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G Levin

Publications and source records attributed to G Levin.

At least 19 recordsLinked to original sources

Low sodium intake induces an increase in renal monoamine oxidase activity in the rat. Involvement of an angiotensin II dependent mechanism.

AIMS: The interplay between natriuretic dopamine and antinatriuretic angiotensin II represents an important mechanism for the regulation of renal sodium and water excretion. Monoamine oxidase is the main metabolizing pathway for dopamine in the renal cortex. In this study, we have analysed the effect of low sodium feeding and AT1 receptor blockade on renal dopamine metabolism by monoamine oxidase. METHODS: Four groups of rats were studied: 1, normal salt diet (NS); 2, low salt diet (LS); 3, NS receiving Losartan (Los, specific AT1 receptor antagonist, 20 mg kg(-1) bwt day(-1), NS + Los); 4, LS receiving Los (LS + Los). RESULTS: Urinary dopamine excretion was lower in LS than in NS rats (543 +/- 32 vs. 680 +/- 34 ng day(-1) 100 g(-1) bwt, P < 0.05). When treated with Los, DOPAC excretion and urinary DOPAC/dopamine ratio fell significantly in the LS + Los group as compared with the LS group (1199 +/- 328 vs. 3081 +/- 681 ng day(-1) 100 g(-1) bwt and 1.90 +/- 0.5 vs. 5.7 +/- 1.2, respectively, both P < 0.02). Losartan increased hydroelectrolyte excretion in the LS group. No changes were found in the NS + Los group. Aromatic L-amino acid decarboxylase activity in cortex was similar in NS and LS rats. Instead, monoamine oxidase activity was higher in cortical homogenates from LS rats (in nmol mg tissue(-1) h(-1): NS 7.66 +/- 0.52; LS 9.82 +/- 0.59, P < 0.05) and this difference was abolished in LS + Los rats (7.34 +/- 0.49 nmol mg tissue(-1) h(-1), P < 0.01, vs. LS). CONCLUSIONS: We have concluded that low levels of dopamine in the urine of LS rats are because of an increase in the activity of renal monoamine oxidase and that angiotensin II mediates this increase through stimulation of AT1 receptors.

3,4-Dihydroxyphenylacetic Acid↗

Swedish dental hygienists' preferences for workplace improvement and continuing professional development.

UNLABELLED: The present study examined factors for workplace improvement and continuing professional development (CPD) for Swedish dental hygienists. Seventy-one per cent of 577 randomly selected members of Sweden's Dental Hygienist Association responded to a questionnaire. The chi-square test, Spearman's rank correlation, and multiple stepwise logistic regression modelling were used in the statistical analysis. The results showed that dental hygienists having more than 10 sick days annually and with a strong commitment to their work increased the preference for workplace improvements, such as peer recognition of dental hygienists' professional qualifications, clinical process quality, and time for reading research articles and participating in projects. In addition, dental hygienists in the 41-52 age group were associated with workplace improvements. This is in contrast to the factors that decreased preferences for workplace improvements: clear work roles, a 1-year training programme, a male clinic manager, and working in the private sector. Practicing dental hygiene in the public sector and lifestyle factors were the most influential determinants for a strong interest in CPD. CONCLUSION: Workplaces should observe people that are obviously committed to their work, those with many sick days, and those in a specific age group, as they indicate different preferences for workplace improvements. CPD seems to be a lower priority than workplace improvements for Swedish dental hygienists.

Adult↗

Effect of implementation of safety measures in tae kwon do competition.

