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Biomedical subjects

R Mori

Publications and source records attributed to R Mori.

At least 91 records · Page 5Linked to original sources
PubMed1993

Frequent isolation of human herpesvirus 7 from saliva samples.

Human herpesvirus 7 (HHV-7) was isolated frequently from saliva specimens. The isolation rates were 81% (13/16) in adults, 70% (7/10) in children over 1 year old, and none (0/7) in children less than 1 year old, respectively, indicating that infection of HHV-7 occurs during early infancy and the virus shedding rate after infection is very high. Human herpesvirus 6 (HHV-6) was not isolated from saliva specimens although some studies on isolation of HHV-6 from saliva was reported previously.

Adult↗
PubMed1993

Necrotizing chorioretinitis in mice inoculated with herpes simplex virus type 1 with or without glycoprotein C: anterior chamber-associated immune deviation does not persist.

BALB/c mice developed contralateral necrotizing retinitis following intracameral inoculation with herpes simplex virus type 1 (HSV-1). The animals showed a positive delayed-type hypersensitivity (DTH) response at 10 days postinoculation, indicating that the anterior chamber-associated immune deviation was transient after HSV-1 inoculation. Since glycoprotein C (gC) of HSV-1 is a major immunogen, we examined DTH and the antibody response induced by a gC-deficient strain TN-1 and compared them with those induced by the recombinant gC-positive mutants. We found that gC was not required for DTH reaction, and that gC was neither necessary for nor protective against the contralateral retinal necrosis. Serial lymphocyte subset analyses of the draining lymph nodes revealed an absolute increase of B cells, CD4-positive T cells, and CD8-positive T cells. CD4-positive T cells but not CD8-positive T cells increased in the contralateral eyes during the inflammation and necrosis. The coincident emergence of the positive DTH and contralateral retinal necrosis of HSV-1-inoculated mice, together with the presence of CD4-positive cells in the retina, indicated that CD4-positive T cells responsible for DTH induction may participate in the retinal necrosis.

Animals↗
PubMed1993

Induction of bilateral retinal necrosis in mice by unilateral intracameral inoculation of a glycoprotein-C deficient clinical isolate of herpes simplex virus type 1.

Herpes simplex virus can cause acute retinal necrosis, a blinding retinal disease in man. A unilateral intracameral inoculation of herpes simplex virus type 1 (HSV-1) in mice induces retinal necrosis primarily in the contralateral eye and provides an experimental model for the disease. Previous studies suggested that a major envelope glycoprotein of HSV-1, glycoprotein C (gC), is required for retinal necrosis. We studied HSV-1 strain TN-1, a gC-deficient clinical isolated from a lesion of herpetic keratitis, for its pathogenicity in mice with an intracameral inoculation of the virus and found that TN-1 could induce severe necrotizing retinitis in both inoculated and uninoculated eyes of BALB/c mice. Inoculation with a lower dose of TN-1 resulted in a unilateral necrotizing retinitis in the uninoculated eyes. Tissue virus titration of infected mice killed at various times after inoculation detected an infectious virus in various organs including the eyeballs, trigeminal ganglia, brain and adrenal glands. Anterior chamber-associated immune deviation (ACAID) was observed in TN-1-inoculated mice as well as in mice inoculated with gC-positive laboratory strain KOS 7 days postinoculation. Our findings suggested that gC of HSV-1 is not necessary for either the induction of retinal necrosis, neural spread of the virus, or ACAID.

Adrenal Glands↗
PubMed1993

Molecular characterization of naturally occurring glycoprotein C-negative herpes simplex virus type 1.

We previously isolated glycoprotein C (gC)-negative herpes simplex virus type 1 (HSV-1) mutants, TN-1, TN-2 and TN-3, from a patient with recurrent herpetic keratitis at one-year intervals. In the present study, the molecular basis for the inability of these clinical isolates to express gC was examined. The nucleotide sequence of the gC gene of the TN-1 strain was compared with that of the HSV-1 KOS strain. In the open reading frame of the gC gene, there were 12 nucleotide differences between the TN-1 and KOS strains, seven of which led to amino acid substitutions. Importantly, one of them was the codon change from CAG for glutamine at position 280 to TAG for the amber termination codon. Accordingly, the TN-1 strain produced a truncated gC with a predicted molecular weight, which was secreted into the extracellular fluid. These results suggest that this amber mutation in the TN-gC gene results in a premature termination of gC translation and is the cause of the gC-negative phenotype of the TN strains. It is expected that these extremely rare HSV-1 strains will provide us with valuable information concerning the in vivo functions of gC, especially in ocular diseases.

