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Biomedical subjects

T Hotokebuchi

Publications and source records attributed to T Hotokebuchi.

54 records · Page 3Linked to original sources
PubMed1989

Limb allografts in rats immunosuppressed with cyclosporine: as a whole-joint allograft.

We performed limb allografts in three inbred rat strains immunosuppressed with cyclosporine. As controls, 10 autografts and 10 isografts exhibited an excellent result. In minor-mismatched allografts (Lewis to Fischer, n = 45), with the use of cyclosporine, the grafted limbs survived and the articular cartilage retained normal architecture and cell viability 52 weeks after grafting, but without cyclosporine treatment severe degeneration and destruction of articular cartilage were shown by 16 weeks after operation. In major-mismatched allografts (Brown Norway to Fischer, n = 35), the articular cartilage of cyclosporine-treated animals maintained normal architecture and cell viability 52 weeks after operation despite the gross appearance of skin rejection, while that of non-cyclosporine-treated animals was degenerated and destroyed by 6 weeks. These results suggest the possibility of whole-joint allografts in humans with the use of cyclosporine, as well as other organ transplantations.

Animals↗
PubMed1988

Collagen arthritis in rats: the importance of humoral immunity in the initiation of the disease and perpetuation of the disease by suppressor T cells.

Arthritis could be passively transferred with a serum concentrate from collagen arthritic rats to nude rats and cyclosporin-treated, type II collagen-tolerant rats. These findings suggest that collagen arthritis could be inducible by humoral immunity alone in the absence of cellular immunity to type II collagen or functional T cells. In addition, passive arthritis induced by anticollagen antibody is a mild, transient disease from which the animals normally recover and the rats that have recovered from passive arthritis are resistant to develop a second phase of arthritis following a second administration of anticollagen antibody or the subsequent challenge with type II collagen. However, when a serum concentrate was transferred while cyclosporin was administered continuously, transferred arthritis in cyclosporin-treated, type II collagen-tolerant rats lasted as long as cyclosporin treatment and arthritis was significantly enhanced compared to those of naive recipients. Further, enhancement and prolongation of passively transferred arthritis in nude rats was observed. Furthermore, treatment with cyclophosphamide reversed acquired resistance to collagen arthritis subsequent to recovery from passive arthritis. These findings suggest that suppressor T cells might, at least in part, affect the clinical course of collagen arthritis and reverse acquired resistance to arthritis.

Animals↗
PubMed1987

Enhancing effects of tilorone on collagen arthritis and humoral immune response to type II collagen.

The effect of tilorone, which is known to suppress adjuvant arthritis, on the induction of collagen arthritis in rats was investigated. Combined data of the present experiments show that all of the tilorone-treated rats except one in the lowest dosage group developed arthritis but that the incidence of arthritis in the tilorone-treated groups was not significantly different from that of the control group. The results also show that the two higher dosages (12.5 and 25 mg/kg/day) of tilorone caused a significant increase in the severity of collagen arthritis. Humoral immune response to type II collagen was significantly augmented in these two higher dosage groups; however, delayed-type hypersensitivity response to type II collagen was suppressed while tilorone was administered continuously. In addition, treatment with tilorone caused a significant increase in the concentration of anticollagen IgG extractable from the joint tissue. Anticollagen IgG subclass analysis revealed that the major subclass was IgG2a in both the serum and paw extract, with minor amounts of IgG2b, IgG2c, and IgG1. The response of all these subclasses was almost equally activated by tilorone treatment.

Animals↗
PubMed1987

Reversal of antigen-induced resistance to collagen arthritis by cyclophosphamide.

Treatment of rats with intravenous injection of 1 mg of soluble native type II collagen induced resistance against the subsequent induction of active arthritis by type II collagen immunization. This resistant state was accompanied by suppressed antibody response and delayed-type hypersensitivity (DTH) skin reaction to type II collagen. However, pretreatment of rats with 20 mg/kg of cyclophosphamide (CY), an agent reputed to damage suppressor T-cell function, 2 days before intravenous injection of soluble type II collagen abrogated the antigen-induced resistance against the subsequent induction of active arthritis. The DTH skin reaction to type II collagen was completely restored and the antibody response to type II collagen was significantly though not completely restored by CY pretreatment. These results provide evidence that antigen-induced resistance to collagen arthritis is mediated, at least in part, under the control of CY-sensitive events.

Animals↗
PubMed1987

Effect of cyclophosphamide and its analogs on collagen arthritis in rats.

