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PubMed2000

The size of occlusal rest seats prepared for removable partial dentures.

OBJECTIVE: The aim of this study was to test whether rest seats cut by a group of general dental practitioners for a removable partial denture differed in size and shape from those prepared by either a group of postgraduate students or their academic teachers. METHOD: The occlusal surfaces of a number of plastic teeth were scanned by a laser profilometer. Each tooth was then placed in a set of articulated phantom head dental arches. 30 dental practitioners, 16 postgraduates and 11 dental academics were asked to cut a rest seat preparation in the mesial marginal ridge suitable for the construction of a removable chromium cobalt partial denture. The tooth was removed from the models, rescanned, and this data converted to grey level images for measurement of the width, length and area of each rest seat. Depth was calculated as the difference between the pre and post preparation scanned profiles. RESULTS: There was a wide variation in the size of the individual rest seat preparations. There was no significant difference between the measured parameters from the images of the preparations made by academic staff and postgraduate students. The two sets of data were therefore combined. The length, width and area of the rest seats prepared by the staff and postgraduate group were significantly greater than those cut by the dental practitioner group. However, there was no significant difference in the depths measured. The outline form of the rests prepared by the dental practitioners was often round with sharply defined margins contrasting with the smooth triangular preparation the staff and postgraduates prepared. CONCLUSION: A 'refresher' in tooth modification for GDPs designing partial dentures would improve the long term success of the prosthesis.

Clinical Competence↗
PubMed1997

Response of normoxic pulmonary arteries of the rat in the resting and contracted state to NO synthase blockade.

1. The pulmonary vasculature is normally in a low resting state of tone. It has been hypothesized that this basal tone is actively maintained by the continuous release of a vasodilator in the resting state. However, evidence for basal release of nitric oxide (NO) is inconclusive. 2. We studied the release of NO in arteries from the pulmonary circulation of male Wistar-Kyoto rats by examining the effects of the L-arginine analogue NG-nitro-L-arginine methyl ester (L-NAME) on resting pulmonary arteries and on vessels pre-contracted with prostaglandin F2(alpha) (PGF2 alpha). 3. Rats (n = 21) were killed by an overdose with pentobarbitone. Pulmonary arteries were dissected (mean internal diameter 459 +/- 11 microns) and mounted in a small vessel wire myograph. Resting tensions were to set to stimulate transmural pressures of 17.5 mmHg. 4. L-NAME (100 microM) was found to produce a contraction of 0.64 +/- 0.09 mN mm-1 in resting pulmonary arteries when added alone to the myograph bath. This contraction was not produced following removal of the endothelium. Vessel contraction to PGF(2 alpha) (100 microM) was found to be significantly greater when carried out in the presence of L-NAME (100 microM) -1.37 +/- 0.15 mN mm-1 compared with 1.96 +/- 0.17 mN mm-1. Dilation following acetylcholine (ACh) (1 microM) was abolished in the presence of L-NAME (100 microM). 5. Rat pulmonary artery contraction in response to the addition of L-NAME and the absence of contraction upon removal of the endothelium provides supportive evidence of the active release of nitric oxide for the maintenance of resting tone.

Animals↗
PubMed1997

Resting membrane potential of skeletal muscle calculated from plasma and muscle electrolyte and water contents.

1. A method is described that enables the calculation of resting membrane potential from the electrolyte and water contents in blood plasma and in a sample of human muscle tissue obtained by the percutaneous needle-biopsy technique. In this calculation, the previously described equations for calculating resting membrane potential via the intra- and extra-cellular distribution of chloride were combined with the equation utilizing potassium distribution over the cell membrane. 2. The method of calculation was applied to 60 healthy subjects divided into three groups aged 19-40, 41-60 and 61-85 years. The calculated resting membrane potential in the subjects as a whole was -88.4 mV (SD 1.35; n = 60). A lower value was observed in the group aged 61-85 years (-87.7 mV, SD 1.0; n = 12) than in the group aged 19-40 years (-88.6 mV; SD 1.4; n = 32). No difference was observed between female and male subjects. 3. The RMP calculated with the present method in 60 healthy subjects was also compared with previously published values in healthy subjects, measured by the Clarke electrode method, and with values calculated from electrolyte and water distribution measured by isotope-dilution techniques. The results obtained in healthy subjects with different techniques were very similar. Data were analysed from earlier published studies in experimental animals in which resting membrane potential ranged from -91 to -65 mV. The resting membrane potential calculated from electrolytes in plasma and muscle showed a very good agreement with resting membrane potential recorded directly.

