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Biomedical subjects

S M Wang

Publications and source records attributed to S M Wang.

At least 91 records · Page 5Linked to original sources
PubMed1998

Morphological changes induced by prostaglandin E in cultured rat osteoblasts.

Prostaglandin E (PGE)-induced morphological changes of osteoblasts and its possible mechanisms were investigated in cultured calvaria and isolated osteoblasts from long bone fragments of neonatal rats. The control osteoblasts, either on the calvaria or isolated from the long bone fragments, were flat, polygonal in shape, and arranged in a monolayer under scanning electron microscopy (SEM) or phase contrast microscopy. Treatment with 1 mumol/L of prostaglandin E2 (PGE2, 2 h) caused these bone cells to contract a soma, whereas 10 and 100 mumol/L PGE2 (2 h) caused 18%-30% of the bone cells to elongate and expose the undersurface. Incubation of the cultured osteoblasts with PGE2 at different time periods showed a bell-shaped pattern with the optimal response at 2 h of incubation. A similar reaction can be induced by treatment with prostaglandin E1 (PGE1) or dibutyryl cyclic adenosine monophosphate (DBcAMP) in combination with 3-isobutyl-1-methylxanthine (IBMX). Furthermore, we assessed the percentage of responsive isolated bone cells to investigate interactions with other agents. The morphological changes induced by PGEs were inhibited by H-8, a protein kinase inhibitor. On the other hand, elevated intracellular calcium enhanced the PGE-induced morphological changes. Fluorescence labeling showed that PGEs caused the breakdown of the actin microfilaments, but spared the microtubules and vimentin filaments in the isolated osteoblast-like cells. These results suggest that the morphological changes of osteoblasts induced by PGEs may be related to the intracellular cAMP and calcium levels.

1-Methyl-3-isobutylxanthine↗
PubMed1998

Water-soluble contrast study predicts the need for early surgery in adhesive small bowel obstruction.

BACKGROUND: The optimal period of conservative treatment for adhesive small bowel obstruction remains controversial. This study sought to determine whether a 24-h abdominal radiograph after oral Urografin is a reliable indicator for operation in patients with adhesive small bowel obstruction. METHODS: One hundred and sixty-one patients who suffered from adhesive intestinal obstruction without clinical evidence of strangulation or gangrene underwent a Urografin study. Some 40 ml Urografin mixed with 40 ml distilled water was administered either orally or via a nasogastric tube to each patient. Serial plain abdominal radiographs were taken 4, 8, 16 and 24 h later. If an earlier plain radiograph showed that contrast medium had reached the ascending colon, subsequent radiographs were not taken. RESULTS: Contrast medium reached the colon within 24 h in 112 patients (70 per cent). These patients were all treated successfully with non-operative methods. Contrast medium was not observed in the colon within the first 24 h in 49 patients (30 per cent). Operation was performed in 47 of these patients and non-operative treatment was given in two. The sensitivity, specificity, accuracy, positive predictive value and negative predictive value of Urografin reaching the colon within 24 h as an indicator for non-operative treatment were 98, 100, 99, 100 and 96 per cent respectively. CONCLUSION: All patients with evidence of Urografin reaching the colon within 24 h were treated successfully with non-operative methods. The results of this prospective study suggest that patients with adhesive intestinal obstruction in whom contrast medium fails to reach the colon within 24 h should receive prompt surgical intervention.

Adult↗
PubMed1998

Characterization of ADG1, an Arabidopsis locus encoding for ADPG pyrophosphorylase small subunit, demonstrates that the presence of the small subunit is required for large subunit stability.

Two mutants of Arabidopsis have been isolated that affect ADPG pyrophosphorylase (ADGase) activity. Previously, it has been shown that ADG2 encodes the large subunit of ADGase. This study characterizes the adg1 mutant phenotype and ADG1 gene structure. RNA blot analyses indicate that the adg1-1 mutant accumulates transcripts encoding both the large and small subunits of ADGase, while the adg1-2 mutant accumulates only large subunit transcripts. RFLP analysis and complementation of adg1 mutants with the ADGase small subunit gene demonstrate that ADG1 encodes the small subunit. Sequence analysis indicates that adg1-1 represents a missense mutation within the gene. Western blot analysis confirms that adg1 mutants contain neither the large nor the small subunit proteins, suggesting that the presence of functional small subunits is required for large subunit stability.

