bluuebunny/crossref_metadata_2025_split huggingface dataset:
The effect of physical exercise on parameters of gastrointestinal function
Authors: Van Nieuwenhoven  , Brouns  , Brummer  
Published: March 2003

Exercise decreases splanchnic bloodflow. Therefore exercise may induce alterations in gastrointestinal (GI) function. In the present study we investigated the effect of high‐intensity exercise on oesophageal motility, gastro‐oesophageal reflux, gastric pH, gastric emptying, orocaecal transit time (OCTT), intestinal permeability and glucose absorption simultaneously, using an ambulatory protocol.Ten healthy well‐trained male subjects underwent a rest–cycling–rest, and a rest–rest–rest protocol (60–90–210 min). Oesophageal motility, gastro‐oesophageal reflux and intragastric pH was measured using a trans‐nasal catheter. OCTT was measured via breath H2 measurement. A sugar absorption test was applied to determine intestinal permeability and glucose absorption. Gastric emptying was measured using the 13C‐acetate breath test.Peristaltic velocity was increased during cycling, compared to rest (4.92 (2.86) vs. 4.03 (1.48) cm s–1, P = 0.015). Peristaltic contraction pressure at the mid‐oesophagus and the duration of the peristaltic contractions at the mid‐ and distal oesophagus was lower during cycling. There were no differences between the pre‐exercise, the exercise and the post‐exercise episodes for gastric pH or for both the number and duration of reflux episodes, in both the rest and cycling trials. Neither gastric emptying nor OCTT showed differences between rest and cycling. The lactulose/rhamnose ratio and intestinal glucose absorption were significantly decreased in the cycling trial.Our model enables multiple GI‐measurements during exercise. Cycling at 70% Wmax does not lead to differences in reflux, gastric pH or gastrointestinal transit in healthy trained individuals. The distal oesophageal pressure decreases and peristaltic velocity increases. The lactulose/rhamnose ratio and jejunal glucose absorption are decreased during exercise.
Impaired egress rather than increased access: an important independent predictor of erosive oesophagitis
Authors: Jones M. P. , Sloan S. S. , Jovanovic B. , Kahrilas P. J. 
Published: March 2003

Abstract Oesophagitis severity is related to total oesophageal acid exposure, which is in turn dependent upon both the number reflux events and the rate of refluxate clearance. This study examined differences in the frequency of reflux events and the characteristics of oesophageal acid exposure in asymptomatic controls and gastro‐oesophageal reflux disease (GORD) patients both with and without oesophagitis. Nine controls and 38 patients with GORD were studied. All patients underwent upper endoscopy, videofluoroscopy, determination of resting lower oesophageal sphincter pressure (LOSP) and 24 h pH monitoring. Analysis was performed with subjects grouped as controls, non‐erosive GORD and oesophagitis. A second analysis was performed with subjects grouped by hiatal hernia size. Statistical comparisons were made using anovaand unpairedt‐tests. Patients with oesophagitis had significantly larger hiatal hernias, greater oesophageal acid exposure, more prolonged episodes of reflux and longer acid clearance times than did controls and patients with non‐erosive GORD. No significant difference was seen in the number of reflux events. Increasing hiatal hernia size was significantly associated with increasing oesophageal acid exposure, number of prolonged reflux events and prolonged acid clearance times. Oesophagitis patients have significantly greater oesophageal acid exposure than subjects with non‐erosive GORD. Increased oesophageal acid exposure in oesophagitis is attributable to impaired acid clearance and the greatest impairments in refluxate clearance occur in patients with large hiatal hernias.
Gastric electrical stimulation at proximal stomach induces gastric relaxation in dogs
Authors: Xing J. H. , Brody F. , Brodsky J. , Larive B. , Ponsky J. , Soffer E. 
Published: March 2003

Abstract Gastric electrical stimulation (GES) improves symptoms in patients with gastroparesis. However, the underlying mechanisms remain unclear. To determine if GES at proximal and distal stomach could affect the biomechanical properties of the stomach, thus contributing to the beneficial effect of GES. Four pairs of electrodes were implanted along the greater curvature of the stomach in seven dogs. Gastric tone and compliance was assessed with a barostat. Measurements were obtained randomly during control and proximal and distal stimulation (4 mA, 375 ms and 6/18 cpm). Data as mean or median (25–75th percentiles). Gastric compliance was not affected by proximal and distal GES. Gastric tone was significantly reduced during proximal GES: 82.0 (66.8, 89.1) mL vs control 49.7 (39.6,75.9) mL at 6 cpm (P = 0.016), and 90.6 (54.5, 117.9) mL vs control 62.8 (39.6, 75.9) mL at 18 cpm (P = 0.031). Tone was not affected by distal GES at 6 cpm: 95.8 (46.3, 106.7) mL vs control 75.2 (49.7, 86.1) mL (P = 0.47) and at 18 cpm: 80.4 (38.1, 170.3) mL vs control 62.8 (44.6, 156.3) mL (P = 0.44). Proximal GES induces gastric relaxation. This effect, if seen also in humans, may explain, in part, the symptomatic improvement associated with GES therapy in patients with gastroparesis.
Endothelial changes in muscle and skin biopsies in patients with CADASIL
Authors: Ruchoux  , Maurage  
Published: March 2003

