bluuebunny/crossref_metadata_2025_split huggingface dataset:
Restorative Effects of GDNF on Striatal Dopamine Release in Rats Treated with Neurotoxic Doses of Methamphetamine
Authors: CASS WAYNE A. , MANNING MICHAEL W. , BAILEY SHERRY L. 
Published: July 2010

AbstractRepeated methamphetamine (METH) administration to animals can result in long‐lasting decreases in striatal dopamine (DA) release and content. Glial cell line‐derived neurotrophic factor (GDNF) has pronounced effects on dopaminergic systemsin vivo, including neuroprotective effects against METH. The present experiments were designed to examine the ability of GDNF to reverse, or accelerate recovery from, METH‐induced alterations in striatal DA release. Male Fischer‐344 rats were administered METH (5 mg/kg, s.c.) or saline 4 times in one day at 2‐hour intervals. Seven days later the animals were anesthetized and given a single injection of 10 μg GDNF, or vehicle, into the right striatum. Three weeks later microdialysis experiments were carried out in both the right and left striata to examine basal and evoked levels of DA and its metabolites 3,4‐dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA). In animals treated with METH followed by vehicle 7 days later, there were significant reductions in potassium‐ and amphetamine‐evoked overflow of DA, and in basal levels of DOPAC and HVA, compared to control animals. In rats treated with METH followed 7 days later with GDNF, there were significant increases in potassium‐ and amphetamine‐evoked overflow of DA on the right, GDNF‐treated, side of the brain compared to the left side. Basal levels of DOPAC and HVA were also elevated on the GDNF‐treated side of the brain. These results suggest that GDNF can accelerate recovery of dopaminergic release processes in the striatum of rats treated with neurotoxic doses of METH.
Methamphetamine‐induced Oxidative Stress in Cultured Mouse Astrocytes
Authors: LAU JOSEPHINE W.S. , SENOK SOLOMON , STADLIN ALFREDA 
Published: July 2010

AbstractMethamphetamine (METH) is a monoaminergic toxin that destroys dopamine terminals and causes astrogliosisin vivo. Oxidative stress has been shown to play an important role in the toxic effects of METH. In the present study, we sought to determine whether astrocytes are involved in METH‐induced oxidative stress. Reactive oxygen species (ROS), ATP, and change in mitochondria membrane potential (ΔΨm) were examined in cultured striatal, mesencephalic, and cortical astrocytes after 4 to 48 h of 4 mM METH treatment. Results showed that only striatal and mesencephalic astrocytes showed a significant increase in ROS formation from 8 and 12 h, respectively. At 48 h treatment, there was a 55 and 53% increase in ROS content in striatal and mesencephalic astrocytes, respectively, whereas cortical astrocytes showed only a 25% (not significant) increase. JC‐1, a ΔΨm‐sensitive dye, showed a decrease in ΔΨm at 8 h treatment for striatal and mesencephalic astrocytes and at 12 h for cortical astrocytes. Astrocytes from all three regions showed a similar pattern of initial increase followed by a decrease in ATP content, with striatal astrocytes resulting in a maximum depletion (39% of control value) at 48 h treatment. These findings showed that METH treatment resulted in the formation of ROS in the order of striatal > mesencephalic > cortical astrocytes. Although the formation of ROS did not severely interfere with ATP production, a depolarization of mitochondria was observed. The present study suggested that astrocytes may be an important element governing the selective vulnerability to the striatum to METH‐induced oxidative stress.
Pharmacology of MDMA in Humans
Authors: DE LA TORRE R. , FARRÉ M. , ROSET P. N. , LÓPEZ C. HERNÁNDEZ , MAS M. , ORTUÑO J. , MENOYO E. , PIZARRO N. , SEGURA J. , CAMÍ J. 
Published: July 2010

AbstractMDMA given at recreational doses (range tested 50 to 150 mg) to healthy volunteers, produced mydriasis and marked increases in systolic and diastolic blood pressure, heart rate, and pupillary diameter. MDMA induced changes on oral temperature. The time course of this observation was biphasic, as a slight decrease at 1 h and a slight increase at 2 and 4 h were observed. MDMA induced a slight dose‐dependent impairment on psychomotor performance. MDMA produced a marked rise in plasma cortisol and prolactin concentrations. The elimination half‐life of MDMA was about 8‐9 h. Drug concentrations increased, and a parallel increase in physiologic and hormonal measures was observed. Both peak concentrations and peak effects were obtained between 1 and 2 h and decreased to baseline values 4‐6 h after drug administration.
Susceptibility to Subsequent Episodes in Spontaneous Recurrence of Methamphetamine Psychosis
Authors: YUI KUNIO , ISHIGURO TAKEO , GOTO KIMIHIKO , IKEMOTO SHIGENORI 
Published: July 2010

