PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Recovery phases”

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 847 records · Page 47Linked to original sources

A functional model of the hair cell-primary fiber complex.

A model is proposed containing three parallel systems; system 1 is a single channel consisting of an inhibitory circuit being fed by a fixed permeability responsible for spontaneous activity in parallel with a displacement-driven permeability, while systems 2 and 3 each consist of a number of identical permeability-volume-permeability channels with on/off switches activated at levels specific for each channel. The (continuous) output of each system drives a Poisson generator whose output "events" are delivered to a firing mechanism in the form of a "leaky integrator" delivering actual "firings" in simulated real time. The model quite accurately reproduces (1) stimulation and recovery phases of PST histograms obtained at six levels of stimulation for six auditory fibers (including "dead" period after stimulation), (2) single-exponential functions of recovery from adaptation for both onset and steady-state part of probe tone, (3) increments in response as independent of time of application of stimulus increment, (4) a specified hazard function for firings, (5) interval histograms of driven activity, (6) loss of phase locking with increasing frequency of stimulation, and (7) extended dynamic range for onset of response. The model fails in reproducing specific characteristics for response to decrements, and for response to AM.

Animals↗

Bethanechol chloride in neurogenic bladder dysfunction.

Representative case summaries of patients with different types of neurogenic bladder diagnosed by combined cystometric-perineal electromyography and treated with bethanechol (Urecholine) are presented. Determination of the activity of the periurethral striated muscle in relation to bladder dysfunction is extremely important in the selection of patients for bethanechol therapy. In the absence of structural obstruction, bethanechol can be used in patients with (1) the early phase of coordinated reflex neurogenic bladder and sphincter when there is incomplete bladder emptying due to feeble or unsustained detrusor contractions, (2) recovery phase of spinal shock when the periurethral striated muscle has recovered and is under voluntary control, (3) incomplete motor paralytic bladder with coordinated sphincter, and (4) sensory paralytic bladder with decompensation. The bethanechol regimen will vary in accordance with the type of bladder being treated.

Achondroplasia↗

Autologous transplantation in chronic myeloid leukaemia using peripheral blood stem cells.

Forty-three patients with chronic myeloid leukaemia in first chronic phase were recruited to study intensive chemotherapy (idarubicin plus cytarabine; IdAC) followed by collection of peripheral blood stem cells (PBSC) in the recovery phase. PBSC autografting was performed on 32 patients. One patient died during mobilization and three died following autograft. All procedural deaths occurred in patients who received IdAc more than a year from diagnosis. Nine further patients died, eight following progression of CML. 72% of transplanted patients showed a major cytogenetic response but most cases have returned to Philadelphia-positive haemopoiesis. 62% of autografted patients remain alive (median survival from diagnosis 52 months). Four of the 11 patients who did not receive a transplant remain in chronic phase.

Adult↗

Nicotine attenuates morphological deficits in a contusion model of spinal cord injury.

Protection against the progression of secondary injury appears to be an effective therapeutic strategy in spinal cord injury (SCI). Evidence indicates that nicotine can induce potent neuroprotective effects against injury to spinal cord neurons. Therefore, the present study was focused on the effects of nicotine on the behavioral and morphological recovery associated with SCI. Adult male Long-Evans rats were subjected to a moderate contusion model of SCI and received subcutaneous injections of nicotine for 14 days at the dose of 0.35 or 7 mg/kg/day. The rats were examined using the BBB locomotor rating scale for 6 weeks. At the end of the BBB recording, spinal cords were examined for the volumetric tissue sparing of gray and white matters. All SCI rats demonstrated a loss of hindlimb function followed by a recovery phase that peaked at 2-3 weeks after the trauma. Compared to untreated SCI rats, chronic nicotine administration appeared to improve the recovery of the locomotor functions. Indeed, nicotine-treated animals scored consistently higher on the BBB scale indicating that the treatment altered animal behavior. However, when taking under consideration correction factors for multiple comparisons, these data did not reach significance at overall experimental levels of significance 0.05. Nevertheless, nicotine administration was effective in sparing tissue at injury epicenter and a lower dose of nicotine also resulted in significant sparing of white matter of the injured spinal cord. These results suggest that agonists of neuronal nicotinic receptors can be attractive candidates for SCI therapy.

