ANALISA PRAKIRAAN KEBUTUHAN BAHAN BAKAR SEKTOR RUMAH TANGGA KOTA PEKANBARU TAHUN 2016-2025 MENGGUNAKAN PERANGKAT LUNAK LEAP

Kebutuhan bahan bakar sektor rumah tangga kota Pekanbaru pastinya akan meningkat setiap tahunnya seiring dengan besarnya aktivitas pemakaian bahan bakar dan besarnya pemakaian bahan bakar per aktivitas. Tingkat perekonomian dan jumlah penduduk sangat berpengaruh terhadap aktivitas pemakaian bahan bakar. Semakin tinggi tingkat pertumbuhan ekonomi dan pertumbuhan penduduk akan menyebabkan aktivitas pemakaianenergi semakin tinggi. Namun kebiakan yang dilakukan pemerintah tentang peralihan bahan bakar dari mitan ke gas mengakibatkan semakin tingginya angka kebutuhan bakar bakar dengan dampak Indonesia harus melakukan impor disetiap tahunnya, disisi lain masih banyaknya penggunaan bahan bakar dengan tingkat polutan yang tinggi seperti kayu bakar, arang dan minyak tanah. Untuk itu diharapkan pada tahun 2025 penelitian ini dapat melihat seberapa penggunaan bahan bakar sektor rumah tangga dan tingkat efisien masyarakat kota Pekanbaru dalam menggunakan bahan bakar. Oleh sebab itu salah satu tahapan yang harus dilakukan adalah dengan melakukan prakiraan untuk melihat seberapa besar pemakaian bahan bakar ditahun mendatang, dalam melakukan prakiraan dibutuhkan data sekunder dan pengolahan selanjutnya yang akan digunakan sebagai asumsi dasar. Penelitian ini menggunakan bantuan perangkat lunakLEAP, jangka waktu prakiraan sepuluh tahun kedepan dengan beberapa faktor yang mempengaruhinya yaitu jumlah penduduk, rumah tangga,PDRB, pertumbuhan penduduk, pertumbuhan rumah tangga dan pertumbuhan PDRB. Prakiraan permintaan bahan bakar dilakukan berdasarkan data historis aktivitas dan intensitas bahan bakar.Hasil penelitian ini menunjukkan bahwa prakiraan kebutuhan bahan bakar sektor rumah tangga kota Pekanbaru periode 2016-2025 memiliki hasil prakiraan yang beragam. Dimana peningkatan pemakaian terjadi pada jenis bahan bakar LPG, gas kota dan lainnya dengan jumlah prakiraan ditahun 2025 untuk pemakaian LPG sebesar 13.300.708,43 SBM, gas kota 3.640,15 SBMdan lainnya 1.152,80SBM. Beberapa jenis bahan bakarterjadi penurunan yaituuntuk jenis bahan bakar minyak tanah, arang dan kayu bakar dengan jumlah prakiraan ditahun 2025 untuk jenis minyak tanah sebesar 13,78 SBM, arang 2,08 SBM dan kayu bakar 0,64 SBM. Dengan hasil prakiraan kebutuhan bahan bakar maka dapat dihasilkannilaielastisitas energi atau tingkat efisiensi penggunaan bahan bakar sektor rumah tangga kota Pekanbaru.Angka elastisitas kota Pekanbaru menunjukkkanmenunjukkan bahwa kota Pekanbaru bersifat boros dalam penggunaan bahan bakaryaitu 1,6.Kata kunci:Prakiraan, Bahan Bakar Sektor Rumah Tangga, Prangkat Lunak LEAP, Intensitas, Elastisitas

Investigating the importance of B cells and antibodies during Trichuris muris infection using the IgMi mouse

