SEARCH · PubMed Health

Results for “Recovery”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 685 records · Page 38Linked to original sources

PubMed1998

The effect of heat exposure on performance of and recovery from high-intensity, intermittent exercise.

Environmental heat is known to hamper aerobic performance. The purpose of this study was to examine the effect of heat on the performance of anaerobic exercise and the recovery from such exercise. Eleven trained men underwent two identical exercise-recovery protocols in neutral (22 degrees C, N) and hot (35 degrees C, H) conditions, in a cross-balanced order. Exercise consisted of a series of five 15 s bouts separated by 30 s of active recovery between bouts. The 60 min resting recovery was evaluated with a subsequent exercise series. Subjects were kept euhydrated with water. Peak power developed in the initial exercise series was higher in H compared with N (720 +/- 80 vs 664 +/- 74 W, respectively, p < 0.05). In the second series of exercise, peak power slightly improved in N but decreased in H (6.1 vs -4.1 %, respectively). Mean power was higher in the initial exercise series in H compared with N (636 +/- 83 vs 584 +/- 60 W, respectively, p < 0.05). No significant change occurred in the subsequent series of exercise. There was no difference in peak lactate following the initial series, nor in the decrease of lactate during recovery between the two conditions. Likewise, there were no differences in the changes in electrolyte concentrations and serum osmolality during recovery. VO2 and heart rate decreased following exercise in a similar manner in the two conditions. Rectal temperature increased similarly but remained elevated during H compared with N (p<0.05). In conclusion, the results of this study suggest that heat exposure may improve anaerobic performance but does not appear to affect the physiological responses during 60 min of recovery. Future research should examine the effect of more extreme heat stress, as well as shorter recovery periods.

Adult↗

PubMed1998

Effect of carbohydrate supplementation on plasma glutamine during prolonged exercise and recovery.

Muscle glycogen and glucose have been suggested to be carbon-chain precursors for glutamine synthesis in skeletal muscle. Therefore, the aim of the present study is to investigate whether carbohydrate supplementation affects plasma glutamine and other amino acids during exercise and 7 h of recovery. Eight well-trained subjects cycled at an alternating workload of 50 and 80% Wmax until exhaustion (59 to 140 min). During the exercise bout the subjects received either water (control) or a carbohydrate (CHO) drink (83 g CHO x l(-1), 2 ml x kg(-1) per kg body weight every 15 min). Plasma glutamine concentration appeared not to be affected by exercise, as a significant increase was only observed at some points in time during the control test. During recovery, however, plasma glutamine concentration decreased from 682+/-24 and 685+/-19 micromol x l(-1) at exhaustion to 552+/-19 and 534+/-12 micromol x l(-1) after 2 h of recovery for the control and CHO test, respectively. Plasma glutamine concentration returned to pre-exercise values after 7 h of recovery. Alanine concentration increased during exercise in both tests. During the recovery period the concentration of alanine (48%), and total amino acids (23%) decreased below the pre-exercise level. The plasma alanine and the total amino acid concentration was still suppressed after 7 h of recovery. In conclusion, carbohydrate supplementation had neither an effect during exercise nor during recovery on the concentration of plasma glutamine or other amino acids. Exercise, however, causes a substantial decrease in the plasma amino acid concentration during recovery.

Adult↗

PubMed2000

Midterm follow-up of patients who underwent removal of a left ventricular assist device after cardiac recovery from end-stage dilated cardiomyopathy.