Animals↗

Immature platelet fraction measurement: a future guide to platelet transfusion requirement after haematopoietic stem cell transplantation.

summary. The decision to prophylactically transfuse platelets is dependent on the platelet count, careful regular clinical assessment and agreed local protocol. The ability to predict when platelet recovery will occur should allow a more reasoned approach to platelet transfusion. An increase in reticulated platelets demonstrates impending platelet recovery. A new rapid automated method to assess reticulated platelets, the immature platelet fraction (IPF), is described, and its clinical utility assessed. The IPF is identified by flow cytometry with the use of a nucleic acid specific dye in the reticulocyte channel on the Sysmex XE-2100. Fifty healthy adult volunteers were used to establish the normal range. Patients where platelet marrow production or destruction might be abnormal were studied, and some patients followed serially during treatment. Thirty patients receiving cytotoxic chemotherapy were tested, and 13 of these patients followed serially. Fifteen patients post-autologous or allogeneic transplant were followed daily for platelet count and IPF percentage to monitor platelet recovery. The method demonstrates good reproducibility and stability. The recovery phase of thrombocytopenia in most chemotherapy and transplant patients was preceded by a rise in IPF percentage several days prior to platelet recovery. In particular, patients undergoing autologous transplantation (n = 8) using peripherally collected stem cells have a characteristic IPF percentage motif, with a rise one or two days prior to engraftment. The automated IPF is a useful parameter in the clinical evaluation of the thrombocytopenic patient and has the potential to allow optimal transfusion of platelet concentrates.

Adult↗

Transcriptional and translational regulation of major heat shock proteins and patterns of trehalose mobilization during hyperthermic recovery in repressed and derepressed Saccharomyces cerevisiae.

Patterns of heat shock gene transcription and translation, as well as trehalose content, were investigated in both glucose (repressed) and acetate (derepressed) grown cells of Saccharomyces cerevisiae during heat shock and subsequent return of cells to 25 degrees C. Heat-shocked cells (37 degrees C for 30 min), grown in either glucose- or acetate-supplemented media, initially acquired high thermotolerance to a 50 degrees C heat stress, which was progressively lost when cultures were allowed to recover at 25 degrees C and subsequently exposed to a second heat stress. In all cases, with the notable exception of repressed cells of a relatively thermosensitive strain, inhibition of protein synthesis and coincident decrease in trehalose accumulation during the heat shock had little effect on the kinetics of loss of thermotolerance. Heat shock at 37 degrees C elicited a marked increase in transcription and translation of genes encoding major heat shock proteins (hsps). During recovery at 25 degrees C, both metabolic activities were suppressed followed by a gradual increase in hsp mRNA transcription to levels observed prior to heat shock. De novo translation of hsp mRNAs, however, was no longer observed during the recovery phase, although immunodetection analyses demonstrated persistence of high levels of hsps 104, 90, 70, and 60 in cells throughout the 240-min recovery period. In addition, while heat shock induced trehalose was rapidly degraded during recovery in repressed cells, levels remained high in derepressed cells. Results therefore indicated that the progressive loss of induced thermotolerance exhibited by glucose- and acetate-grown cells was not closely correlated with levels of hsp or trehalose. It was concluded that both constitutive and de novo synthesized hsps require heat shock associated activation to confer thermotolerance and this modification is progressively reversed upon release from the heat-shocked state.

Acetates↗

Role of cytokines in neurological disorders.