BACKGROUND: Previous reviews of tae kwon do (TKD) tournaments have documented injury rates of 25/1000 to 12.7/100 athlete exposures. Most injuries have been reported to be to the head and the neck and are occasionally very serious. Many of these studies involved high level TKD competitions with minimal safety precautions. Recently, safety measures have been implemented in many TKD competitions. OBJECTIVE: To evaluate retrospectively the incidence of injuries in TKD competitions involving a wide range of participants and featuring extensive safety precautions. METHODS: A total of 2498 participants ranged in age from 18 to 66, included both men and women, and ranged in rank from yellow to black belt. Traumas, defined as any event requiring interaction with medical staff, were documented with respect to mechanism, diagnosis, treatment, and follow up recommendations. An injury was defined as a trauma that prevented a contestant from resuming competition on the day that the trauma occurred, according to National Collegiate Athletic Association criteria. RESULTS: The injury rate was 0.4/1000 athlete exposures. This is lower than reported in previous studies of TKD tournaments and in many other sports. CONCLUSION: TKD tournaments that emphasise limited contact, protective equipment, and medical supervision are relatively safe and compare favourably with other sports.

Adolescent↗

Comparative effects of indomethacin on cell proliferation and cell cycle progression in tumor cells grown in vitro and in vivo.

Considerable research effort is currently being directed towards understanding the mechanisms mediating the antiproliferative effects of non-steroidal anti-inflammatory drugs (NSAIDs) and, more recently, of cyclooxygenase (COX)-2 inhibitors as well. A key question is whether NSAIDs (excluding sulindac) exert their anticarcinogenic effects in vivo by a mechanism that is dependent on their capacity to inhibit COX activity. Some studies with cultured tumor cells in vitro have argued against such a linkage, showing that NSAIDs inhibit cell replication and/or augment apoptosis only at concentrations that exceed those required to inhibit COX activities 10- to 100-fold. The significance of these results for the observed anticarcinogenic effects of NSAIDs in vivo has not yet been evaluated. We addressed this question by comparing, for the same tumor cells, the effects of the NSAID indomethacin on cell growth parameters when the cells were grown in culture to the effects seen in the in vivo growing tumor in the mouse. Indomethacin added to cultured Lewis lung carcinoma cells exerted a potent antiproliferative effect ((3)H thymidine assay) and reduced cell viability (MTT[3-(4,5-dimethyl(thiazol-2-yl)-2,5 diphenyl tetrazolium bromide] assay) at low doses (10-20 microM) in parallel with its inhibitory effect on cellular cyclooxygenase. These effects of indomethacin appeared to arise from a clear antiproliferative shift in the profile of the cell cycle parameters towards a reduced percentage of cells at the S and G(2)/M phases, together with an increased percentage of cells at the G(1) phase. Significantly, similar results were seen when indomethacin was given in vivo at the low dose of 2 mg per kg/day, which blocked blood platelet COX activity and at the same time produced a delay in tumor growth initiation and attenuation of apparent primary tumor growth as well as growth of lung metastases. These results thus provide strong support for the notion that COX inhibition is a major determinant in the antitumorigenic effect of indomethacin in vivo.

Analysis of Variance↗

Surgical treatment of chronic lower extremity neuropathic pain.

The current authors retrospectively reviewed 147 lower extremity peripheral nerve procedures in 114 patients (average age, 42 years) with chronic lower extremity neuropathic pain to determine whether surgical treatment based on an empirically derived algorithm could reduce pain and improve function. This algorithm assigns crush, stretch, and chronic transection injuries to treatment with transection and containment. Peripheral nerve stimulation was used in conjunction with transection and containment for patients with more chronic presentations for whom previous transections had been unsuccessful. Patients with adhesive neuralgia underwent revision neurolysis with vein wrapping. Patients with repetitive nerve trauma (overuse) underwent primary or revision neurolysis. Duration of symptoms averaged 37 months, and mechanisms of nerve injury included chronic transection, crush, adhesive neuralgia, stretch, repetitive trauma, and idiopathic etiology. Time to followup averaged 38 months. Pain and dysfunction were ranked from 0 points (no pain or dysfunction) to 10 points (pain prompting request for amputation or functional deficit warranting wheelchair use); preoperative and followup work status were documented. Average pain and dysfunction scores improved: 8.8 to 5.6 points and 7.6 to 5.0 points, respectively. Of the 114 patients, 52 (46%) patients improved their work status, including 35 of 87 (40%) involved in workers' compensation. There were no statistically significant differences in outcome based on mechanism of nerve injury or type of procedure. The consistent average improvement suggests this algorithm assigns the appropriate procedure to a given mechanism of injury.

