182 research outputs found

    PENDIDIKAN KESEHATAN DALAM MENURUNKAN RESIKO HIPERTENSI PADA REMAJA DUSUN PUNDONG II DESA TIRTOADI KABUPATEN SLEMAN YOGYAKARTA

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    Penyakit tidak menular merupakan penyakit kronis pembunuh pertama di dunia dan tidak ditularkan melalui orang ke orang. Menurut WHO, hampir tiga perempat jumlah kematian diakibatkan oleh PTM. Salah satu PTM dengan prevalensi tinggi Indonesia yaitu hipertensi. Laporan Puskesmas Mlati II (2017) menyatakan penyakit hipertensi merupakan salah satu penyakit dengan penderita tertinggi yaitu 1032 kasus. Berdasarkan data, faktor risiko hipertensi di Pundong II diakibatkan gaya hidup seperti perilaku merokok, kurang konsumsi sayur buah, dan kurang aktivitas fisik. Oleh karena itu, diperlukan intervensi dalam menurunkan risiko Hipertensi khususnya pada remaja yang merupakan usia rentan terhadap hipertensi melalui pendidikan kesehatan penyuluhan dan whats app grup. Tujuan penelitian meningkatkan pengetahuan, sikap, dan intensi remaja untuk memiliki pola hidup sehat seperti tidak merokok dalam rumah, konsumsi buah dan sayur, dan melakukan aktivitas fisik. Metode penelitian, mix method Sekuensial Eksplanatori dan rancangan quasi experiment dengan desain one group pre test dan post test. Hasil penelitian terjadi peningkatan pengetahuan, sikap, dan intensi remaja setelah dilakukan pendidikan kesehatan terhadap pola hidup sehat seperti tidak merokok dalam rumah, konsumsi buah dan sayur, dan melakukan aktivitas fisik. Kesimpulan, pendidikan kesehatan melalui penyuluhan dan whats app grup pada remaja dapat menurunkan risiko hipertensi.Suhartin Haringi, Muhammad Cahyo Wicaksono, Rifqi Utari, Raehal AkalAbstrak Hipertensi merupakan salah satu penyakit tidak menular dengan jumlah penderita terbanyak di dunia bahkan di Indonesia. Di Yogyakarta prevalensi hipertensi cukup tinggi seperti di Pundong II. Dari laporan Puskesmas Mlati II bahwa hipertensi menjadi salah satu penyakit dengan penderita tertinggi yaitu sebanyak 1032 kasus dan banyak diakibatkan oleh perilaku hidup tidak sehat. Penelitian bertujuan meningkatkan pengetahuan, sikap, dan intensi remaja untuk memiliki pola hidup sehat seperti tidak merokok dalam rumah, konsumsi buah dan sayur, dan melakukan aktivitas fisik. Penelitian menggunakan mix method Sekuensial Eksplanatori dan rancangan quasi experiment dengan desain one group pre test dan post test. Penelitian dilakukan pada akhir bulan Mei hingga Juni dari penyuluhan tatap muka dan diskusi online (grup whatsapp). Subjek penelitian yaitu 50 remaja dusun Pundong II. Berdasarkan hasil kuantitatif terdapat peningkatan pengetahuan (5,38%) mengenai perilaku rokok dan terjadi peningkatan sikap terhadap bahaya merokok bagi kesehatan (6,52%) dan bahaya merokok di dekat wanita hamil dan anak-anak (3,7%). Namun, terjadi penurunan sikap terhadap Rumah Bebas Asap Rokok (RBAR) (6,54%) dan merokok merugikan ekonomi keluarga (13%). Hasil kualitatif bahwa terdapat peningkatan pengetahuan, sikap positif dan terbentuk intensi (niat dan keinginan) terhadap perilaku rokok, meningkatkan konsumsi buah dan sayur, dan dalam aktivitas fisik. Kesimpulan, pendidikan kesehatan melalui penyuluhan dan diskusi online melalui grup whatsapp dapat meningkatkan pengetahuan, sikap, dan intensi remaja terhadap faktor resiko dari kejadian hipertensi yang banyak terjadi di dusun Pundong II

    Endocytosis as a biological response in receptor pharmacology: evaluation by fluorescence microscopy

