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101.
102.
小檗碱对培养大鼠神经细胞内游离Ca^2+的影响 总被引:3,自引:1,他引:2
以Fura2/AM为细胞内钙离子的荧光指示剂,用ARCMMIC阳离子测定系统,直接测定了体外培养的新生大鼠神经细胞内游离钙([Ca2+]i)值,并观察了小檗碱(Ber)的影响。结果表明,Ber对神经细胞静息[Ca2+]i无明显影响,Ber1~100μmol·L-1能剂量依赖地抑制去甲肾上腺素和H2O2引起的[Ca2+]i升高,其IC50分别为39.9和17.9μmol·L-1。高剂量Ber(10~100μmol·L-1)能抑制高K+引起的[Ca2+]i升高。姐果提示,Ber对去甲肾上腺素,高K+及H2O2引起的[Ca2+]i升高的抑制作用可能是其抗脑缺血作用机制之一。 相似文献
103.
Darcy MD; Lund GB; Smith TP; Hunter DW; Castaneda-Zuniga WR; Amplatz K 《Radiology》1987,163(3):819-821
Percutaneous techniques to manage urinary fistulas have had limited success. To overcome this, self-closing metallic clips were developed to occlude the ureter. The clips are applied through a percutaneously placed 30-F Teflon sheath. A case is reported in which the clips and new technique were successfully used. 相似文献
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C W Vaughan P D Neilson N J O''Dwyer 《Journal of neurology, neurosurgery, and psychiatry》1988,51(4):534-539
Voluntary control of the masseter and orbicularis oris superioris muscles was examined in able bodied and cerebral palsied subjects using visual tracking tasks. A smoothed measure of muscle activity (the full-wave rectified and low-pass filtered electromyogram) was presented as a marker on a computer display screen and the subjects could control the vertical position of the marker by voluntarily altering the level of isometric contraction of one of the muscles. A target marker was also displayed on the screen and the subjects were required to follow or "track" the irregular movements of this target with the response marker. Their success in aligning the response marker with the target was analysed for these orofacial muscles. The masseter is influenced by muscle spindle based reflexes, while the orbicularis oris superioris lacks such reflex control. The cerebral palsied subjects displayed similarly poor control over both muscles, implying that their voluntary motor deficits are not related to abnormal muscle spindle based reflexes. It is suggested that the impairment may be related to perceptual-motor integration. 相似文献
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Genomic imprinting: potential function and mechanisms revealed by the Prader-Willi and Angelman syndromes 总被引:4,自引:0,他引:4
The Prader-Willi (PWS) and Angelman (AS) syndromes are two clinically
distinct syndromes which result from lack of expression of imprinted genes
within chromosome 15q11-q13. These two syndromes result from 15q11-q13
deletions, chromosome 15 uniparental disomy (UPD), imprinting centre
mutations and, for AS, probable mutations in a single gene. The
differential phenotype results from a paternal genetic deficiency in PWS
patients and a maternal genetic deficiency in AS patients. Within
15q11-q13, four genes (SNRPN, IPW, ZNF127, FNZ127) and two expressed
sequence tags (PAR1 and PAR5) have been found to be expressed only from the
paternally inherited chromosome, and therefore all must be considered
candidate genes involved in the pathogenesis of PWS. A candidate AS gene
(UBE3A) has very recently been identified. The mechanisms of imprinted gene
expression are not yet understood, but it is clear that DNA methylation is
involved in both somatic cell expression and inheritance of the imprint.
The presence of DNA methylation imprints that distinguish the paternally
and maternally inherited alleles is a common characteristic of all known
imprinted genes which have been studied extensively, including SNRPN and
ZNF127. Recently, several PWS and AS patients have been found that have
microdeletions in a region upstream of the SNRPN gene referred to as the
imprinting centre, or IC. Paternal IC deletions in PWS patients and
maternal IC deletions in AS patients result in uniparental DNA methylation
and uniparental gene expression at biparentally inherited loci. The IC is a
novel genetic element which controls initial resetting of the parental
imprint in the germline for all imprinted gene expression over a 1.5-2.5 Mb
region within chromosome 15q11-q13.
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