Biomedical subjects
Publications and source records attributed to T Kuwabara.
A new technique for percutaneous imaging of a one-piece lumboperitoneal shunt is described. Patency of the shunt can be assessed by the intraperitoneal spread of contrast medium which is injected intrathecally via the lumbar route. No special equipment or instrumentation is required other than a typical lumbar puncture tray and a general examination tilt table for fluoroscopy.
Peritumoral edema is one of the most serious complications of intracranial neoplasms; however, the exact pathogenesis of this condition is still unknown. To explore the effect of macrophages in brain tumors on the pathogenesis of peritumoral edema, 42 specimens of primary or metastatic brain tumors were studied. Frozen sections were examined by an immunoperoxidase staining technique with anti-Leu-M3 monoclonal antibody. Eight of 14 gliomas demonstrated Leu-M3-positive cell (macrophage) infiltration. The two glioblastomas showed a moderate or marked degree of macrophage infiltration. Twelve of 16 meningiomas demonstrated varying degrees of macrophage infiltration. All six metastatic brain tumors exhibited prominent macrophages in intra- and peritumoral tissues. Four acoustic neurinomas and two hemangioblastomas showed a slight to moderate degree of macrophage infiltration. Excellent correlation was found between the degree of macrophage infiltration seen on immunoperoxidase staining and the peritumoral edema detected on computerized tomography brain scans of patients with supratentorial tumors, especially meningiomas. Macrophages are known to secrete various substances (including arachidonate metabolites) that may interfere with vascular permeability. These data suggest that macrophages infiltrating brain tumors may play an important role in the pathogenesis of peritumoral edema.
Urine specimens obtained from 19 patients with primary brain tumors were examined for the activity of transforming growth factors (TGF's). Urine was assayed for TGF's by soft agar colony formation and iodine-125 (125I)-epidermal growth factor (EGF)-binding competition. Two nontransformed cell lines, clonal NRK49F and BALB/3T3 A31-1-1 cells, were used as indicator cells for the soft agar colony assay, while EGF receptor-rich A431 cells were used for 125I-EGF-binding competition assay. Urine samples were dialyzed against acetic acid, then lyophilized, prepared with gel-permeation chromatography, and assayed. All 19 patients and a control group of healthy individuals showed high levels of alpha-type TGF's with low molecular weight (4 to 8 kD) in all urine samples. In addition, alpha-type TGF's of high molecular weight (20 to 50 kD) were detected at high levels in urine from all 10 patients with high-grade astrocytoma; at intermediate levels in urine from one of two patients with low-grade astrocytoma and from two of four patients with meningioma; and at low levels in urine from one of two patients with low-grade astrocytoma, from two of four patients with meningioma, from one patient with oligodendroglioma, from two patients with neurinoma, and from all healthy control individuals. The high level of alpha-type TGF's with high molecular weight detected in urine from patients with high-grade astrocytoma could be useful as a tumor marker.
We encountered 8 cases of cystitis probably caused by Tranilast. Bladder biopsy performed on 6 of the 8 cases revealed eosinophilic cystitis in 3 cases. In the lymphocyte stimulation test using Tranilast as an antigen, a positive and false positive reaction was seen in one case each. This disease seemed to occur as a result of allergy of the bladder specific to Tranilast.
A 48-year-old man had his left eye ball enucleated by fingers of an assailant. The optic nerve, measuring 4 cm in length, was attached to the enucleated eye ball, but there was neither a wound in his eyelids nor cerebrospinal fluid leakage from inside the orbit. He was confused, but responsive and was able to recognize other persons with his right eye. His right-eye vision deteriorated within 24 hours and was almost totally lost for about one month. Three months after the trauma his vision recovered to 0.1, but his visual field showed severe concentric narrowing. An emergency CT on admission showed a small subarachnoid hemorrhage in the suprasellar cistern, and follow-up CT scanning on day 7 demonstrated a small infarction in the left globus pallidus and putamen. Cerebral angiography performed on day 17 showed residual vasospasm of the horizontal portion of left anterior cerebral artery. Left ophthalmic artery was patent and there was no aneurysm formation either on the intracranial or on the intraorbital arteries. Literature review yielded only three cases of eye ball enucleation by an assailant. Intracranial complications reported in the literature, including those associated with eye ball enucleation caused by other mechanisms, are; contralateral visual field defect: seven cases, hypothalamic involvement: two cases, subarachnoid hemorrhage: two cases, cerebrospinal fluid leakage: one case, and meningitis: one case. The optic nerve, from just behind the eye ball to the chiasm, is reported to be 40-50 mm long, and eye ball enucleation with the optic nerve measuring 4 cm or more is quite likely to cause intracranial complications such as are cited above.
