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Biomedical subjects

M S Chen

Publications and source records attributed to M S Chen.

At least 19 recordsLinked to original sources
PubMed2006

NO adsorption and dissociation on Rh(111): PM-IRAS study.

We have used in situ polarization-modulation infrared reflection absorption spectroscopy to study the adsorption/dissociation of NO on Rh(111). While these studies have not been conclusive regarding the detailed surface structures formed during adsorption, they have provided important new information on the dissociation of NO on Rh(111). At moderate pressures (< or =10(-6) Torr) and temperatures (<275 K), a transition from 3-fold hollow to atop bonding is apparent. Data indicate that this transition is not due to the migration of the 3-fold hollow NO but rather to the adsorption of gas-phase NO that is directed toward the atop position due to the presence of NO decomposition products, particularly chemisorbed atomic O species at the hollow sites. These results indicate that NO dissociation occurs at temperatures well below the temperature previously reported. Additionally, high pressure (1 Torr) NO exposure at 300 K results in only atop NO, calling into question the surface structures previously proposed at these adsorption conditions consisting of atop and 3-fold hollow sites.

Journal Article↗
PubMed2005

Primary placement of a titanium sleeve in hydroxyapatite orbital implants.

BACKGROUND: To study a new surgical option of primary placement of a titanium sleeve into hydroxyapatite implants during enucleation or evisceration. METHODS: A standard enucleation or cornea preserved evisceration was performed, followed by preplacement of a titanium sleeve into the hydroxyapatite implant by a hand drill sleeve driver. Care must be taken to ensure that the titanium sleeve is positioned centrally when the implant is put inside the orbital socket or eviscerated shell. The Tenon capsule and conjunctiva were meticulously closed with minimal tension. Complications such as sleeve exposure, coralline exposure, and infection of the titanium sleeve were closely observed. RESULTS: In all, 30 patients were treated in the above fashion with 10 enucleation and 20 evisceration procedures. The follow-up period ranged from 9 to 24 months. Three of the sleeves were found to have exposed spontaneously at 5 and 7 weeks following original surgery. They had no further complication except one sleeve loosening. The remaining 27 sleeves that did not spontaneously expose pursued secondary exposure of the titanium sleeve and peg insertion by conjunctival cutdown procedure 3 months after original surgery. Two sleeves were found to be oblique positioned after the conjunctival cutdown procedure. Fortunately, all the 30 patients were successfully fit with a peg-coupled prosthesis with good motility. CONCLUSION: Primary placement of a titanium sleeve into hydroxyapatite implants has several advantages, including high patient acceptance, technical simplicity, and office-based conjunctival cutdown pegging procedure. By avoiding the expense of postoperative imaging study and additional prosthetic modification, a more rapid and efficient rehabilitation is possible.

Adult↗
PubMed2004

The structure of catalytically active gold on titania.

The high catalytic activity of gold clusters on oxides has been attributed to structural effects (including particle thickness and shape and metal oxidation state), as well as to support effects. We have created well-ordered gold mono-layers and bilayers that completely wet (cover) the oxide support, thus eliminating particle shape and direct support effects. High-resolution electron energy loss spectroscopy and carbon monoxide adsorption confirm that the gold atoms are bonded to titanium atoms. Kinetic measurements for the catalytic oxidation of carbon monoxide show that the gold bilayer structure is significantly more active (by more than an order of magnitude) than the monolayer.

Journal Article↗
PubMed2001

Multiple alternative splicing forms of human RAD17 and their differential response to ionizing radiation.

In this study, we have identified four alternatively spliced RAD17 RNAs, FM1, FM2, FM3, and FM4, which are produced through alternative splicing within the first 300 base-pairs of the coding region. FM3 and FM4 are two novel forms that have not been reported before. All four alternatively spliced RAD17 RNAs were detected in the tissues we examined. However, the levels of these forms varied from tissue to tissue. The expression of these four forms was also found to differ in different phases of the cell cycle and following exposure to X-irradiation. FM2, FM1, FM4, and FM3 encode putative polypeptides consisting of 681, 670, 596, and 516 amino acids, respectively. To determine if these polypeptides were expressed in cells, we generated a polyclonal antibody using a synthetic peptide. A major band around 71 kDa and two minor bands around 73 and 62 kDa were detected in human normal fibroblasts on Western blots. These three bands appear to represent the proteins encoded by FM2 (the 73 kDa band), FM1 (the 71 kDa band), and FM4 (the 62 kDa band) since the apparent molecular weights are close to their theoretical weights of the predicted amino acid sequences. The abundance of the 71 kDa protein was not significantly affected by X-irradiation, while the abundance of the 73 and the 62 kDa proteins was increased at least 5-fold 14 h postirradiation. The differential expression of these four alternatively spliced forms in different tissues, in different phases of the cell cycle, and their differential response to X-irradiation suggest that they may perform different functions in cell-cycle regulation and in the response to irradiation.