AbstractThe relation is examined between increased sensitivity to stress associated with noradrenergic hyperactivity and dopaminergic changes, and susceptibility to subsequent spontaneous recurrences of methamphetamine (MAP) psychosis (i.e., flashbacks). Plasma monoamine metabolite levels were assayed in 23 flashbackers, 19 nonflashbackers with a history of MAP psychosis, 10 subjects with persistent MAP psychosis, and 21 MAP user and 9 nonuser controls. All 23 flashbackers had undergone frightening stressful experiences during previous MAP use. Mild psychosocial stressors then triggered flashbacks. The 12 flashbackers with further episodes had markedly increased norepinephrine levels and slightly increased plasma levels of 3‐methoxytyramine, an index of dopamine release. While the 11 flashbackers with a single episode displayed small increases in norepinephrine and 3‐methoxytyramine levels. Thus, robust noradrenergic hyperreactivity, involving increased dopamine release in response to mild stress may predispose to further episodes of flashbacks.
Behavioral Responses to Repeated Cocaine Exposure in Mice Selectively Bred for Differential Sensitivity to Pentobarbital
Authors: PARK KWANKYUN , HUBER JASON , KOLTA MALAK G. , STINO FARID K.R. , SAMAAN SABER S. , SOLIMAN KARAM F.A. 
Published: July 2010

AbstractMice from the 20th generation of three lines divergently selected for response to pentobarbital‐induced sedation times [long‐sedation time (LST), short sedation time (SST), and randomly bred control (RBC)] were used to study cocaine‐induced behavioral sensitization. These lines showed variable degrees of locomotor activities in response to cocaine. At a low cocaine dose and long withdrawal period (10 mg/kg, twice a day for 5 days followed by a 14‐day withdrawal), the LST mice showed tolerance development. In response to cocaine, the locomotor activities of the SST were not significantly different from the RBC group. At a higher dose and a shorter withdrawal period (20 mg/kg, daily for 7 days followed by a 3‐day withdrawal), the SST mice showed behavioral sensitization similar to the RBC mice, but the LST mice did not develop sensitization. The different responses in locomotor activity induced by cocaine suggest that genetic factors may play a role in determining the magnitude of response to this drug. Dopamine (DA) levels did not differ significantly in either striatum (STR) or nucleus accumbens (NAC) for the cocaine‐treated animals to their corresponding saline‐treated controls. The affinity (Kd) of D2in the NAC decreased significantly, without changes in density (Bmax), in the cocaine‐treated SST and RBC mice. On the other hand, the density of D2binding sites in the SST and the RBC mice in the STR was significantly increased in cocaine‐treated groups without change in Kd. The LST mice did not show any changes in the Kdand Bmaxin either the STR or the NAC. Taken together, these findings suggest that the changes in the Kdof D2in the NAC and the Bmaxof D2in the STR may contribute to the differences in locomotor responses to cocaine exposure in these mouse lines.
Effects of Neonatal Exposure to Cocaine in the Development of the Neurotransmitters Retinal Systems: An Immunocytochemical and Neurochemical Study
Authors: SUMMAVIELLE TERESA , SILVA‐ARAÚJO ANTÓNIO , SILVA MARIA C. , TAVARES MARIA AMÉLIA 
Published: July 2010

