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PubMed1998

Water and electrolyte intake and output in conditioned Thoroughbred horses transported by road.

The objectives of this trial were to measure the water and electrolyte intake and loss, of horses during road transportation in relatively hot environmental conditions. Six mature, Thoroughbred horses in full training were used in a balanced crossover design. The horses were conditioned on a treadmill for 6 weeks before the start of the trial in order to simulate the type of horse that is transported most often over long distances in South Africa. The horses were assigned randomly to one of 2 treatment groups. On a particular day 3 horses were transported, while the other horses served as controls. One month was allowed before the crossover. Horses in the 'transport group' were transported by tarred road in a circular route over 600 km. This allowed the standardisation of measurements and use of the same instruments in both groups. Data were collected in each treatment group during transportation that lasted for 8 h (transport phase) and for 6 h after travelling (recovery phase). The following data were collected or calculated: Water and electrolyte (sodium, potassium and chloride) intake and output, changes in bodyweight and feed consumption. Although water was always available, the transport group failed to drink during transit. Based on bodyweight, the transported horses were 3% dehydrated at the end of transit. This bodyweight loss was corrected within one hour after their return due to a significantly higher water intake compared to control horses. The feed intake in the transported horses was unaffected during travelling, but was decreased for 6 h following transportation. Urinary water loss was similar in the 2 treatment groups during and following transportation. The faecal water loss decreased in the transported horses and remained lower than the control group for 6 h following transit. Total sodium and chloride intake were unaffected, while the potassium intake was decreased during transportation. Sodium and potassium loss via the faeces and urine during the transport period were similar in the 2 treatment groups, whereas potassium output in the transport group was significantly decreased during the recovery period of the study. It was concluded that transportation by road affected the water and electrolyte balance of conditioned horses for a period up to 6 h after travelling.

Animals↗

PubMed1994

Baseline and fear-potentiated startle in panic disorder patients.

The present study investigated whether patients with panic disorder had an increase in the startle response and whether this effect, if present, was specific to anticipatory anxiety. The eyeblink component of the acoustic startle reflex was measured in a paradigm involving the anticipation of electric shocks (fear-potentiated startle) in 34 patients with panic disorder and 49 healthy controls. Startle was also recorded in the absence of specific threat at the beginning and at the end of the testing. The testing consisted of three phases: adaptation, fear-potentiated startle, and recovery. In the adaptation and recovery phases, startle stimuli were delivered in the absence of threat. In the fear-potentiated startle phase, startle stimuli were delivered in threat conditions, when subjects anticipated shocks, and in safe conditions that predicted the absence of shocks. Startle was larger in the younger patients (age < 40 years old) compared to the younger controls throughout the testing. The difference reached significance only during the fear-potentiated startle phase, however. Startle was nonsignificantly reduced in the older patients (age > or = 39 years old), compared to the older controls. The results are discussed in terms of the contextual effects of the experimental setting.

Adolescent↗

PubMed1998

The pattern of cytokine gene expression in lymphoid organs and peripheral blood mononuclear cells of mice with experimental allergic encephalomyelitis.

We previously observed Th1-dominated response in the central nervous system (CNS) of mice during the course of experimental allergic encephalomyelitis (EAE) with a semiquantitative reverse transcriptase-polymerase chain reaction (RT/PCR) analysis. We report here that mRNA levels for both inflammatory cytokines including interleukin (IL)-1beta, IL-2, IL-6, interferon (IFN)-gamma, tumor necrosis factor (TNF)-alpha and TNF-beta and immunoregulatory cytokines including IL-4, IL-10 and transforming growth factor (TGF)-beta were up-regulated in the preclinical and/or acute phase but down-regulated in the recovery phase of EAE in lymph node (LN) of mice. Similar profiles for cytokine mRNA levels were also observed in spleen and peripheral blood mononuclear cells (PBMC). The present study also showed that a significant down-regulation of the mRNA level for IL-6 in the acute phase as compared with the preclinical phase, and a significant reduction of the mRNA level for TGF-beta in the preclinical and acute phase as compared with the corresponding mRNA levels in the control mice treated with complete Freund's adjuvant alone were characteristic in peripheral immune organs of mice with EAE. These results indicate that no particular bias in cytokine production occurred in peripheral immune organs of mice with actively induced relapsing EAE, and that the relative reduction in production of TGF-beta or IL-6 in peripheral circulation might participate in the induction or remission of EAE, respectively. Our results using the animal model of multiple sclerosis (MS) suggested that the mRNA levels for IL-6 and TGF-beta in PBMC from patients with MS may be a good indicator to assess the disease activity or to predict relapse.

Animals↗

PubMed1992

Steady-state and dynamic properties of cardiac sodium-calcium exchange. Sodium-dependent inactivation.