Ruchoux M.‐M. & Maurage C.‐A. (1998) Neuropathology and Applied Neurobiology24, 60–65Endothelial changes in muscle and skin biopsies in patients with CADASILCerebral autosomal dominant arteriopathy with subcortical infarcts and leucoencephalopathy (CADASIL) is characterized by the deposition of granular osmiophilic material in association with vascular smooth muscle cells in many different organs. However, the cause of the subsequent destruction of smooth muscle cells that are surrounded by granular osmiophilic material is unclear. In the present study, the ultrastructural changes that occur in endothelial cells in CADASIL have been evaluated by examining blood vessels in six skin biopsies and seven muscle biopsies belonging to three different CADASIL pedigrees. The appearances have been compared with five skin biopsies and five muscle biopsies from age‐matched controls without vascular disease. The most striking features observed in vessels in the skin of CADASIL patients were attenuation of endothelial cells and increased density of endothelial cytoplasm, accompanied by the presence of compact bundles of microfilaments within the cytoplasm of endothelial cells. Endothelial cells in muscle biopsies from CADASIL patients, on the other hand, were swollen until destruction of tight junctions were observed. These findings suggest that impaired permeability of vascular endothelium may play a role in the destruction of vascular smooth muscle cells in CADASIL. Furthermore, the results of this study suggest that further fine structural investigation of blood vessel endothelium and underlying smooth muscle may lead to a better understanding of the pathophysiology of CADASIL.
Local expression of cytokines in idiopathic inflammatory myopathies
Authors: Lepidi  , Frances  , Figarella‐Branger  , Bartoli  , Machado‐Baeta  , Pellissier  
Published: March 2003

H. Lepidi, V. Frances, D. Figarella‐Branger, C. Bartoli, A. Machado‐Baeta & J‐F. Pellissier (1998) Neuropathology and Applied Biology, 24, 73–79Local expression of cytokines in idiopathic inflammatory myopathiesThe idiopathic inflammatory myopathies (IIM), including dermatomyositis (DM), polymyositis (PM), and inclusion body myositis (IBM), are regarded as autoimmune diseases. They are characterized by chronic lymphocytic and macrophagic infiltration in muscle tissue. Of particular importance in understanding the immune response to IIM is the specific pattern of locally produced cytokines. Frozen muscle tissues from IIM (5 DM, 3 PM, and 1 IBM) were used to investigate the cytokine responses. The RT‐PCR technique was instrumental to determine the pattern of expression of pro‐inflammatory (IL‐1β, IL‐6, TNF‐α), Th1 (IFN‐γ IL‐2), and Th2 (IL‐4) cytokines. Immunohistochemistry was also used to localize morphologically IFN‐γ and IL‐4. Our results show that pro‐inflammatory cytokines and Th1 cytokines are mainly expressed in IIM. The accumulation of mononuclear inflammatory cells and the inflammatory syndrome in IIM are probably related in part to the production of pro‐inflammatory cytokines. Moreover, the pattern of local cytokine expression is consistent with a Th1 immune response related to autoimmune diseases.
Nijmegen breakage syndrome: a neuropathological study
Authors: Lammens M. , Hiel J. A. P. , Gabreëls F. J. M. , Weemaes C. M. R. ,   introduced by, Chakrabarty A. 
Published: March 2003

