Biomedical subjects

M Yano

Publications and source records attributed to M Yano.

At least 343 records · Page 19Linked to original sources

PubMed1997

Modulation of circadian expression of D-site binding protein by the schedule of parenteral nutrition in rat liver.

The aim of this study was to investigate the changes in the circadian rhythm of the expression of liver-specific genes caused by different schedules of parenteral nutrition (PN). Rats received PN continuously throughout the day or intermittently during the night or day for 7 days. They were examined for gene expression of D-site binding protein (DBP), albumin, and cytochrome P450 cholesterol 7alpha-hydroxylase (CYP7) in the liver. The nocturnal PN group showed circadian expression of DBP messenger RNA (mRNA) and protein with a peak at 10 PM, in the same manner as the control rats receiving normal chow feeding. However, the diurnal PN group showed inverted expression of DBP mRNA and protein with a peak at 10 AM. CYP7 mRNA levels exhibited good synchronization with the levels of DBP mRNA in all groups, whereas albumin mRNA levels did not show such synchronization. Gel mobility-shift assay disclosed that the binding activity of the nuclear extracts to the CYP7 gene promoter was changed by the PN schedule in accordance with the expression of CYP7 mRNA. The PN schedule modulates the circadian rhythm of DBP expression and may have an effect on hepatic bile acid formation through transcriptional regulation of the CYP7 gene.

Albumins↗

PubMed1997

Effects of cyclic and continuous parenteral nutrition on albumin gene transcription in rat liver.

To evaluate schedule-dependent effects of parenteral nutrition on albumin gene expression and regulation, mRNA levels for albumin and its promoter-binding nuclear factors in the liver were measured in rats receiving cyclic or continuous parenteral nutrition. Rats were divided into three groups: the control group (n = 5) received a nonpurified diet, the continuous parenteral nutrition group (n = 5) received a continuous infusion of a defined parenteral nutrition formula, and the cyclic parenteral nutrition group (n = 5) received a cyclic (between 2000 and 0800) infusion of the same formula. After 7 d, rats were killed to obtain serum and liver. The serum albumin concentrations were 44 +/- 3 g/L in the controls, 31 +/- 2 g/L in the continuous parenteral nutrition group, and 33 +/- 3 g/L in the cyclic parenteral nutrition group. The mRNA for albumin and D site binding protein (DBP) was more abundant and mRNA for CCAAT/enhancer binding protein beta (C/EBP beta) was less abundant in the cyclic parenteral nutrition group than in the continuous parenteral nutrition group. Gel-shift assay for D site and gel-shift Western blotting of DBP carried out using another three rats in each group revealed an increase of DBP in rats receiving cyclic parenteral nutrition compared with continuous parenteral nutrition. In conclusion, although parenteral nutrition decreases serum albumin concentrations, cyclic parenteral nutrition maintains transcription of the albumin gene to a greater extent than does continuous parenteral nutrition. Cyclic parenteral nutrition, in contrast with continuous parenteral nutrition, sustains the mRNA and concentrations of DBP.

Albumins↗

PubMed1997

Gene expression of albumin and liver-specific nuclear transcription factors in liver of protein-deprived rats.

Protein-energy malnutrition causes hypoalbuminemia. Recent work has suggested that this may be partly due to decreased transcription of the albumin gene. This study examined the role of cis-acting and transacting elements of the albumin gene during protein deprivation. Male 7-wk-old Donryu rats were fed a protein-free diet (0% casein diet) for 10 d or given restricted (pair-fed control) or free access (freely fed control) to a 25% casein diet. Serum albumin concentrations were significantly lower in the protein-deprived rats (29 +/- 1 g/L) than in the pair-fed controls (42 +/- 3 g/L) or the freely fed controls (45 +/- 3 g/L). The albumin mRNA level was also significantly lower in livers of protein-deprived rats (36% of pair-fed control). However, gel mobility shift analysis using liver nuclear extracts did not show any significant difference between the protein-deprived rats and the pair-fed controls in the binding activity to the B and D sites of the albumin promoter. Furthermore, gel mobility shift-Western blot analysis showed no significant difference between the two groups in the protein levels of nuclear transcription factors binding to the D sites. The amounts of mRNA of hepatocyte nuclear factor-1 binding to the B site were not significantly different between these two groups. These results suggest that the proximal promoter region may not play a major role in the down-regulation of the albumin gene during protein deprivation.

