PERAN ORANG TUA DALAM MEMBINA NILAI KARAKTER ANAK DI KECAMATAN SIMPANG TIGA ACEH BESAR

ABSTRAKRahmayanti KS, Sri. 2016. Peran Orang Tua Dalam Membina Nilai Karakter Anak di Kecamatan Simpang Tiga Kabupaten Aceh Besar. Skripsi, Jurusan Pendidikan Kesejahteraan Keluarga, Fakultas Keguruan dan Ilmu Pendidikan, Universitas Syiah Kuala. Pembimbing:(1)Dr. Anizar Ahmad, M.Pd., (2). Dra. Fitriana, M.SI.Kata Kunci: Nilai Karakter Anak, Peran Orang TuaPeran orang tua adalah partisipasi atau kesadaran jiwa orang tua untuk memperdulikan anaknya, terutama dalam hal memberikan dan memenuhi kebutuhan hidup anaknya baik dari segi sosial maupun material. Penelitian ini untuk mengetahui usaha orang tua dalam membina nilai karakter anak di Kecamatan Simpang Tiga Kabupaten Aceh Besar. Penelitian ini bertujuan untuk (1) mengetahui usaha yang dilakukan orang tua dalam membina nilai karakter anak dan (2) mengetahui sistem pengawasan yang diterapkan oleh orang tua terhadap anak. Metode yang digunakan dalam penelitian ini adalah metode deskriptif kuantitatif. Data penelitian ini bersumber dari orang tua yang memiliki anak usia 4 sampai 10 tahun berjumlah 28 keluarga, pengumpulan data menggunakan kuisioner. Pengolahan data penelitian ini menggunakan rumus persentase. Simpulan penelitian ini berpengaruh pada usaha orang tua dalam membina nilai karakter anak, walau sebagian kecil yang mengetahui nilai-nilai karakter, tetapi sebagian besar sudah berusaha menanamkan nilai karakter tersebut. Lebih dari setengah responden menanamkan nilai religius kepada anak dengan tujuan agar anak mempunyai akhlak yang mulia kedepannya. Sedangkan yang berperan dalam membina nilai karakter anak adalah suami dan istri. Sistem pengawasan yang diterapkan orang tua berpengaruh terhadap pembentukkan nilai karakter anak. Seluruh anak termasuk kedalam katagori anak yang mudah bersahabat. Penanaman nilai karakter pada anak di mulai pada awal masa kanak-kanak ketika berumur 2-6 tahun. Responden juga menerapkan perilaku disiplin kepada anak karena usia awal kanak-kanak merupakan usia yang masih rentan, dan akan meniru semua yang dikerjakan oleh orang tuanya. Saran untuk orang tua agar dapat mendidik anaknya dengan baik, tidak mengedepankan emosi, dapat meluangkan waktu, adanya komunikasi yang dibina orang tua dengan anak, dan jangan bersikap apatis terhadap apa yang dikerjakan sianak

Anandamide Induces Sperm Release from Oviductal Epithelia through Nitric Oxide Pathway in Bovines

Mammalian spermatozoa are not able to fertilize an egg immediately upon ejaculation. They acquire this ability during their transit through the female genital tract in a process known as capacitation. The mammalian oviduct acts as a functional sperm reservoir providing a suitable environment that allows the maintenance of sperm fertilization competence until ovulation occurs. After ovulation, spermatozoa are gradually released from the oviductal reservoir in the caudal isthmus and ascend to the site of fertilization. Capacitating-related changes in sperm plasma membrane seem to be responsible for sperm release from oviductal epithelium. Anandamide is a lipid mediator that participates in the regulation of several female and male reproductive functions. Previously we have demonstrated that anandamide was capable to release spermatozoa from oviductal epithelia by induction of sperm capacitation in bovines. In the present work we studied whether anandamide might exert its effect by activating the nitric oxide (NO) pathway since this molecule has been described as a capacitating agent in spermatozoa from different species. First, we demonstrated that 1 µM NOC-18, a NO donor, and 10 mM L-Arginine, NO synthase substrate, induced the release of spermatozoa from the oviductal epithelia. Then, we observed that the anandamide effect on sperm oviduct interaction was reversed by the addition of 1 µM L-NAME, a NO synthase inhibitor, or 30 µg/ml Hemoglobin, a NO scavenger. We also demonstrated that the induction of bull sperm capacitation by nanomolar concentrations of R(+)-methanandamide or anandamide was inhibited by adding L-NAME or Hemoglobin. To study whether anandamide is able to produce NO, we measured this compound in both sperm and oviductal cells. We observed that anandamide increased the levels of NO in spermatozoa, but not in oviductal cells. These findings suggest that anandamide regulates the sperm release from oviductal epithelia probably by activating the NO pathway during sperm capacitation