Introduction:  Nijmegen breakage syndrome (NBS) is an autosomal recessive disorder, which belongs to the DNA repair disorders. It is characterized by microcephaly, typical facial appearance, immunodeficiency, X‐ray hypersensitivity and predisposition of cancer.Material and methods:  Neuropathological examination of the brain was performed on a male NBS patient with moderate mental retardation, who was successfully treated for non‐Hodgkin's lymphoma at the age of 19 years. He died at the age of 31 years as a result of carcinomatous peritonitis.Results:  Severe microcephaly (> 3SD< mean) especially pronounced in the frontal lobe was observed. There was a very simplified gyral pattern with reduction of the tertiary gyri. A myelinated bundle 6 × 3.5 mm thick considered to be a large remnant of the striae longitudinales mediales and laterales was found over the whole length on top of the corpus callosum. There was an incomplete enrolling of the hippocampus and hypoplasia of the inferior vermis.Conclusions:  The neuropathological findings in this patient are concurrent with radiological findings in NBS patients and with limited earlier neuropathological studies. These findings suggest a role for a DNA‐repair gene in corticogenesis in man as has already been suggested in animal studies of other DNA‐repair genes before.
Guidelines for the pathoanatomical examination of the lower brain stem in ingestive and swallowing disorders and its application to a dysphagic spinocerebellar ataxia type 3 patient
Authors: Rüb U. , Brunt E. R. , Del Turco D. , De Vos R. A. I. , Gierga K. , Paulson H. , Braak H. 
Published: March 2003

U. Rüb, E. R. Brunt, D. Del Turco, R. A. I. de Vos, K. Gierga, H. Paulson and H. Braak (2003) Neuropathology and Applied Neurobiology 29, 1–13

Guildelines for the pathoanatomical examination of the lower brain stem in ingestive and swallowing disorders and its application to a dysphagic spinocerebellar ataxia type 3 patientDespite the fact that considerable progress has been made in the last 20 years regarding the three‐phase process of ingestion and the lower brain stem nuclei involved in it, no comprehensive descriptions of the ingestion‐related lower brain stem nuclei are available for neuropathologists confronted with ingestive malfunctions. Here, we propose guidelines for the pathoanatomical investigation of these nuclei based on current knowledge with respect to ingestion and the nuclei responsible for this process. The application of these guidelines is described by drawing upon the example of the lower brain stem of a male patient with spinocerebellar ataxia type 3, also known as Machado‐Joseph disease, who displayed malfunctions during the preparatory phase of ingestion, as well as lingual and pharyngeal phases of swallowing. By way of the representative application of the recommended investigation procedure to 100 µm serial sections through the patient's brain stem stained for lipofuscin pigment and Nissl material, we observed neuronal loss together with astrogliosis in nearly all of the ingestion‐related lower brain stem nuclei (motor, principal and spinal trigeminal nuclei; facial nucleus; parvocellular reticular nucleus; ambiguus nucleus, motor nucleus of the dorsal glossopharyngeal and vagal area; gelatinous, medial, parvocellular and pigmented solitary nuclei; hypoglossal nucleus). In view of their known functional role in the three‐phase process of ingestion, damage to these nuclei not only offers an explanation of the patient's malfunctions related to the preparatory phase of ingestion and lingual and pharyngeal phases of swallowing, but also suggests that the patient may have suffered from additional esophageal phase swallowing malfunctions not mentioned in his medical records.
Placental abruption and perinatal death
Authors: Kyrklund‐Blomberg Nina B. , Gennser Gerhard , Cnattingius Sven 
Published: March 2003

SummaryStudies of risk factors for abruptio placentae (AP) are partly conflicting and studies of risk factors for perinatal death in these pregnancies are scarce. Using the population‐based Swedish Birth Registry from 1987 to 1993, we were able to study these risks in 795 459 singleton pregnancies. Logistic regression analysis was used to estimate odds ratios (OR) for risk of AP and risk of perinatal death in pregnancies with and without AP. Risk factors for AP were: age, primiparity, high parity, not cohabiting with infant’s father, low education, smoking, infertility, pregestational diabetes, essential hypertension, pregnancy‐induced hypertensive diseases, preterm premature rupture of membranes, preterm birth and small‐for‐gestational‐age (SGA) births. Risk factors for perinatal death in pregnancies with placental abruption were smoking (1–9 and ≥10 cigarettes/day; OR 1.4 and 1.7 respectively), severe pre‐eclampsia (OR 2.0) and SGA (OR 1.9), whereas in pregnancies without abruption, risks were also increased in maternal age ≥35 years, primiparity, infertility, essential hypertension and pregestational diabetes. These findings support the theory that, in cases of AP, a general impairment of the placenta and/or a defect placentation may be fatal.
Survival of infants with spina bifida: a population study, 1979–94
Authors: Wong Lee‐Yang C. , Paulozzi Leonard J. 
Published: March 2003

