Relationship between Lymphocytes, IL2 and the Hormones E2, LH, PRG and FSH in Menopausal and Postmenopausal Women

Proble

Which is Better: Stainless Steel or Titanium Alloy?

WOS: 000437251200018AIM: To investigate immunologic reactions after implantation of stainless steel (SS) alloy and titanium (Ti) alloy in a rat model. Macrophage and cytokine responses have been reported after in vivo and in vitro application of different biomaterials. MATERIAL and METHODS: Wistar albino rats were used. After an exploration of the thoracolumbar paravertebral muscle tissue of the subjects, Group I underwent sham surgery, and Groups II and III underwent implantation of Ti alloy and SS alloy rods respectively. The CD4, CD8, CD25 (IL-2R) (lymphocyte and CD4 gate), CD4+CD8+ and CD4+CD25+Foxp3+ (Tregs), IL-4, IL-10, IL-6, IL-17A, TGF-beta,TNF-alpha in the blood were analyzed. RESULTS: CD4, CD25 (IL-2R), CD4+CD8+ and Tregs levels were lower in Group III compared to Group I (sham) and Group II. IL-6, IL-17A, TGF-beta and TNF-alpha levels in Group III showed a significant increase on all days in comparison with Group I and Group II. IL-4 and IL-10 levels were lower in Group III than those in Group II; and a significant decrease was observed in the IL-10 level. There was a reduction in IL-6 and IL-17A levels in Group II as opposed to Group I. CONCLUSION: As opposed to SS alloy, Ti alloy suppresses the development of inflammation by inhibiting the pro-inflammatory response; strengthens the humoral immune system by intensifying the antibody-dependent immune response; triggers the development of immune tolerance by regulating the immune response; and activates the mechanism that prevents immune response-related damage from occurring

beta-carotene treatment alters the cellular death process in oxidative stress-induced K562 cells

Oxidizing agents (e.g., H2O2) cause structural and functional disruptions of molecules by affecting lipids, proteins, and nucleic acids. As a result, cellular mechanisms related to disrupted macro molecules are affected and cell death is induced. Oxidative damage can be prevented at a certain point by antioxidants or the damage can be reversed. In this work, we studied the cellular response against oxidative stress induced by H2O2 and antioxidant-oxidant (-carotene-H2O2) interactions in terms of time, concentration, and treatment method (pre-, co-, and post) in K562 cells. We showed that co- or post-treatment with-carotene did not protect cells from the damage of oxidative stress furthermore co- and post-beta-carotene-treated oxidative stress induced cells showed similar results with only H2O2 treated cells. However, -carotene pre-treatment prevented oxidative damage induced by H2O2 at concentrations lower than 1,000 mu M compared with only H2O2-treated and co- and post-beta-carotene-treated oxidative stress-induced cells in terms of studied cellular parameters (mitochondrial membrane potential [Delta psi(m)], cell cycle and apoptosis). Prevention effect of beta-carotene pre-treatment was lost at concentrations higher than 1,000 mu M H2O2 (2-10mM). These findings suggest that beta-carotene pre-treatment alters the effects of oxidative damage induced by H2O2 and cell death processes in K562 cells

K562 cells display different vulnerability to H2O2 induced oxidative stress in differing cell cycle phases

Oxidative stress can be defined as the increase of oxidizing agents like reactive oxygen and nitrogen species, or the imbalance between the antioxidative defense mechanism and oxidants. Cell cycle checkpoint response can be defined as the arrest of the cell cycle functioning after damaging chemical exposure. This temporary arrest may be a period of time given to the cells to repair the DNA damage before entering the cycle again and completing mitosis. In order to determine the effects of oxidative stress on several cell cycle phases, human erytroleukemia cell line (K562) was synchronized with mimosine and genistein, and cell cycle analysis carried out. Synchronized cells were exposed to oxidative stress with hydrogen peroxide (H2O2) at several concentrations and different times. Changes on mitochondria membrane potential (m) of K562 cells were analyzed in G(1), S, and G(2)/M using Rhodamine 123 (Rho 123). To determine apoptosis and necrosis, stressed cells were stained with Annexin V (AnnV) and propidium iodide (PI) for flow cytometry. Changes were observed in the m of synchronized and asynchronized cells that were exposed to oxidative stress. Synchronized cells in S phase proved resistant to the effects of oxidative stress and synchronized cells at G(2)/M phase were sensitive to the effects of H2O2-induced oxidative stress at 500M and above

IMPORTANCE OF ALDH ACTIVITY IN HEMATOPOIETIC STEM CELL ISOLATION

Objective: The preferred method for the purification of hematopoietic stem cells (HSCs), which can easily differentiate into blood cells, is the selection of CD34(+) cells by flow cytometry or magnetic discrimination. Methods are needed that effectively determine human stem cells without entirely relying on phenotypic cell surface markers. One of these methods is cytosolic aldehyde dehydrogenase (ALDH), which plays a role in retinoid metabolism and resistance of HSCs to alkylating agents such as cyclophosphamide. The prospective isolation of human hematopoietic stem and progenitor cells with different functions, as well as surface markers, are also recommended by ALDH and flow cytometry. In the above findings, ALDH(+) cells can be isolated from other cells and the most primitive hematopoietic stem cells can be isolated and used in clinical applications

Hemin-dependent induction and internalization of CD38 in K562 cells.

