bluuebunny/crossref_metadata_2025_split huggingface dataset:
A rat model of neonatal post‐haemorrhagic ventricular dilatation
Authors: Cherian S. , Silver I. A. , Love S. , Whitelaw A. , Thoresen M. 
Published: March 2003

Introduction:  Post‐haemorrhagic ventricular dilatation (Phvd) complicates 30% of cases of severe intraventricular haemorrhage (Ivh) in preterm infants. The majority require shunt surgery and are disabled. The mechanism by which Ivh leads to Phvd is not understood, and no satisfactory neonatal model exists. We have developed a neonatal rat model of Phvd to study the mechanisms of Phvd.Methods:  Mixed sex, 7‐day‐old (P7) Wistar rats were anaesthetized with halothane and placed in a stereotactic frame. Ivh was simulated by injection of citrated rat blood into alternate lateral ventricles on two consecutive days (P7, P8). Survivors were killed on P22 and their brains fixed by immersion in 4% formaldehyde. H&E‐stained 5 µm sections were examined for pathological changes. Glial reaction was assessed by immunohistochemistry for glial fibrillary acidic protein, and ventricular area in standard coronal planes through the cerebrum was measured using Nih Image software.Results:  Increased ventricular size, focal ependymal disruption, reactive changes and accumulation of haemosiderin in scattered parenchymal cells were observed in 30% of the experimental animals. Injection of blood also caused a narrow zone of dense periventricular gliosis.Conclusion:  This rat pup model of Phvd may be useful for ascertaining the mechanism of post‐haemorrhagic ventricular dilatation.
CADASIL in monozygotic twins
Authors: Kalimo H. , Viitanen M. , Carlström C. , Nordberg A. , Bronge L. 
Published: March 2003

Introduction:  The cause of the highly variable clinical course in CADASIL is unknown, independent of the type of mutation.Patients and clinical findings:  The age of onset in the mother of monozygotic twins was 70 years. At 73 years MMSE was 22 with impairment of executive functions. T2w MRI showed grade D hyperintensities and T1w MRI infarcts in basal ganglia. She died at 73 years. Her geminus‐B twin son had first symptoms at 39 years, 30 years earlier than his mother. At 47 years he scored 29 in MMSE. T2w MRI disclosed grade C hyperintensities and T1w MRI infarcts in basal ganglia. Detection of GOM in dermal arteries established CADASIL diagnosis. The A twin is subjectively healthy at 48 years with MMSE 30. His T2w MRI showed grade B hyperintensities, but no infarcts in T1w MRI. In PET, the B twin's CBF was more markedly diminished than that of the A twin.Conclusion:  The clinical course in CADASIL can vary markedly despite the same gene defect or even identical genome. No anticipation or gender difference has been reported. The B twin is a smoker. Elucidation of reasons for the variation may reveal important pathogenetic factors.
Tau load is associated with apolipoprotein E genotype and the amount of amyloid β protein, Aβ40, in sporadic and familial Alzheimer's disease
Authors: Thaker U. , McDonagh A. M. , Iwatsubo T. , Lendon C. L. , Pickering‐Brown S. M. , A. Mann D. M. 
Published: March 2003

U. Thaker, A. M. McDonagh, T. Iwatsubo, C. L. Lendon, S. M. Pickering‐Brown and D. M. A. Mann (2003) Neuropathology and Applied Neurobiology 29, 35–44

Tau load is associated with apolipoprotein E genotype and the amount of amyloid β protein, Aβ40, in sporadic and familial Alzheimer's diseaseThe total amount of hyperphosphorylated tau protein (p‐tau load), present as neurofibrillary tangles (NFTs), neuropil threads or plaque neurites, was quantified in the frontal cortex of 109 cases of sporadic Alzheimer's disease (AD) and 35 cases of familial AD due to missense mutations in the presenilin‐1, presenilin‐2 and amyloid precursor protein genes. p‐tau load was inversely correlated with age at onset of illness in both sporadic and familial AD but not with duration of disease. There was no difference in p‐tau load between cases of familial AD and others with sporadic AD, matching the familial cases for apolipoprotein E (APO E) genotype. However, p‐tau was greater in cases of familial and sporadic AD in the presence of APO E ɛ4 allele and increased with gene dose. Conversely, p‐tau load tended to be lower when ɛ2 allele was present. In sporadic AD, tau load was highly significantly correlated with amyloid β40 (Aβ40), but not Aβ42(43), load. These data indicate that the burden of pathological tau deposited in the brain in both familial and sporadic AD is favoured in the presence of APO E ɛ4 allele and also related to the amount of Aβ40, this also being higher when ɛ4 allele is present. Aβ40 plaques are rich in microglial cells and it is possible that p‐tau pathology in AD is triggered by reaction of microglial cells to the presence of Aβ40 and not this peptide directly.
Maternal age, anthropometrics and pregnancy oestriol
Authors: Kaijser Magnus , Jacobsen Geir , Granath Fredrik , Cnattingius Sven , Ekbom Anders 
Published: March 2003

SummaryIt has been hypothesised that oestrogen exposure in utero influences the risk for breast cancer in adult life. Although several studies report associations between breast cancer and maternal factors associated with birthweight of the offspring – a marker for antenatal oestriol exposure – little is known about the relations between maternal oestrogen levels and these factors per se. We therefore analysed the association between oestriol levels in 188 women in the 17th, 25th, 33rd and 37th weeks of pregnancy, and maternal age, prepregnancy weight, height and pregnancy weight gain.Both maternal prepregnancy body mass index and maternal height were, after controlling for infant birthweight, independently and inversely associated with oestriol levels (P = 0.0021 and P = 0.0006 respectively). We found no association between maternal age or pregnancy weight gain and pregnancy oestriol levels. These findings suggest that the previously reported associations between maternal age and maternal pregnancy weight gain and the offspring’s risk of breast cancer are due to factors other than antenatal exposure to oestriol.
West Coast study of childhood brain tumours and maternal use of hair‐colouring products
Authors: Holly Elizabeth A , Bracci Paige M , Hong Mi‐Kyung , Mueller Beth A , Preston‐Martin Susan 
Published: March 2003

SummaryThe immature nervous system of the fetus is characterised by rapid cell growth and division and is particularly vulnerable to carcinogens and mutagens. Several epidemiological studies have reported an increased risk for childhood brain tumours (CBT) associated with exposure to N‐nitroso compounds (NOC). Hair‐colouring products (hair ‘dyes’) that contain NOC‐related aromatic amines have shown mutagenicity in vitro and carcinogenic properties in vivo. The potential public health impact of the relationship between hair dye use and carcinogenesis has prompted epidemiological research, given that a large proportion of American women have used hair dyes.A large population‐based case–control study was conducted on the west coast of the USA to investigate risk factors for CBT including exposure to NOC. Eligible CBT patients (<20 years of age and diagnosed between 1984 and 1991) were identified from cancer registries in Los Angeles County, the San Francisco Bay Area in California and the Seattle area in Washington state. A total of 540 biological mothers of these children were interviewed, and 801 control subjects who were frequency matched to the CBT patients on birth year and sex were obtained using random digit dialling. Mothers were asked details about personal use of hair dyes during the index pregnancy including frequency of use, trimester of use and type of dye used.Results from age‐ and sex‐adjusted unconditional logistic regression analyses showed no association between risk for CBT and use of hair dyes 1 month before and/or during pregnancy nor during specific trimesters. A nearly twofold increased risk for CBT was associated with single‐interval use during the 1 month before pregnancy, but the confidence interval (CI) was imprecise and the estimate was not different from unity (OR = 1.9, 95% CI [0.5, 7.0]). Exclusive use of permanent dye, temporary dye or hair darkeners was not associated with risk for CBT. A twofold increased risk (OR = 2.0, 95% CI [0.83, 4.7]) was observed with exclusive use of semi‐permanent dye during the month before or during pregnancy. Exclusive use of semi‐permanent dye during the month before pregnancy and/or first trimester also was associated with an elevated risk for CBT, again not different from unity and with an imprecise CI (OR = 2.5, 95% CI = [0.58, 10.3]). There was no evidence of an association between risk for CBT by histological subtypes and use of hair dyes during the index pregnancy or the month before conception. Together with results from previous studies, these results provide no consistent evidence of an association between risk for CBT and use of hair dyes during pregnancy.
The autopsy: experience of a regional neonatal intensive care unit
Authors: Okah Felix A. 
Published: March 2003

