. On the other hand, in some diseases, i.e. essential hypertension, Bartter's syndrome and acute pancreatitis, alterations of the chromatographic and electrophoretic patters were observed and are assumed to correspond to glycosylation changes in each HUK molecule.

Chromatography, Affinity↗

Characterization of human pancreatic kallikrein.

Human pancreatic kallikrein (H.Panc.K.) was purified from human pancreas by ion exchange chromatography on DEAE-cellulose, affinity chromatographies on p-aminobenzamidine Sepharose 6B and aprotinin aminocellulofine, followed by gel filtration on Sephacryl S-200. The final preparation had a specific activity of 9.2 AU/A280 (AU; amidase unit for H-Pro-Phe-Arg-MCA) and its N-terminal sequence coincided with the reported sequence for H.Panc.K.. In HPLC (gel filtration), one symmetrical peak corresponding to a molecular weight of 48,000 was obtained. In SDS-PAGE without 2-mercaptoethanol (2-ME), one band corresponding to a molecular weight of 52,000 was obtained, but with 2-ME, 2 bands, 52,000 and 30,000, were obtained. Km value for MCA was 4.9 x 10(-2) mM. Proteinase inhibitor specificities of H.Panc.K. were the same as those of human urinary kallikrein (HUK) and hog pancreatic kallikrein (hog Panc.K.), while anti-HUK antibody inhibited the activities of H.Panc.K. and HUK, but not that of hog Panc.K.. From the analysis of affinity for concanavalin A (Con A) and erythroagglutinating phytohemagglutinin (E-PHA), the carbohydrate parts of H.Panc.K. are relatively rich in biantennary complex type sugar chains with bisecting GlcNAc compared with those of human salivary kallikrein (H.Saliv.K.) and HUK.

Amino Acid Sequence↗

Enzyme-linked immunosorbent assays for human tissue kallikrein and analysis of immunoreactive kallikrein in the plasma by them.

In order to study immunoreactive tissue kallikrein (TK) in human plasma, three kinds of enzyme-linked immunosorbent assay (ELISA) systems for human urinary kallikrein (HUK) were developed. All three types of TK in the plasma, i.e., active kallikrein, prokallikrein and kallikrein-alpha 1 antitrypsin (alpha 1 AT) complex, could be measured by the competitive ELISA (C-ELISA). However, the sandwich ELISA (S-ELISA) showed more strict specificity. Namely, both active and prokallikreins were able to be measured by the S-ELISA, while kallikrein-alpha 1 AT complex was hardly measurable. Measurement of this kallikrein-alpha 1 AT complex was made possible by using horseradish peroxidase (HRP)-labeled anti-alpha 1 AT IgG instead of HRP-labeled anti-HUK Fab' as the second antibody (HS-ELISA). Using these ELISAs we studied TK in plasma and the following observations were made. 1) The greater part of TK in the plasma was found in a form of a complex with alpha 1 AT. 2) The amount of free type TK was very small and the most part of this type TK in normal plasma was prokallikrein.

Chromatography, Affinity↗

Significance of D-mannose as a sperm receptor site on the zona pellucida in human fertilization.

The role of monosaccharides in human fertilization was studied by testing their effects on penetration of spermatozoa into mature human oocytes (zona penetration test). When oocytes were pretreated with concanavalin A, wheat germ agglutinin, or Ricinus communis agglutinin-I at a concentration of 100 micrograms/ml, no spermatozoa were found to bind to or penetrate through the zona pellucida. Penetration of spermatozoa was restored when the zona pellucida pretreated with wheat germ agglutinin and Ricinus communis agglutinin-I were rinsed with N-acetyl-D-glucosamine (wheat germ agglutinin inhibitor) and D-galactose (Ricinus communis agglutinin inhibitor), respectively. Conversely, the blocking effect of concanavalin A on sperm penetration was not reversed by treatment with D-mannose (concanavalin A inhibitor). Furthermore, pretreatment of spermatozoa with D-mannose (50 mmol/L) completely inhibited sperm penetration through the zona pellucida. However, sperm penetration was clearly demonstrated when the zona pellucida was pretreated with D-mannose. These data suggest that D-mannose residues are essential in, or sterically closely related to, the sperm receptor site on the human zona pellucida.

Carbohydrates↗

Treatment of malignant ascites with allogeneic and autologous lymphokine-activated killer cells.

Two cases of peritonitis carcinomatosa with gynecological cancer, which did not respond to conventional treatment, were treated by intraperitoneal adoptive immunotherapy with allogeneic or autologous lymphokine-activated killer (LAK) cells plus interleukin-2. In case 1, reduction of acute ascites and disappearance of malignant cells from the peritoneal fluid and decreased levels of tumor markers (CA12-5 and CA19-9) were demonstrated during the treatment. In case 2, which also received additional treatment for pleuritis carcinomatosa, reduction of ascites and pleural effusion and disappearance of malignant cells from the pleural fluid were noted. In these cases allogeneic LAK therapy was well tolerated. This therapy did not prolong the patients' lives, but the findings indicate that it had appreciable local antitumor effects on peritonitis and pleuritis carcinomatosa in these patients with gynecological cancer.

Ascites↗

[Purification of human pancreatic kallikrein and organ-specificities of human glandular kallikreins].

