Vestibular Rehabilitation for Children (review) / 中国康复理论与实践

Vestibular rehabilitation has been applied in children with benign paroxysmal positional vertigo, cerebral palsy and central coordination disorder successfully. However, training intensity and methods are various with diseases and therapeutic purposes. This paper reviewed the recovery mechanisms, the assessment and rehabilitation of vestibular dysfunction, and discussed the problems and prospects of vestibular rehabilitation for children.

Expression of renin/prorenin receptor in rat kidney and cultured mesangial cells / 生理学报

The renin/prorenin receptor (RnR) has recently been cloned and demonstrated to exist in different cells in the cardiovascular and renal systems, playing an important role in physiological and pathophysiological situations. In the present study, we used immunofluorescence method to identify whether and where the RnR expressed in cultured rat renal mesangial cells (MCs) and rat kidney. By using the prorenin handle region peptide (HRP) as a decoy peptide of the RnR, we observed the distribution of the HRP-RnR complex in the MCs. Our results showed that the RnR was localized in the perinuclear zone and plasma membrane of the MCs. At the organ level, the RnR was observed in the mesangium of cortical glomeruli in rat kidney. The FITC-labeled HRP (FITC-HRP) translocated from cell culture medium into the cytoplasm within 30 s. Colocalization of the HRP and RnR was observed mainly on the cell membrane and in the perinuclear zone of cytoplasm by using immunofluorescence and confocal microscopy. At 30 min the FITC-HRP was mainly observed in the nucleus while the RnR remained in the perinuclear zone of cytoplasm. Taken together, our results confirm the expression of RnR in the renal MCs. It is suggested that internalization of the RnR after binding with its ligand is at least one of the pathways through which the RnR exerts its biological actions.

Analysis of MYOC gene mutation in a Chinese glaucoma family with primary open-angle glaucoma and primary congenital glaucoma / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Glaucoma is one of the leading causes of blindness in the world. Primary open-angle glaucoma (POAG) and primary congenital glaucoma (PCG) are subtypes of glaucoma. Myocillin is the first gene identified to be involved in POAG. Recently, myocillin mutation has been found in PCG. In this context, we reported a special glaucoma pedigree, which was composed of both PCG and POAG patients, and analyzed the mutation of myocillin in this pedigree.</p><p><b>METHODS</b>The family was composed of the parents, a son and a daughter. All members of the family underwent the complete ophthalmologic examinations. All coding exons 1 - 3 and flanking introns of myocilin gene were screened for sequence alterations by polymerase chain reaction and direct DNA sequencing.</p><p><b>RESULTS</b>The son was the proband, who was diagnosed as PCG in both eyes. The father was diagnosed as POAG in the right eye, the left eye was still normal. Both the sister and the mother of the proband had normal intraocular pressure without glaucomatous optic disc changes. The mutations in intron 2 of myocilin gene were detected in the family. While the proband and the father were homozygous, the mother and the sister were heterozygous for the mutation.</p><p><b>CONCLUSIONS</b>Homozygous mutation in intron 2 of myocilin gene is involved in both POAG and PCG. It is suggested that the pathogenesis might be overlapping in POAG and PCG.</p>

Okadaic acid induces the expression of glutamate transporter EAAT1 in the neurons of rat brain / 生理学报

To study the relationship between tau hyperphosphorylation and the function of glutamate transporter okadaic acid (OA), a protein phosphatase inhibitor, 20 ng in a 0.5 microl volume, was injected into the frontal cortex of rat brain and immunostaining was used to observe the phosphorylation of tau protein and the expression of excitatory amino acid transporter 1 (EAAT1) in the brain following the injection. The results showed that (1) the neurons in the center of the injection region displayed cytoplasmic shrinkage, swelling, nuclear pyknosis, and dislocation at the early stage, and necrosis appeared 3 d after the injection. However, most neurons in the peri-injected areas showed normal morphological characters with immuno positive reaction for AT8, a tau phosphorylated marker; (2) morphological analysis showed that tau hyperphosphorylation caused by OA treatment was mainly observed in the axons and dendrites of neuronal cells at 6 h in the cell body at 1 d, which brought about dystrophic neurites and neurofibrillary tangle (NFT)-like pathological changes; (3) the induction of glutamate transporter EAAT1 was observed in the involved areas corresponding to that with AT8 immunopositive staining, and the number of EAAT1-positive staining cells markedly increased at 12 h (P<0.01), peaked at 1 d (P<0.001), then decreased at 3 d following the injection. Combined with a confocal laser scanning microscopic analysis, double fluorescent immunostaining showed that EAAT1 positive staining appeared in neurons as well as astrocytes in the peri-injected areas of the frontal cortex. These results demonstrate that OA increases glutamate transporter EAAT1 expression in neurons while it induces tau hyperphosphorylation. However, the mechanism and significance of the induction of glutamate transporter EAAT1 expression remain to be further elucidated.

The expression of nestin in ischemia-injured brain of adult rat / 生理学报

Immunohistochemistry and double immunofluorescent labeling techniques combined with confocal laser scanning microscope analysis were used to investigate the characteristic spatial induction profile of nestin following a transient middle cerebral artery occlusion in adult rat brain. The results showed that nestin was induced in ischemic core at 1 day after reperfusion. In addition to ischemic core, the expression of nestin increased in peri-ischemic I, II and III regions at 3 days and 1 week, then it decreased and narrowed along the rim of ischemic core 2 weeks after reperfusion. Double immunofluorescent labeling showed that nestin positive cells were mostly co-stained with GFAP,a astrocyte marker, in peri-ischemic I region 3 days after reperfusion. At 2 weeks, however nestin cells showed a long process and the cells double stained with nestin and NSE,a neuonal specific marker,increased in the ischemic brain. The results suggest that cerebral ischemia induces nestin expression in damaged neurons which might favor the neuroprotection against ischemic damage.