This paper presents a novel position-based routing protocol for vehicular ad hoc networks (VANETs) to enhance traffic safety and traffic organization and facilitate driving through a smart transportation system. The protocol is referred to as the traffic flow-oriented routing (TFOR) protocol for VANETs. It considers a real-time urban scenario with multi-lane and bi-directional roads. It chooses junction optimally considering vehicular traffic flows to accomplish robust routing paths and thereby forwarding the data packets. The new junction selection mechanism and routing between the junctions is based on two-hop neighbor information, which increases packet-delivery ratio and decreases end-to-end delay. We designed, implemented, and compared TFOR against existing routing protocols of VANETs (greedy-perimeter stateless routing (GPSR), geographic source routing (GSR), and enhanced greedy traffic-aware routing (E-GyTAR)). Simulation outcomes in urban scenarios show that TFOR minimizes average end-to-end delay and routing overhead by on average 15.3% and 19.5%, respectively, compared to GPSR. It reduces routing overhead up to 17% compared to GSR. TFOR maximizes packet-delivery ratio on an average of 17.5%, 10.7%, and 7.2% compared to GPSR, GSR, and E-GyTAR, respectively.

Aim: To study the comparative hepatoprotective effect of Virgin Coconut Oil (VCO) and Neem (Azadirachta indica) leaf extract in acetaminophen (Paracetamol) induced liver toxicity. Methods: About 60 mixed population of rats (male/female) of Wistar and Sprague-Dawley species were randomly selected for the proposed study and are segregated into four equal groups. Every group contains 15 animal subjects. Group A was the control group given normal diet. In Group B, the rats were treated with a single dose of 2gm / kg body weight paracetamol, orally. Simultaneously, Group C were given an oral Neem extract of 500mg/kg body weight for 2 weeks days in combination with single dose of Paracetamol, while Group D were provided with 6.7ml/Kg/body weight Virgin Coconut Oil (VCO) for 15 days. Data was analyzed using SPSS Version 20.0 with level of significance being kept at p-value ≤0.05. Results: The mean values of ALT were 23.1, 100.5, 29.85, and 31.09 U/L in Group A, B, C, and D respectively. While, the mean values of AST were 25.6 U/L (Group A), 41 U/L (Group B), 19.3 U/L (Group C), and 15.2 U/L (Group D). The ALP showed maximum response indicated by the mean values of 221 U/L, 444 U/L, 241 U/L, and 243 U/L in Group A, B, C, and D respectively. Group B suggested the paracetamol induced liver toxicity indicated by the increase in hepatic DMEs right after the acetaminophen induction. Conclusion: Azadirachta Indica and Virgin Coconut Oil displayed hepatoprotective effects on the Wistar and Sprague-Dawley rats that were subjected to Paracetamol. Keywords: hepatic, Drug Metabolizing enzymes, Acetaminophen, Virgin coconut oil, Neem extract, Paracetamol, Wistar

The present study was aimed to investigate oxidative stress, DNA damage, and histopathological alterations in hepatic tissues of splenectomized Wistar rats experimentally infected with Babesia bigemina. Rats were challenged with 5x10 6 infected erythrocytes. Babesia infection was confirmed both with Giemsa's staining blood smears and nested-PCR amplified region of apical membrane antigen-1 (AMA-1) gene. Parasitemia reached approximately 10 % at day 5 post-infection. Livers of infected rats were enlarged and darker in color, became extremely brittle with marked congestion. Microscopic evaluation showed cytoplasmic clearing of hepatocytes and severe hydropic changes with significantly dilated sinusoids containing macrophages and also intrasinosoidal parasitized erythrocytes. Severe infiltration of lymphoplasma cells was also present throughout the liver parenchyma. Furthermore, Kupffer cells were enlarged and, occasionally, containing Babesia-parasitized erythrocytes. The activity of Glutathione (GSH) and catalase (CAT), and total antioxidant capacity (TAC) were also significantly decreased (p < 0.05) after infection of rats with B. bigemina. B. bigemina infection also induced a significant increase (p < 0.05) in hepatic malondialdehyde (MDA) and nitric oxide-derived products (NOx) concentrations as well as amount of endogenous hepatocytes DNA damage. Hepatic damage was also reflected through the measurement of lactic acid dehydrogenase (LDH) and protein carbonyl content (PCO) in liver cells. These two indices of liver injury were also significantly elevated (p < 0.5) during B. bigemina infection. Evaluation of correlation between assayed variables in infected rats revealed that MDA levels were positively correlated with PCO, NOx, LDH and DNA damage in the infected group and negatively correlated with GSH, CAT and TAC. There was also an inverse relationship between the antioxidant enzymes activities of GSH, CAT and TAC with PCO, NOx and DNA damage in infected rats. However, NOx showed positive correlation with PCO and DNA damage in infected rats. On the basis of the above results it can be concluded that the Babesia infection increases oxidative stress markers, protein carbonyl content and DNA damage and decreases antioxidant enzymes activities in the liver. These results suggest that B. bigemina infection could alter the liver histopathology and causes DNA damage following oxidative stress in hepatic tissue. Further studies are needed to precisely define how hepatic tissue damage takes place in B. bigemina infection.

ABSTRACT… Objectives:To investigate the histological changes in gastric mucosa of liver cirrhosis patients. Study design: Cross sectional study. Place and Duration: Department of Anatomy and Medicine, Gastroenterology unit, Isra University Hospital (June to December 2012). Subjects and Methods: 85 diagnosed cases of liver cirrhosis were selected according to inclusion and exclusion criteria. Specimen of 2 mm thickness was taken by punch biopsy from gastric body and antrum by endoscope. Tissues were fixed in 10% formaldehyde, 3-5 µ sections were stained with H & E for microscopy. Data was analyzed on SPSS version 21.0. Results: Age (mean ±SD) was noted as 47±11.5 years. Of 85, 56 (65.8%) were male and 29 (34.1%) female. Frequency of mild, moderate, severe and no gastropathy were noted in 52.94%, 34.12%, 4.71%, and 8.24% respectively. 9.4% of cases show capillary dilation and edematous lamina propria. Conclusion: Microscopy shows gastropathy in majority of specimens. Thick gastric mucosa, increased gland size and mucosa capillary dilation was noted. Key words:Liver Cirrhosis, Portal Gastropathy, Histology, Isra University.

Objectives: To investigate the histological changes in gastric mucosa of livercirrhosis patients. Study design: Cross sectional study. Place and Duration: Department ofAnatomy and Medicine, Gastroenterology unit, Isra University Hospital (June to December2012). Subjects and Methods: 85 diagnosed cases of liver cirrhosis were selected accordingto inclusion and exclusion criteria. Specimen of 2 mm thickness was taken by punch biopsyfrom gastric body and antrum by endoscope. Tissues were fixed in 10% formaldehyde, 3-5 μsections were stained with H & E for microscopy. Data was analyzed on SPSS version 21.0.Results: Age (mean ±SD) was noted as 47±11.5 years. Of 85, 56 (65.8%) were male and29 (34.1%) female. Frequency of mild, moderate, severe and no gastropathy were notedin 52.94%, 34.12%, 4.71%, and 8.24% respectively. 9.4% of cases show capillary dilationand edematous lamina propria. Conclusion: Microscopy shows gastropathy in majority ofspecimens. Thick gastric mucosa, increased gland size and mucosa capillary dilation wasnoted.