Amino Acid Sequence↗
PubMed1998

Congenital fibrosis of the extraocular muscles type 2, an inherited exotropic strabismus fixus, maps to distal 11q13.

The extraocular fibrosis syndromes are congenital ocular-motility disorders that arise from dysfunction of the oculomotor, trochlear, and abducens nerves and/or the muscles that they innervate. Each is marked by a specific form of restrictive paralytic ophthalmoplegia with or without ptosis. Individuals with the classic form of congenital fibrosis of the extraocular muscles (CFEOM1) are born with bilateral ptosis and a restrictive infraductive external ophthalmoplegia. We previously demonstrated that CFEOM1 is caused by an autosomal dominant locus on chromosome 12 and results from a developmental absence of the superior division of the oculomotor nerve. We now have mapped a variant of CFEOM, exotropic strabismus fixus ("CFEOM2"). Affected individuals are born with bilateral ptosis and restrictive ophthalmoplegia with the globes "frozen" in extreme abduction. This autosomal recessive disorder is present in members of three consanguineous Saudi Arabian families. Genetic analysis of 70 individuals (20 affected individuals) reveals linkage to markers on chromosome 11q13, with a combined LOD score of 12.3 at the single nonrecombinant marker, D11S1314. The 2.5-cM CFEOM2 critical region is flanked by D11S4196/D11S4162 and D11S4184/1369. Two of the three families share a common disease-associated haplotype, suggesting a founder effect for CFEOM2. We hypothesize that CFEOM2 results from an analogous developmental defect to CFEOM1, one that affects both the superior and inferior divisions of the oculomotor nerve and their corresponding alpha motoneurons and extraocular muscles.

Blepharoptosis↗
PubMed1998

Parental presence during induction of anesthesia versus sedative premedication: which intervention is more effective?

BACKGROUND: Both midazolam and parental presence during induction of anesthesia are routinely used to treat preoperative anxiety in children. The purpose of this investigation was to determine which of these two interventions is more effective. METHODS: Anxiety of the child during the perioperative period was the primary end point. Secondary end points included anxiety of the parent and compliance of the child during induction. Children (n = 88) were randomly assigned to one of three groups: (1) 0.5 mg/kg oral midazolam; (2) parental presence during induction of anesthesia; or (3) control (no parental presence or premedication). Using multiple behavioral measures of anxiety, the effect of the intervention on the children and their parents was assessed. RESULTS: Observed anxiety in the holding area (T1), entrance to the operating room (T2), and introduction of the anesthesia mask (T3) differed significantly among the three groups (P = 0.032). Post hoc analysis indicated that children in the midazolam group exhibited significantly less anxiety compared with the children in the parental-presence group or control group (P = 0.0171). Similarly, parental anxiety scores after separation were significantly less in the midazolam group compared with the parental-presence or control groups (P = 0.048). The percentage of inductions in which compliance of the child was poor was significantly greater in the control group compared with the parental-presence and midazolam groups (25% vs. 17% vs. 0%, P = 0.013). CONCLUSIONS: Under the conditions of this study, oral midazolam is more effective than either parental presence or no intervention for managing a child's and parent's anxiety during the preoperative period.

Adaptation, Psychological↗
PubMed1998

Central nervous system candidiasis in very low-birth-weight premature neonates and infants: US characteristics and histopathologic and MR imaging correlates in five patients.

PURPOSE: To analyze the high-resolution (i.e., 5.0- or 7.5-MHz) ultrasonographic (US) imaging characteristics of central nervous system (CNS) candidiasis and their histopathologic and magnetic resonance (MR) imaging correlates in very low-birth-weight (VLBW) premature neonates and infants with systemic candidiasis. MATERIALS AND METHODS: The US images obtained in one VLBW neonate (age, 24 days; weight, 846 g) and four VLBW infants (age range, 36-161 days; weight range, 800-1, 360 g) with proved CNS candidiasis complicating systemic candidiasis and the clinical (n = 5), histopathologic (n = 3), and MR imaging (n = 2) correlates were retrospectively reviewed. RESULTS: The cranial US findings consisted of parenchymal abnormalities in four and ventricular lesions in three patients. The most common findings were multiple echogenic, rim-like microabscesses (four patients) scattered in the subcortical, periventricular, and basal ganglial areas. Confluent macroabscess formation, seen as echogenic mass-like lesions with hypoechoic centers in the periventricular regions and/or thalami, was noted on the US images obtained in two patients. The ventricles showed dilatation in two, increased ependymal echogenicity in three, the presence of intraventricular echogenic septa in two, and a lumpy choroid plexus or the presence of debris in two patients. US findings correlated well with MR imaging and autopsy findings. The histopathologic changes in the posterior fossa were well demonstrated on MR images but not demonstrated on 5.0- or 7.5-MHz US images. CONCLUSION: CNS candidiasis in VLBW neonates and infants has characteristic US features that may help in the early diagnosis of CNS involvement in systemic candidiasis.