The effects of cyclophosphamide (CY) and its structurally related analogs, ifosfamide (Ifo), sufosfamide (Sufo), and mafosfamide (Mafo), on collagen arthritis in Sprague-Dawley rats were examined. Prophylactic treatment with 7.5-10 mg/kg/day of CY. 15 mg/kg/day of Ifo, and 10-15 mg/kg/day of Sufo for the first 10 days starting on the same day as the type II collagen immunization suppressed arthritis induction as well as humoral immune response to type II collagen. Prophylactic treatment with Mafo at doses ranging from 10 to 40 mg/kg/day for 10 days was ineffective in suppressing the disease development. When drug treatment was started only during the immediate preclinical phase of arthritis, the development of arthritis was suppressed in the animals treated with 10 mg/kg/day of CY and 15 mg/kg/day of Ifo from Day 5 to Day 14. Additional studies demonstrated that treatment with 10 mg/kg/day of CY and 15 mg/kg/day of Ifo started at the time of disease onset significantly suppressed the severity of arthritis compared with the control group. These results show the effectiveness of Ifo and CY on this animal model of polyarthritis and suggest the possibility of clinical use of Ifo for the treatment of human arthritides similar to CY.

Animals↗
PubMed1987

Suppression of collagen arthritis in rats by heterologous anti-idiotypic antisera against anticollagen antibodies.

Affinity-purified rat anti-type II collagen antibodies were used to prepare anti-idiotypic antibodies in rabbits. It has been demonstrated that such anti-idiotypic antibodies are capable of binding to anti-type II collagen antibodies in vitro. Intravenous administration of heterologous anti-idiotypic antisera at the time of immunization with type II collagen resulted in a significant suppression of anti-type II collagen antibody formation and the development of arthritis, although delayed-type hypersensitivity skin test response to type II collagen was not affected. However, treatment of rats with heterologous anti-idiotypic antisera at Day 7 after immunization was ineffective in altering disease expression. On the other hand, treatment with heterologous anti-idiotypic antisera had no significant suppressive effect on the incidence or severity of adjuvant arthritis. These results indicate that the effect of heterologous anti-idiotypic antisera directed toward anti-type II collagen antibodies is disease specific and is restricted to collagen arthritis.

Animals↗
PubMed1986

Treatment with cyclophosphamide reverses acquired resistance to collagen arthritis subsequent to recovery from passive arthritis.

Passive arthritis induced by anticollagen antibody was a mild, transient disease from which the animals normally recovered and the rats that had recovered from passive arthritis were resistant to develop a second phase of arthritis following a second administration of anticollagen antibody or the subsequent challenge with type II collagen. However, treatment of the recovered rats with cyclophosphamide (CY) shortly before a second administration of a serum concentrate induced a second episode of acute polyarthritis in 82% of the rats. In addition, CY treatment without further administration of a serum concentrate induced a recurrence of arthritis in 25% of the recovered rats. Similarly, treatment of the recovered rats with CY shortly before the challenge with type II collagen induced a second episode of arthritis in 83% of the rats. However, treatment with CY shortly before the challenge was unable to restore the suppressed humoral response to type II collagen. These results provide evidence that the resistant state is mediated, at least in part, by CY-sensitive events.

Animals↗
PubMed1986

Effects of cyclosporin on collagen induced arthritis in mice.

We have studied the effect of the immunosuppressive agent cyclosporin on collagen induced arthritis in mice. Cyclosporin, when given prophylactically, was capable of suppressing the development of collagen induced arthritis and the immunological response to native type II collagen in a dose dependent manner. Furthermore, treatment with cyclosporin, started on the same day as the booster injection with type II collagen, also resulted in inhibition of development of arthritis and of immunity to collagen. These findings suggest that the time of a booster injection, three weeks after the initial immunisation, might be still within the induction phase of arthritis since reinoculation is required to produce a high incidence of arthritis in mice. In addition, therapeutic treatment with cyclosporin did not affect the clinical course of the disease or the immune response to collagen.

Animals↗
PubMed1985

Serum transfer of collagen arthritis to cyclosporin-treated, type II collagen-tolerant rats.

