bluuebunny/crossref_metadata_2025_split huggingface dataset:
Evaluating the visual experience: visual acuity and the visual analogue scale
Authors: Pointer Jonathan S. 
Published: November 2003

AbstractPurpose:  To attempt a comparison of the visual experience [assessed using a visual analogue scale (VAS)] with visual acuity in a group of normally‐sighted adult optometric patients.Methods:  A single‐item 100 mm paper VAS was administered to a sequence of 142 normally‐sighted pre‐presbyopic patients. Each individual was invited to indicate their recent subjective distance visual experience between the extremes of ‘dreadful’ (0 mm) and ‘perfect’ (100 mm). Each patient's binocular visual acuity was then determined at 6 m using a high‐contrast logMAR chart under usual consulting room conditions.Results:  A weak association was revealed between the subjective indication of recent visual experience and the actual level of binocular acuity recorded in this normally‐sighted group of subjects. On the basis of group responses a statistically significant discontinuity in the scores recorded with the VAS was demonstrated between patients who attained a clinical acuity better or worse than 0.10 logMAR units (6/7.5). Patient gender, age, and whether spectacles were habitually worn for distance viewing, were each revealed to be not statistically significant features.Conclusions:  For normally‐sighted optometric patients the subjective criterion of visual satisfaction would appear to be only loosely associated with the contemporaneous record of clinical acuity.
The relation between tear film tests in patients with dry eye disease
Authors: Nichols Kelly K. , Nichols Jason J. , Lynn Mitchell G. 
Published: November 2003

AbstractPurpose:  The purpose of this report was to investigate the relation between dry eye diagnostic tests.Methods:  Dry eye patients were enrolled to complete a clinical examination, including the following dry eye tests: a meibomian gland evaluation, tear meniscus height, fluorescein tear breakup time, fluorescein staining of the cornea, the Schirmer 1 test, the phenol red thread test, and rose bengal staining of the conjunctiva. Statistical analyses, including correlation coefficients, the Wilcoxon sign rank test, chi‐square test, and logistic regression were used to address the relation between these clinical tests of dry eye.Results:  There was a strong relation between the Schirmer test and fluorescein staining in all four statistical analyses. Similarly, there was also a strong relation between the phenol red thread test and both fluorescein and rose bengal staining. Finally, the results of the Schirmer test were associated with the tear breakup time test in three of four analyses.Conclusions:  The results indicate that tests of aqueous deficiency (volume or production) are associated with ocular surface desiccation. This important relation should be recognized when choosing dry eye tests as outcomes in clinical trials and epidemiological studies.
Proximity factor in image size magnification for optical instruments in general
Authors: Harris W. F. 
Published: November 2003

AbstractA general expression is derived for the proximity factor in near image size magnification for an arbitrary instrument in front of an arbitrary eye. The proximity factor is a 2 × 2 matrix. The instrument and eye may be astigmatic and have decentred elements. The image on the retina may be blurred or not. The analysis is exact within the limitations of linear optics. The general results are specialized for the case of a stigmatic instrument and a stigmatic eye. The results are applied to the case of a thick, possibly bitoric, spectacle lens. The Appendix treats two numerical examples.
Hepatic Encephalopathy: An Update of Pathophysiologic Mechanisms
Authors: Hazell Alan S. , Butterworth Roger F. 
Published: November 2003