Alternative Splicing↗
PubMed2001

Surface patterning of polychloromethylstyrene films.

We describe and characterize a simple process for the fabrication of patterned materials on polychloromethylstyrene thin film surfaces under ambient conditions. Patterned deep UV exposure (approximately 60 mJcm(-2), 193 nm) efficiently oxidizes the surface C-Cl bonds of the polymer film, producing an aldehyde species as the major photoproduct. Reductive amination in the presence of ammonium ion and cyanoborohydride reductant selectively converts the aldehyde into an alkylamine, which leads to an amine reactivity template on the film surface. The amines formed are sufficiently reactive to selectively and covalently bind fluorescent dye or electroless Ni metal to the template, which results in negative tone features with micron-scale resolutions (mask limited) in each case. Spectroscopic characterizations of the polymer surface following the photochemical transformation, reductive amination, and grafting steps are presented in support of the process. A key advantage of the method is the use of safe solvents, such as water or simple alcohols, to effect the reductive amination and grafting reactions. This approach mitigates waste disposal and associated environmental concerns, increasing the attractiveness of our method for use with high-throughput track-line processing equipment.

Journal Article↗
PubMed2001

Absence of apparent phenotype in mice lacking Cdc25C protein phosphatase.

The Cdc25 family of protein phosphatases positively regulate the cell division cycle by activating cyclin-dependent protein kinases. In humans and rodents, three Cdc25 family members denoted Cdc25A, -B, and -C have been identified. The murine forms of Cdc25 exhibit distinct patterns of expression both during development and in adult mouse tissues. In order to determine unique contributions made by the Cdc25C protein phosphatase to embryonic and adult cell cycles, mice lacking Cdc25C were generated. We report that Cdc25C(-/-) mice are viable and do not display any obvious abnormalities. Among adult tissues in which Cdc25C is detected, its transcripts are most abundant in testis, followed by thymus, ovary, spleen, and intestine. Mice lacking Cdc25C were fertile, indicating that Cdc25C does not contribute an essential function during spermatogenesis or oogenesis in the mouse. T- and B-cell development was also found to be normal in Cdc25C(-/-) mice, and Cdc25C(-/-) mouse splenic T and B cells exhibited normal proliferative responses in vitro. Finally, the phosphorylation status of Cdc2, the timing of entry into mitosis, and the cellular response to DNA damage were unperturbed in mouse embryo fibroblasts lacking Cdc25C. These findings indicate that Cdc25A and/or Cdc25B may compensate for loss of Cdc25C in the mouse.

Animals↗
PubMed2001

Lenticular opacities in populations exposed to chronic low-dose-rate gamma radiation from radiocontaminated buildings in Taiwan.

Chen, W-L., Hwang, J-S., Hu, T-H., Chen, M-S. and Chang, W. P. Lenticular Opacities in Populations Exposed to Chronic Low-Dose-Rate Gamma Radiation from Radiocontaminated Buildings in Taiwan. Radiat. Res. 156, 71-77 (2001). Epidemiological and experimental studies have revealed the cataractogenic potential of large acute doses of radiation. However, studies on the dose-response effect and the incidence of lenticular changes after exposure to chronic low doses of radiation have seldom been conducted. To evaluate quantitatively the lenticular changes in a population exposed to chronic low-dose-rate gamma radiation in their daily living or school environment in steel buildings contaminated with (60)Co in Taiwan, a total of 114 exposed individuals participated in a thorough ophthalmological examination in 1998. The lenticular opacities were evaluated by slit-lamp biomicroscopy after full pupil dilatation and were scored by the Lens Opacities Classification System III (LOCS III) and a modified subclinical minor lenticular focal defects system. These individuals were further divided into those less than 20 years old, those between 20 and 40 years old, and those more than 40 years old to evaluate the effects of age. The cumulative doses were assessed for each individual using the Taiwan Cumulative Dose (TCD) estimation system. A significant dose-dependent increase in the numbers of focal lens defects in those less than 20 years old was demonstrated, while less significant changes were observed in the other two age groups or by the LOCS III scoring. Results suggested that chronic low-dose-rate irradiation might induce minor lenticular changes, especially in lenses of young subjects. The delayed clinical changes in these young exposed subjects warrants further long-term follow-up.

