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Biomedical subjects

Y Katada

Publications and source records attributed to Y Katada.

At least 19 recordsLinked to original sources
PubMed2006

Growth hormone therapy and scoliosis in patients with Prader-Willi syndrome.

Growth hormone (GH) therapy for short stature in patients with Prader-Willi syndrome (PWS) has started worldwide, and various favorable effects have been reported. However, the possibility of progression of scoliosis arises as a new problem of the GH therapy. In this study, we analyzed whether 72 patients who have been followed up in our hospital have such a problem. They included 46 males and 26 females (41 patients with the GH therapy and 31 without it) aged from one to 49 years. Consequently, 33 (45.8%) of 72 patients had scoliosis with the Cobb angle of >10 degrees. Twenty (48.8%) of forty-one patients who received a GH therapy and 13 (41.9%) of 31 patients without the therapy had scoliosis, the frequency of scoliosis between the two groups showing no statistical difference (P = 0.56). Height velocity of scoliotic and non-scoliotic patients during the first year of the therapy was 8.59 +/- 1.92 and 10.70 +/- 2.54 cm, respectively, showing a significant difference (P < 0.001). This shows that accelerated height velocity may not induce scoliosis. Comparison of starting age of a GH treatment revealed that non-scoliotic patients received the therapy earlier than scoliotic patients (P = 0.021). Among 20 scoliotic patients who received the GH therapy, the degree of scoliosis progressed during the therapy in six patients, improved in three and fluctuated in one. Many patients showed progression of scoliosis with age irrespective of the use of GH, and some patients improved their scoliosis during the GH therapy. These findings showed that a GH therapy increases height velocity of PWS patients but does not necessarily develop scoliosis, and early start of the therapy may not be an exacerbating factor of scoliosis.

Adolescent↗
PubMed2005

Cause of sudden, unexpected death of Prader-Willi syndrome patients with or without growth hormone treatment.

Patients with Prader-Willi syndrome (PWS) are recognized to have a tendency of sudden, unexpected death (SED), but its exact cause is unknown because of paucity of such case reports. Since growth hormone (GH) treatment was applied to PWS patients worldwide, several cases of death have been reported. However, whether the therapy is directly related to their SED remains unknown, too. We collected 13 deceased PWS patients (Group A, aged 9 months to 34 years) who had never received GH therapy, and seven deceased patients (Group B, all boys aged 0.7-15 years) having received the therapy from the registration in PWS-patient-support associations and from the literature, respectively. We then compared the cause of SED between the two groups. Irrespective of GH therapy, SED of infants under age 1 year was associated with milk aspiration or hypothalamic dysregulation of respiration, while SED of patients in early childhood or adolescence occurred at sleeping in association with preceding viral infections. In contrast, SED of four adult (>20 years of age) patients who never received GH therapy was associated with complications, such as leg cellulites and pulmonary embolism, secondary to massive obesity and diabetes mellitus (DM). Two Group-B patients (aged 14 and 20 years) without any obesity-related or diabetes-related complications died of drowning in a bath tub, and their drowning death could be related to poor respiratory control. These findings indicated that the cause of SED is not essentially different between PWS patients with and without GH treatment. Deceased PWS patients may have had underlying respiratory dysregulation and hypothalamic dysfunction, and GH therapy might have led to certain obstructive respiratory disturbances that exacerbated the respiratory conditions. This will call clinicians' attention when using GH in PWS patients, for example, careful determination of the dose of GH and careful monitoring of patient's respiratory conditions, especially in male obese patients with respiratory problems.

Adolescent↗
PubMed2004

Coronary risk factors in Kawasaki disease treated with additional gammaglobulin.

AIMS: To assess the hypothesis that an additional intravenous gammaglobulin (IVGG) infusion, if administered early, may prevent coronary artery lesions (CAL) in patients with Kawasaki disease (KD) who do not respond to initial IVGG therapy. METHODS: Forty four KD patients (17 with CAL and 27 without CAL), treated with additional IVGG because of persistent or recrudescent fever after initial IVGG therapy, were studied. Main outcome measures were the presence of CAL by echocardiography and the number of febrile days before and after start of additional IVGG infusion (pre- and post-additional IVGG). RESULTS: In univariate analyses, risk factors for CAL were the number of febrile days pre-additional IVGG, the number of febrile days post-additional IVGG, the number of days that initial IVGG was divided over, the white blood cell count pre- and post-additional IVGG, and the C reactive protein concentration pre-additional IVGG. In a multivariate analysis, the only independent risk factor was the number of febrile days pre-additional IVGG (> or =10 days; odds ratio 7.86; 95% CI 1.44 to 42.8; p = 0.02). CONCLUSIONS: Among KD patients with persistent or recrudescent fever after initial IVGG therapy, administration of additional IVGG before the first 10 febrile days was associated with a decreased prevalence of CAL, when compared with the prevalence in those who were retreated later. An additional IVGG infusion, if administered early, may prevent CAL in initial IVGG non-responders.

