Biomedical subjects

C Chen

Publications and source records attributed to C Chen.

At least 1,369 records · Page 76Linked to original sources

PubMedDate not supplied

Epidemic keratoconjunctivitis caused by a new genotype of adenovirus type 8 (Ad8)-a chronological review of Ad8 in Southern Taiwan.

PURPOSE: To understand the pathogenic evolution of viral keratoconjunctivitis in Kaohsiung, Taiwan, a retrospective molecular and clinical analysis was conducted. METHODS: From January 1990 to December 1994, conjunctival swab samples from patients suspected of having viral conjunctivitis were collected for viral culture isolation, neutralization test (NT), and endonuclease cleavage analysis. Six restriction endonucleases, comprising HindIII, BamHI, SalI, SstI, SmaI, and PstI, were used for cleavage. Clinical examinations of patients were performed by two senior ophthalmologists. RESULTS: Twenty-one cases of a new genotype of adenovirus (Ad) type 8, designated as Ad8H, were discovered in the 27 detected adenovirus cases. The Ad8H has a distinct cleavage pattern, especially by HindIII and SalI. The Ad8H keratoconjunctivitis induced more subconjunctival hemorrhage (33.3%), keratitis (33.3%), and lymphadenopathy (85.7%) than other genotypes of Ad8 previously isolated in Kaohsiung, Taiwan. CONCLUSION: We have discovered a new genotype, Ad8H, which was prevalent as the main pathogen of the adenoviral keratoconjunctivitis in Kaohsiung, Taiwan from 1990 to 1994. Adenovirus type 8 is evolving into more genotypes with a trend towards more severe symptoms, including subconjunctival hemorrhage, keratitis, and lymphadenopathy.

Adenoviridae Infections↗

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Biplane transesophageal color Doppler echocardiography for assessment of mitral valve area with mitral inflow jet widths.

Biplane transesophageal color Doppler echocardiography can image the mitral valve orifice in two orthogonal views. If the maximal stenotic jet width through the mitral valve obtained with the vertical transducer represents the major axis, the stenotic jet width dissected by the horizontal transducer should be the minor axis of the mitral orifice. Thus the mitral valve area can be calculated assuming an oval shape of mitral orifice. Nineteen patients with mitral stenosis were investigated. Maximal mitral stenotic jet width (JW1) was searched on a vertical plane and the jet width from the orthogonal view (JW2) was obtained on a horizontal plane. Mitral valve areas from the color Doppler jet widths were calculated by pi.JW1/2.JW2/2 and compared with those derived from Gorlin's formula. Adequate quality of echocardiographic images could be obtained in all patients for transesophageal color Doppler jet width measurements or Doppler pressure half-time determinations and in 16 of 19 patients for transthoracic planimetery of the mitral orifice at the parasternal short axis. Mitral valve areas derived from biplane transesophageal color Doppler imaging (1.31 +/- 0.53 cm2) were not different from those calculated according to Gorlin's formula from the catheterization data (1.25 +/- 0.50 cm2), those determined by transthoracic echocardiographic planimetery (1.38 +/- 0.5 cm2), or those calculated from the Doppler pressure half-time method (1.32 +/- 0.41 cm2) (difference not significant by analysis of variance). There was a very strong correlation between transesophageal echocardiographic mitral valve areas and those derived from catheterization data (r = 0.94; standard error of the estimate = 0.13 cm2). A similar correlation was obtained for the planimetric echocardiographic method (r = 0.94; standard error of the estimate = 0.14 cm2). A slightly less strong correlation was found between mitral valve areas derived from the Doppler pressure half-time method and those derived from Gorlin's formula (r = 0.83; standard error of the estimate = 0.24 cm2). The pressure half-time method accurately predicted the mitral valve area in most (15/19) patients, but it significantly (> 0.4 cm2) overestimated mitral valve area in two patients with aortic regurgitation and underestimated (< 0.4 cm2) mitral valve area in two patients with left ventricular hypertrophy. Determination of mitral valve area by color Doppler biplane transesophageal echocardiography is an alternative for accurate estimation of mitral valve area and may be most useful in intraoperative monitoring during surgical or balloon mitral commissurotomy or in the case of inadequate imaging quality of transthoracic echocardiography.

