A Survey On Various Methods To Detect Forgery And Computer Crime In Transaction Database

Abstract: A computer forensic method can be used for detecting the different types of forgeries and computer crime. Forgeries and computer crime are the most major concern of the digital world. Lots of techniques and methods have been used to find a proper solution to these problems. Nowadays, digital forensics are an important topic for research articles. In this paper a general survey has been carried out for different methods used in computer forensics to track the evidences which can be useful for detecting the computer crime and forgery. Forensic tools can be used for making any changes to data or tampering of data. Different rules sets or methods are defined to detect the various errors regarding the changes and the tampering of the data in different windows file system. Digital evidence can also be used to detect forgery or computer crime

DETERMINATION OF TRAZODONE IN HUMAN PLASMA BY REVERSED-PHASE LIQUID CHROMATOGRAPHY-MASS SPECTROMETRY WITH ELECTROSPRAY IONISATION

Objective: The development and validation of LC-MS/MS method for quantification of Trazodone (a serotonin antagonist and reuptake inhibitor (SARI), which is a second generation antidepressant compound belonging to the class of phenyl piperazine) in human plasma is described. Methods: The method involves protein precipitation (extraction) using Trazodone d6 as an internal standard (IS). Chromatographic separation is achieved on Zorbax eclipse XDB C8 150×4.6 mm, 5 μm column with a mobile phase consisting of 2 mM ammonium formate (pH 3.0) and methanol (30:70 v/v) at a flow rate of 1.0 mL / min and the total run time was 2.5 minute. Detection was carried out by AB Sciex API 3200 tandem mass spectrometer using positive electro-spray ionization mode by multiple reactions monitoring method at m/z 372.00→176.10 and 378.20→182.10 for Trazodone and Trazodone d6 (ISTD) respectively with dwell times of 300 msecs for each of the transitions. Results: The standard curve was linear from 5.203 ng / mL to 3025.166 ng / mL with goodness of fit (r2) greater than 0.990 observed during the method validation batches. This assay allows quantification of Trazodone at a concentration as low as 5 ng / mL in human plasma. The observed mean recovery was 88% for the drug. Conclusions: The method described here is found to be simple, cost effective and suitable for the use in bioequivalence and bioavailability studies

Patterns of injuries in homicidal cases

Death, an inevitable part of life, prompts an exploration into the manner and method by which it occurs. This study aims to analyze the patterns of injuries in homicidal cases brought for postmortem examination. In 2019, a total of 28,918 murder cases were registered in India, showing a slight decrease of 0.3% in comparison to 2018 (29,017 cases). The study aims to understand the different injury patterns in homicide. At the Department of Forensic Medicine, Gandhi Medical College, Bhopal, India, a total of 62 males and 12 females, along with one unknown gender person, where submitted to postmortem examination. The majority of cases belonged to urban, with leading causes of death being shock and hemorrhage followed by craniocerebral damage. This study concludes that sharp edges and deep cuts were the primary injury patterns in homicide cases. Morte, uma inevitável parte da vida, incita uma exploração a respeito da maneira e do método de sua ocorrência. Este estudo tem por objetivo analisar os padrões de lesões em casos de homicídios verificados em exames post-mortem. Em 2019, registrou-se um total de 28.918 casos de assassinato na India, mostrando um leve decréscimo de 0,3% em comparação com 2018 (29.017 casos). Este estudo objetiva entender os diferentes padrões de lesão em homicídios. No Departamento de Medicina Forense da Gandhi Medical College, em Bhopal, India, um total de 62 homens, 12 mulheres e uma pessoa de gênero não identificado, foram submetidas à análise post mortem. A maioria dos casos pertencia a áreas urbanas, com principal causa de morte sendo choque e hemorragia seguida de dano crânio cerebral. Este estudo conclui que arestas afiadas e cortes profundos foram os principais padrões de lesões em casos de homicídio. 