Abstract.Hepatic encephalopathy (HE) is a neuropsychiatric disorder that occurs in both acute and chronic liver failure. Although the precise pathophysiologic mechanisms responsible for HE are not completely understood, a deficit in neurotransmission rather than a primary deficit in cerebral energy metabolism appears to be involved. The neural cell most vulnerable to liver failure is the astrocyte. In acute liver failure, the astrocyte undergoes swelling resulting in increased intracranial pressure; in chronic liver failure, the astrocyte undergoes characteristic changes known as Alzheimer type II astrocytosis. In portal‐systemic encephalopathy resulting from chronic liver failure, astrocytes manifest altered expression of several key proteins and enzymes including monoamine oxidase B, glutamine synthetase, and the so‐called peripheral‐type benzodiazepine receptors. In addition, expression of some neuroneal proteins such as monoamine oxidase A and neuronal nitric oxide synthase are modified. In acute liver failure, expression of the astrocytic glutamate transporter GLT‐1 is reduced, leading to increased extracellular concentrations of glutamate. Many of these changes have been attributed to a toxic effect of ammonia and/or manganese, two substances that are normally removed by the hepatobiliary route and that in liver failure accumulate in the brain. Manganese deposition in the globus pallidus in chronic liver failure results in signal hyperintensity on T1‐weighted Magnetic Resonance Imaging and may be responsible for the extrapyramidal symptoms characteristic of portal‐systemic encephalopathy. Other neurotransmitter systems implicated in the pathogenesis of hepatic encephalopathy include the serotonin system, where a synaptic deficit has been suggested, as well as the catecholaminergic and opioid systems. Further elucidation of the precise nature of these alterations could result in the design of novel pharmacotherapies for the prevention and treatment of hepatic encephalopathy.
Effect of Pentachlorophenol (PCP) on Frog Cornea Epithelium
Authors: Carrasquer Gaspar , Li Ming , Yang Shen , Schwartz Manuel , Dinno Mumtaz A. 
Published: November 2003

Abstract.Pentachlorophenol (PCP) is a toxic substance that affects many tissues adversely. Present experiments, using an in vitro preparation, were designed to study whether PCP affected the electrophysiological parameters of the bullfrog cornea epithelium, specifically, the Na+/K+ ATPase pump and the K+ conductance located in the basolateral membrane and the Cl− conductance located in the apical membrane. For this purpose, corneas were impaled with microelectrodes and experiments were done under short‐circuit current (Isc) conditions. Addition of PCP to a concentration of 5 × 10−5M to the tear solution gave a marked decrease in Isc; a marked depolarization of the intracellular potential, Vo; and minimal but significant decreases in the apical membrane fractional resistance, fRo, and in the transepithelial conductance, gt. Isc experiments in Cl−‐free solutions with amphotericin B in the tear solution confirm results indicating that PCP inhibits the active transepithelial transport mechanism and produces a small increase in the basolateral membrane resistance due to a decrease in the K+ conductance.
Dehydroepiandrosterone Protects Hippocampal Neurons Against Neurotoxin‐Induced Cell Death: Mechanism of Action2
Authors: Cardounel Arturo , Regelson William , Kalimi Mohammed 
Published: November 2003

Abstract.Dehydroepiandrosterone (DHEA), an adrenal cortex hormone secreted in large quantities in humans, protects cells of the clonal mouse hippocampal cell line HT‐22 against the excitatory amino acid glutamate (5 mM), and amyloid β‐protein (2 μM) toxicity in a dose‐dependent manner with optimum protection obtained at 5 μM concentration of DHEA. The protective effects of DHEA appear to be specific in that other related steroids and metabolites of DHEA, such as 5‐androstene‐3β,17β‐diol, etiocholan‐3α‐ol‐17‐one, etiocholan‐3β‐ol‐17‐one, testosterone, and 5α‐androstane‐3,17‐dione, offered no protection even at 50 μM concentrations. In addition, using immunocytochemical techniques, we observed that 20 hr of treatment with 5 mM glutamate remarkably increased glucocorticoid receptor (GR) nuclear localization in neuronal cells. Interestingly, 5 μM DHEA treatment for 24 hr, followed by 5 mM glutamate treatment for 20 hr almost completely reversed the copious nuclear localization of GR observed by glutamate treatment alone. Results obtained suggest that DHEA protects hippocampal neurons, at least in part, by its antiglucocorticoid action via decreasing hippocampal cells nuclear GR levels.
Butyrate‐Induced G2/M Block in Caco‐2 Colon Cancer Cells is Associated with Decreased p34cdc2 Activity
Authors: Harrison Lawrence E. , Wang Qing Mei , Studzinski George P. 
Published: November 2003

