Background: Atorvastatin and remote ischemic preconditioning (RIPC) have beneficial cardiovascular protective effects. The aimof the studywas to investigate possible effect of this drug alone and in combinationwith RIPC on the biochemical changes induced by ischemic/reperfusion injury (I/R) in a combined study with a clinical and experimental animal arm. Methods: Thirty consecutive patients undergoing elective percutaneous coronary intervention (PCI)were divided into three groups (10 each): group I (control group without any preconditioning), group II (patients who were maintained on atorvastatin (80 mg/day) for one month before PCI), and group III (similar to group II but PCI was preceded by RIPC). On the other hand, sixty adultmaleNewZealandwhite rabbitswere divided into 6 groups (10 each): group I (control), group II (sham), group III (I/R as 30 min ischemia followed by 120 min reperfusion), group IV (regular atorvastatin 10 mg/kg for 40 days orally followed by I/R), group V (I/R preceded by RIPC) and group VI (similar to group IV but I/R was preceded by RIPC). Tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), nitric oxide (NO), troponin I (cTnI), creatine kinase MB (CK-MB) and C-reactive protein (CRP) were measured in blood for all study groups. Results: Clinical and experimental parts showed that groups with RIPC combinedwith atorvastatin pre-treatment showed a synergistic protective effect against I/R injury as evidenced by significant reduction (P b 0.001) in the levels of TNF-α, cTnI (in patients) and IL-6, CK-MB and CRP (in rabbits) while the level of NO was significantly (P b 0.001) increased compared with other groups. Conclusions: Pretreatment with atorvastatin combined with RIPC can exert a synergistic cardioprotective effects by reducing the possible biochemical changes related to ischemic reperfusion injury.

Background: Atorvastatin and remote ischemic preconditioning (RIPC) have beneficial cardiovascular protective effects. The aimof the studywas to investigate possible effect of this drug alone and in combinationwith RIPC on the biochemical changes induced by ischemic/reperfusion injury (I/R) in a combined study with a clinical and experimental animal arm. Methods: Thirty consecutive patients undergoing elective percutaneous coronary intervention (PCI)were divided into three groups (10 each): group I (control group without any preconditioning), group II (patients who were maintained on atorvastatin (80 mg/day) for one month before PCI), and group III (similar to group II but PCI was preceded by RIPC). On the other hand, sixty adultmaleNewZealandwhite rabbitswere divided into 6 groups (10 each): group I (control), group II (sham), group III (I/R as 30 min ischemia followed by 120 min reperfusion), group IV (regular atorvastatin 10 mg/kg for 40 days orally followed by I/R), group V (I/R preceded by RIPC) and group VI (similar to group IV but I/R was preceded by RIPC). Tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), nitric oxide (NO), troponin I (cTnI), creatine kinase MB (CK-MB) and C-reactive protein (CRP) were measured in blood for all study groups. Results: Clinical and experimental parts showed that groups with RIPC combinedwith atorvastatin pre-treatment showed a synergistic protective effect against I/R injury as evidenced by significant reduction (P b 0.001) in the levels of TNF-α, cTnI (in patients) and IL-6, CK-MB and CRP (in rabbits) while the level of NO was significantly (P b 0.001) increased compared with other groups. Conclusions: Pretreatment with atorvastatin combined with RIPC can exert a synergistic cardioprotective effects by reducing the possible biochemical changes related to ischemic reperfusion injury.