Adrenal Cortex Hormones↗
PubMed2003

Association between interleukin-18 gene polymorphism 105A/C and asthma.

BACKGROUND: IL-18 has been shown to exert anti-allergic or allergy-promoting activities, but the existence of genetic polymorphisms in the coding regions of IL-18 gene has not been demonstrated. OBJECTIVE: The aim of this study was to investigate whether polymorphism is present in the coding regions of the IL-18 gene and, if so, to further analyse the association between polymorphism and asthma in a case-control study. METHODS: We screened the coding regions of the IL-18 gene for polymorphisms by using PCRsingle-stranded conformation polymorphism and direct sequencing of PCR products, followed by analysis of the association between polymorphism and asthma. RESULTS: We identified one polymorphism (105A/C) in the coding regions. The frequency of the 105A allele was significantly higher in asthmatic patients than in controls (P<0.01; odds ratio (OR)=1.83 (1.37-2.26)). Significant linkage disequilibrium was observed between the 105A/C and -137G/C polymorphisms in the 5' flanking region of the IL-18 gene (D=0.58, P<0.0001). However, in asthmatic patients the 105A allele was not associated with either total serum IgE or IL-18 levels. CONCLUSION: The 105A/C polymorphism of the IL-18 gene may be associated with the pathogenesis of asthma.

Adolescent↗
PubMed2002

Bronchomalacia associated with pulmonary atresia, ventricular septal defect and major aortopulmonary collateral arteries, and chromosome 22q11.2 deletion.

Respiratory distress is one of the major complications in young infants with pulmonary atresia, ventricular septal defect and major aortopulmonary collateral arteries (PA-VSD-MAPCA); however, its aetiology remains obscure. We have previously reported an association of bronchomalacia with PA-VSD-MAPCA in patients with a hemizygous deletion of chromosome 22q11.2 (del.22q11). To clarify the clinical relevance of bronchomalacia in patients with PA-VSD-MAPCA and del.22q11, we reviewed the clinical and laboratory records of four patients with PA-VSD-MAPCA who had del.22q11 and bronchomalacia. External bronchial compression by anomalous patterning of the aorta and MAPCA was documented in three of the four patients, using combinatorial examination of angiocardiography, bronchography, fibreoptic bronchoscopy and magnetic resonance imaging. One of the four patients died suddenly of severe respiratory distress at 4 years of age, while the remaining three were inoperable for complete surgical repair. Our study indicates that bronchomalacia as a result of external vascular compression may be an aetiology of early-onset respiratory distress in some patients with PA-VSD-MAPCA and del.22q11, and can significantly affect the clinical outcome.

Airway Obstruction↗
PubMed2001

Enhancement of T helper2 response in the absence of interleukin (IL-)6; an inhibition of IL-4-mediated T helper2 cell differentiation by IL-6.

Functional roles of interleukin (IL-)6 in T cell response were investigated. Mice deficient in IL-6 and wild mice were immunized with antigens (myelin oligodendrocyte glycoprotein or methylated BSA) and production of IL-4 and interferon (IFN)-gamma by regional lymph nodes was measured. IL-6 deficiency led to an enhancement of IL-4 and an inhibition of IFN-gamma production. Moreover, polyclonal stimulation of spleen T cells from unimmunized IL-6-deficient mice with anti-CD3 plus anti-CD28 antibodies (Abs) demonstrated an enhancement of T helper (Th)(2)responses. The presence of IL-6, however, augmented IL-4 production but it inhibited IFN-gamma expression by spleen T cells in response to polyclonal stimulation and by antigen-primed spleen T cells in response to re-challenge with the antigen. In contrast, the induction of spleen CD4-positive T cells into Th(2)cells in vitro by the anti-CD3 plus IL-4 was completely suppressed by exogenously added IL-6, whereas Th(1)differentiation of T cells by the anti-CD3 plus IL-12 was not inhibited by the presence of IL-6. Thus, these results indicate that IL-6 physiologically could modulate qualitative T cell response and suggest that it augments Th(1)responses partly through its inhibitory capability of IL-4-induced Th(2)differentiation of naive T cells.

