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I Sun

Publications and source records attributed to I Sun.

16 recordsLinked to original sources
PubMed2005

Ectopic pituitary adenoma located at the pituitary stalk. Case report.

Suprasellar located ectopic pituitary adenomas are unusual tumors. We report a rare case of suprasellar prolactinoma arising from the pars tuberalis in a 37-year-old woman. Menstrual disregulation and bitemporal hemianopsia were the main complaints. Blood tests revealed hyperprolactinemia. In magnetic resonance the tumor was totally supradiaphragmatic. Pterional craniotomy and total tumor excision was performed. The pituitary stalk was preserved. Histopathologic diagnosis was a pituitary adenoma immunoreactive for prolactin. Pituitary hormonal functions returned to normal at 6 months postoperatively. No complications were seen in the postoperative period. An ectopic adenoma should be suspected in a patient with suprasellar tumor and hyperprolactinemia. Surgical excision of this tumor may result with normal pituitary functions and normal visual acuity.

Adult↗
PubMed2002

Identification and regulation of the IGFBP-4 protease and its physiological inhibitor in human trophoblasts and endometrial stroma: evidence for paracrine regulation of IGF-II bioavailability in the placental bed during human implantation.

The IGF family plays an important role in implantation and placental physiology. IGF-II is abundantly expressed by placental trophoblasts, and IGF binding protein (IGFBP)-4, a potent inhibitor of IGF actions, is the second most abundant IGFBP in the placental bed, expressed exclusively by the maternal decidua. Proteolysis of IGFBP-4 results in decreased affinity for IGF peptides, thereby enhancing IGF actions. In the current study, we have identified the IGFBP-4 protease and its inhibitor in human trophoblast and decidualized endometrial stromal cell cultures, and we have investigated their regulation in an effort to understand control of IGF-II bioavailability at the placental-decidual interface in human implantation. IGFBP-4 protease activity was detected in conditioned media (CM) from human trophoblasts and decidualized endometrial stromal cells using (125)I-IGFBP-4 substrate. Identification of the IGFBP-4 protease as pregnancy-associated plasma protein-A (PAPP-A) was confirmed by specific immunoinhibition and immunodepletion of the IGFBP-4 protease activity with specific PAPP-A antibodies. The IGFBP-4 protease activity was IGF-II-dependent in trophoblast CM. In decidualized stromal CM, PAPP-A/IGFBP-4 protease activity was also IGF-II-dependent, but was evident only when IGF-II was added in molar excess of the predominant IGFBP in decidualized stromal cell CM, IGFBP-1, supporting bioavailable IGF-II as a key cofactor of IGFBP-4 proteolysis by PAPP-A. Cultured first and second trimester human trophoblasts (n = 5) secreted PAPP-A into CM with mean +/- SEM levels of 172.4 +/- 32.8 mIU/liter.10(5) cells, determined by specific ELISA. PAPP-A in trophoblast CM (n = 3) and did not change in the presence of IGF-II (1-100 ng/ml). Cultured human endometrial stromal cells (n = 4) secreted low levels of PAPP-A (6.25 +/- 3.6 mIU/liter.10(5) cells). A physiological inhibitor of PAPP-A, the proform of eosinophil major basic protein (proMBP), was detected in trophoblast CM at levels of 1853 +/- 308 mIU/liter.10(5) cells, determined by specific ELISA, and was nearly undetectable in CM of human endometrial stromal cells. Upon in vitro decidualization of endometrial stromal cells with progesterone, PAPP-A levels in CM increased nearly 9-fold without a concomitant change in proMBP. In contrast to the experiments with trophoblasts, IGF-II and the IGF analogues, Leu(27) IGF-II, and Des (1-6) IGF-II, resulted in a dose-dependent decrease of PAPP-A levels in decidualized endometrial stromal CM by 70-90%, and a dose-dependent increase in proMBP of 14- to 41-fold. The data demonstrate conclusively that the IGF-II-dependent IGFBP-4 protease of human trophoblast and decidual origin is PAPP-A. Furthermore, the differential regulation of decidual PAPP-A and proMBP by insulin-like peptides supports a role for trophoblast-derived IGF-II as a paracrine regulator of these maternal decidual products that have the potential to regulate IGF-II bioavailability at the trophoblast-decidual interface. Overall, the data underscore potential roles for a complex family of enzyme (PAPP-A), substrate (IGFBP-4), inhibitor (proMBP), and cofactor (IGF-II) in the placental bed during human implantation.