Background: Atorvastatin and remote ischemic preconditioning (RIPC) have beneficial cardiovascular protective effects. The aimof the studywas to investigate possible effect of this drug alone and in combinationwith RIPC on the biochemical changes induced by ischemic/reperfusion injury (I/R) in a combined study with a clinical and experimental animal arm. Methods: Thirty consecutive patients undergoing elective percutaneous coronary intervention (PCI)were divided into three groups (10 each): group I (control group without any preconditioning), group II (patients who were maintained on atorvastatin (80 mg/day) for one month before PCI), and group III (similar to group II but PCI was preceded by RIPC). On the other hand, sixty adultmaleNewZealandwhite rabbitswere divided into 6 groups (10 each): group I (control), group II (sham), group III (I/R as 30 min ischemia followed by 120 min reperfusion), group IV (regular atorvastatin 10 mg/kg for 40 days orally followed by I/R), group V (I/R preceded by RIPC) and group VI (similar to group IV but I/R was preceded by RIPC). Tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), nitric oxide (NO), troponin I (cTnI), creatine kinase MB (CK-MB) and C-reactive protein (CRP) were measured in blood for all study groups. Results: Clinical and experimental parts showed that groups with RIPC combinedwith atorvastatin pre-treatment showed a synergistic protective effect against I/R injury as evidenced by significant reduction (P b 0.001) in the levels of TNF-α, cTnI (in patients) and IL-6, CK-MB and CRP (in rabbits) while the level of NO was significantly (P b 0.001) increased compared with other groups. Conclusions: Pretreatment with atorvastatin combined with RIPC can exert a synergistic cardioprotective effects by reducing the possible biochemical changes related to ischemic reperfusion injury.

Background: Atorvastatin and remote ischemic preconditioning (RIPC) have beneficial cardiovascular protective effects. The aimof the studywas to investigate possible effect of this drug alone and in combinationwith RIPC on the biochemical changes induced by ischemic/reperfusion injury (I/R) in a combined study with a clinical and experimental animal arm. Methods: Thirty consecutive patients undergoing elective percutaneous coronary intervention (PCI)were divided into three groups (10 each): group I (control group without any preconditioning), group II (patients who were maintained on atorvastatin (80 mg/day) for one month before PCI), and group III (similar to group II but PCI was preceded by RIPC). On the other hand, sixty adultmaleNewZealandwhite rabbitswere divided into 6 groups (10 each): group I (control), group II (sham), group III (I/R as 30 min ischemia followed by 120 min reperfusion), group IV (regular atorvastatin 10 mg/kg for 40 days orally followed by I/R), group V (I/R preceded by RIPC) and group VI (similar to group IV but I/R was preceded by RIPC). Tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), nitric oxide (NO), troponin I (cTnI), creatine kinase MB (CK-MB) and C-reactive protein (CRP) were measured in blood for all study groups. Results: Clinical and experimental parts showed that groups with RIPC combinedwith atorvastatin pre-treatment showed a synergistic protective effect against I/R injury as evidenced by significant reduction (P b 0.001) in the levels of TNF-α, cTnI (in patients) and IL-6, CK-MB and CRP (in rabbits) while the level of NO was significantly (P b 0.001) increased compared with other groups. Conclusions: Pretreatment with atorvastatin combined with RIPC can exert a synergistic cardioprotective effects by reducing the possible biochemical changes related to ischemic reperfusion injury.

Background: Atorvastatin and remote ischemic preconditioning (RIPC) have beneficial cardiovascular protective effects. The aimof the studywas to investigate possible effect of this drug alone and in combinationwith RIPC on the biochemical changes induced by ischemic/reperfusion injury (I/R) in a combined study with a clinical and experimental animal arm. Methods: Thirty consecutive patients undergoing elective percutaneous coronary intervention (PCI)were divided into three groups (10 each): group I (control group without any preconditioning), group II (patients who were maintained on atorvastatin (80 mg/day) for one month before PCI), and group III (similar to group II but PCI was preceded by RIPC). On the other hand, sixty adultmaleNewZealandwhite rabbitswere divided into 6 groups (10 each): group I (control), group II (sham), group III (I/R as 30 min ischemia followed by 120 min reperfusion), group IV (regular atorvastatin 10 mg/kg for 40 days orally followed by I/R), group V (I/R preceded by RIPC) and group VI (similar to group IV but I/R was preceded by RIPC). Tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), nitric oxide (NO), troponin I (cTnI), creatine kinase MB (CK-MB) and C-reactive protein (CRP) were measured in blood for all study groups. Results: Clinical and experimental parts showed that groups with RIPC combinedwith atorvastatin pre-treatment showed a synergistic protective effect against I/R injury as evidenced by significant reduction (P b 0.001) in the levels of TNF-α, cTnI (in patients) and IL-6, CK-MB and CRP (in rabbits) while the level of NO was significantly (P b 0.001) increased compared with other groups. Conclusions: Pretreatment with atorvastatin combined with RIPC can exert a synergistic cardioprotective effects by reducing the possible biochemical changes related to ischemic reperfusion injury.

