EARTH QUAKE PROGNOSTICATION USING DATA MINING AND CURVE FITTING TECHNIQUES

The title “EARTHQUAKE PROGNOSTICATION” is a Global Earthquake prediction, that is used to predict that an earthquake of a specific magnitude will occur in a particular place at a particular time, we however cannot tell the exact time and date the earthquake is going to occur but we can well predict that an earthquake will affect a given location over a certain number of years. The “Gutenberg Richter power-law distribution of earthquake sizes” implies that the largest events are surrounded by a large number of small events, with this statement we collected the data sets of all the EARTHQUAKES of magnitude ranging from small to big since 1900 to 2010 all over the world. After collecting this data we performed clustering techniques to the datasets available with latitude, longitude and time as parameters, which helped to find similarities between them and discovered patterns using non-linear regression functions that helped to forecast earthquakes. This prediction is based on both the historical seismic catalogue and the structural zoning

Investigating transportation research based on social media analysis: A systematic mapping review

Social media is a pool of users’ thoughts, opinions, surrounding environment, situation and others. This pool can be used as a real-time and feedback data source for many domains such as transportation. It can be used to get instant feedback from commuters; their opinions toward the transportation network and their complaints, in addition to the traffic situation, road conditions, events detection and many others. The problem is in how to utilize social media data to achieve one or more of these targets. A systematic review was conducted in the field of transportation-related research based on social media analysis (TRRSMA) from the years between 2008 and 2018; 74 papers were identified from an initial set of 703 papers extracted from 4 digital libraries. This review will structure the field and give an overview based on the following grounds: activity, keywords, approaches, social media data and platforms and focus of the researches. It will show the trend in the research subjects by countries, in addition to the activity trends, platforms usage trend and others. Further analysis of the most employed approach (Lexicons) and data (text) will be also shown. Finally, challenges and future works are drawn and proposed

High ALDH Activity Identifies Chemotherapy-Resistant Ewing's Sarcoma Stem Cells That Retain Sensitivity to EWS-FLI1 Inhibition

Cancer stem cells are a chemotherapy-resistant population capable of self-renewal and of regenerating the bulk tumor, thereby causing relapse and patient death. Ewing's sarcoma, the second most common form of bone tumor in adolescents and young adults, follows a clinical pattern consistent with the Cancer Stem Cell model - remission is easily achieved, even for patients with metastatic disease, but relapse remains frequent and is usually fatal.We have isolated a subpopulation of Ewing's sarcoma cells, from both human cell lines and human xenografts grown in immune deficient mice, which express high aldehyde dehydrogenase (ALDH(high)) activity and are enriched for clonogenicity, sphere-formation, and tumor initiation. The ALDH(high) cells are resistant to chemotherapy in vitro, but this can be overcome by the ATP binding cassette transport protein inhibitor, verapamil. Importantly, these cells are not resistant to YK-4-279, a small molecule inhibitor of EWS-FLI1 that is selectively toxic to Ewing's sarcoma cells both in vitro and in vivo.Ewing's sarcoma contains an ALDH(high) stem-like population of chemotherapy-resistant cells that retain sensitivity to EWS-FLI1 inhibition. Inhibiting the EWS-FLI1 oncoprotein may prove to be an effective means of improving patient outcomes by targeting Ewing's sarcoma stem cells that survive standard chemotherapy

Evaluation of bioactive glass and demineralized freeze dried bone allograft in the treatment of periodontal intraosseous defects: A comparative clinico-radiographic study

Aim: The purpose of this study was to evaluate the efficacy of demineralized freeze dried bone allograft (DFDBA) and bioactive glass by clinically and radiographically in periodontal intrabony defects for a period of 12 months. Materials and Methods: Ten systemically healthy patients diagnosed with chronic periodontitis, with radiographic evidence of at least a pair of contralateral vertical osseous defects were included in this study. Defect on one-side is treated with DFDBA and the other side with bioactive glass. Clinical and radiographic measurements were made at baseline 6 month and 12 month after the surgery. Results: Compared to baseline, the 12 month results indicated that both treatment modalities resulted in significant changes in all clinical parameters (gingival index, probing depth, clinical attachment level (CAL) and radiographic parameters (bone fill); P < 0.001FNx01). However, sites treated with DFDBA exhibited statistically significantly more changes compared to the bioactive glass in probing depth reduction (2.5 ± 0.1 mm vs. 1.8 ± 0.1 mm) CAL gain 2.4 ± 0.1 mm versus 1.7 ± 0.2 mm; ( P < 0.001FNx01). At 12 months, sites treated with bioactive glass exhibited 56.99% bone fill and 64.76% bone fill for DFDBA sites, which is statistically significant ( P < 0.05FNx01). Conclusion: After 12 months, there was a significant difference between the two materials with sites grafted with DFDBA showing better reduction in probing pocket depth, gain in CAL and a greater percentage of bone fill when compared to that of bioactive glass

Chlorzoxazone reduced the paracetamol-induced toxicity via competitive inhibition of CYP2E1-mediated metabolism

