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H Yoshida

Publications and source records attributed to H Yoshida.

At least 253 records · Page 14Linked to original sources

Three-dimensional computer-aided diagnosis scheme for detection of colonic polyps.

We have developed a three-dimensional (3-D) computer-aided diagnosis scheme for automated detection of colonic polyps in computed tomography (CT) colonographic data sets, and assessed its performance based on colonoscopy as the gold standard. In this scheme, a thick region encompassing the entire colonic wall is extracted from an isotropic volume reconstructed from the CT images in CT colonography. Polyp candidates are detected by first computing of 3-D geometric features that characterize polyps, folds, and colonic walls at each voxel in the extracted colon, and then segmenting of connected components corresponding to suspicious regions by hysteresis thresholding based on these geometric features. We apply fuzzy clustering to these connected components to obtain the polyp candidates. False-positive (FP) detections are then reduced by computation of several 3-D volumetric features characterizing the internal structures of the polyp candidates, followed by the application of discriminant analysis to the feature space generated by these volumetric features. The locations of the polyps detected by our computerized method were compared to the gold standard of conventional colonoscopy. The performance was evaluated based on 43 clinical cases, including 12 polyps determined by colonoscopy. Our computerized scheme was shown to have the potential to detect polyps in CT colonography with a clinically acceptable high sensitivity and a low FP rate.

Algorithms↗

Apoptosis of muscle cells causes weight loss prior to impairment of DNA synthesis in tumor-bearing rabbits.

The mechanism of weight loss induced by the growth of malignant tumors is still unknown. We investigated it by focusing on apoptosis of skeletal muscle. VX2-tumor was implanted into rabbits and the apoptotic index (AI) of skeletal muscle was measured by in situ end-labeling assay. Plasma of the tumor-bearing rabbits was perfused repeatedly through non-coated charcoal resin. The AI reached 54.6% early after tumor implantation, when weight loss amounted to an 18% decrease in lean body mass (LBM) without change in muscle DNA synthesis or urinary 3-methylhistidine / creatinine ratio (3-MH / Cr). When the decrease of LBM reached 30%, DNA synthesis was decreased by 48% and 3-MH / Cr was increased by 104%, whereas AI was only 4.7%. The plasma perfusion did not prevent apoptosis in muscle, but improved LBM, DNA synthesis, and 3-MH / Cr. There may be two mechanisms of muscle depletion during the tumor growth: apoptosis in the early stage and metabolic abnormalities in muscle in the late stage.

Animals↗

Expression of apoptosis regulatory proteins in the skeletal muscle of tumor-bearing rabbits.

We reported finding that apoptosis occurred in skeletal muscle in the early stage after implantation. In the present study, we investigated expression of the apoptosis-related proteins Bax and Bcl-2 to determine the mechanism of the apoptosis. In the early stage of tumor bearing, 20 days after implantation, lean body mass (LBM) was reduced by 5.06 +/- 1.10% in the tumor-bearing group, compared with an increase of 4.96 +/- 1.26% in the control group. The apoptotic index (AI) of the skeletal muscle in the tumor-bearing group increased to 40.5 +/- 3.20% but was 0% in the control group, and Bax expression was strongly positive in 5 of the 10 rabbits in the tumor-bearing group, and significantly stronger than in the control group (P = 0.0002). In the late stage of tumor bearing, 40 days after implantation, the AI had declined to 0.93 +/- 0.96% in the tumor-bearing group, but was still 0% in the control group. Bax expression was rarely detected in either the tumor-bearing group or the control group, and there was no significant difference between the two groups (P = 0.706). No significant changes in Bcl-2 were observed in either group. The above results showed that apoptosis via Bax played a role in muscle wasting associated with progression of the malignant tumor. However, the apoptosis and expression of Bax were seen only in the early stage, within 20 days after implantation, not in the late stage. This suggested that the muscle wasting in the early stage might be caused by a different mechanism from that in the late stage.

Animals↗

Large-scale analysis of mutations in RET exon 16 in sporadic medullary thyroid carcinomas in Japan.

Germline mutations in the RET proto-oncogene are the cause of multiple endocrine neoplasia type 2 (MEN 2A and 2B) and familial medullary thyroid carcinoma (FMTC). Some cases of sporadic medullary thyroid carcinoma (MTC) have also been reported to have mutations in the RET gene. However, two previous reports have given discrepant results on the frequency of the mutations in RET in sporadic MTCs in Japan. To clarify this problem, we analyzed mutations in RET exon 16 in 72 sporadic MTCs by means of the two methods used in the previous studies, direct sequencing and polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). Mutations in exon 16 were detected in only 2 of 72 cases of sporadic MTC. These results suggest that when a MTC has a mutation in RET exon 16, it is more likely to be a hereditary MTC than a sporadic one in Japan.