SummaryAutopsy rates have declined steadily throughout the 1970s and 1980s. This trend, if not reversed, could negatively affect information provided to families as well as the training of physicians. In the 1980s, low autopsy rates among neonatal deaths, 50–72%, were attributed to limited parental understanding and to physicians’ attitudes. In the early 1990s, alternatives to the routine autopsy, such as limited endoscopic/needle autopsies, were widely popularised, and the physician's education about autopsy vigorously addressed. The effects of these efforts on autopsy rates in the latter part of the 1990s have not been well studied.The study population consisted of 643 infants who died at an Ohio, USA, neonatal intensive care unit (NICU) between 1 January 1986 and 31 December 1998. Neonatologists obtained consent for autopsy. Information obtained from the computer database included birth hospital, gestational age, age at death, birth and death weight, race, sex, death year and maternal age, religion, gravidity and parity. The overall autopsy rate during the 13‐year study period was 54% [95% CI 44.1%, 63.1%]. There was a trend towards progressive decrease in autopsy rates, 59% in 1986–89, 52% in 1990–94 and 47% in 1995–98 (P = 0.078). Autopsy was associated with increasing gestational age (P < 0.001) and decreasing parity [OR = 0.53 for >2 compared with ≤2, 95% CI 0.36, 0.99], but not with other variables. Autopsy rates remain suboptimum and may be declining despite efforts at educating the medical and general community about its benefits. Among infants who die in the NICU, autopsy is more likely the more mature the infant at birth and the fewer children the mother has. Physicians need to seek autopsy more conscientiously, with consideration for the emotional well‐being of the family, and for its potential diagnostic and research value to science.
Non‐response bias as a likely cause of the association between young maternal age at the time of delivery and the risk of cancer in the offspring
Authors: Schüz Joachim 
Published: March 2003

SummarySome epidemiological studies have shown an association between young maternal age at the time of delivery and risk of cancer in the offspring. In a recent German case–control study, there was a twofold increase in the leukaemia risk for children whose mothers were aged < 20 years at the time of delivery. As the prevalence of younger mothers among control families was particularly low, data on maternal age distributions for the general population of Germany were obtained in order to examine the representativeness of the control sample. Despite the excellent sampling frame based on data from complete and up‐to‐date population registries and a satisfactory response rate among controls (≈71%), there seemed to be a material deficit of young mothers in the control sample. The prevalence of young mothers in the control group was 1.4%[95% CI 0.8%, 2.0%] compared with 2.9% in the general population and 3.3%[1.8%, 4.8%] among leukaemia cases. The most likely cause of this deficit was non‐participation. Non‐participation bias is hard to identify if no information is available on non‐responders and if it results from only small subgroups among the total control sample. Maternal age and childhood leukaemia are an example where differential non‐participation creates a spurious moderate association for a relatively rare exposure situation. But nowadays, many epidemiological studies target the detection of small to moderate risk increases for rare exposures. Therefore, the choice of a representative control group as well as the achievement of an excellent response rate are of prime importance.
Down's syndrome: occurrence and outcome in the north of England, 1985–99
Authors: Bell Ruth , Rankin Judith , Donaldson Liam J. 
Published: March 2003

SummaryThis study reports changes in the prevalence and outcome of Down's syndrome pregnancies within a 15‐year period in a defined geographical population in the north of England. Cases of Down's syndrome in births and terminations of pregnancy occurring between 1985 and 1999, were identified from the Northern Congenital Abnormality Survey. The total prevalence for the 15 years was 15.2 per 10 000 births and terminations of pregnancy [95% CI 14.2, 16.2]. Total prevalence showed an upward trend over time, due largely to increasing maternal age. Sixty‐seven per cent of cases resulted in live births, and the overall live birth prevalence was 10.3 per 10 000 live births [95% CI 9.4, 11.1]. The proportion of cases resulting in termination of pregnancy rose from 15% in 1985–89 to 38% in 1995–99; the rate of increase was greater in women aged < 35 years. Forty‐five per cent of live born infants had an additional anomaly recorded. Survival at 1 year was 78% for those with an additional anomaly recorded, and 96% for those without. There was a non‐significant trend towards improved survival in all infants with Down's syndrome, from 87% in 1985–94 to 92% in 1995–99. Despite increasing termination of Down's syndrome pregnancies resulting from the greater availability of antenatal screening and diagnosis, there has been no significant reduction in live birth prevalence. These infants have high rates of co‐existing structural anomalies and are at high risk of death in the first year of life. There is a continuing need to address the reasons for poor survival for Down's syndrome infants, and to plan for their complex health and social care needs. These findings are useful for parents deciding on prenatal screening, as well as for clinicians and health service managers.
A previous infection withToxoplasma gondiidoes not protect against a challenge withNeospora caninumin pregnant sheep
Authors: Innes E.A. , Lundén A. , Esteban I. , Marks J. , Maley S. , Wright S. , Rae A. , Harkins D. , Vermeulen A. , McKendrick I.J. , Buxton D. 
Published: March 2003

