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Biomedical subjects

Y Endo

Publications and source records attributed to Y Endo.

At least 181 records · Page 10Linked to original sources
PubMed1999

Inhibition of inflammatory actions of aminobisphosphonates by dichloromethylene bisphosphonate, a non-aminobisphosphonate.

1. When injected intraperitoneally into mice in doses larger than those used clinically, all the amino derivatives of bisphosphonates (aminoBPs) tested induce a variety of inflammatory reactions such as induction of histidine decarboxylase (HDC, the histamine-forming enzyme), hypertrophy of the spleen, atrophy of the thymus, hypoglycaemia, ascites and accumulation of exudate in the thorax, and an increase in the number of macrophages and/or granulocytes in the peritoneal cavity of blood. On the other hand, dichloromethylene bisphosphonate (Cl2MBP) a typical non-aminoBP, has no such inflammatory actions. In the present study, we found that this agent can suppress the inflammatory actions of aminoBPs. 2. Cl2MBP, when injected into mice before or after injection of 4-amino-1-hydroxybutylidene-1,1-bisphosphonic acid (AHBuBP; a typical aminoBP), inhibited the induction of HDC activity by AHBuBP in a dose- and time-dependent manner. The increase in HDC activity induced by AHBuBP was largely suppressed by the injection of an equimolar dose of Cl2MBP. Cl2MBP also inhibited other AHBuBP-induced inflammatory reactions, as well as the inflammatory actions of two other aminoBPs. However, Cl2MBP did not inhibit the increase in HDC activity induced by lipopolysaccharide (LPS). 3. We have previously reported that AHBuBP augments the elevation of HDC activity and the production of interleukin-1beta (IL-1beta) that are induced by LPS. These actions of AHBuBP were also inhibited by Cl2MBP. 4. Based on these results and reported actions of bisphosphonates, the mechanisms underlying the contrasting effects of aminoBPs and Cl2MBP, a non-aminoBP are discussed. The results suggest that combined administration of Cl2MBP and an aminoBP in patients might be a useful way of suppressing the inflammatory side effects of aminoBPs.

Animals↗
PubMed1999

Enhancement by galactosamine of lipopolysaccharide(LPS)-induced tumour necrosis factor production and lethality: its suppression by LPS pretreatment.

1. D-Galactosamine (GalN) depletes UTP primarily in the liver, resulting in decreased RNA synthesis in hepatocytes. Co-injection of GalN and lipopolysaccharide (LPS) into mice produces fulminant hepatitis with severe hepatic congestion, resulting in rapid death. Although the underlying mechanism is uncertain, GalN enhances the sensitivity to tumour necrosis factor (TNF). Administration of uridine (a precursor of UTP) prior injection of either LPS itself or interleukin-1 (IL-1) reduces the lethality of GalN+LPS. The present study focused on the effects of these agents on TNF production. 2. Intraperitoneal injection of GalN+LPS into mice greatly elevated serum TNF. Although large doses of LPS alone also greatly elevated serum TNF, LPS itself induced neither hepatic congestion nor rapid death. Administration of a macrophage depletor, liposomes encapsulated with dichloromethylene bisphosphonate, reduced both the TNF production and mortality induced by GalN+LPS. 3. Uridine, when injected 0.5 h after the injection of GalN+LPS, reduced the production of TNF. Prior injection of LPS, but not of IL-1, also reduced this TNF production. 4. Serum from LPS-injected mice reduced the TNF production induced by GalN+LPS, but it was less effective at reducing the lethality. Its ability to reduce TNF production was abolished by heat-treatment. 5. We hypothesize that a factor inhibiting TNF production by macrophages is produced by hepatocytes in response to LPS. Possibly, production of this hepatocyte-derived TNF-down-regulator (TNF-DRh) may be: (i) inhibited by GalN, causing over-production of TNF by macrophages and (ii) stimulated by LPS-pretreatment (and restored by uridine), causing reduced TNF production.

Animals↗
PubMed1999

A time kinetic study of the effect of aminobisphosphonate on murine haemopoiesis.