Adult↗

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Analysis of mitral inertance: a factor critical for early transmitral filling.

The upslope of the transmitral E wave depends on the combined influence of the rate of change of the atrioventricular gradient and the inertial mass of blood within the mitral apparatus (inertance). To use observed transmitral velocity to predict the atrioventricular pressure (delta p) difference requires knowledge of the magnitude of mitral inertance (M, inertial mass divided by effective orifice area), closely related to the length over which blood accelerates and decelerates on passing through the valve. To define the magnitude and determining factors for mitral inertance in typical valvular geometries, we used an in vitro model in which a known atrioventricular gradient (delta p, range 3.8 to 39 mm Hg) was applied instantaneously to orifices (areas of 0.5, 1, 1.5, 2, and 2.5 cm2) and conduits (volume 2.5 to 24 ml). Continuous wave Doppler spectra were recorded and the slope (dv/dt) of the tangent to the upslope was measured manually. From slope and pressure difference, inertance was calculated as delta p/(dv/dt). In 103 combinations of pressure gradients and orifices or conduits, inertance ranged between 1.9 and 12.7 gm/cm2. Linear regression showed that inertance M was highly correlated with orifice diameter D (M = 3.17 D; r = 0.84; p < 0.0001) and, in the conduits, with diameter and length L (M = 4.1 D + 0.7 L-1.8; r = 0.87; p < 0.0001). Inertance was not significantly related to the pressure gradient. In conclusion, inertance depends mainly on the mitral apparatus geometry and most strongly on orifice diameter. Knowledge of mitral inertance should help to extract quantitative data on atrioventricular pressure difference from the upslope of the transmitral E wave.

Binomial Distribution↗

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Impact of delayed reperfusion of myocardial hibernation on myocardial ultrastructure and function and their recoveries after reperfusion in a pig model of myocardial hibernation.

UNLABELLED: This study examined the effect of delayed reperfusion of myocardial hibernation from 24 hours to 7 days on myocardial ultrastructural and functional changes and their recoveries after reperfusion. BACKGROUND: We have previously shown in pigs that after reperfusion the functional and structural alterations in short-term myocardial hibernation which was reperfused in 24 hours can recover in 7 days. The effect of delayed reperfusion of hibernating myocardium on the extent and severity of cellular and extracellular structural changes of hibernating myocardium, and their recoveries after reperfusion is not known. METHODS AND RESULTS: A severe LAD stenosis was created in 27 pigs, reducing resting flow by 30-40% immediately after placement of the stenosis and producing acute ischemia as evidenced by regional lactate production, a decrease in regional coronary venous pH, reduced regional wall thickening (from 38.5 +/- 5.1% to 10.4 +/- 8.0%) and a 33% reduction of regional oxygen consumption. The stenosis was maintained either for 24 hours in 9 pigs (group 1) with LAD flow of 0.65 +/- 0.13 ml/min/g (38% reduction), or for 7 days in 17 pigs (group 2) with LAD flow of 0.67 +/- 0.14 ml/min/g (36% reduction). There were no differences (p = NS) in the reduction of wall thickening, rate-pressure product, lactate production, or regional oxygen consumption between group 1 and group 2. Quantitative morphometric evaluation of the ultrastructure on electromicrographs revealed a greater decrease in sarcomere volume and a higher incidence of myocytes with reduced sarcomere volume in 7-day than in 24-hour hibernating regions (53 +/- 19% versus 33 +/- 14%, p < 0.05). Patchy myocardial necrosis with replacement fibrosis was common, but 6 of the 18 pigs had no myocardial necrosis or replacement fibrosis in the 7-day hibernating group, and 4 of 9 pigs had no patchy myocyte necrosis in the 24 hour hibernating group. In 6 pigs in group 1 in which the stenosis was then released and hibernating myocardium reperfused in 24 hours, regional wall thickening recovered to 30 +/- 6% (p = NS compared to baseline) after one week of reperfusion. In 12 pigs in group 2 in which the stenosis was released and hibernating myocardium reperfused in 7 days, regional wall thickening recovered slowly, from 10.1 +/- 7.2% to 18.1 +/- 8.3% at one week (n = 5) and to 28.0 +/- 3.6% at 3-4 weeks of reperfusion (n = 7, p < 0.05 compared to baseline). Similarly, the sarcomere volume or myofilament recovered significantly (p < 0.01) and was not different compared to the normal region (p = NS) in the 24-hour hibernating region of group 1, but the recovery was much slower and was incomplete at 4 weeks (p < 0.01) compared to baseline in the 7-day hibernating region of group 2. Recovery of regional wall thickening correlated with ultrstructural recovery (p < 0.01). By multivariate stepwise regression analysis, the degree of LAD flow reduction, the extent of fibrosis, and myofilament loss were independent predictors of the extent of functional recovery. CONCLUSIONS: In a porcine model of myocardial hibernation with myocardial hypoperfusion, systolic dysfunction, and metabolic adaptations, a longer period of myocardial hibernation with delayed reperfusion was associated with more severe abnormalities of myocytes. an increasing interstitial fibrosis, and more protracted myofibrillar and functional recoveries after reperfusion. The extent of functional recovery is related to the degree of coronary flow reduction, the severity of the ultrastructural changes, and the extent of interstitial fibrosis.

