bluuebunny/crossref_metadata_2025_split huggingface dataset:
SERUM PROLACTIN AND GONADOTROPHIN LEVELS BEFORE AND AFTER LUTEINIZING HORMONE‐RELEASING HORMONE IN THE INVESTIGATION OF AMENORRHOEA
Authors: Bergh T. , Nillius S. J. , Wide L. 
Published: August 2005

SummaryAn intravenous luteinizing hormone‐releasing hormone (LRH) test was performed in 287 women with amenorrhoea. Prolactin, progesterone and oestrogens in serum were also measured. Twenty‐four women with premature ovarian failure and 9 with gonadal dysgenesis had raised basal follicle‐stimulating hormone (FSH) levels. Neither the basal luteinizing hormone (LH) level nor the gonadotrophin responses after LRH gave a better separation of this group of women with irreversible ovarian failure. Measurement of prolactin levels were valuable in that 15 of 42 patients with hyperprolactinaemia had a radiologically abnormal pituitary fossa, whereas pituitary fossa abnormalities were found in only 11 of 245 normoprolactinaemic women. It was thought that 181 women had functional amenorrhoea; 54 per cent of these women had developed amenorrhoea in relation to weight loss and 32 per cent in relation to discontinuation of oral contraceptives. A strong correlation was found between the body weight and the basal gonadotrophin levels. The basal LH levels were correlated with serum oestrogen levels, the basal FSH level and the LH response to LRH. Most of the patients with low basal LH values had developed amenorrhoea in relation to self‐imposed weight loss. The responses to LRH were often impaired in the underweight patients but became normal after weight gain. The polycystic ovary syndrome (PCO) could not be diagnosed by measuring either basal or LRH‐stimulated gonatrophin levels. Single FSH and prolactin determinations in serum seemed to be the only indispensible hormone assays in the routine clinical evaluation of amenorrhoea.
THE OUTCOME OF PREGNANCY AFTER CONE BIOPSY OF THE CERVIX: A CASE‐CONTROL STUDY
Authors: Jones Jane M. , Sweetnam P. , Hibbard B. M. 
Published: August 2005

SummaryWe investigated the outcome of pregnancy after cone biopsy of the cervix. We found that preterm delivery and low birth weight were commoner and the mean duration of labour longer in women who had a cone biopsy than amongst matched controls. Rapid labour (under two hours) was not significantly more common after cone biopsy.
A STUDY OF CRYOSURGERY FOR DYSPLASIA AND CARCINOMA IN SITU OF THE UTERINE CERVIX
Authors: Elmfors B. , Stormby N. 
Published: August 2005

SummaryWe studied 22 patients with a histopathological diagnosis of severe dysplasia and 89 patients with a diagnosis of carcinoma in situ of the uterine cervix. Twenty patients (18 per cent) had negative cervical smears for four to six years after diagnosis by biopsy of the cervix. The 91 patients with persistently abnormal smears were treated by cryosurgery, using a double freeze technique with nitrous oxide. Seventy‐four (86 per cent) had persistently normal cervical smears after one treatment and eight after a second treatment while nine patients required coni‐zation for recurrently abnormal cervical smears. The duration of follow‐up was five or six years in 48 patients (53 per cent). In a subsidiary study, material was obtained for histological examination from 72 patients with normal smears by endocervical curettage and multiple biopsies of the cervix; 8 showed slight atypia and 2 had residual carcinoma in situ.
CHANGES IN FAT, FAT‐FREE MASS AND BODY WATER IN HUMAN NORMAL PREGNANCY
Authors: Pipe N. G. J. , Smith T. , Halliday D. , Edmonds C. J. , Williams C. , Coltart T. M. 
Published: August 2005