The balance between cytokines with pro- and anti-inflammatory effects contributes to the course of the Guillain-Barré syndrome and chronic inflammatory demyelinating polyneuropathy. TNFalpha seems to be an important factor in the cascade of events leading to demyelination and even axonal damage. During the acute phase, the serum concentrations of TNFalpha and IL-6 are elevated while anti-inflammatory cytokines are up-regulated in the recovery phase. Cytokines also have a key role in the pathogenesis of multiple sclerosis and most data suggest that this effect is mediated by myelin-specific CD4 T lymphocytes secreting Th type 1 cytokines. However, several different immune cells including B lymphocytes, CD8 T lymphocytes and NK T lymphocytes are also involved in the pathogenesis. Both Th1 and Th2 lymphocytes and cytokines probably participate in the development of myasthenia gravis (MG). The IFNalpha production is probably related to the severity of the disease, with clinical improvement associated with decreased production. The serum levels of IL-18 are significantly elevated in MG, with highest concentrations in patients with generalized disease. The immune system may be involved in the pathogenesis of AD by the effect of microglia, which can induce microglial activation with subsequent release of pro-inflammatory cytokines. In parkinsonism, there is evidence of chronic inflammation in the substantia nigra and striatum. Activated microglia, producing proinflammatory cytokines, surround the degenerating dopaminergic neurons and may contribute to the dopaminergic neuron loss. Studies of patients with epilepsy and animals with experimentally induced seizures indicate that cytokines may also influence the electrophysiological properties of neurons.

Alzheimer Disease↗

Elevated sweat sodium associated with pulmonary oedema in meningococcal sepsis.

BACKGROUND: We observed a temporary positive sweat test with sodium and chloride levels greater than 60 mmol L(-1) following meningococcal septicaemia. Objective was to investigate whether this finding is reproducible and whether this disturbance in epithelial sodium transport is related to sepsis-induced pulmonary oedema. MATERIALS AND METHODS: Twenty-four children with a diagnosis of meningococcal septicaemia and 10 controls with noninfectious critical illness admitted to the Royal Liverpool Children's Hospital were included. Sweat collection was by pilocarpine iontophoresis in the acute phase of the illness (days 1-5) and on follow up. Sodium and chloride concentrations were determined by flame photometry. RESULTS: In patients with meningococcal septicaemia, sweat sodium and chloride concentrations were significantly higher in the acute compared with the recovery phase, with a mean (SD) of 31.0 (14.6) mmol L(-1) in the acute vs. 19.6 (10.2) mmol L(-1) on recovery for sodium and 21.0 (12.1) mmol L(-1) in the acute vs. 11.8 (4.9) mmol L(-1) on recovery for chloride (P < 0.01, t-test, for sodium and chloride). Sweat sodium and chloride were significantly higher in patients with meningococcal disease compared with controls and in the acute phase in patients with septicaemia-related pulmonary oedema [mean (SD) sodium: 41.0 (15.4) mmol L(-1) and chloride: 28.8 (14.3) mmol L(-1)] compared with septic patients without [mean (SD) sodium: 24.5 (10.1) mmol L(-1) and chloride: 15.3 (7.9) mmol L(-1)] (P < 0.01 for sodium and chloride). CONCLUSIONS: This is the first study to provide in vivo evidence of reduced epithelial sodium transport in children with septicaemia and of its association with pulmonary oedema.

Child↗

Postpartum thyroiditis. A clinical, histologic, and immunopathologic study of 15 cases.

Fifteen specimens from 15 patients with clinically and laboratory-proven postpartum thyroiditis were examined histologically; 8 specimens were obtained during the hypothyroid phase and the other 7 during the recovery euthyroid phase. All specimens showed focal or diffuse chronic thyroiditis. In the eight specimens taken during the hypothyroid phase and four specimens during the early recovery phase, follicular disruption and hyperplastic change of the follicle were common and characteristic histologic features. In the three specimens taken during the late recovery phase, only focal infiltration of lymphocytes was observed. This histologic change resembled that in spontaneous silent thyroiditis, as shown in the authors' previous study. The authors believe that postpartum thyroiditis and spontaneous silent thyroiditis may fit the same category clinically and histologically. In addition to performing the histologic examination, the authors examined the intrathyroidal lymphocyte subsets and HLA-DR antigen expression in the follicular cells immunohistochemically and compared them with those in chronic thyroiditis (usual type). In postpartum thyroiditis, a significant increase of helper-T-cell numbers and increased expression of HLA-DR antigen in the follicular cells were observed, suggesting an enhancement of autoimmune reactivity.

Adult↗

Pharmacodynamics of subarachnoid hyperbaric 5% lignocaine.