Autopsy↗
PubMed1998

Group B streptococcal infections in children: the changing spectrum of infections in infants.

During a 9-year period from January 1988 to December 1996, 36 patients less than 18 years of age with Lancefield group B streptococcal infections were seen in the National Cheng Kung University Hospital. Among 33 infants with invasive group B streptococcal infections, 3 (9%) were early onset disease (EOD), 27 (82%) late onset disease (LOD) and 3 (9%) onset beyond the third month of life. All cases of EOD were detected during the first day of life and 2 of them were premature births. In the infants with LOD, a high incidence of meningitis occurred (78%). The most common clinical presentation in group B streptococcal infections was fever (81%), followed by irritable crying (42%) and poor feeding (39%). Seizure was noted in 57% of meningitis cases. Obstetric and neonatal risk factors were compared between EOD and LOD, with prematurity and low birth weight significantly (P=0.01) more common among infants with EOD compared with LOD. Of the strains tested, the sensitivity to penicillin, ampicillin and erythromycin were 83%, 74%, and 75%, respectively. All strains were resistant to tetracycline and gentamicin. There were 2 case fatalities (6%) and 6 (17%) had major neurologic sequelae. These data provide that the vast majority of EOD are recognized on the first day of life and prematurity is an important risk factor. In comparison to the previous report in Taiwan, a changing spectrum of GBS infections in infants occurs during the study period. The observed incidence of EOD is decreased and meningitis is still predominantly in LOD. It is suggested early recognition and aggressive therapy have resulted in a much lower mortality rate than previously reported.

Adolescent↗
PubMed1997

Cure of malignant ascites and generation of protective immunity by monoclonal antibody-targeted activation of a glucuronide prodrug in rats.

We examined the in vivo efficacy of targeting beta-glucuronidase (betaG) to activate a glucuronide prodrug (BHAMG) of p-hydroxyaniline mustard (pHAM) at hepatoma ascites in Sprague-Dawley rats. Injection i.p. of 500 microg RH1-betaG, a conjugate formed between recombinant betaG and monoclonal antibody RH1 with specificity for an antigen expressed on AS-30D rat hepatoma cells, into rats bearing AS-30D ascites resulted in the accumulation of 54 microg conjugate per 10(9) tumor cells after 2 hr. Ascites fluid and serum contained 0.53 and 0 microg/ml, respectively, RH1-betaG 2 hr after injection of the conjugate. Conjugate binding to AS-30D cells was heterogeneous and non-saturated, as determined by flow cytometry. BHAMG was less toxic than pHAM to SD rats based on measures of animal mortality, weight loss and hematological toxicity. Treatment of rats bearing established hepatoma ascites with 500 microg RH1-betaG followed 2 hr later with a single i.p. injection of 30 mg/kg BHAMG or 3 i.p. injections of 10 mg/kg BHAMG 2, 3 and 4 hr later resulted in the cure of 6/8 and 8/8 animals, respectively. Treatment with BHAMG or pHAM alone did not produce cures, whereas treatment with a control antibody-betaG conjugate and BHAMG produced significantly greater hematological toxicity compared to treatment with RH1-betaG and BHAMG. All cured rats were completely protected from rechallenge with 2 x 10(7) AS-30D cells, indicating that successful treatment of animals induced protective immunity.

Aniline Mustard↗
PubMed1997

Reorganization of a novel vimentin-associated protein in 3T3-L1 cells during adipose conversion.