SummaryMeasurements of body weight, total body water and total body potassium (40K) were made serially on three occasions during pregnancy and once post partum in 27 normal pregnant women. Skinfold thickness and fat cell diameter were also measured. A model of body composition was formulated to permit the estimation of changes in fat, lean tissue and water content of the maternal body. Total maternal body fat increased during pregnancy, reaching a peak towards the end of the second trimester before diminishing. Serial measurements of fat cell diameter showed poor correlation, whilst total body fat calculated from skinfold thickness correlated well with our estimated values for total body fat in pregnancy.
INTRAPARTUM FETAL MONITORING WITH THE CEREBRAL FUNCTION MONITOR
Authors: Maynard D. E. , Cohen R. J. , Viniker D. A. 
Published: August 2005

SummaryWe report a trial of the technical feasibility of monitoring the state of the fetal brain during labour using the Cerebral Function Monitor (CFM). This device was developed for long‐term monitoring of the electroencephalogram (EEG). A tripolar scalp electrode allows removal of the fetal electrocardiograph (ECG) from the fetal EEG. Technically satisfactory recordings were obtained from 15 fetuses during labour for periods of up to 6½ hours before delivery. There were alterations of CFM trace with fetal distress and also during general anaesthesia for Caesarean section.
CONTINUOUS MEASUREMENT OF TRANSCUTANEOUS FETAL OXYGEN TENSION DURING LABOUR
Authors: Weber T. , Secher N. J. 
Published: August 2005

SummaryTranscutaneous scalp oxygen tension (tcPO2) was measured during labour in 40 fetuses, using a modified Clark electrode (Radiometer, Copenhagen). In 24 of the fetuses the recordings were of good quality during the second stage of labour. After delivery the acid‐base status and oxygenation of the umbilical cord blood was measured. A correlation was found between the tcPO2 and umbilical artery oxygen saturation (r = 0.56, p<0.01) and umbilical artery PO2 (r = 0.56, p<0.01). Furthermore, a positive correlation was found between the area beneath the recorded tcPO2 curve during the last 10 minutes and the umbilical artery pH (r = 0.50, p <0.05). The data suggest that continuous transcutaneous PO2 measurement may be of value in monitoring high risk patients during labour.
AMNIOTIC FLUID PALMITIC ACID/STEARIC ACID RATIOS, LECITHIN/SPHINGOMYELIN RATIOS AND PALMITIC ACID CONCENTRATIONS IN THE ASSESSMENT OF FETAL LUNG MATURITY IN DIABETIC PREGNANCIES
Authors: Anderws A. G. , Brown J. B. , Jeffery P. E. , Horacek I. 
Published: August 2005

SummaryThe lecithin/sphingomyelin (L/S) ratio, palmitic acid concentration and palmitic to stearic acid (P/S) ratio were estimated on samples of amniotic fluid obtained from 66 patients with diabetes. These were compared with similar estimates on amniotic fluid obtained from 127 non‐diabetic patients. At 35 to 40 weeks, significant differences were observed between the L/S ratio and palmitic acid concentration in diabetics and non‐diabetics, whereas the P/S ratio was similar in the two groups. The amniotic fluid L/S ratio, palmitic acid concentration, and P/S ratio were estimated on amniotic fluid obtained from 20 diabetic patients within 48 hours of induction, and the clinical outcome of the newborn infant was used to assess the predictive value of the three parameters. In 19 out of the 20 diabetics the P/S ratio correctly predicted fetal lung maturity, whereas the palmitic acid concentration was correct in 12 patients and the L/S ratio in only 10 patients.
CIRCULATING LEVELS OF PREGNANCY SPECIFIC β1 GLYCOPROTEIN IN PREGNANCIES COMPLICATED BY DIABETES MELLITUS
Authors: Grudzinskas J. G. , Gordon Y. B. , Davies Humphreys J. , Brudenell M. , Chard T. 
Published: August 2005

