Biomedical subjects

S B Jou

Publications and source records attributed to S B Jou.

8 recordsLinked to original sources

PubMed2001

Virtual reality orthopedic surgery simulator.

This paper describes a highly interactive virtual reality orthopedic surgery simulator. The simulator allows surgeons to use various surgical instruments to operate on virtual rigid anatomic structures, such bones, prostheses and bone grafts, to simulate every procedure on the rigid structures for complex orthopedic surgeries, including arthroplasty, corrective or open osteotomy, open reduction of fractures and amputation. A comparative study of the simulator with paper simulation was performed and showed that interns and residents found the simulator to be a useful learning tool, and that visiting doctors could use it effectively for planning verification and rehearsal of operations.

Amputation, Surgical↗

PubMed2001

Protein kinase C and changes in manganese superoxide dismutase gene expression in cultured glial cells.

1. To study the role of protein kinase C (PKC) in the increase in manganese superoxide dismutase (Mn-SOD) gene expression following transient hypoxia in glial cells, we examined the mRNA levels of Mn-SOD using northern blot analysis. 2. The Mn-SOD mRNA levels were markedly increased after exposure to nitrogen gas for 5 min. 3. Pretreatment with chelerythrine or GF109203x, inhibitors of PKC, attenuated the increase in Mn-SOD mRNA following hypoxia in a concentration-dependent manner. 4. Incubation with phorbol 12-myristate 13-acetate, the PKC activator, enhanced the increase in Mn-SOD gene expression in response to transient hypoxia. 5. The results suggest that hypoxia increases Mn-SOD gene expression in cultured glial cells mainly through activation of a PKC pathway.

Cell Hypoxia↗

PubMed2001

Delineation of CTG repeats and clinical features in a Taiwanese myotonic dystrophy family.

Myotonic dystrophy (DM) is an inherited, autosomal dominant muscular disease which is primarily caused by a CTG trinucleotide expansion mutation on chromosome 19q13.3. The size of this trinucleotide repeat is related both to the age of onset and to the severity of the clinical manifestation. This disease is very rare in Taiwan, and clinical and genetic study on DM has not yet been documented in this area. Here, we present both clinical features and degrees of CTG expansion for a Taiwanese DM family. All of the DM patients examined in this family showed obvious clinical manifestations by age 30, which included facial and limb muscle weakness with atrophy, myotonia, and ptosis. In addition, individual DM members also exhibited variable phenotypes, which may reflect the complexity of the pathogenic mechanism. Because the collection of blood specimens was considered to be an invasive procedure, a genetic study on this DM family was performed using buccal cells. Our results confirmed that four members showing classic symptoms of DM had CTG repeat expansion in the DMI locus, and that one member with ptosis and minor muscle weakness in the right foot was a normal homozygote for CTG repeat. These data demonstrate that buccal cells can provide clear and reliable results, and thus, are suitable for a family study of DM.

Alleles↗

PubMed2000

Decrease of adenosine A-1 receptor gene expression in cerebral cortex of aged rats.

Changes of adenosine A-1 receptor (A1-AR) gene expression in aging were investigated in cerebral cortex using the rat aged from 2 months (adult) to 24 months (aged). Quantification of A1-AR protein level by immunoblotting analysis showed an age-related decrease of A1-AR in cerebral cortex of Wistar rats. Compared to the preparations from 2-month-old animals, the levels of A1-AR in the 6-, 12-, and 24-month-old rats were reduced by 14.3+/-5.2, 32.5+/-4.5 and 28.2+/-5.7%, respectively. Similar decrease of mRNA level in A1-AR was also obtained using Northern blotting analysis. Two representative spots of mRNA, a 3.4-kb transcript and a 5.6-kb transcript, were observed in X-ray film from cerebral cortex of rat hybridized with rat A1-AR cDNA probe. Compared to the 2 month-old rats, levels of the 5.6-kb transcript were decreased by 17.9+/-2.5, 27.4+/-3.2 and 23.1+/-2.1% in the 6-, 12- and 24-month-old rats, respectively. These results indicated an age-related decrease of A1-AR in cerebral cortex of the rat that seems responsible for the change of response to adenosine.

Aging↗

PubMed1999

Application of FTA sample collection and DNA purification system on the determination of CTG trinucleotide repeat size by PCR-based Southern blotting.

