In this paper, mm-Pose, a novel approach to detect and track human skeletons in real-time using an mmWave radar, is proposed. To the best of the authors' knowledge, this is the first method to detect >15 distinct skeletal joints using mmWave radar reflection signals. The proposed method would find several applications in traffic monitoring systems, autonomous vehicles, patient monitoring systems and defense forces to detect and track human skeleton for effective and preventive decision making in real-time. The use of radar makes the system operationally robust to scene lighting and adverse weather conditions. The reflected radar point cloud in range, azimuth and elevation are first resolved and projected in Range-Azimuth and Range-Elevation planes. A novel low-size high-resolution radar-to-image representation is also presented, that overcomes the sparsity in traditional point cloud data and offers significant reduction in the subsequent machine learning architecture. The RGB channels were assigned with the normalized values of range, elevation/azimuth and the power level of the reflection signals for each of the points. A forked CNN architecture was used to predict the real-world position of the skeletal joints in 3-D space, using the radar-to-image representation. The proposed method was tested for a single human scenario for four primary motions, (i) Walking, (ii) Swinging left arm, (iii) Swinging right arm, and (iv) Swinging both arms to validate accurate predictions for motion in range, azimuth and elevation. The detailed methodology, implementation, challenges, and validation results are presented.

Acute ischemic stroke (AIS), as the third leading cause of death worldwide, is characterized by its high incidence, mortality rate, high incurred disability rate, and frequent reoccurrence. The neuroprotective effects of Ginkgo biloba extract (GBE) against several cerebral diseases have been reported in previous studies, but the underlying mechanisms of action are still unclear. Using a novel in vitro rat cortical capillary endothelial cell-astrocyte-neuron network model, we investigated the neuroprotective effects of GBE and one of its important constituents, Ginkgolide B (GB), against oxygen-glucose deprivation/reoxygenation and glucose (OGD/R) injury. In this model, rat cortical capillary endothelial cells, astrocytes, and neurons were cocultured so that they could be synchronously observed in the same system. Pretreatment with GBE or GB increased the neuron cell viability, ameliorated cell injury, and inhibited the cell apoptotic rate through Bax and Bcl-2 expression regulation after OGD/R injury. Furthermore, GBE or GB pretreatment enhanced the transendothelial electrical resistance of capillary endothelial monolayers, reduced the endothelial permeability coefficients for sodium fluorescein (Na-F), and increased the expression levels of tight junction proteins, namely, ZO-1 and occludin, in endothelial cells. Results demonstrated the preventive effects of GBE on neuronal cell death and enhancement of the function of brain capillary endothelial monolayers after OGD/R injury in vitro; thus, GBE could be used as an effective neuroprotective agent for AIS/reperfusion, with GB as one of its significant constituents.

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Ginseng, the famous plant drug, has been used as an expensive traditional medicine in oriental countries. The main ginsenosides in the drug ginseng are the ginsenoside Rb 1 , Rb 2 , Rc, Rd, Re, Rf and Rg 1 , and other ginsenoside content was low, the ginsenosides such as Rg 3 , Rg 2 , Rg 5 , Rh 2 , Rh 1 , Rh 3 and Rh 4 are minor ginsenosides in the red ginseng or wild ginseng. These minor ginsenoside Rg 3 , Rg 5 , Rg 2 , Rg 4 , Rh 2 , Rh 3 , Rh 1 and Rh 4 have special physiological activities: for example, the ginsenoside Rh 2 , Rh 3 , Rg 3 and Rh 1 have a good anticancer property, but haven't sideeffects; the ginsenoside Rg 3 and Rg 2 have anti-thrombus and mediating endothelium. So, the minor ginsenosides are very useful for the drug and health food. However, it is very difficult to obtain the minor ginsenoside from the red and wild ginseng, because the contents in the red ginseng and wild ginseng are very low. 1)The metabolism of ginsenosides by human intestinal bacteria was reported to express the ginsenoside hydrolyzing behaviors in human intestinal, to prove the ginseng saponin hy- So, when the ginsenosidase type I hydrolyzed ginsenosides, the enzyme selected ginsenoside-aglycone type, can hydrolyze different glycosides of PPD type ginsenoside; however no selected glycoside type, can hydrolyze multi-glycosides of PPD type ginsenosides. These properties were novel properties, and differentiated with the other previously described glycosidases.