Adult↗

[Five cases of erythema infectiosum in adults].

The similarities between clinical features of erythema infectiosum and collagen disease or other viral infections prompted us to investigate clinical manifestations and laboratory data of parvovirus B19 (B19) infection in adults. We diagnosed all five patients as acute B19 infection by antibody assays. The age of patients ranged from 18 to 39 years old (mean 29), and all patients were female. All five patients showed high fever, arthralgia and edema of the extremities. Four of the five patients showed skin rash of the extremities or cheeks. Two patients were diagnosed as erythema infectiosum by family physicians before coming to us. The three remaining patients were suspected to be systemic lupus erythematosus, adult Still disease or rubella indivisually and referred to our hospital. A-27-old female (case 5) visited our hospital because of polyarthralgia and butterfly rash on her face. A test for antinuclear antibodies (ANA) was positive at a dilution of 1:320. Rheumatoid factor (RF) was also detected by latex fixation test. Her AST was 51 IU/L, ALT 68 IU/L and LDH 568 IU/L. Her symptoms persisted for 3 weeks and hepatic dysfunction recovered within 3 weeks. Five months later. ANA was negative at the dilution of less than 1:40. We suggest that the similarities between some symptoms of B19 infection and clinical and serological manifestation of collagen diseases merit closer attention.

Adolescent↗

[Longitudinal study of serological response to Bartonella henselae by indirect fluorescence assay in cat scratch disease].

Sequential serologic testing for IgG and IgM titers to Bartonella henselae were evaluated by an indirect fluorescence assay (IFA) in patients with CSD. The IFA test for the detection of IgG and IgM antibodies to B. henselae in 52 CSD patients showed that 40 (76.9%) were positive for IgG antibody and 9 (17.3%) were positive for IgM antibody. Two or more consecutive serum samples from 30 patients with CSD were assessed. In regard to the detection of IgG antibody, 5 patients had rapidly elevated titers in the acute phase, 12 patients had high titers from the acute phase, and 5 patients had a positive titer 24 weeks after the onset. B. henselae IgM antibody kinetics varied widely between patients with CSD. The seropositive rate for the antibody to B. henselae was analyzed at overtime after the onset and we found that the IgG-seropositive rate was high from 2 weeks after the onset and low after 25 weeks. The sensitivity of the IgM IFA was low, and IgM antibody to B. henslelae was not detected from 9 weeks. The detection from consecutive serum samples of antibodies to B. henselae by IFA is very useful for diagnosis in the case of clinically suspected CSD.

Antibodies, Bacterial↗

Effects of lansoprazole and amoxicillin on uptake of [(14)C]clarithromycin into gastric tissue in rats.

Triple therapy consisting of clarithromycin (CLR), lansoprazole (LPZ), and amoxicillin (AMZ) is effective as eradication therapy for patients with peptic ulcer disease and Helicobacter pylori infection. We evaluated the effects of LPZ and AMZ on the uptake of [(14)C]CLR into the gastric tissue of rats. After administration of [(14)C]CLR alone or in combination with LPZ and AMZ, the distributions of [(14)C]CLR in the main organs and gastrointestinal tissues were compared. LPZ and AMZ had no effect on the distribution of [(14)C]CLR in any tissue except gastric tissue. The concentration of radioactivity in gastric tissue was several times higher when [(14)C]CLR was administered orally together with LPZ than when it was administered alone. The gastric emptying of [(14)C]CLR became smaller in the case of the coadministration of LPZ. AMZ had no apparent influence on the disposition of [(14)C]CLR. After the intravenous administration of [(14)C]CLR, no effects of drug coadministration were evident. In vitro uptake of [(14)C]CLR into gastric tissue was enhanced in the case of a high-pH environment. The uptake was not influenced by the concurrent presence of LPZ and AMZ. These results suggest that the penetration of [(14)C]CLR possibly depends on elevated gastric pH, as gastric acid secretion was inhibited by LPZ, and this may be a primary factor in explaining why the concentration of [(14)C]CLR at the target site, gastric tissue, was enhanced by the coadministration of LPZ.