Collagen arthritis has been passively transferred with a serum concentrate from immunized donors to immunologically naive recipients as well as cyclosporin-treated, type II collagen-tolerant rats. These findings point to an important role for anticollagen antibody and appear to rule out a role for cellular immunity to type II collagen in the initiation of this disease. The passively transferred arthritis was a transient lesion in the majority of naive recipients and in the cyclosporin-treated, type II collagen-tolerant rats as well when a serum concentrate was transferred after the cessation of cyclosporin treatment. When cyclosporin-treated, type II collagen-tolerant rats received transfer concentrate while cyclosporin was administered continuously, arthritis was significantly enhanced, and lasted as long as cyclosporin was administered and in the majority of rats up to 2 weeks after the cessation of cyclosporin treatment. These results, together with a rapid clearance of anticollagen antibody from the serum, suggest that anticollagen antibody is not the sole regulatory factor and that a cellular suppressor system, sensitive to cyclosporin, might participate in the regulation of this disease process.

Animals↗
PubMed1985

Serum transfer of collagen arthritis in congenitally athymic nude rats.

The role of cellular immunity in collagen arthritis was investigated with congenitally athymic nude rats (rnu/rnu) and their heterozygous littermates (rnu/+). Immunization with type II collagen induced polyarthritis and definite immunity to type II collagen in rnu/+ rats, whereas rnu/rnu rats did not develop arthritis or immunity to collagen. An additional study demonstrated that collagen arthritis could be passively transferred with a serum concentrate from arthritic Sprague-Dawley rats to naive rnu/rnu rats as well as to rnu/+ rats. Histopathologically, the passively transferred arthritis in rnu/rnu rats resembled that in rnu/+ rats. Despite no difference in clearance of anti-type II collagen antibody after transfer between them, the passively transferred arthritis in rnu/rnu rats was significantly enhanced and prolonged in comparison with that in rnu/+ rats. These results indicate that arthritis may be inducible by humoral immunity in the absence of functional T cells and also suggest that anti-type II collagen-antibody is not the sole regulatory factor and that the suppressor cell system might regulate the clinical course of the disease.

Animals↗
PubMed1984

Pathogenetic difference between collagen arthritis and adjuvant arthritis.

Daily treatment with cyclosporin at a dose of 25 mg/kg for 14 d gave complete suppression of the development of collagen arthritis and adjuvant arthritis in Sprague-Dawley rats during an observation period of 45 d. To study whether the immunologic unresponsiveness produced by cyclosporin is antigen specific, we rechallenged the cyclosporin-protected rats with either type II collagen or complete Freund's adjuvant (CFA) after discontinuation of cyclosporin treatment. Type II collagen-immunized, cyclosporin-protected rats did not develop arthritis in response to reimmunization with type II collagen, but, they did develop arthritis in response to a subsequent injection of CFA. Similarly, CFA-injected, cyclosporin-protected rats showed a suppressed arthritogenic reaction in response to reinjection of CFA, whereas their response to a subsequent immunization with type II collagen was unaffected. On the other hand, the rats that were treated with cyclosporin without any prior antigenic challenge could develop arthritis in response to a subsequent injection of CFA or type II collagen after cessation of cyclosporin treatment. These results indicate that specific immunologic unresponsiveness can be induced by cyclosporin in the two experimental models of polyarthritis, collagen arthritis and adjuvant arthritis, and that there is no cross-reactivity between type II collagen and the mycobacterial cell wall components. The results further indicate that immunity to type II collagen plays a critical role in the pathogenesis of collagen arthritis but that its pathogenetic role in adjuvant arthritis is insignificant.

Animals↗
PubMed1983

Paradoxical effects of cyclosporin A on collagen arthritis in rats.

The effect of the immunosuppressive agent cyclosporin A (CS-A) on collagen arthritis in Sprague-Dawley rats is investigated. A 14-d course of CS-A treatment at doses of 15 mg/kg per day or more, begun on the same day as type II collagen immunization, suppressed the development of arthritis as well as humoral and delayed-type hypersensitivity (DTH) skin test responses to type II collagen, possibly by interfering with helper T cells. Additional studies demonstrated that CS-A treatment only during the induction phase of immunity proved to be successful. When CS-A treatment was started only during the immediately preclinical phase of arthritis or after the disease onset, a significant enhancement of the disease was obtained in a dose-dependent manner. This enhancement was accompanied by an augmentation of DTH skin reactions, while antibody responses were either suppressed or unaffected. These results appear to be attributable at least in part to a suppressive effect of CS-A on a population of suppressor T cells, thus resulting in a T cell-mediated helper effect. It is therefore reasonable to assume that the paradoxical effects of CS-A on collagen arthritis in rats might be caused by an altering of the sensitive balance of the two regulatory subpopulations of T cells. It is also possible that cell-mediated immune responses may play an important role in influencing the course of the disease.

