Allergic contact dermatitis from colistin.
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Biomedical subjects
Publications and source records attributed to A Inoue.
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We determined the distribution frequency of angiotensin-converting enzyme insertion/deletion (I/D) polymorphism in 111 Japanese patients with non-insulin-dependent diabetes mellitus (NIDDM) of at least 10 years duration (80 patients with diabetic nephropathy and 31 patients without nephropathy) and 76 healthy Japanese controls. Patients with diabetic nephropathy showed an excess of the ID genotype compared with patients without nephropathy (p < 0.02) and less of the II genotype compared with healthy controls (p < 0.01) and patients without nephropathy (p < 0.01). NIDDM patients with the II genotype have a decreased risk for the development of diabetic nephropathy.
The ligand for CD40 (CD40L) is a membrane protein on activated T cells that induces B cell proliferation and differentiation. Several mutations of the CD40L gene were reported responsible for defective class switching of B cells in an X-linked immunodeficiency with hyper IgM (X-HIM). We studied four affected males from three families and found three independent mutations including new mutations of CD40L gene. In every X-HIM patient tested, however, anti-CD40 plus IL-10 did not induce class switching from IgM to IgG or IgA, even in the presence of Staphylococcus aureus Cowan I strain (SAC). CD4+ T cell clones, expressing CD40L on their surface, also did not rescue IgG or IgA induction by X-HIM peripheral blood B cells in vitro. But signaling through CD40 induced both B cell proliferation and IgE secretion when IL-4 was added to the culture. Taken together, these results show that in vitro signaling through CD40 rescues IgE but not IgG or IgA secretion by peripheral blood X-HIM B cells and suggest that in vivo CD40 and CD40L interaction might be necessary for IgG and IgA differentiation in X-HIM.
We isolated three organic solvent (OS)-tolerant bacterial strains DS-1051, DS-1902, and DS-313 from a depth of 1,168 m in Sagami Bay, Japan. These isolates were tolerant to various kinds of toxic OSs such as benzene, toluene, and p-xylene. They also could degrade polyaromatic hydrocarbons, naphthalene or biphenyl, in a medium-OS (9:1) two-liquid-phase system. Percentage degradation of polyaromatic hydrocarbons in OS by these strains were higher than those obtained from cultures in which substrates were in the medium without OS.
The outer membrane protein profiles of a toluene-tolerant mutant, Pseudomonas aeruginosa, strain PAK103, were compared with those of its parent strain PAO1161. Protein F (OprF), the most abundant outer membrane protein in the parental strain PAO1161, was missing in the toluene-tolerant strain PAK103. The absence of OprF may lead to the loss of toluene diffusion across in the outer membrane of the mutant cells.
Cranioplasty with autogenous split-thickness calvarial bone was performed in 10 patients. Follow-up for a mean of 19 months (range 2-43 mos) showed satisfactory protection of the brain and cosmetic reconstruction. No serious complication was seen except in one patient with postoperative epidural abscess. Split-thickness calvarial bone graft is recommended in patients with previous infection or high risk of infection, in poorly vascularized recipient sites resulting from multiple operations or irradiation, and in younger patients aged more than 7 years.
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Idiopathic chondrolysis of the hip is characterized by pain, limping and a progressive restriction in the range of motion of the hip. The paper describes the case of two female patients, age 28 and 37, who were referred to our hospital in October 1985 and May 1991 for pain and limitation of movement in the right hip. Neither patient had a previous history of systemic illness or trauma or medication such as steroids. On admission they underwent clinical and X-ray examinations. Both required an open biopsy to confirm the diagnosis. They have been followed for 4 years and 8 years, respectively.
Chronic inflammatory cells are key components in the progression of atherosclerotic plaques and restenosis after coronary angioplasty. Adhesion molecules are fundamental in inflammatory processes. Therefore, the distributions of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule (VCAM) were investigated in directional coronary atherectomy specimens obtained from 14 patients, in 6 with acute coronary syndromes (myocardial infarction and unstable angina within 1 month), 6 with old myocardial infarction and 2 with stable effort angina. There were eight primary lesions and six restenotic lesions. Atherectomy tissue fragments were snap frozen and cut into 4 microns thick cryostat sections for immunohistochemical staining by avidin-biotin complex immunoperoxidase techniques using adhesion molecule specific monoclonal antibodies BBIG-I1 (ICAM-1) and BBIG-V1 (VCAM). The cells of lesions were characterized in sequential sections by macrophage marker KP1 (CD68), endothelial marker JC/70A (CD31), and smooth muscle cell marker 1A4 (alpha-smooth muscle actin). Four restenotic lesions that had undergone a prior balloon angioplasty within a few months consisted of intimal proliferation and the other lesions were atherosclerotic plaque. Macrophage-rich areas were seen in the lesions from acute coronary syndromes and/or early restenotic lesions. Expression of ICAM-1 or VCAM was strongly associated with macrophage-rich areas, but VCAM staining was weaker than ICAM-1 except in one restenotic lesion. Macrophages that express ICAM-1 and/or VCAM may be important in the unstable plaques and restenotic lesions related to disease activity of ischemic heart disease.
