bluuebunny/crossref_metadata_2025_split huggingface dataset:
Progesterone and Caspase‐3 Activation in Equine Cyclic Corpora Lutea
Authors: Ferreira‐Dias G , Mateus L , Costa AS , Solá S , Ramalho RM , Castro RE , Rodrigues CMP 
Published: May 2007

ContentsSoon after ovulation, the newly formed corpus luteum (CL) starts secreting progesterone (P4), necessary for implantation. The CL, an ovarian transient endocrine organ, undergoes growth and regression throughout its life span. The objective of this study was to evaluate if caspase‐3 mediates cell death in the equine cyclic luteal structures and relate it to luteal endocrine function. Blood and luteal tissue were collected during the breeding season after slaughter from 38 randomly assigned cycling mares. Luteal tissues were classified as corpora haemorrhagica (CH; n = 7); mid luteal phase corpora lutea (Mid‐CL; n = 17); late or regressing corpora lutea (Late‐CL; n = 9) and corpora albicans (CA; n = 5). Plasma P4 concentration, determined by radioimmunoassay, showed a significant increase from CH to Mid‐CL (p < 0.001), followed by a decrease to Late‐CL (p < 0.001) and CA (p < 0.001). Caspase‐3 processing and poly (ADP) ribose polymerase (PARP) degradation were assessed by western blotting. Active caspase‐3 was twofold increased in Mid‐CL, Late‐CL and CA as compared with CH (p < 0.05). Immunocytochemistry also showed a significant increase in caspase‐3 expression in large luteal cells in all structures when compared with CH (p < 0.05). Consistently, the endogenous caspase‐3 substrate, PARP, was markedly degraded from CH to CA (p < 0.05). In fact, the ratio of full‐length to degraded PARP showed a significant decrease from CH to Mid‐CL, Late‐CL and CA (p < 0.05). Finally, the decrease in P4 from Mid‐ to Late‐CL coincided with no further increases in apoptosis. In conclusion, these results suggest that the effector caspase‐3 of apoptosis, might play an important role during luteal tissue involution in the mare, even though its relationship with P4 remains to be elucidated.
Procedure for Maximizing Oocyte Harvest for In Vitro Embryo Production in Small Ruminants
Authors: Gibbons A , Bonnet FP , Cueto MI , Catala M , Salamone DF , Gonzalez‐Bulnes A 
Published: May 2007

ContentsPossible effects of repeated hormonal treatments and laparoscopic ovum pick‐up (LOPU) on the efficiency of oocyte recovery rate and quality were determined in sheep and goats. In six adult Merino sheep and five Criolla goats, ovarian status was synchronized by a prostaglandin F2α analogue and the insertion of an intravaginal sponge 48 h later. Follicle development was stimulated by a single dose of FSH (60 mg NIH‐FSH‐P1) plus a single dose of equine chorionic gonadotrophin (eCG; 300 UI). The first FSH/eCG doses were administered 48 h after the sponge insertion, being repeated every 4 days to complete a total of four treatments in sheep and three in goats. Follicles in both ovaries were categorized according to their diameter and follicular fluid was aspirated under laparoscopic observation without a vacuum pump. In sheep, during a 12‐day‐period, a total of 347 follicles were aspirated with a recovery rate of 46.9%. In goats, during an 8‐day‐period, 219 follicles were aspirated with a recovery rate of 45.6%. In both species, there were no significant differences in the number of aspirated follicles, oocyte recovery rate and good quality oocyte recovery rate. However, in sheep the oocyte recovery rate was higher for large follicles, whereas in goats no such effect was detected. In summary, current results indicate that retrieval of oocytes can be maximized, without affecting oocyte quality, by repeating ‘oneshot’ FSH/eCG regimes and LOPUs at intervals as short as 4 days.
Quarter Milking for Improved Detection of Increased SCC
Authors: Berglund I , Pettersson G , Östensson K , Svennersten‐Sjaunja K 
Published: May 2007

