Influence of milking interval on the total bacterial count in a simulated automatic milking system.
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Animals↗
Biomedical subjects
C J Allen
Publications and source records attributed to C J Allen.
Gastro-oesophageal reflux related cough and its response to laparoscopic fundoplication.
BACKGROUND: This study was designed to determine prospectively the rate of cough before and after laparoscopic Nissen fundoplication performed for the control of gastro-oesophageal reflux disease. METHODS: One hundred and ninety five consecutive patients (76 men) of mean (SD) age 46.9 (14.1) years with proven gastro-oesophageal reflux disease, who were either on long term omeprazole (n = 187) or who had not responded to a trial of omeprazole (n = 8), took part in the study which was carried out in a university teaching hospital that included a regional respiratory referral centre. Patients underwent oesophageal manometry, 24 hour oesophageal pH testing, and symptom score evaluation by an independent observer before and six months after laparoscopic Nissen fundoplication. RESULTS: One hundred and thirty three patients presented with reflux symptoms and 62 with respiratory symptoms; 68% of patients complained of cough before surgery (86% with respiratory symptoms, 60% with gastrointestinal symptoms). The percentage reflux time in 24 hours fell significantly (p < 0.0001) from a mean (SD) of 9.38 (10.99)% to 1.22 (2.92)%, lower oesophageal sphincter tone rose significantly (p < 0.0001) from a mean (SD) of 7.71 (5.90) mm Hg to 21.74 (10.84) mm Hg, and the cough score fell from a median value of 8.0 (IQR 12.0) to 0 (IQR 3) following surgery. Of the patients with cough, 51% were cough free after surgery and 31% improved. The patients with respiratory symptoms had a higher cough score before (median 12.0 (IQR 5.5) versus 4.0 (IQR 8.75), p < 0.0001) and after surgery (median 1 (7.5) versus 0.0 (IQR 1.0), p = 0.0045) than those with gastrointestinal symptoms. CONCLUSIONS: Patients who present to gastroenterologists with severe reflux commonly complain of cough. Laparoscopic Nissen fundoplication is effective in the control of cough in patients with gastro-oesophageal reflux disease, with or without primary respiratory disease.
Adolescent↗
Use of cysteine replacements and chemical modification to alter XIP, the autoinhibitory region of the Na-Ca exchanger. Inhibition of the activated plasma membrane Ca pump.
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Amino Acid Sequence↗
Prospective evaluation of dysphagia before and after laparoscopic Nissen fundoplication without routine division of short gastrics.
The incidence and severity of dysphagia before and 6 months after laparoscopic Nissen fundoplication without routine division of short gastric vessels are presented. Laparoscopic Nissen fundoplication was undertaken in 195 patients over 32 months with 116 patients who had prospective follow-up longer than 6 months. Patients underwent a 24-h pH recording, esophageal manometry, and symptom score assessment before and 6 months after surgery. There was a significant (p < 0.0001) improvement in the percent of reflux in 24-h (8.61 +/- 0.74 to 0.68 +/- 0.12), lower esophageal pressure (8.53 +/- 0.51 to 23.11 +/- 1.1 mm Hg), and reflux symptom scores (40.97 +/- 1.13 to 12.11 +/- 1.1) at 6 months. A similar improvement (p < 0.0001) was also observed in the dysphagia symptom score (4.58 +/- 0.38 to 1.96 +/- 0.32), with more than half the patients reporting improvement after surgery. No correlation was observed between the change in dysphagia score and the postoperative lower esophageal pressure or esophageal motor function. These data suggest that the incidence of clinically significant dysphagia after laparoscopic Nissen fundoplication, even without division of short gastric vessels, is low. Improvement in the dysphagia score after surgery is interesting and warrants further investigation.
Adolescent↗
Rapid endocytosis of a G protein-coupled receptor: substance P evoked internalization of its receptor in the rat striatum in vivo.
