bluuebunny/crossref_metadata_2025_split huggingface dataset:
Compliance, tone and sensitivity of the rectum in different subtypes of irritable bowel syndrome
Authors: Steens J. , Van Der Schaar P. J. , Penning C. , Brussee J. , Masclee A. A. M. 
Published: March 2003

Abstract

Irritable bowel syndrome (IBS) consists of various subtypes. It is not known whether these subtypes share a common pathophysiology. Evaluation of motor and sensory function of the rectum using a barostat may help to explore a common pathophysiological background or differences in pathophysiology in subtypes of IBS. We have evaluated compliance, tone and sensitivity of the rectum, in both fasting state and postprandially, using a computerized barostat in 15 patients with diarrhoea‐predominant IBS (IBS‐D), 14 patients with constipation‐predominant IBS (IBS‐C) and compared the results with those obtained in 12 healthy controls. Rectal compliance as calculated over the steep part of the pressure–volume curve (17–23 mmHg) was decreased in both IBS groups (IBS‐D 8.0 ± 1.4 mL mmHg−1; IBS‐C 5.6 ± 1.1 mL mmHg−1) compared with controls (24.7 ± 3.5 mL mmHg−1). The perception of urge was increased only in IBS‐D patients, whereas pain perception was significantly increased in both IBS groups. Spontaneous adaptive relaxation was decreased in IBS‐D patients. Postprandially, rectal volume decreased significantly in the controls and in IBS‐D patients, but not in IBS‐C patients. In conclusion, both rectal motor and sensory characteristics are different between IBS‐D and IBS‐C patients. Therefore, testing of rectal visceroperception, adaptive relaxation and the rectal response to a meal may help distinguish groups of patients with different subtypes of irritable bowel syndrome.
Anisotropic propagation in the small intestine
Authors: Lammers W. J. E. P. , Stephen B. , Slack J. R. , Dhanasekaran S. 
Published: March 2003

Abstract
Measuring propagation anisotropy may help in determining the tissue layers involved in the propagation of electrical impulses in the intestine. We used 240 extracellular electrograms recorded from the isolated feline duodenum. The conduction velocities of slow waves and of individual spikes were measured from their site of origin into all directions. Both slow waves and spikes propagate anisotropically in the small intestine but in different directions and to a different degree. Slow waves propagated anisotropically faster in the circumferential (1.7 ± 0.8 cm s−1) than in the axial direction (1.3 ± 0.5 cm s−1; P < 0.001). Spikes, on the other hand, propagated faster in the longitudinal direction (7.8 ± 4.5 cm s−1) than in the circumferential direction (3.3 ± 4.3 cm s−1; P < 0.001). Furthermore, the average conduction velocity of spikes (6.3 ± 4.5 cm s−1) was significantly higher than that of slow waves (1.5 ± 1.1 cm s−1; P < 0.001). The anisotropic propagation of spikes supports the argument that these propagate in the longitudinal muscle layer. The anisotropic propagation of slow waves may be the result of the interaction between the myenteric layer of interstitial cells of Cajal and their electrotonic connection to both the longitudinal and the circular muscle layer.
Sensory neurone responses to mucosal noxae in the upper gut: relevance to mucosal integrity and gastrointestinal pain
Authors: Holzer P. 
Published: March 2003

Abstract
The digestive tract is supplied by extrinsic and intrinsic sensory neurones that, together with endocrine and immune cells, form a surveillance network that is essential to gut function. This article focuses on the responses of extrinsic afferent neurones to chemical insults of the gastrointestinal mucosa and their pathophysiological relevance to mucosal integrity and abdominal pain. Within the gastroduodenal region, spinal afferents subserve an emergency function because, in case of alarm by influxing acid, they stimulate mechanisms of mucosal protection via an efferent‐like release of transmitters. Other sensory neurones signal chemical noxae to the brain, a task that is not confined to spinal afferents because vagal afferents communicate gastric acid and peripheral immune challenges to the brainstem and in this way elicit autonomic, endocrine, affective and behavioural reactions. Emerging evidence indicates that hypersensitivity of extrinsic afferent pathways to mechanical and chemical stimuli makes an important contribution to the abdominal hyperalgesia seen in functional dyspepsia and irritable bowel syndrome. Sensitization may be brought about by inflammatory processes that lead to up‐regulation and functional alterations of receptors and ion channels on sensory neurones. Such sensory neurone‐specific molecules, which include vanilloid (capsaicin) receptors, may represent important targets for novel drugs to treat abdominal pain.
Effect of cholecystokinin‐A receptor blockade on postprandial insulinaemia and gastric emptying in humans
Authors: Hidalgo L. , Clavé P. , Estorch M. , Rodríguez‐Espinosa J. , Rovati L. , Greeley G. H. , Capellà G. , Lluís F. 
Published: March 2003

