Search PubMed⌕ Search

Biomedical subjects

C Bell

Publications and source records attributed to C Bell.

At least 253 records · Page 14Linked to original sources
PubMed1982

The effect of lifting the lids on corneal astigmatism.

Corneal toricity was measured using a keratometer with the lids in the normal position, and with the lids retracted. Lid retraction usually changed the measured toricity. In corneas with more than 1.00 D of with-the-rule astigmatism, the change was in the direction of less with-the-rule astigmatism. In corneas with astigmatism between 1 D with-the-rule and 1 D against-the-rule, the change was not systematic. The results compare with the original experiment of Masci (1965), who also found that corneas with more with-the-rule toricity show a greater reduction in toricity when the lids are retracted. Clearly the pressure the lids exert on the eyeball is a major factor influencing astigmatism.

Adolescent↗
PubMed1982

V and C genes in creating antibodies directed to alpha (1 replaced by 3)-linked D-glucosyls in dextran. III. Frequency of alpha (1 replaced by 3)-responsive, primary B precursors in a1 high- and b low-receptor allogroups.

An evaluation was made of the frequency of alpha (1 replaced by 3)-responsive, primary B precursors and their reactivity profiles in Igh-1al (al) and Igh-1b (beta) allogroup mice, of dissimilar responsiveness as to quantity of the specific serum antibody produced, its light chain isotype, and its variable-region, ligand-modifiable antigenicity, to alpha (1 replaced by 3) glucosyls in dextran B-1355. al mice, exhibited highly alpha 1-specific serum antibody, with relatedness to the idiotypes (Id) shared by three BALB/c, alpha (1 replaced by 3)-specific, gamma 1 myeloma proteins, possess specific primary splenic B precursors at a frequency of 1/5.5-7.3 x 10(4) cells; beta mice, exhibiting low, k serum, Id- antibody, possess B splenic-specific primary precursors at a frequency of 1/1.0-1.4 x 10(5) cells. A radioimmunoassay analysis showed correlations between the isotype profiles of the serum antibody response and of the primary precursors, namely mu gamma 1 in the al and mu kappa in the beta allogroups, but also delineated minor primary mu gamma lambda 1 and mu kappa precursors in al and mu gamma kappa and mu gamma 1 in b, at frequencies of 1/3 x 10(5) to 1/6.5 x 10(6). The al, gamma 1 precursors exhibited defined reactivity patterns for 3-mono-O-3,6-di-O-glucosyls and non-reducing end groups in the B-1355. The beta, kappa precursors recognized the sequential residues.

Animals↗
PubMed1982

Benztropine-induced prolongation of responses to vasodilator nerve stimulation in the canine paw pad.

After blockade of noradrenergic transmission with guanethidine in anaesthetized dogs, stimulation of the peripheral end of the cut tibial nerve (1 Hz, 10 pulses) produces a vasodilator response which is localized to the circulation of the paw pads. The time course of the response is considerably prolonged after systemic administration of the dopamine-uptake blocking drug, benztropine (1 mg/kg). This effect is not due to inhibition of Uptake 1, as benztropine, unlike desmethylimipramine, does not prolong responses to noradrenergic vasoconstrictor nerve stimulation. The results support previous evidence suggesting that the dilator response to tibial nerve stimulation involves neural release of dopamine.

Animals↗
PubMed1981

Effect of colestipol and clofibrate, singly and in combination, on plasma lipid and lipoproteins in type IIb hyperlipoproteinemia.