Analysis of Variance↗

PubMed1997

Expression of recombinant human glutamic acid decarboxylase (GAD) in myeloma cells and enzyme-linked immunosorbent assay (ELISA) for autoantibodies to GAD.

Detection of serum autoantibodies to glutamic acid decarboxylase (GAD) is a new method to differentiate insulin-dependent diabetes mellitus (IDDM) and non-insulin-dependent diabetes mellitus (NIDDM). We established a transformed mouse myeloma cell line, SPG14, which expresses recombinant human GAD65, a major isomer of 65 kDa, inside the cells. GAD65 was partially purified by affinity chromatography using the mouse anti-GAD antibody (Ab). We also established a sandwich ELISA for anti-GAD Ab of the IgG class using GAD65 for coating and the anti-human IgG for detection and examined 54 sera of the IDDM patients and 45 sera of normal individuals. When the mean +2 SD of the color development of the sera of normal individuals was used as a cut-off level, 59.2% of patients with IDDM were positive. This indicates that the ELISA was effective to differentiate IDDM and NIDDM. The result also indicates that the autoantibody to GAD does not dissociate from the recombinant GAD rapidly, even when unbound anti-GAD Ab was fully removed. By using a perfusion culture system, we obtained as many as 4.2 x 10(10) SPG14 cells, from which 5 mg of GAD65 could be obtained; this is sufficient for 5,000 assays. This system could be clinically useful for large-scale diagnosis of IDDM.

Animals↗

PubMed1997

Coexpression studies with endothelin receptor subtypes indicate the existence of intracellular cross-talk between ET(A) and ET(B) receptors.

Human Girardi heart cells expressing endothelin ET(B) receptors (GH(B) cells) were transfected with human ET(A) cDNA, and coexpression of ET(A) and ET(B) in the ratio of 4:6 was demonstrated by Scatchard analysis. [125I]Endothelin (ET)-1 binding to ET(A)-transfected GH cells (GH(AB) cells) was displaced by an ET(A) antagonist, BQ-123, in a biphasic manner. An ET(B) agonist, BQ-3020, and an ET(B) antagonist, BQ-788, inhibited [125I]ET-1 binding to GH(AB) cells in a monophasic manner with low affinities (IC50 = 2,800 and 890 nM, respectively); IC50 values for ET(B) receptors seemed to be as weak as those for ET(A) receptors. However, BQ-3020 and BQ-788 had a high affinity for ET(B) receptors in a binding experiment using [125I]ET-1 in the presence of 1 microM BQ-123, where ET(A) receptors are masked (IC50 = 0.49 and 0.89 nM, respectively). The ET(B)-mediated increase in intracellular calcium concentrations in GH(AB) cells was not affected by 0.1 microM BQ-788 alone but was inhibited significantly by the same concentration of BQ-788 in combination with 10 microM BQ-123. ET-1 suppressed forskolin-stimulated accumulation of cAMP through the activation of ET(A) and ET(B) in GH(AB) cells; 1 microM BQ-123 or BQ-788 inhibited the suppression by only 20%, whereas a mixture of BQ-123 and BQ-788 (1 microM each) completely inhibited the cAMP decrease. These findings suggest that the stimulation of ET(A) receptors with ET-1 results in a lowering of the affinity of BQ-3020 and BQ-788 for ET(B) receptors in GH(AB) cells. We conclude that there is intracellular cross-talk between ET(A) and ET(B) receptors in GH(AB) cells.

Amino Acid Sequence↗

PubMed1997

Involvement of interleukin-6 in activation of lysosomal cathepsin and atrophy of muscle fibers induced by intramuscular injection of turpentine oil in mice.

