Non-Einstein Viscosity Phenomenon of Acrylonitrile–Butadiene–Styrene Composites Containing Lignin–Polycaprolactone Particulates Highly Dispersed by High-Shear Stress

Lignin powder was modified via ring-opening polymerization of caprolactone to form a lignin–polycaprolactone (LPCL) particulate. The LPCL particulates were mixed with an acrylonitrile–butadiene–styrene (ABS) matrix at an extremely high rotational speed of up to 3000 rpm, which was achieved by a closed-loop screw mixer and in-line melt extruder. Using this high-shear extruding mixer, the LPCL particulate size was controlled in the range of 3395 nm (conventional twin-screw extrusion) down to 638 nm (high-shear mixer of 3000 rpm) by altering the mixing speed and time. The resulting LPCL/ABS composites clearly showed non-Einstein viscosity phenomena, exhibiting reduced viscosity (2130 Pa·s) compared to the general extruded composite one (4270 Pa·s) at 1 s–1 and 210 °C. This is due to the conformational rearrangement and the increased free volume of ABS molecular chains in the vicinity of LPCL particulates. This was supported by the decreased glass transition temperature (Tg, 83.7 °C) of the LPCL/ABS composite specimens, for example, giving a 21.8% decrement compared to that (107 °C) of the neat ABS by the incorporation of 10 wt % LPCL particulates in ABS. The LPCL particulate morphology, damping characteristics, and light transmittance of the developed composites were thoroughly investigated at various levels of applied shear rates and mixing conditions. The non-Einstein rheological phenomena stemming from the incorporation of LPCL particulates suggest an interesting plasticization methodology: to improve the processability of high-loading filler/polymer composites and ultra-high molecular weight polymers that are difficult to process because of their high viscosity

Polymorphism of a COLIA1 Gene Sp1 Binding Site in Korean Women with Pelvic Organ Prolapse

PURPOSE: To evaluate the possible influence of G-->T substitution at the Sp1-binding site of the COLIA1 gene on the risk of pelvic organ prolapse (POP). MATERIALS AND METHODS: The study group consisted of 15 women with advanced stage POP. Fifteen control subjects with uterine myomas among the postmenopausal women were matched for age and parity. DNA was obtained from peripheral blood leukocytes. The fragments of the first intron of the COLIA1 gene were amplified by real time polymerase chain reaction. The polymorphism was identified using LightCycler Technology with hybridization probes. Sequencing reactions were performed on each template using commercial primer. RESULTS: Two groups had no significant difference in medical history, surgical, and smoking history. The homozygous peaks in two groups were noted at 57 on melting curve analysis. Sequencing reactions confirmed the G/G alleles in the 30 specimens tested. We could not find any polymorphism at the Sp1-binding site in COLIA1 gene with advanced stage POP. Statistical significance was considered to be p < .05. CONCLUSION: The polymorphism of the Sp1-binding site in the COLIA1 gene did not contribute to the development of POP in Korea.ope

COMPARISON STUDY OF EXPERIMENTS AND PREDICTIONS OF WAVE KINEMATICS FOR ROGUE WAVE

To investigate the wave kinematics under the rogue wave crest, a series of experiments were performed in 2-D wave tank with the application of PIV technique to measure the velocities under the free surface. Three different prediction methods of linear extrapolation, Wheeler stretching, and modified stretching were applied to estimate water wave kinematics and compared with PIV experimental results under the highest wave crest of irregular wave trains satisfying with rogue wave criteria. Also, the cut-off frequency dependence for three prediction methods was investigated with varying spectral peak frequencies to estimate wave kinematics including velocities and accelerations in horizontal and vertical directions. It was suggested that the cut-off frequency for the reasonable prediction of the wave kinematics under the rogue wave crest could be chosen three times of spectral peak wave frequency for the linear extrapolation and higher frequency than four times of spectral peak wave frequency for Wheeler stretching and modified stretching method

An Electrophilic Deguelin Analogue Inhibits STAT3 Signaling in H-Ras-Transformed Human Mammary Epithelial Cells: The Cysteine 259 Residue as a Potential Target

Signal transducer and activator of transcription 3 (STAT3) is a point of convergence for numerous oncogenic signals that are often constitutively activated in many cancerous or transformed cells and some stromal cells in the tumor microenvironment. Persistent STAT3 activation in malignant cells stimulates proliferation, survival, angiogenesis, invasion, and tumor-promoting inflammation. STAT3 undergoes activation through phosphorylation on tyrosine 705, which facilitates its dimerization. Dimeric STAT3 translocates to the nucleus, where it regulates the transcription of genes involved in cell proliferation, survival, etc. In the present study, a synthetic deguelin analogue SH48, discovered by virtual screening, inhibited the phosphorylation, nuclear translocation, and transcriptional activity of STAT3 in H-ras transformed human mammary epithelial MCF-10A cells (MCF10A-ras). We speculated that SH48 bearing an alpha,beta-unsaturated carbonyl group could interact with a thiol residue of STAT3, thereby inactivating this transcription factor. Non-electrophilic analogues of SH48 failed to inhibit STAT3 activation, lending support to the above supposition. By utilizing a biotinylated SH48, we were able to demonstrate the complex formation between SH48 and STAT3. SH48 treatment to MCF10A-ras cells induced autophagy, which was verified by staining with a fluorescent acidotropic probe, LysoTracker Red, as well as upregulating the expression of LC3II and p62. In conclusion, the electrophilic analogue of deguelin interacts with STAT3 and inhibits its activation in MCF10A-ras cells, which may account for its induction of autophagic death.

