Failure of auto-infection with Hymenolepis nana in seven inbred strains of mice initially given beetle-derived cysticercoids.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to A Ito.
Explore the source record for details and available documents.
Effects of prostaglandins on the production of collagenase by rabbit uterine cervical fibroblasts were investigated. Exogenous prostaglandin E2 (PGE2) and PGF2 alpha significantly stimulated the production of collagenase in a dose dependent manner, whereas PGI2 did not. Addition of arachidonic acid in the presence of absence of indomethacin to the cell culture did not show any increase in collagenase production. Recombinant human interleukin-1 (rhIL-1) also promoted the production of cervical collagenase independently of endogenous prostaglandin(s). Furthermore both exogenous PGE2 and PGF2 alpha enhanced the rhIL-1-induced collagenase production whereas PGI2 and/or indomethacin did not. These results suggested that exogenous PGE2 and PGF2 alpha but not endogenous prostaglandin(s) participate in cervical ripening and dilation by enhancing collagenase production by rabbit uterine cervical cells.
We investigated functional aspects of splenic dendritic cells (DC) obtained from MRL/MpJ-lpr/lpr (MRL/l) mice, and their normal counterparts, MRL/MpJ-+/+ (MRL/+) mice. In vitro antigen-presenting activity of DC obtained from MRL/l mice was impaired compared with that of DC from MRL/+ mice. Another major functional aspect of DC, i.e., stimulator cell activity in the allogeneic mixed lymphocyte reaction (MLR), was also found to be impaired in MRL/l mice. MRL/l mice and MRL/+ mice were also examined for co-operation between macrophages (M luminal diameter) and DC. We found peritoneal resident M luminal diameter obtained not only from MRL/+ mice but also from MRL/l mice released a soluble factor which enhanced the activity of DC from the respective mice. Furthermore, DC from both MRL/l and MRL/+ mice responded to the culture supernatant of a mouse macrophage hybridoma clone, S44, which releases a factor that enhances the antigen-presenting activity of DC, and their activity as stimulator cells in the allogeneic MLR was enhanced. However, the degree of enhancement was less in MRL/l mice than in MRL/+ mice.
Chromosome analysis using peripheral lymphocytes is a sensitive and reliable indicator of the biological effect of radiation at low radiation doses. In the present study, using this chromosome aberration analysis, we tried to investigate the radiation dose distribution within and around the radiation field of a 6 MeV neutron beam. The efficient induction of dicentrics and rings at the irradiation of neutrons compared to those of gamma or X rays especially in a lower dose range, results in a dominant linear component in the linear quadratic model in the dose response relation of a chromosome aberration formation. A marked increase of RBE (relative biological effectiveness) in a lower dose range of neutrons was demonstrated. The radiation doses of the neutron beam as a function of depth, estimated from the yields of dicentrics and rings in a water phantom revealed a fairly good agreement with doses that were physically obtained. The radiation portal margin of the neutron beam was demonstrated to be not as sharp due to a wide penumbra. This wide penumbra and high RBE value, especially at lower dose range of the neutron beam may contribute to the induction of secondary malignancies in the normal tissue surrounding the tumor mass.
An antigen histochemically localized in the nuclei and cytoplasmic granules of normal and leukemic human myeloid cells has been identified as myeloperoxidase (MPO; EC 1.11.1.7). The localization and amount of the enzyme was determined by using a murine monoclonal antibody designated H-43-5 raised against nuclear proteins derived from human promyelocytic HL-60 leukemia cells. The highest amount of nuclear MPO (3.5 micrograms per 10(6) nuclei) was found in granulocytes; less than half of this amount was detected in nuclei from HL-60 cells. Still lower levels were found in nuclei from monocytes and a series of human monomyelocytic leukemia cells. MPO from HL-60 cells was purified by immunoaffinity chromatography and fractionated into three components (forms I, II, and III) by CM-cellulose chromatography. Chromatography of these MPO forms on DNA-Sepharose columns confirmed that all three forms of MPO were tightly bound to DNA with apparent relative affinities in the order of form III greater than form II greater than form I. The affinity of MPO form III for DNA was sufficient to enable the formation and elution of DNA-MPO complexes during size-exclusion chromatography at high ionic strength and neutral pH. This form of MPO was also able to shield DNA from strand scission induced by active oxygen species generated by xanthine oxidase acting aerobically on xanthine. These data suggest that intranuclear MPO may help to protect DNA against damage resulting from oxygen radicals produced during myeloid cell maturation and function.