ContentsThe aim of the present study was to investigate whether milk composition and milk yield are changed in relation to a moderate increase in milk somatic cell count (SCC) in separate udder quarters. During a period of 13 weeks, 4158 bulk quarter milk samples from 68 cows were collected and analysed for milk SCC and milk composition. The sampling was done twice weekly. The cows were in different stages of lactation and in different lactation numbers. For calculations, three groups of cows were formed according to their SCC value. Group 1 cows, where all quarters had an SCC <100 000 cells/ml at all sampling occasions, were considered to be non‐affected. Group 2 cows had one udder quarter with an increased SCC >100 000 cells/ml and 1.5‐fold higher than the opposite quarter at one sampling occasion. For group 3 cows, the increase in SCC remained for several consecutive sampling occasions. Data from group 1 cows revealed that front and rear quarters were similar when compared with each other. For group 3 cows, the lactose content in milk decreased significantly, simultaneously with the increase in SCC and remained decreased for two sampling occasions after the initial increase in SCC. It was concluded that deviations in lactose content within front and rear quarters, respectively, may be a useful tool for detection of moderately increased SCC in separate udder quarters.
Oestrus Expression and Ovarian Function in Repeat Breeder Cows, Monitored by Ultrasonography and Progesterone Assay
Authors: Pérez‐Marín CC , España F 
Published: May 2007

ContentsOvarian ultrasonography and plasma progesterone levels were monitored in 37 lactating Holstein cows with a history of repeat breeding; the data obtained were analysed in conjunction with clinical and behavioural signs, to identify the aetiology of the syndrome. Differences were detected between RBCs displaying apparently normal cycles and others with irregular cycles. There were also differences in heat expression; a large number of repeat breeder cows (RBCs, 50%) displayed delayed or silent oestrus. Ovarian disorders were common in RBCs, and included ovarian cysts, mistimed AI, subluteal progesterone levels, luteal dysfunction or ovulation defects. Both ultrasonography and plasma progesterone assays are useful tools for ascertaining the aetiology of the repeat breeder syndrome.
Combination of the ALCR/alcA ethanol switch and GAL4/VP16‐UAS enhancer trap system enables spatial and temporal control of transgene expression in Arabidopsis
Authors: Jia Hongge , Van Loock Bram , Liao Mingjun , Verbelen Jean‐Pierre , Vissenberg Kris 
Published: May 2007

SummaryThe experimental control of gene expression in specific tissues or cells at defined time points is a useful tool for the analysis of gene function. GAL4/VP16‐UAS enhancer trap lines can be used to selectively express genes in specific tissues or cells, and an ethanol‐inducible system can help to control the time of expression. In this study, the combination of the two methods allowed the successful regulation of gene expression in both time and space. For this purpose, a binary vector, 962‐UAS::GUS, was constructed in which the ALCR activator and β‐glucuronidase (GUS) reporter gene were placed under the control of upstream activator sequence (UAS) elements and the alcA response element, respectively. Three different GAL4/VP16‐UAS enhancer trap lines of Arabidopsis were transformed, resulting in transgenic plants in which GUS activity was detected only on ethanol induction and exclusively in the predicted tissues of the enhancer trap lines. As a library of different enhancer trap lines with distinct green fluorescent protein (GFP) patterns exist, transformation with a similar vector, in which GUS is replaced by another gene, would enable the control of the time and place of transgene expression. We have constructed two vectors for easy cloning of the gene of interest, one with a polylinker site and one that is compatible with the GATEWAY™ vector conversion system. The method can be extended to other species when enhancer trap lines become available.
Does the error negativity reflect response conflict strength? Evidence from a Simon task
Authors: Masaki Hiroaki , Falkenstein Michael , Stürmer Birgit , Pinkpank Thomas , Sommer Werner 
Published: May 2007