Adjuvants, Immunologic↗
PubMed1999

Delayed onset and reduced severity of collagen-induced arthritis in interleukin-6-deficient mice.

OBJECTIVE: To investigate the roles of interleukin-6 (IL-6) in the pathogenesis of rheumatoid arthritis (RA) by studying its effect on murine collagen-induced arthritis (CIA). METHODS: IL-6-deficient (IL-6-/-) mice with a genetic background of susceptibility to CIA were generated by backcrossing them with DBA/1J mice for 8 generations. Clinical and immunologic features were compared between these mice and IL-6 wild-type (IL-6+/+) littermates with CIA. RESULTS: Serum IL-6 levels increased during the development of CIA in IL-6+/+ mice. Two prominent peaks were observed. The first was coincident with the onset of arthritis, and the second one was observed during exacerbation of the disease. The onset of arthritis in IL-6-/- mice was delayed for 2 weeks compared with that in IL-6+/+ mice, and the severity of arthritis, as indicated by the arthritis score, remained significantly lower in IL-6-/- mice during the entire followup period (14 weeks), although all IL-6-/- mice developed definite arthritis as did the IL-6+/+ mice. Histologic severity was also reduced in IL-6-/- mice. In addition, radiologic changes such as osteopenia and bone erosion were reduced significantly in these animals. Both humoral and cellular responses to type II collagen (CII) in IL-6-/- mice were reduced to about half those in IL-6+/+ mice. In addition, enhanced production of IL-4 and IL-10 in response to concanavalin A stimulation was observed in IL-6-/- mice. CONCLUSION: IL-6 plays an important role in the development of CIA, and both suppression of specific immune responses to CII and a tendency to a shift toward a Th2 cytokine profile might contribute in part to the attenuation of CIA in IL-6-/- mice. These findings suggest that blockade of IL-6 might be beneficial in the treatment of RA.

Animals↗
PubMed1998

Interleukin 6 plays a key role in the development of antigen-induced arthritis.

To investigate the direct role of interleukin (IL) 6 in the development of rheumatoid arthritis, IL-6-deficient (IL-6 -/-) mice were backcrossed for eight generations into C57BL/6 mice, a strain of mice with a genetic background of susceptibility for antigen-induced arthritis (AIA). Both histological and immunological comparisons were made between IL-6-deficient (IL-6 -/-) mice and wild-type (IL-6 +/+) littermates after the induction of AIA. Although all IL-6 +/+ mice developed severe arthritis, only mild arthritis was observed in IL-6 -/- mice. Safranin O staining demonstrated that articular cartilage was well preserved in IL-6 -/- mice, whereas it was destroyed completely in IL-6 +/+ mice. In addition, comparable mRNA expression for both IL-1beta and tumor necrosis factor alpha, but not for IL-6, was detected in the inflamed joints of IL-6 -/- mice, suggesting that IL-6 may play a more crucial role in cartilage destruction than either IL-1beta or tumor necrosis factor alpha. In immunological comparisons, both antigen-specific in vitro proliferative response in lymph node cells and in vivo antibody production were elicited in IL-6 -/- mice, but they were reduced to less than half of that found in IL-6 +/+ mice. Lymph node cells of IL-6 -/- mice produced many more Th2 cytokines than did IL-6 +/+ mice with either antigen-specific or nonspecific stimulation in in vitro culture. Taken together, these results indicate that IL-6 may play a key role in the development of AIA at the inductive as well as the effector phase, and the blockade of IL-6 is possibly beneficial in the treatment of rheumatoid arthritis.

Animals↗
PubMed1998

[Acute angle-closure glaucoma following surgery for oral cancer].

A 60-year-old woman who had undergone surgery of oral cancer under general anesthesia developed an attack of acute angle-closure glaucoma the next morning. Her intraocular pressure decreased immediately by adequate treatments including surgical procedures (laser iridotomy and trabeculectomy), and her symptom improved. It is considered that this event was induced by several factors such as atropine given before and during general anesthesia, perioperative hypertension and anatomical abnormalities. However the definite cause of this event is unclear. We conclude that it is difficult to predict a glaucoma attack following surgery under general anesthesia, but this complication is an important ophthalmologic emergency. Immediate diagnosis and appropriate treatment should be done to prevent the grave prognosis.

