Biomedical subjects

M Sugimoto

Publications and source records attributed to M Sugimoto.

At least 271 records · Page 15Linked to original sources

PubMed1992

A novel leukotriene antagonist, ONO-1078, inhibits and reverses human bronchial contraction induced by leukotrienes C4 and D4 and antigen in vitro.

ONO-1078, 4-oxo-8(-)[p-(4-phenylbutyloxy)benzoylamino]-2-(tetrazol-5-y l)-4H-1-benzopyran hemihydrate, is a novel compound that has been shown to be a leukotrienes C4 and D4 (LTC4, LTD4) antagonist in the guinea pig airways. We studied the ability of ONO-1078 to inhibit and reverse the contraction of isolated human bronchus induced by LTC4, LTD4, and antigen. The human bronchial tissues were prepared from patients undergoing surgery for lung cancer, and they were placed in organ baths. ONO-1078 (10(-8) to 10(-6) M) produced a concentration-dependent inhibition of LTC4 and LTD4 concentration-response curves. In the presence of l-serine borate complex, which inhibits the conversion of LTC4 to LTD4 by gamma-glutamyl transpeptidase, ONO-1078 significantly inhibited the LTC4-induced contraction, suggesting that ONO-1078 is an antagonist of both LTC4 and LTD4. ONO-1078 (10(-6) M) also significantly reversed an ongoing contraction induced by LTC4 (10(-7) M). The inhibitory effect of ONO-1078 on LTC4-induced contraction was at least 100 times more potent than that of FPL 55712, the first discovered LTC4 and LTD4 antagonist. To study the effect of ONO-1078 on the contraction induced by antigen challenge, bronchial tissues were incubated for 2 h with serum of high specific IgE against house dust from an asthmatic patient. House dust antigen was added to the sensitized bronchial tissues after incubation with ONO-1078 (10(-6) M) or histamine H1 antagonist pyrilamine (10(-6) M), either alone or in combination.(ABSTRACT TRUNCATED AT 250 WORDS)

Antigens↗

PubMed1992

The distribution of tissue insulin receptors in the mouse by whole-body autoradiography.

The distribution of insulin binding sites in the mouse was investigated by in vivo whole-body autoradiography. Male mice were injected intravenously with 125I-insulin in the absence of and, in the presence of, excess unlabeled insulin. Three, 6, 15, 30 and 60 minutes after injection, the animals were perfused and subjected to autoradiographic procedures. Specific insulin binding was observed in the choroid plexus, liver, gastrointestinal tract, spleen, pancreas, deferent duct, and Harderian gland. In the liver and spleen, the distribution of binding sites was heterogeneous. In the liver, the density of the binding was higher around the branches of the portal vein than around the central vein. In the spleen, the marginal zone exhibited a higher density than the white and red pulp. The kidney cortex, and the thyroid gland showed a high degree of insulin binding, but the binding was nonspecific. The binding of insulin to other tissues and organs, including the skeletal muscle and fat, was weak, and most of the binding was nonspecific.

Animals↗

PubMed1992

[Clinical analysis of multiple primary cancers associated with bladder cancer].

Among 321 bladder cancer cases from 1975 to 1989, 43 cases (13.4%) were found to have multiple primary cancers (MPC) and 278 cases without MPC (86.6%). These two groups were compared with regard to their clinical and pathological features. Mean age of patients when the bladder cancer was diagnosed was 68.9 +/- 8.9 in MPC cases and 65.7 +/- 12.3 (mean +/- S.D.) in cases without MPC. The male to female ratio was 3.8 to 1 and 2.6 to 1, respectively. The common sites of MPC were the lung, stomach and rectum, all of them being the organs often involved with cancer. Prostatic cancers in eight of 12 MPC cases were incidentally found in total cystectomy specimens. The sites of the synchronous and metachronous MPC involving lung, stomach and rectum cancers showed relatively even distribution. In males, the most common synchronous MPC included prostatic cancer, but in females, the diagnosis of uterine cancer tended to be made prior to the diagnosis of bladder cancer. In two cases, there was a strong suspicion that the therapy for the first cancer contributed to the occurrence of the second cancer. In the present study, no significant differences were noted with regard to clinicopathological characteristics of bladder cancer between the group with MPC and that without MPC. The five years survival rates from the beginning of bladder cancer treatment were 48.8% and 64.9%, respectively, indicating that the prognosis of the MPC cases was significantly worse (p less than 0.05) than that of cases without MPC. The most common cause of death in MPC cases was due to cancers other than bladder (36%).(ABSTRACT TRUNCATED AT 250 WORDS)

Female↗

PubMed1992

Is necrosis induction therapy relevant to hepatocellular carcinoma? Prognostic evaluation viewed from necrosing feature in HCC occluding the main portal vein after treatment with DBcAMP and MMC.