Blood Proteins↗
PubMed1998

A methodologic issue for ophthalmic telemedicine: image quality and its effect on diagnostic accuracy and confidence.

BACKGROUND: The possibility of ophthalmic telemedicine raises questions as to the quality of images displayed on a video display terminal and its effect on a doctor's accuracy and confidence of diagnosis. This study compares diagnostic accuracy and confidence levels of subjects observing two formats of retinal imaging. METHODS: Test images included 90 conventional 4- x 6-inch retinal fundus photographs and the same set of photographs after they had been scanned, digitized, modified in brightness and contrast, and displayed on a video display terminal. Fifty-six of the images demonstrated one or more retinal anomalies; the remaining 34 were of normal fundi. Abnormalities were selected on the basis of estimates of prevalence in the general population. Twenty optometrists affiliated with the Southern California College of Optometry participated as subjects. One group of 10 was shown the photographs; the remaining ten subjects were shown the digitized images. Both groups were asked if the pictures were "healthy" or "unhealthy," how confident they were of their decision, and, if abnormal, what was the ocular disease. RESULT: T-tests were used to compare the results of the two groups. There was a statistically significant difference in the confidence of a specific diagnosis between the two groups (p = 0.018), as well as tendencies toward significance on other measures. CONCLUSION: Viewing digitally reconstructed photographic images of the retina on a video display caused doctors to lose confidence in making a diagnosis before they lost accuracy.

Adult↗
PubMed1995

Proton release from HeLa cells and alkalization of cytoplasm induced by diferric transferrin or ferricyanide and its inhibition by the diarylsulfonylurea antitumor drug N-(4-methylphenylsulfonyl)-N'-(4-cholorophenyl) urea (LY181984).

Proton release from HeLa cells was stimulated by an external oxidant, potassium ferricyanide, or by the growth factor diferric transferrin. This stimulated proton release was inhibited by the antitumor sulfonylurea LY181984 [N-(4-methylphenylsulfonyl)-N'-(4-chlorophenyl)urea] over the concentration range 10 nM to 1 microM. The antitumor-inactive sulfonylurea analog LY181985 [N-(4-methylphenylsulfonyl)-N'-(phenyl)urea] was without effect at 1 microM and required 10-100 microM concentrations to inhibit proton release. Diferric transferrin-induced alkalization of the cytoplasm estimated by BCECF [2',7'-bis(2-carboxyethyl)-5,(and 6)-carboxyfluorescein] fluorescence also was inhibited by 1 microM LY181984 but not by 1 microM LY181985. The inhibited component appeared to be amiloride resistant. The proton release induced by either ferricyanide or diferric transferrin was inhibited by about 35% at a near optimal amiloride concentration of 0.2 mM or at a dimethylamiloride concentration of 0.075 mM. However, the induced proton release was inhibited further by LY181984. Conversely, when proton release was inhibited fully by LY181984 at a near optimal concentration of 10 microM (50% inhibition), increasing concentrations of amiloride or dimethylamiloride resulted in additional inhibitions of 16 and 23%, respectively. However, the inhibitions by LY181984 and the amilorides were additive, suggesting that amiloride and the sulfonylureas may act independently. Evidence for an action of the sulfonylurea in inhibiting proton efflux differently from that of the amilorides came from measurements of sodium uptake either by fluorometry or by direct measurement with 22Na+. Sodium uptake was not inhibited by either LY181984 or LY181985 in HeLa cells at concentrations of LY181984 sufficient to inhibit proton efflux by 80% or more. The results show LY181984 to be a potent inhibitor of diferric transferrin- or ferricyanide-induced proton efflux and cytoplasmic alkalization in HeLa cells and that the inhibition may involve a component of proton transport that is resistant to amiloride.

Amiloride↗
PubMed1991

Transesophageal echocardiographic features of normal and dysfunctioning bioprosthetic valves.