Adolescent↗

The peripheral vascular response to exercise is impaired in patients with risk factors for coronary artery disease.

BACKGROUND: Abnormal coronary and brachial artery responses have been described in individuals with risk factors for coronary artery disease (CAD). Peripheral arterial tonometry (PAT), a newly developed digital plethysmographic technique was used to assess peripheral vascular response to exercise in healthy controls and individuals with risk factors. METHODS AND RESULTS: Continuous finger PAT during Bruce protocol exercise test was performed in 30 subjects with risk factors for CAD and 30 healthy individuals. Compared with baseline, the PAT wave amplitude at peak exercise decreased in the subjects but increased in the controls: 83 +/- 28% vs. 114 +/- 40% respectively, p < 0.01. CONCLUSIONS: A different pattern of systemic vascular response to exercise was found in individuals with risk factors for atherosclerosis. Since the vascular behavior in these patients is probably related to endothelial dysfunction, it may be that peripheral arterial tonometry can be used as a simple, readily available technique to assess endothelial function.

Adult↗

Correlating a protein structure with function of a bacterial mechanosensitive channel.

MscL, a mechanosensitive channel found in many bacteria, protects cells from hypotonic shock by reducing intracellular pressure through release of cytoplasmic osmolytes. First isolated from Escherichia coli, this protein has served as a model for how a protein senses and responds to membrane tension. Recently the structure of a functionally uncharacterized MscL homologue from Mycobacterium tuberculosis was solved by x-ray diffraction to a resolution of 3.5 A. Here we demonstrate that the protein forms a functional MscL-like mechanosensitive channel in E. coli membranes and azolectin proteoliposomes. Furthermore, we show that M. tuberculosis MscL crystals, when re-solubilized and reconstituted, yield wild-type channel currents in patch clamp, demonstrating that the protein does not irreversibly change conformation upon crystallization. Finally, we apply functional clues acquired from the E. coli MscL to the M. tuberculosis channel and show a mechanistic correlation between these channels. However, the inability of the M. tuberculosis channel to gate at physiological membrane tensions, demonstrated by in vivo E. coli expression and in vitro reconstitution, suggests that the membrane environment or other additional factors influence the gating of this channel.

Bacterial Proteins↗

Technique factors and image quality as functions of patient weight at abdominal CT.

PURPOSE: To investigate how changes in kilovolt peak and milliampere second settings, and patient weight affect transmitted x-ray energy fluence and the image contrast-to-noise ratio (CNR) at abdominal computed tomography (CT). MATERIALS AND METHODS: Cylinders of water were used as patient models, and x-ray spectra, including x-ray tube potentials of 80-140 kVp, were investigated. The mean photon energy and energy fluence transmitted through water cylinders with varying diameters and the image contrast for fat, muscle, bone, and iodine relative to water were determined. The effect of changing the x-ray tube potential on CNR also was investigated. RESULTS: At a constant kVp, increasing patient weight from 10 kg to 120 kg reduced the transmitted energy fluence by two orders of magnitude. Changing the x-ray tube potential from 80 kVp to 140 kVp increased the mean photon energy from approximately 52 keV to approximately 72 keV and thus reduced the image contrast relative to water by 12% for muscle, 21% for fat, 39% for bone, and 50% for iodine (approximate reduction values). Increasing the x-ray tube potential from 80 kVp to 140 kVp increased the CNR by a factor of 2.6 for muscle and by a factor of 1. 4 for iodine. CONCLUSION: With changes in patient weight at abdominal CT, x-ray tube potentials must be varied to maintain a constant detector energy fluence. Increasing the x-ray tube potential generally improves CNR.

Body Weight↗

Prophylaxis against respiratory syncytial virus in high-risk infants: administration of immune globulin and epidemiological surveillance of infection.