Serum IL-6 level increased after the injection of turpentine oil into the right gastrocnemius muscle in mice. The mRNA level of IL-6 was highest in the injected muscle at 12 h after injection, but was not identified in the opposite muscle. The activities of cathepsins B and B+L started to elevate after 12 h in the injected muscle and markedly increased after day 3. Likewise, the mRNA levels of cathepsins B and L markedly increased from day 1 to day 5 in the injected muscle. However, a very mild increase was also observed in the opposite muscle. Immunohistochemical staining of cathepsins B and L exhibited positive reactions as fine granules in myofibers at 12 h and strong positive reactions in the infiltrating macrophages at 3 days. Atrophy of myofibers type 1 and 2 was evident in a time-dependent manner in the injected muscle. Treatment with rat anti-mouse IL-6 receptor monoclonal antibody inhibited the increase in cathepsin activities in the injected muscle. We conclude that IL-6 produced in the inflamed muscle is involved in the process of muscle degeneration, especially through the activation of lysosomal cathepsins.

Animals↗

PubMed1997

Cardiovascular and renal actions of the endothelin(B) receptor in pigs.

Previously we showed that blocking the endothelin (ET)A receptor subtype with BQ-153 inhibited the vasoconstrictor effects of intravenously administered ET-1. In the presence of the ET(A) antagonist, ET-1 produced marked reductions in myocardial contractility and renal blood flow. We postulated that either the ET(B) receptor, or some other, as yet unidentified, ET-receptor subtype mediated the observed hemodynamic changes. In anesthetized pigs, this hypothesis was tested by using a recently developed selective, high-affinity antagonist to the ET(B) receptor, BQ-788, and sarafotoxin S6c, a selective ET(B) agonist, to determine the contribution of this receptor subtype to cardiovascular function. Endothelin-1 (0.4 nmol/kg, i.v.) produced the characteristic biphasic hemodynamic responses, consisting of an initial transient reduction in mean arterial pressure (MAP; 83 +/- 3 to 72 +/- 4 mm Hg; n = 9) followed by a prolonged increase (112 +/- 4 mm Hg; p < 0.01). As well, cardiac output (-58%; p < 0.05), myocardial contractility (-19%; p < 0.01), and renal blood flow (63%; p < 0.05) decreased. Sarafotoxin S6c produced marked but transient reductions in MAP (p < 0.001), cardiac output (p < 0.01), myocardial contractility (p < 0.001), and renal blood flow (p < 0.05). BQ-788 (1.0 mg/kg, i.v.), administered 3 min before sarafotoxin S6c, inhibited its effects. BQ-788 also inhibited the initial transient reduction in MAP seen after the injection of ET-1, but the subsequent sustained pressor responses were enhanced as reflected in the greater increases in left ventricular pressure (p < 0.02), myocardial contractility (p < 0.05), MAP (p < 0.01), and a larger reduction in cardiac output (p < 0.05). The heart rate was not changed after the initial ET injection, but it increased 54% when the peptide was administered in the presence of BQ-788. The reduction in renal blood flow was still evident, and its magnitude (64%) remained the same (p < 0.01) after treatment with BQ-788. Only the combined administration of both the ET(A) (BQ-123) and ET(B) (BQ-788) receptor antagonists blocked the effects of ET-1 on renal blood flow (p < 0.05). These data confirm that BQ-788 is a selective and effective antagonist of the ET(B) receptor and show that activation of this receptor subtype is involved in the transient vasodilation provoked by ET-1. Additionally, the ET(B) receptor appears to oppose the vasoconstrictor effects of the ET(A) receptor, which clearly mediates vasoconstriction. Combined treatment with BQ-123 and BQ-788 attenuated the reductions in renal blood flow produced by ET-1. Furthermore, some actions of ET-1 were not blocked by these antagonists and cannot be attributed to either the ET(A) or ET(B) receptors. We hypothesize the existence of an additional ET receptor or a subtype of the ET(B) receptor that is insensitive to BQ-788.

Animals↗

PubMed1997

Quantitative analysis of interferon alpha/beta receptor mRNA in the liver of patients with chronic hepatitis C: correlation with serum hepatitis C virus-RNA levels and response to treatment with interferon.

