bluuebunny/crossref_metadata_2025_split huggingface dataset:
Basic fibroblast growth factor (bFGF) alleviates the scar of the rabbit ear model in wound healing
Authors: Xie Ju Lin , Bian Hui Ning , Qi Shao Hai , Chen Hua De , Li Hou Dong , Xu Ying Bin , Li Tian Zeng , Liu Xu Sheng , Liang Hui Z. , Xin Bang Rong , Huan Yong 
Published: July 2008

ABSTRACTStudies suggest a possible antiscarring effect of basic fibroblast growth factor (bFGF) during wound healing. However, little is known about the precise pathological mechanisms of bFGF. In particular, there is only limited information available about the mechanism of exogenous administration of bFGF to scar formation. To investigate the effect of bFGF on the hypertrophic scar in the rabbit ear model and to clarify the mechanisms of bFGF on treatment for scar in wound healing, the rabbit ear model of wound healing was created and treated topically with bFGF once daily for 3 months; then we examined the changes of macroscopic and histopathological characteristics of scars and the expression of collagen and collagenase‐1 (matrix metalloproteinase‐1). The results of macroscopic and histologic characteristics revealed a significant difference between scars treated with bFGF and control scars. The expression of collagen in the scars treated with bFGF was decreased, as compared with the scars treated with saline. Further study revealed that bFGF could remarkably enhance expression of matrix metalloproteinase‐1. bFGF could improve the quality of wound healing and remarkably alleviate the scar in the rabbit ear model in wound healing, which suggests that bFGF exerted a net negative effecton scar formation in wound healing. The evidence should contribute to a better understanding of the biological activities of bFGF during hypertrophic scar formation.
NON‐CORONARY HEART DISEASE IN DIALYSIS PATIENTS: Sudden Cardiac Death and Dialysis Patients
Authors: Herzog Charles A. , Mangrum J. Michael , Passman Rod 
Published: July 2008

AbstractDialysis patients have extraordinarily high mortality rates. The death rate for all US dialysis patients in 2004 was 230 per 1000 patient‐years. Cardiac disease is the major cause of death in dialysis patients and accounts for 43% of all‐cause mortality. In the United States Renal Data System database 62% of cardiac deaths (or 27% of all deaths) are attributable to arrhythmic mechanisms. The estimated rate of sudden cardiac death in US dialysis patients in 2002 was 7% per year. There are several plausible explanations for the special vulnerability of dialysis patients to sustaining sudden cardiac death. Obstructive coronary artery disease, coupled with diminished tolerance to myocardial ischemia (in the setting of myocardial fibrosis and left ventricular hypertrophy), rapid electrolyte shifts in hemodialysis patients, and derangements in autonomic function may all contribute to this heightened risk of sudden cardiac death. This review focuses on the epidemiology of sudden cardiac death in dialysis patients, underlying mechanisms of sudden death, and potential interventions to reduce the risk of sudden cardiac death in dialysis patients (including medical therapy and defibrillators). It is unlikely that one single therapeutic intervention will prevent sudden cardiac death in dialysis patients; but a more modest (and attainable) goal is the implementation of multiple strategies to reduce the risk of sudden cardiac death in this special high‐risk population.
Recovering the Reptile Community after the Mine‐Tailing Accident of Aznalcóllar (Southwestern Spain)
Authors: Márquez‐Ferrando Rocío , Pleguezuelos Juan M. , Santos Xavier , Ontiveros Diego , Fernández‐Cardenete Juan R. 
Published: July 2008

Abstract Ecosystem restoration requires that habitat requirements of all species be considered. Among animal communities in Mediterranean ecosystems, reptiles, as ectothermic vertebrates, need refuges for avoidance of extreme environmental temperatures, concealment from predators, and oviposition sites. In 1998, a massive amount of tailings broke out of the holding pond of the Aznalcóllar mine (southwestern Spain) and polluted the Guadiamar river valley. After the accident, a soil‐ and vegetation restoration program began, and the Guadiamar Green Corridor was created to connect two huge natural areas, Doñana National Park and the Sierra Morena. Within this corridor, the reptile community remained dramatically impoverished, probably because of elimination of all natural refuges during the soil restoration program. To test this hypothesis, we set an array of artificial refuges (logs) in a large experimental plot. During the 5 years of the experiment (2002–2006), the area managed with artificial refuges exhibited a better and faster recovery of the reptile community in species richness and individual abundance than did the control area with no artificial refuges. Moreover, reptile colonization of the Guadiamar Green Corridor was transverse rather than lineal—that is, it did not act as a corridor for reptiles, at least in the first stages of colonization. This suggests that landscape restoration programs should not neglect refuge availability, a limiting resource for reptile species.
The Effects of Flavonoid Allelochemicals from Knapweeds on Legume–Rhizobia Candidates for Restoration
Authors: Alford Élan R. , Vivanco Jorge M. , Paschke Mark W. 
Published: July 2008