Adult↗
PubMed1993

Nucleotide sequence of the major DNA-binding protein gene of herpes simplex virus type 2 and a comparison with the type 1.

The nucleotide sequence of a region encompassing about 5,200 base pairs (bp) of the left side of the origin of replication in the long unique region of the herpes simplex virus type 2 (HSV-2) has been determined. This region contained the major DNA-binding protein or the infected-cell protein 8 (ICP 8) gene and 5'-part of the counterpart of HSV-1 ICP 18.5 gene. A comparison of the nucleotide sequence of the ICP8 gene between HSV-1 and HSV-2 showed an 89.8% homology. A primer extension analysis for the HSV-2 ICP 8 mRNA showed that the major transcriptional start site was mapped at 315 bp upstream of the initiation codon. A comparison of the predicted functional amino acid sequence of the ICP 8 between HSV-1 and HSV-2 revealed a striking homology (97.2%), the value of which was the highest among those of the other polypeptides encoded by HSV-1 and HSV-2. Some domains, which were shown to be required for the nuclear function, the binding to single-stranded DNA and the nuclear localization were well conserved. In addition, the nucleotide and the functional amino acid sequences of a part of the HSV-2 counterpart of the HSV-1 ICP 18.5 gene were also compared, demonstrating an 88.4% and 95.9% homology, respectively.

Amino Acid Sequence↗
PubMed1993

Molecular analysis of a neurovirulent herpes simplex virus type 2 strain with reduced thymidine kinase activity.

Thymidine kinase (TK) of herpes simplex virus (HSV) has been identified as one of the factors responsible for its virulence. We have previously isolated acyclovir (ACV)-resistant HSV type 2 (HSV-2), strain YS-4 C-1, by simple plaque cloning from a clinical isolate. Although YS-4 C-1 had extremely low TK activity, it retained high virulence in mice. To determine the mechanism of the reduction of TK activity, a molecular analysis of the YS-4 C-1 TK gene was performed. YS-4 C-1 produced TK mRNA, which was indistinguishable both in size and amount from that of wild-type strains. However, the YS-4 C-1 TK had a single amino acid change from serine to asparagine at amino acid residue 182 of the TK polypeptide, which was caused by a single nucleotide mutation. It was situated within a highly conserved region (162-194) and close to the putative nucleoside-binding site (169-177), one of the three active centers of TK. In order to confirm the effect of this missense mutation on both the TK activity and neurovirulence, the mutation was introduced into the TK genes of wild-type strains. Although all the recombinants were altered to ACV-resistant viruses with reduced TK activity, they retained high neurovirulence for mice. Our study thus suggested that this mutant TK, in spite of low activity, might play a role in the neurovirulence of HSV-2.

Acyclovir↗
PubMed1993

Do anger and aggression affect carotid atherosclerosis?

BACKGROUND AND PURPOSE: Although a number of metabolic and psychosocial factors have been identified as coronary risk factors, no studies have evaluated the relation between personality and cerebrovascular disease. The purpose of the present study was to elucidate the relation between the characteristics of anger or aggression and the severity of carotid atherosclerosis on the basis of the findings of B-mode ultrasonography. METHODS: The Cornell Medical Index was used to measure anger in 34 patients with signs of atherosclerosis or at least one of four recognized risk factors for atherosclerosis (hypertension, hypercholesterolemia, diabetes mellitus, and cigarette smoking). The Rosenzweig Picture Frustration Study and Yatabe-Guilford Personality Test were used to evaluate aggression. High-resolution B-mode ultrasonography was performed, and the severity of carotid atherosclerosis was determined by plaque score. The occurrence of risk factors for carotid atherosclerosis was compared among the patients. RESULTS: The correlation of plaque score with one item that endorses anger was r = .65 (P < .01) and with "extrapersistive" in aggression was r = .50 (P < .01). Multivariate analysis identified significant correlations between plaque score and age, hypercholesterolemia, and anger. CONCLUSIONS: Our results suggest that anger and, perhaps, aggression may be risk factors for cerebrovascular disease.