AbstractThe error (‐related) negativity (Ne or ERN) has been related to detecting the mismatch between incorrectly executed and appropriate responses or, alternatively, to the degree of conflict between different response alternatives. In this study different levels of response conflict were generated by manipulating task difficulty in a Simon task. According to the product of incorrect and subsequent correct EMG activation, the amount of conflict in error trials was indeed larger for the easy than for the hard condition. In contrast, Ne/ERN amplitudes did not differ between difficulty conditions, nor was the amount of conflict mirrored by Ne/ERN amplitude. Therefore, the present data are at variance with the hypothesis that the Ne/ERN reflects the degree of response conflict.
Predictive information and error processing: The role of medial‐frontal cortex during motor control
Authors: Krigolson Olav E. , Holroyd Clay B. 
Published: May 2007

AbstractWe have recently provided evidence that an error‐related negativity (ERN), an ERP component generated within medial‐frontal cortex, is elicited by errors made during the performance of a continuous tracking task (O.E. Krigolson & C.B. Holroyd, 2006). In the present study we conducted two experiments to investigate the ability of the medial‐frontal error system to evaluate predictive error information. In two experiments participants used a joystick to perform a computer‐based continuous tracking task in which some tracking errors were inevitable. In both experiments, half of these errors were preceded by a predictive cue. The results of both experiments indicated that an ERN‐like waveform was elicited by tracking errors. Furthermore, in both experiments the predicted error waveforms had an earlier peak latency than the unpredicted error waveforms. These results demonstrate that the medial‐frontal error system can evaluate predictive error information.
Range of sensory gating values and test–retest reliability in normal subjects
Authors: Fuerst Darren R. , Gallinat Jürgen , Boutros Nash N. 
Published: May 2007

AbstractThis article characterizes gating in normal subjects using P50, N100, and P200 components in a paired‐click paradigm and compares the test–retest reliabilities of the three components. Sixty‐seven normal subjects had gating data from a standard paired‐click paradigm; 30 had test–retest data. The test–retest reliability of the amplitudes, latencies, and sensory gating indices derived from the P50, N100, and P200 responses were compared. Measured gating ratios showed either normal or positively skewed distributions. Test–retest reliability of the P50 gating ratio did not reach significance, but N100 and P200 ratios showed better reliability (.50 and .64). The P50 difference score was more reliable (.61), and the N100 and P200 test–retest reliabilities of difference scores were high (.83 and .81, respectively). N100 and P200 attenuation is reliable; further work is needed to develop more reliable P50 gating measures.
Estimating heart rate and RSA from the mattress‐recorded kinetocardiogram
Authors: Woodward Steven H. , Arsenault Ned J. , Voelker Karin , Nguyen Tram , Lynch Janel , Leskin Greg , Sheikh Javaid 
Published: May 2007

AbstractThis article describes a method for extracting heart rate (HR) and respiratory sinus arrhythmia (RSA) from the kinetocardiogram (KCG) recorded from accelerometers embedded in a mattress topper. Validation has been performed via comparison with simultaneously recorded ECG. All‐night estimates of HR and RSA magnitude derived from both methods were highly correlated. KCG‐derived estimates of HR were slightly lower, and those of RSA magnitude higher, than those derived from ECG. These biases are consistent with the need to constrain KCG estimation to periods free of body movement. Mattress actigraphy represents a zero‐burden method of obtaining intensive longitudinal indices of cardiac status.
A cell‐biological model of p75NTR signaling
Authors: Blöchl A. , Blöchl R. 
Published: May 2007