The effect of colestipol, clofibrate and a combination of these two drugs on plasma lipid and lipoprotein levels was evaluated in 14 adult male patients with Type IIb hyperlipoproteinemia. A crossover design with each patient receiving all three treatments was utilized. Twenty g of colestipol per day reduced total and LDL cholesterol by 39.1 and 51.5 mg/dl, respectively (p less than 0.001). There was an associated rise in total triglycerides of 63.5 mg/dl (p less than 0.01) with no significant change in HDL cholesterol. Clofibrate, 2.0 g per day, did not significantly lower either total (-7.9 mg/dl) or LDL cholesterol (+8.7 mg/dl). There was marked interpatient variability in terms of the LDL cholesterol response to clofibrate, but the majority of patients demonstrated an increase. HDL cholesterol levels increased by 6.7 mg/dl (p less than 0.01) and total triglycerides were reduced by 94.6 mg/dl (p less than 0.001). Utilizing the same dosages of both drugs, the combination of colestipol and clofibrate were less effective in lowering total and LDL cholesterol than colestipol therapy alone, and increases in HDL cholesterol and decreases in triglycerides similar to those obtained with clofibrate were observed.

Adult↗
PubMed1981

Dopamine and noradrenaline levels in peripheral tissues of several mammalian species.

Tissue levels of dopamine (DA) and noradrenaline (NA) have been compared in atrium, spleen, mesenteric artery, vas deferens and renal cortex of sexually mature rats, guinea-pigs, ferrets, rabbits and cats. The results suggest the presence of dopaminergic autonomic axons in the cat renal cortex, as has been previously reported for the dog. Such nerves are probably sparse or absent in the kidneys of the other species examined.

Animals↗
PubMed1981

Patient education in the hospital setting.

S.G. Rosenberg outlines three types of problems which occur in the care of the chronically ill. The first of these is clinical failure which occurs with an unavoidable exacerbation of the illness. Second is medical failure which occurs when technology cannot provide a cure. And third is an education failure when the patient will not follow the prescribed regime. This can result from either a choice made by the patient or family not to comply, or from a lack of knowledge on the part of the patient, or the lack of a planned education approach as part of the patient's care. Compliance is often suggested as the outcome to be measured as the result of any educational effort. This is valid, in part, but there are other outcomes equally important. These include the independence achieved through knowledge, and the assumption of responsibility for self-care. It is one thing to present information, and quite another to have the patient and family demonstrate acceptance and make changes in general lifestyle and daily routines. The responsibility for the treatment regime and change in behavior ultimately rests with the patient and family. The health professional is responsible for providing support and ensuring access to the tools (information, skills, and attitudes) which the patient and family require. Patient education is vital. An acute care setting provides numerous opportunities to initiate and continue the education process for both inpatients and outpatients.

Communication↗
PubMed1980

Effect of probucol on plasma lipids and lipoproteins in type IIb hyperlipoproteinemia.

Probucol was administered for 4 months in 20 adult males with Type IIb HLP in a total daily dose of 1.0 g per day. All patients had achieved a stable weight and diet response prior to entering the study. Plasma lipid and lipoprotein determinations were done at monthly intervals. Probucol produced mean reductions to TPC of -38.8 mg/dl (P < 0.0001), in LDL of -26.7 mg/dl (P < 0.001) and HDL of -8.1 mg/dl (P < 0.0001) for the entire treatment period. The mean LDL/HDL ratio increased from 5.43 to 6.08 (P < 0.02). There was no significant change in TG levels. During the study a progressive decrease in mean HDL levels from 38.9 to 29.2 mg/dl was noted. A progressive increase in the LDL/HDL ratio from 5.43 to 6.35 was also observed. These findings suggest that probucol should be used cautiously in patients with Type IIb HLP, because an inverse relationship between HDL levels and IHD incidence has been demonstrated in epidemiologic studies.

Adult↗
PubMed1980

Effects of dopamine on adrenergic neuromuscular transmission in the guinea-pig vas deferens.

1 In the isolated vas deferens of the guinea-pig, contractile responses to adrenergic nerve stimulation at 2 Hz were depressed by exogenous dopamine (5 microM) and this effect was abolished in the presence of phentolamine (0.3 microM), suggesting that it was due to an agonist action of dopamine on alpha-adrenotors. 2 The depression by dopamine (5 microM) of contractile responses to nerve stimulation was correlated with reduction in amplitude of single excitatory junction potentials (e.j.ps) evoked by nerve stimulation, but not with depression of spontaneous junction potentials. 3 By contrast, during repetitive nerve stimulation at 1 Hz the depressant effect of dopamine on e.j.p. amplitude became less pronounced, due to the amount of facilitation being greater than that occurring under control conditions in the same cell. 4 The alpha-adrenoceptor antagonist, phentolamine (10 microM), also increased the amount of facilitation during repetitive nerve stimulation. 5 In the presence of phentolamine (10 microM), the depressant effect of dopamine (5 microM) on single e.j.ps was abolished but its enhancing effect on facilitation was not reduced. 6 It is suggested that the enhancement of facilitation during repetitive stimulation by both dopamine and phentolamine is independent of their actions on presynaptic alpha-adrenoceptors.

