A comparative study on joints with and without gouge fill

Rock is a discontinuous medium and the discontinuity may be in the form of joints or faults. Hence, the strength of rock mass generally depends on the type of discontinuity present in the rock mass. The strength of jointed rock mass generally depends on the joint spacing, inclination parameter and the roughness parameter. This joint roughness is a vital parameter which generally governs the strength of the rock mass. The roughness is usually computed with the help of direct shear test (r = tanφj). The deformation characteristics of rock mass are another parameter which is usually taken care in addition to the strength of rock mass and can be computed with the help of uniaxial compressive strength test. As collection of jointed rock mass and field testing of rock mass is tedious as well as difficult, hence jointed rock mass models are generally made in the laboratory itself. In the present study, plaster of Paris was used for modeling laboratory specimens as it is locally available and at the same time casting of jointed rock mass specimen can be done easily. The joints in rock mass specimen were made at various angles of orientation (β0) which is varying from 00-900. These models were possessing joints with and without gouge fill. Clay was used as gouge material. Here, an attempt was made to compare the results of strength and deformation characteristics of jointed rock mass with and without gouge fill by using model material plaster of Paris. From the experiments it is found that for single jointed rock mass specimen without gouge fill at β= 300 strength was found to be 0.22 MPa which is minimum and at β= 900 strength was found to be 7.34 MPa which is maximum. For single jointed rock mass specimen with gouge , further trend of decrease in strength was found and this is due to decrease in roughness parameter.Here , also at β= 300 strength was found to be 0.11 MPa which is minimum and at β= 900 strength was found to be 6.79 MPa which is maximum. An empirical relationship σcr= e-0.008 x Jf is applicable for joints with gouge

Long haul fleet assignment : models, methods and applications

Thesis (M.S.)--Massachusetts Institute of Technology, Dept. of Civil and Environmental Engineering, 1995.Includes bibliographical references (leaves 60-63).by Rajiv Chellappa Lochan.M.S

The role of gene-environment interaction in the development of pancreatic cancer

M. D. ThesisThe aetiology for sporadic pancreatic adenocarcinoma is poorly characterized. Familial/hereditary causes account for about 10% cases and tobacco smoking is a well- established risk, however it is only responsible for about a third of cases. DNA repair mechanisms restore the genome damage caused by carcinogens including those derived from tobacco smoking. Increasing attention is being focused on single nucleotide polymorphisms, which exist amongst various physiological pathways including DNA repair mechanisms, and account for inter-individual variation in risk for cancer. This study is an effort to investigate the impact of family history of malignancy, tobacco smoking and selected genetic polymorphisms involved in DNA repair on pancreatic ductal adenocarcinoma development. A hospital-based case-control study of pancreatic adenocarcinoma cases and hospital- based controls was undertaken at the Freeman Hospital between 2005-2006. Pancreatic cancer cases were ascertained based on histology, cytology or a combination of clinical findings, tumour marker levels and progressive radiological changes. All participants were interviewed to establish a detailed clinical, family history and tobacco smoking (MONICA questionnaire) A sample of peripheral blood was obtained for genotyping of specific Base Excision repair genotypes – hOGG1, XRCC194, XRCC280, XRCC399 and APE148. Statistical analysis was performed on SPSS v16. Odds ratios (95% CI) were calculated for individual variables. Tobacco smoking was confirmed to be a risk factor for pancreatic cancer [OR (95% CI) on univariate: ever smoker [(present and past smokers) OR 3.01 (95% CI 1.73 to 5.24)] and multivariate analysis: present smokers [OR = 8.531 (3.198 to 22.759) and past smokers OR = 5.862 (2.223 to 15.460)]. Importantly a significantly decreased cumulative tobacco exposure was seen amongst pancreatic cancer cases with a family history of cancer [mean (SD): 30.00 (24.77) pack-years] as compared those who did not have such a history [44.69 (28.47) pack-years p=0/023]. No specific overall increased risk was associated with the individual base excision repair genotypes on both uni- variate and multi-variate analysis. Tobacco smoking is a risk factor and appears to play a more important role (for pancreatic cancer development) in the presence of a family history of cancer. Small risks associated with SNP’s are difficult to tease out from small studies like the current one. Larger multi institutional studies (as have been achieved for e.g. Lung Cancer) are required to confirm this latter finding and perform pooled analysis of data for specific sequence variants within a target biochemical pathway to uncover the risks associated with these genes