Comparative evaluation of efficacy of autogenous platelet rich plasma versus visco supplementation in treatment of early osteoarthritis of knee

Background: Osteoarthritis is a very common chronic degenerative disease most commonly affecting the knee joints. In present study we compared the efficacy of autogenous platelet rich plasma (PRP) versus visco supplementation in treatment of early osteoarthritis of knees.Methods: 30 patients (56 knees) were registered and divided into two groups. Out of which PRP in 28 knees and visco supplementation in 28 knees injected during. Visual analogue scale (VAS) and Western Ontario and McMaster Universities Arthritis Index (WOMAC) scores were measured. These scores were measured at first visit, 6 weeks, 12 weeks and at 24 weeks.Results: All registered patients were randomized in two groups. Group I (total 16 patients and 28 knees) for intraarticular PRP injection and group II (total 14 patients and 28 knees) for intraarticular viscosupplement injection. Out of 28 knees of group I; 12 (42.85%) knees belonged to grade II and 16 (57.15%) of grade III. Out of 28 knees of group II; 15 (53.57%) knees of grade II and 13 (46.45%) of grade III. None of the knees belonged to grade I and grade 0. There was significant difference in outcome of two treatment groups (p<0.05) at 24 weeks.Conclusions: Treatment with PRP showed a significantly better clinical outcome compared with viscosupplemention at 24 weeks follow up. Although patients achieved lower WOMAC and VAS scores in PRP group at 6 and 12 weeks follow up that was statistically insignificant. We conclude that long term results of PRP are better than viscosupplementation

ABCG5 and ABCG8: More Than a Defense Against Xenosterols

The elucidation of the molecular basis of the rare disease, sitosterolemia, has revolutionized our mechanistic understanding of how dietary sterols are excreted and how cholesterol is eliminated from the body. Two proteins, ABCG5 and ABCG8, encoded by the sitosterolemia locus, work as obligate dimers to pump sterols out of hepatocytes and enterocytes. ABCG5/ABCG8 are key in regulating whole-body sterol trafficking, by eliminating sterols via the biliary tree as well as the intestinal tract. Importantly, these transporters keep xenosterols from accumulating in the body. The sitosterolemia locus has been genetically associated with lipid levels and downstream atherosclerotic disease, as well as formation of gallstones and the risk of gallbladder cancer. While polymorphic variants raise or lower the risks of these phenotypes, loss of function of this locus leads to more dramatic phenotypes, such as premature atherosclerosis, platelet dysfunction, and thrombocytopenia, and, perhaps, increased endocrine disruption and liver dysfunction. Whether small amounts of xenosterol exposure over a lifetime cause pathology in normal humans with polymorphic variants at the sitosterolemia locus remains largely unexplored. The purpose of this review will be to summarize the current state of knowledge, but also highlight key conceptual and mechanistic issues that remain to be explored

Selective reconstitution of liver cholesterol biosynthesis promotes lung maturation but does not prevent neonatal lethality in Dhcr7 null mice

BACKGROUND: Targeted disruption of the murine 3β-hydroxysterol-Δ7-reductase gene (Dhcr7), an animal model of Smith-Lemli-Opitz syndrome, leads to loss of cholesterol synthesis and neonatal death that can be partially rescued by transgenic replacement of DHCR7 expression in brain during embryogenesis. To gain further insight into the role of non-brain tissue cholesterol deficiency in the pathophysiology, we tested whether the lethal phenotype could be abrogated by selective transgenic complementation with DHCR7 expression in the liver. RESULTS: We generated mice that carried a liver-specific human DHCR7 transgene whose expression was driven by the human apolipoprotein E (ApoE) promoter and its associated liver-specific enhancer. These mice were then crossed with Dhcr7+/- mutants to generate Dhcr7-/- mice bearing a human DHCR7 transgene. Robust hepatic transgene expression resulted in significant improvement of cholesterol homeostasis with cholesterol concentrations increasing to 80~90 % of normal levels in liver and lung. Significantly, cholesterol deficiency in brain was not altered. Although late gestational lung sacculation defect reported previously was significantly improved, there was no parallel increase in postnatal survival in the transgenic mutant mice. CONCLUSION: The reconstitution of DHCR7 function selectively in liver induced a significant improvement of cholesterol homeostasis in non-brain tissues, but failed to rescue the neonatal lethality of Dhcr7 null mice. These results provided further evidence that CNS defects caused by Dhcr7 null likely play a major role in the lethal pathogenesis of Dhcr7(-/- )mice, with the peripheral organs contributing the morbidity