Transesophageal and transthoracic echocardiography and color flow Doppler were performed in patients with 42 normal and 20 dysfunctioning bioprosthetic mitral and aortic valves. Transesophageal echocardiography was superior to the transthoracic approach in delineating bioprosthetic valve cusps and the presence of valve thickening due to valve degeneration. In 27 clinically normal bioprosthetic mitral valves, regurgitation was demonstrated in three patients by the transthoracic approach and in seven by transesophageal study. Both transesophageal and transthoracic color flow Doppler demonstrated mitral regurgitation in 17 clinically regurgitant valves. The severity of mitral regurgitation was accurately assessed by the transesophageal study in all 13 patients who underwent angiography, whereas the transthoracic imaging underestimated valvular regurgitation in 7 of the 13 cases (54%). Bioprosthetic aortic valves were normal on clinical examination in 15 patients and were regurgitant in three others. Both transthoracic and transesophageal color flow Doppler were of equal value in observing and quantifying aortic regurgitation. In five clinically normal and regurgitant mitral and aortic valves, transesophageal color flow Doppler revealed eccentric regurgitant jets suggestive of paravalvular leak. This feature was not evident by the transthoracic approach. In conclusion, transesophageal echocardiography and color flow Doppler are superior to transthoracic imaging in estimating bioprosthetic mitral, but not aortic regurgitation, in differentiating valvular from paravalvular regurgitation, and in demonstrating thickened valves due to cusp degeneration.

Aortic Valve↗
PubMed1990

A DNA-activated protein kinase from HeLa cell nuclei.

A DNA-activated protein kinase (DNA-PK) was purified from nuclei of HeLa cells. Activity was associated with a single high-molecular-mass (approximately-300,000 Da) polypeptide when analyzed by gel filtration, denaturing polyacrylamide gel electrophoresis, and Western immunoblotting using a monoclonal antibody that also inhibits enzyme activity. Nuclear localization was indicated by subcellular fractionation and confirmed by immunofluorescence on whole cells. Double-stranded DNA stimulated phosphorylation of the 300-kDa polypeptide in purified preparations as well as phosphorylation of the exogenous substrates alpha-casein, simian virus 40 large T antigen, and the human heat shock protein hsp90. Autophosphorylation led to inactivation of the enzyme. The phosphorylation of casein was stimulated over 30-fold by DNA and was specific for serine and threonine residues. Bovine serum albumin and histone H1 were poor substrates for DNA-PK, and no phosphorylation of immunoglobulin G or histones other than H1 was observed. Supercoiled or heat-denatured DNA and synthetic double-stranded RNA or RNA-DNA copolymers did not stimulate casein phosphorylation by DNA-PK. Interaction of the enzyme with DNA in the absence of exogenous substrates was demonstrated by thermal inactivation and gel mobility shifts. These characteristics identify DNA-PK as distinct from other protein kinases described in the literature and suggest that activation by DNA is an important feature of the enzyme's in vivo function.

Antibodies, Monoclonal↗
PubMed1986

NADP phosphatase as a marker in free-flow electrophoretic separations for cisternae of the Golgi apparatus midregion.

Based on cytochemical analysis, the enzyme NADP phosphatase is most concentrated in the so-called intercalary cisternae from the mid-region of the Golgi apparatus stack. Using free-flow electrophoresis to separate different Golgi regions of rat liver Golgi apparatus, the NADP phosphatase activity, based on estimation of the rate of release of inorganic phosphate from NADP under standard conditions, was similarly localized to membrane fractions from the center of electrophoretic separations. Peak specific activities for both a putative cis marker (NADH-cytochrome c reductase) and an established trans marker (galactosyltransferase) coincided with minima in NADP phosphatase activity, in agreement with the cytochemical observations. The pattern of distribution of enzyme activity for NADP phosphatase differed from that of both acid phosphatase and glucose-6-phosphatase. The pH optimum was 5.0, the Km for NADP was 0.6 mM and a corresponding production of NAD and inorganic phosphorus was shown. Taken together with other markers for free-flow electrophoresis separation, the NADP phosphatase will provide considerable utility as a specific marker to help identify intercalary cisternae of the mammalian Golgi apparatus and to monitor electrophoretic separations.

Animals↗
PubMed1985

Decreased NADH-oxidoreductase activities as an early response in rat liver to the carcinogen 2-acetylaminofluorene.