Aggression↗
PubMed1992

Detection of human papillomavirus DNA in esophageal carcinoma in Japan by polymerase chain reaction.

BACKGROUND: Human papillomaviruses (HPV) have been implicated strongly in the pathogenesis of human squamous cell carcinomas, especially of anogenital carcinomas. Some pathologic changes of the esophagus may be one of the candidates for HPV etiology, but the role of HPV infections in the carcinogenesis of the esophagus remains to be clarified. METHODS: To elucidate the association of HPV with carcinogenesis of the esophagus, 45 biopsy samples of esophageal squamous cell carcinomas were examined for the presence of HPV DNA by polymerase chain reaction (PCR). Primers for PCR were (1) consensus primers (CP) for the simultaneous amplification of the E6-E7 regions of cancer-associated HPV types (HPV 16, 18, 31, 33, 52b, and 58), which have been shown to have transforming activities; (2) type-specific primers (SP16, SP18) for the E7 regions of HPV 16 and HPV 18, respectively; and (3) general primers (GP) for the simultaneous amplification of the L1 regions of HPV 6, 11, 16, 18, 31, and 33. RESULTS: PCR using CP first was done for screening and showed that 3 (6.7%) of 45 specimens contained HPV 16 or HPV 18 DNA, the oncogenic high-risk HPV types. This was confirmed by SP16 and SP18 PCR. However, no HPV DNA was detected by PCR using GP. These results suggested that the HPV DNA detected might be integrated into the cell genome with their transforming genes retained and their late regions deleted. CONCLUSIONS: Most oncogenic types of HPV (HPV 16 and HPV 18) were detected by PCR in carcinomas of the esophagus. Thus, HPV might play a role, although at a low frequency, in carcinogenesis of the esophagus.

Base Sequence↗
PubMed1992

Reactivation of cytomegalovirus in patients with cirrhosis: analysis of 122 cases.

Human cytomegalovirus causes severe and often fatal infections in immunocompromised patients. After organ transplantation cytomegalovirus in peripheral blood mononuclear cells is thought to be activated by alloreaction and to spread because of immunosuppression, and it may cause endogenous cytomegalovirus diseases. Patients with cirrhosis, one group of candidates for liver transplantation, often show various grades of immunosuppression before transplantation. To evaluate the status of cytomegalovirus infection in cirrhotic patients and its relevance to the degree of immunosuppression, we examined the presence of cytomegalovirus in mononuclear cells by polymerase chain reaction and immunocytochemical analysis. We studied 122 patients with definite cirrhosis and 43 normal volunteers. All cirrhotic patients (100%) and 40 (93%) of 43 normal controls were seropositive for cytomegalovirus. Cytomegalovirus DNA was detected by polymerase chain reaction in 77 (63.1%) of 122 seropositive cirrhotic patients, but in only 1 (2.5%) of 40 seropositive normal controls (p < 0.01). Cytomegalovirus antigen could not be detected in mononuclear cells by immunocytochemical staining with monoclonal antibodies. Cytomegalovirus DNA-positive patients have a greater impairment of liver function than do cytomegalovirus DNA-negative patients; this fact is manifested by delayed indocyanine green retention rates and elevated serum bilirubin levels (p < 0.05). Lymphocyte proliferative response induced by phytohemagglutinin and natural killer cell activity were also significantly lower in cytomegalovirus DNA-positive patients as compared with cytomegalovirus DNA-negative patients (p < 0.01). Our data suggest that the reactivation of cytomegalovirus may have already occurred in patients with cirrhosis before transplantation.

Adult↗
PubMed1992

Localization of herpes simplex virus type 1 in sebaceous glands of mice.