Late gestational lung hypoplasia in a mouse model of the Smith-Lemli-Opitz syndrome

BACKGROUND: Normal post-squalene cholesterol biosynthesis is important for mammalian embryonic development. Neonatal mice lacking functional dehydrocholesterol Δ7-reductase (Dhcr7), a model for the human disease of Smith-Lemli-Opitz syndrome, die within 24 hours of birth. Although they have a number of biochemical and structural abnormalities, one cause of death is from apparent respiratory failure due to developmental pulmonary abnormalities. RESULTS: In this study, we characterized further the role of cholesterol deficiency in lung development of these mice. Significant growth retardation, beginning at E14.5~E16.5, was observed in Dhcr7(-/- )embryos. Normal lobation but smaller lungs with a significant decrease in lung-to-body weight ratio was noted in Dhcr7(-/- )embryos, compared to controls. Lung branching morphogenesis was comparable between Dhcr7(-/- )and controls at early stages, but delayed saccular development was visible in all Dhcr7(-/- )embryos from E17.5 onwards. Impaired pre-alveolar development of varying severity, inhibited cell proliferation, delayed differentiation of type I alveolar epithelial cells (AECs) and delayed vascular development were all evident in knockout lungs. Differentiation of type II AECs was apparently normal as judged by surfactant protein (SP) mRNAs and SP-C immunostaining. A significant amount of cholesterol was detectable in knockout lungs, implicating some maternal transfer of cholesterol. No significant differences of the spatial-temporal localization of sonic hedgehog (Shh) or its downstream targets by immunohistochemistry were detected between knockout and wild-type lungs and Shh autoprocessing occurred normally in tissues from Dhcr7(-/- )embryos. CONCLUSION: Our data indicated that cholesterol deficiency caused by Dhcr7 null was associated with a distinct lung saccular hypoplasia, characterized by failure to terminally differentiate alveolar sacs, a delayed differentiation of type I AECs and an immature vascular network at late gestational stages. The molecular mechanism of impaired lung development associated with sterol deficiency by Dhcr7 loss is still unknown, but these results do not support the involvement of dysregulated Shh-Patched-Gli pathway in causing this defect

The missense mutation in Abcg5 gene in spontaneously hypertensive rats (SHR) segregates with phytosterolemia but not hypertension

BACKGROUND: Sitosterolemia is a recessively inherited disorder in humans that is associated with premature atherosclerotic disease. Mutations in ABCG5 or ABCG8, comprising the sitosterolemia locus, STSL, are now known to cause this disease. Three in-bred strains of rats, WKY, SHR and SHRSP, are known to be sitosterolemic, hypertensive and they carry a missense 'mutation' in a conserved residue of Abcg5, Gly583Cys. Since these rat strains are also know to carry mutations at other genetic loci and the extent of phytosterolemia is only moderate, it is important to verify that the mutations in Abcg5 are causative for phytosterolemia and whether they contribute to hypertension. METHODS: To investigate whether the missense change in Abcg5 is responsible for the sitosterolemia we performed a segregation analysis in 103 F2 rats from a SHR × SD cross. Additionally, we measured tail-cuff blood pressure and measured intestinal lipid transport to identify possible mechanisms whereby this mutation causes sitosterolemia. RESULTS: Segregation analysis showed that the inheritance of the Gly583Cys mutation Abcg5 segregated with elevated plant sterols and this pattern was recessive, proving that this genetic change is responsible for the sitosterolemia in these rat strains. Tail-cuff monitoring of blood pressure in conscious animals showed no significant differences between wild-type, heterozygous and homozygous mutant F2 rats, suggesting that this alteration may not be a significant determinant of hypertension in these rats on a chow diet. CONCLUSION: This study shows that the previously identified Gly583Cys change in Abcg5 in three hypertension-susceptible rats is responsible for the sitosterolemia, but may not be a major determinant of blood pressure in these rats