Adult↗
PubMed1999

Topical phenylephrine increases anal sphincter resting pressure.

BACKGROUND: Phenylephrine is an alpha1-adrenergic agonist which causes contraction of human internal anal sphincter muscle in vitro. Its intra-arterial administration in animals has been shown to increase resting sphincter pressure in vivo. In this study the effect of topical application of phenylephrine on resting anal pressure in healthy human volunteers was investigated. METHODS: Twelve healthy volunteers had measurements of maximum resting sphincter pressure (MRP) and anodermal blood flow taken before and after topical application of increasing concentrations of phenylephrine gel to the anus. To determine the duration of effect of the agent, readings were taken throughout the day after a single application. RESULTS: There was a dose-dependent rise in the resting anal sphincter pressure, with a small 8 per cent rise after 5 per cent phenylephrine (P = 0.012) and a larger 33 per cent rise with 10 per cent phenylephrine (mean(s.d.) MRP 85(12) cmH2O before versus 127(12) cmH2O after treatment, P < 0.0001). Thereafter no additional response was noted with higher concentrations of phenylephrine. The median duration of action of a single application of 10 per cent phenylephrine was 7 (range from 6 to more than 8) h. CONCLUSION: Topical application of 10 per cent phenylephrine gel to the anus produces a significant rise in the resting anal sphincter pressure in healthy human volunteers. This represents a potential novel therapeutic approach to the treatment of passive faecal incontinence associated with a low resting anal sphincter pressure.

Administration, Topical↗
PubMed1999

ACE inhibition with ramipril improves left ventricular function at rest and post exercise in patients with stable ischaemic heart disease and preserved left ventricular systolic function.

AIMS: To assess the effects of 6 months intervention with +ramipril on resting and post exercise left ventricular function in patients with stable ischaemic heart disease and preserved left ventricular systolic function. METHODS AND RESULTS: Patients (n=98, age 65+/-9 years, 37% women) were randomized to double-blind treatment with ramipril 5 mg. day(-1)(n=32), ramipril 1.25 mg. day(-1)(n=34), or placebo (n=32). Resting and post maximum exercise echocardiography/Doppler examinations were performed at baseline and after 6 months. Changes over 6 months in resting transmitral E-wave deceleration time (Edt) and Edt adjusted for heart rate (Edt/RR) differed between the ramipril 5 mg, ramipril 1.25 mg, and placebo groups: Edt 24+/-82, -1+/-69, and -29+/-64 ms, respectively, P=0. 012; Edt/RR 30+/-105, 2+/-61, and -28+/-69 ms, respectively, P=0.015. Changes in the difference between resting and post exercise Edt/RR also varied between groups: -53+/-137, -28+/-118, and 35+/-101 ms, respectively, P=0.029. No differences in E/A indices were noted. Resting atrioventricular plane displacement improved in the combined ramipril groups vs the placebo group: 0.2+/-0.8 vs -0.2+/-1.3 mm, P<0.05.Conclusion Six months ramipril treatment in patients with stable ischaemic heart disease and preserved left ventricular systolic function improved resting left ventricular function and reduced the exercise induced diastolic filling abnormalities usually seen in these patients.

Aged↗
PubMed1990

[Resting and exercise hemodynamics in essential arterial hypertension].

