Influence of parental obesity on the physical constitution of preschool children in Japan

The objective of this study was to assess the influence of parental obesity on the physical constitution of preschool children. A total of 3187 children aged between 1–6 years and their parents were studied. A child whose per cent obesity (%OB; per cent overweight for age, height and sex) was greater than 15%, and a parent whose body mass index (BMI; kg/m²) was greater than the 95th percentile were defined to be obese (27.40 and 25.97 for a father and a mother, respectively). We found that the incidence of obesity in children with obese fathers (11.5%) was significantly higher than in those with non-obese fathers (6.2%), and a similar difference was obtained between children with obese mothers (14.5%) and with non-obese mothers (6.2%), respectively. The incidence of obesity in children was 6.0% if both parents were non-obese; this incidence rose to 22.7% if one parent was obese, and to 30.8% if both were obese. The %OB of children was more markedly correlated with the mothers' BMI (r = 0.219) than the fathers' BMI (r = 0.165). The %OB of children correlated significantly with fathers' BMI, but only from the age of 3–6 years, whereas mothers' BMI correlated from the age of 1–6 years. We concluded that parental obesity was of significance in determining the development of juvenile obesity even in the preschool period.     

β-Thalassemia with the IVS-l-1 (G → T) mutation in a Japanese girl

We analyzed the hemoglobins of a Japanese girl with β-thalassemia and those of her immediate family. DNA sequencing of the cloned β-globin gene from this patient revealed a point mutation at the IVS-I position 1 (G → T). This rare point mutation has been found in Asian Indians, but this is the first reported Japanese case.     

REDUCTION OF RAT MYOCARDIAL ISCHAEMIA/REPERFUSION INJURY BY A SYNTHETIC SELECTIN OLIGOPEPTIDE

Neutrophils infiltrate into myocardial tissue subjected to ischaemia followed by reperfusion and play a major role in myocardial reperfusion injury. The infiltration of neutrophils begins within 2 h after reperfusion, indicating the engagement of rapidly inducible adhesion molecules, such as P-selectin, on vascular endothelial cells of myocardial tissue. To investigate the essential role of P-selectin in myocardial reperfusion injury, this study examined the expression of P-selectin in rat hearts subjected to 30 min of ischaemia followed by reperfusion. The induction of P-selectin was also evaluated on the surface of cultured rat vascular endothelial cells subjected to 60 min of hypoxia, followed by reoxygenation in vitro . Finally, the effects of in vitro administration of a synthetic selectin oligopeptide on myocardial necrosis were analysed. Reperfusion of ischaemic myocardial tissue resulted in enhanced expression of P-selectin on the luminal surface of vascular endothelium and surface expression of P-selectin was induced on cultured vascular endothelial cells by hypoxia/reoxygenation in vitro . The in vitro administration of a synthetic selectin oligopeptide significantly reduced the area of myocardial infarction produced by 30 min of ischaemia, followed by 48 h of reperfusion. These data offer therapeutic possibilities for acute myocardial infarction.     

Virtual Histology Intravascular Ultrasound Analysis of Attenuated Plaque and Ulcerated Plaque Detected by Gray Scale Intravascular Ultrasound and the Relation Between the Plaque Composition and Slow Flow/No Reflow Phenomenon During Percutaneous Coronary Intervention

Objective

This study aimed to assess the plaque characteristics of attenuated and ulcerated plaques in virtual‐histology intravascular ultrasound (VH‐IVUS) and the incidence of slow flow/no reflow during percutaneous coronary intervention (PCI).

Background

The attenuated and ulcerated plaques are thought as embolic prone plaque; however, the plaque characteristics are unclear.

Methods

Subjects were 119 patient's 121 lesions undergoing VH‐IVUS before coronary stenting. These lesions were divided into the 15 lesions showing attenuated plaque, 24 lesions showing ulcerated plaque, and 82 lesions revealing neither attenuated nor ulcerated plaque (the control group).

Results

Fibro‐fatty tissue in the attenuation group was significantly larger than the control group (27.5 ± 9.5% vs 13.9 ± 8.2%, P < 0.01, 3.5 ± 1.9 mm² vs 1.6 ± 1.2 mm², P < 0.01). Necrotic core in ulceration group was significantly larger than the control group (20.7 ± 9.0% vs 15.9 ± 9.0%, P < 0.05, 2.5 ± 1.3 mm² vs 1.7 ± 1.0 mm², P < 0.01). Dense calcium in ulceration group was significantly larger than the control group (12.3 ± 6.4% vs 8.3 ± 7.1%, P < 0.05, 1.4 ± 0.7 mm² vs 0.9 ± 0.8 mm², P < 0.01). In the ulceration group, the necrotic core area of acute coronary syndrome was significantly larger than the stable angina pectoris (3.0 ± 1.4 mm² vs 1.8 ± 1.0 mm², P < 0.05). The incidence of slow flow/no reflow was significantly higher in the attenuation and ulceration group than the control group (20.0% [3/15], 20.8% [4/24] vs 4.9% [4/82], P < 0.05, 0.05).

Conclusion

The attenuated plaque had significantly larger fibro‐fatty tissue. The ulcerated plaque had significantly larger necrotic core and dense calcium. The lesions with the attenuated and the ulcerated plaque had more frequent slow flow/no reflow during PCI. (J Interven Cardiol 2013;26:295–301)

     

EXPRESSION OF VASCULAR CELL ADHESION MOLECULE-1 IN MURINE HEARTS WITH ACUTE MYOCARDITIS CAUSED BY COXSACKIEVIRUS B3

Cell-mediated autoimmunity has been strongly implicated in the pathogenesis of the myocardial cell damage involved in viral myocarditis. Using a murine model of acute myocarditis caused by Coxsackievirus B3 (CVB3), perforin-expressing killer cells have been shown to infiltrate the heart, and intercellular adhesion molecular-1 (ICAM-1) together with major histocompatibility complex (MHC) antigen was induced on myocardial cells in acute viral myocarditis. To clarify the immunological mechanisms in more detail, the expression of vascular cell adhesion molecular-1 (VCAM-1) has been examined in the heart of acute myocarditis and on cultured cardiac myocytes treated with interferon-gamma (IFN-γ) and tumour necrosis factor-alpha (TNF-α). The effects of in vivo antibody treatment to VCAM-1 on myocardial damage involved in acute myocarditis were also analysed. CVB3-induced myocarditis resulted in enhanced expression of VCAM-1 on myocardial cells. VCAM-1 expression was also induced on cultured cardiac myocytes by treatment with IFN-γ and TNF-α. The in vivo antibody treatment to VCAM-1 decreased the myocardial damage to some extent, but the effects were not statistically significant. These data suggest that the expression of VCAM-1 on myocardial cells may play at least a partial role in the myocardial damage involved in acute viral myocarditis.     

URETHRAL AFFERENT NERVE ACTIVITY AFFECTS THE MICTURITION REFLEX; IMPLICATION FOR THE RELATIONSHIP BETWEEN STRESS INCONTINENCE AND DETRUSOR INSTABILITY

PURPOSE: A causative relationship between stress urinary incontinence (SUI) and detrusor instability has been suspected but never proven. Many women with mixed incontinence have resolution of detrusor instability after surgical correction of SUI. We sought experimental support that stimulation of urethral afferent nerves can induce or change reflex detrusor contractions. MATERIALS AND METHODS: Urethral perfusion pressure and isovolumetric bladder pressure were measured with catheters inserted through the bladder dome in urethane anesthetized female S.D. rats (250 to 300 grams; n = 12). The catheter assembly was seated securely in the bladder neck to block passage of fluid between the bladder and urethra without affecting the nerve supply to the organs. The external urethra was not catheterized. Responses were examined in the control state at a urethral saline perfusion speed of 0.075 ml. per minute. Intraurethral drugs were administered following blockade of striated sphincter activity with intravenous alpha-bungarotoxin (0.1 mg./kg.). RESULTS: Stopping the urethral saline infusion caused a significant decrease in micturition frequency in approximately 50% of the animals studied (n = 12). Intraurethral lidocaine (1%) infused at 0.075 ml. per minute caused a slight decrease in urethral perfusion pressure but no change in detrusor contraction amplitude. However, intraurethral lidocaine caused a significant (45%) decrease in the bladder contraction frequency (n = 5). The micturition frequency returned to baseline 30 minutes after stopping lidocaine infusion. Intraurethral infusion of nitric oxide (NO) donors (S-nitroso-N-acetylpenicillamine [SNAP] (2 mM) or nitroprusside (1 mM) immediately decreased urethral perfusion pressure by 30 to 37% (n = 5). A 45 to 75% decrease (n = 5) in bladder contraction frequency was also seen, which was similar to that observed following lidocaine. Neither NO donor changed the amplitude of bladder contractions. CONCLUSIONS: These results indicate that in the anesthetized rat activation of urethral afferents by urethral perfusion can modulate the micturition reflex. Thus in patients with stress urinary incontinence, leakage of urine into the proximal urethra may stimulate urethral afferents and facilitate voiding reflexes. This implies that stress incontinence can induce and/or increase detrusor instability. These findings have significant implications for the treatment of patients with mixed urge and stress incontinence. Correction of stress incontinence by surgery or pelvic floor exercise in patients with mixed incontinence may resolve the detrusor instability.     

