bluuebunny/crossref_metadata_2025_split huggingface dataset:
17α-Ethinylestradiol alters reproductive behaviors, circulating hormones, and sexual morphology in male fathead minnows (Pimephales promelas)
Authors: Salierno James D. , Kane Andrew S. 
Published: December 2008

AbstractEcologically relevant indicators of endocrine disruption in fish must be linked with measures of reproductive success. The ability of male fathead minnows (Pimephales promelas) to compete for, maintain, and defend a spawning substrateis paramount to reproductive success. The present study quantified alterations in male fathead minnow reproductive behaviors after exposure to environmentally relevant concentrations (0, 10, 20, or 40 ng/L) of 17α-ethinylestradiol (EE2) for 21 d. A video-based behavioral quantification system examined changes in male-male competitive behaviors (chasing and head-butting) and ability of males to maintain spawning substrates (nibbling and scrubbing). Behaviors analyzed included time under the spawning substrate, frequency of substrate cleaning, and conspecific aggression. Plasma hormone levels (11-ketotestosterone [11-KT], testosterone, and estradiol [E2]), vitellogenin (VTG), secondary male characteristics (tubercle count and dorsal nape pad rank), gonadosomatic index (GSI), and gonad histology also were evaluated. Exposure to 40 ng/L of EE2 decreased the ability of exposed males to compete with control males for spawning substrates (p = 0.09). Furthermore, exposed males displayed reduced frequency of substrate cleaning activities as well as chasing male competitors (p ≤ 0.05). 11-Ketotestosterone, testosterone, and E2 were lower, and VTG was notably higher, in EE2-exposed males compared with control males (p ≤ 0.03). 17α-Ethinylestradiol exposure in males also was associated with reductions in tubercles; lower GSI, gonadal maturity ranks, and number of resorbed tubercles; and presence of an ovipositor (p ≤ 0.001). These data reveal alterations in male reproductive behavior that coincide with decreased hormone levels and secondary sex characteristics. Behavioral endpoints to discern potential ecological consequences in fish exposed to low concentrations of endocrine-disrupting chemicals may provide sensitive and functional indices of effect.
Hypothalamic ERK Mediates the Anorectic and Thermogenic Sympathetic Effects of Leptin
Authors: Rahmouni Kamal , Sigmund Curt D. , Haynes William G. , Mark Allyn L. 
Published: December 2008

OBJECTIVE—Leptin is an adipocyte hormone that plays a major role in energy balance. Leptin receptors in the hypothalamus are known to signal via distinct mechanisms, including signal transducer and activator of transcription-3 (STAT3) and phosphoinositol-3 kinase (PI 3-kinase). Here, we tested the hypothesis that extracellular signal–regulated kinase (ERK) is mediating leptin action in the hypothalamus.
RESEARCH DESIGN AND METHODS—Biochemical, pharmacological, and physiological approaches were combined to characterize leptin activation of ERK in the hypothalamus in rats.
RESULTS—Leptin activates ERK1/2 in a receptor-mediated manner that involves JAK2. Leptin-induced ERK1/2 activation was restricted to the hypothalamic arcuate nucleus. Pharmacological blockade of hypothalamic ERK1/2 reverses the anorectic and weight-reducing effects of leptin. The pharmacological antagonists of ERK1/2 did not attenuate leptin-induced activation of STAT3 or PI 3-kinase. Blockade of ERK1/2 abolishes leptin-induced increases in sympathetic nerve traffic to thermogenic brown adipose tissue (BAT) but does not alter the stimulatory effects of leptin on sympathetic nerve activity to kidney, hindlimb, or adrenal gland. In contrast, blockade of PI 3-kinase prevents leptin-induced sympathetic activation to kidney but not to BAT, hindlimb, or adrenal gland.
CONCLUSIONS—Our findings indicate that hypothalamic ERK plays a key role in the control of food intake, body weight, and thermogenic sympathetic outflow by leptin but does not participate in the cardiovascular and renal sympathetic actions of leptin.
Endoplasmic Reticulum Stress Is Reduced in Tissues of Obese Subjects After Weight Loss
Authors: Gregor Margaret F. , Yang Ling , Fabbrini Elisa , Mohammed B. Selma , Eagon J. Christopher , Hotamisligil Gökhan S. , Klein Samuel 
Published: December 2008