Background: The efflux pumps are one of the main mechanisms of the antibiotic resistance in Escherichia coli .The efflux pump inhibitors (chlorpromazine and omeprazole) were tested for their effect on the antibiotic resistance by inhibiting efflux pump activity. Objective: The present study aims to estimate the effect of some efflux pump inhibitors on the antibiotic resistance of some Escherichia coli isolates. Methodology: A total of 100 isolates of Escherichia coli were studied for antibacterial susceptibility pattern by disk diffusion method with and without efflux pump inhibitors chlorpromazine (25 µg) and omeprazole (100 µg), determination of the MIC of amikacin and gentamicin on 60 E.coli resistant isolates, the effect of the efflux pump inhibitors on the MIC of amikacin and gentamicin and PCR amplification of the efflux pump genes AcrD and MdfA genes. Results: The difference between all tested antibiotics in the change of resistance to totally sensitive E.coli isolates after addition of CPZ and OMP by disk diffustion method were statistically highly significant (p value 0.001), in which the highest percentage value were reported for aminoglycoside antibiotics (amikacin and gentamicin). The highest reduction in the MIC of amikacin and gentamicin was observed with chlorpromazine than omeprazole (p0.05) .The proportion of isolates with greater than two-fold reductions in MIC in the presence of CPZ were 69.2% and 50.9% for amikacin and gentamicin respectively (p>0.05) while in the presence of OMP were 46.2% and 30.9% for amikacin and gentamicin respectively, (p>0.05). PCR detection of efflux pump genes detected a high level of AcrD gene detection than MdfA gene (p value 0.05).The percentage of AcrD detection in amikacin and gentamicin resistant isolates were 77% and 87.3% respectively, while for MdfA gene detection in amikacin and gentamicin resistant isolates were 59% and 71% respectively. Conclusion: Antibacterial efflux pumps are involved in establishment of resistance among the tested isolates. Chlorpromazine and Omperazole were capable of inhibiting the efflux pump with higher activity on aminoglycoside antibiotics. Chlorpromazine was more effective than Omeprazole as EPI. PCR results showed that AcrD and MdfA efflux pump genes contributed to the resistance of the tested aminoglycosides

Background: The efflux pumps are one of the main mechanisms of the antibiotic resistance in Escherichia coli .The efflux pump inhibitors (chlorpromazine and omeprazole) were tested for their effect on the antibiotic resistance by inhibiting efflux pump activity. Objective: The present study aims to estimate the effect of some efflux pump inhibitors on the antibiotic resistance of some Escherichia coli isolates. Methodology: A total of 100 isolates of Escherichia coli were studied for antibacterial susceptibility pattern by disk diffusion method with and without efflux pump inhibitors chlorpromazine (25 µg) and omeprazole (100 µg), determination of the MIC of amikacin and gentamicin on 60 E.coli resistant isolates, the effect of the efflux pump inhibitors on the MIC of amikacin and gentamicin and PCR amplification of the efflux pump genes AcrD and MdfA genes. Results: The difference between all tested antibiotics in the change of resistance to totally sensitive E.coli isolates after addition of CPZ and OMP by disk diffustion method were statistically highly significant (p value 0.001), in which the highest percentage value were reported for aminoglycoside antibiotics (amikacin and gentamicin). The highest reduction in the MIC of amikacin and gentamicin was observed with chlorpromazine than omeprazole (p0.05) .The proportion of isolates with greater than two-fold reductions in MIC in the presence of CPZ were 69.2% and 50.9% for amikacin and gentamicin respectively (p>0.05) while in the presence of OMP were 46.2% and 30.9% for amikacin and gentamicin respectively, (p>0.05). PCR detection of efflux pump genes detected a high level of AcrD gene detection than MdfA gene (p value 0.05).The percentage of AcrD detection in amikacin and gentamicin resistant isolates were 77% and 87.3% respectively, while for MdfA gene detection in amikacin and gentamicin resistant isolates were 59% and 71% respectively. Conclusion: Antibacterial efflux pumps are involved in establishment of resistance among the tested isolates. Chlorpromazine and Omperazole were capable of inhibiting the efflux pump with higher activity on aminoglycoside antibiotics. Chlorpromazine was more effective than Omeprazole as EPI. PCR results showed that AcrD and MdfA efflux pump genes contributed to the resistance of the tested aminoglycosides

