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Biomedical subjects

S-Y Lin

Publications and source records attributed to S-Y Lin.

8 recordsLinked to original sources
PubMed2006

Dynamic surface elasticity of polyelectrolyte/surfactant adsorption films at the air/water interface: dodecyltrimethylammonium bromide and copolymer of sodium 2-acrylamido-2-methyl-1-propansulfonate with N-isopropylacrylamide.

The complex dynamic surface elasticity of the solutions of copolymer of sodium 2-acrylamido-2-methyl-1-propansulfonate with N-isopropylacrylamide and dodecyltrimethylammonium bromide was measured as a function of the surfactant concentration and the surface age by the oscillating bubble and drop methods. The kinetic dependencies of the surface elasticity proved to be non-monotonic at low concentrations and the main features of the surface viscoelasticity differed from the results for other polyelectrolyte/surfactant solutions films studied so far. The observed peculiarities were connected with the properties of the copolymer chain.

Journal Article↗
PubMed2006

Dilational viscoelasticity of PEO-PPO-PEO triblock copolymer films at the air-water interface in the range of high surface pressures.

The dynamic dilational elasticity of adsorbed and spread films of PEO-PPO-PEO triblock copolymers at the air-water interface was measured as a function of surface pressure, surface age, and frequency. At low surface pressures (<10 mN/m), the surface viscoelasticity is identical to that of PEO homopolymer films. The results at higher surface pressures can be explained by the desorption of PPO segments from the interface and then mixing with PEO segments in water. Unlike some recent results, the spread and adsorbed films are not identical. Spread films exhibit a maximum real part of the dynamic surface elasticity of about 20 mN/m and probably begin to dissolve in water at surface pressures above 19 mN/m. However, the surface elasticity of the adsorbed films decreases beyond the maximum, indicating the formation of a loose surface structure.

Journal Article↗
PubMed2006

Spermatogenesis does not require the local production of follistatin.

It has been proposed that follistatin can modulate the actions of activins and/or other members of the transforming growth factor-beta superfamily of proteins on testicular function, since mice overexpressing follistatin showed spermatogenic disruption. However, since mice with targeted disruption of the follistatin gene die soon after birth, it is not feasible to determine the effect of the absence of follistatin on testicular function using this model. To further understand the role of follistatin on the development and maintenance of spermatogenesis, fetal testes, collected by Caesarean section at day 18 of gestation from follistatin null mice, were transplanted to the external ear of castrated recombination activating gene 1 immunocompromised male mice. The testicular grafts were then analysed 7-8 weeks after transplantation and showed that full spermatogenesis developed in both the testes of wild-type and follistatin null mice. This study indicates that, if follistatin is required to modulate spermatogenic development, it is not supplied by local testicular production but by circulating follistatin from the host mouse.

Animals↗
PubMed2005

Calcification of senile cataractous lens determined by Fourier transform infrared (FTIR) and Raman microspectroscopies.

A calcified plaque on the surface of a senile cataractous lens (CL) isolated from a 79-year-old male patient was identified and its chemical composition quantified using Fourier transform infrared (FTIR) and confocal Raman microspectroscopies. The noncalcified area of the same CL and hydroxyapatite (HA) were selected as a control. Several unique absorption bands, at 960, 1034 and 1090 cm(-1) assigned to the nu(1) and nu(3) stretching modes of phosphate and at 875 cm(-1) attributed to carbonate, were clearly displayed in the infrared (IR) spectra of calcified plaque and HA. A peak at 961 cm(-1) due to the nu(1) stretching mode of phosphate was also evidenced in the Raman spectra of calcified plaque and HA. The calcified plaque formed within the lens protein was found to mainly consist of a mature HA, in which type-A carbonate apatites (11.4%), type-B carbonate apatites (55.6%) and liable surface carbonate ions (33.0%) were presented. A higher content of the liable carbonate implies that the calcification or mineralization in this calcified lens was incomplete and still in progress. Moreover, calcification seems not to influence the secondary structure of lens protein because both IR and Raman spectra for the lens protein in the noncalcified area and calcified plaque were similar. The result suggests that both microscopic FTIR and Raman spectroscopies were easy to perform and capable of determination of the chemical composition of a calcified CL.

Aged↗
PubMed2004

Increased serum soluble tumor necrosis factor receptor levels are associated with insulin resistance in liver cirrhosis.

