147 research outputs found

    Perencanaan Pengelolaan Sampah Kampus I Institut Teknologi Nasional Malang

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    Sampah yang dihasilkan oleh kampus I ITN Malang berasal dari kegiatan akademik, administrasi, sampah kantin, taman, dan sampah jalan, yang dapat meyebabkan jumlah dan komposisi sampahnya bervariasi. Data yang dibutuhkan dalam menunjang sistem pengelolaan sampah adalah timbulan, komposisi, dan karakteristik sampah. Pengukuran timbulan dan komposisi sampah didasarkan pada modifikasi dari SNI 19-3694-1994 mengenai Metode Pengambilan dan Pengukuran Contoh Timbulan dan Komposisi Sampah Perkotaan. Hasil timbulan sampah kawasan kampus I Institut Teknologi Nasional Malang untuk timbulan kg/orang/hari dan kg/m²/hari adalah untuk gedung biro lembaga dan rektorat adalah sebesar 0,09 kg/orang/hari, gedung teknik lingkungan 0,03 kg/orang/hari, gedung perencanaan wilayah kota 0,11 kg/orang/hari, gedung teknik sipil 0,05 kg/orang/hari, gedung arsitektur 0,04 kg/orang/hari, gedung teknik geodesi 0,09 kg/orang/hari, gedung pasca sarjana 0,40 kg/orang/hari, fasilitas perpustakaan 7,48 kg/m²/hari, fasilitas kantin A 15,5 kg/m²/hari, fasilitas Kantin B 16,5 kg/m²/hari dan taman/jalan sebesar 8,81 kg/m²/hari. Perencanaan aspek teknik operasional di kawasan kampus yang diusulkan untuk mengurangi timbulan sampah di kawasan kampus I ITN Malang sesuai dengan hasil penelitian yaitu, skenario II dan meliputi penggantian jenis wadah sampah untuk memfasilitasi pemilahan sampah sejak dari sumbernya

    Wanker\u27s Corner Saloon & Cafe

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    Cafe & saloon. Bistro & tavern. Creative menu design. Please note trademark statement on menu. Lots of history and humor throughout menu. Geographical location: 2509 Borland Rd., Tualatin, Oregon

    Current State of Preeclampsia Mouse Models: Approaches, Relevance, and Standardization

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    Preeclampsia (PE) is a multisystemic, pregnancy-specific disorder and a leading cause of maternal and fetal death. PE is also associated with an increased risk for chronic morbidities later in life for mother and offspring. Abnormal placentation or placental function has been well-established as central to the genesis of PE; yet much remains to be determined about the factors involved in the development of this condition. Despite decades of investigation and many clinical trials, the only definitive treatment is parturition. To better understand the condition and identify potential targets preclinically, many approaches to simulate PE in mice have been developed and include mixed mouse strain crosses, genetic overexpression and knockout, exogenous agent administration, surgical manipulation, systemic adenoviral infection, and trophoblast-specific gene transfer. These models have been useful to investigate how biological perturbations identified in human PE are involved in the generation of PE-like symptoms and have improved the understanding of the molecular mechanisms underpinning the human condition. However, these approaches were characterized by a wide variety of physiological endpoints, which can make it difficult to compare effects across models and many of these approaches have aspects that lack physiological relevance to this human disorder and may interfere with therapeutic development. This report provides a comprehensive review of mouse models that exhibit PE-like symptoms and a proposed standardization of physiological characteristics for analysis in murine models of PE

    Sequential and Batch Processing Methods of the EBP Learning Algorithm

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    Placental abnormalities can cause Pregnancy-Associated Disorders, including preeclampsia, intrauterine growth restriction, and placental insufficiency, resulting in complications for both the mother and fetus. Trophoblast cells within the labyrinthine layer of the placenta facilitate the exchange of nutrients, gases, and waste between mother and fetus; therefore, the development of this cell layer is critical for fetal development. As trophoblast cells differentiate, it is assumed their metabolism changes with their energy requirements. We hypothesize that proper regulation of trophoblast metabolism is a key component of normal placental development; therefore, we examined the role of AMP-activated kinase (AMPK, PRKAA1/2), a sensor of cellular energy status. Our previous studies have shown that AMPK knockdown alters both trophoblast differentiation and nutrient transport. In this study, AMPKα1/2 shRNA was used to investigate the metabolic effects of AMPK knockdown on SM10 placental labyrinthine progenitor cells before and after differentiation. Extracellular flux analysis confirmed that AMPK knockdown was sufficient to reduce trophoblast glycolysis, mitochondrial respiration, and ATP coupling efficiency. A reduction in AMPK in differentiated trophoblasts also resulted in increased mitochondrial volume. These data indicate that a reduction in AMPK disrupts cellular metabolism in both progenitors and differentiated placental trophoblasts. This disruption correlates to abortive trophoblast differentiation that may contribute to the development of Pregnancy-Associated Disorders

    Mouse models of preeclampsia with preexisting comorbidities

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    Preeclampsia is a pregnancy-specific condition and a leading cause of maternal and fetal morbidity and mortality. It is thought to occur due to abnormal placental development or dysfunction, because the only known cure is delivery of the placenta. Several clinical risk factors are associated with an increased incidence of preeclampsia including chronic hypertension, diabetes, autoimmune conditions, kidney disease, and obesity. How these comorbidities intersect with preeclamptic etiology, however, is not well understood. This may be due to the limited number of animal models as well as the paucity of studies investigating the impact of these comorbidities. This review examines the current mouse models of chronic hypertension, pregestational diabetes, and obesity that subsequently develop preeclampsia-like symptoms and discusses how closely these models recapitulate the human condition. Finally, we propose an avenue to expand the development of mouse models of preeclampsia superimposed on chronic comorbidities to provide a strong foundation needed for preclinical testing

    Diarrheal-associated gut dysbiosis in cancer and inflammatory bowel disease patients is exacerbated by Clostridioides difficile infection

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    IntroductionLow diversity gut dysbiosis can take different forms depending on the disease context. In this study, we used shotgun metagenomic sequencing and gas chromatography–mass spectrometry (GC-MS) to compared the metagenomic and metabolomic profiles of Clostridioides (Clostridium) difficile diarrheal cancer and inflammatory bowel disease (IBD) patients and defined the additive effect of C. difficile infection (CDI) on intestinal dysbiosis.ResultsThe study cohort consisted of 138 case-mix cancer patients, 43 IBD patients, and 45 healthy control individuals. Thirty-three patients were also infected with C. difficile. In the control group, three well-known enterotypes were identified, while the other groups presented with an additional Escherichia-driven enterotype. Bacterial diversity was significantly lower in all groups than in healthy controls, while the highest level of bacterial species richness was observed in cancer patients. Fifty-six bacterial species had abundance levels that differentiated diarrheal patient groups from the control group. Of these species, 52 and 4 (Bacteroides fragilis, Escherichia coli, Klebsiella pneumoniae, and Ruminococcus gnavus) were under-represented and over-represented, respectively, in all diarrheal patient groups. The relative abundances of propionate and butyrate were significantly lower in fecal samples from IBD and CDI patients than in control samples. Isobutyrate, propanate, and butyrate concentrations were lower in cancer, IBD, and CDI samples, respectively. Glycine and valine amino acids were over- represented in diarrheal patients.ConclusionOur data indicate that different external and internal factors drive comparable profiles of low diversity dysbiosis. While diarrheal-related low diversity dysbiosis may be a consequence of systemic cancer therapy, a similar phenotype is observed in cases of moderate to severe IBD, and in both cases, dysbiosis is exacerbated by incidence of CDI
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