Hospitalizations secondary to respiratory syncytial virus (RSV) infection in children were monitored before and after the administration of RSV immune globulin. Monitored also was the effectiveness of prophylaxis in preventing the disease among at-risk children along the Texas-Mexico border. Small premature infants were at the greatest risk of hospitalization; preterm infants and then term infants followed. Prophylaxis does not necessarily prevent RSV bronchiolitis but may reduce the severity of the pulmonary disease.

Hospitalization↗

Arthur levin

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Journal Article↗

Deprenyl monotherapy improves visuo-motor control in early parkinsonism.

Deprenyl is a potent MAO-B inhibitor which is commonly prescribed for treatment of parkinsonism. Despite prevalent use its effects on the symptoms and course of Parkinson's disease (PD) are still debated. The present study was therefore undertaken in order to measure quantitatively changes in visuo-motor control (VMC), consequent to deprenyl monotherapy in early PD. Previous work from our laboratory has shown typical VMC deterioration in PD patients, that correlates with disease severity. Thus, measurements of such changes provides a sensitive tool with which the symptomatic effects of drug treatment can be assessed quantitatively. Fourteen newly diagnosed, PD patients with light symptoms were studied. The VMC of all patients was tested after the first neurological examination, before drug treatment commenced. A second test was done after 30 days of treatment with deprenyl at a dose of 2.5 mg/day. Following this test, dosage was increased to 10 mg/day and a third VMC test was given after 30 more days of treatment. Our results show significant improvement in VMC functions following 30 days of 2.5 mg/day treatment and a continuing improvement after the next 30 days of 10 mg/day treatment. This improvement pertains mainly to directional control of self initiated movements and is smaller for movements that are guided externally. We conclude that deprenyl monotherapy has a clear symptomatic beneficial effect for patients with early PD.

Antiparkinson Agents↗

Agonist-independent inactivation and agonist-induced desensitization of the G protein-activated K+ channel (GIRK) in Xenopus oocytes.

The G-protein-activated K+ channels of the GIRK (Kir 3) family are activated by Gbetagamma subunits of heterotrimeric Gi/Go proteins. Atrial GIRK currents evoked by acetylcholine (ACh)1 via muscarinic m2 receptors (m2R) display prominent desensitization. We studied desensitization of basal and ACh-evoked whole-cell GIRK currents in Xenopus oocytes. In the absence of receptor and/or agonist, the basal GIRK activity showed inactivation which was prominent when the preparation was bathed in a low-Na+, high-K+ extracellular solution (96 mM [K+]out and 2 mM [Na+]out) but did not occur in a normal physiological solution. Ion substitution experiments showed that this basal, agonist-independent inactivation was caused by the decrease in [Na+]out rather than by the increased [K+]out. We hypothesize that it reflects a depletion of intracellular Na+. ACh-evoked GIRK currents desensitized faster than the basal ones. The agonist-induced desensitization was present when the preparation was bathed in all solutions tested, independently of [Na+]out. A protein kinase C (PKC) activator inhibited the GIRK currents both in high and low [Na+]out, apparently mimicking agonist-induced desensitization; however, a potent serine/threonine protein kinase blocker, staurosporine, blocked only a minor part of desensitization. We conclude that basal inactivation and agonist-induced desensitization are separate processes, the former caused by changes in Na+ concentrations, and the latter by unknown factor(s) with only a minor contribution of PKC.

Acetylcholine↗

Peripheral catecholamine alterations in adolescents with polycystic ovary syndrome.