N-Methyl-N'-nitro-N-nitrosoguanidine (MNNG) dissolved in distilled water (5 g/l) was administered orally once by gastric tube at a dose of 0.25 ml/10 g body weight to 5-day-old or 28-day-old Wistar Furth (W/Fu) or ACI rats. Gastric tumors in the glandular stomach were found in 58% of 5-day-old ACI rats, but none were found in the rest of the groups. Forestomach tumors were found in both strains of rats at both age groups with incidences of 68-100%. Lung tumors were induced in 64% of 5-day-old and 6% of 28-day-old W/Fu rats, but not in ACI rats. Besides the tumors, a high frequency of hepatic cysts was also noted in ACI rats. Intestinal metaplastic foci with alkaline phosphatase activity were found in the group of 5-day-old ACI rats and none in the rest of the groups. The results showed that the incidences and the locations of tumors in rats induced by MNNG are greatly influenced by both strain and age.
In vitro synthesized precursors of several mitochondrial proteins, including P-450(SCC), adrenodoxin, and malate dehydrogenase, bound to liposomes prepared from mitochondrial phospholipids, but not to those from microsomal phospholipids. When liposomes were prepared from various pure phospholipids, adrenodoxin precursor was bound only to the liposomes that contained cardiolipin. The liposomes containing other phospholipids did not show the binding affinity for the precursor. The binding was observed only with the precursor peptides of adrenodoxin and malate dehydrogenase, and their mature forms were not bound to the liposomes. The binding of the precursors was dependent on the concentration of cardiolipin in the liposomes. Liposomes containing various cardiolipin derivatives with modified polar head groups showed very different binding affinity for adrenodoxin precursor, suggesting the importance of the structure of the polar head of the cardiolipin molecule. Two or three positively charged amino acid residues in the extension peptide of P-450(SCC) precursor were replaced by neutral amino acid residues by site-directed mutagenesis. The mutated P-450(SCC) precursors did not bind to the liposomes containing cardiolipin. The results indicated that mitochondrial protein precursors have specific affinity for cardiolipin, and the affinity was due to the interaction between the extension peptides of the precursors and the polar head of the cardiolipin molecule.
The production from murine resident peritoneal macrophages (M phi) of a soluble factor, which was capable of enhancing the antigen-presenting (AP) function of dendritic cells (DC), was examined. The supernatants of peritoneal M phi (M phi sup) were prepared by culturing peritoneal M phi with particles, i.e., zymosan A, latex, and sheep red blood cells (SRBC), or antigen-antibody (Ag-Ab) complexes such as keyhole limpet hemocyanin (KLH)-anti-KLH, ovalbumin (OVA)-anti-OVA, and SRBC-anti-SRBC complexes. When exposed to M phi sup during antigen pulsing DC induced a marked antigen-specific T cell proliferation, relative to DC treated with the supernatants from M phi cultured without stimuli (control sup). On the other hand, M phi sup-treated splenic M phi stimulated antigen-specific T cell activation to almost the same extent as did splenic M phi treated with control sup. These results indicated that peritoneal M phi elaborated a soluble factor which preferentially enhanced the AP capacity of DC when stimulated with particles or Ag-Ab complexes. Analytical gel filtration of M phi sup revealed that the factor had an apparent molecular weight of 27,000 daltons which was distinct from interleukin 1.
A mouse macrophage (M phi) hybridoma which produces a soluble factor responsible for the cooperation between M phi and spleen dendritic cells (DC) was constructed. The antigen-presenting activity and the stimulator cell activity in the allogeneic or syngeneic mixed leukocyte reaction of DC were significantly augmented when DC were incubated with the culture supernatant of the hybridoma treated with various stimulants including latex beads. The monokine present in the culture supernatant of the hybridoma, called dendritic cell-activating factor (DCAF), augmented the production of lymphocyte-activating factor by DC while Ia expression of DCAF-treated DC was not altered. DCAF had no effect on the antigen-presenting activity of peritoneal resident M phi or B cell blasts while the antigen-presenting activity of spleen M phi was enhanced, but the degree of the enhancement was much less than that of spleen DC. DCAF was found to have the following properties: its pI value is between pH 4 and 5; it is stable at pH 2 to 10; and it loses its activity on incubation at 75 C for 30 min. When the culture supernatant of the hybridoma stimulated with latex beads was subjected to gel filtration, the DCAF activity was detected in the 20 Kd to 25 Kd, 30 Kd to 40 Kd, and 50 Kd to 60 Kd molecular weight regions. The 30 Kd to 40 Kd fraction, which is the major peak fraction, was further purified by ion-exchange chromatography followed by gel-filtration chromatography. When each fraction was subjected to SDS-PAGE, a 30 Kd band corresponding to the DCAF activity was observed and DCAF was purified to about 90% purity.