OBJECTIVE—Obesity is associated with insulin resistance and type 2 diabetes, although the mechanisms linking these pathologies remain undetermined. Recent studies in rodent models revealed endoplasmic reticulum (ER) stress in adipose and liver tissues and demonstrated that ER stress could cause insulin resistance. Therefore, we tested whether these stress pathways were also present in obese human subjects and/or regulated by weight loss.
RESEARCH DESIGN AND METHODS—Eleven obese men and women (BMI 51.3 ± 3.0 kg/m2) were studied before and 1 year after gastric bypass (GBP) surgery. We examined systemic insulin sensitivity using hyperinsulinemic-euglycemic clamp studies before and after surgery and collected subcutaneous adipose and liver tissues to examine ER stress markers.
RESULTS—Subjects lost 39 ± 9% body wt at 1 year after GBP surgery (P &lt; 0.001), which was associated with a marked improvement in hepatic, skeletal muscle, and adipose tissue insulin sensitivity. Markers of ER stress in adipose tissue significantly decreased with weight loss. Specifically, glucose-regulated protein 78 (Grp78) and spliced X-box binding protein-1 (sXBP-1) mRNA levels were reduced, as were phosphorylated elongation initiation factor 2α (eIF2α) and stress kinase c-Jun NH2-terminal kinase 1 (JNK1) (all P values &lt;0.05). Liver sections from a subset of subjects showed intense staining for Grp78 and phosphorylated eIF2α before surgery, which was reduced in post-GBP sections.
CONCLUSIONS—This study presents important evidence that ER stress pathways are present in selected tissues of obese humans and that these signals are regulated by marked weight loss and metabolic improvement. Hence, this suggests the possibility of a relationship between obesity-related ER stress and metabolic dysfunction in obese humans.
Reproductive aging in captive and wild common chimpanzees: factors influencing the rate of follicular depletion
Authors: Atsalis Sylvia , Videan Elaine 
Published: December 2008

AbstractWe examine and discuss evidence of contrasting differences in fertility patterns between captive and wild female chimpanzees,Pan troglodytes, as they age; in the wild females reproduce in their 40s, but captive studies suggest that menopause occurs around that time. Thus, despite the increased longevity generally observed in captive populations reproductive life span is shortened. We outline a hypothesis to explain the apparent differential pace of reproductive decline observed between wild and captive populations. The breeding schedules of captive primates may contribute to accelerated reproductive senescence because continuous cycling in captive animals results in early depletion of the ovarian stock and premature senescence. Available evidence supports the hypothesis that women with patterns of high oocyte loss experience earlier menopause. Chimpanzees in captivity live longer, and thus, similar to humans, they may experience follicular depletion that precedes death by many years. In captivity, chimpanzees typically have an early age at menarche and first birth, shorter interbirth intervals associated with short lactational periods as young mature faster, and nursery rearing, which allows mothers to begin cycling earlier. Variables typical of wild chimpanzee populations, including late age at menarche and first birth, long interbirth intervals associated with prolonged lactational periods, and a long period of female infertility after immigration, spare ovulations and may be responsible for the later age at reproductive termination. Finally, we describe and discuss the timing of specific reproductive landmarks that occur as female chimpanzees age, distinguishing between functional menopause (age at last birth) and operational menopause (end of cycling). Am. J. Primatol. 71:271–282, 2009. © 2008 Wiley‐Liss, Inc.
Estimated 10‐year stroke risk by region and race in the United States
Authors: Cushman Mary , Cantrell Ronald A. , McClure Leslie A. , Howard George , Prineas Ronald J. , Moy Claudia S. , Temple Ella M. , Howard Virginia J. 
Published: December 2008