Studies on cultured cells have shown that agonists induce several types of G protein-coupled receptors to undergo internalization. We have investigated this phenomenon in rat striatum, using substance P (SP)-induced internalization of the SP receptor (SPR) as our model system. Within 1 min of a unilateral striatal injection of SP in the anesthetized rat, nearly 60% of the SPR-immunoreactive neurons within the injection zone display massive internalization of the SPR--i.e., 20-200 SPR+ endosomes per cell body. Within the dendrites the SPR undergoes a striking translocation from the plasma membrane to endosomes, and these dendrites also undergo a morphological reorganization, changing from a structure of rather uniform diameter to one characterized by large, swollen varicosities connected by thin fibers. In both cell bodies and dendrites the number of SPR+ endosomes returns to baseline within 60 min of SP injection. The number of neurons displaying substantial endosomal SPR internalization is dependent on the concentration of injected SP, and the SP-induced SPR internalization is inhibited by the nonpeptide neurokinin 1 receptor antagonist RP-67,580. These data demonstrate that in the central nervous system in vivo, SP induces a rapid and widespread SPR internalization in the cell bodies and dendrites and a structural reorganization of the dendrites. These results suggest that many of the observations that have been made on the internalization and recycling of G protein-coupled receptors in in vitro transfected cell systems are applicable to similar events that occur in the mammalian central nervous system in vivo.
Analysis of Variance↗
Community resources for psychiatric and psychosocial problems. Family physicians' referral patterns in urban Ontario.
OBJECTIVE: To document the number and pattern of psychiatric and psychosocial referrals to community resources by family physicians (FPs) and to determine whether referral practices correlate with physician variables. DESIGN: Cross-sectional survey of referrals by FPs to 34 key psychiatric and psychosocial community resources identified by a panel of FPs, psychiatric social workers, psychiatric nurses, public health nurses, and the local community information service. SETTING: Regional municipality of 434,000 persons in Ontario. PARTICIPANTS: Twenty-seven of 34 (79%) community agencies identified 261 FPs who made 4487 referrals to participating agencies (range 0 to 65, median 15, mean 17.19 +/- 13.42). MAIN OUTCOME MEASURES: Number of referrals to all agencies; variables, such as physician sex, school of graduation, year of graduation, and certificate status in the College of Family Physicians of Canada, related to referral patterns. RESULTS: Referrals to outpatient psychiatric clinics, support services, and general counseling services accounted for 96% of all referrals. Physicians' average annual referral profile was as follows: 8.6 patients to a support service, 6.3 to an outpatient psychiatric service, 1.6 to a counseling service, and 0.46 to a substance abuse service. Referral profiles of individual physicians varied greatly. Female FPs made fewer referrals than male FPs to support services, but both made similar numbers of referrals to psychiatric, counseling, and substance abuse services. The more recent the year of graduation, the greater the number of referrals to psychiatric (r = 0.158, P = 0.0107) and counseling services (r = 0.137, P = 0.0272) and the higher the fraction of referrals to psychiatric services (r = 0.286, P = 0.0001). CONCLUSIONS: Family physicians in Hamilton-Wentworth made few referrals to psychiatric and psychosocial services. Only physician sex and year of graduation correlated significantly with numbers of referrals made. Recent graduates of both sexes made significantly more referrals to psychiatric clinics and counseling services than their older colleagues.
Community Mental Health Services↗
Beta 2-adrenergic receptors are expressed by glia in vivo in the normal and injured central nervous system in the rat, rabbit, and human.
Previous studies have demonstrated that glial cells in culture express several subtypes of functional adrenergic receptors. To determine if similar receptors are expressed by glia in vivo, we examined the expression of adrenergic receptors in the normal, crushed, and transected optic nerves of the rabbit and rat using quantitative receptor autoradiography. Additionally, we examined the expression of adrenergic receptors in the normal and damaged human optic nerve. High levels of alpha 1-, alpha 2-, beta 1-, and beta 2-adrenergic receptors were identified in the rabbit and rat forebrain. In the normal rabbit, rat, and human optic nerves, only alpha 1 and beta 2 receptors were observed, and these were present in low to moderate densities. Combined immunohistochemistry and autoradiography suggests that the majority of beta 2-adrenergic receptors in the rabbit, rat, and human optic nerve are expressed by astrocytes. After unilateral optic nerve crush or transection, only beta 2- adrenergic receptors were significantly increased. This increase in beta 2 receptors was first detectable at days 7 and 28 post-transection in the rabbit and rat, respectively. The expression of beta 2 receptors in the transected optic nerve continued to increase with time, so that by 90 d post-transection the density of beta 2 receptors in both the rabbit and rat optic nerve was among the highest of any area in the forebrain. Taken together with previous studies, these results suggest that in vivo, beta 2-adrenergic receptors may provide a therapeutic target for regulation of astrocyte functions including glycogen metabolism, cytokine release, and the hypertrophy and proliferation that occurs in response to neuronal injury.
Aged↗
Efficacy of deferoxamine in preventing complications of iron overload in patients with thalassemia major.