AbstractThe visual system of rodents is affected if exposure to drugs, e.g., cocaine, occurs during prenatal or early postnatal development. This study aims to evaluate, in an experimental model of neonatal exposure to cocaine in the rat, the immunocytochemical expression of tyrosine hydroxylase in the retina and the levels of different neurotransmitters and its metabolites. Male Wistar rats were given 15 mg cocaine hydrochloride/kg body weight/day, subcutaneously, in two daily doses, from the day after birth (PND1) to PND6, 13, and 29. Controls were given 0.9% saline. Groups of rats were perfused at PND7, 14, and 30 with fixative, and the retinas were processed as wholemounts, and immunostained with the antibody anti‐TH. Other groups were decapitated, and the retinas were dissected and processed by high performance liquid chromatography with electrochemical detection (HPLC‐EC) for determination of dopamine and metabolites (DOPAC and HVA). A reduction in the retinal surface area was detected in the PND30 cocaine group, and a decrease in the density of the small TH‐IR cells was found in the PND14 cocaine group although not reaching significant levels. The other quantitative parameters did not differ between the control and cocaine groups. The levels of neurotransmitters did not significantly differ between the groups at any age. These results show a differential vulnerability of the dopaminergic system of rats exposed neonatally to cocaine when compared with the effects found after prenatal exposure to the same drug.
West Nile Virus Serosurvey and Assessment of Personal Prevention Efforts in an Area with Intense Epizootic Activity: Connecticut, 2000
Authors: McCARTHY TARA A. , HADLER JAMES L. , JULIAN KATHLEEN , WALSH STEPHEN J. , BIGGERSTAFF BRAD J. , HINTEN STEVEN R. , BAISLEY CAROLINE , ITON ANTHONY , BRENNAN TIMOTHY , NELSON RANDALL S. , ACHAMBAULT GARY , MARFIN ANTHONY A. , PETERSEN LYLE R. 
Published: July 2010

Abstract: West Nile virus (WNV) can cause large outbreaks of febrile illness and severe neurologic disease. This study estimates the seroprevalence of WNV infection and assesses risk perception and practices regarding potential exposures to mosquitoes of persons in an area with intense epizootics in 1999 and 2000. A serosurvey of persons aged ≥12 years was conducted in southwestern Connecticut during October 10‐15, 2000, using household‐based stratified cluster sampling. Participants completed a questionnaire regarding concern for and personal measures taken with respect to WNV and provided a blood sample for WNV testing. Seven hundred thirty persons from 645 households participated. No person tested positive for WNV (95% CI: 0‐0.5%). Overall, 44% of persons used mosquito repellent, 56% practiced ≥ two personal precautions to avoid mosquitoes, and 61% of households did ≥ two mosquito‐ source reduction activities. In multivariate analyses, using mosquito repellent was associated with age <50 years, using English as the primary language in the home, being worried about WNV, being a little worried about pesticides, and finding mosquitoes frequently in the home (P <0.05). Females (OR = 2.0; CI = 1.2‐2.9) and persons very worried about WNV (OR = 3.8; CI = 2.2‐6.5) were more likely to practice ≥ two personal precautions. Taking ≥ two mosquito source reductions was associated with persons with English as the primary language (OR = 2.0; CI = 1.1‐3.5) and finding a dead bird on the property (OR = 1.8; CI = 1.1‐2.8).An intense epizootic can occur in an area without having a high risk for infection to humans. A better understanding of why certain people do not take personal protective measures, especially among those aged ≥50 years and those whose primary language is not English, might be needed if educational campaigns are to prevent future WNV outbreaks.
Cyclin Proteolysis as a Retinoid Cancer Prevention Mechanism
Authors: DRAGNEV KONSTANTIN H. , FREEMANTLE SARAH J. , SPINELLA MICHAEL J. , DMITROVSKY ETHAN 
Published: July 2010

AbstractThe retinoids, natural and synthetic derivatives of vitamin A, are active in cancer therapy and prevention. Their biological effects are mediated through ligand‐dependent interactions with retinoid receptors that associate with specific co‐regulators. A better understanding of retinoid chemopreventive mechanisms is needed. Our prior work revealed that all‐trans‐retinoic acid (RA) prevented tobacco‐specific carcinogenic transformation of cultured human bronchial epithelial cells. RA signaled G1 arrest that permitted repair of genomic DNA damage caused by these carcinogens. RA triggered G1 arrest at least partly through proteasome‐dependent degradation of cyclin D1. Proteasomal inhibitors blocked RA‐mediated cyclin D1 degradation. To confirm that a specific proteolysis pathway was induced by RA‐treatment, a degradation assay was established using in vitro translated cyclin D1 and cellular extracts from RA‐treated or untreated human bronchial epithelial cells. Incubation of RA‐treated but not the control cellular extracts with in vitro translated cyclin D1 led to cyclin degradation. This degradation depended on the PEST domain of cyclin D1, implicating ubiquitination in this retinoid degradation. Retinoid receptor selective agonists demonstrated that retinoic acid receptor (RAR)β and retinoid X receptor (RXR) but not RARα‐ or RARγ‐dependent pathways signaled this cyclin degradation. Findings were extended to the NT2/D1 human embryonal carcinoma differentiation model where a similar pathway was activated by RA‐treatment. To determine whether G1 cyclins were involved directly in bronchial preneoplasia, immunohistochemical expression profiles for cyclins D1 and E were examined. Aberrant expression of these cyclins was frequent in bronchial preneoplasia. Taken together, these findings indicate that ubiquitin‐dependent proteolysis of G1 cyclins is a retinoid chemoprevention mechanism. Whether the retinoids represent the optimal agents to activate this pathway is the subject of ongoing work. These findings provide a rationale for combining the retinoids in chemoprevention trials with other agents that do not activate this proteolysis pathway. What is now known about the retinoids as cancer prevention agents will be reviewed. Emphasis is placed on retinoid effects on cell cycle progression at G1.
Human Experience with Canal Plugging
Authors: AGRAWAL SUMIT K. , PARNES LORNE S. 
Published: July 2010