SummaryThis study aimed to investigate the survival of infants born with spina bifida between 1979 and 1994 from the population‐based Metropolitan Atlanta Congenital Defects Program (MACDP) and to identify clinical and demographic factors associated with survival. Survival status was obtained from MACDP records and the National Death Index. Survival rates were calculated using the Kaplan–Meier method. Risk factors potentially associated with survival were examined by the log‐rank test. We assessed the independent effect of risk factors using the Cox proportional hazards model. Overall, 78.4% of children with spina bifida survived during the study period. Of the 235 infants born with spina bifida, 87.2% survived the first year of life. Survival to age 1 for the 1979–83, 1984–88 and 1989–94 birth cohorts was 82.7%, 88.5% and 91.0% respectively. In multivariable analysis, factors associated with increased mortality were low birthweight (<2500 g) (vs. ≥2500g, relative risk (RR) 2.3 [95% CI 1.1, 4.9]) and high lesions (vs. low lesions, RR 3.4 [95% CI 1.6, 7.1]). This study suggests a continuous improvement in survival among children born with spina bifida in Atlanta. Demographic and clinical factors are associated with length of survival. This information is useful for both clinicians and families who need to plan for the long‐term care of these children.
Analysis by gestational age of cerebral palsy in singleton births in north‐east England 1970–94
Authors: Drummond P. M. , Colver A. F. 
Published: March 2003

SummaryWe report from a well‐established cerebral palsy (CP) register the changes in CP rates by gestational age for singleton births over a 25‐year period in north‐east England. The gestational ages of numerators and denominators are of high accuracy back to 1970 because academic units in paediatrics and obstetrics were studying the assessment of gestational age in individual infants, and the distribution of gestational age across all births in the north‐east from the 1960s. The rate of CP rose between 1970–75 and 1990–94 from 1.6 to 2.3 per 1000 singleton neonatal survivors, a rise of 0.7/1000 [95% CI 0.2, 1.3]. There was little change in the rate of CP in term infants whereas in preterm infants (<37 weeks) it rose from 5.5 to 16.8, a rise of 11.3/1000 [95% CI 5.9, 16.8]. Rises occurred in the three preterm gestational age bands <28, 28–31, 32–36 weeks with the most marked rise in those <28 weeks from 0 to 112.7. The proportion of all cases of CP arising in the preterm group rose from 19% to 45%; and the proportion of the severest cases arising in the preterm group rose from 8% to 55%. In those born after 32 weeks, there is a preponderance of small‐for‐gestation infants, with 10% more than two standard deviations below the mean. All types of CP are more common in infants below average weight for gestation and this is most marked for the non‐spastic types that are almost only seen in term, small‐for‐gestation infants. Gestational age is the crucial determinant of rate of CP and the increase in prevalence seen over the past 25 years is due to increased rates in preterm infants, not term infants. Both conclusions, suspected from birthweight analyses, are now demonstrated conclusively, with the contribution coming from those 32–36 weeks gestation as well as very preterm infants.
Maternal characteristics associated with place of delivery and neonatal mortality rates among very‐low‐birthweight infants, Georgia
Authors: Samuelson Julia L. , Buehler James W. , Norris Dianne , Sadek Ramses 
Published: March 2003

SummaryTo determine whether the Healthy People 2000 objective to deliver very‐low‐birthweight (VLBW) infants at subspecialty perinatal care centres was met, and if improvements in the regional perinatal care system could reduce neonatal mortality further for 2010, we examined place of delivery for VLBW infants, associated maternal characteristics and the potential impact on neonatal mortality. We used linked birth and death records for the 1994–96 Georgia VLBW (i.e. 500–1499 g) birth cohorts. Among 4770 VLBW infants, 77% were delivered at hospitals providing subspecialty perinatal care. The strongest predictor of birth hospital level was the mother's county of residence, defined using three levels: residence in a county with a subspecialty hospital, residence in a county adjacent to one with such a hospital or residence in a non‐adjacent county. Eighty‐nine per cent of infants born to women who resided in counties with subspecialty care hospitals delivered at such hospitals, compared with 53% of infants born to women who resided in a non‐adjacent county. Women were also more likely to deliver outside subspecialty care if they had less than adequate prenatal care [adjusted odds ratio (AOR) 1.5, P‐value = 0.0001]. The neonatal mortality rate varied by level of perinatal care at the birth hospital from 132.1/1000 to 283/1000 live births, with the highest death rate for infants born at hospitals offering the lowest level of care. Assuming that the differences in mortality were due to care level of the birth hospital, potentially 16–23% of neonatal deaths among VLBW infants could have been prevented if 90% of infants born outside subspecialty care were delivered at the recommended level. These findings suggest that a state's support of strong, collaborative, regional perinatal care networks is required to ensure that high‐risk women and infants receive optimal health care. Improved access to recommended care levels should further reduce neonatal mortality until interventions are identified to prevent VLBW births.
Vaccine efficacy of recombinant cathepsin D aspartic protease from Schistosoma japonicum
Authors: Verity Christiana K. , McManus Donald P. , Brindley Paul J. 
Published: March 2003