Abstract.Butyrate, a short‐chain fatty acid, has been reported to inhibit proliferation and stimulate differentiation in multiple cancer cell lines. Whereas the effects of butyrate on cellular differentiation are well documented, the relationship between butyrate‐induced differentiation and its effect on cell cycle traverse is less well understood. The purpose of this study was to investigate the effects of butyrate on the regulatory proteins of the G2/M traverse in the Caco‐2 colon cancer cell model. We demonstrated that the inhibition of proliferation and increased cellular differentiation after treatment of Caco‐2 cells with butyrate were associated with a significant G2/M cell cycle block. Although protein levels of the major G2/M regulatory protein, p34cdc2, were unchanged, a decrease in p34cdc2 activity was noted. Despite this decrease in activity, the inhibitory tyrosine phosphorylation of p34cdc2 was decreased, suggesting that other factors are responsible for the decreased kinase activity. The reduced activity of p34cdc2 provides a possible mechanism for the accumulation of Caco‐2 cells in the G2/M cell cycle compartment following exposure to butyrate. This cell system provides a new model for studies of G2/M cell cycle perturbations.
Postprandial Low‐Density Lipoproteins in Type 2 Diabetes are Oxidized More Extensively Than Fasting Diabetes and Control Samples
Authors: Diwadkar Veda A. , Anderson James W. , Bridges Susan R. , Gowri Maya S. , Oelgten Peter R. 
Published: November 2003

Abstract.This study examined the kinetics of low‐density lipoprotein (LDL) oxidation in the fasting and postprandial states of diabetic and control subjects to determine if LDL oxidation may contribute to accelerated atherosclerosis in diabetes. We compared in vitro oxidation of LDL from 12 control and 13 Type 2 diabetic subjects in the fasting and postprandial states. The extent of oxidation was assessed by length of lag phase, formation of conjugated dienes (CD), lipid peroxides, thiobarbituric acid reactive substances (TBARS), and percentage reduction in free amine groups. Diabetic subjects were significantly older and heavier. Comparisons between control and diabetic subjects in the postprandial state showed that the lag phase was significantly shorter in diabetic subjects than controls (P = 0.005), TBARS were significantly higher (P = 0.006), and levels of CD were higher at 60, 65, and 70 min (P < 0.01). In the fasting state, however, these comparisons were not significant. In diabetic subjects, postprandial samples had a significantly shorter lag phase (P = 0.003), higher TBARS (P = 0.006), and higher levels of CD at 60, 65 (P < 0.001), and 70 min (P = 0.0013) compared to fasting samples. Elevated levels of serum triglycerides in diabetic subjects were negatively correlated to lag phase, in fasting (P = 0.06) and postprandial states (P = 0.002). We conclude that accelerated oxidation of LDL seen in postprandial states in diabetes may be a critical contributor to cardiovascular risks. Elevated levels of serum triglycerides may contribute to the rapid oxidation of LDL seen in diabetic subjects.
Negative Regulation of Human Heme Oxygenase in Microvessel Endothelial Cells by Dexamethasone
Authors: Deramaudt Therese B. , Da silva Jeane‐Louis , Remy Pierre , Kappas Attallah , Abraham Nader G. 
Published: November 2003

Abstract.Heme oxygenase‐1 (HO‐1) is a stress protein, and its induction has been suggested to participate in defense mechanisms against agents that promote oxidative injury such as endotoxins and heme. We have shown that the inflammatory cytokines, interleukin‐6 (IL‐6) and heme‐induced HO‐1 gene expression, were suppressed by dexamethasone (Dex) in a sustained manner. We examined the mechanism by which the anti‐inflammatory agent, Dex, inhibits IL‐6 and heme‐induced HO‐1 expression in rabbit coronary endothelial cells. Endothelial cells treated with heme (10 μM) and IL‐6 (25 ng/ml), increased HO‐1 mRNA 15‐ and 60‐fold, respectively. The activity of HO was increased 3‐fold after such treatment. Although Dex failed to inhibit heme‐mediated HO‐1 mRNA and HO activity, it was able to reverse IL‐6–stimulated HO activity. Several human HO‐1 promoter‐drive chloramphenicol acetyltransferase (CAT) constructs were examined to analyze IL‐6 and Dex‐mediated modulation of the HO‐1 gene in endothelial cells. CAT assays revealed that the HO‐1 promoter region between –180 and –1500 might contain a Dex‐mediated negative regulator. Gel mobility shift assays using nuclear extracts from IL‐6–treated endothelial cells showed a binding to the synthetic 21 base pairs of the HO‐1 sequence that contains the putative STAT3 sequence. STAT3‐specific probe inhibited nuclear binding protein to the putative HO‐1‐STAT3 sequence. This suggests that IL‐6 induction of human HO‐1 is mediated via the JAK‐STAT pathway and that Dex inhibition of gene expression is carried out by activation of a transcriptional protein in competition with the STAT3 binding site.
On the Role of Vitamin C and Other Antioxidants in Atherogenesis and Vascular Dysfunction
Authors: Frei Balz 
Published: November 2003

