DESAIN BANGUNAN BERTINGKAT BETON BERTULANG STUDI KASUS: GEDUNG EIL (ENGINEERING INTEGRATED LABORATORY) UNIVERSITAS NEGERI PADANG

Gedung Laboratorium Universitas Negeri Padang atau disebut juga Engineering Integrated Laboratory (EIL) adalah gedung yang berfungsi sebagai laboratorium, tempat praktek dan penelitian bagi Fakultas Teknik Universitas Negeri Padang. Daerah pembangunan Gedung EIL ini berada di kawasan daerah dengan resiko gempa tinggi dan daerah zona tsunami sehingga dalam mitigasi bencana untuk perencanaan strukturnya harus berdasarkan aturan dan ketentuan yang sesuai untuk daerah dengan resiko gempa tinggi. Perencanaan struktur diawali dengan penentuan jenis struktur, preliminary desain, permodelan struktur, analisis pembebanan, analisis struktur. Hasil akhir dari proyek akhir berupa perencanaan tulangan pada elemen struktur yaitu perencanaan tulangan balok, kolom, dan pelat. Perencanaan tulangan pada dibagi atas perencanaan tulangan lentur dan perencanaan tulangan geser dimana pada masing-masing tulangan telah memenuhi standar dan aturan yang berlaku saat ini

Prarancangan Pabrik Produksi Gliserol Dari Proses Saponifikasi Crude Palm Oil Dengan Alkali NaOH Kapasitas 60.000 Ton/Tahun

Indonesia merupakan negara dengan industri yang termasuk sangat banyak ragamnya, mulai dari idustri kimia, pangan sampai industri domestik. Perkembangan pasar yang semakin banyak kebutuhan untuk masyarakat sehingga industri berlombalomba untuk menyediakan apa yang dibutuhkan oleh masyarakat maupun industri lainnya untuk ketersediaan bahan baku. Salah satu yang masih berkembang saat ini adalah industri untuk pengolahan minyak kelapa sawit atau yangs ering disebut dengan Crude Palm Oil (CPO) dimana di Asia Indonesia merupakan negara pertama terbesar penghasil kelapa sawit yakni sebesar 31.5 ton (Menurut Food and Agricultural Organization PBB, permintaan terhadap minyak sawit akan meningkat dua kali lipat pada 2020 dan tiga kali lipat pada 2050). Gliserol merupakan bahan intermediate yang banyak digunakan industri, baik industri makanan ataupun industri farmasi.Gliserol pun merupakan limbah yang masih bernilai emas. Dimana hasil samping ini yang merupakan limbah dapat diolah kembali dan memiliki nilai jual dan mengurangi limbah industri yang ada di Indonesia dengan memanfaatkan program recycle. Berdasarkan hal tersebut maka mendirikan pabrik glycerol di Indonesia yang sangat diperlukan guna mengurangi jumlah limbah dan memiliki peluang ekspor yang besar. Pabrik Glycerol ini direncanakan didirikan di daerah Kawasan Industri Medan-Sumatera Utara dan menghasilkan produk sebanyak 60.000 Ton/Tahun,Pabrik ini direncanakan sudah mulai beroperasi pada tahun 2025, berdasarkan hasil analisa kelayakan Pabrik glycerol, jangka waktu pengembalian modal adalah 3,4 tahu

A Prevalence and Antimicrobial Resistance Pattern of Bacterial Strains Isolated from Patients with Urinary Tract Infection in Al-Wahda Hospital in Derna City/Libya

Background:       Urinary tract infection (UTI) is One of the most prevalent infectious diseases in human, where the study aimed to identify the most uropathogen that caused UTIs ,and its the antimicrobial resistance pattern. Methods:       the samples were collected from January and December 2021 using a standard data collection form, where  the patient outcome records were mined for information on the patients' gender, age, isolated organisms, and susceptibility test results, then statistical analysis was done. Results:   266 from 463 samples  were identified as S. aureus 14.3% , in addition, the antibacterial resistance rats showed that the highest resistance was against ampicillin/Sulbactam, ceftazidine, and meropenem 79%, while, the lowest was against ciprofloxacin 40%. Conclusion:     The study showed that S. aureus is the primary cause of UTIs in Derna city, as a result of consuming antibiotics randomly, which resulted in an increase in spread and resistance of S. aureus