We have found that the antibody A2, a marker for the capsule of steroidogenic lipid droplets, reacts with an intermediate filament-associated protein, P200, in 3T3-L1 preadipocytes. Supporting evidence came from the colocalization pattern of P200 with vimentin in double label experiments. The association of P200 with vimentin was further confirmed by its copurification with vimentin after high salt extraction and colocalization of these two proteins in high salt-extracted and vinblastine-treated cells. In preadipocytes this protein was distributed on the vimentin filament network. At the early stage of adipose conversion, this protein was found to encircle nascent lipid droplets ranging from 0.1 to 0.2 micron, accompanied with a decreased distribution on the vimentin filament system. This infers a possible translocation of P200 from the vimentin filaments to the droplet surface. Meanwhile, the vimentin filaments remained in a normal distribution in the cytoplasm and were apparently not associated with the nascent droplet. The association of vimentin filaments to droplet surfaces became prominent in lipid droplets larger than 0.2 micron, forming a typical vimentin cage. Immunogold staining also confirmed the translocation of P200 immunoreactivity from the droplet surface to the vimentin cage. The relocation of P200 from the cytoplasmic vimentin filaments to the droplet surface prior to the formation of the vimentin cage, as well as the reorganization of this protein in the vimentin cage, suggests a stabilizing role in the lipid droplet formation and an inducing function of this protein in the formation of the vimentin cage.

3T3 Cells↗
PubMed1997

The surface region of the bifunctional vaccinia RNA modifying protein VP39 that interfaces with Poly(A) polymerase is remote from the RNA binding cleft used for its mRNA 5' cap methylation function.

VP39 is a single-domain, bifunctional viral protein, which acts at both ends of nascent mRNA. At the 5' end, it acts as a cap-specific 2'-O-methyltransferase. At the 3' end, it acts as a poly(A) polymerase processivity factor, requiring its direct association with poly(A) polymerase. Although crystallographic and biochemical data show the catalytic center and associated binding sites for VP39's methyltransferase function to be juxtaposed around a superficial cleft on the protein surface, surface regions required for VP39's mRNA 3' end modifying functions are not known. Here, we identify a surface region that interfaces directly with poly(A) polymerase, taking three independent approaches: (i) development of a direct in vitro dimerization assay, which is applied to numerous VP39 point mutants; (ii) identification of sites within VP39 that become protected from protease cleavage upon dimerization and further mutagenesis based upon these data; (iii) site-specific photo-cross-linking of VP39 to VP55. We find that the dimerization interface lies on a surface region remote from the methyltransferase cleft and contains a 3-5-residue "hot-spot," which is very sensitive to amino acid substitutions. Various other sites within VP39 consistently became hypersensitive to protease cleavage upon interaction with VP55, indicating the occurrence of extensive conformational changes.

Amino Acid Sequence↗
PubMed1997

Mechanism of oxidative stress-induced intracellular acidosis in rat cerebellar astrocytes and C6 glioma cells.

1. Following ischaemic reperfusion, large amounts of superoxide anion (.O2-), hydroxyl radical (.OH) and H2O2 are produced, resulting in brain oedema and changes in cerebral vascular permeability. We have found that H2O2 (100 microM) induces a significant intracellular acidosis in both cultured rat cerebellar astrocytes (0.37 +/- 0.04 pH units) and C6 glioma cells (0.33 +/- 0.07 pH units). 2. Two membrane-crossing ferrous iron chelators, phenanthroline and deferoxamine, almost completely inhibited H2O2-induced intracellular acidosis, while the non-membrane-crossing iron chelator apo-transferrin had no effect. Furthermore, the acidosis was completely inhibited by two potent membrane-crossing .OH scavengers, N-(2-mercaptopropionyl)-glycine (N-MPG) and dimethyl thiourea (DMTU). Since .OH can be produced during iron-catalysed H2O2 breakdown (Fenton reaction), we have shown that a large reduction in pH1 in glial cells can result from the production of intracellular .OH via H2O2 oxidation. 3. We have ruled out the possible involvement of: (i) an increase in intracellular Ca2+ levels; and (ii) inhibition of oxidative phosphorylation. 4. Our results suggest that .OH inhibits glycolysis, leading to ATP hydrolysis and intracellular acidosis. This conclusion is based on the following observations: (i) in glucose-free medium, or in the presence of iodoacetate or 2-deoxy-D-glucose, H2O2-induced acidosis is completely suppressed; (ii) H2O2 and iodoacetate both produce an increase in levels of intracellular free Mg2+, an indicator of ATP breakdown; and (iii) direct measurement of intracellular ATP levels and lactate production show 50 and 55% reductions in ATP content and lactate production, respectively, following treatment with 100 microM H2O2. 5. Inhibition of the pH1 regulators (i.e. the Na(+)-H+ exchange and possibly the Na(+)-HCO3(-)-dependent pH1 transporters) resulting from H2O2-induced intracellular ATP reduction may also be involved in the H2O2-evoked intracellular acidosis in glial cells.