Mice were vaccinated with recombinant Schistosoma japonicum cathepsin D aspartic protease, expressed in both insect cells and bacteria, in order to evaluate the vaccine efficacy of the schistosome protease. Mean total worm burdens were significantly reduced in vaccinated mice by 21–38%, and significant reductions in female worm burdens were also recorded (22–40%). Vaccination did not reduce fecundity; rather, we recorded increased egg output per female worm in vaccinated animals, suggesting a crowding effect. Vaccinated mice developed high levels of antibodies (predominantly IgG1, IgG2a and IgG2b isotypes), but there was no correlation between antibody levels and protective efficacy. Immune sera from vaccinated mice did not inhibit the degradation of human haemoglobin by the recombinant protease, and passive transfer of serum or antibodies from vaccinated animals, before and after parasite challenge, did not significantly reduce worm or egg burdens in recipient animals. These results suggest that antibodies may not play a key role in the protective effect elicited, and that protection may be due to a combination of humoral and cell‐mediated responses
The 14‐3‐3 protein as a vaccine candidate against schistosomiasis
Authors: Schechtman Deborah , Tarrab‐Hazdai Rebecca , Arnon Ruth 
Published: March 2003

We have previously reported on the cloning of the 14‐3‐3 protein of Schistosoma mansoni. Here, we evaluate the potential use of this protein as a vaccine candidate against infection by S. mansoni. Sm14‐3‐3 was expressed and purified either as a free protein or as a fusion protein to SjGST or MBP. Sera from mice infected with S. mansoni recognized both SjGST and 14‐3‐3, indicating that antibodies against these two proteins are induced in the course of the natural infection. Furthermore, mice immunized with either 14‐3‐3, GST or 14‐3‐3‐GST, reacted with cercaria lysate. A cellular immune response was also detected, particularly in mice immunized with 14‐3‐3‐GST. With respect to the effect on biological functions, antibodies to 14‐3‐3 and 14‐3‐3‐GST caused 23–32% complement‐mediated cytotoxcity of S. mansoni schistosomula compared to only 10–11% induced by either normal mouse serum, or GST alone. In challenge infection with S. mansoni, immunization with 14‐3‐3, either as a fusion protein or as a free protein, led to protection ranging from 25–46%, as determined by reduction of adult worm burden, while SjGST alone elicited only 0–8% protection and MBP alone did not elicit any protection.
Arginase I induction in macrophages, triggered by Th2‐type cytokines, supports the growth of intracellular Leishmania parasites
Authors: Iniesta Virginia , Carlos Gómez‐Nieto L. , Molano Isabel , Mohedano Alicia , Carcelén Jesualdo , Mirón Cristina , Alonso Carlos , Corraliza Inés 
Published: March 2003

Summary Leishmania spp. are intracellular protozoan parasites that invade and replicate within macrophages. In a previous report, we have demonstrated that the growth of intracellular amastigotes could be controlled by inhibition of arginase. This enzyme, induced in host cells by Th2 cytokines, synthesizes L‐ornithine which can be used by parasites to generate polyamines and proliferate. In this study, we have designed experiments to better analyse the dependence of parasite proliferation on arginase induction in infected macrophages. Treatment of Leishmania major‐infected BALB/c macrophages with interleukin (IL)‐4, IL‐10 or transforming growth factor‐β, which are all inducers of arginase I in murine macrophages, led to a proportional increase in the number of intracellular amastigotes. Moreover, parasite proliferation and arginase activity levels in macrophages from the susceptible BALB/c mice were significantly higher than those from infected C57BL/6 cells when treated with identical doses of these cytokines, indicating that a strong correlation exist between the permissibility of host cells to L. major infection and the induction of arginase I in macrophages. Specific inhibition of arginase by Nω‐hydroxy‐nor‐L‐arginine (nor‐LOHA) reverted growth, while L‐ornithine and putrescine promoted parasite proliferation, indicating that the parasite cell division depends critically on the level of L‐ornithine available in the host. Therefore, arginase induction in the context of a Th2 predominant response might be a contributor to susceptibility in leishmaniasis.