The distribution of HSV-1 during the development of zosteriform skin lesions in SCID mice was analyzed by immunofluorescence and electron microscopy. The virus initially appeared within certain keratinocytes, sometimes surrounded by keratinocytes whose surfaces were also positive for the antigens, in the lower epidermal layers including the hair follicles, and then extended upward to the entire epidermis and downward to the sebaceous glands 1-2 days later, when no macroscopic skin lesion was seen. The affected epidermal cells subsequently degenerated and lost their viral antigens within a day, when the zosteriform lesion then became evident. This was followed by a degeneration of the dermis. The sebaceous glands eventually degenerated in 10 days, but some glands in the necrotic skin areas preferentially retained HSV-1. The horizontal spread of the virus in the epidermis beyond the first invaded dermatome occurred much later. In mice passively immunized with specific immune serum, viral antigens were observed even 20 days after the infection in sebaceous glands in necrotized areas. Therefore, HSV-1 appears to spread first via the extracellular fluid among the keratinocytes after being shed from nerve endings, and then produces a successive degeneration of the affected keratinocytes which may prevent any further extension of horizontal viral spread. The pilosebaceous apparatus is possibly acting as a site not only for the replication of HSV-1 with a delayed cytopathic effect, but also as an area that is temporarily sheltered from host defense mechanisms.

Animals↗
PubMed1992

Binding characteristics of naftopidil and alpha 1-adrenoceptor antagonists to prostatic alpha-adrenoceptors in benign prostatic hypertrophy.

Binding properties of naftopidil and alpha 1-adrenoceptor antagonists to alpha-adrenoceptors in prostates from benign prostatic hypertrophy (BPH) were characterized by radioreceptor assays using [3H]prazosin and [3H]rauwolscine. Specific binding of [3H]prazosin and [3H]rauwolscine in human prostatic membranes was saturable and of high affinity, and it showed a pharmacological specificity which characterized alpha 1 and alpha 2-adrenoceptors, respectively. Naftopidil and several alpha 1 antagonists competed for prostatic [3H]prazosin binding in order: R-(-)-YM-12617 greater than prazosin greater than bunazosin greater than terazosin greater than naftopidil greater than urapidil, and the inhibitory effect (Ki = 11.6 nM) of naftopidil was 10 to 45 times less potent than quinazoline derivatives such as prazosin, bunazosin and terazosin. The potencies of these antagonists in competing for [3H]prazosin binding sites in human prostates correlated well with their pharmacological potencies (pA2). Scatchard analysis indicated that the decrease of prostatic [3H]prazosin binding by naftopidil was due to a marked increase in the Kd value without a change in the Bmax value. The inhibition of prostatic [3H]prazosin binding by naftopidil was reversible. Naftopidil also inhibited prostatic [3H]rauwolscine binding (Ki = 70.0 nM). Thus, it is suggested that naftopidil antagonizes alpha 1-adrenoceptors in human prostates in a competitive and reversible manner.

Adrenergic alpha-Antagonists↗
PubMed1992

Possible role of cytomegalovirus in the pathogenesis of inflammatory aortic diseases: a preliminary report.

To search for possible evidence of a relationship between human cytomegalovirus and aortic diseases, we examined 41 aortic lesions excised at surgery and 16 aortic tissues obtained at autopsy for the presence of cytomegalovirus DNA, by use of polymerase chain reaction. Cytomegalovirus DNA was present in seven (88%) of eight lesions of inflammatory aortic diseases with periaortic fibrosis, five of six inflammatory aneurysms, and all of two aortic occlusive lesions with inflammation. Cytomegalovirus DNA was detected in 20 (61%) of 33 atherosclerotic aneurysms, whereas it was detected in only five (31%) of 16 autopsy samples that showed neither inflammation nor atherosclerosis. Thus the possibility that cytomegalovirus may play a role in the pathogenesis of inflammatory aortic diseases warrants further attention.

Adult↗
PubMed1992

Latent infection of SCID mice with herpes simplex virus 1 and lethal cutaneous lesions in pregnancy.