OBJECTIVE: Cardiac recovery in end-stage idiopathic dilated cardiomyopathy recently occurred after temporary support with a left ventricular assist device. We report the case histories of patients who underwent removal of the device more than 4 years ago. METHODS: Since June 1994, 23 patients with end-stage idiopathic dilated cardiomyopathy who were supported by a left ventricular assist device or biventricular assist device for 1 to 26 months (mean, 6 months) underwent removal of the device after complete or extensive cardiac recovery, as revealed by echocardiography. RESULTS: Seven patients (group A) had recurrent cardiac failure after 4 to 24 months. Transplantation was performed in 6 patients, and one died while on the waiting list. Three patients died of noncardiac causes within a period of 4 months and 3 days after removal of the assist device. Stable cardiac recovery occurred in 13 patients (group B) for 3 to 49 months (mean, 23 months). At the time of implantation, there were no significant differences between the groups with regard to age, hemodynamics, left ventricular ejection fraction, left ventricular internal diameter in diastole, and autoantibody levels. The increase of ejection fraction and the decrease of left ventricular internal diameter in diastole after 2 months were highly significant. The patients in group A had longer histories of heart failure and first cardiac symptoms and duration of assist when compared with group B. Group B demonstrated a quicker cardiac recovery on the assist device, and thus support was shorter. Also, the degree of recovery at assist device explantation was more complete in group B. The age at the time of device placement was the only influencing factor for duration on the assist device. The probability of recurrence of heart failure was influenced by the duration of heart failure. CONCLUSIONS: In selected patients with idiopathic dilated cardiomyopathy, lasting recovery can be achieved after unloading with a left ventricular assist device. Lasting cardiac recovery seems to be related to functional normalization and a more rapid recovery during the unloading period.

Adolescent↗

PubMed2000

A common muscarinic pathway for diapause recovery in the distantly related nematode species Caenorhabditis elegans and Ancylostoma caninum.

Converging TGF-beta and insulin-like neuroendocrine signaling pathways regulate whether Caenorhabditis elegans develops reproductively or arrests at the dauer larval stage. We examined whether neurotransmitters act in the dauer entry or recovery pathways. Muscarinic agonists promote recovery from dauer arrest induced by pheromone as well as by mutations in the TGF-beta pathway. Dauer recovery in these animals is inhibited by the muscarinic antagonist atropine. Muscarinic agonists do not induce dauer recovery of either daf-2 or age-1 mutant animals, which have defects in the insulin-like signaling pathway. These data suggest that a metabotropic acetylcholine signaling pathway activates an insulin-like signal during C. elegans dauer recovery. Analogous and perhaps homologous cholinergic regulation of mammalian insulin release by the autonomic nervous system has been noted. In the parasitic nematode Ancylostoma caninum, the dauer larval stage is the infective stage, and recovery to the reproductive stage normally is induced by host factors. Muscarinic agonists also induce and atropine potently inhibits in vitro recovery of A. caninum dauer arrest. We suggest that host or parasite insulin-like signals may regulate recovery of A. caninum and could be potential targets for antihelminthic drugs.

Ancylostoma↗

PubMed1975

Recovery of blood lead concentration and of red cell 8-aminolevulinic acid dehydrase activity in dogs following return to normal diets after 75 weeks of lead feeding.

Blood lead concentration and red cell delta-aminolevulinic acid dehydrase (ALAD) activity were determined at intervals for eight months after symptom-free dogs, which had received 100 ppm or 500-1000 ppm of lead, by weight, in their diets for 75 1/2 weeks, were returned to a lead-free diet. Statistical treatment of the data disclosed a linear relationship between the logarithm of blood lead concentration or of ALAD activity and the logarithm of time (experimental week) during the recovery period. The calculated regressions predict that recovery of ALAD will occur before recovery of the blood lead concentration. Predicted recovery times depend on the levels selected as those which must be attained for recovery to be complete, as well as on the dosage of lead. The logarithm of the slope of the ALAD recovery regression of the individual dog has a linear relation to the percentage reduction in ALAD due to the lead, the regression accounting for 92% of the variance in the recovery rates. The slope of the blood lead recovery regression has a linear relation to the increase in blood lead for the dogs which received the low lead diet, but not for those which received the high lead diet.

Animals↗

PubMed1993

Beliefs about the world and recovery from myocardial infarction.

Seventy male, Hindu Myocardial Infarction (MI) patients were interviewed twice--4 to 5 days after their first heart attack (Time 1) and a month after their first heart attack (Time 2). The patients' beliefs about the world (world beliefs), about the causes of the disease (causal beliefs), and about the factors contributing to their recovery (recovery beliefs) were measured. Each category of beliefs was concerned with three domains: karma, God, and just world (or self). The patients' physical and psychological recovery was evaluated. World and recovery beliefs were intercorrelated, but these beliefs were only weakly correlated with causal beliefs. Furthermore, world beliefs and recovery beliefs were positively associated with recovery from MI at both Time 1 and Time 2. Attribution of causality to God was negatively correlated with medical recovery, perceived recovery, and mood state at Time 2. This trend was in the reverse direction for attribution of causality to self.

