Transforming growth factor- beta1 has been implicated in the pathogenesis of keloids and was reported to be the target of several therapeutic modalities. However, the effect of cryosurgery on its expression in keloid tissue has not been yet investigated. In this cohort study, 26 consecutive keloid patients were treated with cryosurgery for 2-6 sessions. Keloids were biopsied before starting cryosurgery and after two treatment sessions for the immunohistochemical evaluation of the expression of Transforming growth factor- beta1. The average volume reduction, after two treatment sessions (in 22 patients completed the study) was 68.77±15.82%. Dermal over expression of Transforming growth factor- beta1 was demonstrated in all keloid specimens before treatment. Following therapy, significant reduction of that expression was detected in all keloid specimens (P=0.016). In addition to attesting the clinical value of cryosurgery, our findings indicate that cryosurgery effectively suppressed Transforming growth factor- beta1 expression contributing to keloid regression.

Transforming growth factor- beta1 has been implicated in the pathogenesis of keloids and was reported to be the target of several therapeutic modalities. However, the effect of cryosurgery on its expression in keloid tissue has not been yet investigated. In this cohort study, 26 consecutive keloid patients were treated with cryosurgery for 2-6 sessions. Keloids were biopsied before starting cryosurgery and after two treatment sessions for the immunohistochemical evaluation of the expression of Transforming growth factor- beta1. The average volume reduction, after two treatment sessions (in 22 patients completed the study) was 68.77±15.82%. Dermal over expression of Transforming growth factor- beta1 was demonstrated in all keloid specimens before treatment. Following therapy, significant reduction of that expression was detected in all keloid specimens (P=0.016). In addition to attesting the clinical value of cryosurgery, our findings indicate that cryosurgery effectively suppressed Transforming growth factor- beta1 expression contributing to keloid regression.

Transforming growth factor- beta1 has been implicated in the pathogenesis of keloids and was reported to be the target of several therapeutic modalities. However, the effect of cryosurgery on its expression in keloid tissue has not been yet investigated. In this cohort study, 26 consecutive keloid patients were treated with cryosurgery for 2-6 sessions. Keloids were biopsied before starting cryosurgery and after two treatment sessions for the immunohistochemical evaluation of the expression of Transforming growth factor- beta1. The average volume reduction, after two treatment sessions (in 22 patients completed the study) was 68.77±15.82%. Dermal over expression of Transforming growth factor- beta1 was demonstrated in all keloid specimens before treatment. Following therapy, significant reduction of that expression was detected in all keloid specimens (P=0.016). In addition to attesting the clinical value of cryosurgery, our findings indicate that cryosurgery effectively suppressed Transforming growth factor- beta1 expression contributing to keloid regression.

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These findings should be useful for preoperative risk estimations, patient counseling, and to inform strategies aimed at minimizing wound complications following these procedures.

Objective. Systemic administration of folic acid (FA) in rats was used for studying the pathogenesis associated with acute renal damage. However, the mechanism by which FA induces renal damage remains poorly understood. Up to our knowledge, no effective preventive or therapeutic drugs have been developed to protect against acute kidney injury. Curcumin (CUR) is commonly used worldwide as a spice and has been demonstrated to possess various biological activities. The present study was planned to investigate the effect of folic acid administration on renal function, inflammatory cytokines and associated histological changes in renal tissue. In addition, we examined the possible protective effect of curcumin on a rat model of folic acid (FA)-induced acute kidney injury (AKI). Methods. Rats were divided into 3 groups; (FA) folic acid treated group rats were exposed to FA (250 mg/kg) i.p. injection as a single dose. (FA+CUR) folic acid plus curcumin treatment group rats were given curcumin (200 mg/kg) administered by gavage daily for 11 days prior to folic acid (250 mg/kg) i.p injection and the last dose of curcumin was given one day after folic acid injection. Control group are given distilled water by gavage daily for 12 days and saline i.p. as a single dose on the 11th day. Animals were scarified one day following i.p. injection in all groups. Deterioration of kidney function was detected by blood urea and creatinine levels. Inflammatory response was monitored with blood levels of interleukin-6 (IL-6), interleukin-10 (IL-10), and tumor necrosis factor (TNF-α). Results. We found that FA treatment significantly raised blood urea, creatinine, IL-6, IL-10, TNF-α levels and caused marked structural changes of the kidney. CUR treatment for 12 days significantly reduced blood urea, IL-6, IL-10, TNF- α, and protected partially against renal structural damage. Conclusion. These findings suggest that curcumin is a promising protective agent against AKI induced by FA.