BACKGROUND: To determine whether deferoxamine prevents the complications of transfusional iron overload in thalassemia major, we evaluated 59 patients (30 were female and 29 male; age range, 7 to 31 years) periodically for 4 to 10 years or until death. METHODS: At each follow-up visit, we performed a detailed clinical and laboratory evaluation and measured hepatic iron stores with a noninvasive magnetic device. RESULTS: The body iron burden as assessed by magnetic measurement of hepatic iron stores was closely correlated (R = 0.89, P < 0.001) with the ratio of cumulative transfusional iron load to cumulative deferoxamine use (expressed in millimoles of iron per kilogram of body weight, in relation to grams of deferoxamine per kilogram, transformed into the natural logarithm). Each increase of one unit in the natural logarithm of the ratio (transfusional iron load to deferoxamine use) was associated with an increased risk of impaired glucose tolerance (relative risk, 19.3; 95 percent confidence interval, 4.8 to 77.4), diabetes mellitus (relative risk, 9.2; 95 percent confidence interval, 1.8 to 47.7), cardiac disease (relative risk, 9.9; 95 percent confidence interval, 1.9 to 51.2), and death (relative risk, 12.6; 95 percent confidence interval, 2.4 to 65.4). All nine deaths during the study occurred among the 23 patients who had begun chelation therapy later and used less deferoxamine in relation to their transfusional iron load (P < 0.001). CONCLUSIONS: The early use of deferoxamine in an amount proportional to the transfusional iron load reduces the body iron burden and helps protect against diabetes mellitus, cardiac disease, and early death in patients with thalassemia major.
Adolescent↗
Cholecystokinin and neuropeptide Y receptors on single rabbit vagal afferent ganglion neurons: site of prejunctional modulation of visceral sensory neurons.
A [125I]cholecystokinin (CCK) analog and [125I]peptide YY (PYY) were used to localize and characterize CCK and neuropeptide Y (NPY) receptor binding sites in the rabbit vagal afferent (nodose) ganglion. High concentrations of CCK and NPY binding sites were observed in 10.6% and 9.2% of the nodose ganglion neurons, respectively. Pharmacological experiments using CCK or NPY analogs suggest that both subtypes of CCK (CCK-A and CCK-B) and NPY (Y1 and Y2) receptor binding sites are expressed by discrete populations of neurons in the nodose ganglion. These results suggest sites at which CCK or NPY, released in either the nucleus of the solitary tract or a peripheral tissue, may modulate the release of neurotransmitters from a select population of visceral primary afferent neurons. Possible functions mediated by these receptors include modulation of satiety, opiate analgesia, and the development of morphine tolerance.
Amino Acid Sequence↗
Some sensory neurons express neuropeptide Y receptors: potential paracrine inhibition of primary afferent nociceptors following peripheral nerve injury.
Neuropeptide Y (NPY) has been suggested to exert antinociceptive actions by inhibiting the release of neurotransmitters from trigeminal and dorsal root ganglia (DRG) neurons, but the site of direct NPY action in vivo and the NPY receptor subtype mediating these effects are unknown. 125I-peptide YY (PYY) was used to localize and characterize NPY receptor binding sites in trigeminal ganglia, DRG, and spinal cord of the rat, rabbit, and monkey. In the rat, rabbit, and monkey, 5-20% of trigeminal ganglia and DRG neurons express NPY binding sites. Unilateral cuff-induced neuropathy or transection of the rat sciatic nerve did not significantly alter the density or number of DRG neurons expressing NPY receptors. A unimodal size distribution for L4 and L5 DRG neurons expressing NPY binding sites in the rat was determined, with a mean cross-sectional area of 947 microns 2. In the spinal cord the highest concentration of NPY receptors is found in laminae I, II, V, X, and Onuf's nucleus. Pharmacological experiments using selective Y1 and Y2 receptor antagonists suggest that Y2 is the prominent NPY receptor subtype expressed in trigeminal ganglia neurons, DRG neurons, and spinal cord. Previous studies have demonstrated that a population of large-diameter, presumably myelinated primary afferents express NPY after peripheral nerve injury. NPY released from these injured large-diameter DRG neurons may act in a paracrine fashion to block the transmission of nociceptive information from the small- and medium-diameter DRG neurons that constitutively express NPY receptors. NPY receptors are therefore uniquely positioned to inhibit primary afferent nociceptors directly, especially after peripheral nerve injury.
Animals↗
Hepatic iron stores and plasma ferritin concentration in patients with sickle cell anemia and thalassemia major.