Adaptation, Psychological↗

PubMed2004

Carbohydrates and fat for training and recovery.

An important goal of the athlete's everyday diet is to provide the muscle with substrates to fuel the training programme that will achieve optimal adaptation for performance enhancements. In reviewing the scientific literature on post-exercise glycogen storage since 1991, the following guidelines for the training diet are proposed. Athletes should aim to achieve carbohydrate intakes to meet the fuel requirements of their training programme and to optimize restoration of muscle glycogen stores between workouts. General recommendations can be provided, preferably in terms of grams of carbohydrate per kilogram of the athlete's body mass, but should be fine-tuned with individual consideration of total energy needs, specific training needs and feedback from training performance. It is valuable to choose nutrient-rich carbohydrate foods and to add other foods to recovery meals and snacks to provide a good source of protein and other nutrients. These nutrients may assist in other recovery processes and, in the case of protein, may promote additional glycogen recovery when carbohydrate intake is suboptimal or when frequent snacking is not possible. When the period between exercise sessions is < 8 h, the athlete should begin carbohydrate intake as soon as practical after the first workout to maximize the effective recovery time between sessions. There may be some advantages in meeting carbohydrate intake targets as a series of snacks during the early recovery phase, but during longer recovery periods (24 h) the athlete should organize the pattern and timing of carbohydrate-rich meals and snacks according to what is practical and comfortable for their individual situation. Carbohydrate-rich foods with a moderate to high glycaemic index provide a readily available source of carbohydrate for muscle glycogen synthesis, and should be the major carbohydrate choices in recovery meals. Although there is new interest in the recovery of intramuscular triglyceride stores between training sessions, there is no evidence that diets which are high in fat and restricted in carbohydrate enhance training.

Dietary Carbohydrates↗

PubMed2002

Correction of analytical results for recovery: a comparison of the method performance characteristics from recent collaborative trials studies for aflatoxin quantification using conventional and robust statistics.

Results from recently conducted collaborative trials on the determination of aflatoxin B(1) in various matrices have been evaluated to establish whether the use of recovery data would result in a distinct change of the relative between-laboratory standard deviation (RSD(R)) of the corrected data compared with the uncorrected data. In addition, we applied conventional and robust statistics to evaluate whether the impact of the use of recovery data on the estimation of RSD(R) depended on the statistical method applied for data analysis. This investigation was based on means before and after correction for recovery. The method performance characteristics were calculated using results from naturally contaminated test materials, while the results from test materials fortified with the target analytes were used to estimate the recovery. The study revealed that applying conventional and robust statistics in general led to comparable estimates for RSD(R). The comparison about the use of recovery data showed that in most cases, the RSD(R) obtained from the analysis of aflatoxin B(1) decreased after correction of the results for recovery. This tendency was similar when the comparison was done using robust or conventional statistics. However, in three cases, conventional statistics yielded a higher RSD(R) for the corrected data, whereas robust statistics showed the opposite. Looking carefully at the data, the treatment of conventional statistics indicated that the way outliers are detected and removed could result in an under- or overestimation of RSD(R). Applying the law of error propagation revealed that most likely the correlation between the uncorrected data and the recovery rate led to a reduced variability of the data corrected for recovery.

Aflatoxin B1↗

PubMed1988

Postirradiation recovery of haemopoiesis in Steel mutant mice.

The recovery of haemopoiesis in Steel mutant mice following 1 Gy sublethal irradiation is described. Steel homozygotes (S1/S1) did not display the abortive phase of erythropoietic recovery while the secondary phase of erythropoietic recovery was more pronounced in S1/S1 than in control (+/+) animals. On the contrary, the neutrophilopoietic recovery in S1/S1 mice was defective only during the secondary phase of recovery. Steel heterozygotes (S1/+) manifested similar, albeit less pronounced, defects. In the course of studies of recovery of eosioniphils it was observed that neither wild-type nor mutant animals expressed the abortive rise. Moreover, the kinetics of recovery of eosinophils was essentially different from both erythropoietic and neutrophilopoietic recovery, and the preirradiation level was reached in both normal and mutant animals on day 60 postirradiation as opposed to 24 and 35 days for erythropoiesis and neutrophils respectively.

Animals↗

PubMedDate not supplied

How effective is therapy for childhood stuttering? Dissecting and reinterpreting the evidence in light of spontaneous recovery rates.

BACKGROUND: Similar positive results (e.g. immediate decreases in stuttering frequency and a 60-80% recovery rate from stuttering) have been reported for numerous therapeutic protocols for treating childhood stuttering, many of which have been diametrically opposite in their orientations and implementations. For example, Johnson advocated indirect treatments that simply advocated refraining from drawing any negative attention to childhood disfluencies as persistent and chronic stuttering was thought to progress via negative parental reactions to normal disfluencies. In contrast, direct interventionists sought immediately to eliminate stuttered speech patterns by training 'corrected' speech models that usually involved some form of prolonged speech. However, reports from speech and language therapists around North Carolina, USA, suggest much lower recovery rates in the children they treat (i.e. 13.9% over a median therapeutic period of 3 years, which to the present authors is an indicator of therapeutic inefficiency and ineffectiveness). AIMS: The discrepancy between these recovery rates calls for a re-examination of the efficacy of stuttering therapy for children, especially in light of recent statements from some therapies suggesting that therapy might be curative in nature. MAIN CONTRIBUTION: Spontaneous and complete recovery (removing all overt and covert markers of the pathology) occurs in 60-80% of all children who display incipient stuttering behaviours. As such, it appears that many claims of therapeutic success in children who stutter are confounded by the possibility of spontaneous recovery during the testing and intervention period. Simply put, it is impossible to discriminate between recovery that would occur naturally over time, and what may have been simply accelerated via therapy. Based on stable prevalence rates and the data in the present paper, it is suggested that therapy does little to boost recovery rates from incipient stuttering. Therapy can provide 'inhibitory' symptomatic relief with varying degrees of success with respect to decreasing stuttering severity and the need for continued therapy. However, it must be made clear that curing stuttering is not a likely outcome of therapy, although successful management can decrease the severity of the problem. It is argued that all forms of stuttering inhibition, including those at work during spontaneous recovery, are all mediated by the degree of mirror neuron engagement in the brain. CONCLUSIONS: It is proposed that in children who stutter, the best source of relief from stuttering is in the effective and efficient engagement of mirror neurons via methods that best replicate choral speech. In order to induce natural sounding, fluent speech, it is suggested that one uses primarily derivations of choral speech such as altered auditory feedback. Motoric techniques might also be used synergistically to provide supplementary sources of mirror neuron engagement.

Child↗

PubMed1978

Intergrated stereological and biochemical studies of hepatocytic membranes. I. Membrane recoveries in subcellular fractions.

Previous attempts to relate the structure and function of hepatocytic membranes have compared biochemical data of fractions to morphological data derived from either intact tissue or fractions. The effects of the original homogenization aside, biochemical recoveries comparing membrane marker enzymes of the homogenate to subsequent fractions suggest a general conservation of activity. A sterological study was undertaken to estimate membrane surface areas in the intact tissue, homogenate, and fractions of the same livers and then to test the comparability of these data with membrane marker enzymes by calculating both morphological and biochemical recoveries. The sterological data were corrected for errors due to section thickness and compression. The average total membrane sufrace area per 1 g of liver was 9.3 m2 in the intact tissue (T), 7.8 m2 in the homogenate (H), and 7.4 m2 in the fractions (F); recoveries for the membrane surface areas thus averaged 96% for the (F/H) and 81% for the (F/T) comparisons. In homogenate and fractions, the differentiability of membranes by morphological criteria was limited to rough- and smooth- surfaced membranes, as well as outer and inner mitochondrial membranes. The recoveries of rough-surfaced membranes were 101% for F/H and 92% for F/T; those of smooth-surface membranes were 89% for F/H and 107% for F/T. For mitochondrial membranes, a recovery of 100% for F/H was obtained, whereas it amounted to only 54% for F/T. With respect to F/H, the membrane recoveries compare well with the marker enzyme recoveries obtained biochemically. The extension of recovery calculations to the intact tissue (F/T) revealed satisfactory conservation of the procedures of homogenization and fractionation; it indicates, however, that a shift of a substantial part of mitochondrial membranes to the pool of unidentifiable smooth membranes may occur on homogenization.