Various haemodynamic functions were studied in 70 patients (51 men and 19 women; mean age 53.0 +/- 7.0 years) with essential hypertension. The following parameters were measured, at rest and on exercise: systolic and diastolic blood pressure, heart rate, mean pulmonary artery pressure, cardiac output and peripheral vascular resistance. 15 normotensive subjects (11 men and four women; mean age 54.4 +/- 7.2 years) without significant cardiovascular disease served as controls. Resting peripheral vascular resistance (PAP) in the hypertensives was, at 1634.7 +/- 239.0 dyn/s.cm-5, higher by 41%, on exercise at 1029.4 +/- 105.9 higher by 14%, than in the controls (at rest 1157.1 +/- 118.9 dyn/s.cm-5, on exercise 706.9 +/- 94.1 dyn/s.cm-5; P less than 0.0001). Cardiac output at rest was 9.6% lower, on exercise 8.0% lower than in the controls (neither change significant). Thus the increased peripheral vascular resistance was the sole cause of the increased blood pressure. Mean PAP, as a measure of left-ventricular filling pressure, in hypertensives was 14.7 +/- 3.9 mm Hg at rest, 34.9 +/- 7.8 mm Hg on exercise, an increase of 14% and 40%, respectively, over the control values of 12.7 +/- 1.9 mm Hg at rest and 24.4 +/- 2.8 mm Hg on exercise (P less than 0.0001). The raised left-ventricular filling pressure is an indication of early hypertensive heart disease.

Blood Pressure↗
PubMed1982

[5-isosorbide mononitrate at rest and on exercise in coronary heart disease: acute and long-term effect].

Haemodynamic effects of 5-isosorbide mononitrate (5-ISMN) were studied at rest and on exercise in 31 patients with angiographically confirmed coronary heart disease. A decrease in arterial blood pressure and mean pulmonary artery pressure without significant change in heart rate, cardiac output and stroke volume occurred both at rest and on exercise after 20 mg of 5-ISMN to 12 patients. Administration of 50 mg 5-ISMN to 19 patients achieved greater decrease in mean pulmonary artery pressure; cardiac output and stroke volume were highly significantly reduced at rest, while on exercise both cardiac output and stroke volume remained unchanged. Ten patients, in whom after a single dose of 50 mg 5-ISMN the mean pulmonary artery pressure at rest and on exercise had decreased 28% and 45%, respectively, with a definite rise in exercise tolerance, repeat acute administration of a single dose of 50 kmg 5-ISMN produced a fall in mean pulmonary artery pressure at rest by 20% after 50 mg three times daily for four weeks. On exercise the fall was only 14% below the control levels before treatment. In addition, exercise tolerance was reduced. These results indicate that acute administration of 5-ISMN at rest and on exercise decreases cardiac work load. But on chronic administration of high doses, tolerance to the drug may develop.

Adult↗
PubMedDate not supplied

Consideration of perfusion reserve in viability assessment by myocardial Tl-201 rest-redistribution SPECT: a quantitative study with dual-isotope SPECT.

BACKGROUND: To optimize the use of thallium 201 rest-redistribution study in Tl-201/technetium 99m sestamibi dual-isotope single photon emission computed tomography (SPECT), the predictability of Tl-201 rest-redistribution for viable myocardium was examined according to the degree of perfusion reserve. METHODS AND RESULTS: Twenty patients with both unstable angina and left ventricular dysfunction were enrolled. Tl-201 rest-dipyridamole stress Tc-99m sestamibi gated SPECT/Tl-201 24-hour redistribution SPECT was performed before and 3 months after coronary artery bypass grafting. Through use of a 20-segment model, segmental stress perfusion, rest perfusion, and systolic thickening were quantified on gated SPECT by means of automatic quantitation software. Perfusion was expressed as the average percentage of maximal radioactivity uptake. To represent perfusion reserve, the perfusion difference score (PDS) was defined as rest perfusion minus stress perfusion. A low PDS indicated little or no inducible ischemia, and a high PDS indicated inducible ischemia. In dysfunctional myocardium, viability was defined by the improvement of thickening after coronary artery bypass grafting. The overall predictability of Tl-201 redistribution for viability was 0.709 of the area under the curve (AUC) in receiver operating characteristic analysis. With a cutoff of 7, predictability was significantly better in the low PDS group (AUC = 0.785) than in the high PDS group (AUC = 0.582). CONCLUSIONS: The predictability of Tl-201 rest-redistribution for viability differs according to perfusion reserve. It was more reliable for dysfunctional myocardium with persistent perfusion decrease. On the basis of the continuum hypothesis of chronic stunning and hibernation, we suggest that dysfunctional myocardium with persistent perfusion decrease should be assessed by Tl-201 redistribution SPECT.

