青蒿琥酯皮肤擦剂在小鼠和兔体内的药代动力学研究

将青蒿琥酯溶于苯二甲酸二甲酯,加适量氨酮制成皮肤擦剂。给兔脱毛后,皮肤涂抹此擦剂25mg/kg后,血药浓度达峰时间平均为2 h,峰浓度平均为1.80μg/ml。药物在兔体内平均驻留时间为3.54 h,清除半衰期约为2.46 h。给小鼠脱毛皮肤涂抹擦剂6.7,31.3和71.4 mg/kg,血药浓度在给药后0.5～4 h达高峰,峰浓度分别为0.82,2.05和7.11μg/ml,体内药物平均驻留时间为3.39,2.79及3.54 h,清除半衰期为2.35,1.93及2.45 h。可见,给兔及小鼠皮肤擦剂后,青蒿琥酯吸收良好,血药浓度维持时间较长。     

Detection of the carrier state of X-linked retinoschisis

We determined the extent of suppressive rod-cone interaction in 11 obligate carriers and eight potential carriers of X-linked retinoschisis from eight families. Despite otherwise normal ophthalmoscopic and functional testing, all of the obligate heterozygous carriers demonstrated a complete absence of normal rod-cone interaction. Of the potential heterozygous carriers, three had normal rod-cone interactions, two had no detectable interaction, and two yielded technically unsatisfactory results. This lack of rod-cone interactions allows heterozygous individuals to be identified clinically and has implications concerning the origin of this inherited disorder.     

Separable evoked retinal and cortical potentials from each major visual pathway: preliminary results.

Single cell experiments in primates show that there are two major parallel pathways named after the lamination in the lateral geniculate nucleus. Each of these systems can be preferentially excited by appropriate stimuli. Here we report that in man the polarity of the evoked potentials both in retina and in cortex depends on which of these pathways is stimulated. The identification of the resulting waveforms is thereby simplified--a matter of practical importance. The fact that at retina and cortex there are characteristic potentials may reflect the different cell biology of the two pathways.     

Autosomal dominant retinitis pigmentosa mapping to chromosome 7p exhibits variable expression.

The genetic locus causing autosomal dominant retinitis pigmentosa (adRP) has recently been mapped in a large English family to chromosome 7p. Eight affected members of this family were studied electrophysiologically and psychophysically with dark adapted static threshold perimetry and dark adaptometry. The phenotypes observed fell into three categories: minimally affected with no symptoms, and normal (or near normal) electrophysiology and psychophysics; moderately affected with mild symptoms, abnormal electroretinograms, and equal loss of rod and cone function in affected areas of the retina; and severely affected with extinguished electroretinograms and barely detectable dark adapted static threshold sensitivities. The mutation in the gene on 7p causing adRP in this family causes regional retinal dysfunction with greatly variable expressivity ranging from normal to profoundly abnormal in a manner not explained by age.