Intraarterial infusion therapy combining dibutyryl adenosine 3',5'-monophosphate and mitomycin C was administered to 27 patients with hepatocellular carcinoma (HCC) occluding the main portal vein. Twelve patients (44%) survived more than 6 months, among them nine (75%) whose tumors were non-necrosing before treatment. When patients were compared for the presence or absence of necrosis in the tumor, those with necrosis responded poorly to treatment; only 3 of 11 (27%) survived more than 6 months. Although the combination therapy exerted a salutary effect on HCC occluding the main portal vein, the presence of necrosis in the tumor was an unfavorable sign for the prognosis, which casts doubt upon the use of the necrosis-inducing method for the treatment of HCC.

Adult↗

PubMed1992

Long-lasting tolerance of articular cartilage after experimental intraoperative radiation in rabbits.

In experimental intraoperative irradiation, 18 adult rabbits received a single, 50-Gy dose of x-radiation at a unilateral knee joint, and subsequent changes in the articular cartilage were examined over a 15-month period by histology, scanning electron microscopy, and autoradiography. Although the subchondral bone showed histologically typical findings of osteonecrosis three to nine months postirradiation, the articular cartilage revealed no obvious degenerative changes during the entire study period. Scanning electron microscopy revealed normal collagen architecture in the irradiated cartilage for as long as 15 months postirradiation. Autoradiography demonstrated active RNA synthesis by the irradiated chondrocytes during the same period. These results indicate that articular cartilage tissue tolerates intraoperative radiotherapy without sustaining serious degenerative changes, unless possible collapse or contracture disturbs its biomechanical integrity. The survival of articular cartilage can be advantageous for this type of limb-salvage surgery in the treatment of malignant bone tumors around a synovial joint.

Animals↗

PubMed1992

[Seasonal variation of intraocular pressure after trabeculotomy].

The author reviewed the seasonal variation of intraocular pressure (IOP) in primary open angle glaucoma or late type developmental glaucoma to investigate possible relationships among seasonal variation of IOP, progression of visual field defects and the follow-up period between 53 eyes of 39 subjects with successful trabeculotomy (trabeculotomy group) and 45 eyes of 31 subjects with only medication (no operation group). IOPs in both groups were inclined to be low in summer and high in winter. Maximum seasonal variation of IOP and standard deviation of IOP during all follow-up periods which showed the degree of seasonal variation of IOP had no significant difference between the trabeculotomy group and the no operation group. These results showed that seasonal variation of IOP was not reduced even by successful trabeculotomy. The maximum seasonal variation of IOP and standard deviation of IOP had a tendency to be bigger in cases with progression of visual field defects than in cases with no progression of visual field defects, in both groups. Therefore, seasonal variation of IOP may be an important factor influencing the progression of visual field defects.

Follow-Up Studies↗

PubMed1992

[A case of bucillamine-induced interstitial pneumonia].

Bucillamine [N-(2-mercapto-2-methylpropionyl)-L-cysteine] is an anti-rheumatic drug which was developed in Japan. Interstitial pneumonia induced by bucillamine has been reported in two patients with rheumatoid arthritis. In this report, we describe another patient who developed bucillamine-induced interstitial pneumonia. In August 1990, a 53-year-old man was admitted because of fever, dry cough and dyspnea on exertion (DOE). Five months previously, he had noted polyarthritis, and treatment with bucillamine was started in May 1990. His polyarthritis improved about 2.5 months after starting bucillamine, but he developed fever, dry cough, and DOE in August 1990. Chest X-ray on admission showed diffuse acinar and interstitial shadows predominantly in the bilateral upper lung fields. Pulmonary function tests revealed decreased vital capacity and diffusing capacity. Arterial blood gas (ABG) analysis revealed moderate hypoxemia with PaO2 67 Torr. After stopping bucillamine, the fever, dry cough, and DOE improved gradually, and the abnormal shadows on chest X-ray and ABG analysis showed moderate improvements. Bronchoalveolar lavage studies showed that total cell counts and proportion of lymphocytes were increased, and CD4+/CD8+ ratio of T cell subsets was decreased to 0.56. Transbronchial lung biopsy specimen revealed lymphocytic alveolitis and mild interstitial thickening. Lymphocyte stimulation test to bucillamine was negative, but patch test with bucillamine was positive. From the patient's clinical course, laboratory data, and pathologic findings, we concluded that this is a case of bucillamine-induced interstitial pneumonia. After treatment with corticosteroid, his chest X-ray and pulmonary function test showed marked improvements.(ABSTRACT TRUNCATED AT 250 WORDS)