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Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Experimental occlusion of the central retinal vessels in albino rats followed by reperfusion for 2 or 4 days resulted in a highly active proliferative response. Mitotic figures were produced in retinal vascular cells, presumed Müller cells, retinal pigment epithelial cells, and possibly other cell populations in the retina. A large number of mitoses were observed in 60-100% of 50 experimental eyes with 2, 4 or 6 hr of experimental ischemia and 2 or 4 days of reperfusion and in none of the 37 control eyes. Autoradiography demonstrated 3H-thymidine uptake in the retina and in vascular cells on a trypsin digest preparation of the retina. Retinal ischemia followed by reperfusion leads to mitosis of retinal cells. This suggests a causal relationship in proliferative retinopathies where ischemia and cell proliferation coincide.
We studied histopathologic and immunohistopathologic features of an eye from a patient who had hypopigmented choroidal lesions with subsequent development of progressive subretinal fibrotic tissue associated with minimal signs of vitreal inflammation. A 24-year-old woman had a rapid and severe onset of the disease, which led to blindness within a few months despite treatment with corticosteroids and cyclophosphamide. Histopathologic studies disclosed a marked gliotic retina and thick subretinal fibrotic tissue as well as a granulomatous lymphocytic infiltration in the choroid. Electron microscopy demonstrated that the subretinal tissue was derived from retinal pigment epithelial cells. The immunoperoxidase staining showed similar proportions of T and B lymphocytes, indicating a relative increase of B cells. There was a predominance of the helper/inducer T lymphocyte subset in the infiltrating area. The Müller cells in the retina expressed class II antigens of the major histocompatibility complex.
We have shown previously that immunization with bovine interphotoreceptor retinoid-binding protein (IRBP) induces in rats severe eye disease, experimental autoimmune uveoretinitis (EAU). This study examined the uveitogenic capacity of IRBP of another species, the monkey, and tested the cross-antigenicity between these two proteins by a battery of immunological assays. Monkey IRBP was found to be approximately 20 times less uveitogenic in Lewis rats than bovine IRBP. High levels of cross-reactivity between bovine and monkey IRBP were demonstrated by antibodies as measured by the enzyme-linked immunosorbent assay, and by the radiometric ear test of delayed-type hypersensitivity, by using rats immunized with either one of the IRBP. On the other hand, lymphocytes from these rats failed to detect the cross-reactivity between the two IRBP by the proliferation response in culture. Yet, such lymphocytes did recognize the nonimmunizing IRBP when activated in culture for acquiring the capacity to adoptively transfer EAU into naive recipients. The data are discussed with regard to the limited usefulness of the lymphocyte proliferation assay for detection of immunopathogenic processes and the role of cross-reacting antigens in initiation of autoimmune responses.
In patients with nephropathic cystinosis, corneal crystals develop by one year of age; they progressively accumulate and eventually cause recurrent corneal erosions and photophobia. After an in vitro study of cystinotic corneal stromal cells showed cystine depletion by cysteamine and after topical cysteamine was determined to be nontoxic in rabbits, we performed a controlled double-blind clinical trial of 10 mM cysteamine eyedrops in young patients with cystinosis, using one eye for treatment and the other as the control. Two children begun on the protocol before two years of age had a striking decrease in the number of corneal crystals in the cysteamine-treated eye within four to five months of entering the study. Cysteamine eyedrops appear to be safe and efficacious in the short-term treatment of patients with cystinosis who are under two years of age. The long-term value of such treatment and its effectiveness in older patients remain to be determined.