Abstract.Oxidative stress has been implicated as an important etiologic factor in atherosclerosis and vascular dysfunction. Antioxidants may inhibit atherogenesis and improve vascular function by two different mechanisms. First, lipid‐soluble antioxidants present in low‐density lipoprotein (LDL), including α‐tocopherol, and water‐soluble antioxidants present in the extracellular fluid of the arterial wall, including ascorbic acid (vitamin C), inhibit LDL oxidation through an LDL‐specific antioxidant action. Second, antioxidants present in the cells of the vascular wall decrease cellular production and release of reactive oxygen species (ROS), inhibit endothelial activation (i.e., expression of adhesion molecules and monocyte chemoattractants), and improve the biologic activity of endothelium‐derived nitric oxide (EDNO) through a cell‐ or tissue‐specific antioxidant action. α‐Tocopherol and a number of thiol antioxidants have been shown to decrease adhesion molecule expression and monocyte‐endothelial interactions. Vitamin C has been demonstrated to potentiate EDNO activity and normalize vascular function in patients with coronary artery disease and associated risk factors, including hypercholesterolemia, hyperhomocysteinemia, hypertension, diabetes, and smoking.
Opposing Effects of Estrogen and Progestins on LDL Oxidation and Vascular Wall Cytotoxicity: Implications for Atherogenesis
Authors: Zhu Xiaodong , Bonet Bartolome , Gillenwater Hiedi , Knopp Robert H. 
Published: November 2003

Abstract.Estrogens are widely regarded as beneficial to arterial wall health. Among the mechanisms of this benefit are antioxidant effects on LDL and the arterial wall. Because progestins oppose the effect of estrogen in several systems, we asked if progestins oppose the antioxidant effect of estrogen. To study this question, LDL and various female sex hormones were incubated alone and combined in the absence or presence of bovine aortic endothelial cells, placental trophoblast, or macrophages, and LDL oxidation and cytotoxicity were quantitated. In the absence of cells, LDL incubated with copper in phosphate‐buffered saline enhanced the oxidation of LDL. When 17β‐estradiol was added to this system, an antioxidant effect was observed. Progestins inhibited this protective estrogenic effect. In endothelial cell culture, progestins also opposed the antioxidant effect of estrogen, with the strongest antiestrogenic effect seen with the synthetic progestins, levonorgestrel and medroxyprogesterone acetate (MPA). Endothelial cell cytotoxicity was proportional to the enhanced lipid peroxide formation observed with progestins or estrogen. Similar opposing effects were seen when estrogen and progesterone were added to primary cultures of placental trophoblast or macrophages. Thus, three cell culture systems modeling circulating arterial blood contact with cell surfaces demonstrated opposing effects of estrogens and progestins on LDL oxidation and cell cytotoxicity. These studies are in keeping with published reports that female sex steroids influence LDL oxidation in vivo and consequent arterial wall injury.
Oxidative Stress in the Pathogenesis of Preeclampsia
Authors: Hubel Carl A. 
Published: November 2003