We analysed the expression of interferon (IFN) alpha/beta receptor mRNA in the liver of patients with chronic hepatitis C and examined the relationship between the expression of this receptor gene and the level of hepatitis C virus (HCV)-RNA as well as the response to 16 weeks of 6 x 10(6) units IFN. The mean level of IFN alpha/beta receptor mRNA in patients with chronic HCV infection (expressed as delta cycle; 10.8 +/- 1.9 (mean +/- SD); n = 39) was significantly higher than that of control subjects (9.4 +/- 0.5; n = 6; P < 0.01). There was a significant negative correlation between the level of IFN alpha/beta receptor mRNA and serum HCV-RNA in 39 patients with chronic hepatitis C (R = -0.546; P < 0.01). The mean level of IFN alpha/beta receptor mRNA in six patients who showed a complete response to IFN therapy (12.3 +/- 1.6) was higher than that of 15 patients who failed to respond to therapy (10.1 +/- 1.5; P < 0.01). Our results are consistent with the suggestion that the anti-viral activity of IFN depends on the level of the IFN alpha/beta receptor on hepatocytes in patients with chronic hepatitis C.

Adult↗

PubMed1997

Duration of chronic HCV infection and efficacy of interferon in chronic hepatitis C patients with a history of blood transfusion. The Study Group for Treatment of Hepatitis in the Kyushu Area.

To investigate correlations between the interval between blood transfusion and the start of IFN therapy, and IFN efficacy, we studied chronic hepatitis C patients with a history of blood transfusion. The subjects were 122 patients with chronic hepatitis C and a history of blood transfusion at 64 institutions. The patients were treated with high or low-dose IFN. High-dose therapy consisted of intramuscular injection of human lymphoblastoid interferon (HLBI), 6 x 10(6) IU daily for 2 weeks, then 3 times a week for 22 weeks, and low-dose interferon therapy of intramuscular injection of HLBI, 6 x 10(6) IU daily for 2 weeks, then 3 x 10(6) IU 3 times a week for 22 weeks. Normal serum ALT levels for 6 months or more after completing IFN (complete response) were found in 44/122 (36.2%) patients and HCV RNA was no longer detectable after completing IFN therapy in 19/68 (27.9%). Patients in whom the interval between blood transfusion and the start of IFN therapy was less than 20 years had significantly higher rates of HCV RNA-negative complete response than those in whom the interval was 20 years or more (p < 0.039). When chronic HCV infection is caused by blood transfusion, the efficacy of IFN depends on the duration of chronic HCV infection. Since the duration of HCV infection is a factor in predicting efficacy, early IFN therapy may be more effective.

Adult↗

PubMed1997

In vivo aortic wall characteristics at the early stage of atherosclerosis in rabbits.

To assess whether vascular responsiveness to alpha-receptor agonist is altered at the early stage of atherosclerosis, in vivo aortic pressure-diameter relationship of the aorta over a wide range of pressures was analyzed before and after the acute administration of alpha-receptor agonist (phenylephrine) in nine hypercholesterolemic fat-fed (7-wk-old) rabbits and eight normal diet-fed (7-wk-old) rabbits. In hypercholesterolemic fat-fed rabbits, there was no major structural change in the aortic wall except fatty streak, despite a marked increase in the level of plasma cholesterol, indicating the early stage of atherosclerosis of the aorta. By using a modified three-element Maxwell model, diastolic stress-strain relationship was computed after applying several assumptions to the actual aortic pressure-diameter relationship. After the intravenous administration of phenylephrine at a rate of 5 micrograms.kg-1.min-1, the stress (ordinate)-strain (abscissa) relationship curves were shifted to the left, indicating the activation of aortic smooth muscle by phenylephrine. The difference between the stress before and after phenylephrine showed a single peak at a certain strain. The peak difference in the stress was smaller in hypercholesterolemic fat-fed rabbits than in normal diet-fed rabbits, indicating the reduction of vascular responsiveness at the early stage of atherosclerosis of the aorta.

Adrenergic alpha-Agonists↗

PubMed1997

Dose-dependent effect of ANG II-receptor antagonist on myocyte remodeling in rat cardiac hypertrophy.