Animals↗

PubMed1986

Destruction and reorganization of the receptor membrane in labellar chemosensory cells of the blowfly. Recovery of responses to sugar after destruction.

Recovery from destruction by sodium deoxycholate (DOC) was studied with the receptor membrane of the blowfly, Phormia regina. The recovery can be divided into two processes, colchicine dependent and colchicine independent. The colchicine-dependent process was completely depressed by pretreatment with colchicine at 5 mM for 2 min (partially at 0.1 mM for 10 min), but the colchicine-independent one persisted. Vinblastine also caused depression but lumicolchicine did not. Records of responses obtained from the DOC-treated sugar receptor showed long response latencies that gradually became indistinct with recovery. Colchicine also affected this change in response latency after the DOC treatment. These results suggest that the colchicine-dependent recovery process is related to microtubules in the distal process of the receptor cell. The recovery time course and the change in response latency could be quantitatively explained by the simple assumptions that DOC underwent desorption from the receptor membrane (colchicine-independent recovery process) and that regeneration of the disrupted distal process of the receptor cell accompanied recovery in the number of available receptor sites (colchicine-dependent recovery process).

Animals↗

PubMed1997

Secondary cytokines interact in sequence with interleukin-1alpha (IL-1alpha) with or without macrophage colony-stimulating factor (M-CSF) to further accelerate granulopoietic recovery in myelosuppressed animals.

Interleukin-1alpha (IL-1), by itself, accelerates both granulopoietic and thrombopoietic recovery in the 5-fluorouracil (5-FU) myelosuppressed mouse (FUM). As a primary cytokine, IL-1 also interacts in concert with macrophage colony-stimulating factor (M-CSF) to synergistically enhance hematopoietic recovery in the FUM. As part of our continuing interest in cytokine sequencing, studies were carried out to determine whether the addition of several secondary cytokines (GM-CSF, IL-3, and IL-6) to IL-1 (+/-M-CSF) would further enhance the stimulatory effects of the primary cytokine(s) on hematopoietic recovery in FUM. Throughout these studies, IL-1 (+/-M-CSF) was administered for 2 days to the FUM, and the secondary cytokines were given either in concert (days 1 and 2) or in sequence (days 3-6) or both with the primary cytokine(s). Based on the magnitude of 7-day post-5-FU granulocyte recovery, the results demonstrated that the synergistic effects of IL-1 + M-CSF treatment on granulopoietic recovery in FUM could not be duplicated by substituting either IL-3, IL-6, or GM-CSF for M-CSF. Nonetheless, the secondary cytokines were observed to enhance the stimulatory effects of IL-1 under the following administration schedules: (1) 2 days of IL-1, followed by a sequential treatment (days 3-6) with either IL-3 or IL-6, (2) 2 days of IL-1 + GM-CSF followed by an additional 4 days of GM-CSF alone, and (3) 2 days of IL-1 + GM-CSF followed by 3-4 days of a combination of GM-CSF and either IL-3 or IL-6. Although these cytokine treatment schedules led to an enhanced granulocyte recovery (vs. IL-1 alone) in FUM, the day 7 granulocyte numbers never exceeded those observed after 2 days of IL-1 + M-CSF. Similarly, granulocyte recovery in FUM receiving 2 days of IL-1 + M-CSF followed by either GM-CSF or IL-3 also was significantly greater than that observed with IL-1 + M-CSF alone. In contrast, however, the sequential administration of IL-6 with IL-1 + M-CSF, unlike IL-1, failed to further enhance granulopoietic recovery, suggesting that there may be an antagonism between IL-6 and M-CSF in the FUM. In summary, therefore, the secondary cytokines were found to interact more effectively when they were administered in sequence, rather than in concert, with both IL-1 and IL-1 + M-CSF.