Reduced nicotinamide adenine dinucleotide (NADH):ferricyanide reductase and DT-diaphorase specific activity in total homogenates of rat liver are markedly decreased as a very early biochemical event of hepatocarcinogenesis induced by the carcinogen 2-acetylaminofluorene (AAF). A 50 to 75% decrease in NADH:ferricyanide reductase was observed after 1 day of AAF (0.025% in the diet) feeding and persisted throughout a 7-week continuum of AAF administration. Carcinogen added directly to cell extracts had no effect. Similar results were obtained with single injections of either AAF or diethylnitrosamine. Xanthine dehydrogenase was also reduced in liver following AAF administration to nearly the same extent as NADH:ferricyanide reductase and DT-diaphorase. Total NADH-cytochrome c reductase and mitochondrial activity as estimated from succinic dehydrogenase were not affected by carcinogen administration relative to basal dietary controls. The reduced nicotinamide adenine dinucleotide phosphate:cytochrome c reductase that functions in drug detoxification was elevated. With livers of animals fed 4-acetamidophenol, a hepatotoxin chemically related to AAF, small decreases were noted in NADH:ferricyanide reductase, but not in xanthine dehydrogenase nor in DT-diaphorase. Initial lowering of these activities in the livers of the carcinogen-treated animals is preceded by or concomitant with a reduction in the levels of extramitochondrial pyridine nucleotides known from other studies to result from DNA damage.

2-Acetylaminofluorene↗
PubMed1984

Monodehydroascorbate as an electron acceptor for NADH reduction by coated vesicle and Golgi apparatus fractions of rat liver.

Coated vesicles were isolated from rat liver in about 80% fraction purity as determined from electron microscopy and analyses of marker enzymes and compared with Golgi apparatus and other membrane fractions isolated in parallel. The fractions were enriched in NADH-monodehydroascorbate reductase, ascorbate oxidase and ascorbic acid. The NADH-monodehydroascorbate reductase and ascorbate oxidase of the Golgi apparatus and coated vesicles differed from that of the endoplasmic reticulum in being inhibited by the sodium selective ionophore, monensin, at physiological concentrations while these activities were stimulated by ethylenediaminetetraacetic acid in coated vesicles but not in Golgi apparatus. Activities of both coated vesicles and Golgi apparatus fractions depleted in the coat protein, clathrin, were activated by the addition of clathrin-rich supernatant fractions. The results are discussed in the context of monodehydroascorbate as an acceptor for electron transport-mediated transfer of electrons from NADH by coated vesicles as part of a possible mechanism to drive membrane translocations or to acidify the interiors of vesicles.

Animals↗
PubMedDate not supplied

Transesophageal echocardiographic evaluation of left atrial mass lesions.

Transesophageal echocardiography with color flow Doppler studies was performed on 12 consecutive patients who had left atrial mass identified by transthoracic echocardiography. In two patients with atrial myxoma, transesophageal study identified the tumor by its attachment to the atrial septum. In all instances, the tumors were larger and more mobile by transesophageal study and influenced the decision to operate early on an asymptomatic patient. In six instances the masses in the atria were deemed to be thrombi because of associated spontaneous echo contrast, location in the left atrial appendage, mitral valvular disease or prosthesis, atrial fibrillation, congestive heart failure, and enlarged left atrial chamber. In two patients the left atrial masses on transesophageal imaging were large vegetations attached to the mitral valve with ruptured chordae tendineae. In two patients, because of superior quality images obtained by transesophageal imaging, the atrial mass lesions were deemed to be a prominent muscle band between the left atrial appendage and left upper pulmonary vein. In conclusion, transesophageal echocardiography is superior to transthoracic imaging in elucidating the cause and significance of atrial mass lesions and helps in guiding appropriate therapy.

Adult↗
PubMedDate not supplied

Transesophageal echocardiographic evaluation of right atrial mass lesions.

Transesophageal echocardiography with color flow Doppler studies was performed on 10 consecutive patients who had right atrial masses identified by transthoracic echocardiography. In one patient with right atrial myxoma, transesophageal study identified the tumor by its attachment to the atrial septum and ruled out the transthoracic finding of possible additional tumor mass in the right ventricle. In two instances the mass in the atria were deemed to be thrombi because of lack of attachment to the atrial septum, atrial fibrillation, and enlarged right atrial chambers. In all patients, the thrombi appeared larger by transesophageal study and was associated in one instance with atrial septal defect. The atrial septal defect was not identified by the transthoracic study and probably accounted for stroke of the patient through paradoxical emboli. In six patients, because of superior quality images rendered by transesophageal imaging, the right atrial mass lesions were deemed to be anatomic variants, which included prominent eustachian valves, remnants of Chiari network, and thickened atrial septum. We concluded that transesophageal echocardiography is superior to transthoracic imaging in elucidating the cause and significance of right atrial mass lesions and that it helps in guiding appropriate therapy.

Adolescent↗