Abstract: Canal occlusion/plugging is a very effective technique with a low risk to hearing. The series of posterior semicircular canal occlusions described in this review now becomes the largest in the literature to date. It continues to support this procedure as the treatment of choice for intractable benign paroxysmal positional vertigo (BPPV). All 44 operated ears were relieved of BPPV, with one patient having an atypical late recurrence. Of the 40 ears with normal preoperative hearing, one had a delayed (3‐month) sudden and permanent profound loss, while one other had a mild (20 dB) loss. Six patients had protracted courses of imbalance and motion sensitivity.Canal plugging has led to several new and innovative developments including the partial labyrinthectomy for difficult‐to‐access skull base lesions and superior semicircular canal plugging for dehiscence. These new procedures and their development are reviewed in this paper.
Gonadotropin‐Releasing Hormone Antagonists
Authors: GORDON KEITH 
Published: July 2010

AbstractUntil recently, gonadotropin‐releasing hormone (GnRH) agonists were the only choice available to physicians for prevention of premature luteinizing hormone (LH) surges in women undergoing controlled ovarian stimulation. The recent FDA approval of GnRH antagonists for this indication gives clinicians some new options. Results of clinical trials to date suggest that, with GnRH antagonists, much shorter treatment regimens with fewer injections and possibly less gonadotropin can achieve good clinical results. In most of the trials performed to date, however, the GnRH antagonist regimens have been associated with a slightly lower pregnancy and implantation rate than the established GnRH agonist protocols. This remains the biggest hurdle to their more general acceptance. Herein, the possible contributing factors are discussed, and the proposal made that differences in serum estradiol patterns preceding oocyte retrieval are the most likely contributing factor.
Understanding Preterm Labor
Authors: CHALLIS JOHN R. G. , LYE STEPHEN J. , GIBB WILLIAM , WHITTLE WENDY , PATEL FALGUNI , ALFAIDY NADIA 
Published: July 2010

AbstractIncreased uterine contractility at term and preterm results from activation and then stimulation of the myometrium. Activation can be provoked by mechanical stretch of the uterus and by an endocrine pathway resulting from increased activity of the fetal hypothalamic‐pituitary‐adrenal (HPA) axis. In fetal sheep, increased cortisol output during pregnancy regulates prostaglandin H synthase type 2 (PGHS2) expression in the placenta in an estrogen‐independent manner, resulting in increased levels of PGE2 in the fetal circulation. Later increases in maternal uterine expresssion of PGHS2 require elevations of estrogen and lead to increased concentrations of PGF2α in the maternal circulation. Thus, regulation of PGHS2 at term is differentially controlled in fetal (trophoblast) and maternal (uterine epithelium) tissue. This difference may reflect expression of the glucocorticoid receptor (GR), but not estrogen receptor (ER), in placental trophoblast cells. In women, cortisol also contributes to increased PG production in fetal tissues through upregulation of PGHS2 (amnion and chorion) and downregulation of 15‐OH PG dehydrogenase (chorion trophoblasts). The effect of cortisol on chorion expression of PGDH reverses a tonic stimulatory effect of progesterone, potentially through a paracrine or autocrine action. We have interpreted this interaction as a reflection of “progesterone withdrawal” in the primate, in relation to birth. Other agents, such as proinflammatory cytokines, similarly upregulate PGHS2 and decrease expression of PGDH, indicating the presence of several mechanisms by which labor at term or preterm may be initiated. These different mechanisms need to be considered in the development of strategies for the detection and management of the patient in preterm labor.
A Critical Birth Weight and Other Determinants of Survival for Infants with Severe Intrauterine Growth Restriction
Authors: LEE MEN‐JEAN , CONNER ELLEN L. , CHARAFEDDINE LAMA , WOODS JAMES R. , Del PRIORE GIUSEPPE 
Published: July 2010

