Neutral-pion photoproduction on protons near threshold.
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Biomedical subjects
Publications and source records attributed to R Davidson.
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The effects of flexion and extension exercises on lumbar discs and low-back pain are controversial. Our goals were to develop a technique and program for digitizing and analyzing discograms and to study the motion of intradiscal dye in response to flexion and extension. Thirty-five patients following awake discography were evaluated with lateral radiographs obtained in an extension position and a flexion position. Fifty-three segments with normal morphology and 47 segments with abnormal morphology were studied. Discograms with normal morphology showed numerically significant change in position with a more anterior position occurring during extension. Changes in the position of intradiscal dye in discs with abnormal morphology were less predictable. Digitizing was an advantageous technique.
Four patients with acquired immunodeficiency syndrome (AIDS) (CDC group IV) were investigated for biliary disease because of the presence of both severe upper abdominal pain and raised levels of serum alkaline phosphatase. None was clinically jaundiced. Upper abdominal ultrasound was abnormal in three. All had endoscopic retrograde cholangiographic evidence of both an intrahepatic sclerosing cholangitis suggestive of primary sclerosing cholangitis and an irregular suprapapillary common bile duct dilation suggestive of papillary stenosis. Three had evidence of gastrointestinal cryptosporidiosis and two of disseminated cytomegalovirus infection. Endoscopic sphincterotomy, performed in two patients, gave good pain relief. We propose the name 'AIDS sclerosing cholangitis' for this form of secondary cholangitis. The cause of this disorder remains unclear. Recent evidence is discussed which suggests that it is not due to HIV itself but to an opportunistic infection. Cryptosporidium appears to be the most likely candidate.
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1. The withdrawal of tricyclic antidepressants (TCAs) produces symptoms suggesting cholinergic rebound. 2. Amitriptyline (AMI), the most potent antimuscarinic agent among this class of drugs, produces supersensitivity to the muscarinic agonist, oxotremorine. 3. Enhancement of the sensitivity of cholinoceptive neurons to acetylcholine as a consequence of treatment with TCAs would account for many of the symptoms following the withdrawal of these drugs. 4. Desipramine (DMI) is the least potent antimuscarinic compound among the TCAs, yet its withdrawal produces withdrawal symptoms. 5. Recently, it was reported that amoxapine (AMX) weakly binds to muscarinic acetylcholine receptors (mAchR) in vitro. This may indicate that this drug lacks the effects antimuscarinic effects in vivo, and that it will not supersensitize cholinergic networks. 6. A thermoregulation paradigm was used to assess the sensitivity of a central muscarinic mechanism to oxotremorine before and after treatment with DMI and AMX. Treatment with either drug increased the hypothermic response to this agonist. 7. Mechanisms whereby drugs can produce cholinergic system supersensitivity, and the use of thermoregulation paradigms in assessing the properties of therapeutic agents is discussed.
The development of the alcohol dependence syndrome and its inclusion in the International Classification of Diseases in January 1979 led to a demand for brief, easy-to-administer screening questionnaires explicitly based on the syndrome. The present review considers some of the conceptual, methodological and psychometric problems faced by the authors of such questionnaires. The five major self-report scales which have been published since 1979 are critically appraised and the usefulness of each scale for different populations and contexts is noted.
Of 98 patients studied prospectively during admission to the psychiatric ward of a general hospital, 13% showed an initial transient elevation of the serum thyroxine (T4) level (range 142-174 nmol/l) with the incidence increasing to 15% on serial testing at days five and fourteen. There was no clinical evidence of a thyrometabolic disorder and, as the mild hyperthyroxinaemia normalised rapidly, recourse to other thyroid function tests was not required. The possible causes of the transient hyperthyroxinaemia are discussed, but examination of the hyperthyroxinaemic patients' diagnoses did not reveal anything in common. These data indicate that the results of routine thyroid function tests in acute psychiatric admissions should be interpreted with care, and that historical and physical examination remains the primary avenue of diagnosis of thyroid disorders.
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An increase in the number of cases of gram-negative ventriculomeningitis in patients followed with intracranial pressure monitors when compared with patients with craniotomy alone was revealed by routine surveillance data. A study was undertaken at four area institutions to describe the infections, risk factors, and management. Two hundred fifty-five patients with diagnoses of intracerebral hemorrhage (n = 86), closed trauma (n = 66), open trauma (n = 21), tumor (n = 66), and miscellaneous other conditions were compared with their nonmonitored counterparts for type of intracranial pressure monitor used, use of drains, prophylactic antibiotics, and steroids, and remote presence of infection. The presence of intracranial pressure monitor with craniotomy was associated with an 11 percent infection rate whereas craniotomy alone demonstrated a 6 percent rate. Of the intracranial pressure monitors used, the subarachnoid screw was associated with the lowest infection rate (7.5 percent) followed by the subdural cup catheter (14.9 percent) and the ventriculostomy catheter (21.9 percent). Regardless of the monitor used, infection was twice as likely to develop in patients with open trauma or hemorrhage. The use of bacitracin flush solutions for maintenance of lumen patency was more often associated with infections. Use of prophylactic antibiotics did not significantly influence outcome.