Characterization of a Novel Missense Mutation in the Pore of HERG in a Patient with Long QT Syndrome

INTRODUCTION: A new strategy to elucidate the molecular mechanisms underlying the long QT syndrome (LQTS) is now available with genetic mutational analyses and characterization of ion channel mutations. METHODS AND RESULTS: In a 26-year-old woman with LQTS, we identified a novel missense mutation in the pore of HERG by using polymerase chain reaction/single-strand conformation polymorphism (PCR/SSCP) and sequencing of her genomic DNA. The mutation resulted in an amino acid substitution of a positively charged lysine for a highly conserved uncharged asparagine at codon 629 (N629K). Whole cell, patch clamp studies were conducted in COS7 cells by transfecting with wild-type (WT) and/or the mutant N629K HERG. The WT HERG produced an I(Kr)-like, E-4031-sensitive conductance with an inward rectification. In contrast, the cells transfected with the N629K HERG did not display any time-dependent current. Cotransfection of WT and N629K HERG (at a ratio of 1:1) produced a significantly smaller conductance when compared with WT HERG (WT 59.9 +/- 7.3 pA/pF [n = 22] vs WT+N629K 5.5 +/- 2.3 pA/pF [n = 11]; P < 0.01), but did not alter K+ ion selectivity and tail current-voltage dependence. Because aprindine hydrochloride was effective in preventing ventricular tachycardias, we also tested the effect of the drug on WT HERG (I(Kr)) and KvLQT1/KCNE1 (I(Ks)) currents expressed in COS7. CONCLUSION: Functional analyses of a novel missense mutation in the pore of HERG suggest that the mutation causes marked reduction of I(Kr) via a dominant negative effect.     

Micropapillary variant of transitional cell carcinoma of the bladder

A 77-year-old man visited the Kobe City General Hospital complaining of macroscopic hematuria. A computed tomography scan found a bladder tumor with left iliac and para-aortic lymph node metastasis. Two courses of cisplatin, cyclophosphamide and doxorubicin chemotherapy resulted in a minimal response. Radical cystectomy and a retroperitoneal lymph node dissection with bilateral ureterocutaneostomy reconstruction were then performed. A pathological examination revealed a micropapillary variant of transitional cell carcinoma (Grade 3, pT1pN2M1). The patient died of pelvic recurrence 7 months after the initiation of chemotherapy. Peritonitis carcinomatosa and lung metastases were observed at autopsy.     

Dependency on Atrial Electrophysiological Properties of Appearance of Paroxysmal Atrial Fibrillation in Patients with Wolff-Parkinson-White Syndrome: Evidence from Atrial Vulnerability Before and After Radiofrequency Catheter Ablation and Surgical Cryoablation

The pathogenesis of paroxysmal atrial fibrillation in patients with Wolff-Parkinson-White syndrome and the effects of elimination of accessory pathways on the appearance of atrial fibrillation are still controversial. Fifty-four patients with Wolff-Parkinson-White syndrome were classified into three groups: a No AFgroup (n = 24), patients without paroxysmal atrial fibrillation; an RF-AF Group (n =12), patients with paroxysmal atrial fibrillation whose accessory pathways were eliminated using radiofrequency catheter ablation; and a Cryo-AF Group (n = 18), patients with paroxysmal atrial fibrillation whose accessory pathways were eliminated with surgical Cryoablation. The electrophysiological characteristics of each group were evaluated prior to and following the elimination of their accessory pathways. As indices of atrial vulnerability, the presence of fragmented atrial activity and repetitive atrial firing zones were assessed. Deducibility of atrial fibrillation was significantly reduced following ablation of accessory pathways in the Cryo-AF group (83.3%-5.6%, P < 0.0001), while it was unchanged in the RF-AF group (83.3%-75%). In preablation studies, the effective refractory periods of the atrium in the RF-AF group and the Cryo-AF group were significantly shorter compared with the No AF group (204 ± 18 ms, 197 ± 16 ms vs 246 ± 44 ms, respectively, P < 0.0001). Following ablation, the effective refractory period for patients in the Cryo-AF group was significantly prolonged compared with before ablation (197 ± 16 ms to 232 ± 24 ms, P < 0.0001). As a result of this prolongation of the effective refractory period of the atrium, the fragmented atrial activity and repetitive atrial response zones narrowed following ablation in the Cryo-AF group, but not in the RF-AF group. Therefore, the pathogenesis of atrial fibrillation in patients with Wolff-Parkinson-White syndrome may depend on the refractory period of the atrium rather than on the presence of accessory pathways.     

Type la glycogen storage disease with focal nodular hyperplasia in siblings

Glycogen storage disease type I (GSD-I) is an inherited disorder that is due to a glucose-6-phosphatase (G6Pase) deficiency. There have been recent reports of hepatocellular tumors in adults with this disease. Hepatic adenoma is the most common tumor described but others, including hepatocellular carcinomas, hepatoblastomas, and focal nodular hyperplasia (FNH) have been reported. FNH of the liver is a rare benign lesion that has been reported in eight patients with GSD-I. Three of these eight patients, in addition to the patient in our study, had been treated with portacaval shunts. When these patients were compared with patients who had not received such treatment, it appeared that the portacaval shunts may have induced the development of FNH and may have been associated with earlier complications. FNH is a benign tumor that may coexist with adjacent fibrolamillar carcinomas and/or adenomas and requires careful follow-up.