A Computational Model of the Temperature-dependent Changes in Firing Patterns in Aplysia Neurons

We performed experiments using Aplysia neurons to identify the mechanism underlying the changes in the firing patterns in response to temperature changes. When the temperature was gradually increased from 11℃ to 31℃ the firing patterns changed sequentially from the silent state to beating, doublets, beating-chaos, bursting-chaos, square-wave bursting, and bursting-oscillation patterns. When the temperature was decreased over the same temperature range, these sequential changes in the firing patterns reappeared in reverse order. To simulate this entire range of spiking patterns we modified nonlinear differential equations that Chay and Lee made using temperature-dependent scaling factors. To refine the equations, we also analyzed the spike pattern changes in the presence of potassium channel blockers. Based on the solutions of these equations and potassium channel blocker experiments, we found that, as temperature increases, the maximum value of the potassium channel relaxation time constant, τn(t) increases, but the maximum value of the probabilities of openings for activation of the potassium channels, n(t) decreases. Accordingly, the voltage-dependent potassium current is likely to play a leading role in the temperature-dependent changes in the firing patterns in Aplysia neurons

Enzymatic synthesis of chlorogenic acid glucoside using dextransucrase and its physical and functional properties

Chlorogenic acid, a major polyphenol in edible plants, possesses strong antioxidant activity, anti-lipid peroxidation and anticancer effects. It used for industrial applications; however, this is limited by its instability to heat or light. In this study, we, for the first time synthesized chlorogenic acid glucoside (CHG) via transglycosylation using dextransucrase from Leuconostoc mesenteroides and sucrose. CHG was purified and its structure determined by nuclear magnetic resonance and matrix-associated laser desorption ionization–time-of-flight mass spectroscopy. The production yield of CHG was 44.0% or 141 mM, as determined by response surface methodology. CHG possessed a 65% increase in water solubility and a 2-fold browning resistance and it displayed stronger inhibition of lipid peroxidation and of colon cancer cell growth by MTT assay, compared to chlorogenic acid. Therefore, this study may expand the industrial applications of chlorogenic acid as water-soluble or browning resistant compound (CHG) through enzymatic glycosylation

Fasting Plasma Glucose Cutoff Value for the Prediction of Future Diabetes Development: A Study of Middle-Aged Koreans in a Health Promotion Center

We determined optimal fasting plasma glucose (FPG) cutoff values predictive of future diabetes development in a group of middle-aged Koreans who visited a health promotion center. The medical records of 2,964 subjects, who attended the Health Promotion Center in 1998 and 2003, were examined. Subjects were classified into four groups according to their baseline FPG values (Group 1:FPG <5.0 mM/L; Group 2: 5.0≤FPG <5.6 mM/L; Group 3: 5.6≤FPG <6.1 mM/L; Group 4: 6.1≤FPG <7.0 mM/L). No significant difference was observed between Group 1 and Group 2 in terms of diabetes incidence. However, incidence in Group 3 was significantly higher than that in Group 1 [hazards ratio 4.88 (1.65-14.41), p=0.004] and the hazards ratio in Group 4 for diabetes was 36.91 (13.11-103.61), p<0.001, versus Group 1. Receiver operator characteristics curve analysis showed that an FPG of 5.97 mM/L represents the lower limit and gives the best combination of sensitivity and specificity. Our data shows that the risk of future diabetes development started to increase below an FPG of 6.1 mM/L and suggests the importance of efforts to modify diabetes development risk factors at lower impaired fasting glucose levels

HOXB13 promotes androgen independent growth of LNCaP prostate cancer cells by the activation of E2F signaling

<p>Abstract</p> <p>Background</p> <p>Androgen signaling plays a critical role in the development of prostate cancer and its progression. However, androgen-independent prostate cancer cells emerge after hormone ablation therapy, resulting in significant clinical problems. We have previously demonstrated that the HOXB13 homeodomain protein functions as a prostate cancer cell growth suppressor by inhibiting androgen-mediated signals. However, the role of the HOXB13 in androgen-independent growth of prostate cancer cells remains unexplained.</p> <p>Results</p> <p>In this report, we first demonstrated that HOXB13 was highly overexpressed in hormone-refractory tumors compared to tumors without prostate-specific antigen after initial treatment. Functionally, in an androgen-free environment minimal induction of HOXB13 in LNCaP prostate cancer cells, to the level of the normal prostate, markedly promoted cell proliferation while suppression inhibited cell proliferation. The HOXB13-mediated cell growth promotion in the absence of androgen, appears to be mainly accomplished through the activation of RB-E2F signaling by inhibiting the expression of the p21^waftumor suppressor. Indeed, forced expression of HOXB13 dramatically decreased expression of p21^waf; this inhibition largely affected HOXB13-mediated promotion of E2F signaling.</p> <p>Conclusions</p> <p>Taken together, the results of this study demonstrated the presence of a novel pathway that helps understand androgen-independent survival of prostate cancer cells. These findings suggest that upregulation of HOXB13 is associated with an additive growth advantage of prostate cancer cells in the absence of or low androgen concentrations, by the regulation of p21-mediated E2F signaling.</p

Two Lung Masses with Different Responses to Pemetrexed

We described here a patient who had two lung masses. Although the two masses had the same histology and a similar good response to initial chemotherapy with gemcitabine and carboplatin, the response to pemetrexed as a second-line treatment was different after re-growth of the tumors. These two lung masses could have originated from different clones or they could have progressed through different paths of molecular pathogenesis after metastasis, which would lead to different tumor characteristics, including their chemosensitivity. Regardless of their pathogenetic mechanisms, it seems important to recognize that tumors with the same histology that develop in one patient can have different responses to drugs