Sikap Keuangan Pada Perusahaan Keluarga: Peran Moderasi Komitmen Keluarga

This study aims to examine the moderating role of family commitment to the influence of the financial knowledge, positive experience with debt suppliers, and   economic  goal  orientation  to  owner- managers’ attitudes toward debt financing in family firms. This study was conducted through a questionnaire survey of 66 owners of family firms, operated in Special Region of Yogyakarta. This study used moderated regression analysis. The results of this study found several important things as follows.  First, the high family commitment toward business strengthened the positive effect of the positive experience with debt suppliers to owner-managers’ attitudes toward debt financing in family firms. Second, the result of the interaction coefficient of economic goal  orientation  and family Commitment was negative and not significant. Third, the result of the interaction coefficient of financial knowledge and family commitment toward business was positive and not significant. This result was opposite to the direction of prediction of the hypothesi

The Role of Tobacco-Derived Carcinogens in Pancreas Cancer

The extremely poor outcome from pancreas cancer is well known. However, its aetiology less well appreciated, and the molecular mechanisms underlying this are poorly understood. Tobacco usage is one of the strongest risk factors for this disease, and this is a completely avoidable hazard. In addition, there are well described hereditary diseases which predispose, and familial pancreas cancer. We have sought here to summarise the role of tobacco-derived carcinogens and the mode of their tumorigenic action on the pancreas. There is compelling evidence from animal and human studies (laboratory including cell line studies and epidemiologic) that tobacco derived carcinogens cause pancreas cancer. However, the manner in which they do so is not entirely apparent. There is also compelling evidence that synergism with genetic and other life-style factors—like diet obesity—results in a multifactorial causation of the disease. Ascertaining the role of tobacco carcinogens in the development of this cancer and their interaction with other risk factors will enable novel therapeutic and preventative strategies to improve outcome from this appalling malignancy

Minimally invasive and endoscopic versus open necrosectomy for necrotising pancreatitis: a pooled analysis of individual data for 1980 patients

Minimally invasive surgical necrosectomy and endoscopic necrosectomy, compared with open necrosectomy, might improve outcomes in necrotising pancreatitis, especially in critically ill patients. Evidence from large comparative studies is lacking. We combined original and newly collected data from 15 published and unpublished patient cohorts (51 hospitals; 8 countries) on pancreatic necrosectomy for necrotising pancreatitis. Death rates were compared in patients undergoing open necrosectomy versus minimally invasive surgical or endoscopic necrosectomy. To adjust for confounding and to study effect modification by clinical severity, we performed two types of analyses: logistic multivariable regression and propensity score matching with stratification according to predicted risk of death at baseline (low: <5%; intermediate: ≥5% to <15%; high: ≥15% to  <35%; and very high: ≥35%). Among 1980 patients with necrotising pancreatitis, 1167 underwent open necrosectomy and 813 underwent minimally invasive surgical (n=467) or endoscopic (n=346) necrosectomy. There was a lower risk of death for minimally invasive surgical necrosectomy (OR, 0.53; 95% CI 0.34 to 0.84; p=0.006) and endoscopic necrosectomy (OR, 0.20; 95% CI 0.06 to 0.63; p=0.006). After propensity score matching with risk stratification, minimally invasive surgical necrosectomy remained associated with a lower risk of death than open necrosectomy in the very high-risk group (42/111 vs 59/111; risk ratio, 0.70; 95% CI 0.52 to 0.95; p=0.02). Endoscopic necrosectomy was associated with a lower risk of death than open necrosectomy in the high-risk group (3/40 vs 12/40; risk ratio, 0.27; 95% CI 0.08 to 0.88; p=0.03) and in the very high-risk group (12/57 vs 28/57; risk ratio, 0.43; 95% CI 0.24 to 0.77; p=0.005). In high-risk patients with necrotising pancreatitis, minimally invasive surgical and endoscopic necrosectomy are associated with reduced death rates compared with open necrosectom

Hepatic arterial communicating arcades—Case series and review of literature

This case series describes the hepatic arterial communicating arcades and their importance in the endovascular management of hepatic artery pseudoaneurysm, pediatric post liver transplant lobar arterial occlusion, and lobar arterial stenosis due to gall bladder carcinoma. We describe new types of arterial communicating arcades which have not been described earlier

Cyclooxygenase-2 Polymorphisms and Pancreatic Cancer Susceptibility

Objectives: DNA sequence variants in the cyclooxygenase-2 (COX-2) gene may lead to altered COX-2 production and/or activity, resulting in interindividual differences in susceptibility to pancreatic cancer. To test this hypothesis, we investigated the relationship between polymorphisms in the COX-2 gene and the risk of pancreatic cancer in a European population