OBJECTIVE: Polycystic ovary syndrome (PCO) is one of the most common endocrine disorders affecting women. Several lines of evidence have suggested the involvement of the sympathetic nervous system (SNS) in this condition. The present work was designed to assess neurochemically SNS activity in patients during the early stages of PCO. DESIGN AND PATIENTS: Fourteen patients with PCO (aged 14 to 21 years) were studied on a random day and 9 normal regularly cycling adolescents (aged 14 to 20 years) were studied during the early follicular phase (days 2 to 5). MEASUREMENTS: Hormonal profile was determined in basal conditions. LH and FSH were also measured after i.v. administration of 100 micrograms GnRH. Plasma concentrations of dihydroxyphenylalanine (Dopa), noradrenaline (NA), adrenaline (A), total dopamine (DA) and dihydroxyphenylglycol (DHPG) were determined in basal conditions and in response to GnRH by HPLC with electrochemical detection or a radioenzymatic method. Basal urinary Dopa, catecholamines and catechol metabolites (DHPG, vanillylmandelic acid (VMA), 3-methoxy-4-hydroxyphenylglycol (MHPG), homovanillic acid (HVA), metanephrine (MN) and normetanephrine (NMN)) were determined by HPLC with electrochemical detection. RESULTS: Basal plasma LH, testosterone, androstenedione, oestrone and LH/FSH ratio were higher (P < 0.01) and serum sex hormone-binding globulin (SHBG) were lower (P < 0.01) in PCO patients than in control subjects. Basal and GnRH-stimulated plasma free Dopa, A, NA and total DA were similar in patients and controls. Plasma DHPG was lower (P < 0.01) in PCO patients (4.20 +/- 0.30 nmol/l) than in controls (8.0 +/- 1.0 nmol/l) throughout the study. Urinary A, NA, DA, Dopa, MN, MHPG, HVA, and VMA were similar in patients and controls. Urinary DHPG was lower (P < 0.01) in PCO patients (0.50 +/- 0.02 mumol/d) than in controls (0.73 +/- 0.09 mumol/d). On the other hand PCO patients had a higher urinary excretion of NMN than controls (PCO: 1.20 +/- 0.10; C: 0.78 +/- 0.10 mumol/d, P < 0.05). CONCLUSIONS: Our results show the same endocrinological features in adolescent PCO patients as those reported in adults. The results also demonstrate a peripheral catecholaminergic alteration which suggests an alteration in noradrenaline deamination and/or uptake in adolescent patients. This study however does not permit us to conclude that PCO is primarily caused by this sympathetic alteration.

Adolescent↗

In vivo antiperoxidative effect of 9-cis beta-carotene compared with that of the all-trans isomer.

It has been implied that the antiperoxidative activity of beta-carotene is important for its ability to prevent malignant and cardiovascular diseases. In vitro studies have shown that 9-cis beta-carotene is a better antioxidant than the all-trans isomer. In the present study the antiperoxidative biopotency of 9-cis beta-carotene was studied in vivo. For three weeks, weanling female rats were fed diets containing 10% fresh or oxidized soybean oil. The experimental diets were supplemented with beta-carotene at 1 g/kg with the synthetic all-trans isomer or with a carotene extract of Dunaliella bardawil containing 75% 9-cis beta-carotene. Both carotene sources prevented to the same extent hepatic and erythrocyte peroxidation associated with the consumption of oxidized oil. However, this beneficial effect was accompanied, in most of the groups, by a reduction in the hepatic carotene stores. Only in the animals fed Dunaliella extract combined with oxidized oil were the hepatic stores of beta-carotene and vitamin A maintained. The enhanced degradation of 9-cis beta-carotene observed in the livers of these animals might indicate that, like the effect observed under in vitro conditions, this isomer has a greater affinity toward free radicals and therefore might be a more efficient antioxidant than the all-trans form under in vivo conditions. The activity of glutathione peroxidase, glucose-6-phosphate dehydrogenase, and glutathione reductase as affected by the two carotene sources was also studied.

Animals↗

Evidence for a direct interaction of superoxide anion radical with carnosine.

Using photochemiluminescence, the interaction between carnosine and superoxide anion was measured directly. Carnosine at physiological concentrations decreased the amplitude of luminol chemiluminescence like superoxide dismutase (SOD) did, and prolonged the lag-period of the chemiluminescence similar to the effect of ascorbic acid. From the interaction of nitro blue tetrazolium with superoxide anion generated by the xanthine oxidase system, the constant for interaction of carnosine with 02-. was calculated to be 10(5) M-1.sec-1. The possible biological significance of the quenching of superoxide anion by carnosine is discussed.

