BACKGROUND: Cardiac hypertrophy is the compensatory response of the myocadium to increased workload. Compensatory mechanisms come into play when the hypertrophied heart can no longer accommodate the increased demand or persistent stimuli. Although it has been reported that the molecular changes in hypertrophied hearts that initially mediate enhanced function may contribute to the development of heart failure, the structural/biochemical/molecular basis for myocardial contractile failure is still obscure. This study was aimed to clarify the structural basis for relation between hypertrophy and failure. METHOD: Nine pairs of rabbits were sacrificed at 8,12,24,48 hours and 1,2,4,6,8 weeks after experiment aortic constriction. There hearts were studied with routine histopathology. Each heart was weighed and compared with total body weight. Multiple sections were embedded in paraffin, sectioned at 5um, and stained with hematoxylin and cosin and Masson's trichrome and analysed. RESULTS: The heart weight to body weight ratio(g/Kg) increased progressively with time after aortic banding. Banding of the aorta in the rabbit resulted in multifocal areas of myofiber degeneration, necrosis and fibrosis through the wall of the left ventricle, in the papillary muscles of the left ventricle and in the left ventricular portions of the interventricular septum in rabbit of 6 and 8 weeks after aortic banding. By 4 weeks after banding, the foci of necrosis were not observed. CONCLUSION: There findings suggest that the increased necrosis, fibrosis in animals with cardiac hypertrophy induced by banding the aorta may play a role in progression to heart failure.
Animals ; Aorta ; Body Weight ; Cardiomegaly ; Constriction ; Fibrosis ; Heart Failure ; Heart Ventricles ; Heart* ; Hematoxylin ; Hypertrophy ; Necrosis* ; Papillary Muscles ; Paraffin ; Rabbits

No abstract available.
Female ; Laparoscopy* ; Methotrexate* ; Pregnancy ; Pregnancy, Ectopic*

Multidirectional shoulder instability is often difficult to diagnose and treat and can be cause of significant disability. Nonoperative rehabilitations and life tyle modifications are the primary treatments. Hiwever, the inferior capsular shift procedure, performed either from an anterior or posterior approach, as described by Neer and Foster, is recommended for symptomatic multidirectional instability that is unresponsive to nonoperative therapy. Twenty-seven shoulders in twenty-seven patients with inferior and multidirectional instability were managed with Neer s inferior capsular shift, through anterior or posterior approach depending on the direction in which the shoulder is most unstable. All of the patients were followed up for an average of 3 years (range one to seven years). The postoperative range of motion of the shoulders was well maintained except 1 patient. Three patients had recurrence of symptomatic and disabling multidirectional instability, but twenty-four (89%) of the shoulders continued to function well with no instability, no pain, no recurrence and no remarkable limitation of motion.
Humans ; Range of Motion, Articular ; Recurrence ; Shoulder*

No abstract available.
CA-125 Antigen* ; Female ; Pregnancy ; Pregnancy, Ectopic*

No abstract available.
Female ; Obstetric Labor, Premature* ; Pregnancy ; Ritodrine* ; Tocolytic Agents*

No abstract available.
Nephrosis, Lipoid*

No abstract available.
Appendicitis* ; Child* ; Humans

BACKGROUND: Cardiac hypertrophy is an adaptive mechanisms in response to an increased cardiac work load. Alterations in gene expression play an important role in this adaptive process. Recent investigations have indicated that the alpha-1 adrenergic stimulation in vitro induces hypertrophic change of neonatal cardiomyocytes. The signalling mechanisms of this alpha-1 agonist induced cardiomyocyte hypertrophy are largely unknown. however, recent evidence favors an effector pathway that involves phospholipase C(PLC) mediated hydrolysis of phosphatidylinositol 4,50 bisphosphate. It should be recognized that the demonstration of enhanced phosphoinositol turnover in the presence of alpha-1 adrenergic agonist in vitro does not necessarily imply that a similar response is operative in vivo. Furthermore, the role of subtypes of phospholipase C in this system should be determined. In this context, we produced in vivo cardiac hypertrophy by repeated injection of alpha-1 adrenergic agonist, phenylephrine, and tried to evaluate any change of phospholipase C subtypes by immunohistochemistry and immunoblotting technique and also measured the phosphatidylinositol hydrolyzing activity of the enzyme. METHOD: To produce cardiac hypertrophy, we injected phenylephrine 12mg/kg i.p. to the 28 female S-D rats weighing 150-250g daily for 5 days. This measures produced 22% increase of heart weight/body weight ratio. After 5 days. rats were sacrificed and hearts were rapid excised and freezed for next procedure. The immunohistochemical stainings of myocardium were carried out using monoclonal antibodies against PLC-beta1,-gamma1,-delta1 with Avidine-Biotin Complex method. Immunoblotting was done with monoclonal anti-PLC-gamma1 antibody after immnoprecipitation. The activity of PLC-gamma1 was determined in the assay mixture containing [3H] phosphatidylinositol of 20,000 cpm. The reaction was performed by incubating with resuspended immunoprecipttol of 20,000 cpm. The reaction was performed by incubating with resuspended immunoprecipitate for 10 min and supernatant was collected for -scintillation counting. RESULTS: Immunohistochemical staining demonstrated increased staining of PLC-gamma1 in the phenylephrine induced hypertrophied heart as compared with normal control heart. PLC-beta1 and-o1 did not showed any change. Elghteen out of 20 hypertrophied cardiac tissue(90%) demonstrated increased expression of the PLC-gamma1 compared with control heart tissue in immunoblotting. [3H] PI hydrolyzing activity of PLC-gamma1 in the immunoprecipitates of the hypertrophied hearts(4650+/-614 cpm) were increased consistently in 6 samples as compared with control normal hearts (2387+/-651 cpm). CONCLUSION: In the present experiments we demonstrated that Phospholipase C-gamma1 was overexpressed compared with control normal heart of rat by immunohistochemistry and immunoblotting technique and showed that the activity of this isoenzyme was elevated. Our findings of increased PLC-gamma1 expression in the alpha1-adrenergic agonist induced cardiac hypertrophy tissue suggest that the phosphatidylinositol signalling pathway is important in the genesis of cardiac hypertrophy and the isoenzyme of PLC-gamma1 may play a central role in this mechanism.
Adrenergic Agonists ; Animals ; Antibodies, Monoclonal ; Cardiomegaly* ; Female ; Gene Expression ; Heart ; Humans ; Hydrolysis ; Hypertrophy ; Immunoblotting ; Immunohistochemistry ; Myocardium ; Myocytes, Cardiac ; Phenylephrine* ; Phosphatidylinositols ; Phospholipases* ; Rats* ; Signal Transduction ; Type C Phospholipases

Kallmann syndrome is characterized by hypogonadotropic hypogonadism resulting from insufficient release of GnRH and associated with anosmia or hyposmia. We experienced two cases of Kallmann syndrome with abnormal brain MRI findings(olfactory bulb aplasia) & secondary sexual dysfunction.
Brain ; Gonadotropin-Releasing Hormone ; Hypogonadism ; Kallmann Syndrome* ; Magnetic Resonance Imaging ; Olfaction Disorders

Kallmann syndrome is characterized by hypogonadotropic hypogonadism resulting from insufficient release of GnRH and associated with anosmia or hyposmia. We experienced two cases of Kallmann syndrome with abnormal brain MRI findings(olfactory bulb aplasia) & secondary sexual dysfunction.
Brain ; Gonadotropin-Releasing Hormone ; Hypogonadism ; Kallmann Syndrome* ; Magnetic Resonance Imaging ; Olfaction Disorders