Twenty male patients (55 to 85 yr) undergoing cystoscopy received spinal anaesthesia with either 75 mg (n = 10) or 100 mg of hyperbaric lignocaine 5% under standardised conditions. Plantar flexion muscle power was recorded during onset and offset of anaesthesia using a load cell interfaced with a computer (PFPD) and these data were compared with intermittent clinical assessments of spinal anaesthesia. Onset of paralysis was rapid and complete with motor power declining exponentially to 5% of preoperative values by 5 minutes in all patients. Extent of block to cold and pinprick was similar in both dosage groups (median T4), as was the rate of block onset. Block regression was complete by three hours in all patients and restitution of plantar flexion motor power was associated with normal thermosensibility at L1 and recovery of the patient's ability to walk and micturate. Recovery of plantar flexion motor power occurred at 95.5 +/- 7.38 min in patients given 75 mg compared with 129 +/- 9.5 min in those given 100 mg lignocaine (P < 0.05). The time between onset and full motor recovery in the 75 mg group (7.2 +/- 1.2 min) was less than the 100 mg lignocaine group (29 +/- 5.1 min) (P < 0.001). The larger dose of lignocaine did not confer any clinical advantage in block onset or intensity and made the onset of recovery less predictable. The Bromage grading, while clinically appropriate during anaesthesia onset, does not provide data relating to the density of block and the PFPD was therefore useful for describing the anaesthesia recovery phase.

Aged↗

Infections and immunodeficiency in bone marrow transplantation.

After allogeneic bone marrow transplantation certain patterns of infectious complications emerge that follow the clinical course, are correlated to the immunobiology of transplantation and are almost predictable in their character and expression. The preparative regimen, designed to generate complete aplasia, will be associated with severe and sometimes life-threatening bacterial infections, predominantly with Gram-negative organisms derived from bowel flora, but also Gram-positive skin saprophytes. In this early aplastic phase, life-threatening viral infections are less common, consisting mainly of herpes simplex and possibly Epstein-Barr stomatitis and BK papovavirus cystitis. Systemic infections with invasive filamentous fungi are rare and are seen only when the induced aplasia is markedly prolonged. Once early marrow recovery has been achieved, systemic infections will generally disappear unless acute graft-vs.-host disease develops. This complication, which will lead to the breakdown of natural barriers such as skin and gastrointestinal epithelium and the marked impairment of all systemic defense mechanisms, can cause polymicrobial infections as well as set the stage for life-threatening viral infections. Such opportunistic viral infections, leading to either interstitial pneumonia or hemorrhagic gastroenteritis, are the major threat in the early recovery phase after engraftment has taken place. Usually caused by cytomegalovirus and rotavirus, respectively, these infections are the primary expression of the severe combined immunodeficiency post transplant, statistically associated with the presence of acute graft-vs.-host disease and amenable to immunologic manipulations. With the recovery of cellular and humoral immune function derived from transplanted donor lymphoid cells, the third phase of infectious complications is reached, covering 3 months to 2 years post grafting.(ABSTRACT TRUNCATED AT 250 WORDS)

Anti-Bacterial Agents↗

Temporal evolution of body surface map patterns following acute inferior myocardial infarction.

We studied the evolution of body-surface potential map (BSPM) patterns in 32 patients following first acute inferior myocardial infarction. Initial BSPMs were obtained at a mean of 79 hours post-infarction; follow-up BSPMs, a mean of eight months post-infarction. Temporal area-of-difference maps, constructed by subtracting initial from follow-up group-mean BSPMs, revealed reciprocal changes over the superior and inferior torso for both Q-zone and ST-segment time-integral distributions. The temporal changes in Q-zone patterns were small but definite: over the inferior torso there was a relative gain in Q-zone values and, over the superior torso, a relative decrease. In contrast, there were marked spatial and quantitative changes of ST-segment distributions during the follow-up period. Over the superior torso, particularly anteriorly, there was a gain in ST-segment values; over the inferior torso, a decrease. With the small temporal changes in Q-zone time-integral distributions, individual Q-zone maps continued to reflect a pattern of inferior myocardial infarction at follow-up. In contrast, the marked temporal changes in ST-segment time-integral distributions resulted in individual map patterns at follow-up that were nearly indistinguishable from normal ST-segment maps. The relatively small changes in depolarization time-integral patterns during the early post-infarction period suggest that the Q-zone patterns of the acute phase of myocardial infarction reflect near-irreversible or completed myocardial damage. The marked normalization of repolarization time-integral patterns during the recovery phase suggests, however, that there are also considerable areas of myocardium-at-risk during the early phase of the infarction process which stabilize with time.