Animals↗
PubMed1979

Regulation of tumor growth and antibody clone expression by antigen and anti-idiotype antibody ligands with specificity for receptor-binding sites.

Dextran ligands, modified to increase epitope reactivity with receptors, were more effective in suppressing BALB/c mouse plasmacytomas MOPC 104 E and J-558, which bind alpha (1 leads to 3) dextran and have an idiotype (Id) in the common, than autoantibody (Ab) against the Id unique to each of the proteins secreted by the two tumors (the (IdI). BALC/c immunized with 104 E myeloma protein and expressing an antibody response to the 104 E IdI exhibited a specific, anti-104 E IdI transplantation resistance to lethal grafts of 104 E, but not J-558, tumors notwithstanding the shared common Id and similar ability to bind alpha(1 leads to 3) dextran. This autoantibody did not prevent modulation of the 104 E tumor to variant forms or the growth of the variants. On challenge with alpha (1 leads to 3) dextran, the immunized mice expressing the anti-104 C IdI responses failed to express the 104 D IdI-like antibody clone present in the normal, anti-alpha (1 leads to 3) dextran antibody repertoire. Passive, iso-anti-104 E IdI antibody had a transitory suppressive effect on the normal, 104 E IdI-like antibody clone but failed to circumvent 104 E tumor growth. It is apparent that the greater effectiveness of ligands strongly reactive in a nonphysiological manner with the tumor receptors lies in the stabilization of the tumor load without inducing variant escape or a disturbance of the immune network, and that receptor expression and malignancy state are not necessarily co-extensive functions.

Animals↗
PubMed1979

Dependence of deoxycorticosterone/salt hypertension in the rat on the activity of adrenergic cardiac nerves.

1. Chronic hypertension was induced in Wistar rats with intact kidneys by subcutaneous implantation of 50 mg of deoxycorticosterone acetate (DOCA) in wax and addition of sodium chloride (9 g/l) to the drinking water. 2. The development of DOCA/salt hypertension, as monitored by tail-cuff plethysmography, was prevented by: (a) destruction of the peripheral adrenergic nerves with neonatal administration of guanethidine (80 mg/kg subcutaneously for the first 14 days postnatally); (b) bilateral stellate ganglionectomy; (c) oral administration of the beta-adrenoreceptor antagonists propranolol or atenolol (1 mg day-1 kg-1) during the period of DOCA/salt treatment. 3. The dose of DOCA used was sufficient to inhibit the atrial Uptake2 pathway completely: this process appears to participate in termination of action of neurally released noradrenaline in the heart. 4. It is suggested that this model of DOCA/salt hypertension is due to adrenergic enhancement of cardiac output in the presence of an increased sodium load. The enhancement may be partly due to deficient myocardial inactivation of noradrenaline.

Adrenergic Fibers↗
PubMed1979

V and C gene contribution in creating anti-alpha-1,3 dextran antibodies in mice. I. Characteristics of Ig-lal prototype responses.