Polarized P-glycoprotein expression by the immortalised human brain endothelial cell line, hCMEC/D3, restricts apical-to-basolateral permeability to rhodamine 123

P-glycoprotein (P-gp) expression at the blood-brain barrier prevents unwanted blood-borne toxins and signalling molecules from entering the brain. Primary and immortalised human brain endothelial cells (BECs) represent two suitable options for studying P-gp function in vitro. The limited supply of primary human BECs and their instability over passage number makes this choice unattractive for medium/high throughput studies. The aim of this study was to further characterise the expression of P-gp by an immortalised human BEC line, hCMEC/D3, in order to evaluate their use as an in vitro human blood-brain barrier model. P-gp expression was stable over a high passage number (up to passage 38) and was polarised on the apical plasma membrane, consistent with human BECs in vivo. In addition, hCMEC/D3 cell P-gp expression was comparable, albeit slightly lower to that observed in primary isolated human BECs although P-gp function was similar in both cell lines. The P-gp inhibitors tariquidar and vinblastine prevented the efflux of rhodamine 123 (rh123) from hCMEC/D3 cells, indicative of functional P-gp expression. hCMEC/D3 cells also displayed polarised P-gp transport, since both tariquidar and vinblasine selectively increased the apical-to-basolateral permeability of hCMEC/D3 cells to rh123. The results presented here demonstrate that hCMEC/D3 cells are a suitable model to investigate substrate specificity of P-gp in BECs of human origin

The critical role of ERK in death resistance and invasiveness of hypoxia-selected glioblastoma cells

<p>Abstract</p> <p>Background</p> <p>The rapid growth of tumor parenchyma leads to chronic hypoxia that can result in the selection of cancer cells with a more aggressive behavior and death-resistant potential to survive and proliferate. Thus, identifying the key molecules and molecular mechanisms responsible for the phenotypic changes associated with chronic hypoxia has valuable implications for the development of a therapeutic modality. The aim of this study was to identify the molecular basis of the phenotypic changes triggered by chronic repeated hypoxia.</p> <p>Methods</p> <p>Hypoxia-resistant T98G (HRT98G) cells were selected by repeated exposure to hypoxia and reoxygenation. Cell death rate was determined by the trypan blue exclusion method and protein expression levels were examined by western blot analysis. The invasive phenotype of the tumor cells was determined by the Matrigel invasion assay. Immunohistochemistry was performed to analyze the expression of proteins in the brain tumor samples. The Student T-test and Pearson Chi-Square test was used for statistical analyses.</p> <p>Results</p> <p>We demonstrate that chronic repeated hypoxic exposures cause T98G cells to survive low oxygen tension. As compared with parent cells, hypoxia-selected T98G cells not only express higher levels of anti-apoptotic proteins such as Bcl-2, Bcl-X_L, and phosphorylated ERK, but they also have a more invasive potential in Matrigel invasion chambers. Activation or suppression of ERK pathways with a specific activator or inhibitor, respectively, indicates that ERK is a key molecule responsible for death resistance under hypoxic conditions and a more invasive phenotype. Finally, we show that the activation of ERK is more prominent in malignant glioblastomas exposed to hypoxia than in low grade astrocytic glial tumors.</p> <p>Conclusion</p> <p>Our study suggests that activation of ERK plays a pivotal role in death resistance under chronic hypoxia and phenotypic changes related to the invasive phenotype of HRT98G cells compared to parent cells.</p

Residues contributing to drug transport by ABCG2 are localised to multiple drug-binding pockets

Multidrug binding and transport by the ATP binding cassette transporter ABCG2 is a factor in the clinical resistance to chemotherapy in leukaemia, and a contributory factor to the pharmacokinetic profiles of many other prescribed drugs. Despite its importance, the structural basis of multidrug transport, i.e. the ability to transport multiple distinct chemicals, has remained elusive. Previous research has shown that at least two residues positioned towards the cytoplasmic end of transmembrane helix 3 (TM3) of the transporter play a role in drug transport. We hypothesised that other residues, either in the longitudinal span of TM3, or a perpendicular slice through the intracellular end of other TM helices would also contribute to drug binding and transport by ABCG2. Single point mutant isoforms of ABCG2 were made at approximately 30 positions and were analysed for effects on protein expression, localisation (western blotting, confocal microscopy) and function (flow cytometry) in a mammalian stable cell line expression system. Our data were interpreted in terms of recent structural data on the ABCG protein subfamily and enabled us to propose a surface binding site for the drug mitoxantrone as well as a second, buried site for the same drug. Further mutational analysis of residues that spatially separate these two sites prompt us to suggest a molecular and structural pathway for mitoxantrone binding by ABCG2

