DISCUSSION OF MECHANISM ON LUMBAR DISC HERNIATION TREATED WITH BLOODLETTING ON W■IZH■NG(委中BL40)

Objective To observe the changes of sciatic nerve conduction velocity （SNCV） and interleukin-1α （IL-1α）, phospholipase A2 （PLA2） and prostaglandin E2 （PGE2） in neucleus pulposus tissue in experimental rabbits with lumbar disc herniation （LDH） ; and discuss the mechanism of LDH treated with bloodletting on Wěizhōng （委中 BL40）. Methods 40 normal named control group, LDH model group, BL40 group New Zealand rabbits were randomized into 4 groups, and comparative point group. The experimental LDH model was prepared by the self-made LDH animal pathological modeling device. Bloodletting on BL40 or on comparative point was applied for 7 days. BL-410 physiological signal recorder was used to record SNCV. Enzyme-linked immunosorbent assay （ELISA） and radioimmunology methods were used to determine the contents of IL-1α and PLA2 in neucleus pulposus tissue and PGE2 in serum. Results In BL40 group, SNCV was significantly increased after treatment comparing with that before treatment （P〈0. 01 ）, and the difference in SNCV value before and after treatment was significantly bigger than that in model group and comparative point group （P〈0.05）. Bloodletting on BL40 reduced the contents of IL-1α and PLA2 in neucleus pulposus tissue and serum PGE2 in LDH rabbits, which indicated significant difference or very significant results in the comparison with model and comparative point groups （P〈0.01 or 0. 05）. Conclusion Bloodletting speeded up rapidly SNCV and reduced the contents of inflammatory factors, i.e. IL-1α, PLA2 and serum PGE2 in LDH rabbits, which indicated that alleviation of local inflammatory reaction is probably one of the mechanisms on LDH treated by bloodletting on BL40.

Temperature dependence of heat conduction coefficient in nanotube/nanowire networks

Studies on heat conduction are so far mainly focused on regular systems such as the one-dimensional（1D） and twodimensional（2D） lattices where atoms are regularly connected and temperatures of atoms are homogeneously distributed.However, realistic systems such as the nanotube/nanowire networks are not regular but heterogeneously structured, and their heat conduction remains largely unknown. We present a model of quasi-physical networks to study heat conduction in such physical networks and focus on how the network structure influences the heat conduction coefficient κ. In this model,we for the first time consider each link as a 1D chain of atoms instead of a spring in the previous studies. We find that κ is different from link to link in the network, in contrast to the same constant in a regular 1D or 2D lattice. Moreover, for each specific link, we present a formula to show how κ depends on both its link length and the temperatures on its two ends.These findings show that the heat conduction in physical networks is not a straightforward extension of 1D and 2D lattices but seriously influenced by the network structure.

First principles insights into oxide/polymer composites: SrTiO_(3) /polyaniline/graphene

A detailed computational investigation,based on density functional theory,of the interaction of polyani-line(PANI)and graphene nanoribbons(GNRs)with SrTiO_(3) is presented.The adsorption of PANI in var-ious oxidation states and co-adsorption with GNRs is found to be thermodynamically favourable.Ad-sorbed PANI introduces N and C 2p states into the SrTiO_(3) bandgap,while co-adsorption of PANI and GNRs leads to a bridging of the gap and semi-metallic behaviour,thus rendering the electrical properties highly sensitive to the loading of the GNRs/PANI in the composites.Modelling the lattice dynamics of the composites predicts a 68-88%reduction in the lattice thermal conductivity due to reduced phonon group velocities.Taken together,these findings provide insight into the growing number of experimental studies highlighting the enhanced thermoelectric performance of oxide-polymer composites and indicate co-adsorption with graphene as a facile direction for future research.

Forensic Significance of Messenger RNA and Protein Expression of Genes Downstream of Hypoxia Inducible Factor 2 in Myocardial Tissue for Death Discrimination

Background: As a heterodimeric transcription factor, hypoxia-inducible factor 2 alpha subunit (HIF2A), is an important member of the HIF family. It plays a significant role in the hypoxia adaptation process by regulating the different types of downstream transcription factors and auxiliary regulatory factors. HIF2A-related factors are believed to participate in the progression of myocardial injury or myocardial ischemia, support the protection of ischemic myocardium, and provide guiding significance for the diagnosis and discrimination of sudden cardiac death in forensic pathology. Aim and Objectives: This study aimed to explore the discriminability and applicability of HIF2A-related factors in myocardial infarction cases compared with other causes of death, provide further insights for the forensic diagnosis of heart failure (HF) cases with myocardial infarction, and support the clinical treatment of patients with HF after myocardial infarction. Materials and Methods: The relative expression levels of HIF2A, amphiregulin (AREG), potassium large conductance calcium-activated channel subfamily M β1 (KCNMB1), peroxisome proliferator-activated receptor α (PPARA), vascular endothelial growth factor (VEGF), and VEGFR2 messenger RNAs (mRNAs) in myocardial tissue samples were performed using quantitative reverse transcriptase-polymerase chain reaction. A partial least squares-discriminant analysis model was constructed to select the indicators with better identification effects for myocardial infarction cases. The protein levels of HIF2A, AREG, KCNMB1, and PPARA were further detected by immunohistochemistry. The forensic autopsy cases (27 cases in total, postmortem interval <72 h) included seven cases of acute myocardial infarction and ten cases of myocardial ischemia. There were ten cases in the control group, including four cases of traffic injury, one case of injury by fall from height, and five cases of blunt force injury. Results: Characteristic results were observed in the myocardial ischemia/infarction samples. Compared with the control group, the relative mRNA expression levels of AREG, KCNMB1, and PPARA were significantly increased during the progression of myocardial ischemia, but this was not observed for HIF2A, VEGF, or VEGFR2 mRNA. Immunohistochemistry assays further verified the expression levels of the related factors at the protein level, and H and E staining showed signs of angiogenesis and inflammation in the ischemia/infarction group. Conclusions: By controlling the expression of downstream target genes (AREG, KCNMB1, and PPARA) during myocardial cell hypoxia adaptation, HIF2A has a potential significance in the diagnosis of myocardial infarction in forensic medicine. We believe that HIF2A, AREG, KCNMB1, and PPARA can be used as molecular pathological biomarkers for the discrimination of causes of death in myocardial infarction cases.