Animals↗

PubMed1997

Early time-dependent decompression for spinal cord injury: vascular mechanisms of recovery.

Although surgical decompression is often advocated for acute spinal cord injury, the timing and efficacy of early treatment have not been clinically proven. Our objectives were to determine the importance of early spinal cord decompression on recovery of evoked potential conduction under precision loading conditions and to determine if regional vascular mechanisms could be linked to electrophysiologic recovery. Twenty-one mature beagles were anesthetized and mechanically ventilated to maintain normal respiratory and acid-base balance. Somatosensory-evoked potentials from the upper and lower extremities were measured at regular intervals. The spinal cord at T-13 was loaded dorsally under precision loading conditions until evoked potential amplitudes had been reduced by 50%. At this functional endpoint, spinal cord displacement was maintained for either 30 (n = 7), 60 (n = 8), or 180 min (n = 6). Spinal cord decompression was followed by a 3-h monitoring period. Regional spinal cord blood flow was measured with fluorescent microspheres at baseline (following laminectomy) immediately after stopping dynamic cord compression, 5, 15, and 180 min after decompression. Within 5 min after stopping dynamic compression, evoked potential signals were absent in all dogs. We observed somatosensory-evoked potential recovery in 6 of 7 dogs in the 30-min compression group, 5 of 8 dogs in the 60-min compression group, and 0 of 6 dogs in the 180-min compression group. Recovery in the 30- and 60-min groups varied significantly from the 180-min group (p < 0.05). Regional spinal cord blood flow at baseline, 21.4+/-2.2 ml/100/g/min (combined group mean +/- SE) decreased to 4.1+/-0.7 ml/100 g/min after stopping dynamic compression. Reperfusion flows after decompression were inversely related to duration of compression. Of the 7 dogs in the 30 min compression group, 5 min after decompression the blood flow was 49.1+/-3.1 ml/100 g/min, which was greater than two times baseline. In the 180-min compression group early post-decompression blood flow, 19.8+/-6.2 ml/100 g/min, was not significantly different than baseline. Of the 8 dogs in the 60-min compression group, 5 who recovered evoked potential conduction revealed a lower spinal cord blood flow sampled immediately after stopping dynamic compression, 2.1+/-0.4 ml/100 g/min, compared to the 3 who did not recover where blood flow was 8.4+/-2.1 ml/100 g/min (p < 0.05). Reperfusion flows measured as the interval change in blood flow between the time dynamic compression was stopped to 5, 15, or 180 min after decompression, were significantly greater in those dogs that recovered evoked potential function (p < 0.05). Three hours after decompression, spinal cord blood flow in the 3 dogs in the 60-min compression group with no recovery, 11.1+/-2.1 ml/100 g/min, was significantly less than the spinal cord blood flow of the recovered group (n = 5), 20.5+/-2.2 ml/100 g/min. These data illustrate the importance of early time-dependent events following precision dynamic spinal cord loading and sustained compression conditions. Spinal cord decompression performed within 1 h of evoked potential loss resulted in significant electrophysiologic recovery after 3 h of monitoring. This study showed that the degree of early reperfusion hyperemia after decompression was inversely proportional to the duration of spinal cord compression and proportional to electrophysiologic recovery. Residual blood flow during the sustained compression period was significantly higher in those dogs that did not recover evoked potential function after decompression suggesting a reperfusion injury. These results indicate that, after precise dynamic spinal cord loading to a point of functional conduction deficit (50% decline in evoked potential amplitude), a critical time period exists where intervention in the form of early spinal cord decompression can lead to effective recovery of electrophysiologic function in the 1- to 3-h post-decompression p

Animals↗

PubMed2003

Recovery of phenytoin from feeding formulas and protein mixtures.