Sodium-calcium exchange current was isolated in inside-out patches excised from guinea pig ventricular cells using the giant patch method. The outward exchange current decayed exponentially upon activation by cytoplasmic sodium (sodium-dependent inactivation). The kinetics and mechanism of the inactivation were studied. (a) The rate of inactivation and the peak current amplitude were both strongly temperature dependent (Q10 = 2.2). (b) An increase in cytoplasmic pH from 6.8 to 7.8 attenuated the current decay and shifted the apparent dissociation constant (Kd) of cytoplasmic calcium for secondary activation of the exchange current from 9.6 microM to < 0.3 microM. (c) The amplitude of exchange current decreased synchronously over the membrane potential range from -120 to 60 mV during the inactivation, indicating that voltage dependence of the exchanger did not change during the inactivation process. The voltage dependence of exchange current also did not change during secondary modulation by cytoplasmic calcium and activation by chymotrypsin. (d) In the presence of 150 mM extracellular sodium and 2 mM extracellular calcium, outward exchange current decayed similarly upon application of cytoplasmic sodium. Upon removal of cytoplasmic sodium in the presence of 2-5 microM cytoplasmic free calcium, the inward exchange current developed in two phases, a fast phase within the time course of solution changes, and a slow phase (tau approximately 4 s) indicative of recovery from sodium-dependent inactivation. (e) Under zero-trans conditions, the inward current was fully activated within solution switch times upon application of cytoplasmic calcium and did not decay. (f) The slow recovery phase of inward current upon removal of cytoplasmic sodium was also present under the zero-trans condition. (g) Sodium-dependent inactivation shows little or no dependence on membrane potential in guinea pig myocyte sarcolemma. (h) Sodium-dependent inactivation of outward current is attenuated in rate and extent as extracellular calcium is decreased. (i) Kinetics of the sodium-dependent inactivation and its dependence on major experimental variables are well described by a simple two-state inactivation model assuming one fully active and one fully inactive exchanger state, whereby the transition to the inactive state takes place from a fully sodium-loaded exchanger conformation with cytoplasmic orientation of binding sites (E1.3Ni).

Adenosine Triphosphate↗

PubMed1990

Analgesic efficacy of i.m. alfentanil.

We have studied the analgesic, respiratory, cardiovascular and sedative effects of alfentanil 30 micrograms kg-1 i.m. in two experiments in six healthy volunteers. In the first experiment, recordings were made up to 120 min after injection. Thresholds (sensory and pain) and pain-related evoked potentials (amplitude and latency) to cutaneous argon laser stimulation were used for quantitative assessment of onset, efficacy and duration of analgesia. Pain was significantly reduced from 5 to 60 min after injection. The onset phase of analgesia was faster than the recovery phase. In the second experiment, the alfentanil-induced analgesia was antagonized by naloxone 0.4 mg i.v. The reaction time to pain was prolonged significantly 15 min after injection, whereas the latency of the pain-related potential remained constant. No clinically significant changes were observed in respiratory and cardiovascular measurements.

Adult↗

PubMed1989

Development of behavioral distress in reaction to acute pain in two cultures.

Studied developmental and gender differences in distress behavior during separate phases of a medical treatment in 2 cultures. Distress reactions of 175 children with cancer (age 8 months-18 years 7 months) were observed during bone marrow aspirations (BMA) in 2 different treatment centers (one in the United States, one in The Netherlands) using a behavioral checklist (Procedure Behavioral Rating Scale). The BMAs contained a preparatory phase, the actual needle introduction, and a recovery period. In both cultures almost all separate distress behaviors occurred less in older children, except for increasing muscle tension during the actual puncture. Distress was highest during the needle introduction and significantly lower during the preparatory and recovery phases; in addition, somewhat different patterns of distress behavior were found in separate phases. Culture and sex differences were found. The latter were less robust than developmental and phase differences.

Adolescent↗

PubMed2002

Use of dynamic negative airway pressure (DNAP) to assess sedative-induced upper airway obstruction.

BACKGROUND: Traditional methods of assessing ventilatory effects of sedative agents do not measure their propensity to cause upper airway obstruction (UAO). The primary objective of this study was to develop a method, using dynamic negative airway pressure (DNAP), for replicating UAO during deep sedation. METHODS: A state of deep sedation (defined as an Observer Assessment of Alertness and Sedation score of 3 and a bispectral index < 80) was attained in 10 healthy volunteers, aged 19-41, using midazolam. Volunteers breathed through a chamber connected to a regulated source of negative pressure that was gradually adjusted downward to produce UAO based on maximal inspiratory flow. The study consisted of three phases: A control phase while awake, a study phase during midazolam deep sedation, and a recovery phase after flumazenil administration. RESULTS: During the control phase no subject demonstrated airway obstruction at negative pressures to -30-cm H2O. All subjects exhibited complete UAO during DNAP episodes while sedated. Negative pressures required to cause complete UAO (Pcrit) ranged from -2 to -14 cm H2O. After administration of flumazenil, all subjects attained full consciousness within 5 min and did not demonstrate UAO at negative pressures to -30-cm H2O. CONCLUSIONS: Dynamic Negative Airway Pressure is a useful method for provoking midazolam-induced UAO, and may potentially be used to compare the potential for different sedatives and patient factors to cause UAO. Flumazenil was completely effective in reversing the potential for midazolam to cause UAO.

Adult↗

PubMed1999

Short-term potentiation of carotid chemoreflex: an NMDAR-dependent neural integrator.

Repetitive stimulation of the carotid sinus nerve (CSN) elicits a short-term potentiation (STP) of the reflex response in respiratory motor output in mammals. The input-output transformation approximates a leaky integrator with a time constant of several seconds. Here, we showed that STP induced by CSN stimulation in rats was manifested in the reflex response in the amplitude of rhythmic phrenic nerve activity as well as its duration. Moreover, pharmacological blockade of NMDA receptors (NMDAR) resulted in marked increases in the time constants of the equivalent neural integrator in both the STP induction phase (by 10- to 20-fold) and recovery phase (by 1- to 5-fold). Thus, NMDAR serves as a molecular switch that facilitates the integrative processing of CSN inputs by STP.

Animals↗

PubMed2003

Role of neutralizing antibody in the pathogenesis of zoster and the correlation of severity with anti-gE: gI antibody response.

Antibody response to varicella-zoster virus glycoproteins and neutralizing antibodies were examined to correlate them with the severity of the zoster. