No abstract available.
Brain* ; Child* ; Humans ; Magnetic Resonance Imaging* ; Seizures*

No abstract available.
Holoprosencephaly*

No abstract available.
Adrenocorticotropic Hormone* ; Humans ; Infant ; Infant, Newborn ; Spasms, Infantile*

No abstract available.
Spinal Muscular Atrophies of Childhood*

No abstract available.

No abstract available.
Congenital Hypothyroidism*

BACKGROUND: No-reflow is a specific type of vascular damage occuring when removal of coronary occlusion dose not lead to restoration of coronary flow. There are three major explanations for the no-reflow phenomenon such as endothelial cell edema, microvascular plugging by platelets or thrombi and coronary occlusion by ischemic contracture of the myocardium. But detailed mechanisms of no-reflow phenomenon are not known. The objects of this study are to elucidate the possibility whether elevation of cytosolic Ca2+ concentration during ischemic cardioplegic period is mechanism of no-reflow phenomenon or not. METHODS: Changes in cytosolic Ca2+ concentration were measured under varying experimental condition. Free [Ca2+] in the cytosole [Ca2+]i of single rabbit coronary artery cells was measured with fluorescent Ca2+ indicator, Fura-2. RESULTS: Resting [Ca2+]i was 134.2+/-34 nM (n=43). When single cells were perfused with cardioplegic or ischemic cardioplegic solution, [Ca2+]i was significantly increased and degree of [Ca2+]i elevation was further augmented by ischemic cardioplegic solution. Pretreatment of sarcoplasmic reticulum emptying agent (20mM caffeine) had no effect on cardioplegia-induced [Ca2+]i change, but application of Ca2+ channel blocker (5x10-7M nifedipine) or an antagonist of Na+/Ca2+ exchange (5mM Ni2+ ) partially (nifedipine) or completely (nickel) inhibited the [Ca2+]i elevation. Pretreament of caffeine had no effect on ischemic cardioplegia-induced [Ca2+]i change, but application of nifedipine or nickel partially inhibited the [Ca2+]i elevation. Magnitude of ischemic cardioplegia-induced [Ca2+]i elevation was dependent on the Ca2+ concentration of perfusate from 0 to 2.5mM. When Ni2+ was added to reperfusion solution, recovery of ischemic cardioplegia-induced [Ca2+]i elevation was very rapid compared with control. CONCLUSIONS: From the above results, it may be speculated that ischemic cardioplegia-induced [Ca2+]i elevation may act as one of the mechanism of no-reflow phenomenon in rabbit coronary artery.
Caffeine ; Cardioplegic Solutions ; Coronary Occlusion ; Coronary Vessels* ; Cytosol* ; Edema ; Endothelial Cells ; Fura-2 ; Ischemic Contracture ; Muscle, Smooth* ; Myocardium ; Myocytes, Smooth Muscle* ; Nickel ; Nifedipine ; No-Reflow Phenomenon ; Reperfusion ; Sarcoplasmic Reticulum

No abstract available.
Diverticulum*

No abstract available.

No abstract available.
Methylprednisolone* ; Purpura, Thrombocytopenic, Idiopathic*