AbstractNeurotrophin stimulation of tropomyosin‐related kinase (Trk) and p75 receptors influences cellular processes such as proliferation, growth, differentiation, and other cell‐specific functions, as well as regeneration. In contrast to Trk receptors, which have a well‐defined trophic role, p75 has activities ranging from trophism to apoptosis. Continued neurotrophin stimulation of differentiating neurons transforms the initially trophic character of p75 signaling into negative growth control and overstimulation leads to apoptosis. This function shift reflects the signaling effects of ceramide that is generated upon stimulation of p75. The use of ceramide signaling by p75 may provide a key to understanding the cell‐biological role of p75. The review presents arguments that the control of cell shape formation and cell selection can serve as an organizing principle of p75 signaling. Concurrent stimulation by neurotrophins of p75 and Trk receptors constitutes a dual growth control with antagonistic and synergistic elements aimed at optimal morphological and functional integration of cells and cell populations into their context.
Brain energy metabolism and neurotransmission at near‐freezing temperatures: in vivo1H MRS study of a hibernating mammal
Authors: Henry Pierre‐Gilles , Russeth Kevin P. , Tkac Ivan , Drewes Lester R. , Andrews Matthew T. , Gruetter Rolf 
Published: May 2007

AbstractThe brain of a hibernating mammal withstands physiological extremes that would result in cerebral damage and death in a non‐hibernating species such as humans. To examine the possibility that this neuroprotection results from alterations in cerebral metabolism, we used in vivo1H NMR spectroscopy at high field (9.4 T) to measure the concentration of 18 metabolites (neurochemical profile) in the brain of 13‐lined ground squirrels (Spermophilus tridecemlineatus) before, during, and after hibernation. Resolved in vivo1H NMR spectra were obtained even at low temperature in torpid hibernators (∼7°C). The phosphocreatine‐to‐creatine ratio was increased during torpor (+143%) indicating energy storage, and remained increased to a lesser extent during interbout arousal (IBA) (+83%). The total γ‐aminobutyric acid concentration was increased during torpor (+135%) and quickly returned to baseline during IBA. Glutamine (Gln) was decreased (−54%) during torpor but quickly returned to normal levels during IBA and after terminal arousal in the spring. Glutamate (Glu) was also decreased during torpor (−17%), but remained decreased during IBA (−20% compared with fall), and returned to normal level in the spring. Our observation that Glu and Gln levels are depressed in the brain of hibernators suggests that the balance between anaplerosis and loss of Glu and Gln (because of glutamatergic neurotransmission or other mechanisms) is altered in hibernation.
‘Mild Uncoupling’ does not decrease mitochondrial superoxide levels in cultured cerebellar granule neurons but decreases spare respiratory capacity and increases toxicity to glutamate and oxidative stress
Authors: Johnson‐Cadwell L. I. , Jekabsons M. B. , Wang A. , Polster B. M. , Nicholls D. G. 
Published: May 2007

AbstractCultured rat cerebellar granule neurons were incubated with low nanomolar concentrations of the protonophore carbonylcyanide‐p‐trifluoromethoxyphenyl hydrazone (FCCP) to test the hypothesis that ‘mild uncoupling’ could be neuroprotective by decreasing oxidative stress. To quantify the uncoupling, respiration and mitochondrial membrane potential (Δψm) were determined in parallel as a function of FCCP concentration. Δψm dropped by less than 10 mV before respiratory control was lost. Conditions for the valid estimation of matrix superoxide levels were determined from the rate of oxidation of the matrix‐targeted fluorescent probe MitoSOX. No significant change in the level of matrix superoxide could be detected on addition of FCCP while respiratory control was retained, although cytoplasmic superoxide levels measured by dihydroethidium oxidation increased. ‘Mild uncoupling’ by 30 nmol/L FCCP did not alleviate neuronal dysregulation induced by glutathione depletion and significantly enhanced that due to menadione‐induced oxidative stress. Low protonophore concentrations enhanced N‐methyl‐d‐aspartate receptor‐induced delayed calcium deregulation consistent with a decrease in the spare respiratory capacity available to match the bioenergetic demand of chronic receptor activation. It is concluded that the ‘mild uncoupling’ hypothesis is not supported by this model.
Identification, physiological actions, and distribution of TPSGFLGMRamide: a novel tachykinin‐related peptide from the midgut and stomatogastric nervous system of Cancer crabs
Authors: Stemmler Elizabeth A. , Peguero Braulio , Bruns Emily A. , Dickinson Patsy S. , Christie Andrew E. 
Published: May 2007