Adolescent↗
PubMed2000

Genetic linkage of Bietti crystallin corneoretinal dystrophy to chromosome 4q35.

Bietti crystalline corneoretinal dystrophy (BCD) is an autosomal recessive retinal degeneration characterized by multiple glistening intraretinal dots scattered over the fundus, degeneration of the retina, and sclerosis of the choroidal vessels, ultimately resulting in progressive night blindness and constriction of the visual field. Although BCD has been associated with abnormalities in fatty-acid metabolism and absence of fatty-acid binding by two cytosolic proteins, the genetic basis of BCD is unknown. We report linkage of the BCD locus to D4S426 (maximum LOD score [Z(max)] 4.81; recombination fraction [straight theta] 0), D4S2688 (Zmax=3.97; straight theta=0), and D4S2299 (Zmax=5.31; straight theta=0), on chromosome 4q35-4qtel. Multipoint analysis confirmed linkage to the region telomeric of D4S1652 with a Z(max) of 5.3 located 4 cM telomeric of marker D4S2930.

China↗
PubMed2000

The neurofibromatosis 2 tumor suppressor protein interacts with hepatocyte growth factor-regulated tyrosine kinase substrate.

The neurofibromatosis 2 tumor suppressor protein schwannomin/merlin is commonly mutated in schwannomas and meningiomas. Schwannomin, a member of the 4.1 family of proteins, which are known to link the cytoskeleton to the plasma membrane, has little known function other than its ability to suppress tumor growth. Using yeast two-hybrid interaction cloning, we identified the HGF-regulated tyrosine kinase substrate (HRS) as a schwannomin interactor. We verified the interaction by both immunoprecipitation of endogenous HRS with endogenous schwannomin in vivo as well as by using bacterially purified HRS and schwannomin in vitro. We narrowed the regions of interaction to include schwannomin residues 256-579 and HRS residues from 480 to the end of either of two HRS isoforms. Schwannomin molecules with a L46R, L360P, L535P or Q538P missense mutation demonstrated reduced affinity for HRS binding. As HRS is associated with early endosomes and may mediate receptor translocation to the lysosome, we demonstrated that schwannomin and HRS co-localize at endosomes using the early endosome antigen 1 in STS26T Schwann cells by indirect immunofluorescence. The identification of schwannomin as a HRS interactor implicates schwannomin in HRS-mediated cell signaling.

Adult↗
PubMed2000

Point mutation associated with X-linked dominant Charcot-Marie-Tooth disease impairs the P2 promoter activity of human connexin-32 gene.

Many lines of evidence suggest that connexin-32 gap junction is involved in the exchange of information and metabolites in the peripheral nervous system. It has been shown that connexin-32 protein and mRNA are expressed in Schwann cells that function as myelinating cells of the peripheral nervous system. The physiological importance of connexin-32 gap junctions in regulating the normal function of myelinating Schwann cell is indicated by recent findings that X-linked dominant Charcot-Marie-Tooth disease, a hereditary peripheral neuropathy, is associated with the mutations of connexin-32 gene. Recently, we encountered a Taiwanese family affected with X-linked dominant Charcot-Marie-Tooth neuropathy. Therefore, we investigated the possible mutation in the coding and noncoding regions of the connexin-32 gene of affected members of this family. Our results suggest that a G-to-A transition at the position -215 (in relation to the transcription initiation site) of the nerve-specific P2 promoter region is associated with the pathogenesis of X-linked dominant Charcot-Marie-Tooth disease. Further experiments using the promoter assay indicate that G-to-A mutation at the position -215 greatly impairs the transcriptional activity of connexin-32 P2 promoter. These findings propose that a reduced expression of connexin-32 mRNA and protein in the myelin sheath could be responsible for the development of X-linked dominant Charcot-Marie-Tooth neuropathy.