Adult↗

Calcium-dependent spontaneously reversible remodeling of brain mitochondria.

An exposure of cultured hippocampal neurons expressing mitochondrially targeted enhanced yellow fluorescent protein to excitotoxic glutamate resulted in reversible mitochondrial remodeling that in many instances could be interpreted as swelling. Remodeling was not evident if glutamate receptors were blocked with MK801, if Ca(2+) was omitted or substituted for Sr(2+) in the bath solution, if neurons were treated with carbonylcyanide p-trifluoromethoxyphenylhydrazone to depolarize mitochondria, or if neurons were pretreated with cyclosporin A or N-methyl-4-isoleucine-cyclosporin (NIM811) to inhibit the mitochondrial permeability transition. In the experiments with isolated brain synaptic or nonsynaptic mitochondria, Ca(2+) triggered transient, spontaneously reversible cyclosporin A-sensitive swelling closely resembling remodeling of organelles in cultured neurons. The swelling was accompanied by the release of cytochrome c, Smac/DIABLO, Omi/HtrA2, and AIF but not endonuclease G. Depolarization with carbonylcyanide p-trifluoromethoxyphenylhydrazone or inhibition of the Ca(2+) uniporter with Ru360 prevented rapid onset of the swelling. Sr(2+) depolarized mitochondria but failed to induce swelling. Neither inhibitors of the large conductance Ca(2+)-activated K(+) channel (charybdotoxin, iberiotoxin, quinine, and Ba(2+)) nor inhibitors of the mitochondrial ATP-sensitive K(+) channel (5-hydroxydecanoate and glibenclamide) suppressed swelling. Quinine, dicyclohexylcarbodiimide, and Mg(2+), inhibitors of the mitochondrial K(+)/H(+) exchanger, as well as external alkalization inhibited a recovery phase of the reversible swelling. In contrast to brain mitochondria, liver and heart mitochondria challenged with Ca(2+) experienced sustained swelling without spontaneous recovery. The proposed model suggests an involvement of the Ca(2+)-dependent transient K(+) influx into the matrix causing mitochondrial swelling followed by activation of the K(+)/H(+) exchanger leading to spontaneous mitochondrial contraction both in situ and in vitro.

Animals↗

High levels of circulating haemopoietic stem cells in very early remission from acute non-lymphoblastic leukaemia and their collection and cryopreservation.

Circulating myeloid progenitor cells (PB CFU-GM) were measured in the peripheral blood of 13 patients with acute non-lymphoblastic leukaemia (ANLL) as they entered first remission. The mean of the recorded peak levels was 2796 X 10(3) CFU-GM/l, representing a 25-fold increase above the mean value in normal subjects. These elevated levels of PB CFU-GM occurred regularly during the very early remission phase when platelet counts rose rapidly. Five of the patients had PB mononuclear cells collected by continuous-flow leukapheresis during this early recovery phase. CFU-GM were assayed as a measure of the number of haemopoietic stem cells in each collection. The cells were concentrated and then cryopreserved in liquid nitrogen. Leukapheresis was also performed on five normal subjects for comparison. Low numbers of CFU-GM were harvested from normal subjects, mean 0.33 +/- 0.06 X 10(4) CFU-GM/kg body weight for each leukapheresis. In ANLL patients entering remission, however, very large numbers of CFU-GM were regularly harvested. A mean of 11 +/- 2 X 10(4) CFU-GM/kg body weight were cryopreserved after each leukapheresis, representing 5 times the number of CFU-GM considered necessary for successful autologous haemopoietic reconstitution. Haemopoietic stem cell viability was assessed after varying periods of cryopreservation. There was no significant stem cell loss after up to 24 months storage. Thus, it is possible to collect and cryopreserve large numbers of CFU-GM and by inference pluripotent haemopoietic stem cells from the peripheral blood of patients with ANLL during very early remission. The possible biological and therapeutic implications are discussed.