AbstractIn most invertebrates, multiple species‐specific isoforms of tachykinin‐related peptide (TRP) are common. In contrast, only a single conserved TRP isoform, APSGFLGMRamide, has been documented in decapod crustaceans, leading to the hypothesis that it is the sole TRP present in this arthropod order. Previous studies of crustacean TRPs have focused on neuronal tissue, but the recent demonstration of TRPs in midgut epithelial cells in Cancer species led us to question whether other TRPs are present in the gut, as is the case in insects. Using direct tissue matrix assisted laser desorption/ionization Fourier transform mass spectrometry, in combination with sustained off‐resonance irradiation collision‐induced dissociation, we found that at least one additional TRP is present in Cancer irroratus, Cancer borealis, Cancer magister, and Cancer productus. The novel TRP isoform, TPSGFLGMRamide, was present not only in the midgut, but also in the stomatogastric nervous system (STNS). In addition, we identified an unprocessed TRP precursor APSGFLGMRG, which was detected in midgut tissues only. TRP immunohistochemistry, in combination with preadsorption studies, suggests that APSGFLGMRamide and TPSGFLGMRamide are co‐localized in the stomatogastric ganglion (STG), which is contained within the STNS. Exogenous application of TPSGFLGMRamide to the STG elicited a pyloric motor pattern that was identical to that elicited by APSGFLGMRamide, whereas APSGFLGMRG did not alter the pyloric motor pattern.
Caffeic acid phenethyl ester reduces neurovascular inflammation and protects rat brain following transient focal cerebral ischemia
Authors: Khan Mushfiquddin , Elango Chinnasamy , Ansari Mubeen A. , Singh Inderjit , Singh Avtar K. 
Published: May 2007

AbstractIschemic stroke is a neurovascular disease treatable by thrombolytic therapy, but the therapy has to be initiated within 3 h of the incident. This therapeutic limitation stems from the secondary injury which results mainly from oxidative stress and inflammation. A potent antioxidant/anti‐inflammatory agent, caffeic acid phenethyl ester (CAPE) has potential to mitigate stroke’s secondary injury, and thereby widening the therapeutic window. We observed that CAPE protected the brain in a dose‐dependent manner (1–10 mg/kg body weight) and showed a wide therapeutic window (about 18 h) in a rat model of transient focal cerebral ischemia and reperfusion. The treatment also increased nitric oxide and glutathione levels, decreased lipid peroxidation and nitrotyrosine levels, and enhanced cerebral blood flow. CAPE down‐regulated inflammation by blocking nuclear factor kappa B activity. The affected mediators included adhesion molecules (intercellular adhesion molecule‐1 and E‐selectin), cytokines (tumor necrosis factor‐α and interleukin‐1β) and inducible nitric oxide synthase. Anti‐inflammatory action of CAPE was further documented through reduction of ED1 (marker of activated macrophage/microglia) expression. The treatment inhibited apoptotic cell death by down‐regulating caspase 3 and up‐regulating anti‐apoptotic protein Bcl‐xL. Conclusively, CAPE is a promising drug candidate for ischemic stroke treatment due to its inhibition of oxidative stress and inflammation, and its clinically relevant wide therapeutic window.
Mitochondrial aspartate aminotransferase: a third kynurenate‐producing enzyme in the mammalian brain
Authors: Guidetti Paolo , Amori Laura , Sapko Michael T. , Okuno Etsuo , Schwarcz Robert 
Published: May 2007