Background: The efflux pumps are one of the main mechanisms of the antibiotic resistance in Escherichia coli .The efflux pump inhibitors (chlorpromazine and omeprazole) were tested for their effect on the antibiotic resistance by inhibiting efflux pump activity. Objective: The present study aims to estimate the effect of some efflux pump inhibitors on the antibiotic resistance of some Escherichia coli isolates. Methodology: A total of 100 isolates of Escherichia coli were studied for antibacterial susceptibility pattern by disk diffusion method with and without efflux pump inhibitors chlorpromazine (25 µg) and omeprazole (100 µg), determination of the MIC of amikacin and gentamicin on 60 E.coli resistant isolates, the effect of the efflux pump inhibitors on the MIC of amikacin and gentamicin and PCR amplification of the efflux pump genes AcrD and MdfA genes. Results: The difference between all tested antibiotics in the change of resistance to totally sensitive E.coli isolates after addition of CPZ and OMP by disk diffustion method were statistically highly significant (p value 0.001), in which the highest percentage value were reported for aminoglycoside antibiotics (amikacin and gentamicin). The highest reduction in the MIC of amikacin and gentamicin was observed with chlorpromazine than omeprazole (p0.05) .The proportion of isolates with greater than two-fold reductions in MIC in the presence of CPZ were 69.2% and 50.9% for amikacin and gentamicin respectively (p>0.05) while in the presence of OMP were 46.2% and 30.9% for amikacin and gentamicin respectively, (p>0.05). PCR detection of efflux pump genes detected a high level of AcrD gene detection than MdfA gene (p value 0.05).The percentage of AcrD detection in amikacin and gentamicin resistant isolates were 77% and 87.3% respectively, while for MdfA gene detection in amikacin and gentamicin resistant isolates were 59% and 71% respectively. Conclusion: Antibacterial efflux pumps are involved in establishment of resistance among the tested isolates. Chlorpromazine and Omperazole were capable of inhibiting the efflux pump with higher activity on aminoglycoside antibiotics. Chlorpromazine was more effective than Omeprazole as EPI. PCR results showed that AcrD and MdfA efflux pump genes contributed to the resistance of the tested aminoglycosides