AbstractOur objective was to assess the perinatal management and neonatal outcomes of premature, severely intrauterine growth‐restricted (IUGR) neonates. A cohort of neonates <1000 grams, ≤ first percentile for weight, and <37 weeks' gestation was identified and matched 2:1 to two control sets of premature, appropriate‐for‐gestational age (AGA) infants—one with similar gestational age (AGA‐GA group) and the other with similar birth weight (AGA‐BW group) to determine the effect of IUGR on the outcome of the premature infant. The IUGR group was then examined in detail for descriptive statistics. Data were analyzed by t‐tests and Chi‐square analyses where appropriate. The IUGR infants had worse outcomes than AGA‐GA controls but had somewhat better results than the AGA‐BW controls. In the IUGR group, a birth weight less than 550 grams was significantly associated with neonatal death (p < 0.001). However, increasing gestational age was not associated with neonatal survival (p= 0.661) if birthweight remained below 550 grams. Classical cesarean delivery was associated with neonatal death (p= 0.003). Neonatal variables associated with poor outcome included patent ductus arteriosus (p= 0.034), feeding intolerance (p= 0.046), and failure to thrive (p= 0.05). Overall, neonatal survival was 73%. Of the surviving neonates, 69% had evidence of neurodevelopmental delay when tested at 6 and 12 months. Premature, growth‐restricted neonates with birth weights of <550 grams versus those of >550 grams have dismal outcomes despite a gestational age that is compatible with survival.
The Embryo Question
Authors: FLAMIGNI CARLO 
Published: July 2010

AbstractIn Italy, the seat of the Vatican, the problem of the “rights of the embryo” has been particularly felt and has caused bitter debate between laymen and clergy. The disagreement has focused primarily on the definition of “person,”“individual,” and the “beginning of life.” Catholics, for the most part, have contested the concept of the “pre‐embryo” and have tried to have a law passed that would impede the production and freezing of supernumerary embryos (according to the hypothesis of the “simple case”). In the same way, Catholics have strongly opposed the possible manipulation of embryos, including pre‐implant genetic investigations. In addition to Catholic teachings, the National Committee for Bioethics has also declared itself favorable to the protection of the “waking life.” It published a special document on the theme in a period in which the Committee was composed only of strict Catholics, following action taken by the then Prime Minister, Berlusconi, who believed it necessary to exclude and remove all lay members from the Committee. The document of the National Committee for Bioethics, which distinguishes itself for having declared that “the embryo is one of us,” has been the cause of a transversal political aggregation that has gathered Catholic parliamentarians from different political parties and that has begun a campaign to acknowledge the prerogatives and rights of the embryo which Italian law attributes only to the baby after its birth. An intense debate continues on all these themes, and in back of all this is the warning from the Church to re‐examine the Italian law dealing with the voluntary interruption of pregnancy.
Non‐gaussianity Versus Nonlinearity of Cosmological Perturbations
Authors: Verde Licia 
Published: July 2010

Abstract: Following the discovery of the cosmic microwave background, the hot big‐bang model has become the standard cosmological model. In this theory, small primordial fluctuations are subsequently amplified by gravity to form the large‐scale structure seen today. Different theories for unified models of particle physics, lead to different predictions for the statistical properties of the primordial fluctuations, that can be divided in two classes: gaussian and non‐gaussian. Convincing evidence against or for gaussian initial conditions would rule out many scenarios and point us toward a physical theory for the origin of structures.The statistical distribution of cosmological perturbations, as we observe them, can deviate from the gaussian distribution in several different ways. Even if perturbations start off gaussian, nonlinear gravitational evolution can introduce non‐gaussian features. Additionally, our knowledge of the Universe comes principally from the study of luminous material such as galaxies, but galaxies might not be faithful tracers of the underlying mass distribution. The relationship between fluctuations in the mass and in the galaxies distribution (bias), is often assumed to be local, but could well be nonlinear. Moreover, galaxy catalogues use the redshift as third spatial coordinate: the resulting redshift‐space map of the galaxy distribution is nonlinearly distorted by peculiar velocities. Nonlinear gravitational evolution, biasing, and redshift‐space distortion introduce non‐gaussianity, even in an initially gaussian fluctuation field.I investigate the statistical tools that allow us, in principle, to disentangle the above different effects, and the observational datasets we require to do so in practice.