AbstractThe tryptophan metabolite kynurenic acid (KYNA), which is produced enzymatically by the irreversible transamination of l‐kynurenine, is an antagonist of α7 nicotinic and NMDA receptors and may thus modulate cholinergic and glutamatergic neurotransmission. Two kynurenine aminotransferases (KAT I and II) are currently considered the major biosynthetic enzymes of KYNA in the brain. In this study, we report the existence of a third enzyme displaying KAT activity in the mammalian brain. The novel KAT had a pH optimum of 8.0 and a low capacity to transaminate glutamine or α‐aminoadipate (the classic substrates of KAT I and KAT II, respectively). The enzyme was inhibited by aspartate, glutamate, and quisqualate but was insensitive to blockade by glutamine or anti‐KAT II antibodies. After purification to homogeneity, the protein was sequenced and the enzyme was identified as mitochondrial aspartate aminotransferase (mitAAT). Finally, the relative contributions of KAT I, KAT II, and mitAAT to total KAT activity were determined in mouse, rat, and human brain at physiological pH using anti‐mitAAT antibodies. KAT II was most abundant in rat and human brain, while mitAAT played the major role in mouse brain. It remains to be seen if mitAAT participates in cerebral KYNA synthesis under physiological and/or pathological conditions in vivo.
Involvement of KCNQ2 subunits in [3H]dopamine release triggered by depolarization and pre‐synaptic muscarinic receptor activation from rat striatal synaptosomes
Authors: Martire Maria , D’Amico Monia , Panza Elisabetta , Miceli Francesco , Viggiano Davide , Lavergata Francesco , Iannotti Fabio Arturo , Barrese Vincenzo , Preziosi Paolo , Annunziato Lucio , Taglialatela Maurizio 
Published: May 2007

AbstractKCNQ2 and KCNQ3 subunits encode for the muscarinic‐regulated current (IKM), a sub‐threshold voltage‐dependent K+current regulating neuronal excitability. In this study, we have investigated the involvement of IKMin dopamine (DA) release from rat striatal synaptosomes evoked by elevated extracellular K+concentrations ([K+]e) and by muscarinic receptor activation. [3H]dopamine ([3H]DA) release triggered by 9 mmol/L [K+]ewas inhibited by the IKMactivator retigabine (0.01–30 μmol/L;Emax = 54.80 ± 3.85%; IC50 = 0.50 ± 0.36 μmol/L). The IKMblockers tetraethylammonium (0.1–3 mmol/L) and XE‐991 (0.1–30 μmol/L) enhanced K+‐evoked [3H]DA release and prevented retigabine‐induced inhibition of depolarization‐evoked [3H]DA release. Retigabine‐induced inhibition of K+‐evoked [3H]DA release was also abolished by synaptosomal entrapment of blocking anti‐KCNQ2 polyclonal antibodies, an effect prevented by antibody pre‐absorption with the KCNQ2 immunizing peptide. Furthermore, the cholinergic agonist oxotremorine (OXO) (1–300 μmol/L) potentiated 9 mmol/L [K+]e‐evoked [3H]DA release (Emax = 155 ± 9.50%; EC50 = 25 ± 1.80 μmol/L). OXO (100 μmol/L)‐induced [3H]DA release enhancement was competitively inhibited by pirenzepine (1–10 nmol/L) and abolished by the M3‐preferring antagonist 4‐diphenylacetoxyN‐methylpiperidine methiodide (1 μmol/L), but was unaffected by the M1‐selective antagonist MT‐7 (10–100 nmol/L) or by Pertussis toxin (1.5–3 μg/mL), which uncouples M2‐ and M4‐mediated responses. Finally, OXO‐induced potentiation of depolarization‐induced [3H]DA release was not additive to that produced by XE‐991 (10 μmol/L), was unaffected by retigabine (10 μmol/L), and was abolished by synaptosomal entrapment of anti‐KCNQ2 antibodies. Collectively, these findings indicate that, in rat striatal nerve endings, IKMchannels containing KCNQ2 subunits regulate depolarization‐induced DA release and that IKMsuppression is involved in the reinforcement of depolarization‐induced DA release triggered by the activation of pre‐synaptic muscarinic heteroreceptors.