Insulin resistance is present in nearly all patients with liver cirrhosis, but its etiology remains unclear. Recent studies have shown that tumor necrosis factor-alpha (TNF-alpha) system is involved in the insulin resistance of human obesity. Serum concentrations of TNF-alpha, and 2 soluble TNF receptors (sTNF-RI and sTNF-RII) are increased in cirrhotic patients. This study explored whether TNF-alpha system activity was associated with insulin resistance in liver cirrhosis. A total of 26 male nondiabetic patients with liver cirrhosis (mean age, 59 +/- 3 years; body mass index, 23.7 +/- 0.4 kg/m2) and 25 male control subjects (age, 65 +/- 2 years; body mass index, 24.4 +/- 0.5 kg/m2) were studied. Serum insulin, c-peptide, TNF-alpha, sTNF-RI, and sTNF-RII concentrations were determined by immunoassay. The insulin resistance was estimated by homeostasis assessment model (HOMA IR). In cirrhotic patients, serum levels of TNF-alpha, sTNF-RI, and sTNF-RII were all higher than those in the controls, and correlated with disease severity. Also, the serum c-peptide, insulin concentrations, and the HOMA IR were higher in liver cirrhosis with comparable blood glucose to control subjects, indicating a degree of insulin insensitivity. In the whole population, there was a moderate, but statistically significant, correlation between serum sTNF-RI or sTNF-RII, and HOMA IR. Also, body mass index was associated with HOMA IR, but not related to serum TNF-alpha, and sTNF-Rs levels. In multiple regression analysis, both sTNF-RII and body mass index jointly contributed to 30% variance of HOMA IR. Our study demonstrated that elevated sTNF-RII levels were associated with insulin resistance in liver cirrhosis. The data indicated that TNF-alpha system might play a role in modulating insulin action in patients with liver cirrhosis.

Aged↗
PubMed2003

Endostatin induces autophagic cell death in EAhy926 human endothelial cells.

Endostatin, a proteolytic fragment of collagen XVIII, is a potent inhibitor of angiogenesis and suppresses neovascularization and tumor growth. However, the inhibitory mechanism of endostatin in human endothelial cells has not been characterized yet. Electron microscopic analysis revealed that endostatin induced formation of numerous autophagic vacuoles in endothelial in 6 to 24 h after treatment. Moreover, there was only a 2- to 3-fold increase in intracellular reactive oxygen species after endostatin treatment. Endostatin-induced cell death was not prevented by antioxidants (vitamin C, vitamin E, or propyl gallate) or caspase inhibitors, suggesting that the increase of oxidative stress or the activation of caspases may not be the crucial factors in the anti-angiogenic mechanism of endostatin. However, the cytotoxicity of endostatin was significantly reduced by 3-methyladenine (a specific inhibitor of autophagy) and serine and cysteine lysosomal protease inhibitors (leupeptin and aprotinin). Taken together, these results suggest that in human endothelial cells: (1) endostatin predominantly causes autophagic, rather than apoptotic, cell death, (2) endostatin-induced autophagic cell death occurs in the absence of caspase activation and through an oxidative-independent pathway, and (3) endostatin-induced "autophagic cell death" or "type 2 physiological cell death" is regulated by serine and cysteine lysosomal proteases.

Acridine Orange↗
PubMedDate not supplied

Sweet hyperopia: refractive changes in acute hyperglycemia.

PURPOSE: A prospective study was performed to evaluate refractive and ocular biometric changes in acute hyperglycemic status in patients with diabetes mellitus. METHODS: From January to August 2002, 48 eyes of 24 patients with persistent diabetes and a plasma glucose level>or=17 mmol/L or HbA1c>or=10.0% on admission were enrolled in this prospective study. Upon admission to Tri-Service General Hospital in Taipei, Taiwan, these patients underwent intensive glycemic control. The basic ophthalmic examinations, including visual acuity, intraocular pressure measurement, slit lamp, and fundus examinations, were conducted. The ocular parameters including refraction, anterior chamber depth, lens thickness, axial length, mean keratometry, and thinnest corneal thickness were evaluated by A-mode scan and Orbscan II. Each patient underwent clinical follow-up visits at 1, 2, and 4 weeks after the acute hyperglycemic episode. RESULTS: Of the 24 patients, 18 were male and 6 were female. The mean age of the patients was 55 years (range: 38 to 69). Comparing the refractive status on admission and at week 4, the authors found that 8 cases (16 eyes, 33%) showed hyperopia during hyperglycemia (+1.9+/-0.8 D), but in the other 16 cases (32 eyes, 67%), there were no significant changes. In addition, there were also no significant changes in anterior chamber depth, lens thickness, axial length, thinnest corneal thickness, or mean keratometry in the follow-up period. CONCLUSIONS: Transitory hyperglycemia produces hyperopia. The alteration in refractive index in the lens may contribute to the hyperopic change, but no change of ocular biometrics in lens or cornea is observed.

Acute Disease↗