2-Pyridinylmethylsulfinylbenzimidazoles↗

Determination of Helicobacter pylori virulence by simple gene analysis of the cag pathogenicity island.

Nucleic acid amplification was performed for five loci in the cag pathogenicity island (PAI) of Helicobacter pylori (comprising cagA, the cagA promoter region, cagE, cagT, and the left end of cagII [LEC]), and gastric inflammation in patients was evaluated. Of 204 H. pylori isolates from Japanese patients (53 with peptic ulcer, 55 with gastric cancer, and 96 with chronic gastritis), 197 (96.6%) were positive for all five loci. Two isolates (1%) were negative for all five loci, and five isolates (2.4%) were positive for only cagA and LEC. These latter seven isolates were all from patients with mild chronic gastritis. Neutrophil infiltration in gastric mucosa was significantly milder in patients infected with partially or totally deleted-PAI strains than in those with intact-PAI strains. The cagE gene was a more accurate marker of an intact cag PAI than the cagA gene, and cagE seemed to be more useful in discriminating between H. pylori strains causing different rates of disease progression.

Adult↗

Helicobacter pylori activates the cyclin D1 gene through mitogen-activated protein kinase pathway in gastric cancer cells.

Helicobacter pylori induces cellular proliferation in host cells, but the mechanism remains unclear. Thus, we examined the effect of H. pylori on cyclin D1, an important regulator of the cell cycle, especially in relation to intracellular signaling pathways. In a Northern blot analysis, cyclin D1 transcription in gastric cancer (AGS) cells was enhanced by coculture with H. pylori strain TN2 in a time-dependent and multiplicity-of-infection-dependent manner. An isogenic mutant form of vacA also increased cyclin D1 transcription, but mutant forms of cagE or the entire cag pathogenicity island did not enhance cyclin D1 transcription. These effects were confirmed with a luciferase assay of the cyclin D1 promoter (pD1luc). Cyclin D1 promoter activation by H. pylori was inhibited by MEK inhibitors (U0126 and PD98059), indicating that the mitogen-activated protein kinase pathway may be involved in intracellular signal transduction. In contrast, transfection of a reporter plasmid having any point mutations of the NF-kappaB binding sites in the promoter (pD1-kappaB1M, pD1-kappaB2M, or pD1-kappaB1/2M) or cotransfection of dominant negative IkappaBalpha did not affect cyclin D1 activation by H. pylori. In conclusion, H. pylori activates cyclin D1 through the mitogen-activated protein kinase pathway and not through NF-kappaB activation in AGS cells. This activation of cyclin D1 is partly dependent on the cag pathogenicity island but not on vacA.

Cyclin D1↗

Endoplasmic reticulum stress-induced formation of transcription factor complex ERSF including NF-Y (CBF) and activating transcription factors 6alpha and 6beta that activates the mammalian unfolded protein response.

The levels of molecular chaperones and folding enzymes in the endoplasmic reticulum (ER) are controlled by a transcriptional induction process termed the unfolded protein response (UPR). The mammalian UPR is mediated by the cis-acting ER stress response element (ERSE), the consensus sequence of which is CCAAT-N(9)-CCACG. We recently proposed that ER stress response factor (ERSF) binding to ERSE is a heterologous protein complex consisting of the constitutive component NF-Y (CBF) binding to CCAAT and an inducible component binding to CCACG and identified the basic leucine zipper-type transcription factors ATF6alpha and ATF6beta as inducible components of ERSF. ATF6alpha and ATF6beta produced by ER stress-induced proteolysis bind to CCACG only when CCAAT is bound to NF-Y, a heterotrimer consisting of NF-YA, NF-YB, and NF-YC. Interestingly, the NF-Y and ATF6 binding sites must be separated by a spacer of 9 bp. We describe here the basis for this strict requirement by demonstrating that both ATF6alpha and ATF6beta physically interact with NF-Y trimer via direct binding to the NF-YC subunit. ATF6alpha and ATF6beta bind to the ERSE as a homo- or heterodimer. Furthermore, we showed that ERSF including NF-Y and ATF6alpha and/or beta and capable of binding to ERSE is indeed formed when the cellular UPR is activated. We concluded that ATF6 homo- or heterodimers recognize and bind directly to both the DNA and adjacent protein NF-Y and that this complex formation process is essential for transcriptional induction of ER chaperones.

Activating Transcription Factor 6↗

Helicobacter pylori induced transactivation of SRE and AP-1 through the ERK signalling pathway in gastric cancer cells.