We previously showed that aminobisphosphonates (aminoBPs), potent inhibitors of bone resorption, increased the number of osteoclasts and granulocytes, and enhanced the cell size of osteoclasts in vivo, indicating that aminoBPs have a profound effect on murine haemopoiesis. The possible effect of an aminoBP (4-amino-1-hydroxybutylidene-1,1-bisphosphonate; AHBuBP) on murine haemopoiesis in vivo was examined in more detail. Macroscopically, AHBuBP induced the whitened bone marrow (BM) and splenomegaly. Flow cytometric analysis indicated that in BM, AHBuBP reduced the number of mature monocyte-macrophage lineage cells and erythroid cells 1 and 2 d after treatment, respectively, whereas it enhanced granulopoiesis on day 4. In the spleen, both erythropoiesis and granulopoiesis were significantly increased. BM haemopoietic progenitors of granulocyte lineage and of monocyte-macrophage lineage (CFU-G, CFU-M and CFU-GM) were well maintained by the injection of AHBuBP, and even a small increment in these progenitors was observed 2-4 d after treatment. Immunohistochemical examination of BM demonstrated that residential macrophages of erythroblastic islands disappeared. Increased numbers of osteoclasts, as well as enlarged cell size, was confirmed up to 7 d after the treatment, implicating that the inhibition of bone resorption was not due to the reduced generation of osteoclasts by AHBuBP. These results suggest (1) that AHBuBP treatment in vivo rapidly deleted mature residential macrophages from BM, (2) that mature macrophages once deleted did not reappear even when CFU-M and CFU-GM increased in number and the number of Mac-1+/Gr-1- cells recovered to normal, (3) that BM erythropoiesis was significantly decreased due to the lack of erythroblastic islands, and (4) that compensatory erythropoiesis was evoked in the spleen to induce splenomegaly.

Animals↗
PubMed1999

Acute pancreatitis and parotitis induced by methimazole in a patient with Graves' disease.

A wide variety of adverse effects of methimazole (MMI) have been reported. Here we report a new MMI-induced disorder, acute pancreatitis and parotitis. Three weeks after a woman started MMI treatment for Graves' disease, she developed a high fever, painful parotid swelling and dull pain in the upper abdomen with elevation of the serum levels of salivary and pancreatic enzymes. These abnormalities disappeared soon after the withdrawal of MMI. However, the same abnormalities were rapidly provoked when MMI was reintroduced. Marked increases in the leucocyte count and CRP were also observed during these episodes. The possible mechanisms of MMI-induced pancreatitis/parotitis are discussed.

Acute Disease↗
PubMed1999

Multiple pulmonary leiomyomatous hamartoma with secondary ossification.

A 31-year-old woman presented with multiple pulmonary leiomyomatous hamartoma (MPLH) with secondary ossification. She had a past history of parosteal osteosarcoma. The pulmonary lesions were composed of spindle-shaped cells arranged in interlacing fascicles, among which glands or duct-like spaces were scattered. As some lesions contained bony tissues, it was unclear whether or not the pulmonary lesions were metastases of parosteal osteosarcoma. However, the majority of spindle-shaped cells were positive for alpha-smooth muscle actin, including cells proliferating around the bony tissues. Clonality analysis using a target of human androgen receptor (HUMARA) gene disclosed that the pulmonary nodules were polyclonal. These findings do not indicate that the lesions were metastatic. We would like to emphasize that MPLH can show osseous metaplasia.

Adult↗
PubMed1999

Ameloblastoma with basal cell carcinoma-like feature emerging as a nasal polyp.

A case of a 63-year-old man with ameloblastoma with basal cell carcinoma (BCC)-like features clinically emerging as a nasal polyp is reported. The left nasal cavity was filled with a solid mass, which seemed to be a sinusitis-associated nasal polyp. The polyp was covered by parakeratotic squamous epithelium which was directly connected to the BCC-like tumor nest. The BCC-like features gradually changed to adamantinoid features. The polyp was connected with a huge mass filling the maxillary sinus and the molar area, which consisted of conventional ameloblastoma features. Although the tumor was finally diagnosed as an ameloblastoma of the maxilla, the biopsy specimen forced us to face the problem of differential diagnosis, ameloblastoma with BCC-like features or adamantinoid basal cell carcinoma (BCC). Immunohistochemical examination revealed that tumor cells of the ameloblastoma reacted with anticytokeratin antibody KL-1 but not with antiepithelial antibody Ber-EP4, and these reaction patterns were completely contrary to those of BCC. It is emphasized that immunohistochemical examination using anticytokeratin antibody KL-1 and antiepithelial antibody Ber-EP4 is a good tool for distinguishing ameloblastoma with BCC-like features from adamantinoid BCC.

Ameloblastoma↗
PubMed1999

Mucinous carcinoma of the breast: a multifaceted study with special reference to histogenesis and neuroendocrine differentiation.