Myotonic dystrophy (DM) is caused by a CTG trinucleotide expansion mutation at exon 15 of the myotonic dystrophy protein kinase gene. The clinical severity of this disease correlates with the length of the CTG trinucleotide repeats. Determination of the CTG repeat length has been primarily relied on by Southern blot analysis of restriction enzyme-digested genomic DNA. The development of PCR-based Southern blotting methodology provides a much more sensitive and simpler protocol for DM diagnosis. However, the quality of the template and the high (G+C) ratio of the amplified region hamper the use of PCR on the diagnosis of DM. A modified PCR protocol to amplify different lengths of CTG repeat region using various concentrations of 7deaza-dGTP has been reported (1). Here we describe a procedure including sample collection, DNA purification, and PCR analysis of CTG repeat length without using 7-deaza-dGTP. This protocol is very sensitive and convenient because only a small number of nucleate cells are needed for detection of CTG expansion. Therefore, it could be very useful in clinical and prenatal diagnosis as well as in prevalence study of DM.

Blood Specimen Collection↗

PubMed1998

Modification of superoxide dismutase (SOD) mRNA and activity by a transient hypoxic stress in cultured glial cells.

In order to understand the role of superoxide dismutase (SOD) in response to transient hypoxia or hypoxia-reperfusion in astrocytes, the present study performed an in vitro investigation using rat glial cells in culture. Hypoxia was induced by an incubation with nitrogen gas for 10 min and that followed a further reperfusion with air for 10 min was indicating as hypoxia-normoxia. Activity of SOD was determined by the reduction of nitroblue tetrazolium (NTB). Changes of mRNA for Cu,Zn-SOD or Mn-SOD were also characterized using Northern blotting analysis. Transient hypoxia increased the activity of Mn-SOD but not that of Cu,Zn-SOD in glial cells. Expression of mRNA for SOD was also elevated in cells received hypoxia and the mRNA level for Mn-SOD raised higher than that for Cu,Zn-SOD. In cells received hypoxia-reperfusion, these changes of SOD both the activity and the mRNA level were not observed. Otherwise, the SOD protein amount, both Cu,Zn-SOD and Mn-SOD, identified by Western blotting was not changed in glial cells receiving hypoxic stress or not. The obtained results suggest that gene expression and activity of Mn-SOD in glial cells can be activated in response to the transient hypoxic stress.

Animals↗

PubMed1997

The role of free radicals in the release of noradrenaline from myenteric nerve terminals of guinea-pig ileum.

In an attempt to understand the role of free radicals in the regulation of sympathetic neurotransmission, the in vitro secretion of noradrenaline (NA) from synaptosomal preparations of guinea-pig ileum was investigated. Release of endogenous NA was quantified by an electrochemical detection (HPLC-ECD). In the presence of superoxide dismutase (SOD) and catalase at concentrations sufficient to scavenge the free radicals, secretion of NA was attenuated in samples with stimulation of 4-aminopyrine (4-AP) or not (spontaneous release). However, inducing superoxide radicals via the reaction of hypoxanthine with xanthine oxidase failed to modify the secretion of NA, both the 4-AP-stimulated release and the spontaneous secretion. Then, free radicals were induced in synaptosomes using hypoxia-normoxia exposure. Secretion of NA was markedly increased in samples receiving this treatment in a calcium-dependent way because it was attenuated by the removal of calcium chloride from bathing medium. An increase of SOD activity, both Mn-SOD and Cu, Zn-SOD, was also obtained by this exposure. Changes of SOD activities in response to free radicals produced by hypoxia-normoxia exposure in ileal synaptosomes can thus be considered. In conclusion, these results suggest that free radicals are formed to involve in the regulation of sympathetic neurotransmission via an increase of calcium influx to enhance the NA release in guinea-pig ileum.

Animals↗

PubMed1997

Changes of superoxide dismutase (SOD) mRNA and activity in response to hypoxic stress in cultured Wistar rat glioma cells.

In an attempt to understand the change of superoxide dismutase (SOD) in tumor cells by hypoxia and hypoxia-normoxia exposure, the present study performed an in vitro investigation using rat glioma cell line in culture. Hypoxia was induced by an incubation with nitrogen gas for 15 h followed the normoxia exposure with air for 30 min. Activity of SOD in cytosolic and particulate of cells was determined by the reduction of nitroblue tetrazolium. Changes of mRNA for Cu,Zn-SOD or Mn-SOD were also characterized using Northern blotting analysis. Hypoxic stress decreased the activity of SOD, both Cu,Zn-SOD and Mn-SOD, in glioma cells. Expression of mRNA for SOD was elevated by hypoxic stress and the increase of mRNA level for Cu,Zn-SOD was more marked than that for Mn-SOD. In response to hypoxia-normoxia exposure, an increase of activity with a lower mRNA level for Mn-SOD was observed in glioma cells. However, changes of Cu,Zn-SOD both the activity and the level of mRNA were not found in glioma cells by hypoxia-normoxia. The obtained results suggest that the SOD in glioma cells can be activated to compensate the damage from free radicals during hypoxic stress.

Animals↗