Acidosis↗
PubMed1997

Studies on the function of rho A protein in cardiac myofibrillogenesis.

The aim of this study was to provide morphological evidence for the presence of rho A protein in developing cardiomyocytes and to investigate its possible role in myofibrillogenesis. Immunostaining with a monoclonal anti-rho antibody gave a diffuse pattern in the cytosol of cultured cardiomyocytes. Introduction of C3 exoenzyme into the cells by electroporation was used to inactivate rho A protein by ADP-ribosylation. An immunostaining with anti-vinculin, anti-talin, and anti-integrin antibodies showed the focal adhesions in electroporation control cardiomyocytes to be evenly distributed in the ventral sarcolemma; the costameric structure was also detected using these antibodies. In contrast, in C3 exoenzyme treated cells, focal adhesions were disassembled and costamere were absent; in addition, beta-actin-positive, non-striated fibrils were lost and assembly of M-protein, titin, and alpha-actinin into myofibrils was poor, as shown by diffuse and filamentous staining pattern. C3 exoenzyme treatment had a less marked effect on mature cardiomyocytes than on immature cells; in this case, cells became distorted and few myofibrils were seen. The intensity of anti-phosphotyrosine antibody staining of the focal adhesion was also decreased or diffuse in C3 exoenzyme-treated cardiomyocytes, suggesting dephosphorylation of focal adhesion components. We therefore conclude that small G protein rho A plays an important role in myofibril assembly in cardiomyocytes.

ADP Ribose Transferases↗
PubMed1997

Cloning of the human twist gene: its expression is retained in adult mesodermally-derived tissues.

We have previously reported on the isolation of several differentially expressed genes derived from young and senescent non growing WI-38 human fetal lung-derived fibroblasts. A 0.8-kb cDNA clone, isolate EPC-A2 (early population doubling cDNA-A2), encodes the 3' end of the human homolog of the Twist protein. Twist genes encode basic helix-loop-helix DNA-binding transcription factors that play crucial roles in mesoderm development. Here, we report the cloning and sequencing of the genomic human twist gene. It encodes a protein of 201 amino acids with 96% amino acid sequence identity to mouse Twist, and 100% sequence conservation in the DNA-binding region among all species in which it has been characterized. We further show that expression of human twist is retained in mesodermally-derived tissues and cell lines derived from adult donors.

Adult↗
PubMed1997

Characterization of a novel filament system in goldfish xanthophores.

We report the presence of a novel filament system in goldfish xanthophores using a monoclonal antibody (A2) made against 40-70 kD proteins derived from cytoskeletal preparations. On Western blots, this antibody recognized a 45 kD protein in xanthophore cell extracts. In cells with dispersed pigment, immunofluorescence staining of xanthophores revealed a uniform distribution of A2-reactive filaments. In cells with aggregated pigment, these filaments assumed a distinctively radial orientation, such that filaments emanated from the central pigment mass (CPM). At the electron microscopic level, immunogold labeling identified a filament system with a diameter of 7 nm. Overall, the cellular distribution of A2-reactive filaments was distinctly different from that of the other known components of the cytoskeleton, such as intermediate filaments, actin filaments, and microtubules. A2-reactive filaments also appeared resistant to agents known to perturb the cytoskeleton such as cytochalasin B, which depolymerized the actin filaments. When xanthophores were treated with vinblastine, shown to depolymerize microtubules and induce the collapse of intermediate filaments (vimentin and keratin) in other cell types, no effect on the A2 filament distribution was observed. On the other hand, treatment with calyculin A, a phosphatase inhibitor, converted A2 filaments into a wavy bundles, the effect of which was completely reversible by the removal of the drug from culture medium. These novel properties of A2 filaments, together with their reorganization in response to pigment translocation suggest that A2 filaments might play a yet unidentified role in intracellular organelle transport in these cells.

Actin Cytoskeleton↗