AbstractObjectiveBlack individuals younger than 75 years have more than twice the risk for stroke death than whites in the United States. Regardless of race, stroke death is approximately 50% greater in the “stroke belt” and “stroke buckle” states of the Southeastern United States. We assessed geographic and racial differences in estimated 10‐year stroke risk.MethodsThe Reasons for Geographic and Racial Differences in Stroke study is a population‐based cohort of men and women 45 years or older, recruited February 2003 to September 2007 at this report, with oversampling of stroke belt/buckle residents and blacks. Racial and regional differences in the Framingham Stroke Risk Score were studied in 23,940 participants without previous stroke or transient ischemic attack.ResultsThe mean age‐, race‐, and sex‐adjusted 10‐year predicted stroke probability differed slightly across regions: 10.7% in the belt, 10.4% in the buckle, and 10.1% elsewhere (p <0.001). Geographic differences were largest for the score components of diabetes and use of antihypertensive therapy. Blacks had a greater age‐ and sex‐adjusted mean 10‐year predicted stroke probability than whites: 11.3% versus 9.7%, respectively (p <0.001). Race differences were largest for the score components of hypertension, systolic blood pressure, diabetes, smoking, and left ventricular hypertrophy.InterpretationAlthough blacks had a greater predicted stroke probability than whites, regional differences were small. Results suggest that interventions to reduce racial disparities in stroke risk factors hold promise to reduce the racial disparity in stroke mortality. The same may not be true regarding geographic disparities in stroke mortality. Ann Neurol 2008;64:507–513
A critical evaluation of the Braak staging scheme for Parkinson's disease
Authors: Burke Robert E. , Dauer William T. , Vonsattel Jean Paul G. 
Published: December 2008

AbstractBraak and colleagues have proposed that, within the central nervous system, Parkinson's disease (PD) begins as a synucleinopathy in nondopaminergic structures of the lower brainstem or in the olfactory bulb. The brainstem synucleinopathy is postulated to progress rostrally to affect the substantia nigra and cause parkinsonism at a later stage of the disease. In the context of a diagnosis of PD, made from current clinical criteria, the pattern of lower brainstem involvement accompanying mesencephalic synucleinopathy is often observed. However, outside of that context, the patterns of synucleinopathy that Braak described are often not observed, particularly in dementia with Lewy bodies and when synucleinopathy occurs in the absence of neurological manifestations. The concept that lower brainstem synucleinopathy represents “early PD” rests on the supposition that it has a substantial likelihood of progressing within the human lifetime to involve the mesencephalon, and thereby cause the substantia nigra pathology and clinical parkinsonism that have heretofore defined the disease. However, the predictive validity of this concept is doubtful, based on numerous observations made in populations of aged individuals who, despite the absence of neurological signs, have brain synucleinopathy ranging up to Braak stages 4 to 6 at postmortem. Furthermore, there is no relation between Braak stage and the clinical severity of PD. We conclude that the relation between patterns of abnormal synuclein immunostaining in the human brain and the disease entity now recognized as PD remains to be determined. Ann Neurol 2008;64:485–491
Mutation in BAG3 causes severe dominant childhood muscular dystrophy
Authors: Selcen Duygu , Muntoni Francesco , Burton Barbara K. , Pegoraro Elena , Sewry Caroline , Bite Anna V. , Engel Andrew G. 
Published: December 2008

AbstractObjectiveMyofibrillar myopathies (MFMs) are morphologically distinct but genetically heterogeneous muscular dystrophies in which disintegration of Z disks and then of myofibrils is followed by ectopic accumulation of multiple proteins. Cardiomyopathy, neuropathy, and dominant inheritance are frequent associated features. Mutations in αB‐crystallin, desmin, myotilin, Zasp, or filamin‐C can cause MFMs and were detected in 32 of 85 patients of the Mayo MFM cohort. Bag3, another Z‐disk–associated protein, has antiapoptotic properties, and its targeted deletion in mice causes fulminant myopathy with early lethality. We therefore searched for mutations in BAG3 in 53 unrelated MFM patients.MethodsWe searched for mutations in BAG3 by direct sequencing. We analyzed structural changes in muscle by histochemistry, immunocytochemistry, and electron microscopy, examined mobility of the mutant Bag3 by nondenaturing electrophoresis, and searched for abnormal aggregation of the mutant protein in COS‐7 (SV‐40 transformed monkey kidney fibroblast‐7) cells.ResultsWe identified a heterozygous p.Pro209Leu mutation in three patients. All presented in childhood, had progressive limb and axial muscle weakness, and experienced development of cardiomyopathy and severe respiratory insufficiency in their teens; two had rigid spines, and one a peripheral neuropathy. Electron microscopy showed disintegration of Z disks, extensive accumulation of granular debris and larger inclusions, and apoptosis of 8% of the nuclei. On nondenaturing electrophoresis of muscle extracts, the Bag3 complex migrated faster in patient than control extracts, and expression of FLAG‐labeled mutant and wild‐type Bag3 in COS cells showed abnormal aggregation of the mutant protein.InterpretationWe conclude mutation in Bag3 defines a novel severe autosomal dominant childhood muscular dystrophy. Ann Neurol 2008
Relative impacts of native and non‐native crayfish on shelter use by an indigenous benthic fish
Authors: Bubb Damian H. , O'Malley Oliver J. , Gooderham Angela C. , Lucas Martyn C. 
Published: December 2008

