Studi Potensi Jumlah Penumpang Bus Pemadu Moda Rute Malang – Bandar Udara Juanda Pp

Bandar Udara Malang yang belum melayani banyak tujuan penerbangan membuat pengguna moda pesawat memilih Bandar Udara Juanda. Disisi lain angkutan yang melayani rute Malang-Juanda PP hanya angkutan travel. Untuk itu dibutuhkan moda lain yang lebih ekonomis dan memiliki kapasitas lebih banyak dibandingkan angkutan travel. Bus pemadu moda adalah moda alternatif yang dapat memenuhi kebutuhan tersebut.Pengumpulan data dilakukan dengan penyebaran kuisioner karakteristik sosial-ekonomi, karakteristik perjalanan serta kuisioner dengan teknik penyusunan stated preference. Stated preference memiliki atribut biaya perjalanan, waktu tempuh dan frekuensi keberangkatan. Sedangkan untuk prediksi tarif bus pemadu moda yang direncanakan diperoleh dari perhitungan BOK. Tarif yang telah diperoleh dari perhitungan BOK dibandingkan dengan nilai ATP dan WTP yang diperoleh dari kuisioner yang telah disebarkan. Sehingga didapatkan tarif ideal yang akan diberlakukan apabila bus pemadu moda tersebut direalisasikan.Setelah melakukan perhitungan tarif berdasarkan BOK diperoleh tarif sebesar Rp 23.374,- serta berdasarkan ATP dan WTP diperoleh tarif sebesar Rp 43.675,-. Dengan demikian perkiraan awal tarif bus pemadu moda sebesar Rp 40.000,- dapat diberlakukan. Hasil dari pemodelan pemilihan moda dengan metode stated preference untuk selisih biaya perjalanan Malang-Juanda: dan Juanda-Malang : , untuk selisih waktu tempuh perjalanan () rute Malang-Juanda : dan rute Juanda-Malang : , sedangkan untuk selisih Frekuensi Keberangkatan () rute Malang-Juanda : dan rute Juanda-Malang : .Potensi perpindahan pengguna travel ke bus pemadu moda rute Malang-Juanda sebanyak 705 orang per hari (83,97%). Sedangkan untuk rute Juanda-Malang sebanyak 1516 orang per hari (90,24%)

Analysis of the ability of HA to activate the NOP, DOP, MOP,

<p><b>and </b><b>KOP </b><b>receptors.</b> CHO stable clones expressing NOP (<b>a</b>), DOP (<b>b</b>), MOP (<b>c</b>), or KOP (<b>d</b>) receptors were transfected with a mitochondrial targeted aequorin probe and stimulated with different HA concentrations as indicated in the figure. The mitochondrial Ca²⁺ responses are expressed as percentage of mitochondrial Ca²⁺ response compared to receptors stimulation with canonic agonist as indicated in the figure.</p

HA-dependent activation of the KOP receptor.

<p>(<b>a</b>) Dose response curve of HA on the CHO cells stably expressing KOP receptors. Cells were stimulated with 200 kDa HA at increasing concentrations ranging from 0,005 to 5 mg/ml. (<b>b</b>) Inhibition response curves of norbinaltor-phimine vs 200 kDa HA (5 mg/ml) in CHO cells stably expressing KOP receptors. (<b>c</b>) Dose response curve of dynorphin A on CHO cells stably expressing KOP receptors. (<b>d</b>) Inhibition response curves of norbinaltor-phimine vs dynorphin A (10⁻⁹ M) in CHO cells stably expressing KOP receptors. In all curves (<b>a–d</b>), the mitochondrial Ca²⁺ responses represent the percentage of probe discharged.</p

Analysis of cytosolic and mitochondrial Ca²⁺ responses on rat DRG neurons.

<p>(<b>a–b</b>) Rat DRG neurons were co-transfected with the mtAEQ probe and the promiscuous G protein Gα_qi5. At 36 h post-transfection, the rat DRG neurons were stimulated with either 200 kDa HA (5 mg/ml) or dynorphin A as indicated. (<b>a</b>) [Ca²⁺] values, (<b>b</b>) percentage of probe discharged during the stimulation. (<b>c–d</b>) rat DRG neurons were transfected with the promiscuous G protein Gα_qi5, loaded with Fura-2/AM and stimulated with either 200 kDa HA (5 mg/ml) or dynorphin A as indicated (<b>c</b>) in presence of extracellular Ca²⁺ or (<b>d</b>) first stimulated in a medium without [Ca²⁺] (with EGTA 100 µM), and then with the addition of Ca²⁺ to the extracellular medium. The kinetic behavior of the cytosolic Ca²⁺ response is presented as the 340 nm/380 nm ratio.</p

Cytosolic Ca²⁺ responses in CHO cell lines expressing human OPr.