SummaryCirculating levels of SP1 were measured in 20 insulin dependent diabetic women during the third trimester of pregnancy. With one exception, SP1 levels were between the 80 percent confidence limits of the normal range. The exception was a patient who was delivered of a normal infant at 37 weeks but had consistently low levels of SP1 from 32 weeks until delivery, suggesting a specific defect in SP1 synthesis.
PRIMARY CARCINOMA OF THE FALLOPIAN TUBE ASSOCIATED WITH TUBERCULOUS SALPINGITIS A CASE REPORT
Authors: Vinall P. S. , Buxton N. , Cowen P. N. 
Published: August 2005

SummaryA patient with co‐existent carcinoma and tuberculosis of the Fallopian tube is described. Tuberculosis was diagnosed by the finding of numerous typical granulomata throughout the uterus, tubes and ovaries, and by exclusion of other possible causes of these; and carcinoma by the finding of solid tumour, with a marked anisocytic appearance, invading submucosa. Despite the well recognised epithelial hyperplasia seen in tuberculous salpingitis, there remains no evidence that the occurrence of carcinoma in such cases is other than fortuitous.
Down‐regulation of muscarinic acetylcholine receptor M2 adversely affects the expression of Alzheimer's disease‐relevant genes and proteins
Authors: Zuchner Thole , Schliebs Reinhard , Perez‐Polo J. Regino 
Published: August 2005

AbstractBeta‐amyloid peptides play a major role in the pathogenesis of Alzheimer's disease (AD). Therefore, preventing beta‐amyloid formation by inhibition of the beta site amyloid precursor protein‐cleaving enzyme (BACE) 1 is considered as a potential strategy to treat AD. Cholinergic mechanisms have been shown to control amyloid precursor protein processing and the number of muscarinic M2‐acetylcholine receptors is decreased in brain regions of patients with AD enriched with senile plaques. Therefore, the present study investigates the effect of this M2 muscarinic receptor down‐regulation by siRNA on total gene expression and on regulation of BACE1 in particular in SK‐SH‐SY5Y cells. This model system was used for microarray analysis after carbachol stimulation of siRNA‐treated cells compared with carbachol stimulated, non‐siRNA‐treated cells. The same model system was used to elucidate changes at the protein level by using two‐dimensional gels followed by Matrix Assisted Laser Desorption Ionization Time‐of‐Flight Mass Spectrometry (MALDI‐TOF) analysis. Taken together, the results indicate that the M2 acetylcholine receptor down‐regulation in brains of patients with AD has important effects on the expression of several genes and proteins with major functions in the pathology of AD. This includes beta‐secretase BACE1 as well as several modulators of the tau protein and other AD‐relevant genes and proteins. Moreover, most of these genes and proteins are adversely affected against the background of AD.
A model for dynamic regulation of choline acetyltransferase by phosphorylation
Authors: Dobransky Tomas , Rylett R. Jane 
Published: August 2005

AbstractCholine acetyltransferase (ChAT) synthesizes the neurotransmitter acetylcholine (ACh) and is a phenotypic marker for cholinergic neurons. Cholinergic neurons in brain are involved in cognitive function, attentional processing and motor control, and decreased ChAT activity is found in several neurological disorders including Alzheimer's disease. Dysregulation of ChAT and cholinergic communication is also associated with some spontaneous point‐mutations in ChAT that alter its substrate binding kinetics, or by disruption of signaling pathways that could regulate protein kinases for which ChAT is a substrate. It has been identified recently that the catalytic activity and subcellular distribution of ChAT, and its interaction with other cellular proteins, can be modified by phosphorylation of the enzyme by protein kinase‐C and Ca2+/calmodulin‐dependent protein kinase II; these kinases appear also to mediate some of the effects of β‐amyloid peptides on cholinergic neuron functions, including the effects on ChAT. This review outlines a new model for the regulation of cholinergic transmission at the level of the presynaptic terminal that is mediated by hierarchically‐regulated, multi‐site phosphorylation of ChAT.
Calpain‐mediated truncation of dihydropyrimidinase‐like 3 protein (DPYSL3) in response to NMDA and H2O2 toxicity
Authors: Kowara Renata , Chen Qianfa , Milliken Melissa , Chakravarthy Balu 
Published: August 2005