Some SCID mice survived primary infection with herpes simplex virus 1 without the development of peripheral lesions but established coculture-positive ganglionic latency when a low dose of a wild-type strain was inoculated intracutaneously. The latency was also evidenced by the development of the fatal zosteriform skin lesions and the isolation of the virus during pregnancy. We consider that the viral entry into neurons without successive replication, rather than the arrest of the lytic infection within the cells, is an important mechanism in the establishment of latency.

Animals↗
PubMed1992

Neutralizing antibodies against HTLV-I in HTLV-I-associated myelopathy/tropical spastic paraparesis (HAM/TSP) patients and asymptomatic carriers.

We tested serum specimens from patients with HAM/TSP and asymptomatic HTLV-I carriers from endemic areas of Japan, Jamaica, Colombia, and Chile for neutralizing antibodies against HTLV-I. The data suggest a trend for neutralizing activity to be found more frequently in the sera from HAM/TSP patients than in sera from asymptomatic carriers. The result of this study emphasizes the importance of determining biologic properties of the envelope glycoprotein of HTLV-I.

Carrier State↗
PubMed1992

[An unusual chronic microvasculitis: Goodpasture's syndrome with late myocardial involvement].

We describe a disease, started in a female young adult patient as an apparent pulmonary siderosis, followed nine years later by an extracapillary proliferative nephritis, which developed to uremia in a few months. Later an intra-myocardial vasculitis, responsible of heart failure, appeared. Immune-histochemistry and serological tests exclude a disease mediated by anti-GMB antibodies, and pathologic features suggest a vasculitis mainly affecting lungs and kidneys.

Adult↗
PubMed1991

Rapid detection of a point mutation in thyroid-stimulating hormone beta-subunit gene causing congenital isolated thyroid-stimulating hormone deficiency.

Previous study showed that congenital isolated TSH deficiency in Japan is resulted exclusively from a G-A transition at nucleotide 145 in exon 2 of the TSH beta-subunit gene. All reported cases were from the inbred in Shikoku Island. We describe here a 10-year-old boy with hereditary TSH deficiency in the same area. The patient was born with a weight of 3,225 g to non-consanguineous parents. Evaluation at age 2 months revealed typical manifestations of cretinism without goiter. Serum T4, T3, and TSH values were 2.53 micrograms/dl, 107 ng/dl, and 0.5 microU/ml, respectively. A TRH stimulation test showed no increment of serum TSH value. Other anterior pituitary hormone levels were all within the normal range. Two oligonucleotide primers T1a and T1b were synthesized according to the sequence data. Amplified 169 bp nucleotides in exon 2 of the TSH beta gene with this primer set were digested with MaeI. Both the phenotypically normal brother and normal controls showed only the 169 bp fragment, whereas the proband showed 140 and 29 bp fragments and both parents showed three fragments; 169, 140, and 29 bp. These results were consistent with the point mutation of TSH beta gene in Japanese patients with congenital isolated TSH deficiency. Our PCR method with MaeI digestion contributes to the rapid detection of the homozygous patient and the heterozygous carrier.

Child↗
PubMed1991

Glycoprotein C of herpes simplex virus type 1 is essential for the virus to evade antibody-independent complement-mediated virus inactivation and lysis of virus-infected cells.

Glycoprotein C (gC) of herpes simplex virus type 1 (HSV-1) is a receptor for the complement component C3b. We have previously isolated HSV-1 gC- strains (TN1, TN2 and TN3) from a patient with recurrent keratitis at three different times. These are very rare isolates because gC was thought to be essential for the virus in vivo. To determine whether gC modifies the interaction of complement with cell-free virus or virus-infected cells, we constructed gC+ recombinant viruses in which the intact gC gene of strain KOS was inserted into the TN1 virus genome. TN1 virus was inactivated by complement and TN1 virus-infected cells were lysed by complement; however, gC+ recombinant viruses became resistant to these effects of complement. These results suggest a role for gC in protection of both the virion envelope and the infected cell surface against damage by complement. TN1 virus was inactivated by complement from rats (Wistar, WKA, F344 and SD), guinea-pigs (Hartley) and humans, but not by complement from mice (C3H, DDD and BALB/c), which indicates that mice seem to be inappropriate as an experimental model for the study of HSV infection in which complement factors need to be considered.

Animals↗