BACKGROUND AND AIMS: Helicobacter pylori infection induces expression of proinflammatory cytokines such as interleukin (IL)-8 and tumour necrosis factor alpha (TNF-alpha) in gastric mucosa, and their genes have AP-1 binding sites in the promoter region. c-Fos is important for transactivation of AP-1 which has SRE in the promoter region. We conducted this study to confirm H pylori induced transactivation of these binding sites. METHODS: Transactivation of SRE and AP-1 was evaluated in human gastric cancer cells TMK1 and MKN45 by luciferase reporter assay in transient transfection. We compared the effects of coculture with four H pylori strains, a cag pathogenicity island (PAI) positive strain TN2, its isogenic vacA negative (TN2-DeltavacA) or cagE negative (TN2-DeltacagE) mutants, and a cag PAI negative clinical isolate T68. Phosphorylation of ERK1/2, JNK, and c-Jun was measured by immunoblot, induction of IL-8 secretion by ELISA, and the effects of MEK by inhibitor U0126. RESULTS: Both SRE and AP-1 were transactivated by coculture with TN2. Although TN2-DeltavacA induced comparable transactivation, TN2-DeltacagE and T68 showed decreased transactivation of SRE (65% and 51%) and AP-1 (71% and 54%, respectively, of TN2). Heat killed TN2 or indirect contact using a permeable membrane inhibited transactivation. Levels of phosphorylated ERK1/2, JNK, and c-Jun were increased by coculture with TN2. MEK inhibitor U0126 reduced TN2 induced transactivation of SRE and AP1, as well as secretion of IL-8, by 83%, 87%, and 53%, respectively, of TN2. CONCLUSIONS: Transactivation of SRE and AP-1, through ERK/MAPK and JNK/SAPK cascades, respectively, was found in gastric cancer cells cocultured with H pylori. Direct contact with viable bacteria possessing intact cag PAI is a prerequisite for the onset of intracellular signalling leading to AP-1 transactivation.

Animals↗

Inverse background of Helicobacter pylori antibody and pepsinogen in reflux oesophagitis compared with gastric cancer: analysis of 5732 Japanese subjects.

BACKGROUND: The relationship between Helicobacter pylori and reflux oesophagitis remains controversial. AIMS: To evaluate the relationship between H pylori and reflux oesophagitis in a large number of Japanese subjects. SUBJECTS: A total of 5732 consecutive Japanese subjects during a health screening were enrolled. METHODS: Gastrointestinal endoscopy was performed on all subjects. We simultaneously measured serum anti-H pylori antibody and pepsinogen as markers of H pylori infection together with gastric atrophy. The risk of reflux oesophagitis was evaluated in relation to these markers, and the results were compared with those of gastric cancer. RESULTS: Reflux oesophagitis was found in 108 subjects. Both positivity for H pylori antibody (adjusted odds ratio (OR) 0.67 (95% confidence interval 0.45-1.0)) and "low" pepsinogen indicating gastric atrophy (OR 0.35 (0.18-0.68)) were negatively associated with reflux oesophagitis. After subjects were classified into four groups based on positivity or negativity for H pylori antibody and "low" pepsinogen, the prevalence of reflux oesophagitis showed a decreasing trend as H pylori induced gastric atrophy became more severe. The risk of gastric cancer showed an increasing trend, exactly the opposite to that of reflux oesophagitis. CONCLUSIONS: Analysis of a large series of Japanese subjects revealed a decreasing prevalence of reflux oesophagitis in conjunction with progress of gastric atrophy induced by H pylori infection. This pattern was completely opposite to that of gastric cancer cases. A protective role of H pylori for reflux oesophagitis through the development of gastric atrophy has been suggested.

Adult↗

Long working hours and risk for hypertension in Japanese male white collar workers.

