High levels of endothelial progenitor cells and circulating endothelial cells in patients with Behçet's disease and their relationship to disease activity.

BACKGROUND: Behçet's disease is a multisystemic vasculitis, associated with vascular endothelial dysfunction. Currently, the prognosis is unpredictable, because there is still no valid laboratory marker indicating the disease activity in Behçet's disease. Endothelial progenitor cells and circulating endothelial cells are newly introduced hematological markers which are presumed to take part in the pathogenesis of vasculitis. OBJECTIVES: To evaluate the levels of endothelial progenitor cells and subtypes and circulating endothelial cells in patients with Behçet's disease and to describe their relationship with the disease activity. METHODS: A total of 45 patients with Behçet's disease and 28 healthy controls were included in the study. Endothelial progenitor cells (CD34+CD133+KDR+ as early endothelial progenitor cells and CD34+KDR+ as late endothelial progenitor cells), and circulating endothelial cells (CD34+CD133+) were measured by flow cytometry. RESULTS: The mean plasma level of endothelial progenitor cells and circulating endothelial cells, vascular endothelial growth factor, matrix metalloproteinase-9, C-reactive protein, and erythrocyte sedimentation rate were significantly higher in patients with Behçet's disease. All of these parameters except circulating endothelial cells were also found to be higher in patients with active disease than in patients with inactive disease. Early endothelial progenitor cells showed significant correlations with C-reactive protein and circulating endothelial cells. STUDY LIMITATIONS: The cross-sectional nature of the study and patient characteristics such as being under treatment, which can affect endothelial progenitor cells numbers. CONCLUSION: The increase in endothelial progenitor cells may play an essential role in the repair of endothelial injury in Behçet's disease, especially in the active period of the disease. Thus, endothelial progenitor cells can indicate the disease activity. In addition, endothelial progenitor cells and circulating endothelial cells can be used as endothelial repair and injury markers for Behçet's disease, respectively.

¿El licopeno puede eliminar los efectos perjudiciales de la hiperoxia en los cerebros inmaduros? / Can lycopene eliminate the harmful effects of hyperoxia in an immature brain?

Objetivos: Al ser un antioxidante, el licopeno protege a las células contra el daño causado por los radicales libres, fortalece los enlaces intercelulares y mejora el metabolismo celular. Este estudio analiza los efectos del licopeno sobre los trastornos neurodegenerativos por hiperoxia en ratas recién nacidas a término. Métodos: Estas ratas se dividieron en cuatro grupos: grupo 1 de referencia con normoxia, grupo 2 con normoxia + licopeno, grupo 3 de referencia con hiperoxia y grupo 4 con hiperoxia + licopeno. Los grupos 1 y 2 se supervisaron en condiciones de aire ambiental, y los grupos 3 y 4 se supervisaron con un nivel de oxígeno > 85 % O2. Los grupos 2 y 4 recibieron inyecciones intraperitoneales de licopeno de 50 mg/kg/día; los otros grupos recibieron inyecciones intraperitoneales de aceite de maíz con el mismo volumen. Las ratas se sacrificaron en el día 11, después de 10 días con hiperoxia. Se extrajeron los cerebros, y se evaluaron los parámetros del sistema oxidativo. Resultados: Se detectaron lesiones cerebrales por hiperoxia en sustancia blanca, regiones corticales y tálamo. Aumentó la cantidad de células apoptóticas y disminuyó la cantidad de células PCNA positivas en los grupos 3 y 4, comparados con el grupo 1. No se observó una mejora significativa en la cantidad de células apoptóticas y células PCNA positivas en los grupos 3 y 4; además, aumentó la apoptosis. Conclusión: Se halló que el licopeno no mostró efectos terapéuticos para el daño cerebral en ratas recién nacidas. Además, se demostró que el licopeno podría causar efectos tóxicos.