Abstract Background Drug metabolism is crucial to attaining the therapeutic index of any drug. The metabolism and elimination of the drugs are governed mainly by P-glycoprotein (P-gp) and Cytochrome P450 (CYP). Paracetamol is mostly used as analgesic and antipyretic agent. The metabolism of paracetamol is primarily via Glucuronidation and sulphation at therapeutic doses. About 5–10% of paracetamol is metabolized via CYP mediated pathway. Cytochrome P450 2E1 (CYP2E1) is primarily responsible for forming a toxic metabolite of paracetamol called N-acetyl-p-benzoquinoneimine (NAPQI). Even at therapeutic doses, long-term usage of paracetamol leads to the hepatic and nephrotoxicity because of NAPQI. Several in-vitro and in-vivo studies conducted by different research groups and reported that chlorzoxazone is a substrate and inhibitor of CYP2E1. However, the effect of chlorzoxazone on the paracetamol (CYP2E1 substrate) metabolism via the CYP2E1 has not yet been reported. This study investigated the effect of chlorzoxazone on the CYP2E1-mediated metabolism of Paracetamol and NAPQI formation in Wistar rats. Results For 15 days, animals were orally administered with Paracetamol (300 mg/kg) with and without Silymarin (100 mg/kg) (standard CYP2E1 inhibitor) and Chlorzoxazone (50 and 100 mg/kg). Analysis was performed using RP-HPLC on the 15th day to determine paracetamol and NAPQI concentration in the plasma. Paracetamol combination with chlorzoxazone (50 and 100 mg/kg) showed a dose-dependent increase in the AUC0–∞ and the peak plasma concentration (Cmax) of Paracetamol and a dose-dependent decrease of AUC0–∞ and Cmax of NAPQI compared to paracetamol control (p < 0.001). Chlorzoxazone significantly decreased the elevated liver and renal markers compared to paracetamol control. Simultaneously, Hepatic and nephrotic tissue studies showed that compared to the paracetamol control group, the combination of chlorzoxazone significantly ameliorated paracetamol-induced hepatotoxicity and nephrotoxicity. Conclusion Finally, this study revealed that paracetamol in combination with chlorzoxazone led to a significant decrease in the plasma levels of NAPQI and enhanced absorption of paracetamol in rats via the inhibition of CYP2E1- mediated metabolism. In addition, chlorzoxazone significantly ameliorated paracetamol-induced hepatotoxicity and nephrotoxicity

Critical interactions between TGF-β signaling/ELF, and E-cadherin/β-catenin mediated tumor suppression

Inactivation of the transforming growth factor-β (TGF-β) pathway occurs often in malignancies of the gastrointestinal (GI) system. However, only a fraction of sporadic GI tumors exhibit inactivating mutations in early stages of cancer formation, suggesting that other mechanisms play a critical role in the inactivation of this pathway. Here, we show a wide range of GI tumors, including those of the stomach, liver and colon in elf+/- and elf+/-/Smad4+/- mutant mice. We found that embryonic liver fodrin (ELF), a β-Spectrin originally identified in endodermal stem/ progenitor cells committed to foregut lineage, possesses potent antioncogenic activity and is frequently inactivated in GI cancers. Specifically, E-cadherin accumulation at cell-cell contacts and E-cadherin-β-catenin-dependent epithelial cell-cell adhesion is disrupted in elf+/- Smad4 +/- mutant gastric epithelial cells, and could be rescued by ectopic expression of full-length elf, but not Smad3 or Smad4. Subcellular fractionation revealed that E-cadherin is expressed mainly at the cell membrane after TGF-β stimulation. In contrast, elf+/- /Smad4+/- mutant tissues showed abnormal distribution of E-cadherin that could be rescued by overexpression of ELF but not Smad3 or Smad4. Our results identify a group of common lethal malignancies in which inactivation of TGF-β signaling, which is essential for tumor suppression, is disrupted by inactivation of the ELF adaptor protein. © 2006 Nature Publishing Group All rights reserved

RING finger-dependent ubiquitination by PRAJA is dependent on TGF-β and potentially defines the functional status of the tumor suppressor ELF

In gastrointestinal cells, biological signals for transforming growth factor-beta (TGF-β) are transduced through transmembrane serine/threonine kinase receptors that signal to Smad proteins. Smad4, a tumor suppressor, is often mutated in human gastrointestinal cancers. The mechanism of Smad4 inactivation, however, remains uncertain and could be through E3-mediated ubiquitination of Smad4/adaptor protein complexes. Disruption of ELF (embryonic liver fodrin), a Smad4 adaptor protein, modulates TGF-β signaling. We have found that PRAJA, a RING-H2 protein, interacts with ELF in a TGF-β-dependent manner, with a fivefold increase of PRAJA expression and a subsequent decrease in ELF and Smad4 expression, in gastrointestinal cancer cell lines (P \u3c 0.05). Strikingly, PRAJA manifests substantial E3-dependent ubiquitination of ELF and Smad3, but not Smad4. Δ-PRAJA, which has a deleted RING finger domain at the C terminus, abolishes ubiquitination of ELF. A stable cell line that overexpresses PRAJA exhibits low levels of ELF in comparison to a Δ-PRAJA stable cell line, where ELF expression is high compared to normal controls. The alteration of ELF and/or Smad4 expression and/or function in the TGF-β signaling pathway may be induced by enhancement of ELF degradation, which is mediated by a high-level expression of PRAJA in gastrointestinal cancers. In hepatocytes, half-life (t1/2) and rate constant for degradation (kD) of ELF is 1.91 h and 21.72 min-1 when coupled with ectopic expression of PRAJA in cells stimulated by TGF-β, compared to PRAJA-transfected unstimulated cells (t1/2 = 4.33 h and kD = 9.6 min-1). These studies reveal a mechanism for tumorigenesis whereby defects in adaptor proteins for Smads, such as ELF, can undergo degradation by PRAJA, through the ubiquitin-mediated pathway. © 2006 Nature Publishing Group All rights reserved