The goal of this study was to examine the effect of an angiotensin II type 1 (AT1)-receptor antagonist (TCV-116) on left ventricular (LV) geometry and function during the development of pressure-overload LV hypertrophy. A low (LD; 0.3 mg x kg(-1) x day(-1)) or a high (HD; 3.0 mg x kg(-1) x day(-1)) dose of TCV-116 was administered to abdominal aortic-banded rats over 4 wk, and hemodynamics and morphology were then evaluated. In both LD and HD groups, peak LV pressures were decreased to a similar extent compared with the vehicle-treated group but stayed at higher levels than in the sham-operated group. In the LD group, both end-diastolic wall thickness (3.08 +/- 0.14 mm) and myocyte width (13.3 +/- 0.1 microm) decreased compared with those in the vehicle-treated group (3.67 +/- 0.19 mm and 15.3 +/- 0.1 microm, respectively; both P < 0.05). In the HD group, myocyte length was further decreased (HD: 82.6 +/- 2.6, LD: 94.1 +/- 2.9 microm; P < 0.05) in association with a reduction in LV midwall radius (HD: 3.36 +/- 0.12, LD: 3.60 +/- 0.14 mm; P < 0.05) and peak midwall fiber stress (HD: 69 +/- 8, LD: 83 +/- 10 x 10(3) dyn/cm2; P < 0.05). There was no significant difference in cardiac output among all groups. The AT1-receptor antagonist TCV-116 induced an inhibition of the development of pressure-overload hypertrophy. Morphologically, not only the width but also the length of myocytes was attenuated with TCV-116, leading to a reduction of midwall radius and hence wall stress, which in turn may contribute to a preservation of cardiac output.

Angiotensin Receptor Antagonists↗

PubMed1997

Study of the structure of struvite stones with scanning electron microscopy and energy-dispersive X-ray microanalysis.

Topographic features of eight struvite calculi were investigated with scanning electron microscopy (SEM) equipped with energy-dispersive X-ray microanalysis (EDX). Perpendicularly cracked fragments showed concentric laminations composed of compact and loosely packed strata alternately. Magnesium and phosphorus were detected in the compact strata with their characteristic dispersive X-ray spectra. There existed numerous spherular crystals with smooth or porous surfaces and scattered penta- or hexa-hedral coffin-lid shaped crystals in the loosely packed strata. The former crystals showed the dispersive X-ray spectra of calcium and phosphorus, and were estimated to be calcium phosphate (CaP). The latter ones were presumed to be magnesium ammonium phosphate (MAP) with EDX. The surfaces of the fragments were cracked like eggshells and displayed numerous CaP crystals and scattered MAP crystals in most cases, while in only 1 case some faces of pieces demonstrated wavy MAP phases, sundry areas which were rimmed with aggregated CaP spherulites. The mean molar ratios of Mg/P and Ca/P in each case were 0.88-1.03 and 1.25-1.52, respectively. Though EDX was inadequate to determine the accurate chemical formula of CaP and MAP crystals by detecting their molar ratios of Ca/P and Mg/P with EDX, SEM/EDX is useful to observe these urolith crystals and to surmise them to be CaP or MAP crystals by detecting their atomic elements with EDX.

Adult↗

PubMed1997

Effects of angiotensin AT1 receptor antagonist on volume overload-induced cardiac gene expression in rats.

The present study was undertaken to examine the effects of volume overload on cardiac gene expression and the possible role of angiotensin AT1 receptor in such expression. Cardiac volume overload was prepared by abdominal aortocaval shunt in rats. Rats with aortocaval shunt were treated with 1) vehicle, 2) an angiotensin AT1 receptor antagonist, CS-866 (10 mg/kg/d), or 3) an angiotensin-converting enzyme inhibitor, temocapril (10 mg/kg/d), for 7 days. Cardiac tissue mRNA was measured by Northern blot analysis with specific probes. Aortocaval shunt not only caused cardiac hypertrophy but also upregulated the gene expression of atrial natriuretic polypeptide, collagen III, and downregulated Ca(2+)-ATPase expression in the left ventricle. These changes were prevented by treatment with CS-866, while temocapril failed to normalize left ventricular Ca(2+)-ATPase expression. Unlike the left ventricle, the significant downregulation of alpha-myosin heavy chain and transforming growth factor-beta 3 by aortocaval shunt was observed in the right ventricle, and CS-866 normalized this decreased expression of transforming growth factor-beta 3. The left and right atria showed increased expression of collagen type I as well as of collagen type III and atrial natriuretic polypeptide, and these increases were more effectively prevented by CS-866 than by temocapril. Thus, the effects of cardiac volume overload on cardiac performance-related gene expression differ between the ventricles and atria. Our results suggest that AT1 receptor partially contributed to volume overload-induced changes in cardiac gene expression and that AT1 receptor antagonists and angiotensin-converting enzyme inhibitors have different effects in this model of cardiac hypertrophy.