Anandamide Capacitates Bull Spermatozoa through CB1 and TRPV1 Activation

Anandamide (AEA), a major endocannabinoid, binds to cannabinoid and vanilloid receptors (CB1, CB2 and TRPV1) and affects many reproductive functions. Nanomolar levels of anandamide are found in reproductive fluids including mid-cycle oviductal fluid. Previously, we found that R(+)-methanandamide, an anandamide analogue, induces sperm releasing from bovine oviductal epithelium and the CB1 antagonist, SR141716A, reversed this effect. Since sperm detachment may be due to surface remodeling brought about by capacitation, the aim of this paper was to investigate whether anandamide at physiological concentrations could act as a capacitating agent in bull spermatozoa. We demonstrated that at nanomolar concentrations R(+)-methanandamide or anandamide induced bull sperm capacitation, whereas SR141716A and capsazepine (a TRPV1 antagonist) inhibited this induction. Previous studies indicate that mammalian spermatozoa possess the enzymatic machinery to produce and degrade their own AEA via the actions of the AEA-synthesizing phospholipase D and the fatty acid amide hydrolase (FAAH) respectively. Our results indicated that, URB597, a potent inhibitor of the FAAH, produced effects on bovine sperm capacitation similar to those elicited by exogenous AEA suggesting that this process is normally regulated by an endogenous tone. We also investigated whether anandamide is involved in bovine heparin-capacitated spermatozoa, since heparin is a known capacitating agent of bovine sperm. When the spermatozoa were incubated in the presence of R(+)-methanandamide and heparin, the percentage of capacitated spermatozoa was similar to that in the presence of R(+)-methanandamide alone. The pre-incubation with CB1 or TRPV1 antagonists inhibited heparin-induced sperm capacitation; moreover the activity of FAAH was 30% lower in heparin-capacitated spermatozoa as compared to control conditions. This suggests that heparin may increase endogenous anandamide levels. Our findings indicate that anandamide induces sperm capacitation through the activation of CB1 and TRPV1 receptors and could be involved in the same molecular pathway as heparin in bovines

Effects of estrogen replacement therapy on plasma levels of nitric oxide in postmenopausal women

Our purpose was to assess the effects of estrogen replacement therapy on plasma levels of nitric oxide in postmenopausal women. STUDY DESIGN: The study, designed as a randomized, double-blind placebo-controlled crossover trial, involved 28 healthy postmenopausal women who had previously undergone hysterectomy. Women received either transdermal estradiol (50 g/day) (estradiol group) or placebo (placebo group) for 6 months continuously. At the end of month 6 the treatment allocations were opened, and then the treatments were exchanged for 1 month. The serum concentration of estradiol was measured at baseline before treatment and at the end of months 6 and 7. The plasma concentration of the stable oxidation products of nitric oxide was assessed before treatment and monthly until month 7. RESULTS: The mean baseline concentrations of nitric oxide metabolites in the estradiol and placebo groups were similar (mean and SD: 19+/-4.3 vs 21+/-5.6 micromol/L, respectively). At subsequent measurements from months 1 to 6, the mean concentration of nitric oxide metabolites increased significantly in the estradiol group alone, in which the concentration ranged between 33 6.4 and 36 8.5 micromol/L. At the end of month 7 the mean level of nitric oxide metabolites in women previously treated with estradiol fell to baseline value (19 2.6 micromol/L), whereas in the placebo group the level increased significantly (34 4.4 micromol/L). CONCLUSION: Estrogen replacement therapy induces a sustained increase in plasma levels of nitric oxide in postmenopausal women; the suspension of estrogen replacement therapy is followed by a significant reduction in nitric oxide levels. The results of this study suggest that a nitric oxide-related mechanism may help to explain the cardioprotective effect of estrogen replacement therapy in the postmenopausal perio

Different plasma levels of nitric oxide in arterial and venous blood

Experimental investigations suggest that a basal release of nitric oxide (NO) occurs in arterial but not in venous endothelium. We therefore decided to compare plasma levels of NO in the arterial and venous circulation. Parallel blood samples were drawn from the radial artery and brachial vein in 15 healthy drug-free women. Nitric oxide levels were assessed by measuring plasma levels of nitrite and nitrate, the two stable oxidation products of NO metabolism. Plasma levels of NO metabolites in arterial blood were signi®cantly higher than in the paired venous blood samples (45á1 17á7 versus 22á5 8á5 lmol lA1, respectively, mean SD). The results of this preliminary study strongly suggest that the endothelial release of NO is probably different in arteries and veins in vivo; this is also consistent with previous literature indicating that basal release of NO occurs mainly from the endothelium of arteries but not from that of veins