The recovery of phenytoin from mixtures containing different phenytoin formulations and protein mixtures was studied. Three phenytoin solutions (40 mg/microL) were prepared, each in triplicate, from phenytoin tablets, phenytoin suspension, and bulk phenytoin powder. These solutions were mixed with equivalent volumes of two commercially available feeding formulas (Replete and Ultracal) and two isolated protein mixtures (casein protein mixture and why protein isolates mixture) and placed in ultrafiltration tubes. The mixtures were centrifuged, and phenytoin recovery was determined by using high-performance liquid chromatography. Control data were also obtained before and after the experiment. There was no difference in phenytoin recovery when comparing phenytoin tablets versus phenytoin suspension in any of the protein media. There was a significant difference in phenytoin recovery when comparing the standard phenytoin solution mixed with Replete (32.51%) versus Ultracal (37.71%). There was also a significant difference in recovery when comparing the standard solution mixed with the calcium caseinate mixture (48.41%) versus the whey protein isolates mixture (82.01%). While the difference in recovery between Replete and Ultracal was expected, the significantly higher recovery of phenytoin from the whey protein mixture versus the calcium caseinate mixture indicated a much lower binding affinity between phenytoin and whey protein than with phenytoin and casein. The recovery of unbound phenytoin from feeding formulas and solutions of protein isolates did not differ with phenytoin formulations. Ultracal had a lower level of binding to phenytoin than Replete; whey protein had a lower level of binding than casein.

Anticonvulsants↗

PubMed1988

32P-adduct assay: comparative recoveries of structurally diverse DNA adducts in the various enhancement procedures.

A 32P-adduct assay for the measurement of low levels (1 adduct per 10(7) nucleotides) of binding of carcinogens to DNA has been reported previously. In this procedure, DNA is enzymatically hydrolyzed to 3'-monophosphates of normal nucleosides and adducts, which are 5'-32P-labeled by T4 polynucleotide kinase and [gamma-32P]ATP. Labeled adducts are resolved by TLC. Enrichment of adducts by extraction in 1-butanol [Gupta, R.C. (1985) Cancer Res., 45, 5656] or digestion with nuclease P1 [Reddy, M.V. and Randerath, K. (1986) Carcinogenesis, 7, 1543] prior to 32P-labeling, however, increased the sensitivity of detection for many adducts to a level of 1 per 10(9-10) nucleotides, although adduct recovery particularly in the latter assay depended on the chemical nature of adducts. We have now compared recoveries for greater than 70, different carcinogen-DNA adducts of known and unknown chemical nature in the two enrichment procedures as well as in a new procedure in which polynucleotide kinase is substituted for nuclease P1. When compared with the butanol extraction procedure, arylamines (such as 2-aminofluorene, 2-aminophenanthrene, 2-naphthylamine, 4-aminobiphenyl, 4-azoaminobenzene and N'-acetylbenzidine) bound to the C8 position of guanine were lost almost completely (0.2-4% recovery) in the nuclease P1-mediated assay, but the presence of a polar group in the aromatic amine moiety (such as 2-acetylaminofluorene, 2-acetylamino-phenanthrene and methyl-4-azoaminophenyl) rendered similar recovery. In contrast, aromatic amines (2-amino-phenanthrene, 2-acetylaminophenanthrene, 2-acetylaminofluorene and methyl-4-azoaminobenzene) and polycyclic aromatic hydrocarbons (benzo[a]pyrene, bromomethylbenzanthracene and benzanthracene) bound to the exocyclic positions of guanine or adenine showed extensive or as complete recovery in the nuclease P1 procedure as in the extraction procedure. Some of the unknown presumably polar adducts showed a lower recovery (30-70%) in the butanol procedure as compared to the nuclease P1 enrichment. The recovery pattern of most adducts examined in the polynucleotide kinase-enrichment assay was essentially the same as found in nuclease P1-mediated assay, except that overall lower values were obtained. Our data suggest that a given DNA sample should be analyzed by different versions of the 32P-adduct assay, particularly, DNA of specimens of humans exposed to low levels of unknown carcinogens. The observation that chemical structure of an adduct may be detrimental in its recovery in the enzyme- and extraction-mediated enrichment procedures may serve as a probe in the structural characterization of adducts of unknown carcinogens.