Abstract Russian knapweed (Acroptilon repens) and Spotted knapweed (Centaurea maculosa) are allelopathic weeds invasive in North American grasslands. Both species contain at least one phytotoxic flavonoid root exudate with demonstrated negative influences on other plants. Previous findings indicated that Silky lupine (Lupinus sericeus), among other legumes, was relatively resistant to Spotted knapweed invasion and allelochemistry. We hypothesized that legume species may exhibit resistance to flavonoids in knapweed root exudates and may serve as candidate species for management efforts. Because legumes form symbiotic relationships with rhizobia, these bacteria must also be evaluated for allelochemical resistance before legumes can be recommended for restoration. In this study, we examined four legume species for effects of 7,8‐benzoflavone (from Russian knapweed) and (±)‐catechin (from Spotted knapweed) on rhizosphere interactions involving legume roots and associated rhizobia. Pure cultures of four rhizobia strains exhibited varied responses when grown with 7,8‐benzoflavone or (±)‐catechin. Alfalfa (Medicago sativa) and its bacterial symbiont, Sinorhizobium meliloti, exhibited allelochemical resistance that varied with (±)‐catechin concentration when grown in vitro. Four legume species were grown under greenhouse conditions. Plants that were inoculated and nodulated generally exhibited no response to 7,8‐benzoflavone or (±)‐catechin treatments. Plants that were not inoculated exhibited stronger responses. Therefore, inoculation and nodulation may confer resistance to allelochemicals. These results, when coupled with previous research and field observations, suggest that legumes may not be susceptible to knapweed allelopathy and may be good choices in restoration of knapweed infestations when inoculated, particularly on sites with low soil nitrogen.
Evaluation of Restoration Measures in a Shallow Lake through a Comparison of Present Day Zooplankton Communities with Historical Samples
Authors: Louette Gerald , Declerck Steven , Vandekerkhove Jochen , De Meester Luc 
Published: July 2008

Abstract Many shallow lakes have lost a large part of their ecological value during the past decades. Human‐induced factors such as eutrophication and inappropriate fish stock management are generally the main causes for this loss. To restore such degraded habitats, several measures are taken, typically involving a reduction of nutrient loading and interventions in the aquatic food web functioning (biomanipulation). In this study, we report on the joint effects of a series of restoration measures in a shallow lake (Lake Kraenepoel, Belgium, 22 ha) and evaluate these effects via three different criteria. The first criterion is that the target condition, being a clearwater phase with submerged macrophytes, was successfully achieved and persisted for a period of at least 5 years after restoration. Second, we detected a substantial change in community structure of cladoceran zooplankton and an associated increase in species richness and conservation value following restoration measures. Finally, we observed that the general structure of the present day cladoceran zooplankton community resembles well that of the preeutrophication period (1929–1931). Current species richness, however, tends to be lower than in the reference period, and some rare species are still lacking. It is conceivable that, when submerged macrophytes develop further, a subset of specialist species may reappear. Overall, the use of historical habitat‐specific samples offers a major opportunity for evaluating restoration success in great detail. Community structures may directly be compared, the gain or loss of specific species can accurately be documented, and more insights in the observed patterns be obtained.
Familial Clustering of Migraine: Further Evidence From a Portuguese Study
Authors: Lemos Carolina , Castro Maria‐José , Barros José , Sequeiros Jorge , Pereira‐Monteiro José , Mendonça Denisa , Sousa Alda 
Published: July 2008