Comparative analysis of novel and conventional Hsp90 inhibitors on HIF activity and angiogenic potential in clear cell renal cell carcinoma: implications for clinical evaluation

<p>Abstract</p> <p>Background</p> <p>Perturbing Hsp90 chaperone function targets hypoxia inducible factor (HIF) function in a von Hippel-Lindau (VHL) independent manner, and represents an approach to combat the contribution of HIF to cell renal carcinoma (CCRCC) progression. However, clinical trials with the prototypic Hsp90 inhibitor 17-AAG have been unsuccessful in halting the progression of advanced CCRCC.</p> <p>Methods</p> <p>Here we evaluated a novel next generation small molecule Hsp90 inhibitor, EC154, against HIF isoforms and HIF-driven molecular and functional endpoints. The effects of EC154 were compared to those of the prototypic Hsp90 inhibitor 17-AAG and the histone deacetylase (HDAC) inhibitor LBH589.</p> <p>Results</p> <p>The findings indicate that EC154 is a potent inhibitor of HIF, effective at doses 10-fold lower than 17-AAG. While EC154, 17-AAG and the histone deacetylase (HDAC) inhibitor LBH589 impaired HIF transcriptional activity, CCRCC cell motility, and angiogenesis; these effects did not correlate with their ability to diminish HIF protein expression. Further, our results illustrate the complexity of HIF targeting, in that although these agents suppressed HIF transcripts with differential dynamics, these effects were not predictive of drug efficacy in other relevant assays.</p> <p>Conclusions</p> <p>We provide evidence for EC154 targeting of HIF in CCRCC and for LBH589 acting as a suppressor of both HIF-1 and HIF-2 activity. We also demonstrate that 17-AAG and EC154, but not LBH589, can restore endothelial barrier function, highlighting a potentially new clinical application for Hsp90 inhibitors. Finally, given the discordance between HIF activity and protein expression, we conclude that HIF expression is not a reliable surrogate for HIF activity. Taken together, our findings emphasize the need to incorporate an integrated approach in evaluating Hsp90 inhibitors within the context of HIF suppression.</p

Multidrug transporters : a study of drug interactions using a photoactive analogue of rhodamine 123

The emergence of multidrug resistance is a serious medical problem that has significantly affected the treatment of tumor cells and infectious diseases. This multidrug resistance phenotype is mediated by the action of a large family of membrane proteins that act as active transporters or energy driven efflux pumps in both of prokaryotic and eukaryotic cells. Most eukaryotic multidrug efflux pumps belong to the ATP binding cassette (ABC) family of transport proteins that include P-glycoprotein (P-gp1), Multidrug Resistance Associated Protein (MRP1), and Breast Cancer Resistance Protein (BCRP). In prokaryotic cells, Lactococcus lactis LmrA, a homolog of P-gp1, mediates drug resistance to antibiotics and cytotoxic drugs. The transport function of these proteins is facilitated by the hydrolysis of ATP. However, the mechanism by which these proteins bind to, and are able to transport structurally dissimilar drugs across the cell membrane remains poorly understood. In this thesis we have attempted to characterize the interactions of various ABC transporters (MRP1, BCRP, and LmrA) with structurally diverse drugs, using a well characterized photoreactive drug analogue of Rhodamine 123, [125I] iodoaryl azido-rhodamine 123 (IAARh123). In the case of MRP1 interaction with Rhodamine 123, it was of interest to determine the nature of MRP1 drug interactions. In that study, our results show that CHAPS (1-[(3-cholamidopropyl) dimethylamino]-1-propansulfate) and Brij35 inhibited the photolabeling of MRP1 with IAARh123, and this interaction occurred outside the lipid bilayer. These results were unexpected in light of previous results with another ABC transporter which also binds to Rhodamine 123. Consequently, we show that non-toxic concentrations of CHAPS and Brij35 potentiate the toxicity of two MRP1 substrates, vincristine and etoposide (VP16). In the second chapter, we have used IAARh123 to demonstrate for the first time that the BCRP mediates drug res