Anti-Inflammatory Agents, Non-Steroidal↗

PubMed1992

[A case of intractable hemoptysis due to malignant hemangioendothelioma].

A 65-year-old man who died of respiratory failure due to malignant hemangioendothelioma is reported. He was admitted to our hospital because of intractable hemoptysis. Chest roentgenogram revealed multiple patchy shadows in both lungs, but we could not make a diagnosis by usual clinical examinations including transbronchial lung biopsy. Since the patient's condition became critical, oxygen therapy, anticoagulants and antibiotics were started. In addition, corticosteroid therapy and double filtration plasmapheresis were performed since immunological disorder was suspected because of positive immunological examinations such as antinuclear antibodies and an increase in circulatory immune complexes. There was little response to the treatments and the patient finally died of respiratory failure. At autopsy, multiple tumor nodules were found throughout the lungs and the liver. Metastasis to mediastinal lymph nodes was also discovered. These findings made it impossible to confirm the primary lesion. Microscopy showed proliferation of anastomosing capillaries encasing tumor cells of unknown origin. Silver staining demonstrated capillaries encompassing the atypical cells, suggesting a vascular origin of the tumor. Furthermore, factor VIII related-antigen in the tumor cells was confirmed by the peroxidase-antiperoxidase (PAP) method. The final diagnosis of malignant hemangioendothelioma was made from these histological findings. Malignant hemangioendothelioma is rare, but is an important cause of intractable hemoptysis.

Aged↗

PubMed1992

[Pathogenesis of T-lymphocyte alveolitis associated with HTLV-I infection].

Pulmonary involvement has been demonstrated in patients with spastic myelopathy associated with HTLV-I infection (HAM/TSP). Pulmonary lesions in these patients are characterized by T-lymphocytosis and increased level of soluble IL-2 receptor in bronchoalveolar lavage fluid. T-lymphocytes from peripheral blood and bronchoalveolar lavage fluid proliferated spontaneously and released IL-2 and IL-2 receptor when cultured in vitro. Spontaneous proliferation of T-lymphocytes was also found in HTLV-I carriers without myelopathy, but less intensely than in HAM/TSP patients. Interestingly, HTLV-I-infected cells were markedly increased in bronchoalveolar lavage fluid from HAM/TSP patients compared to HTLV-I carriers without myelopathy. These results suggest that T-lymphocyte activation and increased HTLV-I-infected cells play an important role in the pathogenesis of pulmonary involvement in patients with HAM/TSP.

Carrier State↗

PubMed1991

Inhibition of prostaglandin production in the inflammatory tissue by loxoprofen-Na, an anti-inflammatory prodrug.