Actins↗

PubMed1997

Glucose tolerance, insulin secretion, and insulin sensitivity in nonobese and obese Japanese subjects.

OBJECTIVE: To investigate the relative contributions of insulin secretion and insulin resistance to the development of glucose intolerance in Japanese subjects. RESEARCH DESIGN AND METHODS: A cross-sectional study of 756 Japanese subjects (530 nonobese, 226 obese) was performed. A 75-g oral glucose tolerance test (OGTT) was given, and subjects were classified according to the World Health Organization (WHO) criteria (normal glucose tolerance [NGT], impaired glucose tolerance [IGT], and diabetes). Early-phase insulin secretion was assessed by the insulinogenic index (the ratio of the increment of insulin to that of plasma glucose [PG] 30 min after a glucose load [delta IRI0-30 min/delta PG0-30 min]). Total insulin secretion was assessed by mean immunoreactive insulin (IRI) during the OGTT, and insulin resistance was assessed by use of the homeostasis model [HOMA(R)]. RESULTS: Early-phase insulin secretion was significantly decreased in IGT, compared with patients with NGT, in both the nonobese and obese subjects (0.70 +/- 0.05 vs. 0.37 +/- 0.03, P < 0.01 and 1.36 +/- 0.19 vs. 0.73 +/- 0.08, P < 0.01, respectively). However, mean IRI and HOMA(R) in both nonobese and obese subjects with IGT and NGT were not statistically different. Subjects with diabetes showed a significant decline in early-phase and total insulin secretion and a significantly higher level of insulin resistance than did subjects with IGT. When the fasting glucose (FPG) exceeded 100 mg/dl, early-phase insulin decreased progressively. The graphed relationship between FPG and mean IRI did not show an inverted U-shape, and mean IRI decreased progressively when FPG exceeded 100-130 mg/dl. The pattern of changes in insulin secretion and insulin resistance associated with the progression of glucose intolerance was similar in both the nonobese and obese subjects. CONCLUSIONS: The worsening from NGT to IGT in Japanese subjects may be associated with a decrease in early-phase insulin secretion in nonobese as well as in obese subjects. Hyperinsulinemia in IGT is not common. We suggest that impaired early-phase insulin secretion may be the initial abnormality in the development of glucose intolerance in Japanese people. Insulin resistance may be a consequence of hyperglycemia and/or obesity.

Adult↗

PubMed1997

Insulin resistance and arteriosclerosis obliterans in patients with NIDDM.

OBJECTIVE: To investigate the risk factors for arteriosclerosis obliterans (ASO) in NIDDM, we measured insulin sensitivity and other risk factors including lipoprotein(a) [Lp(a)] in NIDDM patients with and without ASO. RESEARCH DESIGN AND METHODS: A case-control study in 100 patients with NIDDM, 35 with and 65 without ASO, was performed. Insulin sensitivity was assessed by the short insulin tolerance test's K index (KITT). Duration of diabetes, a history of smoking, prevalence of hypertension, prevalence of coronary artery disease (CAD), serum C-peptide, 24-h urinary C-peptide, serum lipids, and Lp(a) were compared in the two groups. RESULTS: Age, BMI, HbA1c, and fasting plasma glucose were comparable in the two groups. Patients with ASO were significantly more insulin resistant than patients without ASO (KITT 2.16 +/- 0.16 vs. 3.00 +/- 0.13%/min, P < 0.0001, respectively), had a longer duration of diabetes (10.3 +/- 1.2 vs. 7.5 +/- 0.8 years, P < 0.05), included a greater number of smokers (68.6 vs. 40.0%, P < 0.01), had a higher prevalence of CAD (60.0 vs. 16.9%, P < 0.01), and had a greater percentage of insulin therapy (48.6 vs. 29.2%, P < 0.05). However, urinary and serum C-peptide levels, serum lipids, and Lp(a) levels were comparable in the two groups. Multiple logistic regression analysis indicated that a history of smoking (odds ratio 3.70, P = 0.011), insulin resistance (odds ratio 3.68, P < 0.001), and an elevated Lp(a) level (odds ratio 1.03, P = 0.020) were independently related to ASO. When patients with CAD were removed from the logistic regression analysis, insulin resistance was most strongly related to ASO (odds ratio 20.9, P < 0.001). CONCLUSIONS: Patients with ASO were characterized by a higher prevalence of CAD, a greater percentage of smokers, a greater percentage of insulin therapy, and a higher insulin resistance than were patients without ASO. Insulin resistance, especially, may be the most powerfully related to ASO. Lp(a) may play a minor role in the development of ASO.