To examine the relationship between hepatic iron stores and plasma ferritin concentration in individuals treated with red cell transfusion and iron chelation therapy, 37 patients with sickle cell anemia and 74 patients with thalassemia major were studied. In each patient, hepatic iron stores were measured by an independently validated noninvasive magnetic method, and plasma ferritin was determined by immunoassay. The correlation between hepatic iron and plasma ferritin was significant both in patients with sickle cell anemia (R = 0.75, P < 0.0001) and in those with thalassemia major (R = 0.76, P < 0.0001). Regression analysis showed no significant difference between the two groups in the linear relationships between hepatic iron stores and plasma ferritin. Considering all 111 transfused patients as a group, the coefficient of correlation between hepatic iron stores and plasma ferritin was highly significant (R = 0.76, P < 0.0001). Regression analysis found that variation in body iron stores, as assessed by magnetic determinations of hepatic iron, accounted for only approximately 57% of the variation in plasma ferritin, suggesting that the remainder was the result of other factors, such as hemolysis, ineffective erythropoiesis, ascorbate deficiency, inflammation, and liver disease. The 95% prediction intervals for hepatic iron concentration, given the plasma ferritin, were so broad as to make a single determination of plasma ferritin an unreliable predictor of body iron stores. Variability resulting from factors other than iron status limits the clinical usefulness of the plasma ferritin concentration as a predictor of body iron stores.
Adolescent↗
Neuropeptide Y/peptide YY receptor binding sites in the heart: localization and pharmacological characterization.
[125I]Peptide YY was used to localize and characterize peptide YY and neuropeptide Y receptor binding sites in the heart. In the rat and rabbit heart, nearly every artery and arteriole that could be histologically identified also expressed saturable binding sites for [125I]peptide YY. In the arteries, these [125I]peptide YY binding sites were primarily associated with the smooth muscle layer. Pharmacological experiments demonstrated that peptide YY and neuropeptide Y were equipotent in competing for [125I]peptide YY binding in the heart. In another competition series, [Leu31,Pro34]-neuropeptide Y (a Y1 receptor-specific agonist when used with [125I]peptide YY) was significantly more potent than neuropeptide Y (a Y2 receptor-specific agonist when used with [125I]peptide YY) in competing for [125I]peptide YY binding from coronary arteries, suggesting that the receptor binding sites on cardiac arteries and arterioles are of the Y1 subtype. These results demonstrate that smooth muscle cells of the atrial and ventricular arteries and arterioles in rat and rabbit heart express Y1 receptors and suggest a possible direct effect of neuropeptide Y on coronary blood vessels to induce vasoconstriction.
Animals↗
Aluminum, iron, and zinc ions promote aggregation of physiological concentrations of beta-amyloid peptide.
A major pathological feature of Alzheimer's disease (AD) is the presence of a high density of amyloid plaques in the brain tissue of patients. The plaques are predominantly composed of human beta-amyloid peptide beta A4, a 40-mer whose neurotoxicity is related to its aggregation. Certain metals have been proposed as risk factors for AD, but the mechanism by which the metals may exert their effects is unclear. Radioiodinated human beta A4 has been used to assess the effects of various metals on the aggregation of the peptide in dilute solution (10(-10) M). In physiological buffers, 10(-3) M calcium, cobalt, copper, manganese, magnesium, sodium, or potassium had no effect on the rate of beta A4 aggregation. In sharp contrast, aluminum, iron, and zinc under the same conditions strongly promoted aggregation (rate enhancement of 100-1,000-fold). The aggregation of beta A4 induced by aluminum and iron is distinguishable from that induced by zinc in terms of rate, extent, pH and temperature dependence. These results suggest that high concentrations of certain metals may play a role in the pathogenesis of AD by promoting aggregation of beta A4.
Aluminum↗
Intraepithelial mast cells in allergic and nonallergic asthma. Assessment using bronchial brushings.
