Indoor and Outdoor Tests for a Chemi-capacitance Carbon Nanotube Sensor Installed on a Quadrotor Unmanned Aerial Vehicle for Dimethyl Methylphosphonate Detection and Mapping.

Unmanned aerial vehicles (UAVs) have been used as a new chemical reconnaissance platform in chemical, biological, radiological, and nuclear detection and in industrial monitoring and environmental research, owing to their mobility, unconventional accessibility, and safety. Based on the UAV's payload and operational time considerations, the ultralight chip-sized chemical sensor is the most promising candidate for chemical reconnaissance among various chemical sensors. To optimize the UAV's chip-sensor performance, realistic outdoor tests of chemical sensors during UAV flights have to be conducted to verify their performances. In this study, indoor and outdoor experiments were conducted with a carbon nanotube (CNT)-based chip sensor installed on the UAV to detect dimethyl methylphosphonates (DMMPs), commonly used as chemical warfare agent simulants. Based on the indoor tests, DMMP concentrations and the position/direction of the CNT sensor were analyzed to optimize the sensing performances during UAV operations. Based on outdoor tests, we confirmed that the chemical sensor mounted on the UAV could detect DMMP gases by moving designated pathways in realistic conditions.

Anatomical basis of pronator teres for electromyography needle placement using ultrasonography.

OBJECTIVE: To find the optimal needle insertion site for needle electromyography of the pronator teres (PT) muscle among commonly used sites. METHODS: Fifty forearms of 25 healthy subjects were evaluated. Four expected needle insertion points were designated as follows. Point 0 was positioned at the midpoint between the medial epicondyle and medial border of biceps tendon in the elbow crease. Points 1, 2, and 3 were located 2 cm, 3.5 cm and 5 cm distal to point 0, respectively. We assumed that the thickness of PT and the distances between a vertical line from each point to the medial margin of the PT were significant parameters for finding the optimal site. Thus, we measured these parameters through ultrasonographic examination. RESULTS: In men, the PT was thickest at point 2, and in women, at point 1. The distance between the expected needle insertion line and medial margin of PT was longest at point 1 in both men and women, and was statistically significant compared to points 2 and 3. Both men and women had neurovascular bundles located lateral to the expected needle insertion line. CONCLUSION: The most appropriate and safe needle electromyographic insertional site for the PT is 2-3.5 cm distal to the mid-point between the biceps tendon and medial epicondyle in the elbow crease and the needle should be inserted upward and medial.

Ethanolic extract of Taheebo attenuates increase in body weight and fatty liver in mice fed a high-fat diet.

We evaluated whether intake of an ethanolic extract of Taheebo (TBE) from Tabebuia avellanedae protects against body weight increase and fat accumulation in mice with high-fat diet (HFD)-induced obesity. Four-week old male C57BL/6 mice were fed a HFD (25% fat, w/w) for 11 weeks. The diet of control (HFD) mice was supplemented with vehicle (0.5% sodium carboxymethyl cellulose by gavage); the diet of experimental (TBE) mice was supplemented with TBE (150 mg/kg body weight/day by gavage). Mice administered TBE had significantly reduced body weight gain, fat accumulation in the liver, and fat pad weight, compared to HFD mice. Reduced hypertrophy of fat cells was also observed in TBE mice. Mice administered TBE also showed significantly lower serum levels of triglycerides, insulin, and leptin. Lipid profiles and levels of mRNAs and proteins related to lipid metabolism were determined in liver and white adipose tissue of the mice. Expression of mRNA and proteins related to lipogenesis were decreased in TBE-administered mice compared to mice fed HFD alone. These results suggest that TBE inhibits obesity and fat accumulation by regulation of gene expression related to lipid metabolism in HFD-induced obesity in mice.

Influence of Resistance Exercise Training to Strengthen Muscles across Multiple Joints of the Lower Limbs on Dynamic Balance Functions of Stroke Patients.