Aged↗

PubMed1997

[Surgically unsuccessful cases with pulmonary tuberculosis].

Because of the development of effective drugs, surgical treatment for pulmonary tuberculosis has decreased in recent years, but there are some cases which require surgical operation in patients with drug resistant tuberculosis. Between 1979 and 1994, 52 patients with pulmonary tuberculosis underwent surgical operations for the negative conversion of drug resistant bacilli. Pulmonary resection was the principal procedure and when a patient was not tolerant to this procedure, thoracoplasty or cavernostomy was selected. Continuation of bacilli positive sputum after the operation was seen in 12 cases (23.1%). The main causes of the failure were multiple drug resistance and remaining lesions. The unsuccessful rate in the patients with bacilli completely resistant to all of the 5 main drugs (SM, KM, INH, RFP, EB) was extremely high amounting to 57.1%. When 2 or more of the 5 main drugs were effective, the unsuccessful rate was 11.1%. A total of 21 cases had tuberculous lesions remaining in the lung postoperatively, because of bilateral lesions or poor lung function. In such cases, the unsuccessful rate was 42.3%. In the 31 cases that had no remaining lesion, the rate was 9.7%. There was no unsuccessful case in the patients who had 2 or more effective drugs and no remaining lesion. We reoperated on 6 patients and 5 of them got negative conversion. In the 2 of other patients who didn't undergo reoperation, their sputum became negative after long term postoperative chemotherapy, and the other 2 patients had only a few bacilli in ther sputum postoperatively. Nine cases were able to return to normal daily life.

Adult↗

PubMed1997

Leucocytoclastic vasculitis associated with mixed cryoglobulinaemia and hepatitis C virus infection.

Mixed cryoglobulinaemia is frequently associated with chronic hepatitis. We report a patient with mixed cryoglobulinaemia, hepatitis C virus (HCV) infection and palpable purpura. The skin manifestations were diagnosed as leucocytoclastic vasculitis in view of both the clinical appearance and the histological findings. In this study, we demonstrated the presence of IgG-class anti-HCV-antibody, HCV-RNA and IgA-class rheumatoid factor in the cryoprecipitate. These results suggest that the cryoglobulinaemia in this case was caused by aggregation of an immune complex comprised of HCV and anti-HCV antibody with IgA-type-rheumatoid factor, and that this led to a cutaneous vasculitis.

Antigen-Antibody Complex↗

PubMed1997

[Diagnostic criteria for Non-ABCDE hepatitis].

Hepatitis viruses A, B, C, D and E are all well-characterized, molecularly defined agents with unequivocal disease association. Usual diagnosis for these virus infections are established by serological markers which are specific antigens or antibodies for these virus infections. But serological diagnosis occasionally shows pseudonegative results because this method is indirect diagnosis. In contrast, molecular diagnosis catches directly components of viral structure. Molecular diagnosis is also able to show the appearance and disappearance of these hepatitis viruses. Diagnostic criteria for Non-ABCDE hepatitis is the exclusion of hepatitis viruses A, B, C, D and E infections by using not only serological diagnosis but also molecular diagnosis.

Acute Disease↗