Mast cell mediators are known to contribute to the pathogenesis of asthma. There is some disagreement concerning the numbers of mast cells in asthmatic mucosa. In this study a standardized bronchial brush technique was developed and used to assess intraepithelial mast cells and other inflammatory cells in allergic and nonallergic asthmatic and nonasthmatic subjects. A total of 10 nonasthmatic (5 allergic) and 13 asthmatic (8 allergic) subjects with stable controlled asthma treated with beta-agonist only were assessed by history, spirometry, allergy prick tests, and methacholine airway responsiveness. During fiberoptic bronchoscopy, bronchoalveolar lavage (BAL) was performed from the middle lobe and standardized bronchial brushings were taken from the lingula and left lower lobe bronchi. Quantitative cell counts were performed blind to the clinical characteristics of the subjects. The average total cell recovery from the brushings was 1.04 (SEM 0.09) x 10(6) ml, with a cell viability of 64% (5.3%). Reproducible total cell and mast cell counts were obtained from brushings taken from two lobar bronchi (ICC 0.86). Mast cells were significantly elevated in asthmatic compared with nonasthmatic subjects (1.5 +/- 0.34 versus 0.15 +/- 0.06%). Allergic asthmatic subjects had the greatest numbers of mast cells (1.86 +/- 0.48%); however, the numbers present in brushings from nonallergic asthmatic subjects were also increased (1.03 +/- 0.45%). The mast cells had the staining characteristics of mucosal mast cells, with formalin-blockable metachromatic staining and positive staining for tryptase. Both asthmatic groups also had elevated BAL eosinophils, and neutrophils were elevated in nonallergic asthmatic subjects.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Reversible in vitro growth of Alzheimer disease beta-amyloid plaques by deposition of labeled amyloid peptide.
The salient pathological feature of Alzheimer disease (AD) is the presence of a high density of amyloid plaques in the brain tissue of victims. The plaques are predominantly composed of human beta-amyloid peptide (beta A4), a 40-mer whose neurotoxicity is related to its aggregation. Radioiodinated human beta A4 is rapidly deposited in vitro from a dilute (less than 10 pM) solution onto neuritic and diffuse plaques and cerebrovascular amyloid in AD brain tissue, whereas no deposition is detectable in tissue without performed plaques. This growth of plaques by deposition of radiolabeled beta A4 to plaques is reversible, with a dissociation half-time of approximately 1 h. The fraction of grey matter occupied by plaques that bind radiolabeled beta A4 in vitro is dramatically larger in AD cortex (23 +/- 11%) than in age-matched normal controls (less than 2%). In contrast to the human peptide, rat/mouse beta A4 (differing at three positions from human beta A4) does not affect the deposition of radiolabeled human beta A4. beta A4 has no detectable interaction with tachykinin receptors in rat or human brain. The use of radioiodinated beta A4 provides an in vitro system for the quantitative evaluation of agents or conditions that may inhibit or enhance the growth or dissolution of AD plaques. This reagent also provides an extremely sensitive method for visualizing various types of amyloid deposits and a means for characterizing and locating sites of amyloid peptide binding to cells and tissues.
Aged↗
Membrane cofactor protein (CD46) protects cells from complement-mediated attack by an intrinsic mechanism.
The cleavage of C3 is a critical step for complement (C) activation in the classical and alternative pathways. This reaction is controlled by the regulators of C activation protein family. Membrane cofactor protein (MCP) is a cofactor for the factor I-mediated inactivation of C3b and C4b. As a widely distributed membrane protein, MCP may protect host cells from inadvertent C activation. Human MCP has recently been shown to protect transfected rodent cells from human C-mediated lysis. In this report the relationship of MCP expression to C3b deposition and cytoprotection was examined using NIH/3T3 cells transfected with human MCP and exposed to human serum as a source of C and naturally occurring anti-mouse antibody. MCP inhibited C3b deposition in a dose-dependent fashion and inhibited lysis of the mouse cells expressing it. MCP did not inhibit lysis on bystander cells. These results demonstrate the protective role of MCP, at the cellular level, by an intrinsic mechanism.
3T3 Cells↗
Receptor binding sites for cholecystokinin, galanin, somatostatin, substance P and vasoactive intestinal polypeptide in sympathetic ganglia.
Sympathetic ganglia are innervated by neuropeptide-containing fibers originating from pre- and postganglionic sympathetic neurons, dorsal root ganglion neurons, and in some cases, myenteric neurons. In the present report receptor autoradiography was used to determine whether sympathetic ganglia express receptor binding sites for several of these neuropeptides including bombesin, calcitonin gene-related peptide-alpha, cholecystokinin, galanin, neurokinin A, somatostatin, substance P, and vasoactive intestinal polypeptide. The sympathetic ganglia examined included the rat and rabbit superior cervical ganglia and the rabbit superior mesenteric ganglion. High levels of receptor binding sites for cholecystokinin, galanin, somatostatin, substance P, and vasoactive intestinal polypeptide were observed in all sympathetic ganglia examined, although only discrete neuronal populations within each ganglion appeared to express receptor binding sites for any particular neuropeptide. These data suggest that discrete populations of postganglionic sympathetic neurons may be regulated by neuropeptides released from pre- and postganglionic sympathetic neurons, dorsal root ganglion neurons, and myenteric neurons.
Animals↗