AbstractDihydropyrimidinase‐like protein 3 (DPYSL3), a member of TUC (TOAD‐64/Ulip/CRMP), is believed to play a role in neuronal differentiation, axonal outgrowth and, possibly, neuronal regeneration. In primary cortical cultures, glutamate (NMDA) excitotoxicity and oxidative stress (H2O2) caused the cleavage of DPYSL3, resulting in the appearance of a doublet of 62 kDa and 60 kDa. Pre‐treatment of cell cultures with calpain inhibitors, but not caspase 3 inhibitor, before exposure to NMDA or H2O2 completely blocked the appearance of the doublet, suggesting calpain‐mediated truncation. Furthermore, in vitro digestion of DPYSL3 in cell lysate with purified calpain revealed a cleavage product identical to that observed in NMDA‐ and H2O2‐treated cells, and its appearance was blocked by calpain inhibitors. Analysis of the DPYSL3 protein sequence revealed a possible cleavage site for calpain (Val‐Arg‐Ser) on the C‐terminus of DPYSL3. Collectively, these studies demonstrate for the first time that DPYSL3 is a calpain substrate. The physiological relevance of the truncated DPYSL3 protein remains to be determined.
Dopamine release in PC12 cells is mediated by Ca2+‐dependent production of ceramide via sphingomyelin pathway
Authors: Jeon Hyung Jun , Lee Dong Hoon , Kang Mi Sun , Lee Mi‐Ock , Jung Kwang Mook , Jung Sung Yun , Kim Dae Kyong 
Published: August 2005

AbstractA presynaptic membrane disturbance is an essential process for the release of various neurotransmitters. Ceramide, which is a tumor suppressive lipid, has been shown to act as a channel‐forming molecule and serve as a precursor of ceramide‐1‐phosphate, which can disturb the cellular membrane. This study found that while permeable ceramide increases the rate of dopamine release in the presence of a Ca2+‐ionophore, A23187, permeable ceramide‐1‐phosphate provoked its release even without the ionophore. The treatment of PC12 cells with the ionophore at concentrations < 2 µm produced ceramide via the sphingomyelin (SM) pathway with a concomitant release of dopamine, and no cell damage was observed. The addition of a Ca2+ chelator, EGTA, to the medium inhibited the increase in the release of both the ceramide and dopamine. This suggests that ceramide might be produced by Ca2+ and is implicated in the membrane disturbance associated with the release of dopamine as a result of its conversion to ceramide‐1‐phosphate. Consistent with these results, this study detected a membrane‐associated and neutral pH optimum sphingomyelinase (SMase) whose activity was increased by Ca2+. Together, these results demonstrate that ceramide can be produced via the activation of a neutral form of SMase through Ca2+, and is involved in the dopamine release in concert with Ca2+.
The endocannabinoid system in the brain of Carassius auratus and its possible role in the control of food intake
Authors: Valenti M. , Cottone E. , Martinez R. , De Pedro N. , Rubio M. , Viveros M. P. , Franzoni M. F. , Delgado M.J. , Di Marzo V. 
Published: August 2005