Animals↗
PubMed1983

Hurler-Scheie phenotype with parental consanguinity. Report of an additional case supporting the concept of genetic heterogeneity.

The Hurler-Scheie phenotype in a 27-year-old woman of first-cousin parentage is possibly the first reported in the orthopedic literature. The patient exhibited short stature, coarse facies, corneal clouding, multiple stiff joints, normal intelligence, and a long history of bilateral carpal tunnel syndrome, which has not been relieved after operation. The irreversible nerve damage was apparently produced by the marked thickening of the transverse carpal ligament. Surgical findings in this case and data from published reports emphasize the need for early surgical treatment of the associated carpal tunnel syndrome in patients with the Hurler-Scheie phenotype. Parental consanguinity present in this patient is further evidence supporting the concept of a third mutant allele different from both the Hurler gene and the Scheie gene.

Adult↗
PubMed1982

Generalized enchondromatosis with unusual complications of soft tissue calcifications and hemangiomas. Follow-up for over a twelve-year period.

Generalized enchondromatosis is a newly delineated type of enchondromatosis. Radiographically there are multiple enchondromata in almost all metaphyses of the long and short tubular bones and the lesions are in almost the same stage of development with mild platyspondyly and skull deformity. The pelvic changes are characteristic and, together with the metaphyseal changes of the long and short tubular bones, are probably diagnostic of this disorder. The present case demonstrates advanced radiographic features of this disorder associated with unusual soft tissue calcifications and hemangiomas. The presence of hemangiomas in our case as well as three cases in the literature suggests this feature is more than a coincidence.

Bone Neoplasms↗
PubMed1982

Intermediate form of osteopetrosis with recessive inheritance.

The clinical and radiographic features of the intermediate form of osteopetrosis in two sibs are presented in which the disorder appears to have been inherited as a recessive trait. Although this form of osteopetrosis has been poorly delineated, its recognition is practically important in order to give an accurate prognosis. This paper also presents an unusual complication of bilateral avascular necrosis of the femoral head in the younger sib. Radiographic changes of the femoral heads suggest those of Legg-Calvé-Perthes disease, though the possibility of avascular necrosis following unrecognized femoral neck fracture is not completely excluded.

Adolescent↗
PubMed1982

Transtrochanteric rotational osteotomy of the femoral head for the treatment of osteonecrosis. Follow-up statistics.

Transtrochanteric rotational osteotomy of the femoral head was technically established as a surgical procedure in 1972. This procedure has been successfully performed on 250 hips in 204 patients. In the treatment of idiopathic and steroid-induced osteonecrosis of the femoral head, the results of 128 hips in 90 patients followed two to nine years were reviewed. In 98 of 128 hips, excellent results were obtained clinically and roentgenographically. Progressive collapse in the newly created weight-bearing area occurred in 25 hips where the lesions had been extensive. In 35 of 39 Grade I or II hips, excellent results were obtained in every respect (success rate: 90%). Following the analysis of results on the preoperative lateral roentgenograms of the femoral head, 76 of the 80 hips in the group in which the intact area was greater than one third of the total articular surface showed no collapse of the newly created weight-bearing area, thus accounting for a 95% success rate. In cases when a further collapse was prevented, the necrotic lesions were smaller at follow-up. Excellent results were obtained when the osteotomy was performed during the early stage of necrosis and in the absence of an advanced collapse, even in extensive lesions. In advanced cases with an extensive lesion, adequate anterior rotation is essential and intentional varus position should be designed. These results suggest that this procedure will inhibit progressive collapse of the femoral head and restore the joint more effectively than other surgical procedures.

Femur Head Necrosis↗
PubMed1981

Phalangeal microgeodic syndrome in childhood: report of seven cases and review of the literature.

Seven cases of phalangeal microgeodic syndrome in childhood are reported. Reviewing the literature, we have found a total of thirty Japanese cases, including the cases of our own. On the other hand, only ten cases have been reported outside Japan. The mean age of onset of the Japanese was six and a half years, which is older than that in the initial description. Of further interest is the fact all the cases in Japan occurred sporadically and exclusively in winter, and regressed spontaneously and fairly rapidly within six months. Furthermore, most of the cases reported in Europe also occurred in the winter months. These facts imply an etiological relationship between the lowered temperature and the bone lesions.

Bone Diseases↗