Carnosine↗

Phosphorylation of a K+ channel alpha subunit modulates the inactivation conferred by a beta subunit. Involvement of cytoskeleton.

Voltage-gated K+ channels isolated from mammalian brain are composed of alpha and beta subunits. Interaction between coexpressed Kv1.1 (alpha) and Kvbeta1.1 (beta) subunits confers rapid inactivation on the delayed rectifier-type current that is observed when alpha subunits are expressed alone. Integrating electrophysiological and biochemical analyses, we show that the inactivation of the alphabeta current is not complete even when alpha is saturated with beta, and the alphabeta current has an inherent sustained component, indistinguishable from a pure alpha current. We further show that basal and protein kinase A-induced phosphorylations at Ser-446 of the alpha protein increase the extent, but not the rate, of inactivation of the alphabeta channel, without affecting the association between alpha and beta. In addition, the extent of inactivation is increased by agents that lead to microfilament depolymerization. The effects of phosphorylation and of microfilament depolymerization are not additive. Taken together, we suggest that phosphorylation, via a mechanism that involves the interaction of the alphabeta channel with microfilaments, enhances the extent of inactivation of the channel. Furthermore, phosphorylation at Ser-446 also increases current amplitudes of the alphabeta channel as was shown before for the alpha channel. Thus, phosphorylation enhances in concert inactivation and current amplitudes, thereby leading to a substantial increase in A-type activity.

Animals↗

Modulation by protein kinase C activation of rat brain delayed-rectifier K+ channel expressed in Xenopus oocytes.

The modulation by protein kinase C (PKC) of the RCK1 K+ channel was investigated in Xenopus oocytes by integration of two-electrode voltage clamp, site-directed mutagenesis and SDS-PAGE analysis techniques. Upon application of beta-phorbol 12-myristate 13-acetate (PMA) the current was inhibited by 50-90%. No changes in the voltage sensitivity of the channel, changes in membrane surface area or selective elimination of RCK1 protein from the plasma membrane could be detected. The inhibition was mimicked by 1-oleoyl-2-acetyl-rac-glycerol (OAG) but not by alphaPMA, and was blocked by staurosporine and calphostin C. Upon deletion of most of the N-terminus a preceding enhancement of about 40% of the current was prominent in response to PKC activation. Its physiological significance is discussed. The N-terminus deletion eliminated 50% of the inhibition. However, phosphorylation of none of the ten classical PKC phosphorylation sites on the channel molecule could account, by itself or in combination with others, for the inhibition. Thus, our results show that PKC activation can modulate the channel conductance in a bimodal fashion. The N-terminus is involved in the inhibition, however, not via its direct phosphorylation.

Alkaloids↗

Deletion of the N-terminus of a K+ channel brings about short-term modulation by cAMP and beta 1-adrenergic receptor activation.

On deletion of the N-terminus of RCK1 K+ channel, acute modulation of the channel by cAMP-elevating treatments is revealed. This modulation is studied in Xenopus oocytes using two-electrode voltage-clamp, site-directed mutagenesis, and SDS-PAGE analyses. Treatments by Sp-8-Br-cAMPS, a membrane-permeant cAMP analog, and by isoproterenol, a beta 1-adrenergic receptor (beta 1R) agonist, both increased the current amplitudes with no effect on the voltage dependency of activation. The effect of isoproterenol was blocked by coexpression of either G alpha S or G alpha i3 proteins. The channel protein is phosphorylated on the Sp-8-Br-cAMPS treatment at Ser446; however, a phosphorylation-deficient variant in which this site has been altered is still modulated by Sp-8-Br-cAMPS and isoproterenol. Expression of the full-length channel with Kv beta 1.1 auxiliary subunit renders the channel at the same modulation as that of the truncated one. Taken together, the RCK1 channel can be acutely modulated by cAMP and beta 1R activation possibly through protein kinase A (PKA) activation, but not through direct channel phosphorylation; the involvement of the N-terminus in this modulation is discussed.

Adrenergic beta-Agonists↗