AbstractCannabinoid receptors and the endocannabinoids anandamide and 2‐arachidonoylglycerol have been suggested to regulate food intake in several animal phyla. Orthologs of the mammalian cannabinoid CB1 and CB2 receptors have been identified in fish. We investigated the presence of this endocannabinoid system in the brain of the goldfish Carassius auratus and its role in food consumption. CB1‐like immunoreactivity was distributed throughout the goldfish brain. The prosencephalon showed strong CB1‐like immunoreactivity in the telencephalon and the inferior lobes of the posterior hypothalamus. Endocannabinoids were detected in all brain regions of C. auratus and an anandamide‐hydrolysing enzymatic activity with features similar to those of mammalian fatty acid amide hydrolase was found. Food deprivation for 24 h was accompanied by a significant increase of anandamide, but not 2‐arachidonoylglycerol, levels only in the telencephalon. Anandamide caused a dose‐dependent effect on food intake within 2 h of intraperitoneal administration to satiated fish and significantly enhanced or reduced food intake at low (1 pg/g body weight) or intermediate (10 pg/g) doses, respectively, the highest dose tested (100 pg/g) being inactive. We suggest that endocannabinoids might variously contribute to adaptive responses to food shortage in fish.
Effects of CAG repeat length, HTT protein length and protein context on cerebral metabolism measured using magnetic resonance spectroscopy in transgenic mouse models of Huntington's disease
Authors: Jenkins Bruce G. , Andreassen Ole A. , Dedeoglu Alpaslan , Leavitt Blair , Hayden Michael , Borchelt David , Ross Christopher A. , Ferrante Robert J. , Beal M. Flint 
Published: August 2005

AbstractHuntington's disease is a neurodegenerative illness caused by expansion of CAG repeats at the N‐terminal end of the protein huntingtin. We examined longitudinal changes in brain metabolite levels using in vivo magnetic resonance spectroscopy in five different mouse models. There was a large (>50%) exponential decrease in N‐acetyl aspartate (NAA) with time in both striatum and cortex in mice with 150 CAG repeats (R6/2 strain). There was a linear decrease restricted to striatum in N171‐82Q mice with 82 CAG repeats. Both the exponential and linear decreases of NAA were paralleled in time by decreases in neuronal area measured histologically. Yeast artificial chromosome transgenic mice with 72 CAG repeats, but low expression levels, had less striatal NAA loss than the N171–82Q mice (15% vs. 43%). We evaluated the effect of gene context in mice with an approximate 146 CAG repeat on the hypoxanthine phosphoribosyltransferase gene (HPRT). HPRT mice developed an obese phenotype in contrast to weight loss in the R6/2 and N171–82Q mice. These mice showed a small striatal NAA loss (21%), and a possible increase in brain lipids detectable by magnetic resonance (MR) spectroscopy and decreased brain water T1. Our results indicate profound metabolic defects that are strongly affected by CAG repeat length, as well as gene expression levels and protein context.
Serofendic acid prevents 6‐hydroxydopamine‐induced nigral neurodegeneration and drug‐induced rotational asymmetry in hemi‐parkinsonian rats
Authors: Inden Masatoshi , Kitamura Yoshihisa , Kondo Jun‐ichi , Hayashi Kousuke , Yanagida Takashi , Takata Kazuyuki , Tsuchiya Daiju , Yanagisawa Daijiro , Nishimura Kaneyasu , Taniguchi Takashi , Shimohama Shun , Sugimoto Hachiro , Akaike Akinori 
Published: August 2005

AbstractSerofendic acid was recently identified as a neuroprotective factor from fetal calf serum. This study was designed to evaluate the neuroprotective effects of an intranigral microinjection of serofendic acid based on behavioral, neurochemical and histochemical studies in hemi‐parkinsonian rats using 6‐hydroxydopamine (6‐OHDA). Rats were injected with 6‐OHDA in the presence or absence of serofendic acid, or were treated with serofendic acid on the same lateral side, at 12, 24 or 72 h after 6‐OHDA lesion. Intranigral injection of 6‐OHDA alone induced a massive loss of tyrosine hydroxylase (TH)‐immunopositive neurons in the substantia nigra pars compacta (SNpc). Either simultaneous or 12 h post‐administration of serofendic acid significantly prevented both dopaminergic neurodegeneration and drug‐induced rotational asymmetry. Immunoreactivities for oxidative stress markers, such as 3‐nitrotyrosine (3‐NT) and 4‐hydroxy‐2‐nonenal (4‐HNE), were markedly detected in the SNpc of rats injected with 6‐OHDA alone. These immunoreactivities were markedly suppressed by the co‐administration of serofendic acid, similar to the results in vehicle‐treated control rats. In addition, serofendic acid inhibited 6‐OHDA‐induced α‐synuclein expression and glial activation in the SNpc. These results suggest that serofendic acid protects against 6‐OHDA‐induced SNpc dopaminergic neurodegeneration in a rat model of Parkinson's disease.
γ‐Secretase complexes containing N‐ and C‐terminal fragments of different presenilin origin retain normal γ‐secretase activity
Authors: Strömberg Kia , Hansson Emil M. , Laudon Hanna , Bergstedt Susanne , Näslund Jan , Lundkvist Johan , Lendahl Urban 
Published: August 2005