Abstract.The etiology and pathogenesis of the pregnancy syndrome preeclampsia remain poorly understood. There is substantial evidence to suggest that the diverse manifestations of preeclampsia, including altered vascular reactivity, vasospasm, and discrete pathology in many organ systems, are derived from pathologic changes within the maternal vascular endothelium. With the theme of endothelial cell dysfunction emphasized, this review focuses on the role of oxidative stress (an imbalance favoring oxidant over antioxidant forces) in the pathogenesis of preeclampsia. Data are summarized regarding 1) the role of the placenta in preeclampsia; 2) evidence and mechanisms of oxidative stress in the preeclampsia placenta; 3) markers of oxidative stress in the maternal circulation; and 4) the potential role of maternal dyslipidemia in generation of oxidative stress. A recurrent theme is that free radical reactions, promoted by “cross‐talk” between the diseased placenta and maternal dyslipidemia, promote a vicious cycle of events that make cause and effect difficult to distinguish but likely contribute to the progression of preeclampsia.
Mechanisms of DNA Oxidation
Authors: Aust Ann E. , Eveleigh Jamie F. 
Published: November 2003

Abstract.Oxidative damage of DNA caused by a variety of chemical and physical agents appears to be linked to cancer. However, it is becoming increasingly clear that endogenous generation of oxidants, such as hydroxyl radical and peroxynitrite, lead to oxidation of DNA, and this may cause cancer in individuals where no obvious exposure to chemical or physical agents known to be carcinogenic has occurred. The mechanisms for generation of these two oxidants in living organisms will be discussed and their reactivities with DNA to produce oxidized products (e.g., 8‐oxo‐dG) will be presented with special emphasis on the individual characteristics of the generation and reactivity of each oxidant.
Oxidants and Skeletal Muscle Function: Physiologic and Pathophysiologic Implications
Authors: Clanton Thomas L. , Zuo Li , Klawitter Paul 
Published: November 2003

Abstract.Previous studies have demonstrated that skeletal muscles generate considerable reactive oxygen during intense muscle contraction. However, the significance of this phenomenon and whether it represents normal physiology or pathology are poorly understood. Treatment with exogenous antioxidants suggests that normal redox tone during contraction is influencing ongoing contractile function, both at rest and during intense exercise. This could represent the influence of redox‐sensitive proteins responsible for excitation‐contraction coupling or redox‐sensitive metabolic enzymes. Some conditions associated with intense exercise, such as local tissue hypoxia or elevated tissue temperatures, could also contribute to reactive oxygen production. Evidence that muscle conditioning results in upregulation of antioxidant defenses also suggests a close relationship between reactive oxygen and contractile activity. Therefore, there appears to be a significant role for reactive oxygen in normal muscle physiology. However, a number of conditions may lead to an imbalance of oxidant production and antioxidant defense, and these, presumably, do create conditions of oxidant stress. Ischemia‐reperfusion, severe hypoxia, severe heat stress, septic shock, and stretch‐induced injury may all lead to oxidant‐mediated injury to myocytes, resulting in mechanical dysfunction.
The Antioxidant Function of Metallothionein in the Heart
Authors: Kang Y. James 
Published: November 2003

Abstract.The antioxidant function of metallothionein (MT) was first suggested in the early 1980s. Studies in vitro have revealed that MT reacts directly with reactive oxygen species, including superoxide and hydroxyl radicals and hydrogen peroxide. These reactions have never been demonstrated in intact animal studies. Nevertheless, both pharmacologic and genetic studies have shown that MT functions in protection against oxidative injury in vivo. In particular, the antioxidant function of MT in the heart has been explored extensively. The data gathered from recent studies using a cardiac‐specific, MT‐overexpressing transgenic mouse model have provided direct evidence to support this physiological role of MT. Under acute and chronic oxidative stress conditions such as treatment with doxorubicin, ischemia‐reperfusion, and dietary copper restriction, MT‐overexpressing transgenic mouse hearts displayed a marked resistance to the injurious consequences, including biochemical, pathological, and functional alterations. This protective action of MT correlates with its inhibition of reactive oxygen species–induced lipid peroxidation. A critical elucidation of the mechanism of action of MT as an antioxidant in vivo remains to be achieved. However, the combination of recent understanding of the zinc cluster structure of MT and novel molecular genetic approaches has provided the basis for further advancement in this field.