http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
Vladimír Šámal,Jan Krhut,Vít Paldus,Jana Műllerová,Jan Mečl 대한배뇨장애요실금학회 2020 International Neurourology Journal Vol.24 No.1
Purpose: To evaluate intravesical loss of onabolunumtoxinA (onaBTA) during endoscopic injection into the bladder wall for treatment of neurogenic detrusor overactivity (NDO). The intraluminal loss of onaBTA cannot be determined directly, therefore we added methylene blue (MB) to reconstitute onaBTA. Subsequently we used spectrophotometry to determine the total amount of MB in the irrigation fluid, which allowed us to calculate total intraluminal loss of onaBTA. Methods: The study population was consisted of 48 patients with NDO. The mean age was 36.6±8.9 years. Forty-two patients suffered from NDO due to spinal cord injury and 6 patients suffered from multiple sclerosis. Each patient received 200 units of onaBTA administered by 30 endoscopic injections (1 mL per injection) using a 23-G needle. The entire volume of irrigation fluid was collected and spectrophotometry was used to determine the MB concentration. The total amount of injected onaBTA, total amount of irrigation solution and the known amount of MB used during reconstitution, allowed for the determination of intravesical loss of onaBTA. Results: Forty-five patients were included in the final analysis. The mean volume of irrigation fluid was 603.33±400.14 mL. The mean absorbance was 0.14±0.12 with the mean MB concentration 0.19±0.18 mg/L. The mean calculated loss of onaBTA was 4.14±4.11 units. Conclusions: The endoscopic injection of onaBTA marked by MB into the bladder wall is associated with minimal intravesical loss of the agent, representing less than 3% of the administered dose of MB. This may reflect the amount of the onaBTA detected in the irrigation fluid.
Jana Essing,Ewgeni Jakubovski,Nikolas Psathakis,Sinan N Cevirme,James F Leckman,Kirsten R Müller-Vahl 대한파킨슨병및이상운동질환학회 2022 Journal Of Movement Disorders Vol.15 No.1
In patients with Tourette syndrome and other primary tic disorders (PTDs), tics are typically preceded by premonitory urges (PUs). To date, only a few studies have investigated the location and frequency of PUs, and contrary to clinical experience, the results suggest that PUs are not located in the same anatomic region as the tics. This study aimed to further explore PU location and frequency in detail, differentiating the kind and complexity of the corresponding tics, in a large sample of patients with PTD.
Neutral beam injector system for Steady State Tokamak -1
S. K. Mattoo,A.K. Chakraborty,B. Prajapati,BVSNNP Sridhar,C. Rotti,Ch. Chakrapani,G. Patel,M. Bandyopadhyay,M.J. Singh,M.R. Jana,N.P. Singh,P. Bharati,P.J. Patel,P.K. Jayakumar,R. Onali,S. Ramababu,S. 한국물리학회 2006 THE JOURNAL OF THE KOREAN PHYSICAL SOCIETY Vol.49 No.III
This paper discusses the experimental results obtained from the various components developed for a 1.7 MW neutral beam injector (NBI). Several technologies related to fabrication of back plate, extractor grids, high-current filament feedthru’s, heat-transfer elements, ceramic insulators, cryopumps, rectangular vessels and power supplies have been developed in collaboration with the Indian industry. Control experiments on the prototype plasma box are described.
Mutations in <i>ATP1A1</i> Cause Dominant Charcot-Marie-Tooth Type 2
Lassuthova, Petra,Rebelo, Adriana P.,Ravenscroft, Gianina,Lamont, Phillipa J.,Davis, Mark R.,Manganelli, Fiore,Feely, Shawna M.,Bacon, Chelsea,Brož,ková,, Dana Š,afka,Haberlova, Jana,M University of Chicago Press [etc.] 2018 American journal of human genetics Vol.102 No.3
<P>Although mutations in more than 90 genes are known to cause CMT, the underlying genetic cause of CMT remains unknown in more than 50% of affected individuals. The discovery of additional genes that harbor CMT2-causing mutations increasingly depends on sharing sequence data on a global level. In this way—by combining data from seven countries on four continents—we were able to define mutations in <I>ATP1A1</I>, which encodes the alpha1 subunit of the Na<SUP>+</SUP>,K<SUP>+</SUP>-ATPase, as a cause of autosomal-dominant CMT2. Seven missense changes were identified that segregated within individual pedigrees: c.143T>G (p.Leu48Arg), c.1775T>C (p.Ile592Thr), c.1789G>A (p.Ala597Thr), c.1801_1802delinsTT (p.Asp601Phe), c.1798C>G (p.Pro600Ala), c.1798C>A (p.Pro600Thr), and c.2432A>C (p.Asp811Ala). Immunostaining peripheral nerve axons localized ATP1A1 to the axolemma of myelinated sensory and motor axons and to Schmidt-Lanterman incisures of myelin sheaths. Two-electrode voltage clamp measurements on <I>Xenopus</I> oocytes demonstrated significant reduction in Na<SUP>+</SUP> current activity in some, but not all, ouabain-insensitive ATP1A1 mutants, suggesting a loss-of-function defect of the Na<SUP>+</SUP>,K<SUP>+</SUP> pump. Five mutants fall into a remarkably narrow motif within the helical linker region that couples the nucleotide-binding and phosphorylation domains. These findings identify a CMT pathway and a potential target for therapy development in degenerative diseases of peripheral nerve axons.</P>