Objectives. In addition to protecting cells against free radical harm thanks to its anti-oxidant nature, lycopene strengthens the bonds among cells and improves cell metabolism. This study focuses on analyzing therapeutic effects of lycopene in hyperoxia-induced neurodegenerative disorders in newborn rats. Methods. Term newborn rats were divided into four groups as the normoxia control group (group-1), normoxia+lycopene group (group-2), hyperoxia control group (group-3) and hyperoxia+lycopene group (group-4). Group-1 and group-2 were monitored in room air while the group-3 and group-4 were monitored at > 85% O2. The group-2 and group-4 were injected with lycopene intrapertioneally (i.p. ) at 50mg/kg/day while the other groups were injected with corn oil i.p. at the same volume. The rats we sacrificed on the 11th day following the 10-day hyperoxia. The brains were removed and oxidant system parameters were assessed. Results. Injury resulting from hyperoxia was detected in the white matter, cortical regions, and thalamus of the brains. It was observed that the number of apoptotic cells increased and the number of proliferating cell nuclear antigen (PCNA) positive cells decreased in the groups-3 and 4 compared to the group-1. No significant improvement in the number of apoptotic cells and PCNA positive cells was observed in the groups-3 and 4, and apoptosis increased as well. Conclusion. This study found that lycopene, did not show any therapeutic effects for brain damage treatment in newborn rats. In addition, this study demonstrated that lycopene might lead to toxic effects.

Can lycopene eliminate the harmful effects of hyperoxia in an immature brain? / ¿El licopeno puede eliminar los efectos perjudiciales de la hiperoxia en los cerebros inmaduros?

OBJECTIVES: In addition to protecting cells against free radical harm thanks to its anti-oxidant nature, lycopene strengthens the bonds among cells and improves cell metabolism. This study focuses on analyzing therapeutic effects of lycopene in hyperoxia-induced neurodegenerative disorders in newborn rats. METHODS: Term newborn rats were divided into four groups as the normoxia control group (group-1), normoxia+lycopene group (group-2), hyperoxia control group (group-3) and hyperoxia+lycopene group (group-4). Group-1 and group-2 were monitored in room air while the group-3 and group-4 were monitored at > 85% O2. The group-2 and group-4 were injected with lycopene intrapertioneally (i.p. ) at 50mg/kg/day while the other groups were injected with corn oil i.p. at the same volume. The rats we sacrificed on the 11th day following the 10-day hyperoxia. The brains were removed and oxidant system parameters were assessed. RESULTS: Injury resulting from hyperoxia was detected in the white matter, cortical regions, and thalamus of the brains. It was observed that the number of apoptotic cells increased and the number of proliferating cell nuclear antigen (PCNA) positive cells decreased in the groups-3 and 4 compared to the group-1. No significant improvement in the number of apoptotic cells and PCNA positive cells was observed in the groups-3 and 4, and apoptosis increased as well. CONCLUSIONS: This study found that lycopene, did not show any therapeutic effects for brain damage treatment in newborn rats. In addition, this study demonstrated that lycopene might lead to toxic effects.

Objetivos: Al ser un antioxidante, el licopeno protege a las células contra el daño causado por los radicales libres, fortalece los enlaces intercelulares y mejora el metabolismo celular. Este estudio analiza los efectos del licopeno sobre los trastornos neurodegenerativos por hiperoxia en ratas recién nacidas a término. Métodos: Estas ratas se dividieron en cuatro grupos: grupo 1 de referencia con normoxia, grupo 2 con normoxia + licopeno, grupo 3 de referencia con hiperoxia y grupo 4 con hiperoxia + licopeno. Los grupos 1 y 2 se supervisaron en condiciones de aire ambiental, y los grupos 3 y 4 se supervisaron con un nivel de oxígeno > 85 % O2. Los grupos 2 y 4 recibieron inyecciones intraperitoneales de licopeno de 50 mg/kg/día; los otros grupos recibieron inyecciones intraperitoneales de aceite de maíz con el mismo volumen. Las ratas se sacrificaron en el día 11, después de 10 días con hiperoxia. Se extrajeron los cerebros, y se evaluaron los parámetros del sistema oxidativo. Resultados: Se detectaron lesiones cerebrales por hiperoxia en sustancia blanca, regiones corticales y tálamo. Aumentó la cantidad de células apoptóticas y disminuyó la cantidad de células PCNA positivas en los grupos 3 y 4, comparados con el grupo 1. No se observó una mejora significativa en la cantidad de células apoptóticas y células PCNA positivas en los grupos 3 y 4; además, aumentó la apoptosis. Conclusión: Se halló que el licopeno no mostró efectos terapéuticos para el daño cerebral en ratas recién nacidas. Además, se demostró que el licopeno podría causar efectos tóxicos.