Animals↗

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Reversibility and pathohistological basis of left ventricular remodeling in hibernating myocardium.

The phenomenon of left ventricular (LV) remodeling with dilatation, wall thinning, and increased muscle mass has previously been reported in pigs with 7-day myocardial hibernation. This study investigated cellular and extracellular basis and reversibility of the structural LV remodeling with hibernating myocardium. Five groups of pigs were included: Group A: 7-day myocardial hibernation with a fixed coronary stenosis; Group B: 7-day hibernation with subsequent 3-week reperfusion by release of the stenosis; Group C: control group with sham operation; Group D: 24-hour myocardial hibernation to define structural mechanism of initial wall thinning in the hibernating region without confounding factors of cell loss or hypertrophy, Group E: 4-week myocardial hibernation to exclude the possibility of spontaneous regression of LV remodeling with hibernation. LAD flow decreased by 38+/-12% (p<0.01) with a significant decrease in systolic wall thickening at 7 days of hibernation with severe coronary stenosis (Group A). End-diastolic wall thickness decreased by 19% (p<0.01) accompanied by a decrease in myocyte number across the wall (44%) and in myocyte density (24%), a significant increase in myocyte width (17%), a mild increase in interstitial tissues in hibernating region, and significant increases in LV diastolic volume and in LV mass at 7 days. After reperfusion (Group B), LV volume decreased, LV ejection fraction improved, and myocyte hypertrophy regressed with a decreased LV mass index without a significant change in interstitial tissue. LV remodeling progressed with further increases in LV volume, mass, and interstitial fibrosis in 4-week hibernation. In pigs undergoing 24 hours of myocardial hibernation (Group D), end-diastolic LV wall thickness decreased significantly in the hibernating region with a proportional decrease in the transmural myocyte number but without changes in myocyte width, myocyte density, or interstitial tissues. Therefore, progressive gross LV remodeling associated with hibernating myocardium is accompanied by increasing myocyte hypertrophy and interstitial fibrosis. In hibernating myocardial region, wall thinning is proportional to a decreased myocyte number across the LV wall, indicating slippage of myocytes as a preponderant mechanism for the wall thinning. Myocyte hypertrophy develops within 7 days in hibernating myocardium, causing an increase in LV mass. These changes are partially reversible after reperfusion.

Animals↗

PubMedDate not supplied

DNA complexing with polyamidoamine dendrimers: implications for transfection.

DNA and polyamidamine (PAMAM) dendrimers form complexes on the basis of the electrostatic interactions between negatively charged phosphate groups of the nucleic acid and protonated (positively charged) amino groups of the polymers. Charge neutralization of both components and subsequent increases of the net positive charge of the complex result in changes in the physicochemistry and biological properties of the complexes. The formation of soluble, low-density and insoluble, high-density complexes was analyzed using UV light absorption and measurements of radioactive labeled DNA. Formation of high molecular weight and high-density complexes depended mainly on the DNA concentration and was enhanced by increasing the dendrimer-DNA charge ratio. Electrostatic charge related effects (attraction or repulsion of charged particles) appeared to be modulated by the generation of dendrimer (size of the polymer). With the progressive increases in the dendrimer-DNA charge ratio (above 20), an increase in the amount of low-density, soluble complexes was observed. Functional analysis revealed that the great majority (>90%) of transfection is carried by low-density, soluble, complexes which only represent approximately 10-20% of total complexed DNA. The ability of the dendrimer to complex and form aggregates with DNA is crucial for efficient transfection and the function of the complexed DNA.