The effect of loxoprofen-Na, a novel non-steroidal anti-inflammatory drug with a prodrug property, on prostaglandin (PG) levels in the inflammatory tissue was investigated with a carrageenin-induced pleurisy model in rats. The intrapleural injection of carrageenin caused a marked increase in the levels of PGE2 and 6-keto-PGF1 alpha in the pleural exudate up to 3 hr after the injection. When [14C]PGE2 was injected into the cavity 2 hr after the carrageenin injection, the PG rapidly disappeared from the cavity (T 1/2 = 5 min). Thus, the PG level determined in the inflammatory exudate represents PG produced in the inflammatory tissue. Loxoprofen-Na, administered orally 2 hr after the carrageenin injection, dose-dependently inhibited the increase in the levels of PGs in the exudate 1 hr after administration (ID50 = 0.07 mg/kg for PGE2 and 0.10 mg/kg for 6-keto-PGF1 alpha). Indomethacin also inhibited PG production, but was less effective (ID50 = 0.24 mg/kg for PGE2 and 0.47 mg/kg for 6-keto-PGF1 alpha). Similar results were obtained 3 hr after the administration of these drugs (ID50 of PGE2 production = 0.14 mg/kg for loxoprofen-Na and 0.28 mg/kg for indomethacin). The time-course analysis of the effect of loxoprofen-Na showed that this drug had more immediate and stronger inhibitory activity than indomethacin. The relative potencies of suppression of protein leakage and leukocyte infiltration correlated well with the inhibition of PG production, but higher doses were needed for an obvious anti-inflammatory effect. The active metabolite (SRS trans-OH) of loxoprofen-Na determined in the inflammatory exudate 1 hr after oral administration of 0.2 and 2 mg/kg of loxoprofen-Na was 0.05 and 0.25 micrograms/mL, respectively. The concentration was sufficient to suppress PG production in the exudate, because the IC50 of the SRS trans-OH for PG production in vitro with leukocytes was 0.02 microgram/mL (0.01 microM). The potency of the SRS trans-OH metabolite to inhibit PGE2 production in leukocytes was about 20 times stronger than that of the parent compound and 3 times stronger than that of indomethacin.

6-Ketoprostaglandin F1 alpha↗

PubMed1991

Factor IX Amagasaki: a new mutation in the catalytic domain resulting in the loss of both coagulant and esterase activities.

Factor IX Amagasaki (AMG) is a naturally occurring mutant of factor IX having essentially no coagulant activity, even though normal levels of antigen are detected in plasma. Factor IX AMG was purified from the patient's plasma by immunoaffinity chromatography with an anti-factor IX monoclonal antibody column. Factor IX AMG was cleaved normally by factor VIIa-tissue factor complex, yielding a two-chain factor IXa. Amino acid composition and sequence analysis of one of the tryptic peptides isolated from factor IX AMG revealed that Gly-311 had been replaced by Glu. We identified a one-base substitution of guanine to adenine in exon VIII by amplifying exon VIII using the polymerase chain reaction method and sequencing the product. This base mutation also supported the replacement of Gly-311 by Glu. In the purified system, factor IXa AMG did not activate factor X in the presence of factor VIII, phospholipids, and Ca2+, and no esterase activity toward Z-Arg-p-nitrobenzyl ester was observed. The model building of the serine protease domain of factor IXa suggests that the Gly-311----Glu exchange would disrupt the specific conformational state in the active site environment, resulting in the substrate binding site not forming properly. This is the first report to show the experimental evidence for importance of a highly conserved Gly-142 (chymotrypsinogen numbering) located in the catalytic site of mammalian serine proteases so far known.

Amino Acid Sequence↗

PubMed1991

Isolation and sequence of rat testis cDNA for a calcium binding polypeptide similar to the regulatory subunit of calcineurin.

We have cloned and sequenced rat testis cDNAs coding for a calcium binding polypeptide similar to calcineurin beta subunit, the Ca(2+)-binding subunit of the Ca2+/calmodulin stimulated protein phosphatase. Rat testis cDNA library was screened with a monoclonal antibody Va1 raised against bovine brain calcineurin beta subunit. The deduced amino acid sequence is similar to that of human brain calcineurin beta subunit with respect to containing four putative calcium binding sites. However, distinct differences were found: 1) The cloned cDNA had six amino acids polypeptide tail at carboxy-terminal which is absent in human brain calcineurin beta subunit. This amino acids tail makes the carboxy-terminal highly hydrophilic in contrast to the human brain beta subunit which is hydrophobic at carboxy-terminal; 2) eleven amino acids at the N terminal of the cloned cDNA were completely different from the corresponding region of the brain calcineurin beta subunit.

Amino Acid Sequence↗

PubMed1991

Identification of discontinuous von Willebrand factor sequences involved in complex formation with botrocetin. A model for the regulation of von Willebrand factor binding to platelet glycoprotein Ib.