Although mucinous carcinoma (MC) of the breast is considered to originate from ductal carcinoma, it is not known whether mucinous growth begins in the intraductal carcinoma or later in the invasive carcinoma. In this study, 33 MC (16 pure without any ductal components, 10 mixed Type I with an intraductal component, seven mixed Type II with a common invasive ductal carcinoma (IDC) component)) were examined to clarify the time when mucinous growth begins. Histochemical and immunohistochemical examinations of mucin revealed that mucinous growth can begin in the intraductal carcinoma and in the common IDC. Histological transition and clonality analysis using microsatellite markers supported that some MC originate from common IDC. The pure type of MC probably originates from the intraductal carcinoma, showing a micropapillary feature. Neuroendocrine differentiation, known to be associated with MC, seemed to create the main progress in the typical MC. Moreover, we analyzed the factors of a worse prognosis of mixed MC Type II, which was strongly suggested by the lymph node status. However, no explainable differences on the cell proliferating ability, or c-erbB-2 and p53 protein overexpression were found.

Adenocarcinoma, Mucinous↗
PubMed1999

Proliferation of parathyroid cells negatively correlates with expression of parathyroid hormone-related protein in secondary parathyroid hyperplasia.

BACKGROUND: Parathyroid hormone-related protein (PTHrP) is now suspected to act as an autocrine or paracrine regulator of cell growth or differentiation, although it was originally reported as a hypercalcemic substance in malignancies. This study was performed to assess the relationship between PTHrP expression and cell proliferation in human parathyroid glands. METHODS: The localization of PTH and PTHrP was studied in 42 samples of hyperplastic parathyroid from 14 long-term hemodialysis cases with immunohistochemistry and in situ hybridization. Results were compared with proliferative activity (proliferating cell nuclear antigen index: counts of proliferating cell nuclear antigen-positive cells/100 cells). The localization of the PTH/PTHrP receptor was also examined. Ten normal glands were studied as controls. RESULTS: In hyperplasia, cells positive for PTH, PTHrP, or both were observed immunohistochemically. The areas expressing PTHrP mRNA completely coincided with those positive for PTHrP immunohistochemically. Oxyphilic or transitional oxyphilic cells were consistently positive for PTHrP. PTH/PTHrP receptors were located in the cytoplasmic membrane in most parathyroid cells. Proliferating cell nuclear antigen-positive cells were rare in normal glands with an index of 0. 22 +/- 0.09 (mean +/- sem). They were significantly increased in hyperplastic cases but less for PTHrP-positive than for -negative cells (1.25 +/- 0.16 as compared with 7.80 +/- 0.52; P < 0.0001). CONCLUSION: The observed low level of proliferation of PTHrP-positive cells suggests a functional role for PTHrP as a possible growth suppressor in the human parathyroid.

Adult↗
PubMed1999

Effects of bilateral jugular vein ligation on local cerebral blood flow.

The authors examined the effect of bilateral jugular vein ligation (JVL) on local cerebral blood flow (CBF). Local CBF was measured in the neocortex of the frontal lobe over a 1-week period in 10 freely moving male rats. Measurements were taken with the hydrogen clearance method before and after the rat underwent either an operation of bilateral JVL or a sham operation. After the sham operation, blood flow values did not change significantly compared with preoperative values. Blood flow values decreased rapidly in rats with JVL. For 3 hours after surgery, JVL values were significantly lower (p <0.05) than preoperative values were, then gradually they recovered and reached preoperative values within 48 hours. Histopathologic study showed no remarkable parenchymal damages in the brain of rats with JVL. These results show that bilateral JVL produces a reversible decrease in the CBF and does not cause histopathologic brain damages.

Journal Article↗
PubMed1999

A truncated form of mannose-binding lectin-associated serine protease (MASP)-2 expressed by alternative polyadenylation is a component of the lectin complement pathway.

The lectin complement pathway is initiated by binding of mannose-binding lectin (MBL) and MBL-associated serine protease (MASP) to carbohydrates. In the human lectin pathway, MASP-1 and MASP-2 are involved in the proteolysis of C4, C2 and C3. Here we report that the human MBL-MASP complex contains a new 22 kDa protein [small MBL-associated protein (sMAP)] bound to MASP-1. Analysis of the nucleotide sequence of sMAP cDNA revealed that it is a truncated form of MASP-2, consisting of the first two domains (i.e. the first internal repeat and the epidermal growth factor-like domain) with four different C-terminal amino acids. sMAP mRNAs are expressed in liver by alternative polyadenylation of the MASP-2 gene, in which a sMAP-specific exon containing an in-frame stop codon and a polyadenylation signal is used. The involvement of sMAP in the MBL-MASP complex suggests that the activation mechanism of the lectin pathway is more complicated than that of the classical pathway.

Amino Acid Sequence↗
PubMed1999

Mechanism of ribosome RNA apurinic site specific lyase.