Sheep immunized with Toxoplasma gondii (Toxovax®) prior to pregnancy were tested for their ability to withstand a challenge at 90 days gestation with 107Neospora caninum (NC1) tachyzoites. The antibody responses in sheep following immunization with T. gondi were specific for T. gondii whereas peripheral blood mononuclear cells responded to both T. gondii and caninumantigen in vitro.This suggested that there was induction of crossreactive immune recognition in the sheep, at least at the cellular level. Following challenge of sheep at mid‐gestation with N caninum, no febrile responses were recorded in the group of sheep which had previously received Toxovax® while significant febrile responses were recorded in the group of sheep which received N challenge alone. Antibody responses to N developed in all sheep following challenge and antibody responses to T,gondii were boosted in the group of sheep which had previously been immunized with Toxovax®. No antibodies to were observed in the sheep which received the challenge alone. Peripheral blood mononuclear cells from both groups of sheep responded to T.gondii N.caninum antigen invitro and interferon gamma was present in the cell‐free supernatant from activated cells. However despite evidence of the induction of crossreactive immunity between T.gondii N.caninum this was not sufficient to prevent foetal death. The group of sheep which had received Toxovax® prior to pregnancy and the group of sheep which only received the N.caninum challenge experienced 100% foetal death compared with 0% in the unchallenged control group. Vaccination prior to pregnancy with Toxovax® did protect against foetal death following oral challenge at 90 days with 2000 oocysts which caused 100% foetal death in a control challenge group.
Immune‐mediated damage is not essential for the expulsion of Nippostrongylus brasiliensis adult worms from the small intestine of mice
Authors: Ishiwata Kenji , Nakao Hiroshi , Nakamura‐Uchiyama Fukumi , Nawa Yukifumi 
Published: March 2003

SummaryNippostrongylus brasiliensis adult worms are expelled from the rat small intestine during a primary infection by two steps. First, host immune responses cause damage to the worms, and then a nonspecific inflammatory response initiates expulsion. We have tested the two‐step expulsion hypothesis in mice infected with N. brasiliensis. After a primary infection in C57BL/6 mice, adult worms started to lay eggs on day 5 postinfection (p.i.) and were expelled around day 9–10 p.i. According to the rat system, 5 day‐ and 8‐day‐old worms were assumed to be ‘normal’ and ‘damaged’, respectively. When 5 day‐ and 8 day‐old worms obtained from C57BL/6 mice were transferred surgically into the small intestine of naive C57BL/6 mice, both 5 day‐ and 8 day‐old worms were almost simultaneously expelled by day 6 postworm implantation (p.w.i.). In contrast, when 5 day‐ and 8 day‐old worms of mouse origin were implanted into naive Wistar rats, 8 day‐old worms were expelled by day 5 p.w.i., while 5 day‐old worms were expelled by day 8 p.w.i. Similar results were obtained when BALB/c mice were used. Therefore, mice can expel N. brasiliensis adult worms as rapidly as rats expel ‘damaged’ worms, regardless of the status of the worms (‘normal’ or ‘damaged’). Stat6‐deficient mice were unable to expel implanted 5 day‐old worms up to day 10 p.w.i., suggesting that cellular mechanisms depending on Stat6‐signalling system are necessary for the expulsion. When N. brasiliensis adult worms obtained from Stat6‐deficient mice 5 and 15 days after a primary infection were implanted into Wistar rats, the former established in the recipient rats for approximately 1 week and were then expelled by day 10 p.w.i., whereas the latter were expelled by day 4 p.w.i. These results suggest that immune‐mediated damage of N. brasiliensis adult worms (first step) is not a prerequisite for expulsion from the small intestine of mice, although adult worms are actually damaged by Stat6‐independent immune mechanisms.
Early response of guinea‐pig lungs toTrichinella spiralisinfection
Authors: Dzik Jolanta M. , Gołos Barbara , Jagielska ELżbieta , Kapała Agnieszka , Wałajtys‐Rode ELżbieta 
Published: March 2003

