An integrated theory and computer program were developed in this study for simulation of shrinkage, warpage, and sink marks of crystalline polymer injection molded parts. The basic theory considers the following items: (1) mold cooling analysis; (2) analysis of the polymeric filling, packing, and cooling processes; (3) viscoelastic behavior of polymeric fluid; (4) influence of thermal and mechanical properties of polymer; (5) pressure‐volume‐temperature relationship of polymer; (6) crystallization kinetics of crystalline polymer; and (7) solid mechanics analysis. Considered are the origins of defects, e.g. nonuniform cooling process, nonuniform volume shrinkage, flow‐induced residual stress, thermal induced residual stress, and crystallization behavior. The boundary element and the finite difference method were applied toward calculating the mold cooling analysis for obtaining the temperature profile at the cavity surface as the boundary conditions in filling and packing analysis. A hybrid finite‐element and finite‐difference methods were employed for simulating the injection molding filling, packing, and cooling processes. A control volume method was applied towards both finding the melt front position and also calculating the temperature and pressure profile at any instant during the filling process. A modified Tait equation provided a description of the pressure‐volume‐temperature relationship of crystalline polymers. The Malkin's kinetics model was employed to describe the behavior of polymer crystallization. The flow‐induced and thermal induced‐residual stresses employed as the initial conditions in the solid mechanics analysis were obtained with the linear thermo‐viscoelastic model. The displacements, including the thickness direction of part, which could not be calculated by the traditional bending moment method, were solved by using the numerical solid mechanics analysis with the three dimensional finite element method. These methods were applied to predict the shrinkage, warpage, and sink marks of crystalline polypropylene and amorphous ABS for the plate cavity. Both the qualitative results for the theoretical prediction correlated sufficiently with the experimental data. The theoretical results were also correlated using the commercial software C‐MOLD.

BackgroundOur previous studies suggested that deoxyschizandrin (DSD) and schisantherin A (STA) may have cardioprotective effects, but information in this regard is lacking. Therefore, we explored the protective role of DSD and STA in myocardial ischemia–reperfusion (I/R) injury.Methodology/Principal FindingsAnesthetized male rats were treated once with DSD and STA (each 40 µmol/kg) through the tail vein after 45 min of ischemia, followed by 2-h reperfusion. Cardiac function, infarct size, biochemical markers, histopathology and apoptosis were measured and mRNA expression of gp91phox in myocardial tissue assessed by RT-PCR. Neonatal rat cardiomyocytes were pretreated with DSD and STA and then damaged by H2O2. Cell apoptosis was tested by a flow cytometric assay. Compared with the I/R group: (i) DSD and STA could significantly reduce the abnormalities of LVSP, LVEDP, ±dp/dtmax and arrhythmias, thereby showing their protective roles in cardiac function; (ii) DSD and STA could significantly attenuate the infarct size and MDA release while increasing SOD activity, suggesting a role in reducing myocardial injury; (iii) tissue morphology and myocardial textual analysis revealed that DSD and STA mitigated changes in myocardial histopathology; (iv) DSD and STA decreased apoptosis (33.56±2.58% to 10.28±2.80% and 10.98±1.99%, respectively) and caspase-3 activity in the myocardium (0.62±0.02 OD/mg to 0.38±0.02 OD/mg and 0.32±0.02 OD/mg, respectively), showing their protective effects upon cardiomyocytes; and (v) DSD and STA had similar protective effects on I/R injury as those seen with the positive control metoprolol. In vitro, DSD and STA could significantly decrease the apoptosis of neonatal cardiomyocytes.Conclusions/SignificanceThese data suggest that DSD and STA can protect against myocardial I/R injury. The underlining mechanism may be related to their role in inhibiting cardiomyocyte apoptosis.

Coamorphous systems using citric acid as a small molecular excipient were studied for improving physical stability and bioavailability of loratadine, a BCS class II drug with low water solubility and high permeability. Coamorphous loratadine-citric acid systems were prepared by solvent evaporation technique and characterized by differential scanning calorimetry, X-ray powder diffraction, and Fourier transform infrared spectroscopy. Solid-state analysis proofed that coamorphous loratadine-citric acid system (1:1) was amorphous and homogeneous, had a higher T over amorphous loratadine, and the intermolecular hydrogen bond interactions between loratadine and citric acid exist. The solubility and dissolution of coamorphous loratadine-citric acid system (1:1) were found to be significantly greater than those of crystalline and amorphous form. The pharmacokinetic study in rats proved that coamorphous loratadine-citric acid system (1:1) could significantly improve absorption and bioavailability of loratadine. Coamorphous loratadine-citric acid system (1:1) showed excellently physical stability over a period of 3 months at 25°C under 0% RH and 25°C under 60% RH conditions. The improved stability of coamorphous loratadine-citric acid system (1:1) could be related to an elevated T over amorphous form and the intermolecular hydrogen bond interactions between loratadine and citric acid. These studies demonstrate that the developed coamorphous loratadine-citric acid system might be a promising oral formulation for improving solubility and bioavailability of loratadine.

A sensitive, fast, and effective method, field-amplified sample stacking (FASS) in capillary electrophoresis, has been established for the separation and determination of corynoxine and corynoxine B. Hydroxypropyl-β-CD (HP-β-CD) and tetrabutylammonium-L-glutamic acid (TBA-L-Glu) were used as additives in the separation system. Electrokinetic injection was chosen to introduce sample from inlet at 10 kV for 50 s after a water plug (0.5 psi, 4 s) was injected to permit FASS. The running buffer (pH 6.1) was composed of 40 mM sodium dihydrogen phosphate solution, 130 mM HP-β-CD, and 10 mM TBA-L-Glu and the separation voltage was 20 kV. Under the optimum conditions, corynoxine and corynoxine B were successfully enriched and separated within 12 min and the sensitivity was improved approximately by 700-900 folds. Calibration curves were in a good linear relationship within the range of 62.5-5.00 × 10 ng/mL for both corynoxine and corynoxine B. The limits of detection (S/N = 3) and quantitation (S/N = 10) were 14.9, 45.2 ng/mL for corynoxine and 11.2, 34.5 ng/mL for corynoxine B, respectively. Finally, this method was successfully applied for the determination of corynoxine and corynoxine B in the stems with hooks of Uncaria rhynchophylla and its formulations.

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