In our previous study rats immunized with bovine retinal interphotoreceptor retinoid-binding protein (IRBP) were found to develop inflammation in the eye and the pineal gland. This inflammatory disease was distinct in several aspects from experimental autoimmune uveoretinitis (EAU) induced by the retinal S-antigen (S-Ag). The current study examined the adoptive transfer of IRBP-induced EAU. We established that lymphocytes from IRBP immunized donor rats were capable of transferring EAU after in vitro stimulation with either IRBP (lymph node or spleen cells) or concanavalin A (spleen cells only). Recipients of these cells developed uveoretinitis and pinealitis identical to the actively induced disease. As compared with the S-Ag system, recipients of IRBP sensitized cells developed disease earlier, and smaller numbers of cells were needed to transfer EAU. Development of inflammation was directly related to a cellular response to the specific retinal antigen used for sensitization. Moreover, the unique nature of ocular inflammation was reestablished in the IRBP system: high proportions of polymorphonuclear leukocytes were found in the inflamed tissue of certain recipients despite a lack of a humoral response to the specific antigen. In contrast to the eye, only mononuclear leukocytes comprised the inflammation in the pineal gland.
An eye from a patient with systemic sarcoidosis and active ocular involvement was studied by the use of monoclonal antibodies and the immunoperoxidase technique to identify the subtypes of infiltrating cells and the presence of lymphokines. Large numbers of lymphoid cells reacting with anti-pan T cell (Leu-4) and anti-T helper/inducer (Leu-3a) subsets were observed around and within sarcoid granulomas. Only rare T suppressor/cytotoxic cells (Leu-2a) were observed. B lymphocytes and plasma cells were present in a few foci. Within the granuloma, T lymphocytes, macrophages, and epithelioid cells showed membrane labeling for interleukin 2 receptors and interferon gamma. We demonstrate the in vivo expression of interleukin 2 receptors and the release of interferon gamma by mononuclear phagocytes and T lymphocytes in ocular sarcoidosis, and we theorize about the activated T helper cell-derived lymphokines in macrophage activation and sarcoid granuloma formation in the eye.
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We describe a 16-year-old Japanese girl with a mitochondrial encephalomyopathy who presented with progressive dementia, limb weakness and atrophy, episodic vomiting, generalized convulsions, myoclonic seizures, and hypertrophic cardiomyopathy. CT scan revealed transient focal low density areas in her occipital and parietal lobes, and cerebellar atrophy. The clinical features were consistent with mitochondrial myopathy, encephalopathy, lactic acidosis, and strokelike episodes (MELAS). Microscopically, most of muscle fibers in the skeletal muscles and heart were occupied by markedly increased mitochondria. Polarographic studies on mitochondria isolated from postmortem heart muscle showed severe impairment of oxidation of NADH-linked substrates in contrast to normal succinate oxidation. The rotenone-sensitive NADH-coenzyme Q reductase activity was markedly decreased in heart, skeletal muscle and liver mitochondria. The biochemical investigations have led to the identification of a defect of complex I in the respiratory chain. Reported cases of a defect of complex I have revealed pure myopathy, encephalopathy or encephalomyopathy. The reason for a varied clinical expression of a single defect remains to be clarified.
Rats immunized with the retinal interphotoreceptor retinoid-binding protein (IRBP) develop an inflammatory eye disease, "experimental autoimmune uveoretinitis" (EAU). The ocular changes which characterize the EAU induced by IRBP resemble those seen in rats which develop EAU by immunization with another retinal protein, S-antigen (S-Ag). Yet, the two antigens do not cross-react antigenically and the two diseases differ by several features: At low doses (less than or equal to 4 micrograms/rat), IRBP was more uveitogenic in Lewis rats than was S-Ag, inducing disease more reproducibly and with earlier onset time. On the other hand, at higher doses (greater than or equal to 20 micrograms/rat) the disease induced by S-Ag was more severe than that induced by the same doses of IRBP. Rats of various inbred strains differed in their susceptibility to EAU induced by these two antigens. In particular, BN rats were more susceptible to IRBP-induced EAU than to the S-Ag-induced disease, while WF and RCS-rdy+ rats developed severe EAU when immunized with S-Ag but showed minimal or no ocular change when immunized with IRBP.