We have retrospectively compared the efficacy of plasma exchange (PE), immunoadsorption plasmapheresis therapy (IAPP), corticosteroid administration and no treatment in the treatment of the Guillain-Barré Syndrome (GBS). Forty-two patients with GBS and clinical functional grades of more than Hughes 3 were admitted to Shinshu University Hospital, Nagano Red-cross Hospital and Saku General Hospital between 1978 and 1994. These patients were treated with either PE, IAPP, corticosteroids or no therapy. Eight were treated with PE, eleven with IAPP, twelve with corticosteroids and eleven were untreated. None of the patients were received combined therapy. The four groups of patients were compared on the following points; duration of the deteliocation in symptoms, duration of the worst symptoms, period of the ability to walk after onset, minimum motor nerve conduction velocity (MCV) over the course, maximum cerebrospinal fluid (CSF) protein concentration over the course, and CSF protein concentration improvement 6 weeks after onset as compared with 2 weeks after onset. The results revealed that the duration of the worst symptoms was shortened more in the IAPP-treated and PE-treated groups than in the other groups. Decreases in CSF protein concentration were more significant in the IAPP-treated and PE-treated groups than in the other groups. There were no significant differences in the other parameters among the groups. Furthermore the clinical symptoms of GBS improved more rapidly with PE and IAPP than with supportive care alone or corticosteroid therapy, especially in the early phase of the disease. IAPP and PE are equally effective.(ABSTRACT TRUNCATED AT 250 WORDS)
We report a patient with myasthenia gravis who experienced a relapse 13 years after apparently successful treatment by mediastinal irradiation and corticosteroid therapy. A 20-year-old male was admitted to Shinshu University Hospital with a chief complain double vision and drooping eyelids. These symptoms had appeared 2 months prior to admission. They tended to be more severe late in the day, and varied from day to day. Prior to this admission the patient had been healthy for the 13 years since undergoing 45-Gy mediastinal irradiation and corticosteroid therapy. MRI and CT studies revealed no thymic hyperplasia. Total thymectomy was performed, and his myasthenic symptoms, including the opthalmoplegia, improved. Histological examination of the resected thymus revealed an active thymus with germinal centers. Immunohistological studies showed an abundance of intracellular adhesion molecule-1 (ICAM-1) in the germinal centers and thymic medullary epithelium, and the presence of lymphoid function-associated antigen-1 (LFA-1) in thymic lymphocytes. ICAM-1 and LFA-1 are ligand of adhesion molecules which interact with each other and play an important role in antigen presentation. Acetylcholine receptor (ACh-R) antigen is known to be present in the thymus. The presence of both ICAM-1 and LFA-1 in the active thymus in this patient suggests that these adhesion molecules may have a role in ACh-R antigen presentation, causing myasthenia. These findings suggest that patients with myasthenia gravis who do not undergo total thymectomy have a risk of recurrence, even after long-term remission.
We here report a case of Miller Fisher syndrome (MFS) in which serum anti-cerebellar antibody was detected by Western blot analysis. The 32-year-old male studied suffered from diplopia, gait ataxia and sensory disturbance in the distal portion of the upper limbs preceded by cold-like symptoms. Neurological examination on admission revealed that he had external ophthalmoplegia with bilateral ptosis, cerebellar ataxia and areflexia. A cerebrospinal fluid examination showed albuminocytologic dissociation with a protein concentration of 60 mg/dl. Brain CT and MRI showed no significant abnormalities. The patient was diagnosed as MFS, and treated it with two sessions of immunoadsorption plasmapheresis (IAPP). After receiving IAPP therapy, the patient's neurological symptoms and signs were improved. Western blot analysis showed the existence of antibody directed against mouse cerebellum but not against mouse cerebrum, brain stem, and spinal cord in his serum, the level of which was decreased after the IAPP therapy. Serum anti-GQ1b antibody was also elevated. As far as we are aware, there have been no reports showing the existence of anti-cerebellar antibodies detected by Western blot analysis. Though the pathogenesis of MFS remains unclear, our findings suggest that anti-cerebellar antibody detected by Western blot analysis may be caused by cerebellar ataxia in MFS.