AbstractThe γ‐secretase complex processes substrate proteins within membranes and consists of four proteins: presenilin (PS), nicastrin, Aph‐1 and Pen‐2. PS harbours the enzymatic activity of the complex, and there are two mammalian PS homologues: PS1 and PS2. PS undergoes endoproteolysis, generating the N‐ and C‐terminal fragments, NTF and CTF, which represent the active species of PS. To characterize the functional similarity between complexes of various PS composition, we analysed PS1, PS2, and chimeric PS composed of the NTF from PS1 and CTF from PS2, or vice versa, in assembly and function of the γ‐secretase complex. Chimeric PSs, like PS1 and PS2, undergo normal endoproteolysis when introduced into cells devoid of endogenous PS. Furthermore, PS2 CTF can, at least partially, restore processing in a truncated PS1, which cannot undergo endoproteolysis. All PS forms enable maturation of nicastrin and cleave full length Notch receptors, indicating that both PS1 and PS2 are present at the cell surface. Finally, when co‐introduced as separate molecules, NTF and CTF of different PS origin reconstitute γ‐secretase activity. In conclusion, these data show that endoproteolysis, NTF–CTF interactions, and the assembly and activity of γ‐secretase complexes are very conserved between PS1 and PS2.
A peptide from the first fibronectin domain of NCAM acts as an inverse agonist and stimulates FGF receptor activation, neurite outgrowth and survival
Authors: Anderson Alexandra A. , Kendal Claire E. , Garcia‐Maya Mitla , Kenny Anna V. , Morris‐Triggs Samantha A. , Wu Teresa , Reynolds Richard , Hohenester Erhard , Saffell Jane L. 
Published: August 2005

AbstractNeural cell adhesion molecule (NCAM) contributes to axon growth and guidance during development and learning and memory in adulthood. Although the Ig domains mediate homophilic binding, outgrowth activity localizes to two membrane proximal fibronectin‐like domains. The first of these contains a site identified as a potential FGF receptor (FGFR) activation motif (FRM) important for NCAM stimulation of neurite outgrowth, but its activity has hitherto remained hypothetical. Here, we have tested the effects of a domain‐specific antibody and peptides corresponding to the FRM in cellular assays in vitro. The first fibronectin domain antibody inhibited NCAM‐stimulated outgrowth, indicating the importance of the domain for NCAM function. Monomeric FRM peptide behaved as an inverse agonist; low concentrations specifically inhibited neurite outgrowth stimulated by NCAM and cellular responses to FGF2, while saturating concentrations stimulated FGFR‐dependent neurite outgrowth equivalent to NCAM itself. Dendrimeric FRM peptide was 125‐fold more active and stimulated FGFR activation, FGFR‐dependent and FGF‐mimetic neurite outgrowth and cell survival (but not proliferation). We conclude that the FRM peptide contains NCAM‐mimetic bioactivity accounted for by stimulation of FGF signalling pathways at the level of or upstream from FGF receptors, and discuss the possibility that FRM comprises part of an FGFR activation site on NCAM.