We have used proteolytic fragments and overlapping synthetic peptides to define the domain of von Willebrand factor (vWF) that forms a complex with botrocetin and modulates binding to platelet glycoprotein (GP) Ib. Both functions were inhibited by the dimeric 116-kDa tryptic fragment and by its constituent 52/48-kDa subunit, comprising residues 449-728 of mature vWF, but not by the dimeric fragment III-T2 which lacks amino acid residues 512-673. Three synthetic peptides, representing discrete discontinuous sequences within the region lacking in fragment III-T2, inhibited vWF-botrocetin complex formation; they corresponded to residues 539-553, 569-583, and 629-643. The 116-kDa domain, with intact disulfide bonds, exhibited greater affinity for botrocetin than did the reduced and alkylated 52/48-kDa molecule, and both fragments had significantly greater affinity than any of the inhibitory peptides. Thus, conformational attributes, though not strictly required for the interaction, contribute to the optimal functional assembly of the botrocetin-binding site. Accordingly, 125I-labeled botrocetin bound to vWF and to the 116-kDa fragment immobilized onto nitrocellulose but not to equivalent amounts of the reduced and alkylated 52/48-kDa fragment; it also bound to the peptide 539-553, but only when the peptide was immobilized onto nitrocellulose at a much greater concentration than vWF or the proteolytic fragments. These studies demonstrate that vWF interaction with GP Ib may be modulated by botrocetin binding to a discontinuous site located within residues 539-643. The finding that single point mutations in Type IIB von Willebrand disease are located in the same region of the molecule supports the concept that this domain may contain regulatory elements that modulate vWF affinity for platelets at sites of vascular injury.

Amino Acid Sequence↗

PubMed1991

Independent assembly and secretion of a dimeric adhesive domain of von Willebrand factor containing the glycoprotein Ib-binding site.

von Willebrand factor (vWF) is a multimeric glycoprotein that supports platelet adhesion on thrombogenic surfaces as part of the normal hemostatic response to vascular injury. We have employed a domain-specific expression strategy to analyze the biosynthetic processing steps and minimum structural requirements for assembly of the platelet receptor glycoprotein Ib-binding domain of vWF. A chimeric cDNA that codes for the vWF signal peptide and a segment of vWF internal primary sequence, residues 441-730, directs the secretion of a functional vWF fragment from mammalian cells. The recombinant molecule intrinsically assembles through intermolecular disulfide bond formation into a dimeric adhesive domain without contributions from other regions of vWF, including propeptide, previously indicated as essential for vWF multimer assembly. Prevention of N-linked glycosylation on the recombinant domain does not impair dimer formation or the ability to support platelet aggregation. These results identify a minimum structural element for vWF subunit assembly and provide new insights into the processing steps to produce vWF multimers and adhesive domains.

Animals↗

PubMed1991

Functional modulation of the isolated glycoprotein Ib binding domain of von Willebrand factor expressed in Escherichia coli.

We have expressed in Escherichia coli the domain of von Willebrand factor (vWF) containing the binding site for platelet glycoprotein (GP) Ib and used it to study the regulation of vWF-platelet interaction. The recombinant fragment, comprising residues 445-733 of the mature vWF subunit and designated rvWF445-733, did not have the native conformation of the corresponding domain in the intact molecule because, in order to prevent formation of random aggregates, the seven cysteine residues in the sequence were reduced and alkylated. Unlike native vWF, rvWF445-733 bound to GP Ib in the absence of any modulator, suggesting that the lack of disulfide bonds and/or carbohydrate side chains within this domain may expose platelet interaction sites. In the presence of two modulators, the glycopeptide ristocetin and the snake protein botrocetin, rvWF445-733 inhibited native vWF binding to GP Ib as well as platelet aggregation mediated by vWF, suggesting that both the fragment and the native molecule interact with the same site on platelets. This conclusion was also supported by the observation that the recombinant fragment competed with the binding to platelets of an anti-GP Ib monoclonal antibody known to inhibit vWF binding. Botrocetin formed a complex with rvWF445-733, but the affinity of this interaction was approximately 25-fold lower than with native vWF. However, the complexes of botrocetin with either rvWF445-733 or multimeric native vWF bound to GP Ib with similar dissociation constant. Therefore, conformational attributes of vWF regulate its affinity for botrocetin, but once the complex is formed, interaction with GP Ib is independent of native vWF conformation. These findings provide insights into the regulation of vWF-platelet interaction.