Acute Disease↗
PubMed1997

In vivo but not in vitro stimulations rescue of the defective class switching to IgG or IgA in B-cells of immunodeficiency with hyper IgM.

In an X-linked immunodeficiency with hyper IgM (X-HIM), several mutations of genes coding for CD40 ligand are responsible for B-cell defects. However, it is controversial whether the defective class switching from IgM to IgG or IgA but not IgE is rescued by in vitro stimulations or not. In six X-HIM patients, signaling through CD40 induced IgE but not IgG or IgA secretion in vitro. When transferred into SCID mice, however, B-cells of X-HIM patients secreted as much IgG and IgA as those of healthy controls. Moreover, sIgG and sIgA expressions were also induced by the in vivo stimulation. These results support that B-cells of X-HIM patients are defective of in vitro class switching from IgM to IgG or IgA and show that the in vivo stimulations rescue the defective class switching and suggest that the class switching of IgE and that of IgG or IgA might be regulated quite differently.

Animals↗
PubMed1996

B cell-B cell interaction through intercellular adhesion molecule-1 and lymphocyte functional antigen-1 regulates immunoglobulin E synthesis by B cells stimulated with interleukin-4 and anti-CD40 antibody.

IgE synthesis by purified human B cells is induced by two signals: a class switching factor, most commonly interleukin (IL)-4, and the engagement of CD40, which is activated through its interaction with CD40 ligand (CD40L) expressed on activated T cells. Thus, the combination of IL-4 and anti-CD40 monoclonal antibody (mAb) has been shown to stimulate IgE production in vitro by highly purified B cells. In this T cell-independent system, strong homotypic aggregation of B cells is observed prior to the production of IgE. Flow cytometric analysis and cell binding assays showed that the stimulation of purified B cells with anti-CD40 mAb plus IL-4 resulted in a striking increase of intercellular adhesion molecule (ICAM)-1(CD54) expression, an induction of CD43 and an avidity change of lymphocyte functional antigen (LFA)-1(CD11a/CD18), with little augmentation of CD18 expression. Addition of anti-ICAM-1 mAb caused an inhibition of homotypic aggregation but augmented IgE synthesis by B cells stimulated with anti-CD40 mAb and IL-4, although it did not affect B cell proliferation or IL-6 production by the B cells. Among the mAb against counter-receptors for ICAM-1 tested, anti-CD11a mAb suppressed IgE synthesis, while anti-CD18 mAb and anti-CD43 mAb had little effect. The enhancing or inhibitory effect of anti-ICAM-1 mAb or anti-CD11a mAb on IgE production was achieved by the increased or decreased expression of germline C epsilon transcripts by B cells stimulated with anti-CD40 mAb and IL-4. These results indicate that B cell-B cell interaction through ICAM-1 and one of its counter receptors, LFA-1, regulates IgE synthesis by modulating C epsilon germ-line transcription.

Antibodies, Monoclonal↗
PubMed1996

Functional disturbance of naive T lymphocytes in very high IgE producers: depletion of interleukin-4-induced interleukin-4-producing cells.

We examined the capacity of T cells from normal individuals and allergic patients with very high IgE to differentiate into interleukin-4(IL-4)-producing cells in vitro. T cells incubated with anti-CD3 monoclonal antibody plus IL-4 or plus anti-IL-4 antibody in the presence of antigen-presenting cells for 7 days were restimulated and their capacity to express IL-4 mRNA was examined by RT-PCR. In T cells from normal individuals, there was a marked increase in the expression of IL-4 mRNA following the addition of IL-4. After fractionation of normal T cells into naive T (CD45RA+) and memory T (CD45RO+) cells, induction of the increase of IL-4 mRNA was restricted to the naive T cell population. In contrast, in T cells from allergic patients, the stimulation of whole or naive T cells with anti-CD 3 monoclonal antibody in the presence of IL-4 induced much less IL-4 mRNA. These findings suggest the presence of a functional abnormality in IL-4-dependent development of IL-4-producing T cells in the peripheral-blood naive T cells from allergic patients.

Adjuvants, Immunologic↗
PubMed1996

Peripheral blood T lymphocytes and basophils, freshly isolated from house-dust-mite-sensitive patients, produce interleukin-4 in response to allergen-specific stimulation.