Acute Disease↗

The effects of propofol anesthesia on transcortical electric evoked potentials in the rat.

The effects of halogenated anesthetic agents on somatosensory and motor evoked potentials (MEP) have been documented previously. Intravenous anesthetic propofol has not yet been used during MEP monitoring. This study investigates the effects of propofol on transcortical MEP in rats during bolus, infusion, and recovery conditions. After baseline MEP recordings, animals received a hetastarch bolus, followed by a propofol (10 mg/kg) bolus dose. A propofol infusion (10 mg/kg/h) and a hetastarch infusion were then begun. MEP recordings were obtained after the propofol bolus, during the infusion, and after a 30-minute recovery phase. Blood pressure readings remained stable. MEP onset latency increased, and amplitude decreased. Response duration diminished. All values returned towards the baseline during recovery. Our results show that the effects of propofol on MEPs are similar to its effects on somatosensory evoked potentials. Propofol seems to be a reasonable agent for use during intraoperative MEP monitoring and should be further investigated for use during spinal cord monitoring in humans.

Anesthesia, General↗

Where are we headed? Facing the challenge of elderly trauma.

1. The elder population, in comparison with younger populations, not only suffers different types of trauma injury, but also responds differently to their injuries. 2. Nursing care in the resuscitation phase includes careful assessment to evaluate physiologic trends and patterns of response. Ideally, this is done, along with treatment of injuries, within the first hour following trauma. 3. During the first 24 hours post-trauma, a hypermetabolic state occurs approximating twice the normal state. Within 24 to 96 hours postinjury, the body remains acutely catabolic and stressed, but hemodynamic stability is achievable. 4. While strict attention is given to the prevention of infection throughout the resuscitation phase, sepsis remains one of the most serious complications facing the trauma patient. Pain also cannot be dissociated from the acute to the recovery phase of the illness.

Aged↗

[Efficacy of anticonvulsants on acute encephalitis with refractory, repetitive partial seizures (AERRPS)].

The first purpose of this study is to propose a new clinical entity, acute encephalitis with refractory, repetitive partial seizures (AERRPS), which satisfy the following five criteria: 1. a prolonged acute phase of more than 2 weeks; 2. partial seizures of the same seminology persisting from the acute phase to the convalescence; 3. seizures frequently evolving into convulsive status especially during the acute phase; 4. marked intractableness of seizures; 5. exclusion of related disorders such as known viral encephalitis or metabolic disorders. The second purpose is to evaluate the efficacy of therapeutic agents on AERRPS. We reviewed 21 cases reported previously, as well as one patient seen by us. Based on the data, we recommend that patients with AERRPS should be under a high dose intravenous barbiturate during the acute phase, followed by a high dose of phenobarbital or phenytoin in the convalescence. Clonazepam, zonisamide, and potassium bromide were sometimes effective during the recovery phase.

Acute Disease↗

[Protein catabolism and tourniquet shock: the role of proteolytic enzymes].

In the plasma and/or serum ultrafiltrates of a 20-year-old patient with tourniquet shock and post-traumatic acute renal failure it was possible to identify free proteolytic activity during the oligoanuric phase. Plasma alpha 2-macroglobulin values were significantly lowered, whereas the plasma concentrations of antithrombin III were unchanged. alpha 1-Antitrypsin values, however, were markedly enhanced. In contrast, urinary excretion of alpha 1-antitrypsin and antithrombin III were enhanced during the oligoanuric phase. Addition of kallikrein and/or trypsin resulted in strong inhibition of urinary proteolytic activity. These effects were not seen during the polyuric and recovery phase. From our results it can be concluded that proteolytic enzymes may be involved in protein catabolism of patients with tourniquet shock and hypercatabolic acute renal failure.

Acute Kidney Injury↗