Abstract
The North American signal crayfish Pacifastacus leniusculus has been widely introduced throughout Europe where it is expanding its range and in many areas replacing the native white‐clawed crayfish Austropotamobius pallipes. There is concern with regards to the impact of this species replacement on benthic fish. Interspecific behavioural interactions and competition for shelter between the benthic fish, bullhead Cottus gobio and A. pallipes and P. leniusculus were measured to assess the comparative impact of native and non‐native crayfish.
Both white‐clawed crayfish and signal crayfish were dominant over bullhead. Bullheads moved away from approaches of crayfish, left shelters on entry of crayfish and rarely entered an occupied shelter. Signal crayfish made significantly more aggressive approaches towards bullheads than white‐clawed crayfish.
Alone, bullheads spent most of their time by day under shelter (median 96%), reflecting a highly entrained behavioural response, which was relaxed by night (median 60%). Both crayfish species reduced shelter use by bullheads although the extent of shelter sharing by bullheads was higher in trials with white‐clawed crayfish than with signal crayfish.
Sampling in the River Wharfe, northern England, where signal and white‐clawed crayfish and bullhead currently exist, demonstrated a negative relationship between the densities of signal crayfish and bullhead, with high bullhead abundance where crayfish were absent or where white‐clawed crayfish were present at low density.
Assuming that shelter is sometimes limited under natural conditions, crayfish are likely to displace bullheads from shelters, which may increase predation risk for bullheads. Although the effects of signal crayfish on bullhead shelter use were more intense, the pattern was highly evident for the native white‐clawed crayfish. The higher fecundity and densities attained by signal crayfish may be more significant than differences in the behaviour of the two crayfish species in determining the impact of crayfish on bullheads.
Copyright © 2008 John Wiley & Sons, Ltd.
Detritus accumulation and decomposition in a coastal lake (Acquatina–southern Italy)
Authors: Costantini M. Letizia , Rossi Loreto , Fazi Stefano , Rossi David 
Published: December 2008

Abstract
Knowledge about processes and dynamics underlying organic matter accumulation in transitional waters is crucial for the protection of these ecologically important coastal habitats. This study investigated the relationship between large particle accumulation and decomposition in a coastal lake included in a Site of Community Interest (SCI) using sediment trap and litterbag techniques.
Two sets of sediment traps were deployed at five sites along the longitudinal axis of the lake. One set was emptied once a month for 12 months, and the other twice a year. The contents of the monthly and the 6‐monthly traps and the superficial sediments were then compared to estimate the organic matter accumulation and loss. To determine the mass loss rate of the three major allochthonous sources of detritus (the reed Phragmites australis, the cordgrass Spartina juncea, and the seagrass Posidonia oceanica), litterbags were placed near the sediment traps at three out of the five sites at the beginning of each 6‐month period and retrieved monthly.
The amount of annual particulate organic matter (POM) deposition in the traps was 1320.2±58.5 g m−2 y−1 and consisted of 25% large particles (CPOM). Allochthonous litter comprised an important fraction of CPOM, and its breakdown rate changed with the plant species, site and season. Loss rate of CPOM accumulated at the lake bottom was significantly related with the mass loss rate of reed and cordgrass litter, but not with that of seagrass.
Due to slow litter breakdown and tidal landward advection, the lake acted as a sediment trap for allochthonous matter, especially from Posidonia. The important role of marine‐derived litter in organic matter sedimentation suggests addressing conservation strategies of the lake functioning towards the selective control of allochthonous CPOM inputs, in particular at the mouth where the incoming tide brings suspended material and salinity decelerates matter flow to the sea and decomposition. This study supports the hypothesis that sedimentation and decomposition dynamics are important factors for coastal lake evolution, and shows litterbag and sediment trap techniques as simple useful investigation tools in management strategies aiming at conserving transitional waters.
Copyright © 2008 John Wiley & Sons, Ltd.
Identification of endo‐ and exo‐polygalacturonase activity in Lygus hesperus (Knight) salivary glands
Authors: Celorio‐Mancera Maria de la Paz , Carl Greve L. , Teuber Larry R. , Labavitch John M. 
Published: December 2008

