Novel polyvinyl chloride composite via hybrid metal-organic framework grafted polyethyleneimine and layered double hydroxide incorporation: Thermal, rheological, and electrical properties

Improving the heat stabilization of polyvinyl chloride (PVC) is of great importance, particularly for its use in electrical insulation. In this study, a novel zeolitic imidazole framework (ZIF-8) was modified using polyethyleneimine (PEI) and layered double hydroxide (LDH) to create a new PVC heat stabilizer. The heat stability of PVC was analyzed using oven, Congo red, and thermogravimetric analysis (TGA) tests, with the dosage of modified ZIF-8 found to have a significant impact on PVC's heat stability (increasing from 33 to 58 min). Additionally, con-calorimetry was performed to evaluate the effect of LDH modification on ZIF-8′s flame retardancy, revealing that LDH delayed flame emission from 255 to 560 s. Lastly, volume resistance and mechanical tests were conducted to assess the effect of the novel ZIF-8 modification on PVC compound properties

Ceramide 1-phosphate enhances calcium entry through voltage-operated calcium channels by a protein kinase C-dependent mechanism in GH4C1 rat pituitary cells.

Sphingomyelin derivatives modulate a multitude of cellular processes, including the regulation of [Ca2+]i (the intracellular free calcium concentration). Previous studies have shown that these metabolites often inhibit calcium entry through VOCCs (voltage-operated calcium channels). In the present study, we show that, in pituitary GH4C1 cells, C1P (C2-ceramide 1-phosphate) enhances calcium entry in a dose-dependent manner. The phospholipase C inhibitor U73122 attenuated the response. C1P invoked a small, but significant, increase in the formation of inositol phosphates. Pre-treatment of the cells with pertussis toxin was without an effect on the C1P-evoked increase in [Ca2+]i. The effect of C1P was critically dependent on extracellular calcium, since no increase in [Ca2+]i was observed when cells in a calcium-free buffer were stimulated with C1P. Furthermore, if the cells were retreated with 300 nM of the VOCC inhibitor nimodipine, the effect of C1P was almost totally abolished. In addition, ceramide C8-1-phosphate evoked an increase in [Ca2+]i, but the onset of the response was slow compared with that of C1P. In cells treated with 1 mM thapsigargin for 15 min, C1P still evoked an increase in [Ca2+]i. In patch-clamp experiments in the whole-cell mode, C1P enhanced calcium entry through the VOCCs compared with vehicle-treated cells. Dialysis of the cells with C1P did not enhance the calcium current. On-cell patch-clamp experiments showed an enhanced probability of the VOCCs being open (P(open)) in the presence of C1P. Inhibition of PKC (protein kinase C) with GF109203X and down-regulation of PKC with PMA attenuated the C1P-evoked increase in [Ca2+]i. Furthermore, down-regulation of PKC abolished the effect of C1P on P(open). This is the first report showing that a sphingomyelin derivative enhances calcium entry through VOCCs

Fetal but not adult Leydig cells are susceptible to adenoma formation in response to persistently high hCG level; a study on hCG overexpressing transgenic mice

We have previously demonstrated that male transgenic (TG) mice overexpressing human chorionic gonadotropin (hCG+) develop reproductive organ defects, but no tumors, in adult age. In this study, the effects of persistently elevated hCG were followed in TG males between day 5 postpartum and adulthood. Leydig cell (LC) adenomas were found in prepubertal mice, most prominently at the age of 10 days, but not in adult age. Serum testosterone concentrations were significantly increased in TG males at all ages studied. The phenotype of the prepubertal hCG+ males resembled that found in boys upon expression of constitutively activating luteinizing hormone (LH) receptor mutations. The temporal expression patterns of the fetal LC marker gene, thrombospondin 2, and those of adult LCs, hydroxysteroid dehydrogenase-6, delta5-3-beta and prostaglandin D synthase, were similar in wild-type and hCG+ males. Hence, the postnatal adenomas resemble functionally fetal LCs, and only these cells are susceptible to hCG-induced tumorigenesis. Our findings demonstrate a novel intriguing difference between the fetal and adult LC populations and provide further insight into the potential tumorigenic effects of gonadotropins.Fil: Ahtianen, Petteri. University of Turku; FinlandiaFil: Rulli, Susana Beatriz. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; ArgentinaFil: Shariatmadari, Ramin. University of Turku; FinlandiaFil: Pelliniemi, Lauri J.. University of Turku; FinlandiaFil: Toppari, Jorma. University of Turku; FinlandiaFil: Poutanen, Matti. University of Turku; FinlandiaFil: Huhtaniemi, Ilpo T.. University of Turku; Finlandia. Imperial College London; Reino Unid