We examined the capacity of interleukin-4 (IL) production from lymphocytes and basophils, isolated from the peripheral blood of allergic patients sensitive to house dust mite, after stimulation with mite extract. IL-4 production was measured by a sensitive bioassay based on coculture with CT.h4S (a human IL-4-responsive cell line). Lymphocytes and basophils from patients with elevated serum IgE specific to mite allergen [radioallergosorbent test (RAST) score > 3] could produce detectable levels of IL-4 in response to mite extract, whereas those from patients with a RAST score of less than 2 or normal volunteers could not. The sensitivity of basophils to mite extract was high, so that a lower concentration of mite extract (1-10 ng/ml) could induce maximal IL-4 production. On the other hand, a higher concentration (10 micrograms/ml) was required for maximal IL-4 production from the lymphocytes. These findings demonstrate that allergen-specific IL-4-producing cells, lymphocytes and basophils, are generated in vivo in allergic patients and also that there exist characteristic differences between lymphocytes and basophils related to the in vivo source of IL-4.

Allergens↗
PubMed1995

Signaling through CD40 rescues IgE but not IgG or IgA secretion in X-linked immunodeficiency with hyper-IgM.

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.

Amino Acid Sequence↗
PubMed1995

[A case of acquired von Willebrand disease due to pulmonary stenosis after Jatene's operation].

The case of a 9-year-old girl with pulmonary stenosis complicated by acquired bleeding tendency after Jatene's operation is reported. Coagulation study revealed that platelet count and von Willebrand factor were reduced. Catheterization study revealed severe pulmonary stenosis, the pressure gradient between the right ventricle (RV) and pulmonary artery (PA) being 190 mmHg. A link between pulmonary stenosis and bleeding tendency was suggested and the patient was diagnosed as having acquired von Willebrand disease due to activated platelet/von Willebrand factor interactions enhanced by "shear stress" at the site of pulmonary stenosis. Right ventricular outflow reconstruction was done when she was 9 years-old. Due to a protocol based on the results of the challenge test that we instituted to determine the efficacy and effective duration of blood derivatives and hemostatic agents, perioperative massive bleeding was avoided. Bleeding tendency disappeared and coagulation study findings normalized with correction of the abnormal hemodynamic state.

Child↗
PubMed1993

[Two cases of Swyer-James syndrome].

Case 1: 55-year-old male was admitted to our hospital for further examination of increased transparency of X-ray in the left lower lung. He had history of pneumonia in his childhood. Left bronchography revealed mild cylindrical bronchi-ectasia in the proximal bronchi but poor filling by contrast in the peripheral bronchi. Case 2: 61-year-old male was referred to our hospital with palpitation and dyspnea. Chest X-ray film revealed hyperlucency of the left lower lung. The ventilation scan showed a marked decrease in ventilation to the left lung and air trapping was present in the left lung. The perfusion scan showed a matched decrease in blood supply to the left lung. In both cases, pulmonary arteriogram showed narrowed and withered-tree-like left pulmonary arteries. From these clinical findings, we diagnosed these two cases as Swyer-James syndrome. We are reporting two cases of Swyer-James syndrome and describing the clinical feature, differential diagnosis and etiology of the syndrome.

Arteriosclerosis↗
PubMed1987

[Experimental analysis of the conscious structure of the sex-role-acceptance in the female adolescents: among the girl students in their final period of moratorium in Hokkaido].

The purposes of this paper are, 1) to determine the dimensions representing the structure of conscious level "sex-role-acceptance" by the female adolescents in relation to the environments within which the subjects were brought up and educated, and 2) to investigate several factors under which the conscious structure of role-acceptance have been deeply influenced: i.e., parents, sibling, boy friends in intimate terms, and others (male or female). Our data were collected from more than 1800 female students, and were subjected to multivariate analyses. The results were: 1) The following three dimensions pertaining to their sex-role-related decision-making were obtained: Biological, Social-motivational, and Self-interest. 2) The difference in the conscious-structure between the role acceptance group and the non-acceptance group was statistically significant. 3) the father-daughter interaction was significantly important in creating an active contributional will in the girls' life-plan, while the mother-daughter interaction turned out to have a rather negative influence upon their will of contribution. 4) The lack of identification with parents was sometimes compensated by their identification with others. The social importance of positive, warm support for the youngsters was clearly demonstrated.

Adult↗