Animals↗
PubMed2000

Sequence-specific interaction between the disintegrin domain of mouse ADAM 2 (fertilin beta) and murine eggs. Role of the alpha(6) integrin subunit.

Little is yet known about the biological and biochemical properties of the disintegrin-like domains of ADAM (a disintegrin and metalloprotease) proteins. Mouse ADAM 2 (mADAM 2; fertilin beta) is a sperm surface protein involved in murine fertilization. We produced recombinant proteins containing the disintegrin-like domain of mADAM 2 in both insect cells and in bacteria. The protein produced in insect cells (baculo D+C) contained a signal sequence followed by the disintegrin-like and cysteine-rich domains; it was purified from the medium of recombinant baculovirus-infected cells. A bacterial construct containing the disintegrin-like domain was produced in Escherichia coli as a glutathione S-transferase chimera. Baculo D+C, as well as the D domain of the bacterial construct (released with thrombin), bound to the microvillar surface of murine eggs. Using concentrations in the range of 1 to 5 microM, both recombinant proteins strongly inhibited sperm-egg binding and fusion; the baculovirus-produced protein exhibited a somewhat greater extent of inhibition (approximately 75 versus approximately 55% maximal inhibition). Substitution of alanine for each of the five charged residues within the disintegrin loop of mADAM 2 revealed a critical importance for the aspartic acid at position nine. Binding of both recombinant proteins to the egg was inhibited by the function blocking anti-alpha(6) monoclonal antibody, GoH3, but not by a nonfunction-blocking anti-alpha(6) monoclonal antibody. Binding was also inhibited by a peptide analogue of, and with an antibody against, the disintegrin loop of mADAM 2.

ADAM Proteins↗
PubMed2000

Nogo-A is a myelin-associated neurite outgrowth inhibitor and an antigen for monoclonal antibody IN-1.

The capacity of the adult brain and spinal cord to repair lesions by axonal regeneration or compensatory fibre growth is extremely limited. A monoclonal antibody (IN-1) raised against NI-220/250, a myelin protein that is a potent inhibitor of neurite growth, promoted axonal regeneration and compensatory plasticity following lesions of the central nervous system (CNS) in adult rats. Here we report the cloning of nogo A, the rat complementary DNA encoding NI-220/250. The nogo gene encodes at least three major protein products (Nogo-A, -B and -C). Recombinant Nogo-A is recognized by monoclonal antibody IN-1, and it inhibits neurite outgrowth from dorsal root ganglia and spreading of 3T3 fibroblasts in an IN-1-sensitive manner. Antibodies against Nogo-A stain CNS myelin and oligodendrocytes and allow dorsal root ganglion neurites to grow on CNS myelin and into optic nerve explants. These data show that Nogo-A is a potent inhibitor of neurite growth and an IN-1 antigen produced by oligodendrocytes, and may allow the generation of new reagents to enhance CNS regeneration and plasticity.

3T3 Cells↗
PubMed2000

Tissue plasminogen activator and gas for diabetic premacular hemorrhage.

PURPOSE: To report the effect of intravitreal injection of tissue plasminogen activator and gas for the treatment of diabetic premacular hemorrhage. METHODS: Five eyes of five consecutive patients with fresh diabetic premacular hemorrhage and previous panretinal photocoagulation were treated with intravitreal injection of 50 microg of tissue plasminogen activator, and 0.3 ml of sulfur hexafluoride. After intravitreal injection, patients maintained a prone position for 3 days and were followed for an average of 7 months (range, 6 to 8 months). RESULTS: All eyes had clearing of the premacular hemorrhage with improved visual acuity. Three eyes with no visible fibrovascular proliferation required 3 weeks to resorb the hemorrhage, and two eyes with active fibrovascular proliferation needed 2 months to resorb the intravitreal hemorrhage. CONCLUSION: Intravitreal injection of tissue plasminogen activator and gas may be an effective way to treat fresh diabetic premacular hemorrhage.

Adult↗