Abstract
Our aim was determine the relationship between cholecystokinin (CCK)‐A receptor blockade, glucose levels, insulin secretion and gastric emptying in humans, and to assess the effect of CCK‐A blockade on pancreatic polypeptide secretion. After a 12‐h fast, six healthy volunteers were given [99mTc]iminodiacetic acid monosodium salt (IDA) intravenously (5 mCi). One hour later they were offered a 577 kcal liquid meal containing [99mTc]diethylenetriaminepentaacetic acid (DTPA) (2 mCi) and glucose (105 g). Scintigraphic gastric and gallbladder activity, and plasma glucose, insulin and pancreatic polypeptide responses were monitored. In a second experiment, a continuous intravenous infusion of loxiglumide (7.5 mg kg h−1) was started 60 min before and continued until 120 min after test meal ingestion to block the CCK‐A receptors. Gallbladder emptying was blocked by loxiglumide. Loxiglumide accelerated gastric emptying, increased insulin secretion without alteration of glucose profiles, and abolished all phases of the postprandial pancreatic polypeptide response. Blockade of peripheral CCK‐A receptors accelerates gastric emptying of liquids with an increase in postprandial insulin levels. The lack of changes in glycaemia suggests that alternative homeostatic mechanisms also control postprandial glucose levels. Inhibition of pancreatic polypeptide release may reflect an independent effect of loxiglumide on vagal control involved in pancreatic polypeptide release.
The effect of glucagon‐induced gastric relaxation on TLOSR frequency
Authors: Chang H. Y. , Pandolfino J. E. , Shi G. , Boeckxstaens G. E. , Joehl R. J. , Kahrilas P. J. 
Published: March 2003

Abstract This study aimed to determine the effect of glucagon‐induced gastric relaxation on the frequency of transient lower oesophageal sphincter relaxations (TLOSRs). Eight normal subjects (four male, age 18–52 y) were studied after a 6‐h fast using a combined manometric barostat assembly. The recording was divided into two 1‐h sessions: (1) a baseline period with the barostat set at minimal distending pressure (MDP) + 2 mmHg and (2) a period with continuous glucagon or placebo infusion with barostat set at MDP + 2 mmHg. Patients were studied on two different days and randomly received glucagon (4.8 μg kg−1 bolus followed by 9.6 μg kg−1 h−1 infusion) on 1 day and placebo (saline) on another. Lower oesophageal sphincter (LOS) pressure, frequency of TLOSRs, and barostat bag volumes were determined for both placebo and glucagon infusion. Glucagon induced significant fundal relaxation compared with placebo (P < 0.05) and significantly decreased baseline LEOS pressure (P < 0.05). The frequency of TLOSRs was not altered by glucagon infusion compared with placebo. Despite causing substantial proximal stomach relaxation, glucagon did not increase TLOSR frequency. This suggests that the relevant gastric mechanoreceptors responsible for triggering TLOSRs do not respond to passive elongation.
Glycosphingolipid lysosomal storage diseases: therapy and pathogenesis
Authors: Jeyakumar M. , Butters T. D. , Dwek R. A. , Platt F. M. 
Published: March 2003

Paediatric neurodegenerative diseases are frequently caused by inborn errors in glycosphingolipid (GSL) catabolism and are collectively termed the glycosphingolipidoses. GSL catabolism occurs in the lysosome and a defect in an enzyme involved in GSL degradation leads to the lysosomal storage of its substrate(s). GSLs are abundantly expressed in the central nervous system (CNS) and the disorders frequently have a progressive neurodegenerative course. Our understanding of pathogenesis in these diseases is incomplete and currently few options exist for therapy.In this review we discuss how mouse models of these disorders are providing insights into pathogenesis and also leading to progress in evaluating experimental therapies.
Factors influencing tumour cell and vascular proliferation in glioblastoma
Authors: Chan P. T. H. , Weller R. O. 
Published: March 2003