Serum antibody responses in two strains of mice infected with embryonated eggs of Hymenolepis nana were analysed by the enzyme-linked immunosorbent assay (ELISA) and immunoprecipitation (IP) using sodium deoxycholate (DOC)-solubilized antigens prepared from embryonated eggs (eggs), mouse-derived cysticercoids (cysts) and adult tapeworms with immature segments only (adults). Highly susceptible dd mice, which harbour mature tapeworms for a long period (greater than 70 days), produced high levels of antibodies to all three different stages of H. nana. BALB/c mice, almost all of which expel adult tapeworms by 30 days after infection, produced high levels of antibody against egg antigens only. The high antibody titres to cyst and adult antigens in dd mice did not lead to expulsion of the worms. However, worms are rejected early in BALB/c mice when there is little or no detectable serum antibody. The antibody responses to eggs seen in BALB/c mice which had long since shed their adult worms were probably due to ingestion of eggs from faeces of other infected mice. Antibodies to eggs were not detected in BALB/c mice which were initially inoculated with eggs (day 0) and then treated with praziquantel on day 6 after the tissue phase of infection only. The different antibody responses to egg antigens and the other two antigens (cyst and adult) in BALB/c mice suggest a difference in antigen specificity between eggs and both cysts and adults. A major antigen component with Mr 32,000 appears to be specific to the egg (or oncosphere) stage of H. nana. Antibody to this major component of eggs was absorbed only with intact eggs, but not with intact cysts nor adults with immature segments only, so that the antigen appears to be on the surface of the oncosphere.
The influence of ranitidine and cysteamine on intestinal metaplasia was examined in 7-month-old male Crj: CD (SD) rats. At the age of 5 weeks, the animals were treated with 10 Gy doses of X-rays at 3-day intervals up to a total of 20 Gy in the gastric region, and 6 months after irradiation, the rats received either ranitidine (0.02% in diet) or cysteamine (0.1% in drinking water) for 2 months. The incidence and number of intestinal metaplasia with alkaline phosphatase-positive foci in rats given X-rays and cysteamine (group 4) were significantly low compared with those in rats given X-rays and ranitidine (group 3) (p less than 0.01). In both the pyloric and the fundic gland mucosae, the average numbers of type C metaplasia (intestinal crypts with Paneth cells) and total numbers of metaplastic foci in rats of group 3 were much higher than those in group 4 (P less than 0.05). The present results showed that the occurrence of intestinal metaplasia was significantly increased after administration of ranitidine and decreased by cysteamine.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
To define the clinical significance of T wave map changes in patients with angina at rest, body surface isopotential T distributions were obtained in 48 patients with single-vessel disease (left anterior descending artery, 34; right coronary artery, eight; left circumflex artery, six) documented angiographically and were compared with those in 120 healthy subjects and those in 19 patients with left ventricular overload whose electrocardiograms showed negative T waves accompanied by an increase in R wave amplitude in left precordial leads. The T wave map abnormalities were observed in 24 of 48 patients (50%) with angina and were classified into three types: (1) type I (18 patients, 37.5%) was characterized by a segmental negative potential in the positive area located at the left thorax and the minimum at the peak of T wave positioned in the upper portion of the left anterior chest, (2) type II (three patients, 6.3%) was characterized by a negative potential with a minimum in the inferior thorax and an indentation of negative potential at the lower margin of the positive potential located over the upper thorax, and (3) type III (three patients, 6.3%) was characterized by a negative potential with a minimum at the back throughout the period of T wave. All patients showing T wave map abnormalities of type I had a significant stenosis of the left anterior descending artery. Likewise, all patients with type II or III had single-vessel disease of the right coronary or left circumflex artery, respectively. All types of T wave map changes observed in patients with angina were different from those in patients with left ventricular overload, whose maps showed the generalized negative potential at the inferior thorax and the left back and the minima clustered at the precordium. In seven patients with lesions of the left anterior descending artery, T wave map abnormalities of type I recovered to normal after successful percutaneous transluminal coronary angioplasty. The behavior of the negative potential and its extrema on the T wave map, which was not available from routine electrocardiography, was indicative of the involved coronary artery and probably of its associated ischemic area in one-half of our patients with angina pectoris.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
We report on an autopsy case of cholangiocarcinoma associated with Caroli's disease. A 38-year-old woman was admitted to our hospital suffering from epigastralgia. A diagnosis of Caroli's disease was made after CT, US, and ERCP testing. Because of diffuse intrahepatic bile duct dilatation, the patient was treated with antibioticus. In August 1985, her CA 19-9 level was 3,800 U/ml. This data suggested the development of a carcinoma secondary to Caroli's disease, but no tumor in the liver had been detected in the US and CT examinations. The patient died on February 1, 1986, of hepatorenal failure, approximately seven years after her first admission. An autopsy revealed diffuse dilatation of the intrahepatic bile duct (Caroli's disease) with a cholangiocarcinoma.