In Egypt, bladder cancer is one of the most popular cancers, accounting for 31% of all cancer cases. It ranks first in males about 16.2% of male cancer. The incidence in rural areas among males is near 32 per 100,000. The exact etiology of bladder cancer is still unknown; K-ras gene is known as a critical DNA target for chemical carcinogens such as pesticide. Some occupational hazard exposure is thought to be directly genotoxic, while others might enhance the mutagenicity and carcinogenicity of directly acting genotoxic agents. Analysis of the relationship between pesticide exposure and mutation in the K-ras gene in human bladder cancer. One hundred patients were diagnosed with bladder cancer and two hundred controls attended the outpatient clinic; after taking consent and filling a questionnaire for age, sex, occupation and pesticide exposure, surgically resected specimens were collected and the samples were used to determine the k-ras mutation. Blood samples were taken to analyze the level of acetylcholinesterase enzyme and level of P. The present study indicated that pesticide exposure may play a great role in malignant transformation of the bladder cells through mutation in the K-ras gene; there was a significant correlation between the acetylcholinesterase enzyme level and k-ras mutation (p < 0.001). The results revealed that the level of P was significantly high in comparison with the control group (p < 0.001). These findings give an alarm to decrease the amount of pesticides used in our area; also, p may be used as an indicator to bladder cancer.

Background: Determination of time passed since burn injury in the living is critical in forensic science. Autophagy biomarkers and vitronectin can play an important role in determination of the age of burn injuries through their levels in the tissue. Objective: The aim of this study was to investigate the role of autophagy biomarkers in dating burn injury and to correlate them with the histopathological effects of deep second-degree thermal burn. Method: Fifty-four male rats were used in this study after infliction of second-degree thermal burns to their skin. Samples were taken from them after 30 minutes and one, four, 24, 48, and 72 hours following burn to be examined histologically and also for autophagy biomarkers and vitronectin. Results: Significant reduction in the autophagy biomarkers (p < 0.001) over the first 24 hours then began to increase but still not reach the normal level up to 72 hours after burn. Vitronectin level increased after burn infliction 1.5-fold after first hour, then up to four-fold after four hours and after that began to decline but still did not reach the normal level up to 72 hours. Conclusion: Autophagy biomarkers can be used as a forensic tool in determination of the time passed since burn infliction in living.

Head trauma is one of common injury related mortality and morbidity. Blood biomarkers are valuable tools for the identification and characterization of initial injury and secondary pathological processes for traumatic brain injury (TBI). This study evaluated the performance of a recently developed visfatin and its genetic marker and its correlation with other blood circulating biomarkers that reflect specific pathological mechanisms including neuro inflammation, neuron injury and oxidative damage in moderate to severe TBI patients. Peripheral blood was taken from TBI patients (n=78) at hospital admission, maximum 6 hours post-injury. Severity and neurological outcome were assessed using the extended Glasgow Coma Scale (GCS) and blood level of: visfatin and its gene, neuron specific enolase (NSE), malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione (GSH). Concentrations of visfatin, NSE and MDA were significantly higher in TBI patients compared to control group, while SOD and GSH were decreased in TBI patients compared to control group. Visfatin was positively correlated with NSE and MDA, while there was negative correlation with SOD and GSH. Regarding visfatin genotype, CC genotype had the highest plasma concentrations of visfatin, NSE and MDA and lowest concentrations of SOD and GSH. These concentrations did not significantly differ between the variant genotypes CT and TT. In conclusion blood level of visfatin and its genetic marker in correlation with other blood biomarkers can be used for prediction of severity of TBI cases.

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Head trauma is one of common injury related mortality and morbidity. Blood biomarkers are valuable tools for the identification and characterization of initial injury and secondary pathological processes for traumatic brain injury (TBI). This study evaluated the performance of a recently developed visfatin and its correlation with other blood circulating biomarkers that reflect specific pathological mechanisms including neuro inflammatory, neuron injury and oxidative damage in moderate to severe TBI patients. Peripheral blood was taken from TBI patients (n = 78) at hospital admission, maximum 6 hours post-injury. Severity and neurological outcome were assessed using the Glasgow Coma Scale (GCS) and blood level of: visfatin, neuron specific enolase (NSE), malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione (GSH). Concentrations of visfatin (28 ± 1.68 µg/L, 25 ± 2.09 µg/L) was significantly higher (p < 0.0001) in sever and moderate groups of TBI patients respectively compared to control group (7.62 ± 0.87 µg/L), NSE concentrations also were significantly higher (p < 0.0001) in both groups of TBI patients (20.47 ± 3 ng/ml, 13.49 ± 2.66 ng/ml) compared to control group (4.3 ± 0.52 ng/ml), MDA was significantly elevated (p < 0.001) in sever TBI patients group (6.88 ± 0.58 µmol/L) compared to control group (5.12 ± 0.76 µmol/L), while SOD (245.12 ± 24.2 U/L, 276.097 ± 30.8 U/L) and GSH (112.07 ± 2.09 µmol/L, 119.26 ± 2.7 µmol/L) were highly significantly decreased (p < 0.0001) in TBI patients compared to control group (304.