Objective. Systemic administration of folic acid (FA) in rats was used for studying the pathogenesis associated with acute renal damage. However, the mechanism by which FA induces renal damage remains poorly understood. Up to our knowledge, no effective preventive or therapeutic drugs have been developed to protect against acute kidney injury. Curcumin (CUR) is commonly used worldwide as a spice and has been demonstrated to possess various biological activities. The present study was planned to investigate the effect of folic acid administration on renal function, inflammatory cytokines and associated histological changes in renal tissue. In addition, we examined the possible protective effect of curcumin on a rat model of folic acid (FA)-induced acute kidney injury (AKI). Methods. Rats were divided into 3 groups; (FA) folic acid treated group rats were exposed to FA (250 mg/kg) i.p. injection as a single dose. (FA+CUR) folic acid plus curcumin treatment group rats were given curcumin (200 mg/kg) administered by gavage daily for 11 days prior to folic acid (250 mg/kg) i.p injection and the last dose of curcumin was given one day after folic acid injection. Control group are given distilled water by gavage daily for 12 days and saline i.p. as a single dose on the 11th day. Animals were scarified one day following i.p. injection in all groups. Deterioration of kidney function was detected by blood urea and creatinine levels. Inflammatory response was monitored with blood levels of interleukin-6 (IL-6), interleukin-10 (IL-10), and tumor necrosis factor (TNF-α). Results. We found that FA treatment significantly raised blood urea, creatinine, IL-6, IL-10, TNF-α levels and caused marked structural changes of the kidney. CUR treatment for 12 days significantly reduced blood urea, IL-6, IL-10, TNF- α, and protected partially against renal structural damage. Conclusion. These findings suggest that curcumin is a promising protective agent against AKI induced by FA.

Objective. Systemic administration of folic acid (FA) in rats was used for studying the pathogenesis associated with acute renal damage. However, the mechanism by which FA induces renal damage remains poorly understood. Up to our knowledge, no effective preventive or therapeutic drugs have been developed to protect against acute kidney injury. Curcumin (CUR) is commonly used worldwide as a spice and has been demonstrated to possess various biological activities. The present study was planned to investigate the effect of folic acid administration on renal function, inflammatory cytokines and associated histological changes in renal tissue. In addition, we examined the possible protective effect of curcumin on a rat model of folic acid (FA)-induced acute kidney injury (AKI). Methods. Rats were divided into 3 groups; (FA) folic acid treated group rats were exposed to FA (250 mg/kg) i.p. injection as a single dose. (FA+CUR) folic acid plus curcumin treatment group rats were given curcumin (200 mg/kg) administered by gavage daily for 11 days prior to folic acid (250 mg/kg) i.p injection and the last dose of curcumin was given one day after folic acid injection. Control group are given distilled water by gavage daily for 12 days and saline i.p. as a single dose on the 11th day. Animals were scarified one day following i.p. injection in all groups. Deterioration of kidney function was detected by blood urea and creatinine levels. Inflammatory response was monitored with blood levels of interleukin-6 (IL-6), interleukin-10 (IL-10), and tumor necrosis factor (TNF-α). Results. We found that FA treatment significantly raised blood urea, creatinine, IL-6, IL-10, TNF-α levels and caused marked structural changes of the kidney. CUR treatment for 12 days significantly reduced blood urea, IL-6, IL-10, TNF- α, and protected partially against renal structural damage. Conclusion. These findings suggest that curcumin is a promising protective agent against AKI induced by FA.