STUDY OBJECTIVE: To evaluate the association of long working hours with the risk for hypertension. DESIGN: A five year prospective cohort study. SETTING: Work site in Osaka, Japan. PARTICIPANTS: 941 hypertension free Japanese male white collar workers aged 35-54 years were prospectively examined by serial annual health examinations. Men in whom borderline hypertension and hypertension were found during repeated surveys were defined as incidental cases of borderline hypertension and hypertension. MAIN RESULTS: 336 and 88 men developed hypertension above the borderline level and definite hypertension during the 3940 and 4531 person years, respectively. After controlling for potential predictors of hypertension, the relative risk for hypertension above the borderline level, compared with those who worked < 8.0 hours per day, was 0.63 (95% confidence intervals (CI): 0.43, 0.91) for those who worked 10.0-10.9 hours per day and 0.48 (95% CI: 0.31, 0.74) for those who worked > or = 11.0 hours per day. The relative risk for definite hypertension, compared with those who worked < 8.0 hours per day, was 0.33 (95% CI: 0.11, 0.95) for those who worked > or = 11.0 hours per day. The multivariate adjusted slopes of diastolic blood pressure (DBP) and mean arterial blood pressure (MABP) during five years of follow up decreased as working hours per day increased. From the multiple regression analyses, working hours per day remained as an independent negative factor for the slopes of systolic blood pressure, DBP, and MABP. CONCLUSIONS: These results indicate that long working hours are negatively associated with the risk for hypertension in Japanese male white collar workers.

Adult↗

Hours of work and the risk of developing impaired fasting glucose or type 2 diabetes mellitus in Japanese male office workers.

OBJECTIVE: To investigate the association between duration of overtime and the development of impaired fasting glucose (IFG) or type 2 diabetes mellitus (DM). METHODS: A cohort of 1266 Japanese male office workers aged 35-59 years and free of IFG (fasting plasma glucose concentration 6.1-6.9 mmol/l), type 2 DM (fasting plasma glucose concentration of 7.0 mmol/l or more or taking hypoglycaemic medication), history of diabetes, or medication for hypertension were re-examined over 5 successive years after their initial examinations in 1994. RESULTS: 138 men developed IFG or type 2 DM during the 5736 person-years of follow up. After controlling for potential predictors of diabetes, the relative risks of IFG or type 2 DM, compared with those who worked <8.0 hours a day, were 0.82 (95% confidence interval (95% CI) 0.54 to 1.26), 0.69 (95% CI 0.38 to 1.26), 0.63 (95% CI: 0.37 to 1.09), and 0.50 (95% CI: 0.25 to 0.98) for those who worked 8.0-8.9, 9.0-9.9, 10.0-10.9, and of 11.0 hours or more a day, respectively (p for trend=0.020). 87 and 54 men developed IFG and type 2 DM during the 5817 and 5937 person-years of follow up, respectively. The multivariate adjusted relative risks of IFG tended to decrease with an increase in hours of overtime work a day, but did not reach significance (p for trend=0.202). On the other hand, the multivariate adjusted relative risks of type 2 DM significantly decreased with an increase in hours of overtime work a day (p for trend=0.014). CONCLUSION: Longer overtime is a negative risk factor for the development of IFG or type 2 DM in Japanese male office workers.

Adult↗

Protective effect of heat shock protein 72 on contractile function of perfused failing heart.

The contribution of heat shock protein 72 (HSP72) to the protection of cardiac function was examined in rats with chronic heat failure (CHF) following coronary artery ligation (CAL). The CAL animals revealed functional deterioration without low cardiac output 2 wk after CAL and with low cardiac output 8 wk after CAL, suggesting that CHF had developed by 8 wk after CAL. The hearts isolated from animals 2 and 8 wk after CAL (2-wk CAL heart and 8-wk CAL heart, respectively) were subjected to hyperthermia (at 42 degrees C) for 15 min, followed by 6-h perfusion (hyperthermia/6-h perfusion). The 2-wk CAL heart showed a 19.0 +/- 3.9% decline in the rate- pressure product (RPP) after hyperthermia/6-h perfusion, similar to the nonoperated control (19.8 +/- 2.9% decline). The production of myocardial HSP72 increased in the 2-wk CAL heart in response to hyperthermia (412.7 +/- 29.5% of each prehyperthermia value). The 8-wk CAL heart showed a reduction in the RPP (45.2 +/- 4.3% decline) after hyperthermia/6-h perfusion, associated with blunting of the production of HSP72 (68.9 +/- 22.6% increase, respectively). The results suggest that functional deterioration of the isolated failing heart may be attributed to a reduction in the production of myocardial HSP72.

Animals↗

Up-regulated TGF-beta mRNA expression in splenic T cells of high IgA-prone mice: a murine model of IgA nephropathy with glomerulosclerosis.