From Springer Nature via Jisc Publications RouterHistory: received 2020-04-24, rev-recd 2020-06-24, registration 2020-07-17, accepted 2020-07-17, pub-electronic 2020-08-10, online 2020-08-10, pub-print 2020-09Publication status: PublishedFunder: Indonesian endowment fund for education, Phd StudentshipFunder: Biotechnology and Biological Sciences Research Council UK, PhD StudenshipFunder: Medical Research Council UK; Grant(s): MR/NO22661/1 to KJEFunder: Biotechnology and Biological Sciences Research Council UK; Grant(s): BB/P018157/1 to KJEAbstract: The IgMi mouse has normal B cell development; its B cells express an IgM B cell receptor but cannot class switch or secrete antibody. Thus, the IgMi mouse offers a model system by which to dissect out antibody-dependent and antibody-independent B cell function. Here, we provide the first detailed characterisation of the IgMi mouse post-Trichuris muris (T. muris) infection, describing expulsion phenotype, cytokine production, gut pathology and changes in T regulatory cells, T follicular helper cells and germinal centre B cells, in addition to RNA sequencing (RNA seq) analyses of wild-type littermates (WT) and mutant B cells prior to and post infection. IgMi mice were susceptible to a high-dose infection, with reduced Th2 cytokines and elevated B cell-derived IL-10 in mesenteric lymph nodes (MLN) compared to controls. A low-dose infection regime revealed IgMi mice to have significantly more apoptotic cells in the gut compared to WT mice, but no change in intestinal inflammation. IL-10 levels were again elevated. Collectively, this study showcases the potential of the IgMi mouse as a tool for understanding B cell biology and suggests that the B cell plays both antibody-dependent and antibody-independent roles post high- and low-dose T. muris infection. Key messages: During a high-dose T. muris infection, B cells are important in maintaining the Th1/Th2 balance in the MLN through an antibody-independent mechanism. High levels of IL-10 in the MLN early post-infection, and the presence of IL-10-producing B cells, correlates with susceptibility to T. muris infection. B cells maintain gut homeostasis during chronic T. muris infection via an antibody-dependent mechanism

Structural epitope profiling identifies antibodies associated with critical COVID-19 and long COVID

Even within a single protein, antibody binding can have beneficial, neutral, or harmful effects during the response to infection. Resolving a polyclonal antibody repertoire across a pathogen’s proteome to specific epitopes may therefore explain much of the heterogeneity in susceptibility to infectious disease. However, the three-dimensional nature of antibody-epitope interactions makes the discovery of non-obvious targets challenging. We implemented a novel computational method and synthetic biology pipeline for identifying epitopes that are functionally important in the SARS-CoV-2 proteome and identified an IgM-dominant response to an exposed Membrane protein epitope which to our knowledge is the strongest correlate of severe disease identified to date (adjusted OR 72.14, 95% CI: 9.71 – 1300.15), stronger even than the exponential association of severe disease with age. We also identify persistence (> 2 years) of this IgM response in individuals with longCOVID, and a correlation with fatigue and depression symptom burden. The repetitive arrangement of this epitope and the pattern of isotype class switching is consistent with this being a previously unrecognized T independent antigen. These findings point to a coronavirus host-pathogen interaction characteristic of severe virus driven immune pathology. This epitope is a promising vaccine and therapeutic target as it is highly conserved through SARS-CoV-2 variant evolution in humans to date and in related coronaviruses (e.g. SARS-CoV), showing far less evolutionary plasticity than targets on the Spike protein. This provides a promising biomarker for longCOVID and a target to complement Spike-directed vaccination which could broaden humoral protection from severe or persistent disease or novel coronavirus spillovers

Monocyte-derived peritoneal macrophages protect C57BL/6 mice against surgery-induced adhesions