Animals↗

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Growth hormone secretagogue actions on the pituitary gland: multiple receptors for multiple ligands?

1. Growth hormone (GH) secretion is thought to occur under the reciprocal regulation of two hypothalamic hormones, namely GH-releasing hormone (GHRH) and somatostatin (SRIF), through their engagement with specific cell-surface receptors on the anterior pituitary somatotropes. 2. In addition to GHRH and SRIF, synthetic GH-releasing peptides (GHRP) or GH secretagogue(s) (GHS) regulate GH release through the activation of a novel receptor, the GHS receptor (GHS-R). 3. The cloning of the GHS-R from human, swine and rat identifies a novel G-protein-coupled receptor involved in the control of GH secretion and supports the existence of an undiscovered hormone that may activate this receptor. 4. Varieties of intracellular signalling systems are suggested to mediate the action of GHS, which include changes in intracellular free Ca2+ ([Ca2+]i), cAMP, protein kinases A and C, phospholipase C etc. 5. With regard to the use of signalling systems by GHS, especially a new form of GHRP or GHRP-2, a clear species difference has been demonstrated, supporting the possibility of more than one type of GHS-R.

Animals↗

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Clinical and economic outcomes of coronary angioplasty alone or in combination with stents in academic health centers: a retrospective database analysis.

OBJECTIVES: Indications for the use of stents are evolving and their optimal place in therapy remains to be defined. The objective was to compare the 1-year clinical and economic outcomes of percutaneous transluminal coronary agioplasty (PTCA) with and without the use of stents. METHODS: This retrospective database analysis was conducted using data from 60 US academic medical centers in 1996 and 1997. Outcomes of interest included in-hospital mortality (both on sentinel and readmission visits), readmission rates, revascularization procedures, length of stay, and the cost of sentinel and readmission hospitalization. RESULTS: A total of 27,020 patients either did (n = 13,254) or did not (n = 13,766) receive coronary stents in conjunction with PTCA. The median cost of hospitalization for the stent group was about dollar 1,409 higher (mean, dollar 1,200) than the no-stent group and the length of stay was similar (4.3 days vs. 4.5 days, respectively, P = .2628). Mortality rates on readmission (0.9% stent vs. 0.8% no-stent, P = NS) did not differ. However, patients in the stent group had better mortality rates compared to the no-stent group during the sentinel visit (1.7% vs. 2.7%, P < .001). Stent use was not associated with a significantly lower risk of a revascularization procedure on readmission to the same institution (OR 0.95, 95% CI 0.87-1.04, P = .28). CONCLUSIONS: Stents were associated with a 1% decrease of inpatient mortality during the sentinel visit without impacting length of stay or readmission rates. This advantage was associated with a dollar 1,409 higher median cost of hospitalization in the stent group.

Journal Article↗

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Molecular and mechanistic validation of delayed healing rat wounds as a model for human chronic wounds.