Butanols↗

PubMed2004

Recovery of evoked potentials, metabolic activity and behavior in a mouse model of somatosensory cortex lesion: role of the neural cell adhesion molecule (NCAM).

Understanding the processes that underlie functional recovery after cortical injury is a major challenge for neurobiology and clinical neurology. The aim of the present study was to establish a mouse model of functional recovery that would facilitate the investigation of the molecular and cellular events involved in cortical dynamics. We show that a focal injury of approximately 0.5 mm of diameter and 1 mm depth made in the barrel cortex of adult mice induced a transitory deficit that could be characterized using somatosensory evoked potential (SEP), metabolic mapping and a behavioral test. SEP recordings of short latency responses using an epicranial multi-array system showed a decreased cortical activity in the peri-lesion regions 2 weeks after the injury and a partial recovery to normal pattern 6 weeks after the lesion. Delayed SEP signals over the motor cortex were not altered by the injury. Metabolic mapping with [14C]deoxyglucose uptake in the surround of the injury reproduced the time course of deficit and recovery. Finally, a deficit in vibrissae related performance in a gap-crossing test 1 week after injury was followed by a functional recovery in the following 2 weeks. We show in addition that the recovery process is deficient and significantly delayed in NCAM knockout mice lacking all isoforms of NCAM (neural cell adhesion molecule)and PSA-NCAM. These results support the hypothesis that impairment and recovery of functions after focal cortical lesion involves remodeling of intact circuits surrounding the lesion and that the NCAM molecule participate in this process. The model opens new possibilities for investigating the role of candidate molecules in functional recovery using genetically modified mice.

Animals↗

PubMed2005

Rates of suppression and recovery of human sperm output in testosterone-based hormonal contraceptive regimens.

BACKGROUND: Practical hormonal male contraceptive regimens are likely to have delayed onset and offset of reliable contraception dictated by the length of the spermatogenic cycle and clearance rate of pre-formed sperm from the ductular system. While delayed onset of contraceptive efficacy is an accepted feature of vasectomy, reliable time estimates for a hormonal male contraceptive of time to onset and offset of reliable contraception and of resumption of normal male fertility are required. METHODS AND RESULTS: We utilized the sperm output data from three male contraceptive efficacy studies to define quantitative estimates of suppression and recovery rates from an androgen alone (testosterone enanthate) and an androgen/progestin (testosterone/depot medroxyprogesterone acetate) study. Using nearly 14,000 semen samples from World Health Organization (WHO) studies #85921 and #89903 with identical protocols, the rate of suppression of sperm output was best modelled as a two-parameter, single exponential decay function with effective half-time to suppression of 5.5 weeks and times of 6.8 weeks to 10 x 10(6)/ml, 8.7 weeks to 5 x 10(6)/ml, 10.0 weeks to 3 x 10(6)/ml and 13.0 weeks to 1 x 10(6)/ml. The rate of recovery using absolute sperm concentration was best modelled as a three-parameter, sigmoidal curve with effective time to reach half of the recovery plateau of 10.5 weeks and times of 9.0 weeks to 3 x 10(6)/ml, 9.9 weeks to 5 x 10(6)/ml, 11.5 weeks to 10 x 10(6)/ml, and 13.6 weeks to 20 x 10(6)/ml. Using relative sperm output, defined as a percentage of the participants' own baseline, recovery approached an asymptotic plateau of approximately 85% of geometric mean pre-treatment sperm concentration. In the combination androgen/progestin study, suppression rate was significantly faster (effective time to reach half maximal suppression of 3.0 weeks) and recovery significantly slower (effective time to reach half of recovery plateau of 14.7 weeks) and less complete (asymptotic recovery plateau of 43% of baseline) than in the androgen-alone WHO studies. CONCLUSION: These findings therefore provide large sample estimates of the suppression and recovery rates from an androgen-alone hormonal male contraceptive regimen as a basis for comparison with other second-generation combination androgen/progestin regimens that are the most promising approach to developing practical male hormonal regimens.

Contraception↗