Binding Sites↗

PubMed1991

Identification of a point mutation in type IIB von Willebrand disease illustrating the regulation of von Willebrand factor affinity for the platelet membrane glycoprotein Ib-IX receptor.

von Willebrand factor (vWF) supports platelet adhesion on thrombogenic surfaces by binding to platelet membrane glycoprotein (GP) Ib in the GP Ib-IX receptor complex. This interaction is physiologically regulated so that it does not occur between circulating vWF and platelets but, rather, only at a site of vascular injury. The abnormal vWF found in type IIB von Willebrand disease, however, has a characteristically increased affinity for GP Ib and binds to circulating platelets. We have analyzed the molecular basis of this abnormality by sequence analysis of a type IIB vWF cDNA and have identified a single amino acid change, Trp550 to Cys550, located in the GP Ib-binding domain of the molecule comprising residues 449-728. Bacterial expression of recombinant fragments corresponding to this vWF domain yielded molecules that, whether containing a normal Trp550 or a mutant Cys550 residue, bound directly to GP Ib in the absence of modulators and with similar affinity. In contrast, mammalian cell expression of the same segment of sequence yielded molecules that, when containing the normal Trp550, did not bind to GP Ib directly but, like native vWF, bound in the presence of ristocetin. However, molecules containing the point mutation (Cys550) behaved like type IIB vWF--namely, bound to GP Ib even without ristocetin modulation and, in the presence of ristocetin, had 10-fold higher affinity than molecules with normal sequence. These results identify a region of vWF that, although not thought to be directly involved in binding to GP Ib, may modulate the interaction through conformational changes.

Cloning, Molecular↗

PubMed1991

Isolation and chemical characterization of two structurally and functionally distinct forms of botrocetin, the platelet coagglutinin isolated from the venom of Bothrops jararaca.

Two distinct forms of botrocetin, the von Willebrand factor (vWF)-dependent platelet coagglutinin isolated from the venom of the snake Bothrops jararaca, were purified and characterized structurally and functionally. The apparent molecular mass of the one-chain botrocetin was 28 kDa before and 32 kDa after reduction of disulfide bonds, while that of the two-chain botrocetin was 27 kDa before and 15/14.5 kDa after reduction. Amino acid composition of the two species revealed a similar high content of potentially acidic residues (greater than 60 Asx and Glx residues/molecule) but significant differences in the content of Cys and Phe residues. The NH2-terminal sequence of the one-chain botrocetin was Ile-Ile/Val-Ser-Pro-Pro-Val-Cys-Gly-Asn-Glu-. Two constituent polypeptides of the two-chain botrocetin showed similar but different NH2-terminal sequences, distinct from that of the one-chain species: (alpha) Asp-Cys-Pro-Ser-Gly-Trp-Ser-Ser-Tyr-Glu- and (beta) Asp-Cys-Pro-Pro-Asp-Trp-Ser-Ser-Tyr-Glu-. The carbohydrate content of both species was less than 2% of the total mass, and the pI was 4.0-4.1 for the one-chain species, and 4.6, 5.3-5.4, and 7.7-7.8 for the two-chain species. No free sulfhydryl group was detected in each species. Both types of botrocetin were resistant to proteolysis at neutral pH. Incubation of 125I-labeled one-chain botrocetin with the crude venom solution resulted in no detectable structural change. On a weight basis, the two-chain botrocetin was 34 times more active than the one-chain form in promoting vWF binding to platelets.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Sequence↗

PubMed1991

Immunological and virological characterization of improved construction of recombinant vaccinia virus expressing rinderpest virus hemagglutinin.

We constructed a recombinant vaccinia virus (RVV) expressing rinderpest virus (RPV) hemagglutinin (H) by modifying the promoter region of the original RVV. The promotor region was modified at three points, i.e., an outframe ATG was eliminated, the sequence between the promoter and initiation codon was shortened and the base sequence just upstream of the initiation codon was changed. As compared with the original RVV, the modified RVV was found to produce a remarkably large amount of H protein in infected rabbit kidney cells cultured in vitro and to induce high titers of anti-RPV-H antibodies in rabbits. The median protective doses in rabbits of the modified and of the original RVVs were 10(2) pfu and 10(3.5) pfu, respectively, indicating that the modified RVV was at least 10-times more effective in protection than the original. The neurovirulence of the modified RVV and the parental LC16mO strain was roughly at the same level, and was much lower than that of WR strain. The modified RVV was as heat-stable as the original one. These results indicate that the modified RVV could be a candidate rinderpest vaccine for further examinations including cattle.

Animals↗