Estimation of permeability of shaly sand from Induced Polarization relaxation time spectra

The Singular Value Decomposition (SVD) method is used to invert induced polarization (IP) decay curve for the IP relaxation time spectrum. A nonnegative restriction is added during inversion for meaningful solution of the amplitude of the relaxation spectrum. The analysis of the experiment design, by comparing results in different range, shows that the appropriate number of relaxation arrangement points in data inversion lies with 32 to 64. The attenuation of noise in this range is better and resolution is good. IP relaxation spectrum indicates the pore size distribution that in turn indicates the permeability of shaly sand reservoir. Combining the average relaxation time (geometric average time) with the porosity can improve the accuracy of estimation of the permeability in comparison to that obtained using total porosity from core measurements

Determination of TL Kinetic parameters of a phosphor

Present paper reports the methods of evaluating the kinetic parameters like trap depth, frequency factor etc. by using the Glow Curve of a phosphor. Peak shape method is found to be suitable amongst all reported methods. This method provides the nearest possible values of all studied kinetic parameters which are discussed in details. MS -Excel sheet is prepared for calculation

Penerapan Model Pembelajaran Numbered Heads Together (Nht) Dalam Upaya Untuk Meningkatkan Keaktifan Dan Hasil Belajar Mahasiswa Prodi Pendidikan IPA Ust YOGYAKARTA Tahun Akademik

: This research has been done to know how NHT as a model of study could increase activity and achievement the students of natural science education department on 2013/2014 of academic year. This was a class action research. This research consisted of two cycles. Each cycles was consist of planning, doing, observing and reflecting. The instruments of this research were lecture-observing papers, students-observing papers, evaluating papers and statements papers. The result showed increasing of students\u27 activity. At first discussion on first cycles, there were 52.5% active students, at last discussion on second cycles there were 90.8% active students. The average of students\u27 achievement has increased 15.3 points, i.e. from 63.2 to 78.5

Minnelide effectively eliminates CD133+ side population in pancreatic cancer

BACKGROUND: Pancreatic Ductal Adenocarcinoma (PDAC) is a devastating disease hallmarked by limited patient survival. Resistance to chemotherapy, a major cause of treatment failure in PDAC patients, is often attributed to Cancer Stem Cells (CSCs). Pancreatic CSCs are a small subset of quiescent cells within a tumor represented by surface markers like CD133. These cells are responsible not only for tumor recurrence, but also poor prognosis based on their “stem-like” characteristics. At present, conventional therapy is directed towards rapidly dividing PDAC cells and thus fails to target the CSC population. METHODS: MIA PaCa-2, S2-013 and AsPC-1 were treated with 12.5 nM triptolide (12 T cells) for 7 days. The surviving cells were recovered briefly in drug-free growth media and then transferred to Cancer Stem cell Media (CSM). As a control, untreated cells were also transferred to CSM media (CSM). The 12 T and CSM cells were tested for stemness properties using RNA and protein markers. Low numbers of CSM and 12 T cells were implanted subcutaneously in athymic nude mice to study their tumorigenic potential. 12 T and CSM cells were sorted for CD133 expression and assayed for their colony forming ability and sphere forming ability. Invasiveness of 12 T cells, CSM and MIA PaCa-2 were compared using Boyden chamber assays. RESULTS: Treated 12 T cells displayed increased expression of the surface marker CD133 and the drug transporter ABCG2 compared to untreated cells (CSM cells). Both 12 T and CSM cells formed subcutaneous tumors in mice confirming their tumor-initiating properties. When tested for invasion, 12 T cells had increased invasiveness compared to CSM cells. CD133(+) cells in both CSM and 12 T showed greater colony and sphere forming ability compared to CD133(−) cells from each group. Consistent with these data, when injected subcutaneously in mice, CD133(−) cells from CSM or 12 T did not form any tumors whereas CD133(+) cells from both groups showed tumor formation at a very low cell number. Despite pre-exposure to triptolide in 12 T CD133(+) cells, treatment of tumors formed by these cells with Minnelide, a triptolide pro-drug, showed significant tumor regression. CONCLUSION: Our results indicated that triptolide enhanced and enriched the “stemness” in the PDAC cell lines at a low dose of 12.5 nM, but also resulted in the regression of tumors derived from these cells. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s12943-015-0470-6) contains supplementary material, which is available to authorized users

Unconventional T Cells in the Pancreatic Tumor Microenvironment: Thinking Outside the Box

Unlike conventional MHC-reactive T cells, unconventional T cells have emerged as an abundant component of the human immune system because of their role in tumor immunology. In this issue of , Hundeyin and colleagues have identified a population of unconventional T cells in pancreatic tumors that can reprogram the immune evasive components of the tumor to promote immunogenicity and thus are critical for the development of novel cell-based therapy in pancreatic cancer.

Pathophysiology of Experimental Pancreatitis

Acute pancreatitis is a significant cause of morbidity, mortality, and hospitalization worldwide. The incidence of acute pancreatitis is on the rise. Owing to an incomplete understanding of the pathophysiology of acute pancreatitis, no targeted therapy is available for this disease. Hence, currently, the treatment revolves largely around supportive measures. Our limited understanding of the pathophysiology of acute pancreatitis is based on studies using experimental animal models and pancreatic cell‐based in vitro experiments. Several experimental models of acute pancreatitis have been developed in different species. However, lately most of the studies have been performed in murine models, for multiple reasons, the most important of which is the availability of strains of mice with different gene deletions. Although studies on these murine models have provided useful information on the initiating events of acute pancreatitis, these models do not mimic the progression of human pancreatitis. Studies suggest that acute pancreatitis begins in the pancreatic acinar cells. Premature activation of zymogens, inhibition of secretion, and activation of inflammatory pathways are observed in the pancreatic acinar cells within minutes of pathologic provocation. Other events such as increased endoplasmic reticulum stress, loss of mitochondrial potential, and autophagy dysfunction are also observed in pancreatic acinar cells, early on during acute pancreatitis. Eventually, these events lead to pancreatic acinar cell death and spread of inflammation to other organs. Uncontrolled systemic inflammation can lead to multiorgan failure. Studies in experimental models suggest that intra‐acinar trypsin activation, which has been considered central to the pathogenesis of acute pancreatitis for decades, results from colocalization of zymogens and lysosomes. Perturbed calcium signaling is believed to be involved in initiating pathologic changes. Although inhibition of trypsin provides significant protection from acinar cell death, recent studies suggest that events other than trypsin activation play a central role in pathogenesis of acute pancreatitis. Emerging evidence suggests that cathepsin B, in addition to playing an important role in trypsin activation, can play a role in activation of cell death pathways. Furthermore, data suggest that trypsin‐independent inflammation plays an important role in local and systemic injury. The ability to modulate the pathophysiology and progression of inflammation might improve the outcomes for patients