AbstractPolygalacturonase (PG) activity found in the salivary gland apparatus of the western tarnished plant bug (WTPB, Lygus hesperus Knight) has been thought to be the main chemical cause of the damage inflicted by this mirid when feeding on its plant hosts. Early viscosity and thermal stability studies of the PG activity in L. hesperus protein extracts were difficult to interpret. Thus, it has been suggested that one or more PG protein(s) with different hydrolytic modes of action are produced by this mirid. In order to understand the quantitative complexity of the WTPB salivary PG activity, PG purification from a protein extract from salivary glands excised from L. hesperus insects was performed using affinity and ion exchange chromatography. To elucidate the qualitative complexity of the purified PGs, the digestion products generated by the PGs were separated using high performance anion exchange chromatography with pulsed amperometric detection. At least five PG proteins were detected; these differing in terms of their glycosylation, mass‐to‐charge ratios, and/or molecular mass. The characterization of the products generated by these PGs showed that endo‐ and exo‐acting PGs are produced by WTPB. Although none of the PGs was purified to homogeneity, the present work provides biochemical evidence of a multiplicity of PGs that degrade the pectin component of the plant tissue in different fashions. The implications of these findings affect the understanding of WTPB feeding damage and, potentially, help identify ways to control this important crop pest. Arch. Insect Biochem. Physiol. 2008. © 2008 Wiley‐Liss, Inc.
Teratology: From science to birth defects prevention
Authors: Rasmussen Sonja A. , Erickson J. David , Reef Susan E. , Ross Danielle S. 
Published: December 2008

AbstractOne of the goals of birth defects research is to better understand risk or preventive factors for birth defects so that strategies for prevention can be developed. In this article, we have selected four areas of birth defects research that have led to the development of prevention strategies. These areas include rubella virus as a cause of congenital rubella syndrome, folic acid as a preventive factor for neural tube defects, cytomegalovirus infection as a cause of birth defects and developmental disabilities, and alcohol as a cause of fetal alcohol spectrum disorders. For each of these areas, we review key clinical and research findings that led to the identification of the risk or preventive factor, milestones in the development of prevention strategies, and the progress made thus far toward prevention. Birth Defects Research (Part A), 2009. © 2008 Wiley‐Liss, Inc.
Maternal asthma, asthma medication use, and the risk of congenital heart defects
Authors: Lin Shao , Herdt‐Losavio Michele , Gensburg Lenore , Marshall Elizabeth , Druschel Charlotte 
Published: December 2008

AbstractBACKGROUND:Asthma is a common problem that complicates pregnancy. Several drugs are considered acceptable for use during pregnancy, although none have been classified as safe. Few studies have assessed the health impact of maternal asthma/medication use on the fetus.METHODS:A population‐based case‐control study was conducted in New York State to determine if cardiac congenital malformations in offspring were associated with maternal use of asthma medication and/or maternal asthma. Cases were cardiac anomalies in the New York State Congenital Malformations Registry. Controls were live births without any major birth defects randomly selected from birth certificates and frequency matched by year of birth. Data were collected through a 30 min telephone interview. Exposure was maternal asthma/medication use, maternal asthma/no medication use, no asthma/medication use, and no asthma/no medication use (reference).RESULTS:A total of 502 (59.4%) cases and 1,066 (53.8%) controls participated. A positive association was seen between any heart defect and women with asthma who used medication (OR 2.38; 95% CI: 1.18, 4.82). No significant associations were observed between heart defects and either women with asthma who did not use medication or women without asthma who used asthma medications. When considering types of medication used, offspring of women with asthma who used bronchodilators had an increased risk of any heart defect (OR 2.20; 95%CI: 1.05, 4.61).CONCLUSIONS:These results suggest that both maternal asthma status (controlled vs. uncontrolled; severe vs. mild) and asthma medication use, particularly bronchodilators, may play a role in cardiac malformations in offspring. Birth Defects Research (Part A), 2009. © 2008 Wiley‐Liss, Inc.