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    The activation of G-protein coupled receptors by agonist compounds results in diverse biological responses in cells, such as the endocytosis process consisting in the translocation of receptors from the plasma membrane to the cytoplasm within internalizing vesicles or endosomes. In order to functionally evaluate endocytosis events resulted from pharmacological responses, we have developed an image analysis method -the Q-Endosomes algorithm- that specifically discriminates the fluorescent signal originated at endosomes from that one observed at the plasma membrane in images obtained from living cells by fluorescence microscopy. Mu opioid (MOP) receptor tagged at the carboxy-terminus with yellow fluorescent protein (YFP) and permanently expressed in HEK293 cells was used as experimental model to validate this methodology. Time-course experiments performed with several agonists resulted in different sigmoid curves depending on the drug used to initiate MOP receptor endocytosis. Thus, endocytosis resulting from the simultaneous activation of co-expressed MOP and serotonin 5-HT2C receptors by morphine plus serotonin was significantly different, in kinetics as well as in maximal response parameters, from the one caused by DAMGO, sufentanyl or methadone. Therefore, this analytical tool permits the pharmacological characterization of receptor endocytosis in living cells with functional and temporal resolution

    Morphine activation of mu opioid receptors causes disinhibition of neurons in the ventral tegmental area mediated by β-arrestin2 and c-Src

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    Abstract The tyrosine kinase, c-Src, participates in mu opioid receptor (MOP) mediated inhibition in sensory neurons in which β-arrestin2 (β-arr2) is implicated in its recruitment. Mice lacking β-arr2 exhibit increased sensitivity to morphine reinforcement; however, whether β-arr2 and/or c-Src participate in the actions of opioids in neurons within the reward pathway is unknown. It is also unclear whether morphine acts exclusively through MOPs, or involves delta opioid receptors (DOPs). We examined the involvement of MOPs, DOPs, β-arr2 and c-Src in the inhibition by morphine of GABAergic inhibitory postsynaptic currents (IPSCs) recorded from neurons in the mouse ventral tegmental area. Morphine inhibited spontaneous IPSC frequency, mainly through MOPs, with only a negligible effect remaining in MOP−/− neurons. However, a reduction in the inhibition by morphine for DOP−/− c.f. WT neurons and a DPDPE-induced decrease of IPSC frequency revealed a role for DOPs. The application of the c-Src inhibitor, PP2, to WT neurons also reduced inhibition by morphine, while the inactive PP3, and the MEK inhibitor, SL327, had no effect. Inhibition of IPSC frequency by morphine was also reduced in β-arr2−/− neurons in which PP2 caused no further reduction. These data suggest that inhibition of IPSCs by morphine involves a β-arr2/c-Src mediated mechanism

    Spinal CX3CL1/CX3CR1 may not directly participate in the development of morphine tolerance in rats

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    CX3CL1 (fractalkine), the sole member of chemokine CX3C family, is implicated in inflammatory and neuropathic pain via activating its receptor CX3CR1 on neural cells in spinal cord. However, it has not been fully elucidated whether CX3CL1 or CX3CR1 contributes to the development of morphine tolerance. In this study, we found that chronic morphine exposure did not alter the expressions of CX3CL1 and CX3CR1 in spinal cord. And neither exogenous CX3CL1 nor CX3CR1 inhibitor could affect the development of morphine tolerance. The cellular localizations of spinal CX3CL1 and CX3CR1 changed from neuron and microglia, respectively, to all the neural cells during the development of morphine tolerance. A microarray profiling revealed that 15 members of chemokine family excluding CX3CL1 and CX3CR1 were up-regulated in morphine-treated rats. Our study provides evidence that spinal CX3CL1 and CX3CR1 may not be involved in the development of morphine tolerance directly

    Pharmacological differentiation of opioid receptor antagonists by molecular and functional imaging of target occupancy and food reward-related brain activation in humans

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    Opioid neurotransmission has a key role in mediating reward-related behaviours. Opioid receptor (OR) antagonists, such as naltrexone (NTX), can attenuate the behaviour-reinforcing effects of primary (food) and secondary rewards. GSK1521498 is a novel OR ligand, which behaves as an inverse agonist at the μ-OR sub-type. In a sample of healthy volunteers, we used [11C]-carfentanil positron emission tomography to measure the OR occupancy and functional magnetic resonance imaging (fMRI) to measure activation of brain reward centres by palatable food stimuli before and after single oral doses of GSK1521498 (range, 0.4–100 mg) or NTX (range, 2–50 mg). GSK1521498 had high affinity for human brain ORs (GSK1521498 effective concentration 50=7.10 ng ml−1) and there was a direct relationship between receptor occupancy (RO) and plasma concentrations of GSK1521498. However, for both NTX and its principal active metabolite in humans, 6-β-NTX, this relationship was indirect. GSK1521498, but not NTX, significantly attenuated the fMRI activation of the amygdala by a palatable food stimulus. We thus have shown how the pharmacological properties of OR antagonists can be characterised directly in humans by a novel integration of molecular and functional neuroimaging techniques. GSK1521498 was differentiated from NTX in terms of its pharmacokinetics, target affinity, plasma concentration–RO relationships and pharmacodynamic effects on food reward processing in the brain. Pharmacological differentiation of these molecules suggests that they may have different therapeutic profiles for treatment of overeating and other disorders of compulsive consumption
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