The purpose of this study was to provide molecular and mechanistic evaluation of an ischemic wound model in rats to determine if it is a valid model for human chronic wounds. Compared to acute wounds, human chronic wounds contain markedly elevated levels of proinflammatory cytokines and matrix metalloproteinases, while matrix metalloproteinase inhibitors and growth factor activity are diminished. Accordingly, tissue from ischemic and normal rat wounds were analyzed for cytokine, proteases and growth factor levels. Dorsal full thickness punch wounds were created in rats using a reproducible template. The ischemic wound group (n = 10) had six uniformly placed wounds within a bipedicled dorsal flap. The control group (n = 10) had the same wounds created without elevation of a flap. On postwound days 3, 6 and 13 wounds were excised and analyzed. Protein levels for tumor necrosis factor-alpha were determined with a rat-specific enzyme-linked immunosorbent assay, while mRNA was determined by RNase protection assay. Matrix metalloproteinases and serine protease detection was done using gelatin and casein zymography, respectively. Significant delay in healing was achieved in the ischemic group: 50% healing for control wounds was at 7 days and 11 days for ischemic wounds (p < 0.001). No significant differences between wound groups were found for interleukin-1beta, and mRNA for tumor necrosis factor-alpha and interleukin-1beta. However, at day 13 ischemic wounds contained significantly more tumor necrosis factor-alpha than controls and normal skin (586 +/- 106 pg/biopsy vs. 79 +/- 7 pg/biopsy vs. 52 +/- 2 pg/biopsy; p < 0. 001). Zymography showed substantially greater quantities of matrix metalloproteinase-2, matrix metalloproteinase-9, and serine proteases in ischemic wounds. This model of delayed healing in rats shares many of the key biochemical, molecular and mechanistic characteristics found in human chronic wounds, namely elevated tumor necrosis factor-alpha and protease levels. As such, this model will likely prove to be useful in chronic wound research, particularly in developing novel therapeutics.

Animals↗

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[Spontaneous subdural hematoma in a 18-day-old male newborn infant with severe hemophilia A].

Most intracranial bleedings in hemophiliacs occur in patients more than 6 months of age. In the neonatal period, this complication is rare and almost always observed in the first week of life. Based on a review of the literature, intracranial hemorrhage is an exceedingly rare occurrence in infants with hemophilia aged 2 weeks-6 months. We report on a male infant with hemophilia A who was referred to our hospital on day 18 because of pallor and jaundice. The neurological examination was normal. A cerebral ultrasound showed a left sided subdural hematoma with a shift of the midline structures to the right. Packed red blood cells (10 ml/kg) and factor VIII replacement (250 IU) were rapidly instituted and a craniotomy with evacuation of the hematoma was performed. The postoperative course was uneventful. On discharge, the neurological examination was considered normal.

Echoencephalography↗

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Intramolecular glycosylation to form 4-methoxy-2,6-dioxopyrimidine nucleosides via O6,5'-cyclonucleosides.

Lewis-acid promoted intramolecular N1 glycosylation to form the novel O6,5'-cyclonucleoside 1a occurs in high yield from the corresponding acyclic thiophenyl-glycoside 12. The relative stability of the O6,5' tether compared with O2,5' and O2,3' tethers is reported. Cleavage of the anhydro bond was effected with aqueous base to yield the 4-methoxybarbituric acid nucleoside analogue 14.

Glycosylation↗

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Induction of xenobiotic enzymes by the MAP kinase pathway and the antioxidant or electrophile response element (ARE/EpRE).

Cellular responses to xenobiotic-induced stress can signal proliferation, differentiation, homeostasis, apoptosis, or necrosis. To better understand the underlying molecular mechanisms after exposure to xenobiotics or drugs, we studied the signal transduction pathways, the mitogen-activated protein kinase (MAPK), and the basic leucine zipper transcription factor Nrf2, activated by different agents in the induction of Phase II drug metabolizing enzymes (DMEs). The MAPKs, characterized as proline-directed serine/threonine kinases, are essential components of signaling pathways that convert various extracellular signals into intracellular responses through serial phosphorylation cascades. Once activated, MAPKs can phosphorylate many transcription factors, such as c-Jun, ATF-2, and ultimately lead to changes in gene expression. Two classes of Phase II gene inducers, which are also cancer chemopreventive agents, were studied: (1) the phenolic antioxidants, namely butylated hydroxyanisole (BHA) and its active de-methylated metabolite t-butylhydroquinone (tBHQ), and phenolic flavonoids such as green tea polyphenols (GTP) and (-)-epigallocatechin-3-gallate (EGCG); and (2) the naturally occurring isothiocyanates, namely phenethyl isothiocyanate (PEITC), and sulforaphane. BHA and tBHQ are both well-known phenolic antioxidants used as food preservatives, and strongly activate c-Jun N-terminal kinase 1 (JNK1), extracellular signal-regulated protein kinase 2 (ERK2), or p38, in a time- and dose-dependent fashion. Free radical scavengers N-acetyl-L-cysteine (NAC), or glutathione (GSH), inhibited ERK2 activation and, to a much lesser extent, JNK1 activation by BHA/tBHQ, implicating the role of oxidative stress. Under conditions where MAPKs were activated, BHA or GTP also activated ARE/EpRE (antioxidant/electrophile response element), with the induction of Phase II genes such as NQO. Transfection studies with various cDNAs encoding wild-type or dominant-negative mutants of MAPKs and/or transcription factor Nrf2, substantially modulated ARE-mediated luciferase reporter activity in the presence or absence of phenolic compounds. Other phytochemicals including PEITC, and sulforaphane, also differentially regulated the activities of MAPKs, Nrf2, and ARE-mediated luciferase reporter gene activity and Phase II enzyme induction. A model is proposed where these xenobiotics (BHA, tBHQ, GTP, EGCG, PEITC, sulforaphane) activate the MAPK pathway via an electrophilic-mediated stress response, leading to the transcription activation of Nrf2/Maf heterodimers on ARE/EpRE enhancers, with the subsequent induction of cellular defense/detoxifying genes including Phase II DMEs, which may protect the cells against toxic environmental insults and thereby enhance cell survival. The studies of these signaling pathways may yield insights into the fate of cells upon exposure to xenobiotics.