[Purpose] The objective of this study was to evaluate the effects of resistance exercise training for strengthening muscles across multiple joints on the dynamic balance function of stroke patients. [Subjects and Methods] Subjects in the training group (n=14) and the control group (n=14) received conservative physical therapy for 30 minutes per day, five days per week, for a period of six weeks. The training group additionally performed three sets (eight to 10 repetitions per set) of resistance exercise at 70% of the 1-repetition maximum (1RM) to strengthen muscles across multiple joints. The control group did the same exercises for the same duration but without resistance. To assess dynamic balance function, before and after the intervention, we measured antero-posterior (A-P) and medio-lateral (M-L) sway distances, the Berg balance scale (BBS), and the timed up and go (TUG) times. [Results] Compared to pre-intervention values, the BBS score showed significant increases in both groups, and A-P and M-L sway distances and TUG times showed significant decreases in both groups. Changes in A-P and M-L sway distances, BBS scores, and TUG times were significantly different between the muscle training group and the control group. [Conclusion] Training involving muscle strength across multiple joints is an effective intervention for improvement of dynamic balance function of stroke patients.

Study on evaporation characteristics of a sessile drop of sulfur mustard on glass.

The evaporation characteristics (evaporation rates and process) of a sessile drop of sulfur mustard on glass has been studied using a laboratory-sized wind tunnel, gas chromatograph mass spectrometry, and drop shape analysis. It showed that the evaporation rates of the droplet increased with temperature and air flow. The effect of temperature on the rates was more pronounced at lower air flow. Air flow was less effective at lower temperature. The contact angle of the droplet was initially observed as θ = 19.5° ± 0.7 and decreased linearly with time until it switched to a constant mode.

Extensive intramuscular venous malformation in the lower extremity.

Typical venous malformations are easily diagnosed by skin color changes, focal edema or pain. Venous malformation in the skeletal muscles, however, has the potential to be missed because their involved sites are invisible and the disease is rare. In addition, the symptoms of intramuscular venous malformation overlaps with myofascial pain syndrome or muscle strain. Most venous malformation cases have reported a focal lesion involved in one or adjacent muscles. In contrast, we have experienced a case of intramuscular venous malformation that involved a large number of muscles in a lower extremity extensively.

Pharmacological stimulation of NADH oxidation ameliorates obesity and related phenotypes in mice.

OBJECTIVE: Nicotinamide adenine dinucleotides (NAD+ and NADH) play a crucial role in cellular energy metabolism, and a dysregulated NAD+-to-NADH ratio is implicated in metabolic syndrome. However, it is still unknown whether a modulating intracellular NAD+-to-NADH ratio is beneficial in treating metabolic syndrome. We tried to determine whether pharmacological stimulation of NADH oxidation provides therapeutic effects in rodent models of metabolic syndrome. RESEARCH DESIGN AND METHODS: We used beta-lapachone (betaL), a natural substrate of NADH:quinone oxidoreductase 1 (NQO1), to stimulate NADH oxidation. The betaL-induced pharmacological effect on cellular energy metabolism was evaluated in cells derived from NQO1-deficient mice. In vivo therapeutic effects of betaL on metabolic syndrome were examined in diet-induced obesity (DIO) and ob/ob mice. RESULTS: NQO1-dependent NADH oxidation by betaL strongly provoked mitochondrial fatty acid oxidation in vitro and in vivo. These effects were accompanied by activation of AMP-activated protein kinase and carnitine palmitoyltransferase and suppression of acetyl-coenzyme A (CoA) carboxylase activity. Consistently, systemic betaL administration in rodent models of metabolic syndrome dramatically ameliorated their key symptoms such as increased adiposity, glucose intolerance, dyslipidemia, and fatty liver. The treated mice also showed higher expressions of the genes related to mitochondrial energy metabolism (PPARgamma coactivator-1alpha, nuclear respiratory factor-1) and caloric restriction (Sirt1) consistent with the increased mitochondrial biogenesis and energy expenditure. CONCLUSIONS: Pharmacological activation of NADH oxidation by NQO1 resolves obesity and related phenotypes in mice, opening the possibility that it may provide the basis for a new therapy for the treatment of metabolic syndrome.