BACKGROUND/AIMS: Recently, we established a high serum IgA-prone inbred (HIGA) mouse strain as a murine model of spontaneous IgA nephropathy by selective mating of high serum IgA ddY mice, and found that they showed enhanced production of glomerular extracellular matrix components with increased expression of TGF-beta mRNA and protein in the kidneys. In this study, we examined the roles of lymphocytes in the development of high serum IgA in this strain. METHODS: We performed flow cytometric analyses of T and B cells in splenic mononuclear cells (SMNCs) from these mice using BALB/c mice as normal controls. We also compared serum TGF-beta1 concentrations and TGF-beta mRNA expression levels in the B-cell-depleted (T-cell-rich) fraction of SMNCs in these mice. RESULTS: HIGA mice showed significantly fewer CD3-positive cells compared with BALB/c mice when young, but not when aged. The CD4/CD8 ratio of HIGA mice was lower than that of BALB/c mice, but this difference was not significant. Although the number of B220-positive cells did not vary significantly, the ratio of surface IgA-positive B cells was significantly increased in both young and adult HIGA mice. The B-cell-depleted SMNCs from HIGA mice exhibited higher levels of expression of TGF-beta and TGF-beta1 mRNA than controls from a young age, which were maintained throughout life, but there were no differences in PDGF, MCP-1 or bFGF expression between these two strains. In contrast to local mRNA expression, serum TGF-beta1 concentration was decreased in HIGA mice compared with BALB/c controls. CONCLUSION: These findings suggest that the mating procedure performed to establish HIGA mice selected for a unique phenotype of local up-regulation of TGF-beta production in the kidneys, as well as T cells that may contribute to both the early and consistently high serum IgA expression and enhanced production of renal extracellular matrix components in HIGA mice. Additionally, TGF-beta1 may act locally, not systemically, in a paracrine or autocrine manner.

Animals↗

Altered cultured mesangial cell phenotypes from RF/J mice: a spontaneous immune complex mediated glomerulonephritis with progressive glomerulosclerosis.

BACKGROUND/AIM: RF/J mice are a model of spontaneous immune complex mediated glomerulonephritis showing massive extracellular matrix accumulation and progressive glomerulosclerosis. The aim of this study was to investigate whether there is an altered cultured mesangial cell (MC) phenotype in RF/J mice associated with these glomerular changes. METHODS: The nature of cultured MCs from RF/J mice in the proliferative response to platelet-derived growth factor (PDGF) BB was compared with that of normal mice (BALB/c) by 3H-thymidine incorporation. The binding of PDGF-BB was examined with Scatchard analysis, and the messenger RNAs (mRNAs) of PDGF beta-receptor, collagen I, collagen IV, and fibronectin were detected using Northern blot analysis in the MCs of each mouse. RESULTS: The 3H-thymidine incorporation of MCs from RF/J mice showed significantly lower responses to PDGF-BB stimulations with concentrations ranging from 0.5 to 10.0 ng/ml in comparison with those of BALB/c mice which exhibited a proportional dose- dependent increase of the incorporation (p < 0.05 for 0.5 ng/ml PDGF-BB, p < 0.01 for 1.0-10.0 ng/ml). According to the Scatchard analysis, MCs from BALB/c mice showed aKD of 105 pM of PDGF-BB binding to its receptors, and the density of receptors was 5.82 fmol/10(5) cells. However, no binding PDGF-BB site on the surface of MCs from RF/J mice was noted. Northern blot analysis of MCs from RF/J mice indicated negative expression of detectable PDGF-beta receptor mRNA. As for matrix protein messages, MCs from RF/J mice did not express mRNA of type I collagen, but did express a higher amount of type IV collagen and fibronectin in comparison with MCs from normal BALB/c mice. CONCLUSIONS: An altered phenotype in MCs of RF/J mice was demonstrated, possibly contributing to the characteristic pathological glomerular changes. However, the precise association remains to be clarified.

Animals↗

Treatment of fetal congenital complete heart block with maternal administration of beta-sympathomimetics (terbutaline): a case report.

We report a case of fetal congenital heart block treated with maternal administration of beta-sympathomimetics. The case was diagnosed as fetal complete heart block associated with maternal anti-Ro/SS-A antibody at 22 weeks of gestation. By fetal sonography, the ventricular rate was revealed to be 60 beats/min and mild cardiomegaly was shown. We initiated maternal administration of a sympathomimetic, specifically terbutaline, to prevent fetal heart failure. An increase in the fetal ventricular rate and an improvement in cardiac function were both achieved during the treatment. A viable infant was delivered by an elective cesarean section without complications at term. Maternal administration of the beta-adrenergic agent terbutaline is suggested to be effective for improving fetal congenital heart block in order to prevent heart failure in utero.

Adult↗