The cell surface antigen, CD38, is a bifunctional ecto-enzyme, which is predominantly expressed on hematopoietic cells during differentiation. In the present study, it is shown that hemin treatment of K562 cells gives rise to induction of enzymatic activities inherent to CD38. GDP-ribosyl cyclase activity, an indicator of CD38, increased initially in response to hemin in a time-dependent manner, reached a maximum level on the 5th day and, thereafter, declined sharply to the initial level. The increase in NAD(+) glycohydrolase and ADP-ribose uptake activities followed a similar time course. However, the decline in the latter activities after the 5th day of induction appeared to be rather slow in contrast to GDP-ribosyl cyclase activity. The time course of these changes was well correlated with the FACScan findings obtained by use of anti-CD38 monoclonal antibody. SDS-PAGE and Western blot analyses by use of the monoclonal antibody OKT10 revealed a transient hemin-dependent appearence of a 43 kDa membrane protein with maximum signal intensity on the first 4 days of incubation. There was subsequently a gradual decrease on the 5th day, concomitant with a reciprocal increase in activity of the internalized protein fraction. The results together indicated that hemin-induced expression of CD38 was followed by its down-regulation. (C) 2003 Wiley-Liss, Inc

CD133+cells are associated with ADIPOCYTOKINES and endothelial dysfunction in hemodialysis patients

Background: Hemodialysis (HD) patients have increased risk of cardiovascular disease (CVD). Impaired stem cell health and adipocytokine metabolism may play important roles in the complex pathophysiological mechanisms of CVD in this patient population. We aimed to investigate the relationships between CD133+ cell counts, adipocytokines and parameters of endothelial dysfunction and atherosclerosis in HD patients

CD133+ cells are associated with ADIPOCYTOKINES and endothelial dysfunction in hemodialysis patients

Abstract Background Hemodialysis (HD) patients have increased risk of cardiovascular disease (CVD). Impaired stem cell health and adipocytokine metabolism may play important roles in the complex pathophysiological mechanisms of CVD in this patient population. We aimed to investigate the relationships between CD133+ cell counts, adipocytokines and parameters of endothelial dysfunction and atherosclerosis in HD patients. Methods In 58 chronic HD patients (male/female:28/30, mean age:58 ± 14 years), serum levels of interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), leptin, adiponectin and resistin were measured by ELISA. Left ventricular mass index (LVMI), carotid intima-media thickness (CIMT), flow-mediated dilatation (FMD) of the brachial artery were measured. CD133+ cells were counted by flow cytometry (BD FACSCalibur-BD Bioscience,CA). Results CD133+ cell counts were inversely associated with FMD (r = −0.39, p = 0.007) and positively correlated with serum resistin (r = 0.45, p < 0.001) and serum TNF-α (r = 0.31, p = 0.02). Serum leptin levels were higher in high CD133 group compared to low CD133 group [32.37(12.74–72.29) vs 15.50(5.38–37.12)ng/mL, p = 0.03]. Serum leptin levels were correlated with TNF-α(r = 0.35, p = 0.009). Serum adiponectin levels were negatively correlated with serum leptin (r = −0.28, p = 0.03). Serum resistin levels were associated with TNF-α (r = 0.54, p < 0.001) and leptin (r = 0.29, p = 0.03). Serum IL-6 levels were significantly associated with LVMI (r = 0.31, p = 0.03). Serum IL-6 levels were significantly higher in patients with carotid plaque compared to patients without plaque [12.75(9.91–28.68) vs 8.27(5.97–14.04) pg/mL, p = 0.02]. In multiple linear regression analysis to determine the factors predicting LogFMD; dialysis vintage, LVMI and LogCD133+ cell counts were included as independent variables(R = 0.57, adjusted R-square = 0.27, p = 0.001). CD133+ cell count and LVMI were found to significantly predict FMD (p = 0.03 and p = 0.04 respectively). Conclusion CD133+ cells were associated with inflammation and endothelial dysfunction in HD patients. Serum leptin, resistin and TNF-α levels were positively related to CD133+ cell count. Impaired regulation of undifferentiated stem cells and adipocytokines might contribute to endothelial dysfunction in HD patients

A stimulatory role of ozone exposure on human natural killer cells

Ozone is claimed to have beneficial effects. While studies revealed the safe therapeutic use of ozone, there are conflicting results for the link between immune system and ozone encounter. Natural killer (NK) cells are important sentinels of immunity with their cytotoxic activity and immune-regulatory potentials. This study aimed to investigate the effects of direct ozone encountering on human immune system, at cellular level. Survival, proliferative capacity and subset content of peripheral blood mononuclear cells (PBMC) were analysed. PBMC of healthy donors (n = 5, mean age: 27 +/- 6 years) were exposed to 1, 5, 10 and 50 mu g/mL doses of medical ozone, directly injected into culture wells, once, initially. 1 and 5 mu g/mL doses didn't show toxic effects while 10 and 50 mu g/mL doses were toxic. PBMC were cultured for 5 days following 1 and 5 mu g/mL ozone encountering. 1 mu g/mL dose increased numbers of CD3(-)CD16(+)/56(+) NK cells among PBMC. Following stimulation with ozone, no difference was observed in basal and phytohemaglutinin-stimulated proliferative capacity. 1 and 5 mu g/mL doses of ozone were found to increase NK cytotoxicity. These data indicates influential effects of transient ozone exposure on NK cells, which in turn may have a role in control of immune responses