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ANALISIS KEBISINGAN LALU LINTAS PADA RUAS JALAN ARTERI (STUDI KASUS JALAN PROF. DR. IB. MANTRA PADA KM 15 s/d KM 16) Wardika, I Ketut; Suparsa, I Gusti Putu; Wedagama, D.M. Priyantha
Jurnal Ilmiah Elektronik Infrastruktur Teknik Sipil Vol 1 No 1 (2012): Vol.1, No.1, Desember 2012
Publisher : Jurnal Ilmiah Elektronik Infrastruktur Teknik Sipil

Show Abstract | Download Original | Original Source | Check in Google Scholar | Full PDF (1188.981 KB)

Abstract

Abstrak: Penelitian ini bermula dari pengamatan volume lalu lintas di Jalan Prof. DR Ida Bagus Mantra  yang bertambah padat serta banyaknya tanjakan yang dijumpai sepanjang jalan tersebut. Sebagai contoh Pada segmen kilometer 15 sampai dengan kilometer 16 berupa tanjakan dengan kelandaian 2,3% yang dijadikan sebagai objek penelitian, hal tersebut tentunya berpengaruh terhadap volume lalu lintas, kecepatan kendaraan dan kebisingan yang terjadi. Penelitian ini dimaksudkan untuk menganalisis tingkat kebisingan kendaraan akibat lalu lintas pada jalan Prof. DR Ida Bagus Mantra, membuat suatu model matematis yang menyatakan hubungan antara tingkat kebisingan dengan volume kendaraan dan menganalisis ekivalensi kebisingan kendaraan akibat lalu lintas. Analisis data  menggunakan metode Regresi Linier Berganda pada program SPSS 17.0 for Windows. Data yang dihasilkan dari proses analisis meliputi :  Nilai Korelasi (hubungan) antara variabel bebas  dengan variabel tidak bebas, Tingkat Keberartian (signifikansi) dari  masing-masing koefisien regresi, Model Tingkat Kebisingan, Uji Kenormalan Data dan Koefisien Determinasi. Berdasarkan hasil analisis maka tingkat kebisingan kendaraan pada jalan Prof. DR Ida Bagus Mantra adalah sebesar 81,0 dBA. Bentuk model tingkat kebisingan lalu lintas terbaik adalah Y4 = L90 = 53,512 + 0,019X1 + 0,043X2 + 0,010X3 dengan nilai R2= 0,853, dimana nilai X1 adalah volume sepeda motor, X2 volume kendaraan ringan dan X3 volume kendaraan berat. Nilai ekivalensi kebisingan dari masing-masing kendaraan adalah untuk sepeda motor : 1,9 ; kendaraan ringan : 1 dan kendaraan berat : 0,12. Model tingkat kebisingan lalu lintas tersebut berlaku untuk  jalan arteri dengan kelandaian memanjang 2,3% dengan kecepatan rata-rata 75 Km/jam.  
Presumed Polymyositis in Chronic Hepatitis C: Navigating Diagnostic Uncertainty and Therapeutic Imperatives in Recurrent Myopathy I Ketut Wardika; Pande Ketut Kurniari
Bioscientia Medicina : Journal of Biomedicine and Translational Research Vol. 9 No. 12 (2025): Bioscientia Medicina: Journal of Biomedicine & Translational Research
Publisher : HM Publisher

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.37275/bsm.v9i12.1446

Abstract

Background: Polymyositis (PM) is a cell-mediated inflammatory myopathy for which viral triggers, particularly the Hepatitis C virus (HCV), are increasingly recognized. The convergence of these conditions creates a formidable clinical scenario, often compelling urgent therapeutic intervention despite incomplete diagnostic data. This report explores the management of such a case, highlighting the pragmatic decision-making required when definitive investigations are deferred. Case presentation: A 48-year-old male with untreated chronic HCV infection (Genotype 1b, viral load 2.8 x 10⁶ IU/mL) presented with a debilitating relapse of severe, symmetric proximal muscle weakness, three years after a similar episode. He exhibited profound weakness (Medical Research Council grade 2/5 in hip flexors) and marked myonecrosis (Creatine Kinase 8,572 U/L). Although comprehensive myositis-specific autoantibodies were negative, a strong clinical and biochemical profile led to a presumptive diagnosis of an acute PM exacerbation. Definitive diagnostics, including muscle biopsy, were deferred by the patient. Empirical treatment with high-dose corticosteroids and azathioprine was initiated, predicated on a careful risk-benefit analysis concerning immunosuppression in active viral infection. This strategy resulted in rapid and significant clinical and biochemical improvement. The patient was subsequently scheduled for direct-acting antiviral therapy to address the underlying viral trigger. Conclusion: This case underscores the critical challenge of managing severe, presumed autoimmune disease in the face of diagnostic ambiguity. It demonstrates that a therapeutic strategy guided by strong clinical evidence can be effective for controlling acute, disabling flares. Furthermore, it champions a necessary dual-paradigm approach: acute immunomodulation to preserve function, followed by targeted antiviral therapy to eradicate the probable etiological trigger, thereby aiming to prevent future recurrence and achieve durable remission.
Presumed Polymyositis in Chronic Hepatitis C: Navigating Diagnostic Uncertainty and Therapeutic Imperatives in Recurrent Myopathy I Ketut Wardika; Pande Ketut Kurniari
Bioscientia Medicina : Journal of Biomedicine and Translational Research Vol. 9 No. 12 (2025): Bioscientia Medicina: Journal of Biomedicine & Translational Research
Publisher : HM Publisher

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.37275/bsm.v9i12.1446

Abstract

Background: Polymyositis (PM) is a cell-mediated inflammatory myopathy for which viral triggers, particularly the Hepatitis C virus (HCV), are increasingly recognized. The convergence of these conditions creates a formidable clinical scenario, often compelling urgent therapeutic intervention despite incomplete diagnostic data. This report explores the management of such a case, highlighting the pragmatic decision-making required when definitive investigations are deferred. Case presentation: A 48-year-old male with untreated chronic HCV infection (Genotype 1b, viral load 2.8 x 10⁶ IU/mL) presented with a debilitating relapse of severe, symmetric proximal muscle weakness, three years after a similar episode. He exhibited profound weakness (Medical Research Council grade 2/5 in hip flexors) and marked myonecrosis (Creatine Kinase 8,572 U/L). Although comprehensive myositis-specific autoantibodies were negative, a strong clinical and biochemical profile led to a presumptive diagnosis of an acute PM exacerbation. Definitive diagnostics, including muscle biopsy, were deferred by the patient. Empirical treatment with high-dose corticosteroids and azathioprine was initiated, predicated on a careful risk-benefit analysis concerning immunosuppression in active viral infection. This strategy resulted in rapid and significant clinical and biochemical improvement. The patient was subsequently scheduled for direct-acting antiviral therapy to address the underlying viral trigger. Conclusion: This case underscores the critical challenge of managing severe, presumed autoimmune disease in the face of diagnostic ambiguity. It demonstrates that a therapeutic strategy guided by strong clinical evidence can be effective for controlling acute, disabling flares. Furthermore, it champions a necessary dual-paradigm approach: acute immunomodulation to preserve function, followed by targeted antiviral therapy to eradicate the probable etiological trigger, thereby aiming to prevent future recurrence and achieve durable remission.