Aged↗
PubMed2001

Mandibular rest position: a reliable position influenced by head support and body posture.

This prospective study was designed to establish how the positions of the molars and the condyles are related to incisor position in the mandibular rest position and how their positions are altered by changing head posture. Measurements of the mandibular rest position were taken on 24 men (age range, 23 to 35) with normal Class I occlusion, skeletal patterns, and temporomandibular joint function. The movements of 5 landmarks (lower incisor, and condyles and molars bilaterally) were tracked from maximum intercuspation into 4 independent rest positions (upright supported, upright unsupported, supine supported, and supine unsupported) using an optoelectric (Optotrak; Northern Digital, Waterloo, Ontario, Canada) computer system. The positions were based on minimal electromyographic and verbal instructions to swallow, lick the lips, and say "Mississippi." The results showed significant (P <.01) movements of the incisors, the molars, and the condyles into each of the 4 rest positions. Movements of the molars and the condyles into the supported upright posture and the unsupported upright posture differed slightly but significantly because of greater movement into the supported posture. Patterns of mandibular movement were entirely different between the upright and the supine rest positions; the mandible rotated anteriorly in the supine position and posteriorly in the upright position. We concluded that movement into the mandibular rest position from the intercuspal position is not a simple opening rotation of the mandible, and that the pattern of movement is influenced by head support and body postures.

Adult↗
PubMed2004

Roles of substrate availability and infection of resting and activated CD4+ T cells in transmission and acute simian immunodeficiency virus infection.

In studies of sexual mucosal transmission and early stages of simian immunodeficiency virus (SIV) and HIV infections, productive infection predominates in CD4(+) T cell populations, in both ostensibly resting and activated cells. The surprising ability of SIV and HIV to replicate in resting cells in vivo, in contrast to propagation of infection in vitro, suggested a model in which during the early stages of infection these viruses exploit the greater availability of resting cells to maintain unbroken chains of transmission from an infected resting cell to another resting cell nearby. Because immune activation in response to infection provides more activated CD4(+) T cells, these viruses take advantage of the greater efficiency of virus production and spread in activated cells for propagation and dissemination of infection. In this article, we report the results of experimental tests of this model, including visualization at the light microscopic level and direct analysis of virus production by cells in tissues. Analysis of tissues of rhesus macaques inoculated intravaginally or i.v. with SIV supports the proposed roles of target cell availability, susceptibility, and virus production by infected resting and activated CD4(+) T cells in mucosal transmission and early infection, and points to a potential role for topical anti-inflammatory agents in moderating the initial propagation of infection.

Acute Disease↗
PubMed2000

Examining the noncompetitive antagonist-binding site in the ion channel of the nicotinic acetylcholine receptor in the resting state.