تهدف هذه الدراسة إلى تقييم مدى انتشار بروتين النسيج الغضروفى في تقييم تدمير الغضروف في المرضى الذين يعانون من التهاب المفاصل الروماتويدي وتأثير العوامل المضادة للروماتيزم على مستوياته.وقد أجريت هذه الدراسة على 50 مريضا من حديثي التشخيص من مرضي الروماتويد المفصلى ، و الذين تم اختيارهم من عيادات الأمراض الباطنة ووحدة الأمراض الروماتيزمية بمستشفى أسيوط الجامعى و20 من الاصحاء كمجموعة ضابطة. جميع المرضى استوفوا معايير الكلية الأمريكية لأمراض الروماتيزم2010 لتشخيص المرض.وقد تم تقسيم المرضى الى مجموعتين:شديدى النشاط (29مريض) ومتوسطى النشاط (21 مريض) وذلك طبقا لمعيار نشاط المرض 28. وقد تم تقسيم المرضى الى مجموعتين أخريين اعتمادا على العلاج بعقار لوفلوناميد لمدة ثلاثة شهور الى مجموعة ما قبل العلاج ومجموعة ما بعد العلاج. حيث تم تجميع كل البيانات الخاصة بالمرض والكشف الطبى وأخذ عينات من الدم لعمل التحاليل الاتية: سرعة الترسيب، بروتين سي التفاعلي ،معامل روماتويد، انتي سي سي بي، بروتين النسيج الغضروفى، والأشعة السينية للمفاصل المصابة عند التشخيص وبعد 3 أشهر من العلاج بأدوية المرحلة الثانية لعلاج الروماتويد(دواء لوفلوناميد). أظهرت نتائج الدراسة ارتفاع نسبة بروتين سي التفاعلي و سرعة الترسيب ارتفاعا ذو دلالة إحصائية مقارنة بالاصحاء.وكذلك أظهرت الدراسة ارتفاع نسبة بروتين النسيج الغضروفى فى مرضى الروماتويدالمفصلي حديثى التشخيص ارتفاعا ذو دلالة إحصائية مقارنة بالأصحاء وأيضا تبين وجود علاقة طردية بين بروتين النسيج الغضروفى ومعدل تأكل الغضروف وضيق المسافة بين عظمتى المفصل باستخدام الأشعة السينية.وهناك علاقة عكسية بينه وبين عامل روماتويد.وقد أثبتت الدراسة تناقص بروتين النسيج الغضروفى للعلاج بعقار لفلونوميد لمدة ثلاثة شهور.

تهدف هذه الدراسة إلى تقييم مدى انتشار بروتين النسيج الغضروفى في تقييم تدمير الغضروف في المرضى الذين يعانون من التهاب المفاصل الروماتويدي وتأثير العوامل المضادة للروماتيزم على مستوياته.وقد أجريت هذه الدراسة على 50 مريضا من حديثي التشخيص من مرضي الروماتويد المفصلى ، و الذين تم اختيارهم من عيادات الأمراض الباطنة ووحدة الأمراض الروماتيزمية بمستشفى أسيوط الجامعى و20 من الاصحاء كمجموعة ضابطة. جميع المرضى استوفوا معايير الكلية الأمريكية لأمراض الروماتيزم2010 لتشخيص المرض.وقد تم تقسيم المرضى الى مجموعتين:شديدى النشاط (29مريض) ومتوسطى النشاط (21 مريض) وذلك طبقا لمعيار نشاط المرض 28. وقد تم تقسيم المرضى الى مجموعتين أخريين اعتمادا على العلاج بعقار لوفلوناميد لمدة ثلاثة شهور الى مجموعة ما قبل العلاج ومجموعة ما بعد العلاج. حيث تم تجميع كل البيانات الخاصة بالمرض والكشف الطبى وأخذ عينات من الدم لعمل التحاليل الاتية: سرعة الترسيب، بروتين سي التفاعلي ،معامل روماتويد، انتي سي سي بي، بروتين النسيج الغضروفى، والأشعة السينية للمفاصل المصابة عند التشخيص وبعد 3 أشهر من العلاج بأدوية المرحلة الثانية لعلاج الروماتويد(دواء لوفلوناميد). أظهرت نتائج الدراسة ارتفاع نسبة بروتين سي التفاعلي و سرعة الترسيب ارتفاعا ذو دلالة إحصائية مقارنة بالاصحاء.وكذلك أظهرت الدراسة ارتفاع نسبة بروتين النسيج الغضروفى فى مرضى الروماتويدالمفصلي حديثى التشخيص ارتفاعا ذو دلالة إحصائية مقارنة بالأصحاء وأيضا تبين وجود علاقة طردية بين بروتين النسيج الغضروفى ومعدل تأكل الغضروف وضيق المسافة بين عظمتى المفصل باستخدام الأشعة السينية.وهناك علاقة عكسية بينه وبين عامل روماتويد.وقد أثبتت الدراسة تناقص بروتين النسيج الغضروفى للعلاج بعقار لفلونوميد لمدة ثلاثة شهور.