A new enzyme, which we named ribosome RNA apurinic site specific lyase (RALyase), has been characterized. The enzyme specifically cleaves a phosphodiester bond at the apurinic site in the sarcin/ricin domain of 28S rRNA in ribosomes. The cut ends of wheat 28S rRNA were determined as 5'---GUACG-alpha-hydroxy-alpha, beta-unsaturated aldehyde and pGAGGA---3' for the 3' fragment, demonstrating that the enzyme catalyzes the beta-elimination reaction.

Apurinic Acid↗
PubMed1999

Radiation-induced inflammatory malignant fibrous histiocytoma of the ileum.

A case of inflammatory malignant fibrous histiocytoma of the ileum seemingly induced by radiation is described. A 50-year-old female with a past history of uterine cervical carcinoma and postoperative radiation therapy presented with abdominal pain, fever and leukocytosis. The subserosa of the distal part of the ileum showed a diffuse dense, neutrophilic and lymphocytic infiltrate with dispersed atypical, short spindle- or plump oval-shaped histiocyte-like cells. Pleomorphic mono- or multinucleated giant cells with bizarre nuclei were also intermingled in the lesion. Immunohistochemically, the tumorous atypical cells were positive for vimentin, alpha-smooth muscle actin, alpha-1 antitrypsin and granulocyte colony-stimulating factor. No EBV genomic sequences were detected by in situ hybridization. Flow cytometry showed an aneuploid DNA content with high S-phase fraction. The patient was well with no evidence of tumor at 5 months after surgery. It is important to include this type of tumor in the differential diagnosis of small intestinal lesions accompanied by fever and leukocytosis following radiation.

Female↗
PubMed1999

Complement-dependent accumulation and degradation of platelets in the lung and liver induced by injection of lipopolysaccharides.

We found unique behaviors among platelets within a few minutes of the intravenous injection of lipopolysaccharide (LPS) into mice. Platelets accumulated primarily in the liver at lower doses of LPS, but at higher doses they accumulated largely in the lungs. When the platelets accumulated in these organs were degraded, there was a rapid anaphylactoid shock. The platelet response depended on the strain of mouse and on the source of LPS. Of various LPSs tested, the LPS from the smooth type of Klebsiella O3 (KO3-S LPS) was the most potent at inducing the platelet response and shock. K-76 monocarboxylic acid, an inhibitor of complement C5, effectively prevented the KO3-S LPS-induced degradation (but not accumulation) of platelets and the ensuing rapid shock in BALB/c mice. Moreover, in DBA/2 mice (which are deficient in complement C5), platelets accumulated in the lungs and liver in response to KO3-S LPS but soon returned to the circulation without degradation, and there was no rapid shock. The LPS from the rough type of KO3 induced an accumulation of platelets in the liver and lungs but not a degradation of platelets. On the basis of these results and those reported by other investigators, we propose that in the platelet response to LPS, the lectin pathway to form C3 convertase from C4 and C2 is involved in the rapid accumulation of platelets in the liver and lungs and that the pathway from C5 to C9 is involved in the destruction of platelets and the consequent anaphylactoid shock.

Anaphylaxis↗
PubMed1999

Amino acid substitutions reveal distinct functions of serine 186 of the ZEBRA protein in activation of early lytic cycle genes and synergy with the Epstein-Barr virus R transactivator.

The ZEBRA protein mediates the switch between the latent and lytic life cycles of Epstein-Barr virus. Z(S186A), a point mutant in ZEBRA's basic domain in which serine 186 is changed to alanine, is unable to induce expression of lytic cycle mRNAs or proteins from the latent EBV genome even though it retains the ability to activate transcription from reporters bearing known ZEBRA-responsive promoters (A. L. Francis et al., J. Virol. 71:3054-3061, 1997). We now describe three distinct phenotypes of ZEBRA mutants bearing different amino acid substitutions at S186. These phenotypes are based on the capacity of the mutants to activate expression of the BRLF1 and BMRF1 genes, which are targets of ZEBRA's action, and to synergize with the BRLF1 gene product Rta (R transactivator) in activating expression of downstream genes. One mutant class, represented by Z(S186T), was similar to the wild type, although reduced in the capacity to activate BRLF1 and BMRF1 early lytic cycle genes from the latent virus. A second class, represented by Z(S186C) and Z(S186G), was impaired in transcriptional activation, unable to activate early lytic cycle products from the latent virus, and not rescued by overexpression of Rta. A third class, Z(S186A), although unable by itself to activate BRLF1 or other lytic cycle genes, synergized with Rta. Rta rescued the capacity of Z(S186A) to activate the BMRF1 early lytic cycle gene from the latent virus. All mutant classes bound to DNA in vitro, although their capacity to bind to different ZEBRA response elements varied. Serine 186 of ZEBRA is a critical residue that is required for the distinct activities of induction of BRLF1 expression and for synergy with Rta. Since only Z(S186T) among the mutants behaved similarly to the wild type, activation of BRLF1 likely requires phosphorylation of S186. However, since Z(S186A) could synergize with Rta, synergy with Rta does not appear to be dependent on phosphorylation of S186. S186 likely mediates DNA recognition on the BRLF1 promoter in the context of the latent virus, protein-protein interactions, or both. The Z(S186) mutants define the amino acid side chains required for these functions.

