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In this study, a new organic nucleating agent N, N -bis(stearic acid)-1,4-dicarboxybenzene dihydrazide (PASH) to improve crystallization behavior of poly(L-lactic acid) (PLLA) along with the effect of PASH on melting behavior, thermal stability of PASH-nucleated PLLA was holistically reported. The melt-crystallization process illustrated that PASH as an effective heterogeneous nucleating agent could boost PLLA�s crystallization rate, but increasing PASH concentration and cooling rate conversely inhibited melt-crystallization process of PLLA in this study. With respect to melt-crystallization process, a larger amount of PASH leaded to a shift of cold-crystallization peak to lower temperature level. Isothermal crystallization revealed, in comparison to pure PLLA, that the half time of overall crystallization of PLLA/PASH was significantly decreased with PLLA containing 3 wt% PASH having the minimum t1/2= 67.3 s at 105şC. The different melting behaviors of PLLA/PASH under different conditions were attributed to the nucleating effect of PASH within PLLA. In particular, the melting behavior at a heating rate of 10�C/min after isothermal crystallization depended primarily on the crystallization temperature. Whereas, the impact of crystallization time on melting behavior was negligible. Nonetheless, the melting behavior was influenced by the heating rate after non-isothermal crystallization. The thermal stability of PLLA was detrimental with the addition of PASH owing to a typical drop in onset thermal decomposition temperature.

An in vitro model to study myocardial cell injury was developed with primary monolayer cultures of rat myocardial cells. Two important conditions associated with myocardial ischemia were simulated by depriving the cultures of oxygen and glucose for a specified period of time. Cellular injury caused by hypoxia and glucose deprivation resulted in significant leakage of lactate dehydrogenase (LDH) from the cells into the culture medium. The cells were not lethally injured by treatments as reflected by a lack of change in cell viability and protein content when compared to controls. Pretreatment of cultures with methylprednisolone for 24 hr provided protection to the cells when challenged by hypoxia and glucose deprivation. Methylprednisolone exhibited a dose-response effect in reducing LDH leakage in cultures, which were subsequently deprived of oxygen and glucose for 4 hr. Similar pretreatment with hydrocortisone had no effect in limiting cellular injury in hypoxic and glucose-deprived cultures.

Primary monolayer cultures of rat myocardial cells were used to study the cellular injury that occurs when calcium is reintroduced after a period of calcium depletion. Cultures were treated with a calcium-free balanced salt solution (BSS) for 2 h and were then incubated for different time periods in the presence of normocalcemic BSS (2.5 mM CaCl2). Myocyte calcium content was determined after the calcium-free period and after incubation in the presence of calcium. Leakage of cytoplasmic lactate dehydrogenase (LDH) into the medium was used as an index of cell injury. At the end of the calcium-free period there was a significant decrease in the total cellular content of calcium, and LDH release was minimal. After incubation in normocalcemic BSS, the myocyte calcium content increased progressively with time and cellular injury was manifested by significant leakage of LDH. The calcium content of treated cells reached control levels 10 min after calcium repletion. Maximal leakage of LDH was observed 60 min after the restoration of calcium. The calcium content of treated cultures was higher than that of control cultures 120 min after incubation in normocalcemic BSS.

Primary cultures of rat myocytes were deprived of oxygen (approximately 5 mm Hg, pO2) for 2 h in the presence or absence of calcium and were subsequently incubated for different time periods under normoxic (approximately 120 mm Hg, pO2) conditions. Myocyte calcium content was determined at the end of the oxygen-free period and after repletion of oxygen. Lactate dehydrogenase (LDH) release from the cells into the medium was used as an index of cell injury. Cultures deprived of oxygen in the absence of calcium showed a significant decrease in myocyte calcium content at the end of the oxygen-free period. However, the calcium content of myocyte cultures deprived of oxygen in the presence of calcium did not change significantly. The enzyme release of both groups of oxygen-deprived cultures was similar to that of controls. A progressive increase in myocyte calcium content was observed 5, 10, 15, and 30 min after repletion of oxygen in both groups. Reoxygenation of cultures subjected to hypoxia in the presence of calcium caused minimal LDH leakage. However, major enzyme release was observed 30 min after oxygen repletion in cultures previously subjected to hypoxia in a calcium-free environment. The present study shows that reoxygenation injury is more severe in myocyte cultures previously deprived of both oxygen and calcium than in cultures deprived of oxygen in the presence of calcium.

The threshold for pentylenetetrazol (PTZ)-induced clonic seizures is below control levels 15 min after administration of apomorphine (APO) but above them 60 min after APO administration. Pretreatment with ascorbic acid (10 mg/kg) or the presence of ascorbic acid in the APO solution (1 mg/ml) inhibited the early (15 min) decrease in seizure threshold caused by 60 mg/kg APO and reversed the increase in seizure threshold 60 min after a 50 mg/kg APO challenge. Ascorbate co-administration concomitant with APO also counteracted the increase in seizure threshold 60 min after 70 mg/kg APO. Results suggest a potential model for modulation of a seizure system through dietary supplementation.

Based on previous work examining the effects of dextroamphetamine on pentylenetetrazol (PTZ)-induced clonic seizure threshold, the objective of the present study was to determine the effects of two other dopamine agonists, apomorphine (AP) and piribedil, on PTZ seizures. TD50 and LD50 values for CD-1 mice were determined initially for the two drugs. Subsequently, dose-and time-response analyses established that AP decreased PTZ seizure threshold 15 min after administration, but increased the threshold at 60 min. Piribedil elevated the seizure threshold, but like AP, did not exhibit a clear dose-response relationship. Subsequent blocker studies with phentolamine, (-)sotalol, pimozide, and atropine suggested the possible neurotransmitter systems involved in the modulation of the PTZ-induced seizures by AP and piribedil. Pimozide blocked the changes in seizure threshold induced by both drugs. Atropine also decreased the AP-induced increase in threshold at 60 min. The pattern of inhibition of seizure threshold changes induced by the neurotransmitter blockers suggested that piribedil blocked seizures by means of indirect actions on several neurotransmitters.

Primary cultures of rat heart endothelial cells were subjected to simulated conditions of ischemia: hypoxia and glucose deprivation for 4 and 24 hr. Cellular injury was evaluated by measuring changes in viability, total protein, cellular morphology, and leakage of cytoplasmic enzymes from the cells into the culture medium. Deprivation of oxygen and glucose for 4 or 24 hr did not lethally injure the cells as noted by no change in cell viability, morphology, and total protein when compared to controls. However, reversible or nonlethal cellular injury was produced as reflected by a significant release of lactate dehydro-genase (LDH) from the cells into the medium after treatment with hypoxia and glucose deprivation for 4 or 24 hr. When the cultures were deprived of glucose, but were oxygenated, cellular injury was not evident after 24 hr. Deprivation of oxygen but not glucose resulted in significant loss of LDH after 4 or 24 hr. When the cultures were allowed to recover after oxygen and glucose deprivation in complete medium containing 1000 mg glucose per l and a normal atmosphere of 20% O2, they had levels of LDH leakage comparable to those of control cultures.