We reported a case of Crow-Fukase syndrome and examined the mechanism of hepatomegaly in Crow-Fukase syndrome. A 67-year-old woman was presented with polyneruopathy, hepatosplenomegaly, pericardial effusion and M proteinemia. On examination, all laboratory data and clinical symptoms were compatible with Crow-Fukase syndrome. The patient was treated with prednisolone and immunoadsorption plasmaphresis therapy. All the clinical manifestations including hepatomegaly gradually improved. In order to examine whether some factors that promote the prolifelation of hepatocyte may exist in the patient's serum, we cultured mouse hepatocyte in the presence of patient's or control serum together. Though the number of hepatocytes decreased after 2 days culture, the number of hepatocytes cultured with patient's serum in active disease stage remained significantly greater than of hepatocytes cultured with either control serum or patient's serum in healing stage. There were no abnormal pathological findings in biopsied liver. Liver suggesting that hepatomegaly was the results of normal hepatocytes proliferation. Taken together, these findings suggest there were some factors that may promote the proliferation of hepatocytes or may have protective effect of hepatocyte in patient's serum. Though the level of human hepatocyte growth factor (h-HGF) in patient's serum in active disease stage was slightly increased, hepatomegaly cannot be attributable solely to h-HGF. Organomegaly is one of the important symptoms of the Crow-Fukase syndrome, however, in so far as we are aware its mechanism is not examined. In this report it is suggested that several unknown factors other than h-HGF may contribute the hepatomegaly of the Crow-Fukase syndrome.
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Quinpirole with D2 agonist activity showed a two-fold increase in the GTPase activity in the 6-hydroxydopamine-lesioned side of the striatum, compared with that in the control side. However, neither qualitative nor quantitative changes were observed in the gene expression of two alternative splicing products derived from dopamine D2 receptor gene or of Gil alpha, in the RNAase protection assay. These results suggest that D2 receptor-mediated supersensitization does not come from the D2 receptor upregulation.
The rate of 6-[14C]D-glucose oxidation in cerebral cells of SAMP8, a substrain of senescence accelerated mouse, was investigated in vitro. The production of 14CO2 in dissociated intact brain cells prepared from the cerebrum of 4-8-week-old SAMP8 was higher than that of age-matched SAMR2 as a control mouse, while no difference between these two strains was observed in the production of 14CO2 in the cerebral homogenates. These results indicated that the increased metabolism of glucose in SAMP8 might be associated with the glucose transport system across the cell membrane. Therefore, 2-deoxy-D-glucose (2-DG) uptake into the brain cells and cytochalasin B (CB) binding to cerebral crude membranes were examined. Both the 2-DG uptake and the CB binding in SAMP8 were much greater than in SAMR2. Furthermore, the increased CB binding in SAMP8 was seen only in the cerebral cortex of 4- to 8-week-old mice, and neither in other regions of the cerebrum nor in other aged mice (2-week- and 40- to 48-week-old mice). These results suggest that the transient overproduction of the glucose transporter protein in the cerebral cortex is involved in the increased glucose metabolism in 4- to 8-week-old SAMP8.
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Thyroid hormone (3,5,3'-tri-iodothyronine; T3) regulates gene expression through binding to its specific receptor in the nucleus. In euthyroid animals, roughly half of all receptors are occupied by the hormone. Nuclear extracts thus yield mixtures of occupied and unoccupied receptors. We present here a simple method for transforming occupied receptors into unoccupied ones. In vitro, the T3-receptor complex dissociated in a half-dissociation time exceeding 100 h at 0 degrees C, and at temperatures that accelerated the dissociation the receptor was quickly inactivated. Long-chain-fatty-acyl-CoAs, on the other hand, greatly accelerated the dissociation of T3-receptor complex at 0 degree C. The receptor was extracted from rat liver nuclei, incubated with oleoyl-CoA to release the bound hormone, and passed through a small column of Lipidex, which strongly adsorbed both oleoyl-CoA and the dissociated hormone. The receptor was recovered in the flow-through fraction in its unoccupied form, as seen by the results of DEAE-Sephadex column chromatography and the loss of all previously bound [125I]T3. The maximum T3-binding capacity of the unoccupied receptor was about 1.5-fold that of the untreated sample, and the dissociation constant was unaltered. The results suggest that most nuclear thyroid-hormone receptors occupied by the hormone were transformed into unoccupied ones. From the T3-binding capacity before and after oleoyl-CoA treatment, the in vivo T3 occupancy of the receptor was estimated. The procedure is easy to perform, and the method should be useful for studies of unoccupied receptors.