Objectives: sleep deprivation is a significant problem among adult men. It is considered to be a risk factor that contributes to several disease. It has been proposed that reactive oxygen species and the resulting oxidative stress may be responsible for some of the effects of sleep deprivation. The present study was performed to determine the impact of sleep deprivation for different periods on serum testosterone, luteinizing hormone, corticosterone and whether sleep deprivation causes oxidative stress indicated by measuring malondialdehyde (MDA) level in testicular tissue as a direct evidence of cellular damage and measuring glutathione (GSH) in testicular tissue to determine possibility of reversible nature of oxidative stress by scavenger antioxidant system. We studied also if sleep recovery after sleep loss could relieve these effects or not. Material and methods: 42 adult male albino rats aged 12 weeks weighing about 200-250 gm were used in this study. They were divided into seven groups, six animals in each group, a control group and six experimental groups. Three experimental groups were used as sleep deprivation (SD) groups and another three experimental groups were used as sleep recovery (SR) groups. The SR groups were also sleep deprived and then returned to home-cages and were allowed to undisturbed and spontaneous sleep. Group I: served as a control group. Group II: rats were subjected to sleep deprivation for one day. Group III: rats were subjected to sleep deprivation for three days. Group IV: rats were subjected to sleep deprivation for five days. Group V: rats were subjected to sleep deprivation for three days followed by a period of sleep recovery for one day. Group VI: rats were subjected to sleep deprivation for three days followed by a period of sleep recovery for three days. Group VII: rats were subjected to sleep deprivation for three days followed by a period of sleep recovery for five days. After each planned SD and SR period, blood samples were collected for hormonal assay. The rats were decapitated and the testes were dissected out and used for the study of malondialdehyde and glutathione. The parameters were measured then analyzed by using Student's t-test. Results: serum testosterone level and luteinizing hormone (LH) showed significant decrease after three days of deprivation. Serum corticosterone level increased significantly from the first day of deprivation in comparison with the control group. After five days of sleep recovery, serum testosterone level and corticosterone returned to the level of the control group. Serum LH level improved after three days of sleep recovery. Sleep deprivation increased the testicular tissue MDA significantly and GSH was significantly decreased after three day of sleep deprivation when comparing with the control. Sleep recovery decreased testicular tissue MDA significantly and significant increase in GSH after the fifth day as non-significant change noticed on comparing their levels on that day with the control. Conclusions: The present study demonstrated the sleep deprivation effects on testosterone, luteinizing hormone, corticosterone levels in serum, malondialdehyde and glutathione in testicular tissue of rat. Sleep recovery was associated with restoration of the serum hormone levels. Also with sleep recovery MDA level was decreased and GSH content was improved in testicular tissue.

Objectives: sleep deprivation is a significant problem among adult men. It is considered to be a risk factor that contributes to several disease. It has been proposed that reactive oxygen species and the resulting oxidative stress may be responsible for some of the effects of sleep deprivation. The present study was performed to determine the impact of sleep deprivation for different periods on serum testosterone, luteinizing hormone, corticosterone and whether sleep deprivation causes oxidative stress indicated by measuring malondialdehyde (MDA) level in testicular tissue as a direct evidence of cellular damage and measuring glutathione (GSH) in testicular tissue to determine possibility of reversible nature of oxidative stress by scavenger antioxidant system. We studied also if sleep recovery after sleep loss could relieve these effects or not. Material and methods: 42 adult male albino rats aged 12 weeks weighing about 200-250 gm were used in this study. They were divided into seven groups, six animals in each group, a control group and six experimental groups. Three experimental groups were used as sleep deprivation (SD) groups and another three experimental groups were used as sleep recovery (SR) groups. The SR groups were also sleep deprived and then returned to home-cages and were allowed to undisturbed and spontaneous sleep. Group I: served as a control group. Group II: rats were subjected to sleep deprivation for one day. Group III: rats were subjected to sleep deprivation for three days. Group IV: rats were subjected to sleep deprivation for five days. Group V: rats were subjected to sleep deprivation for three days followed by a period of sleep recovery for one day. Group VI: rats were subjected to sleep deprivation for three days followed by a period of sleep recovery for three days. Group VII: rats were subjected to sleep deprivation for three days followed by a period of sleep recovery for five days. After each planned SD and SR period, blood samples were collected for hormonal assay. The rats were decapitated and the testes were dissected out and used for the study of malondialdehyde and glutathione. The parameters were measured then analyzed by using Student's t-test. Results: serum testosterone level and luteinizing hormone (LH) showed significant decrease after three days of deprivation. Serum corticosterone level increased significantly from the first day of deprivation in comparison with the control group. After five days of sleep recovery, serum testosterone level and corticosterone returned to the level of the control group. Serum LH level improved after three days of sleep recovery. Sleep deprivation increased the testicular tissue MDA significantly and GSH was significantly decreased after three day of sleep deprivation when comparing with the control. Sleep recovery decreased testicular tissue MDA significantly and significant increase in GSH after the fifth day as non-significant change noticed on comparing their levels on that day with the control. Conclusions: The present study demonstrated the sleep deprivation effects on testosterone, luteinizing hormone, corticosterone levels in serum, malondialdehyde and glutathione in testicular tissue of rat. Sleep recovery was associated with restoration of the serum hormone levels. Also with sleep recovery MDA level was decreased and GSH content was improved in testicular tissue.