Objective.— Our aim was to evaluate familial aggregation of migraine in a large group of Portuguese families, and to assess if familial aggregation differs between MA and MO.Methods.— Familial aggregation was evaluated by estimating relative risk (RR) of migraine in 143 first‐degree relatives of 50 probands with MA, in 196 first‐degree relatives of 94 probands with MO and also in proband's spouses. Probands were enrolled in the study from a clinical sample and a population sample was used as reference.Results.— A significantly increased risk of migraine was found in both first‐degree relatives of MO probands (RR = 3.7; 95% CI: 3.2‐4.3) and of MA probands (RR = 3.6; 95% CI: 3.1‐4.3), comparatively to the general population. Risk for spouses was not increased. First‐degree relatives of MA probands and MO probands had a significantly increased risk of both MA and MO compared to the general population. In the group of MA probands, RR of MA in first‐degree relatives reached a significant 4‐fold increase when compared with RR of MO (RRMA|MA = 12.2, 95%CI: 7.7‐19.5; RRMO|MA = 3.1, 95%CI: 2.5‐3.8), while, in the group of MO probands, RR of MA was not significantly increased when compared with RR of MO (RRMA|MO = 5.3, 95%CI: 3.1‐9.2; RRMO|MO = 4.0, 95%CI: 3.5‐4.7).Conclusions.— The present study focus on familial aggregation of migraine in a Portuguese population. Our results demonstrate a substantial familial risk of migraine with evidence of both common and specific etiologic mechanisms for either migraine subtypes.
Headache Disability in Orofacial Pain Patients Is Related to Traumatic Life Events
Authors: Branch Morris A. 
Published: July 2008

Background.— Headache is commonly reported in patients presenting with orofacial pain. It has only recently been demonstrated that headache‐related disability is high in orofacial pain patients. Traumatic life events (TLEs) such as sexual abuse, physical abuse, and post‐traumatic stress disorder (PTSD) are also common in orofacial pain patients and in the same patients reporting headache. In association with a previously reported study of headache disability in orofacial pain patients, it was noted that Migraine Disability Assessment (MIDAS) scores appeared to be significantly higher in patients with TLEs.Objectives.— To investigate the relationship between TLEs and headache disability in a clinic population of orofacial pain patients.Design.— Retrospective study.Methods.— Four hundred and twenty‐six consecutive orofacial pain patient records were reviewed, composed of new patients seen at the Orofacial Pain Center, National Naval Medical Center, Bethesda, MD, from November 2003 through December 2004.Results.— Of 426 orofacial pain patients reporting headache, 109 or 41.7% reported TLEs. In patients with TLEs, the mean MIDAS score was 28.81 ± 37.2 compared with 13.5 ± 17.9 for patients not reporting TLEs P < .000. MIDAS scores were significantly correlated with TLEs, Spearman correlation coefficient 0.272, P < .010.Conclusions.— This is the first study to demonstrate that headache disability is significantly higher in a group of orofacial pain patients with TLEs and is correlated with that report of traumatic events. These findings clearly demonstrate the necessity for providers to consider a history of TLEs in orofacial pain patients presenting with headache.
Choroid Plexus Dysfunction: The Initial Event in the Pathogenesis of Wernicke’s Encephalopathy and Ethanol Intoxication
Authors: Nixon Peter F. , Jordan Lindsay , Zimitat Craig , Rose Stephen E. , Zelaya Fernando 
Published: July 2008

Background:  In both acute ethanol intoxication and in thiamin deficient glucose metabolism, previous studies have detected blood‐brain barrier (BBB) and/or blood‐CSF‐barrier (BCSFB) impairment but were unable to assess their significance in relation to other changes in the brain.Methods:  Contrast‐enhanced, magnetic resonance imaging (MRI) was used to detect and time any impairment of the BBB or BCSFB in rats given an acute ethanol load or in rats made thiamin deficient to the point of mild ataxia and then given an acute glucose load.Results:  The BCSFB at the choroid plexus (CP) was impaired within 10 minutes by either (i) a single i.p. dose of glucose in thiamin‐deficiency, an effect that was attenuated by prior MK801 and preceded the published onset of exacerbation of motor incoordination and elevation of brain glutamate derivatives; or (ii) a single i.p. dose of ethanol in thiamin‐sufficiency, an effect that was proportional to the blood alcohol concentration and preceded the published onset of signs of intoxication. In contrast to the BCSFB, the BBB remained intact throughout the 90 minutes period of these experiments.Conclusions:  In both ethanol intoxication and thiamin‐deficient glucose metabolism, BCSFB impairment exposes the CSF and hence the brain extracellular fluid to neuroactive substances from the blood. CP impairment is the earliest detected event in both these animal models; and explains the paraventricular location of WE neuropathology and why WE is associated with, but not dependent on, alcoholism.
Acute Alcohol Intake Induces SOCS1 and SOCS3 and Inhibits Cytokine‐Induced STAT1 and STAT3 Signaling in Human Monocytes
Authors: Norkina Oxana , Dolganiuc Angela , Catalano Donna , Kodys Karen , Mandrekar Pranoti , Syed Amber , Efros Marian , Szabo Gyongyi 
Published: July 2008