3-Trifluoromethyl-3-(m-[(125)I]iodophenyl)diazirine ([(125)I]TID) has been shown to be a potent noncompetitive antagonist (NCA) of the nicotinic acetylcholine receptor (AChR). Amino acids that contribute to the binding site for [(125)I]TID in the ion channel have been identified in both the resting and desensitized state of the AChR (White, B.H., and Cohen, J.B. (1992) J. Biol. Chem. 267, 15770-15783). To characterize further the structure of the NCA-binding site in the resting state channel, we have employed structural analogs of TID. The TID analogs were assessed by the following: 1) their ability to inhibit [(125)I]TID photoincorporation into the resting state channel; 2) the pattern, agonist sensitivity, and NCA inhibition of [(125)I]TID analog photoincorporation into AChR subunits. The addition of a primary alcohol group to TID has no demonstrable effect on the interaction of the compound with the resting state channel. However, conversion of the alcohol function to acetate, isobutyl acetate (TIDBIBA), or to trimethyl acetate leads to rightward shifts in the concentration-response curves for inhibition of [(125)I]TID photoincorporation into the AChR channel and a progressive reduction in the agonist sensitivity of [(125)I]TID analog photoincorporation into AChR subunits. Inhibition of [(125)I]TID analog photoincorporation by NCAs (e.g. tetracaine) as well as identification of the sites of [(125)I]TIDBIBA photoincorporation in the deltaM2 segment indicate a common binding locus for each TID analog. We conclude that relatively small additions to TID progressively reduce its ability to interact with the NCA site in the resting state channel. A model of the NCA site and resting state channel is presented.

Animals↗
PubMed2005

Uncoupling the chemical steps of telomere resolution by ResT.

ResT is the telomere resolvase of the spirochete Borrelia burgdorferi, the causative agent of Lyme disease. ResT is an essential cellular function that processes replication intermediates to produce linear replicons terminated by covalently closed hairpin telomeres. ResT generates these hairpin telomeres in a reaction with mechanistic similarities to those catalyzed by type IB topoisomerases and tyrosine recombinases. We report here, that like most of the tyrosine recombinases, ResT requires interprotomer communication, likely in an in-line synapse, to activate reaction chemistry. Unlike the tyrosine recombinases, however, we infer that the cleavage and strand transfer reactions on the two sides of the replicated telomere occur nearly simultaneously. Nonetheless, the chemical steps of the forward and reverse reactions performed by ResT can occur in a non-concerted fashion (i.e. events on the two sides of the replicated telomere can occur independently). We propose that uncoupling of reaction completion on the two sides of the substrate is facilitated by an early commitment to hairpin formation that is imposed by the precleavage action of the hairpin binding module of the ResT active site.

Bacterial Proteins↗
PubMed2000

Effects of activity-rest schedules on physiological strain and spinal load in hospital-based porters.

Workers in physically demanding occupations require rest breaks to recover from physiological stress and biomechanical loading. Physiological stress can increase the risk of developing musculoskeletal disorders and repeated loading of the spine may increase the potential for incurring back pain. The aim of the study was to assess the impact of an altered activity-rest schedule on physiological and spinal loading in hospital-based porters. An existing 4-h activity-rest schedule was obtained from observations on eight male porters. This schedule formed the normal trial, which included two 5- and one 15-min breaks. An alternative 4-h schedule was proposed (experimental condition) that had two breaks each of 12.5 min. It was hypothesized that the experimental trial is more effective in promoting recovery from physiological strain and spinal shrinkage than the normal trial, due to the 5-min breaks being insufficient to allow physiological variables to return to resting levels or the intervertebral discs to reabsorb fluid. Ten males performed both test conditions and oxygen uptake VO2, heart rate, minute ventilation VE, perceived exertion and spinal shrinkage were recorded. There were no significant differences in any of the measured variables between the two trials (p > 0.05). Median heart rates were 78 (range 71-93) and 82 (71-90) beats.min(-1) for the normal trial and the experimental trial respectively, indicating that the activity was of low intensity. The light intensity was corroborated by the oxygen uptakes (0.75, range 0.65-0.94 1.min(-1)). Spinal shrinkage occurred to the same extent in the two trials (2.12 +/- 3.16 mm and 2.88 +/- 2.92 mm in the normal trial and the experimental trial respectively). Varying the length and positioning of the rest breaks did not significantly affect the physiological responses or magnitude of spinal shrinkage between the two trials. More physically demanding work than the porters' schedule should induce greater physiological fatigue and spinal shrinkage. The ratio between activity and rest breaks would then become more important.