Introduction:  This project examines the factors that influence tumour cell and vascular proliferation in glioblastomas.Hypothesis:  Necrosis is a major factor inducing tumour cell and vascular proliferation in glioblastomas.Material and methods:  5 µm paraffin sections from 10 cases of glioblastoma containing areas of normal brain, viable tumour and necrosis were stained with H&E, reticulin and by immunocytochemistry for GFAP, Ki‐67, CD34 for blood vessel endothelium, a combined Ki‐67/CD34, and CD68 for macrophages and microglia. Tumour cell proliferation in Ki‐67 preparations was measured in relation to (a) distance from necrosis and (b) proximity to blood vessels. The density of blood vessels was related to the distance from necrosis, and the presence of macrophages was related to the distance from necrosis and to the proximity to blood vessels. These measurements were effected by an automated computer quantification algorithm and by field‐specific ocular quantification.Results:  The mean tumour proliferation index (PI) was 6.49% (±4.95), with a two‐fold increase in tumour cell PI to 12.36% ± 5.82 (P ≤ 0.001) in the vicinity of blood vessels. The density of blood vessels was increased in the vicinity of areas of necrosis. Macrophages were distributed throughout the tumour, but were increased around areas of necrosis and around blood vessels. No relationship between tumour cell proliferation and necrosis was detected.Conclusions:  Tumour cell proliferation is concentrated around blood vessels in glioblastomas. Blood vessel proliferation, but not tumour cell proliferation, is related to areas of necrosis and the presence of macrophages in glioblastomas. Targeting of blood vessel proliferation and macrophages within glioblastoma may present a therapeutic strategy for treatment of these devastating tumours.
Familial hemi‐polymicrogyria and neurofibromatosis type 1
Authors: McLellan A. , Harding B. , Cross H. 
Published: March 2003

Background:  There have been rare reports of cerebral cortical malformations occurring in individuals with neurofibromatosis type 1 (NF1) but, to our knowledge, none with polymicrogyria. This communication concerns two brothers with right unilateral hemipolymicrogyria, one of who clinically has NF1.Observations:  The index case, a boy, presented at 22 months of age with macrocephaly and developmental delay, cutaneous stigmata of NF1 and a mild left hemiplegia. He developed drug resistant epilepsy, which led to focal resective surgery. Full‐scale IQ was 64 with poor memory performance. MRI demonstrated right hemisphere polymicrogyria, while functional imaging involving passive movement of the left hand showed activation in the dysplastic right sensorimotor cortex. Neuropathological examination of the focal resection confirmed polymicrogyria. His older brother showed mild learning difficulties at school but does not have cutaneous signs of NF1 or epilepsy. Psychometry revealed IQ of 87 with difficulties in working memory. Structural and functional MRI studies were similar to his brother.Comment:  Both brothers show extensive hemipolymicrogyria, with similar functional imaging and neuropsychological profiles, but only one brother has signs of NF1. Several maternal relatives also have NF1, and presently genetic studies are being undertaken to determine possible causal links or an independent mutation.
Third ventricular chordoid glioma: clinicopathological features of two cases
Authors: Kurian K. M. , Statham P. F. X. , Smith C. , Bell J. E. , Ironside J. W. 
Published: March 2003

Introduction:  Primary brain tumours occupying the third ventricle form a heterogenous group of uncommon lesions including colloid cysts, choroid plexus tumours, ependymoma, pilocytic astrocytoma, germinoma and pineal parenchymal tumours. Recently Brat et al. (J Neuropathol Exp Neurol 1998; 57: 238) described a tumour of the third ventricle composed of epithelioid cells with eosinophilic cytoplasm, extracellular mucin as well as a lymphoplasmacytic infiltrate. Although they resembled chordoma and chordoid meningioma histologically, immunohistochemistry demonstrated that these tumours were in fact glial in nature. These tumours have therefore been termed third ventricular chordoid glioma. They characteristically lack the chromosomal and genetic alterations commonly found in other types of gliomas or meningiomas (Reifenberger et al. Brain Pathol 1999; 9: 617). We describe the clinicopathological features of two recent cases of chordoid glioma that presented to the Department of Neuropathology, Western General Hospital, Edinburgh.Results:

Case 1 (238/01)

Case 2 (474/01)

Sex
Female

Female

Age
32 years

37 years

Presentation
Mild but progressive
Acute hydrocephalus

visual failure, weight

increase of 25.5 kg

over 4 years
headache, memory

problems, collapse

Imaging
Lower lateral third
Third ventricular

ventricle/ Hypothalamic

lesion
lesion

Immuno.
Ki67
<1%
<1%

GFAP
+++
+++

VIM
+++
+++

EMA
++
++

Conclusions:  The two cases of chordoid glioma we describe have slightly different clinical presentations and different appearances on histology. Understanding these variations will aid diagnosis of this unusual tumour.
Selective loss of inhibitory neurons in the cerebral cortex in motor neuron disease
Authors: Maekawa S. , Cotter D. , Leigh N. , Al‐Sarraj S. 
Published: March 2003

