This paper presents a novel algorithm to reconstruct parameters of a sufficient number of current dipoles that describe data (equivalent current dipoles, ECDs, hereafter) from radial/vector magnetoencephalography (MEG) with and without electroencephalography (EEG). We assume a three-compartment head model and arbitrary surfaces on which the MEG sensors and EEG electrodes are placed. Via the multipole expansion of the magnetic field, we obtain algebraic equations relating the dipole parameters to the vector MEG/EEG data. By solving them directly, without providing initial parameter guesses and computing forward solutions iteratively, the dipole positions and moments projected onto the xy-plane (equatorial plane) are reconstructed from a single time shot of the data. In addition, when the head layers and the sensor surfaces are spherically symmetric, we show that the required data reduce to radial MEG only. This clarifies the advantage of vector MEG/EEG measurements and algorithms for a generally-shaped head and sensor surfaces. In the numerical simulations, the centroids of the patch sources are well localized using vector/radial MEG measured on the upper hemisphere. By assuming the model order to be larger than the actual dipole number, the resultant spurious dipole is shown to have a much smaller strength magnetic moment (about 0.05 times smaller when the SNR = 16 dB), so that the number of ECDs is reasonably estimated. We consider that our direct method with greatly reduced computational cost can also be used to provide a good initial guess for conventional dipolar/multipolar fitting algorithms.

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Objective The precise relationship between alcohol intake and metabolic syndrome (MetS) is still unclear, and the results from previous studies have been inconclusive. Thus, we examined the effect of alcohol intake on the risk of MetS in men in order to gain more information on a potential relationship. Methods This study included 22,349 men who were divided into four groups according to their average alcohol intake [non-, light (less than 20 g ethanol/day), heavy (equal or more than 20 g and less than 60 g ethanol/day) and very heavy (equal and greater than 60 g ethanol/day) drinkers]. We measured each subject's body mass index (BMI), waist circumference and blood pressure (BP) and conducted a blood test to obtain a complete blood count and biochemical panel. These results were used to obtain the MetS prevalence. Additionally, fatty liver was diagnosed using abdominal ultrasonography. Results Light drinkers had smaller waist circumferences. Heavy and very heavy drinkers had larger waist circumferences, a higher BMI, a higher BP, higher fasting plasma glucose levels, higher triglycerides (TG) levels and higher high-density lipoprotein (HDL) cholesterol levels while they had lower low-density lipoprotein cholesterol levels than nondrinkers. The prevalence of high BP, hyperglycemia and high TG was significantly higher in heavy and very heavy drinkers than in nondrinkers. The prevalence of low HDL cholesterol levels decreased with an increase in alcohol consumption. The prevalence of MetS was significantly lower in light drinkers and higher in very heavy drinkers compared with nondrinkers. Conclusion Alcohol intake significantly influences the risk of MetS in men. A significant association was seen between an alcohol intake of 60 g/day or higher and the prevalence of MetS.

The contribution of P2‐purinoceptors to neurogenic contraction was investigated in rat urinary bladder smooth muscle by measurement of isotonic tension. Contraction of rat urinary bladder smooth muscle induced by electrical stimulation was decreased to 84.19±3.90% of the control (n= 16) in the presence of atropine (1 μm), which was further decreased to 38.80 ±2.75% of the control (n = 49) in the presence of both atropine and 10 μm α,β‐methylene adenosine 5′‐triphosphate (α,β‐Me ATP). The contractile response induced by electrical stimulation in the presence of atropine and α,β‐Me ATP was decreased to 27.81 ±4.07% (n = 23) and 26.63 ±5.01% (n = 15) of the control, by the addition of 100 μm cibacron blue 3GA and 100 μm suramin, respectively. The application of 100 μm adenosine 5′‐0–2‐thiodiphosphate (ADPβS) in the presence of atropine and α,β‐Me ATP decreased the contractile response induced by electrical stimulations to 17.15 ±3.71% (n=15) of the control. Pretreatment of muscle strips with 100 μm ADPβS significantly reduced the response to either 200 μm α,β‐methylene adenosine 5′‐diphosphate or 200 μm ADPβS. Uridine 5′‐triphosphate (100 μm to 1 mM) concentration‐dependently contracted muscle strips, and this contraction was significantly antagonized by desensitization of P2‐receptors with α,β‐Me ATP (10 μm), and completely antagonized by pretreatment of muscle strips with both α,β‐Me ATP and ADPβS (100 μm). Di(adenosine‐5′) tetraphosphate (30 and 100 μm) contracted muscle strips, whereas it failed to contract after desensitization of P2‐receptors. It is suggested that about 20% of the neurogenic contraction of rat urinary bladder smooth muscle is mediated via ADPβS‐sensitive purinoceptors.

A study is made of the crystallization of amorphous antimony film deposited on a glass substrate. The substrate is maintained at a desired temperature between 20°C and 90°C. The crystal growth in the films of thickness 210-550 Å is directly observed through an optical microscope. At any substrate temperature Ts the rate of crystal growth v is found to change with the thickness d in accordance with the expression v=v∞(1-dc/d), where dc is the critical thickness for crystallization of the amorphous antimony film and v∞ the rate of crystal growth for bulk antimony. The critical thickness dc decreases with the rise of Ts. The activation energy of atoms for crystallization Q is found to be 0.32 eV for bulk antimony.