Adult↗
PubMed1996

CD40 and B cell antigen receptor dual triggering of resting B lymphocytes turns on a partial germinal center phenotype.

Phenotypic alterations occur when resting human B lymphocytes become germinal center (GC) cells. These include the induction of surface CD38, CD95 (FAS/APO-1), and carboxy-peptidase-M (CPM), a recently described GC marker. However, the factors that govern the in vivo induction of these surface molecules on B cells remain unknown. Here, we purified resting (CD38-) human B lymphocytes from tonsils in an attempt to establish culture conditions resulting in the induction of these three GC markers. We show that interferon (IFN) alpha or IFN-gamma, as well as antibodies against the B cell antigen receptor (BCR), could induce CD38 on resting B lymphocytes, a phenomenon further enhanced by CD40 stimulation. Concomitantly, CD95 was upregulated by CD40 ligation and, to a lesser extent, by IFN-gamma. By contrast, CPM expression could be upregulated only through BCR triggering. This CPM induction was specifically enhanced by CD19 or CD40 ligation. CD40 + BCR stimulation of resting B cells with CD40 ligand-transfected fibroblastic cells in the presence of cross-linked anti-BCR monoclonal antibodies resulted in the coexpression of CD38, CD95, and CPM. As GC cells, these cells also expressed CD71, CD80 (B7.1), and CD86 (B7.2), but not CD24. However, CD10+ or CD44- B cells could not be detected in these culture conditions, suggesting that yet other signals are required for the induction of these GC markers. Consistent with a GC phenotype, CD40 + BCR-stimulated cells exhibited reduced viability when cultured for 20 h in the absence of stimulus. These results first demonstrate that cotriggering of resting B cells through BCR and CD40 induces both phenotypic and functional GC features. They also show that IFN and CD19 triggering of resting B cells specifically modulate the expression of GC markers.

ADP-ribosyl Cyclase↗
PubMed1997

Interleukin 4 (IL-4) or IL-7 prevents the death of resting T cells: stat6 is probably not required for the effect of IL-4.

Although much is known about the activation, proliferation, and function of CD4(+) T cells, little is known about how they survive as resting T cells in animals. Resting T cells have a half-life in animals of more than a week; however, when they are removed from animals and placed in tissue culture their half-life falls to approximately 24 h. In this paper, we show that the survival of resting T cells in vitro is promoted by two cytokines, interleukins 4 and 7 (IL-4, IL-7). They may do this in part by maintaining levels of survival-promoting proteins such as Bcl-2 in the cells, because the levels of Bcl-2 and Bcl-Xl in resting T cells fall rapidly after the cells are isolated from animals, and are maintained by culture in IL-4. Because the IL-4 receptor is known to signal through the JAK1 and JAK3/Stat6 pathway, we tested whether Stat6 was required for IL-4- dependent T cell survival. Surprisingly, we found that IL-4 rescued T cells from apoptosis in what appeared to be a Stat6-independent manner. These results demonstrate that the survival of resting T cells is an active process that can be affected by signals delivered by cytokines and also suggest that the IL-4 receptor on resting T cells may use a novel signaling pathway to facilitate T cell viability.

Animals↗
PubMed1995

Na+, K+, and Cl- transport in resting pancreatic acinar cells.