Introduction:  Motor neuron disease (MND) is characterized by selective loss of upper and lower motor neurons, although other CNS regions may also be affected (Abrahams et al. Brain 1996; 119: 2105; Lloyd et al. Brain 2000; 123: 2289). We previously demonstrated reduced neuronal density within extra‐motor cortical areas associated with astrocytic and microglial activation. We have now explored whether selective loss of inhibitory (GABAergic) neurones occurs in MND.Material and methods:  The density of inhibitory interneurons immunoreactive for the calcium‐binding proteins calbindin‐D28K (CB), calretinin (CR), and parvalbumin (PV) was determined via quantitative image analysis in the primary motor cortex (PMC; Brodmann's area 4) and dorsolateral prefrontal cortex (DLPFC; Brodmann's area 9) from 13 MND and eight control cases, matched for age and postmortem interval.Results:  There was a significant reduction in CB‐+ve densities within lamina II of both area 4 and 9 in MND (Wilk's lambda multivariate test: P = 0.003). However, post hoc comparisons of individual regions showed that these changes were only significant in area 9 (P = 0.046). PV‐+ve densities within cortical layer VI were significantly reduced in MND in both regions (P = 0.015), whereas the multivariate test showed no significant difference within the two regions (P = 0.951).Conclusions:  These findings reveal a selective loss in the density of subpopulations of GABAergic neurons in PMC and DLPFC in MND.
Central nervous system tumours in children in Costa Rica, 1981–96
Authors: Reutfors Johan , Kramárová Eva , Weiderpass Elisabete , Monge Patricia , Wesseling Catharina , Ahlbom Anders 
Published: March 2003

SummaryIncidence rates of malignant central nervous system (CNS) tumours in children in Costa Rica are presented in an international perspective. For the 16‐year period 1981–96, a total of 256 CNS tumours were registered in children below age 15 years by the National Tumour Registry of Costa Rica. The age‐standardised incidence rate was 15.2 per million person–years, with a male‐to‐female ratio of 1.4. The median age‐standardised incidence rates of selected registries in other Latin American countries were 19.3, in other developing countries 12.0 and in industrialised countries 29.6 per million person–years. The comparatively low incidence rates in Costa Rica were evident in all diagnostic subgroups, most notably in the youngest age group and for tumours in the brain stem. In the Central Valley, where the capital and the only specialised paediatric hospital are situated, the crude incidence rate was 18.1 [95% CI 15.1, 21.1] compared with 10.5 [95% CI 8.3, 12.8] per million person–years in the rest of the country (RR = 1.7, 95% CI 1.3, 2.3). There was no evidence of any increase over time. The data in this study cannot exclude under‐diagnosis and, to a lesser degree, under‐registration as a partial explanation of the low incidence rates of malignant CNS tumours in children in Costa Rica.
Epidemiology of neonatal necrotising enterocolitis: a population‐based study
Authors: Llanos Adolfo R. , Moss Mark E. , Pinzòn Maria C. , Dye Timothy , Sinkin Robert A. , Kendig James W. 
Published: March 2003

SummaryWe examined the birthweight‐, gender‐ and race‐specific incidence as well as the biodemographic and clinical correlates of necrotising enterocolitis (NEC) in a well‐defined six‐county perinatal region in upstate New York. We conducted a retrospective, 8‐year population‐based survey to identify all cases of proven NEC (modified Bell stage II and above) in the area's regional neonatal intensive care unit (NICU). The denominator used to calculate the incidence was obtained from the Statewide Planning Research Cooperative System. Incidence was expressed as cases per 1000 live births. A total of 85 documented cases of proven NEC was identified in a six‐county perinatal region that experienced 117 892 live births during the 8‐year period. The average annual incidence was 0.72 cases per 1000 live births [95% CI 0.57, 0.87 per 1000 live births]. The highest incidence of NEC occurred among infants weighing 750–1000 g at birth and declined with increasing birthweight. The urban county had a 1.53 times higher risk of NEC than rural counties [95% CI 0.9, 2.6]. The overall incidence of NEC for non‐Hispanic blacks was significantly greater than that for non‐ Hispanic whites (2.2 vs. 0.5 cases per 1000 live births, P = 0.00). The differences remained statistically significant even after correction for birthweight. Most cases (93%) in this series were preterm (gestational age <37 weeks). Only two patients were never fed before the diagnosis of NEC was confirmed. Positive blood cultures were documented in 27% of the cases with a predominance of Gram‐negative enteric micro‐organisms. NEC remains an important health problem especially for preterm infants and the non‐Hispanic black population.
The influence of γδ T cells on the CD4+ T cell and antibody response during a primary Plasmodium chabaudi chabaudi infection in mice
Authors: Seixas Elsa , Fonseca Luis , Langhorne Jean 
Published: March 2003