Background:  Acute alcohol consumption is associated with induction of immuno‐inhibitory cytokines and down‐regulation of pro‐inflammatory responses to various pathogens. We previously reported that alcohol activates janus kinase/signal transducer and activator of transcription (JAK/STAT) signaling leading to IL‐10 induction. The JAK‐STAT pathway also activates its own negative regulators, suppressors of cytokine signaling (SOCS) 1 and SOCS3. SOCS proteins are inducible inhibitors that negatively regulate STAT3/STAT1 signaling pathways induced by cytokines, IL‐6 or IFNs. Here we aimed to explore the effect of acute alcohol on induction of SOCS1/SOCS3 and regulation of STAT3/STAT1 pathways induced by IL‐6 or IFNs in human monocytes.Methods:  Blood samples from normal volunteers were collected before and 24 hours after consumption of 2 ml vodka/kg body weight. For in vitro experiments human monocytes were pretreated with ethanol (EtOH) followed by stimulation with cytokines; proteins were analyzed by Western blot, nuclear protein binding to DNA by EMSA, and RNA by real time PCR.Results:  Acute in vivo or in vitro alcohol treatment increased both SOCS1 and SOCS3 RNA expression in monocytes. Alcohol treatment resulted in increased STAT3 and STAT1 DNA binding capacity. Activation of both STAT1 and STAT3 has been shown to induce SOCS1/3. We hypothesized that induction of SOCS proteins by alcohol in turn may lead to modulation of cytokine signaling through STAT1 and STAT3. Indeed, we observed significant down‐regulation of IL‐6‐, IFNα‐ and IFNγ‐induced STAT1 DNA binding as well as inhibition of IL‐6‐ and IFNγ‐induced STAT3 when alcohol was added to monocytes 3 hours prior to the cytokine stimulation. Consistent with inhibition of IL‐6‐induced STAT3 DNA binding in alcohol‐pretreated cells, the levels of IL‐6‐dependent genes, MCP‐1 and ICAM‐1, was reduced after IL‐6 stimulation. Similar to EtOH alone, combined EtOH+IL‐6 simulation resulted in increased expression of both SOCS3 and SOCS1 genes.Conclusion:  While acute alcohol treatment alone activates STAT1/3 signaling pathways and induces SOCS3 and SOCS1 levels in monocytes, alcohol also leads to down‐regulation of IL‐6‐, IFNα‐, and IFNγ‐induced signaling via STAT1/STAT3 pathways, likely through excessive SOCS activation.
Glutamate Export at the Choroid Plexus in Health, Thiamin Deficiency, and Ethanol Intoxication: Review and Hypothesis
Authors: Nixon Peter F. 
Published: July 2008