High levels of endothelial progenitor cells and circulating endothelial cells in patients with Behçet's disease and their relationship to disease activity

Abstract: Background: Behçet's disease is a multisystemic vasculitis, associated with vascular endothelial dysfunction. Currently, the prognosis is unpredictable, because there is still no valid laboratory marker indicating the disease activity in Behçet's disease. Endothelial progenitor cells and circulating endothelial cells are newly introduced hematological markers which are presumed to take part in the pathogenesis of vasculitis. Objectives: To evaluate the levels of endothelial progenitor cells and subtypes and circulating endothelial cells in patients with Behçet's disease and to describe their relationship with the disease activity. Methods: A total of 45 patients with Behçet's disease and 28 healthy controls were included in the study. Endothelial progenitor cells (CD34+CD133+KDR+ as early endothelial progenitor cells and CD34+KDR+ as late endothelial progenitor cells), and circulating endothelial cells (CD34+CD133+) were measured by flow cytometry. Results: The mean plasma level of endothelial progenitor cells and circulating endothelial cells, vascular endothelial growth factor, matrix metalloproteinase-9, C-reactive protein, and erythrocyte sedimentation rate were significantly higher in patients with Behçet's disease. All of these parameters except circulating endothelial cells were also found to be higher in patients with active disease than in patients with inactive disease. Early endothelial progenitor cells showed significant correlations with C-reactive protein and circulating endothelial cells. Study Limitations: The cross-sectional nature of the study and patient characteristics such as being under treatment, which can affect endothelial progenitor cells numbers. Conclusion: The increase in endothelial progenitor cells may play an essential role in the repair of endothelial injury in Behçet's disease, especially in the active period of the disease. Thus, endothelial progenitor cells can indicate the disease activity. In addition, endothelial progenitor cells and circulating endothelial cells can be used as endothelial repair and injury markers for Behçet's disease, respectively.

The importance of risk factors for the prediction of patients with invasive pulmonary aspergillosis.

OBJECTIVE: Invasive pulmonary aspergillosis (IPA) is a major challenge in the management of immunocompromised patients. Despite all the advances in diagnosis, it remains a problem. The purpose of our study was to investigate the risk factors associated with IPA seen in patients with hematological malignancies. METHOD: A total of 152 febrile neutropenia (FEN) patients with hematological malignancies aged over 18 years and receiving high-dose chemotherapy or stem cell transplant between January 1, 2010, and December 31, 2012 were included in the study. Sixty-five (65) cases with IPA according to the European Organization for the Research and Treatment of Cancer and Infectious Diseases Mycoses Study Group criteria were enrolled as the case group, while 87 patients without IPA development during concomitant monitoring were enrolled as the control group. Incidence of IPA was 21.4% (3/14) in patients receiving bone marrow transplant (allogeneic 2, autologous 1) and those cases were also added into the case group. The two groups were compared in terms of demographic, clinical and laboratory findings and risk factors associated with IPA investigated retrospectively. RESULTS: Presence of relapse of primary disease, neutropenia for more than 3 weeks, presence of bacterial infection, and non-administration of antifungal prophylaxis were identified as risk factors associated with IPA. CONCLUSION: It may be possible to reduce the incidence of the disease by eliminating preventable risk factors. Predicting those risks would, per se, enable early diagnosis and treatment and, thus, the mortality rate of these patients would unquestionably decline.

The importance of risk factors for the prediction of patients with invasive pulmonary aspergillosis

Summary Objective: Invasive pulmonary aspergillosis (IPA) is a major challenge in the management of immunocompromised patients. Despite all the advances in diagnosis, it remains a problem. The purpose of our study was to investigate the risk factors associated with IPA seen in patients with hematological malignancies. Method: A total of 152 febrile neutropenia (FEN) patients with hematological malignancies aged over 18 years and receiving high-dose chemotherapy or stem cell transplant between January 1, 2010, and December 31, 2012 were included in the study. Sixty-five (65) cases with IPA according to the European Organization for the Research and Treatment of Cancer and Infectious Diseases Mycoses Study Group criteria were enrolled as the case group, while 87 patients without IPA development during concomitant monitoring were enrolled as the control group. Incidence of IPA was 21.4% (3/14) in patients receiving bone marrow transplant (allogeneic 2, autologous 1) and those cases were also added into the case group. The two groups were compared in terms of demographic, clinical and laboratory findings and risk factors associated with IPA investigated retrospectively. Results: Presence of relapse of primary disease, neutropenia for more than 3 weeks, presence of bacterial infection, and non-administration of antifungal prophylaxis were identified as risk factors associated with IPA. Conclusion: It may be possible to reduce the incidence of the disease by eliminating preventable risk factors. Predicting those risks would, per se, enable early diagnosis and treatment and, thus, the mortality rate of these patients would unquestionably decline.