BackgroundMinor ginsenosides, those having low content in ginseng, have higher pharmacological activities. To obtain minor ginsenosides, the biotransformation of American ginseng protopanaxadiol (PPD)-ginsenoside was studied using special ginsenosidase type-I from Aspergillus niger g.848.MethodsDEAE (diethylaminoethyl)-cellulose and polyacrylamide gel electrophoresis were used in enzyme purification, thin-layer chromatography and high performance liquid chromatography (HPLC) were used in enzyme hydrolysis and kinetics; crude enzyme was used in minor ginsenoside preparation from PPD-ginsenoside; the products were separated with silica-gel-column, and recognized by HPLC and NMR (Nuclear Magnetic Resonance).ResultsThe enzyme molecular weight was 75 kDa; the enzyme firstly hydrolyzed the C-20 position 20-O-β-D-Glc of ginsenoside Rb1, then the C-3 position 3-O-β-D-Glc with the pathway Rb1→Rd→F2→C-K. However, the enzyme firstly hydrolyzed C-3 position 3-O-β-D-Glc of ginsenoside Rb2 and Rc, finally hydrolyzed 20-O-L-Ara with the pathway Rb2→C-O→C-Y→C-K, and Rc→C-Mc1→C-Mc→C-K. According to enzyme kinetics, Km and Vmax of Michaelis–Menten equation, the enzyme reaction velocities on ginsenosides were Rb1 > Rb2 > Rc > Rd. However, the pure enzyme yield was only 3.1%, so crude enzyme was used for minor ginsenoside preparation. When the crude enzyme was reacted in 3% American ginseng PPD-ginsenoside (containing Rb1, Rb2, Rc, and Rd) at 45°C and pH 5.0 for 18 h, the main products were minor ginsenosides C-Mc, C-Y, F2, and C-K; average molar yields were 43.7% for C-Mc from Rc, 42.4% for C-Y from Rb2, and 69.5% for F2 and C-K from Rb1 and Rd.ConclusionFour monomer minor ginsenosides were successfully produced (at low-cost) from the PPD-ginsenosides using crude enzyme.

We have recently reported that Ginsenoside Rh2 (G-Rh2) induces the activation of two initiator caspases, caspase-8 and caspase-9 in human cancer cells. However, the molecular mechanism of its death-inducing function remains unclear. Here we show that G-Rh2 stimulated the activation of both caspase-8 and caspase-9 simultaneously in HeLa cells. Under G-Rh2 treatment, membrane death receptors Fas and TNFR1 are remarkably upregulated. However, the induced expression of Fas but not TNFR1 was contributed to the apoptosis process. Moreover, significant increases in Fas expression and caspase-8 activity temporally coincided with an increase in p53 expression in p53-non-mutated HeLa and SK-HEP-1 cells upon G-Rh2 treatment. In contrast, Fas expression and caspase-8 activity remained constant with G-Rh2 treatment in p53-mutated SW480 and PC-3 cells. In addition, siRNA-mediated knockdown of p53 diminished G-Rh2-induced Fas expression and caspase-8 activation. These results indicated that G-Rh2-triggered extrinsic apoptosis relies on p53-mediated Fas over-expression. In the intrinsic apoptotic pathway, G-Rh2 induced strong and immediate translocation of cytosolic BAK and BAX to the mitochondria, mitochondrial cytochrome c release, and subsequent caspase-9 activation both in HeLa and in SW480 cells. p53-mediated Fas expression and subsequent downstream caspase-8 activation as well as p53-independent caspase-9 activation all contribute to the activation of the downstream effector caspase-3/-7, leading to tumor cell death. Taken together, we suggest that G-Rh2 induces cancer cell apoptosis in a multi-path manner and is therefore a promising candidate for anti-tumor drug development.Electronic supplementary materialThe online version of this article (doi:10.1007/s13238-014-0027-2) contains supplementary material, which is available to authorized users.

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