The light (L) and heavy (H) chain and the antigenic, idiotypic (Id) composition of the antibody (Ab) plaque-forming cells (PFC) and serum Ab specific for alpha-1,3 dextran have been characterized in Ig-lal BALB/c prototype mice, in Ig-la- [30] mice, and in BALB/c congenic and recombinant strains. Four distinct Ab Id specificities were identified by using criteria of Id relatedness to three Id-distinct, alpha-1,3 dextran-binding BALB/c myeloma proteins (MP), all associated, in the Ig-lal mice with the lambda (lambda) chains: a major, common IdX in 40--90% of the molecules; three minor, individual IdI in 1--49% of the molecules; and a fifth, Id-undefined one. These specificities were expressed at the PFC and serum level in the mu and gamma isotypes. A minor, kappa (kappa), Id-negative Ab was discerned only at the PFC level. The Ig-la- CBA and C3H mice responded with anti-alpha-1,3 dextran, kappa Id-negative Ab. The BALB/c, congenic strain CB20 (BALB/c Ig-lb, carrying the C57Bl/Ka, Ig-lb variable H (VH) gene complement and CH phenotype, made anti-alpha-1,3 dextran kappaId-negative Ab of the Ig-lb prototype. The recombinant BAB/14, carrying in the C57Bl/Ka CH-Ig-lb phenotype the BALB/c Ig-lal VH gene(s) controlling anti-alpha-1,3 dextran lambda Ab responsiveness and Id specificity (VH-DEX+), express the BALB/c lambdaId repertoire.

Animals↗
PubMed1979

V and C gene contribution in creating anti-alpha-1,3 dextran antibodies in mice. II. Characteristics of Ig-lb to e prototype responses.

The light (L) and heavy (H) chain and the idiotypic (Id) composition of the antibody (Ab) plaque-forming cells (PFC) and serum Ab specific for alpha-1,3 dextran have been characterized in murine strains exhibiting the CH-Ig-lb to e allotypes and in their F1 hybrids with Ig-la1, BALB/c prototypes. The Ab response of the Ig-lb to e mice to the alpha-1,3 dextran was low in the kappa (kappa) L chain class with only a minor, sporadic Ab in the lambda (lambda) L chain class discernible after prolonged immunization. Two of a total of sixty-eight C57Bl/6 Ig-lb mice, in a total of 318 Ig-lb to e mice tested, exhibited, in late responses, a significantly elevated Ab in the lambda L class at both serum and PFC levels, equalling at the PFC level the total non-specific lambda PFC values. An Id analysis showed this lambda Ab and the kappa Ab to lack the Id relatedness to the three BALB/c alpha-1,3 dextran-binding myeloma proteins (MP) Ab prototypes, J-558, 104 E, and UPC-102, exhibited by the lambda Id+ Ab of the Ig-la1 BALB/c prototypes and their F1 hybrids with the Ig-lb to e prototypes. Furthermore, affinity differences could be detected by alpha-1,3 nigerodextrans, PFC inhibition analysis, between the late C57Bl/6 anti-alpha-1,3 dextran lambda Id--Ab PFC and the lambda Id+ Ab PFC of the BALB/c and their F1 progeny.

Animals↗
PubMed1979

Evidence for dopaminergic vasodilator innervation of the canine paw pad.

1 In chloralose-anaesthetized dogs pretreated with guanethidine and pancuronium, electrical stimulation (0.2 to 5 Hz) of the peripheral end of the cut tibial nerve caused a frequency-dependent increase in femoral blood flow which was restricted to the paw pads. 2 This neurogenic vasodilatation was not attenuated by atropine, mepyramine plus burimamide, indomethacin or propranolol. It was, however, attenuated in a dose-dependent manner by intra-arterial administration of the dopamine receptor antagonist, ergometrine (0.05 to 0.5 mg). 3 The effect of ergometrine could not be explained by non-specific effects on axonal conduction or transmission or by vasospasm of the blood vessels of the paw-pads. 4 In dogs with intact tibial nerves, a pharmacologically similar dilator response localized to the paw-pads could be elicited by electrical stimulation of loci in the ipsilateral diencephalon and midbrain. This response was not due to inhibition of adrenergic vasomotor tone and was abolished by systemic ganglion blockade or by tibial nerve section as well as by femoral arterial administration of ergometrine. 5 It is suggested that the vasculature of the canine paw pads is innervated by a population of autonomic axons which utilize dopamine or a related substance as a transmitter substance and activation of which causes vasodilation.

Animals↗