Peritoneal adhesions commonly occur after abdominal or pelvic surgery. These scars join internal organs to each other or to the cavity wall and can present with abdominal or pelvic pain, and bowel obstruction or female infertility. The mechanisms underlying adhesion formation remain unclear and thus, effective treatments are not forthcoming. Peritoneal macrophages accumulate after surgery and previous studies have attributed either pro- or anti-scarring properties to these cells. We propose that there are complex and nuanced responses after surgery with respect to both resident and also monocyte-derived peritoneal macrophage subpopulations. Moreover, we contend that differences in responses of specific macrophage subpopulations in part explain the risk of developing peritoneal scars. We characterized alterations in peritoneal macrophage subpopulations after surgery-induced injury using two strains of mice, BALB/c and C57BL/6, with known differences in macrophage response post-infection. At 14 days post-surgery, BALB/c mice displayed more adhesions compared with C57BL/6 mice. This increase in scarring correlated with a lower influx of monocyte-derived macrophages at day 3 post-surgery. Moreover, BALB/c mice showed distinct macrophage repopulation dynamics after surgery. To confirm a role for monocyte-derived macrophages, we used Ccr2-deficient mice as well as antibody-mediated depletion of CCR2 expressing cells during initial stages of adhesion formation. Both Ccr2-deficient and CCR2-depleted mice showed a significant increase in adhesion formation associated with the loss of peritoneal monocyte influx. These findings revealed an important protective role for monocyte-derived cells in reducing adhesion formation after surgery

Monocyte-derived peritoneal macrophages protect C57BL/6 mice against surgery-induced adhesions

Peritoneal adhesions commonly occur after abdominal or pelvic surgery. These scars join internal organs to each other or to the cavity wall and can present with abdominal or pelvic pain, and bowel obstruction or female infertility. The mechanisms underlying adhesion formation remain unclear and thus, effective treatments are not forthcoming. Peritoneal macrophages accumulate after surgery and previous studies have attributed either pro- or anti-scarring properties to these cells. We propose that there are complex and nuanced responses after surgery with respect to both resident and also monocyte-derived peritoneal macrophage subpopulations. Moreover, we contend that differences in responses of specific macrophage subpopulations in part explain the risk of developing peritoneal scars. We characterized alterations in peritoneal macrophage subpopulations after surgery-induced injury using two strains of mice, BALB/c and C57BL/6, with known differences in macrophage response post-infection. At 14 days post-surgery, BALB/c mice displayed more adhesions compared with C57BL/6 mice. This increase in scarring correlated with a lower influx of monocyte-derived macrophages at day 3 post-surgery. Moreover, BALB/c mice showed distinct macrophage repopulation dynamics after surgery. To confirm a role for monocyte-derived macrophages, we used Ccr2-deficient mice as well as antibody-mediated depletion of CCR2 expressing cells during initial stages of adhesion formation. Both Ccr2-deficient and CCR2-depleted mice showed a significant increase in adhesion formation associated with the loss of peritoneal monocyte influx. These findings revealed an important protective role for monocyte-derived cells in reducing adhesion formation after surgery

Presentation_1_Monocyte-derived peritoneal macrophages protect C57BL/6 mice against surgery-induced adhesions.pdf

Peritoneal adhesions commonly occur after abdominal or pelvic surgery. These scars join internal organs to each other or to the cavity wall and can present with abdominal or pelvic pain, and bowel obstruction or female infertility. The mechanisms underlying adhesion formation remain unclear and thus, effective treatments are not forthcoming. Peritoneal macrophages accumulate after surgery and previous studies have attributed either pro- or anti-scarring properties to these cells. We propose that there are complex and nuanced responses after surgery with respect to both resident and also monocyte-derived peritoneal macrophage subpopulations. Moreover, we contend that differences in responses of specific macrophage subpopulations in part explain the risk of developing peritoneal scars. We characterized alterations in peritoneal macrophage subpopulations after surgery-induced injury using two strains of mice, BALB/c and C57BL/6, with known differences in macrophage response post-infection. At 14 days post-surgery, BALB/c mice displayed more adhesions compared with C57BL/6 mice. This increase in scarring correlated with a lower influx of monocyte-derived macrophages at day 3 post-surgery. Moreover, BALB/c mice showed distinct macrophage repopulation dynamics after surgery. To confirm a role for monocyte-derived macrophages, we used Ccr2-deficient mice as well as antibody-mediated depletion of CCR2 expressing cells during initial stages of adhesion formation. Both Ccr2-deficient and CCR2-depleted mice showed a significant increase in adhesion formation associated with the loss of peritoneal monocyte influx. These findings revealed an important protective role for monocyte-derived cells in reducing adhesion formation after surgery.</p