In this study, a platinum(II) complex ([Pt(H2L)(PPh3)] complex) containing a thiocarbohydrazone as the ligand was tested as an anti-proliferative agent against ovarian adenocarcinoma (Caov-3) and human colorectal adenocarcinoma (HT-29) through MTT assays. Apoptotic markers were tested by the AO/PI double staining assay and DNA fragmentation test. Flow cytometry was conducted to measure cell cycle distribution, while the p53 and caspase-8 pathways were tested via immunofluorescence assay. Results demonstrated that the cytotoxic effect of the Pt(II)- thiocarbohydrazone complexes against Caov-3 and HT-29 cells was highly significant, and this effect triggered the activation of the p53 and caspase-8 pathways. Besides, apoptosis stimulated by the Pt(II)-thiocarbohydrazone complex was associated with cell cycle arrest at the G0/G1 phase. These findings suggest that the target complex inhibited the proliferation of Caov-3 and HT-29 cells, resulting in the arrest of the cell cycle and induction of apoptosis via the stimulation of the p53 and caspase-8 pathways. The present data suggests that the Pt(II)-thiocarbohydrazone complex could also be a promising chemotherapeutic agent for other types of cancer cells.
SAPO-11 is synthesized from silicoaluminophosphate in the presence of di-n-propylamine as a template. The results show that the sample obtained has good crystallinity, 396m2/g BET surface area, and 0.35 cm3/g pore volume. The hydroisomerization activity of (0.25)Pt (1)Zr (0.5)W/SAPO-11 catalyst was determined using n-decane and base oil. All hydroisomerization experiments of n-decane were achieved at a fixed bed plug flow reactor at a temperature range of 200-275°C and LHSV 0.5-2h-1. The results show that the n-decane conversion increases with increasing temperature and decreasing LHSV, the maximum conversion of 66.7 % was achieved at temperature 275°C and LHSV of 0.5 h-1
... Show MoreThe mean age of AS patients was (35.0 ± 9.8) years.When the patients and control subjects were divided into different age groups (>40, 30-40, <30 years), the differences were not significantin terms of disease prevalence. The results also showed that the percentage of male patients is higher than that of females. There was no significant difference (P?0.05) between patients and controls in the distribution of males and females.Most of the patients had the disease for a period of 5 years or higher, with a disease severity of ? 2.1 and functional disability degree of I, II. The resultsshoweddifferent patterns of distribution for the three tested cytokines. A significant increase in the level of TNF-?, anon-significantincrease i
... Show MoreWe can summarize the main risk factors for type 2 diabetes mellitus (T2DM) by looking at our nutrition, age, and lifestyle. β-cell dysfunction and insulin resistance (IR) are outcomes of the pathophysiology of type 2 diabetes. As an indirect result of IR on important metabolic enzymes, lipid and lipoprotein abnormalities are also a factor in T2DM patients. Recent research has indicated that lipid fluctuation may be the cause of poor glucose metabolism as well as one of its effects. Fatty acids (FAs) affect cell membrane fluidity and permeability, insulin receptor binding and signaling, and the translocation of glucose transporters. Therefore, it is suggested that FAs might play a crucial part in the emergence of IR and T2DM.
We can summarize the main risk factors for type 2 diabetes mellitus (T2DM) by looking at our nutrition, age, and lifestyle. β-cell dysfunction and insulin resistance (IR) are outcomes of the pathophysiology of type 2 diabetes. As an indirect result of IR on important metabolic enzymes, lipid and lipoprotein abnormalities are also a factor in T2DM patients. Recent research has indicated that lipid fluctuation may be the cause of poor glucose metabolism as well as one of its effects. Fatty acids (FAs) affect cell membrane fluidity and permeability, insulin receptor binding and signaling, and the translocation of glucose transporters. Therefore, it is suggested that FAs might play a crucial part in the emergence of IR and T2DM. The cu
... Show MoreWe can summarize the main risk factors for type 2 diabetes mellitus (T2DM) by looking at our nutrition, age, and lifestyle. β-cell dysfunction and insulin resistance (IR) are outcomes of the pathophysiology of type 2 diabetes. As an indirect result of IR on important metabolic enzymes, lipid and lipoprotein abnormalities are also a factor in T2DM patients. Recent research has indicated that lipid fluctuation may be the cause of poor glucose metabolism as well as one of its effects. Fatty acids (FAs) affect cell membrane fluidity and permeability, insulin receptor binding and signaling, and the translocation of glucose transporters. Therefore, it is suggested that FAs might play a crucial part in the emergence of IR and T2DM. The cu
... Show MoreThe reaction of poly (vinyl alcohol) (PV A) with Urea in (DMSO) resulted in uerthanised oxim, wr,ich reacted with diacetylmonoxime in a (DY.ISOfmethanol) to give anew type (N2) polymeric bidentate imine oxime ligand [HL], The ligand was reacted with MCh (where M= Co, Cu, and Hg). Under reflux in a (DMF/Methanol) mixture with (I:1) ratio to give Complexes of the general formula [M (T.)2]X, (where M= Co,Hg, Cu). All .:ompouncs have been characterized by spectroscopic methods [IR, U.V.-Vis, A tomi<;absorption] microanalysis along with conductivity measurements, from the above:: data the proposed molecular structure for Co,Cu, and Hg is a distorted. Tetrahedml
The compound 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), an environmental contaminant, is a potent ligand for aryl hydrocarbon receptor (AhR). In the current study, we made an exciting observation that naive C57BL/6 mice that were exposed i.p. to TCDD showed massive mobilization of myeloid-derived suppressor cells (MDSCs) in the peritoneal cavity. These MDSCs were highly immunosuppressive and attenuated Con A–induced hepatitis upon adoptive transfer. TCDD administration in naive mice also led to induction of several chemokines and cytokines in the peritoneal cavity and serum (CCL2, CCL3, CCL4, CCL11, CXCL1, CXCL2, CXCL5, CXCL9, G-CSF, GM-CSF, VEGF, and M-CSF) and chemokine receptors