To understand the role of Na+, K+, and Cl- transporters in fluid and electrolyte secretion by pancreatic acinar cells, we studied the relationship between them in resting and stimulated cells. Measurements of [Cl-]i in resting cells showed that in HCO3(-)-buffered medium [Cl-]i and Cl- fluxes are dominated by the Cl-/HCO3- exchanger. In the absence of HCO3-, [Cl-]i is regulated by NaCl and NaK2Cl cotransport systems. Measurements of [Na+]i showed that the Na(+)-coupled Cl- transporters contributed to the regulation of [Na+]i, but the major Na+ influx pathway in resting pancreatic acinar cells is the Na+/H+ exchanger. 86Rb influx measurements revealed that > 95% of K+ influx is mediated by the Na+ pump and the NaK2Cl cotransporter. In resting cells, the two transporters appear to be coupled through [K+]i in that inhibition of either transporter had small effect on 86Rb uptake, but inhibition of both transporters largely prevented 86Rb uptake. Another form of coupling occurs between the Na+ influx transporters and the Na+ pump. Thus, inhibition of NaK2Cl cotransport increased Na+ influx by the Na+/H+ exchanger to fuel the Na+ pump. Similarly, inhibition of Na+/H+ exchange increased the activity of the NaK2Cl cotransporter. The combined measurements of [Na+]i and 86Rb influx indicate that the Na+/H+ exchanger contributes twice more than the NaK2Cl cotransporter and three times more than the NaCl cotransporter and a tetraethylammonium-sensitive channel to Na+ influx in resting cells. These findings were used to develop a model for the relationship between the transporters in resting pancreatic acinar cells.

Animals↗
PubMed2002

A polymorphism in the beta1 adrenergic receptor is associated with resting heart rate.

Resting heart rate is significantly associated with cardiovascular morbidity and mortality. However, the extent to which resting heart rate is genetically determined is poorly understood, and no genes have been found that contribute to variation in resting heart rate. Because signaling through the beta1 adrenergic receptor is a key determinant of cardiac function, we tested whether polymorphisms in this receptor are associated with resting heart rate. A cohort of >1,000 individuals of Chinese and Japanese descent, from nuclear families, was genotyped for two polymorphisms, resulting in a serine/glycine substitution at amino acid 49 (Ser49Gly) and an arginine/glycine substitution at residue 389 (Arg389Gly), in the beta1 adrenergic receptor. For comparison, polymorphisms in the beta2 and beta3 adrenergic receptors were also evaluated. The Ser49Gly polymorphism was significantly associated (P=.0004) with resting heart rate, independent of other variables, such as body-mass index, age, sex, ethnicity, exercise, smoking, alcohol intake, hypertension status, and treatment with beta blockers. The data support an additive model in which individuals heterozygous for the Ser49Gly polymorphism had mean heart rates intermediate to those of either type of homozygote, with Ser homozygotes having the highest mean heart rate and with Gly homozygotes having the lowest. Neither the Arg389Gly polymorphism in the beta1 adrenergic receptor nor polymorphisms in the beta2 and beta3 adrenergic receptors were associated with resting heart rate. The heritability of heart rate was 39.7% +/- 7.1% (P<10-7).

Age Factors↗
PubMed1992

Inhibition of HIV infection of resting peripheral blood lymphocytes by nucleosides.

T cells in the peripheral blood are largely in the resting state and represent a significant pool of potential targets for HIV infection. The protection of these cells from infection is an important goal of nucleoside therapy. Resting PBL may not be protected effectively by such nucleosides as azidothymidine (AZT) since anabolic phosphorylation of thymidine nucleosides is reported to be limited in these cells. In this study we used DNA amplification procedures to follow HIV proviral DNA formation in resting T cells and to determine the ability of azidodeoxythymidine (AZT), dideoxyinosine (ddI), and dideoxycytosine (ddC) to inhibit this process. Experiments confirm that resting PBL synthesize HIV proviral DNA sequences. Drug titrations showed that this synthesis could be inhibited by nucleosides. ddC was the most potent drug, inhibiting transcription at the U5 region. ddI and AZT at similar concentrations (10 microM) did not inhibit. ddI in the concentration range of 10-100 microM was able to inhibit production of transcripts containing U3 and env sequences in resting cells. Similar inhibition levels were accomplished by AZT at 10-100-fold lower drug concentrations. These results demonstrate that resting T cells can be protected from HIV infection by nucleosides and that thymidine nucleosides are effective inhibitors despite the limited potential for anabolic phosphorylation.

Base Sequence↗