<p>CHO stable clones expressing NOP, DOP, MOP, or KOP receptors were loaded with Fura-2/AM and stimulated with nociceptin (<b>a</b>), dermorphin (<b>b</b>), [d-Pen2,d-Pen5]-Enkephalin (DPDPE) (<b>c</b>) and dynorphin A (<b>d</b>) respectively, as indicated in figure. The kinetic behavior of the cytosolic Ca²⁺ response is presented as the 340 nm/380 nm ratio.</p

Cytosolic Ca²⁺ homeostasis in CHO cell lines expressing KOP receptors.

<p>CHO cells expressing KOP receptors were loaded with Fura-2/AM and stimulated with either dynorphin A [1 μM] alone (<b>a</b>) or with 200 kDa HA (5 mg/ml) and dynorphin A (<b>b</b>). The kinetic behavior of the cytosolic Ca²⁺ response is presented as the 340 nm/380 nm ratio.</p

Mitochondrial Ca²⁺ responses in CHO cell lines expressing human OPr.

<p>CHO stable clones expressing NOP, DOP, MOP, or KOP receptors were transfected with a mitochondrial targeted aequorin probe and stimulated with nociceptin, [d-Pen2,d-Pen5]-Enkephalin (DPDPE), dermorphin and dynorphin A, respectively. The negative control was the addition of buffer (KRB) without agonist. The mitochondrial Ca²⁺ responses are expressed either as (<b>a</b>) percentage of probe discharged during the stimulation or (<b>b</b>) as [Ca²⁺] values.</p

Discovery of Novel 1,3,8-Triazaspiro[4.5]decane Derivatives That Target the c Subunit of F₁/F_O‑Adenosine Triphosphate (ATP) Synthase for the Treatment of Reperfusion Damage in Myocardial Infarction

Recent cardiology research studies have reported the role, function, and structure of the mitochondrial permeability transition pore (mPTP) and have shown that its opening plays a key role in the progression of myocardial cell death secondary to reperfusion. In this manuscript, we validated a new pharmacological approach as an adjunct to reperfusion in myocardial infarction (MI) treatment and describe the discovery, optimization, and structure–activity relationship (SAR) studies of the first small-molecule mPTP opening inhibitors based on a 1,3,8-triazaspiro[4.5]­decane scaffold that targets the c subunit of the F₁/F_O-ATP synthase complex. We identified three potential compounds with good mPTP inhibitory activity and beneficial effects in a model of MI, including a decreased apoptotic rate in the whole heart and overall improvement of cardiac function upon administration during reperfusion. The selected compounds did not show off-target effects at the cellular and mitochondrial levels. Moreover, the compounds preserved the mitochondrial ATP content despite interacting with the ATP synthase complex

Discovery of Novel 1,3,8-Triazaspiro[4.5]decane Derivatives That Target the c Subunit of F₁/F_O‑Adenosine Triphosphate (ATP) Synthase for the Treatment of Reperfusion Damage in Myocardial Infarction

Recent cardiology research studies have reported the role, function, and structure of the mitochondrial permeability transition pore (mPTP) and have shown that its opening plays a key role in the progression of myocardial cell death secondary to reperfusion. In this manuscript, we validated a new pharmacological approach as an adjunct to reperfusion in myocardial infarction (MI) treatment and describe the discovery, optimization, and structure–activity relationship (SAR) studies of the first small-molecule mPTP opening inhibitors based on a 1,3,8-triazaspiro[4.5]­decane scaffold that targets the c subunit of the F₁/F_O-ATP synthase complex. We identified three potential compounds with good mPTP inhibitory activity and beneficial effects in a model of MI, including a decreased apoptotic rate in the whole heart and overall improvement of cardiac function upon administration during reperfusion. The selected compounds did not show off-target effects at the cellular and mitochondrial levels. Moreover, the compounds preserved the mitochondrial ATP content despite interacting with the ATP synthase complex