Summary A primary infection with Plasmodium chabaudi chabaudi (AS) is characterized by an expansion ofγδcells after the acute phase of infection in mice. This is particularly marked during chronic infections in B cell‐deficient mice. Infections inγδT cell‐deficient mice suggest that, although these cells play some role in the control of parasitaemia and can produce interferon‐γ, they do not appear to be involved in the development of hypoglycaemia, loss of weight and temperature during a P. c. chabaudi infection. However,γδT cells do influence the nature of the CD4+T cell response during infection since, in their absence, Th2‐like responses, such as interleukin (IL)‐4 production and help for malaria‐specific antibody responses, are more pronounced. This alteration in CD4+T cells is reflected in a more rapid and greater immunoglobulin (Ig)G1 and IgG3 antibody response to the parasite. The largeγδT cell expansion normally observed in infected B cell‐deficient mice did not take place in the absence of IL‐2, and double‐knockout mice lacking both B cells and functional IL‐2 were highly susceptible to lethal infection with P. c. chabaudi. The majority of the single IL‐2 knockout mice, in contrast, were able to control and clear a primary infection, suggesting that for the CD4+T cell and antibody response, IL‐2 could be replaced by other cytokines.
Paraflagellar rod protein‐specific CD8+ cytotoxic T lymphocytes target Trypanosoma cruzi‐infected host cells
Authors: Wrightsman Ruth A. , Luhrs Keith A. , Fouts David , Manning Jerry E. 
Published: March 2003

SummaryOur previous studies show that in mice immunized with the paraflagellar rod (PFR) proteins of Trypanosoma cruzi protective immunity against this protozoan parasite requires MHC class I‐restricted T cell function. To determine whether PFR‐specific CD8+ T cell subsets are generated during T. cruzi infection, potential CTL targets in the PFR proteins were identified by scanning the amino acid sequences of the four PFR proteins for regions of 8–10 amino acids that conform to predicted MHC class I H‐2b binding motifs. A subset of the peptide sequences identified were synthesized and tested as target antigen in 51Cr‐release assays with effector cells from chronically infected T. cruzi mice. Short‐term cytotoxic T lymphocyte (CTL) lines specific for two of the peptides, PFR‐1164–171 and PFR‐3123–130, showed high levels of lytic activity against peptide‐pulsed target cells, secreted interferon (IFN)‐γ in response to parasite‐infected target cells, and were found to be CD8+, CD4−, CD3+, TCRαβ+ cells of the Tc1 subset. Challenge of PFR immunized CD8−/− and perforin‐deficient (PKO) mice confirmed that while CD8+ cells are required for survival of T. cruzi challenge infection, perforin activity is not required. Furthermore, while lytic activity of PFR‐specific CD8+ T cell lines derived from PKO mice was severely impaired, the IFN‐γ levels secreted by CTLs from PKO mice were equivalent to that of normal mice, suggesting that the critical role played by CD8+ T cells in immunity to the parasite may be secretion of type 1 cytokines rather than lysis of parasite infected host cells.
Visualizing the postembryonic development ofSarcophaga peregrina(flesh fly) by NMR microscopy
Authors: Price William S. , Kobayashi Ayako , Ide Hiroyuki , Natori Shunji , Arata YojI. 
Published: March 2003

AbstractThe postembryonic development of the flesh fly was studied using high resolution nuclear magnetic resonance imaging. Because this development occurs in a puparium, this process cannot be observed directly using standard histological techniques. The remodelling of histolysing larval tissues to developing imaginal tissues including the yellow body, a transient alimentary structure, and the integration of the developed adult structure were revealed in the images. Most surprisingly it was found that a large gas space that forms in the central region of the prepupa moves to the dorso‐anterial region in less than 5 min due to the larval–pupal apolysis together with separation of the developing pupal epidermis from the puparium.
The structure and surface properties of the eggshell of Megaselia imitatrix Borgmeier (Diptera, Phoridae) in relation to the respiration of the embryo
Authors: Benton Forbes , Claugher Donald 
Published: March 2003

SummaryThe role of the chorion in the mechanism of respiration is examined for the egg of Megaselia imitatrix. An air layer in the chorion is not essential for respiration, and oxygen can be absorbed through a hydrophilic pathway in the chorion by diffusion from the surrounding water. A model based on the diffusion of oxygen through the surface layer of the water down to the depth of the egg is proposed and presented in detail.