Impact of Experiencing Acute Coronary Syndrome Prior to Open Heart Surgery on Psychiatric Status.

Objective: The incidence of depression and anxiety is higher in patients with acute coronary syndrome. The aim of this study is to determine whether experiencing acute coronary syndrome prior to open heart surgery affects patients in terms of depression, hopelessness, anxiety, fear of death and quality of life. Methods: The study included 63 patients who underwent coronary bypass surgery between January 2015 and January 2016. The patients were divided into two groups: those diagnosed after acute coronary syndrome (Group 1) and those diagnosed without acute coronary syndrome (Group 2). Beck depression scale, Beck hopelessness scale, Templer death anxiety scale and death depression scale, State-Trait anxiety inventory and WHOQOL-Bref quality of life scale were applied. Results: There was no significant difference between the two groups in terms of the total score obtained from Beck depression scale, Beck hopelessness scale - future-related emotions, loss of motivation, future-related expectations subgroups, death anxiety scale, the death depression scale, State-Trait Anxiety Inventory - social and environmental subgroups. The mental quality of life sub-scores of group 2 were significantly higher. The patients in both groups were found to be depressed and hopeless about the future. Anxiety levels were found to be significantly higher in all of the patients in both groups. Conclusion: Acute coronary syndrome before coronary artery bypass surgery impairs more the quality of life in mental terms. But unexpectedly there are no differences in terms of depression, hopelessness, anxiety and fear of death.

Impact of experiencing acute coronary syndrome prior to open heart surgery on psychiatric status

Abstract Objective: The incidence of depression and anxiety is higher in patients with acute coronary syndrome. The aim of this study is to determine whether experiencing acute coronary syndrome prior to open heart surgery affects patients in terms of depression, hopelessness, anxiety, fear of death and quality of life. Methods: The study included 63 patients who underwent coronary bypass surgery between January 2015 and January 2016. The patients were divided into two groups: those diagnosed after acute coronary syndrome (Group 1) and those diagnosed without acute coronary syndrome (Group 2). Beck depression scale, Beck hopelessness scale, Templer death anxiety scale and death depression scale, State-Trait anxiety inventory and WHOQOL-Bref quality of life scale were applied. Results: There was no significant difference between the two groups in terms of the total score obtained from Beck depression scale, Beck hopelessness scale - future-related emotions, loss of motivation, future-related expectations subgroups, death anxiety scale, the death depression scale, State-Trait Anxiety Inventory - social and environmental subgroups. The mental quality of life sub-scores of group 2 were significantly higher. The patients in both groups were found to be depressed and hopeless about the future. Anxiety levels were found to be significantly higher in all of the patients in both groups. Conclusion: Acute coronary syndrome before coronary artery bypass surgery impairs more the quality of life in mental terms. But unexpectedly there are no differences in terms of depression, hopelessness, anxiety and fear of death.

Expression of Ghrelin and GHSR-1a in Long Term Diabetic Rat's Kidney

The aim of this work was to study the relative ghrelin and growth hormone secretagogue receptor (GHS-R)1a gene expression in the kidney of long-term diabetic rats. Forty male Wistar albino rats were divided into four groups: C- control group, DI- one month diabetic rats group, DII- two months diabetic rats group, and DIII- three months diabetic rats group. Diabetes was induced by streptozotocin STZ (40mg/kg i.p). The rats were decapitated under ketamine anesthesia and their kidney tissues were removed. Tissue GHS-R mRNA levels, ghrelin expression, and histopathological damage scores were compared. Dilatation in the distal tubules, epithelial desquamation into the lumen of the tubules and transparent tubules showing glycogen vacuolation were observed in all the diabetic groups. Ghrelin immunoreactivity was significantly higher in group DI compared to group C, whereas in groups DII and DIII, ghrelin immunoreactivity was similar with group C. GHSR-1a mRNA level in group DIII was significantly lower than in group C. As a result, ghrelin immunoreactivity increased at the beginning of diabetes; however, with increase in the duration of diabetes ghrelin immunoreactivity approached to the control values. The expression of GHSR-1a mRNA decreased with increase in diabetes duration. It seemed that down-regulation of GHSR-1a contributed to the renal damage induced by long-term diabetes.