Animals↗

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Photolithographic synthesis of high-density oligonucleotide probe arrays.

High-density DNA probe arrays provide a massively parallel approach to nucleic acid sequence analysis that is transforming gene-based biomedical research and diagnostics. Light-directed combinatorial oligonucleotide synthesis has enabled the large-scale production of GeneChip probe arrays which contain several hundred of thousand oligonucleotide sequences on glass "chips" about one cm2 in size. Due to their very high information content, GeneChip probe arrays are finding widespread use in the hybridization-based detection and analysis of mutations and polymorphisms ("genotyping"), and in a wide range of gene expression studies. The manufacturing process integrates solid-phase photochemical oligonucleotide synthesis with lithographic techniques adapted from the microelectronics industry. The present-generation methodology employs MeNPOC photo-activatable nucleoside monomers with proximity photolithography, and is currently capable of printing individual 10 microns 2 probe features at a density of 10(6) probes/cm2.

DNA Probes↗

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Novel nucleoside triphosphate analogs for the enzymatic labeling of nucleic acids.

We have evaluated several novel nucleotide analogs suitable for enzymatic labeling of nucleic acid targets for a variety of array-based assays. Two new reagents in particular, a C4-labeled 1-(2',3'-dideoxy-beta-D-ribofuranosyl) imidazole-4-carboxamide 5'-triphosphate 5 and an N1-labeled 5-(beta-D-ribofuranosyl)-2,4(1H,3H)-pyrimidinedione 5'-triphosphate 3, were found to be excellent substrates for labeling with terminal deoxynucleotidyl transferase and T7 RNA polymerase, respectively.

Biotin↗

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Temporal specificity of long-term depression in parallel fiber--Purkinje synapses in rat cerebellar slice.

The phenomenon of cerebellar long-term depression (LTD), a decrease of synaptic strength between the parallel fibers (PFs) and Purkinje cells after conjunctive activation of PFs and the climbing fibers (CFs), is implicated as a cellular mechanism for motor learning. We have characterized a field-potential recording technique in cerebellar slice and have used the technique to examine the temporal conditions for cerebellar LTD induction in an attempt to examine the relevance of LTD to associative conditioning. Interstimulus intervals (ISIs) between onsets of PF and CF activation and the number of paired stimuli (pairings) were examined. LTD has distinct temporal specificity that seems to be constrained by inhibitory interneurons and can be masked by excessive stimulation. When 100 paired stimuli were given to PFs and CFs, LTD was induced with an ISI of 250 msec (PF activation preceding CF activation). In contrast, a smaller forward (125 msec), simultaneous (0 msec), or backward (-250 msec) ISIs were not effective for inducing LTD. However, the blockade of GABAA receptor-mediated inhibition made it possible to induce LTD with 100 pairs of simultaneous stimulations. Furthermore, by increasing the number of pairings to 600, significant LTD was observed with all four interstimulus intervals. These results suggest that temporal conditions for LTD induction share some similarity to associative learning of discrete motor responses.