SummaryIn order to assess immunological response, induced in guinea‐pig lungs byTrichinella spiralis,cellular infiltration into pulmonary alveolar space and production ofand NO in alveolar macrophages obtained from bronchoalveolar lavage fluid (BALF), as well as accumulation of nitric oxide (NO) metabolites in BALF and serum, were evaluated during the early period of primaryT. spiralisinfection (from 4th to 8th and on 14th day after oral administration of larvae) and on 6th day after secondary infection. Primary infection caused increased infiltration of lymphocytes, macrophages, neutrophils and eosinophils, while secondary infection resulted in raised lymphocyte and eosinophil numbers. In spite of marked cellular infiltration of alveolar space, only very limited activation of effector cells, pointing to a suppressed innate response, was apparent, as (i) BALF supernatant phospholipid/protein concentration ratio, and lung levels of phospholipid peroxidation markers, conjugated dienes and malondialdehyde, did not change during 7 days following infection; (ii) primary, but not secondary, infection caused only a transient increase of superoxide anion production by alveolar macrophages; (iii) despite expression of inducible nitric oxide synthase in macrophages of control, infected and BCG‐treated animals, and of interferon (IFN)‐γ‐like activity in sera of infected animals, macrophage nitric oxide production was not affected by infection, even after additional stimulationin vitro(lipopolisaccharide + hrIFN‐γ) or in vivo (BCG or secondaryT. spiralisinfection); and (iv) increased nitrate concentrations were found in BALF supernatant and serum, but not in lung homogenates, of infected animals.
Venom induces alarm behaviour in the social wasp Polybioides raphigastra (Hymenoptera: Vespidae): an investigation of alarm behaviour, venom volatiles and sting autotomy
Authors: Sledge M. F. , Dani F. R. , Fortunato A. , Maschwitz U. , Clarke S. R. , Francescato E. , Hashim R. , Morgan E. D. , Jones G. R. , Turillazzi S. 
Published: March 2003

SummaryChemicals from the venom gland elicited alarm behaviour and attack in the Asian polistine wasp Polybioides raphigastra. When presented with crushed venom glands workers of this wasp respond with a mass stinging attack. Gas chromatography–mass spectrometry analyses show that the major volatiles in the venom gland are alkanes, monounsaturated alkenes and 2‐alcohols. Several pyrazines, a spiroacetal and aromatics were also identified as trace compounds. The anatomy and morphology of the sting apparatus are reported, and we describe sting autotomy in this wasp. This is the first such report for the Ropalidiinae. The structures responsible for autotomy are likely to be large barbs present on the sting lancets, and a conspicuous tooth present on the medial side of the left lancet. Sting autotomy in P. raphigastra probably plays an important role in the localization of sites of attack by wasps defending the nest.
Behavioural and electrophysiological responses of the phlebotomine sandfly Lutzomyia longipalpis (Diptera: Psychodidae) when exposed to canid host odour kairomones
Authors: Dougherty M. J. , Guerin P. M. , Ward R. D. , Hamilton J. G. C. 
Published: March 2003

SummaryCompounds from the odour‐producing glands of the fox Vulpes vulpes were collected. This complex mixture of compounds was used to stimulate the ‘ascoid’ olfactory organs of female sandflies in single sensillum and gas chromatography‐linked single sensillum recordings. Sixteen of these compounds were identified using gas chromatography‐linked mass spectrometry and amounts present were determined. The compounds fell into four organic classes: ketones, carboxylic acids, alcohols and aldehydes. Specific neurones present in the ascoid sensillum that responded to each of these classes of compound were characterized.A bioassay chamber was developed that gave female sandflies the choice of two odour sources. Female sandflies were attracted upwind by fox odour and were trapped in closer proximity to the fox odour port than the control port. Synthetic compounds were recombined in appropriate quantities to mimic the fox odour. In this bioassay, the synthetic blend attracted sandflies upwind, and again they were caught closer to the test port than the control port. Furthermore, the synthetic fox odour induced an electrophysiological response from neurones in the ascoid sensillum that was very similar to that induced by natural fox odour. No synthetic compound alone induced the same behavioural response from sandflies as did whole fox odour. However, benzaldehyde, 4‐hydroxy‐4‐methyl‐2‐pentanone and 4‐methyl‐2‐pentanone alone did cause sandflies to fly upwind and to be caught closer to the test port than the control.