Presenilin mutations linked to familial Alzheimer's disease cause an imbalance in phosphatidylinositol 4,5-bisphosphate metabolism.

Phosphatidylinositol 4,5-bisphosphate (PIP2) is an important cellular effector whose functions include the regulation of ion channels and membrane trafficking. Aberrant PIP2 metabolism has also been implicated in a variety of human disease states, e.g., cancer and diabetes. Here we report that familial Alzheimer's disease (FAD)-associated presenilin mutations cause an imbalance in PIP2 metabolism. We find that the transient receptor potential melastatin 7 (TRPM7)-associated Mg2+ -inhibited cation (MIC) channel underlies ion channel dysfunction in presenilin FAD mutant cells, and the observed channel deficits are restored by the addition of PIP2, a known regulator of the MIC/TRPM7 channel. Lipid analyses show that PIP2 turnover is selectively affected in FAD mutant presenilin cells. We also find that modulation of cellular PIP2 closely correlates with 42-residue amyloid beta-peptide (Abeta42) levels. Our data suggest that PIP2 imbalance may contribute to Alzheimer's disease pathogenesis by affecting multiple cellular pathways, such as the generation of toxic Abeta42 as well as the activity of the MIC/TRPM7 channel, which has been linked to other neurodegenerative conditions. Thus, our study suggests that brain-specific modulation of PIP2 may offer a therapeutic approach in Alzheimer's disease.

Regulation of magnesium-inhibited cation current by actin cytoskeleton rearrangement.

Magnesium-inhibited, non-selective cation current (I(MIC)) is activated by depletion of intracellular Mg(2+) and ATP. I(MIC) transports various divalent cations including Mg(2+) and Ca(2+), and is involved in cell viability. We investigated the effect of actin dynamics on I(MIC). Formation of a stable cortical actin network by calyculin A inhibited the activation of I(MIC), while the actin depolymerizing reagent, cytochalasin D, reversed the inhibition. Induction of a dense cortical actin layer by transfecting the constitutively active form of RhoA also inhibited the activation of I(MIC). These results suggest that the activation of I(MIC) may be dynamically regulated by actin cytoskeleton rearrangement.

Modulation of delayed rectifier potassium channels by alpha1-adrenergic activation via protein kinase C zeta and p62 in PC12 cells.

When PC12 cells are exposed to nerve growth factor (NGF), they extend neurites and express autonomic ganglion cell properties. We have previously shown that NGF is capable of inducing p62 expression, enabling the formation of the protein kinase C zeta (PKCzeta)-p62-Kvbeta (beta-subunit of delayed rectifier K+ channel) complex, a Kv channel-modulating complex. The formation of this complex results in the shifting of the Kv channel activation curve to the left via PKCzeta activity. During the experiments, we noted that PC12 cells in a high-density culture exhibited a Kv channel activation curve shift similar to that observed in the NGF-treated cells. Therefore, we hypothesized that catecholamines released from PC12 cells may induce p62 expression. In order to test this idea, cells in a low-density culture were treated for 24h with norepinephrine (NE). In these cells, we noted a leftward shift of the activation curve. The presence of the alpha1-adrenergic antagonist specifically prevented the effects of NE. Pre-treatment of the low-density cells with alpha1-agonists induced changes similar to those associated with NE, confirming that NE modulates Kv channels via the alpha1-adrenergic receptor. NE's effects were blocked by treatment with PKCzeta specific inhibitors. Using Western blotting, we observed increased levels of p62 expression in both the high-density cells and the NE-treated low-density cells. These results suggest that locally secreted NE induces an increase in p62 expression, and also exerts a modulatory effect on Kv channels via the PKCzeta-p62-Kvbeta channel modulating complex.