Human pancreatic kallikrein (H. Panc. K.) was purified from human pancreas by serial liquid chromatographies. The final preparation had a specific activity of 9.2 AU/A280 (AU: amidase unit for H-Pro-Phe-Arg-MCA) and its N-terminal sequence coincided with the reported sequence determined from cloned cDNA analysis. In HPLC (gel filtration), one symmetrical peak corresponding to a molecular weight of 48,000 was obtained. In SDS-PAGE without 2-mercaptoethanol, one band corresponding to a molecular weight of 52,000 was obtained. Protease inhibitor specificities of H. Panc. K. were the same as those of human urinary kallikrein (HUK) and hog pancreatic kallikrein (hog Panc. K.), while anti-HUK rabbit antibody inhibited the activities of H. Panc. K. and HUK, but not that of hog Panc. K. From the analysis of affinity for concanavalin A and erythroagglutinating phytohemagglutinin, the carbohydrate parts of H. Panc. K. are relatively rich in bi-(or multi-) antennary complex type sugar chains with bisecting GlcNAc compared with those of human salivary kallikrein and HUK. These findings will be a help to clarify the physiological and pathophysiological roles of H. Panc. K. in the pancreas and pancreatic diseases, especially in acute pancreatitis.

Carbohydrate Conformation↗

Renal lesions in Cockayne syndrome.

Two siblings with typical features of the Cockayne syndrome were studied at autopsy. Many glomeruli revealed a paucity of capillary loops and had thickened capillary walls. Some glomeruli with advanced lesions showed collapse of the glomerular tufts or complete hyalinization. Atrophy of tubules and interstitial fibrosis were also observed. There were no significant arteriosclerotic changes in the vessels. Ultrastructural studies demonstrated thickened glomerular basement membranes with bends and folds. These histopathological findings are different to those previously reported with the exception of the 1966 report by Ohno and Hirooka.

Basement Membrane↗

Clinical and virological observations on swine experimentally infected with Getah virus.

The pathogenicity of Getah virus for swine was examined. All 8 pigs (4 adults and 4 piglets) inoculated with Strains MIP-99 and MI-110 developed pyrexia ranging from 39.4 to 40.7 degrees C and anorexia. Mild depression and diarrhea were observed in 2 of the 4 piglets. These clinical signs were transient. Viremia occurred 1-2 days post-inoculation (p.i.) and the maximum titer was 10(3.0) TCID50 0.1 ml-1. The virus was recovered from a piglet autopsied on Day 3 p.i. from spleen and various lymph nodes. The maximum titer of virus (10(3.75) TCID50 0.1 g-1) was detected in the inguinal lymph node. Seroconversion was demonstrated in all the pigs on Day 6 p.i. These results suggest that Getah virus is mildly pathogenic for swine, which may play a role as an amplifying host in nature.

Alphavirus↗

Transplacental infection in mice inoculated with Getah virus.

Transplacental transmission was demonstrated in pregnant mice subcutaneously inoculated with Getah virus. Viremia was shown in the infected dams, and high-titered virus was detected in the placenta and later in the fetus, suggesting virus invasion of the fetus through hematogenous infection of the placenta. High-titered virus was shown in the fetal brain and muscle and in the brain of the young dying soon after birth. Intrauterine infection resulted in a reduction of the litter size, number of young born alive and survival rate to 1 week of age. These results were further corroborated by necropsy performed several days after virus inoculation. The stage of gestation at the time of virus inoculation greatly influenced these results. Dams inoculated at 12 days of gestation delivered all dead babies, whereas virus inoculation at 5 days of gestation had no effect on the number of young born alive. The dams inoculated at 8 days of gestation had reduced litter sizes and those inoculated at 16 days of gestation produced slightly fewer live babies. Gestational stage at the time of virus inoculation also influenced viral growth in fetuses and placentas. The infection rate was low in dams inoculated at 5 days of gestation, high in dams inoculated at 8 or 16 days of gestation and 100% in dams inoculated at 12 days of gestation. High-titered virus was shown in placentas and fetuses of the dams inoculated at 8, 12 or 16 days of gestation. These results suggest that Getah virus may readily cross the placental barrier through hematogenous infection of the placenta in mice.

Alphavirus↗

Pathogenicity for horses of original Sagiyama virus, a member of the Getah virus group.

Sagiyama virus is a member of the Getah virus group. Its pathogenicity for horses was examined. All the horses infected with the original 4 strains of Sagiyama virus (M6/Mag 33, Mag 121, Mag 132 and Mag 258) developed pyrexia ranging from 39.0 to 40.0 degrees C. Other clinical signs, characterized by eruptions, edema in the hind legs, enlargement of the submandibular lymph node and mild leukopenia, were also manifested. Viremia occurred 1-4 days post-inoculation (p.i.). Virus was recovered from spleen, liver, lung and various lymph nodes of a horse autopsied on Day 4 p.i. The maximum titer of virus (10(6.0) TCID50 g-1) was detected in the inguinal lymph node. Seroconversion was demonstrated in all the infected horses on Day 5 p.i. These clinical signs and virological findings were similar to those of horses infected naturally. The results indicate that Sagiyama virus has pathogenicity for horses and is similar to that of Getah virus.

Alphavirus↗