Selenium protects cerebral cells by cisplatin induced neurotoxicity.

PURPOSE: To evaluate the central nervous system toxicity of cisplatin and neuroprotective effect of selenium. METHODS: Twenty-one male Wistar albino rats were divided into three groups: control (C), cisplatin (CS), cisplatin and selenium (CSE, n=7 in each group). Cisplatin (12 mg/kg/day, i.p.) was administered to CS and CSE groups for three days. Furthermore, CSE group received 3mg/kg/day (twice-a-day as 1.5 mg/kg) selenium via oral gavage five days before cisplatin injection and continued for 11 consecutive days. The same volumes of saline were administered to C group intraperitoneally and orally at same time. RESULTS: Heterochromatic and vacuolated neurons and dilated capillary vessels in the brain were observed in the histochemical examinations of cisplatin treated group. Rats that were given a dose of 3mg/kg/day selenium decreased the cisplatin induced histopathological changes in the brain, indicating a protective effect. In addition, cytoplasmic staining of the cell for bcl-2, both cytoplasmic and nuclear staining for bax were determined to be positive in the all groups. Bax positive cells were increased in the CS group compared to C group, in contrast to decreased bcl-2 positivity. CONCLUSION: Selenium limited apototic activity and histological changes due to the cisplatin related central neurotoxicity.

Selenium protects cerebral cells by cisplatin induced neurotoxicity

PURPOSE: To evaluate the central nervous system toxicity of cisplatin and neuroprotective effect of selenium. METHODS: Twenty-one male Wistar albino rats were divided into three groups: control (C), cisplatin (CS), cisplatin and selenium (CSE, n=7 in each group). Cisplatin (12 mg/kg/day, i.p.) was administered to CS and CSE groups for three days. Furthermore, CSE group received 3mg/kg/day (twice-a-day as 1.5 mg/kg) selenium via oral gavage five days before cisplatin injection and continued for 11 consecutive days. The same volumes of saline were administered to C group intraperitoneally and orally at same time. RESULTS: Heterochromatic and vacuolated neurons and dilated capillary vessels in the brain were observed in the histochemical examinations of cisplatin treated group. Rats that were given a dose of 3mg/kg/day selenium decreased the cisplatin induced histopathological changes in the brain, indicating a protective effect. In addition, cytoplasmic staining of the cell for bcl-2, both cytoplasmic and nuclear staining for bax were determined to be positive in the all groups. Bax positive cells were increased in the CS group compared to C group, in contrast to decreased bcl-2 positivity. CONCLUSION: Selenium limited apototic activity and histological changes due to the cisplatin related central neurotoxicity. .

Selenium protects cerebral cells by cisplatin induced neurotoxicity

PURPOSE:To evaluate the central nervous system toxicity of cisplatin and neuroprotective effect of selenium.METHODS:Twenty-one male Wistar albino rats were divided into three groups: control (C), cisplatin (CS), cisplatin and selenium (CSE, n=7 in each group). Cisplatin (12 mg/kg/day, i.p.) was administered to CS and CSE groups for three days. Furthermore, CSE group received 3mg/kg/day (twice-a-day as 1.5 mg/kg) selenium via oral gavage five days before cisplatin injection and continued for 11 consecutive days. The same volumes of saline were administered to C group intraperitoneally and orally at same time.RESULTS:Heterochromatic and vacuolated neurons and dilated capillary vessels in the brain were observed in the histochemical examinations of cisplatin treated group. Rats that were given a dose of 3mg/kg/day selenium decreased the cisplatin induced histopathological changes in the brain, indicating a protective effect. In addition, cytoplasmic staining of the cell for bcl-2, both cytoplasmic and nuclear staining for bax were determined to be positive in the all groups. Bax positive cells were increased in the CS group compared to C group, in contrast to decreased bcl-2 positivity.CONCLUSION:Selenium limited apototic activity and histological changes due to the cisplatin related central neurotoxicity.(AU)