Animals↗

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Function of estrogen receptor isoforms alpha and beta in endometrial carcinoma cells.

The aim of this study was to explore how to modulate the expression of estrogen receptors (ER) alpha and beta and to verify the role of ERalpha and beta in relationship to estrogen and tamoxifen (TAM). A series of oligodeoxyribonucleotides (ODN) corresponding to regions of the ERalpha or beta was tested in human endometrial cancer cell lines (HEC-1B). The change in HEC-1B proliferation in response to 17beta-estradiol (E(2)) and TAM under the impact of antisense ODN was studied. The results of the study are as follows: 1) transfection with antisense ODN significantly inhibited ERalpha and ERbeta protein production, 2) the cells lost the ability to proliferate in response to E(2) after transfection with ERalpha antisense ODN especially at 24, 48, and 72 h. There was no obvious change in response to E(2) in HEC-1B cell lines that were transfected with ERbeta antisense ODN, and 3) after transfection with ERalpha antisense ODN, HEC-1B cells lost the ability to proliferate in response to TAM at 48 h. This inhibition was also observed after transfection with ERbeta antisense ODN at 24 h. ERalpha may be the primary receptor in the proliferation of HEC-1B cells in response to E(2). Both ERalpha and ERbeta are involved in the agonist impact of TAM on endometrial cancer cells.

Cell Proliferation↗

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Coronary artery bypass grafting in patients with chronic congestive heart failure: a 10-year experience with 203 patients.

From 1983 to 1992, 203 patients with chronic congestive heart failure and no angina underwent primary coronary artery bypass. This represented 3% of patients undergoing coronary artery bypass grafting. Ninety-two percent of the patients were in New York Heart Association (NYHA) functional class III or IV prior to undergoing coronary artery bypass grafting. Thallium perfusion imaging was performed in 21% of the patients, with a reversible defect present in 88%. An internal mammary artery graft was used in 70% of the patients. The hospital mortality was 6.0% and the actuarial survival at 5 years was 59%. An improvement in NYHA functional class occurred in 75% of the surviving patients with a mean improvement of 1.6 +/- 0.6 functional classes. Univariate analysis identified risk factors for hospital death as emergency operation, recent myocardial infarction (< 30 days), and the need for an intra-aortic balloon pump. A trend emerged for nonuse of an internal mammary artery to predict hospital death. A positive thallium perfusion scan was not a predictor of early or late survival, nor did it influence NYHA functional class. The use of the internal mammary artery significantly enhanced late survival (p = 0.01), however, did not affect the functional class of survivors. We conclude that coronary artery bypass grafting is effective in ameliorating symptoms of chronic congestive heart failure in patients suffering from chronic ischemic cardiomyopathy and can be performed with acceptable early and late mortality.

Actuarial Analysis↗

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Fourier transform infrared imaging spectroscopy analysis of collagenase-induced cartilage degradation.

Collagenase treatment of cartilage serves as an in vitro model of the pathological collagen degradation that occurs in the disease osteoarthritis (OA). Fourier transform infrared imaging spectroscopic (FT-IRIS) analysis of collagenase-treated cartilage is performed to elucidate the molecular origin of the spectral changes previously found at the articular surface of human OA cartilage. Bovine cartilage explants are treated with 0.1% collagenase for 0, 15, or 30 min. In situ collagen cleavage is assessed using immunofluorescent staining with an antibody specific for broken type II collagen. The FT-IRIS analysis of the control and treated specimens mirrors the differences previously found between normal and OA cartilage using an infrared fiber optic probe (IFOP). With collagenase treatment, the amide II/1338 cm(-1) area ratio increases while the 1238 cm(-1)/1227 cm(-1) peak ratio decreases. In addition, polarized FT-IRIS demonstrates a more random orientation of the collagen fibrils that correlate spatially with the immunofluorescent-determined regions of broken type II collagen. We can therefore conclude that the spectral changes observed in the collagenase-treated cartilage, and similarly in OA cartilage, arise from changes in collagen structure. These findings support the use of mid-infrared spectral analysis, in particular the minimally invasive IFOP, as potential techniques for the diagnosis and management of degenerative joint diseases such as osteoarthritis.

Animals↗