Antigens, Viral↗
PubMed1999

Interspecies transmission of feline immunodeficiency virus from the domestic cat to the Tsushima cat (Felis bengalensis euptilura) in the wild.

Feline immunodeficiency virus (FIV) was isolated from a wild-caught Tsushima cat (Felis bengalensis euptilura), an endangered Japanese nondomestic subspecies of leopard cat (F. bengalensis). Phylogenetic analysis of the env gene sequences indicated that the FIV from the Tsushima cat belonged to a cluster of subtype D FIVs from domestic cats. FIVs from both the Tsushima cat and the domestic cat showed similar levels of replication and cytopathicity in lymphoid cell lines derived from these two species. The results indicated the occurrence of interspecies transmission of FIV from the domestic cat to the Tsushima cat in the wild.

Amino Acid Sequence↗
PubMed1999

Human and mouse GPAA1 (Glycosylphosphatidylinositol anchor attachment 1) genes: genomic structures, chromosome loci and the presence of a minor class intron.

Many eukaryotic cell surface proteins are anchored to the membrane with glycosylphosphatidylinositol (GPI) that is covalently linked to the carboxyl-terminus. A Saccharomyces cerevisiae gaa1 mutant is defective in posttranslational attachment of GPI to proteins. A recent report demonstrated that the GPAA1 gene encodes a component of a transamidase that mediates GPI-anchor attachment. Here, we report structures and chromosome loci of human and mouse GPAA1 genes. Both genes consist of twelve exons that span about 4 kb. Human and mouse GPAA1s are located at 8q24.3 and 15E, respectively. There is a human pseudo GPAA1 gene (GPAA1P1) that is located at 2q12-->q14. Introns 8 of human and mouse GPAA1s were minor class introns bearing AT at the 5' splice sites and AC and AT at the 3' splice sites, respectively. The 3' splice sites of corresponding introns of African green monkey, Chinese hamster, dog and rat were AC, AT, AT and AA, respectively. The mouse GPAA1 gene (Gpaa1) bearing AG at the 3' splice site prepared by site-directed mutagenesis was functional, indicating that any nucleotide is allowed at the 3' end of a minor class intron.

Animals↗
PubMed1999

Possible involvement of histamine in muscular fatigue in temporomandibular disorders: animal and human studies.

As an approach to clarifying the molecular basis of pain and fatigue in muscles involved in temporomandibular disorders, we examined the activity of histidine decarboxylase (HDC), the enzyme which forms histamine, in the masseter muscles of mice. In the resting muscle, HDC activity was very low. Direct electrical stimulation of the muscle markedly elevated HDC activity. HDC activity rose within 3 hrs of the electrical stimulation, peaked at 6 to 8 hrs, and then gradually declined. Intraperitoneal injection of a small amount of interleukin-1 (IL-1) (from 1 to 10 microg/kg) produced a similar elevation of HDC activity in the masseter muscle. We also examined the effect of an antihistamine, chlorphenylamine (CP), on temporomandibular disorders in humans and compared it with that of an anti-inflammatory analgesic, flurbiprofen (FB). Two groups received one or the other of the drugs daily for 7 days, and they were asked about their signs and symptoms before and after the treatment. A positive evaluation of their treatment was made by 74% of the CP group, but by only 48% of the FB group. Although the effects of CP on the limitation of mouth-opening and on joint noise were negligible, about 50% of the CP group answered positively concerning the drug's effect on spontaneous pain or pain induced by chewing or mouth-opening. The positive evaluation for CP (50%) in relieving associated symptoms (headache or shoulder stiffness) was significantly greater than for FB (13%). FB showed effectiveness similar to but sometimes weaker than that of CP on several symptoms. On the basis of these and previous results and the known actions of histamine, we propose that the histamine newly formed following the induction of HDC activity, which is itself mediated by IL-1, may be involved in inducing pain and, possibly, stiffness in muscles in temporomandibular disorders.

Adult↗