Introduction: The earliest observed effect in the pathogenesis of experimental Wernicke’s encephalopathy and of ethanol intoxication in rats is impairment of the blood cerebrospinal fluid (CSF) barrier at the choroid plexus (CP). For an explanation, these observations direct attention to the role of the CP in maintaining glutamate homeostasis in the CSF.Methods: Characteristics of the CP epithelium (CPE) are reviewed, focusing on its role in removal of glutamate from the CSF and its potential for impairment by ethanol oxidation or by thiamin‐deficient glucose oxidation.Results: The export of glutamate from CSF to blood at the CP is energy dependent, saturable, and stereospecific. However, the incapacity of the CP to convert glutamate to other metabolites makes it vulnerable to glutamate accumulation should α‐ketoglutarate dehydrogenase activity be decreased. Elsewhere ethanol metabolism and thiamin‐deficiency independently decrease the activity of this mitochondrial enzyme. We argue that they have the same effect within the mitochondria‐rich CPE, thereby decreasing energy production necessary for export of glutamate from CSF to blood; diverting its energy metabolism to further glutamate production; and impairing its blood CSF barrier function. This impairment appears to be mediated by glutamate and is attenuated by MK801 but whether it involves one of the CPE glutamate receptors is yet uncertain. This impairment exposes the CSF and hence the paraventricular brain extracellular fluid to neuroactive substances from the blood, including further glutamate, explaining the paraventricular location of neuropathology in Wernicke’s encephalopathy. Other organs normally protected from blood by a barrier are affected also by ethanol abuse and by thiamin deficiency, namely the eye, peripheral nerves, and the testis. Much less is known regarding the function of these barriers.Conclusions: Impairment of the CP by ethanol intoxication and by thiamin‐deficient carbohydrate metabolism has a common, rational explanation that can guide future research.
Insulin and Insulin‐Like Growth Factor Resistance in Alcoholic Neurodegeneration
Authors: De La Monte Suzanne M. , Tong Ming , Cohen Ariel C. , Sheedy Donna , Harper Clive , Wands Jack R. 
Published: July 2008

Background:  Chronic alcohol feeding of adult Long Evans rats causes major central nervous system abnormalities that link neuronal loss and impaired acetylcholine homeostasis to ethanol inhibition of insulin and insulin‐like growth factor (IGF) signaling and increased oxidative stress.Objectives:  We now characterize the integrity of insulin and IGF signaling mechanisms and assess molecular indices of neurodegeneration in the cerebellar vermis and anterior cingulate gyrus of human alcoholics.Results:  Alcoholic cerebella had increased neuronal loss, gliosis, lipid peroxidation, and DNA damage relative to control. Quantitative RT‐PCR studies demonstrated reduced expression of insulin, insulin receptor and IGF‐II receptor in the anterior cingulate, and reduced expression of insulin, IGF‐I, and their corresponding receptors in the vermis. Competitive equilibrium binding assays revealed significantly reduced specific binding to the insulin, IGF‐I, and IGF‐II receptors in both the anterior cingulate and vermis of alcoholic brains. These effects of chronic alcohol abuse were associated with significantly reduced expression of choline acetyltransferase, which is needed for acetylcholine biosynthesis.Conclusions:  The results suggest that alcoholic neurodegeneration in humans is associated with insulin and IGF resistance with attendant impairment of neuronal survival mechanisms and acetylcholine homeostasis.
Trazodone for Sleep Disturbance After Alcohol Detoxification: A Double‐Blind, Placebo‐Controlled Trial
Authors: Friedmann Peter D. , Rose Jennifer S. , Swift Robert , Stout Robert L. , Millman Richard P. , Stein Michael D. 
Published: July 2008

Background:  Trazodone is a commonly prescribed off‐label for sleep disturbance in alcohol‐dependent patients, but its safety and efficacy for this indication is unknown.Methods:  We conducted a randomized, double‐blind, placebo‐control trial of low‐dose trazodone (50 to 150 mg at bedtime) for 12 weeks among 173 alcohol detoxification patients who reported current sleep disturbance on a validated measure of sleep quality or during prior periods of abstinence. Primary outcomes were the proportion of days abstinent and drinks per drinking day over 6‐months; sleep quality was also assessed.Results:  Urn randomization balanced baseline features among the 88 subjects who received trazodone and 85 who received placebo. The trazodone group experienced less improvement in the proportion of days abstinent during administration of study medication (mean change between baseline and 3 months: −0.12; 95% CI: −0.15 to −0.09), and an increase in the number of drinks per drinking day on cessation of the study medication (mean change between baseline and 6 months, 4.6; 95% CI: 2.1 to 7.1). Trazodone was associated with improved sleep quality during its administration (mean change on the Pittsburgh Sleep Quality Index between baseline and 3 months: −3.02; 95% CI: −3.38 to −2.67), but after it was stopped sleep quality equalized with placebo.Conclusions:  Trazodone, despite a short‐term benefit on sleep quality, might impede improvements in alcohol consumption in the postdetoxification period and lead to increased drinking when stopped. Until further studies have established benefits and safety, routine initiation of trazodone for sleep disturbance cannot be recommended with confidence during the period after detoxification from alcoholism.