Although a linear relationship between age and utterance length during the preschool years has been reported, that result was only partially replicated from age 2 to 5 years in two new research samples, one cross-sectional and the other longitudinal in design. Instead, a deceleration in age curves, particularly beyond about 36 months, was observed in each sample. Some explanations and implications of the findings are discussed from normative and developmental viewpoints.
One hundred forty-two patients were treated by the Scolitron method of lateral electric surface stimulation (LESS) for scoliosis. Using 10 degrees progression as a failure point, clinicians reported the following: 56.3% of patients were classified as failures, 26.8% as successes; and 16.9% were still under treatment. When broken down into individual groups, true protocol patients, at risk for progression, had the lowest success rate; whereas those that were nonprotocol, and least at risk, had the highest success rate. This method should still be considered experimental and cannot be considered an alternative to bracing at this time.
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The noradrenaline and dopamine depletion induced by 6-hydroxydopamine (6-OHDA) and pargyline plus 6-OHDA was investigated in the heart, mesenteric, renal, splenic and femoral arteries and saphenous vein of the dog. Catecholamine concentrations in plasma were also analyzed in these two experimental conditions. 6-OHDA and pargyline plus 6-OHDA induced a parallel decrease of the noradrenaline and dopamine content in the main trunk of the mesenteric artery, femoral artery and heart. In the proximal branches of the mesenteric artery, renal and splenic arteries 6-OHDA selectively reduced noradrenaline (by 50%) without changes in dopamine levels. Previous treatment with pargyline abolished this selectivity and depleted the tissue levels of both noradrenaline and dopamine by 75%. The noradrenaline and dopamine levels in the saphenous vein were not significantly reduced by 6-OHDA (15%) and pargyline plus 6-OHDA (40%). 6-OHDA and pargyline plus 6-OHDA increased both noradrenaline and adrenaline concentrations in plasma, without significant changes in dopamine concentrations. The present findings suggest: an independent dopamine presence in the proximal branches of the mesenteric artery, renal artery and splenic artery; that noradrenaline and dopamine are in one and the same structure in the heart, femoral artery and the main trunk of the mesenteric artery; the saphenous vein is more resistant to chemical sympathectomy than arterial blood vessels; the changes in plasma catecholamine concentrations are probably related to a compensatory mechanism initiated at the adrenal medulla.
Dog saphenous vein strips were incubated with 1.4 mumol/l 3H-(--)-noradrenaline for 60 min, after inhibition of the noradrenaline-metabolizing enzymes and of extra-neuronal uptake. At the end of the incubation period the strips were perifused for 150 min; cocaine (10 mumol/l) was added to the perifusion fluid from t = 75 min onwards. In some experiments either phentolamine (10 mumol/l) or clonidine (0.1 mumol/l) was also added at this time. Some strips were subjected to electrical stimulation from t = 100 to 150 min of perifusion (t = 0 being the start of perifusion), with frequencies ranging from 0.5 to 13.5 Hz. A compartmental analysis of spontaneous or electrically-induced efflux of 3H-noradrenaline was made. The spontaneous efflux had a long half time (t/2 = 124 min) and most of the 3H-noradrenaline which had accumulated in the strips did not participate in the efflux ("bound fraction", representing 90% of tissue activity at t = 100 min of perifusion). Neither phentolamine nor clonidine modified the half time or the "bound fraction" observed for spontaneous efflux. Electrical stimulation (greater than 0.5 Hz) mobilized only one compartment of noradrenaline, which represented about 50% of the noradrenaline accumulated in the strips. The half time of 3H-efflux induced by electrical stimulation decreased when the frequency increased from 0.5 Hz up to 13.5 Hz. Phentolamine increased the rate of efflux for all frequencies of stimulation and decreased the half time of efflux. However, the releasable pool of noradrenaline was only increased by phentolamine at 0.5 Hz, but not at higher frequencies.(ABSTRACT TRUNCATED AT 250 WORDS)
In an attempt to determine the incidence of alloimmune neonatal neutropenia, a systematic study was initiated during a period of six months. Complete blood count, differential and absolute neutrophil count of all the newborns were determined to identify the newborns with neutropenia and those with persistent neutropenia were evaluated for the presence of maternal neutrophil antibodies. This resulted in the design and use of a computerized system which was successfully employed to identify several neonates born with this disorder. The system includes a main program and eight functional options, and is operated under a secret authority code so that patients' data are accessible only to the investigators. The major functional options are: create, display, update and delete a record for the newborn; display most recent neutropenic babies; search all records and display name and ID number; search all records for a given year and display data; and perform statistics. The statistical analysis includes the total number of babies, both normal and those with neutropenia, the total number of babies with neutropenia and with/without sepsis, and those with persistent neutropenia. Also included are the hematological data consisting of complete blood count and differential of all of the newborns. Several possibilities exist to expand and extend the program for additional research-related purposes.
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Globin gene mapping of DNA from families with (A gamma delta beta) thalassaemia has revealed a previously unreported gene deletion responsible for this condition. The deletion removes the A gamma, delta and beta genes and while its 5' end is in a similar position to that described in a previous deletion of this type, the 3' ends of the two deletions are quite different. In addition we have observed further examples of two other previously described deletions which result in this disorder. Phenotypic comparisons of families with (A gamma delta beta) thalassaemia, in which the molecular basis has been defined, show a remarkable similarity among the four different deletion defects, with important implications with regard to the mechanism by which deletions allow the continued expression of gamma genes.