Radiofrequency catheter ablation in familial paroxysmal supraventricular tachycardia due to accessory atrioventricular pathways

Radiofrequency catheter ablation (RF-CA) has been widely used to cure paroxysmal supraventricular tachycardia (PSVT). However, its use has never been reported in familial PSVT caused by an accessory atrioventricular pathway (AP), which is known as one of the typical familial cardiovascular diseases. Two cases of using RF-CA for familial PSVT due to APs are presented, in a brother and sister, supporting a potential genetic role in the developmental failure to lose the atrioventricular connection during fetal life. The sister, a 24-year-old woman, had intermittent episodes of palpitation accompanied by chest pain for 2 years. An electrophysiologic study (EPS) confirmed her clinical tachycardia was atrioventricular reentrant tachycardia (AVRT) due to a left lateral concealed AP, which was subsequently successfully ablated with RF-CA. The brother, a 22-year-old man, had a 5-year history of paroxysmal palpitation. A resting electrocardiogram showed a right bundle branch block and left axis deviation with a delta wave. During his EPS, AVRT was reproducibly induced and a manifest AP was localized and then ablated at the left posteroseptal site, resulting in disappearance of the delta wave. PSVT, however, recurred 1 month later and during a repeat EPS the tachycardia was proved to be AVRT due to a right anterior concealed AP. The right anterior AP was successfully ablated with RF-CA. Both patients remained asymptomatic for more than 3 years following the successful ablation procedures.     

Binding of a phosphoprotein to the 3' untranslated region of the mouse protamine 2 mRNA temporally represses its translation

The synthesis of the protamines, the predominant nuclear proteins of mammalian spermatozoa, is regulated during germ cell development by mRNA storage for about 7 days in the cytoplasm of differentiating spermatids. Two highly conserved sequences, the Y and H elements present in the 3' untranslated regions (UTRs) of all known mammalian protamine mRNAs, form RNA-protein complexes and specifically bind a protein of 18 kDa. Here, we show that translation of fusion mRNAs was markedly repressed in reticulocyte lysates supplemented with a mouse testis extract enriched for the 18-kDa protein when the mRNAs contained the 3' UTR of mouse protamine 2 (mP2) or the Y and H elements of mP2. No significant decrease was seen when the fusion mRNAs contained the 3' UTR of human growth hormone. The 18-kDa protein is developmentally regulated in male germ cells, requires phosphorylation for RNA binding, and is found in the ribonucleoprotein particle fractions of a testicular postmitochondrial supernatant. We propose that a phosphorylated 18-kDa protein plays a primary role in repressing translation of mP2 mRNA by interaction with the highly conserved Y and H elements. At a later stage of male gamete differentiation, the 18-kDa protein no longer binds to the mRNA, likely as a result of dephosphorylation, enabling the protamine mRNA to be translated.     

The rationale of argon green laser photocoagulation for diabetic maculopathy

To determine the effect of glycemic control on vitamin B12 (B12) metabolism in diabetes mellitus, we studied B12 metabolism in 19 diabetic patients with poor glycemic control and 15 normal individuals. The diabetic patients had significantly higher total B12 binding capacity (3303 +/- 963 pg/ml), higher serum B12 levels (1173 +/- 503 pg/ml) and unsaturated B12 binding capacity (2131 +/- 902 pg/ml) when compared with the normal controls, but there was no difference in R-binder levels and the B12 binding ratio between the two groups. During a 2-week admission to establish glycemic control, the fructosamine levels in the diabetic patients decreased from 556 to 428 mumol/l and the total B12 binding capacity as well as unsaturated B12 binding capacity were significantly improved to the normal range (P < 0.01), but serum B12 levels, R-binder levels and the B12 binding ratio were not changed. There was a significant association between serum fructosamine levels and the total B12 binding capacity in poorly controlled diabetic patients and the decrease of fructosamine was correlated significantly with the change of total B12 binding capacity and serum B12 levels in diabetic patients. These results indicate the effects of glycemic control on B12 metabolism in diabetes mellitus.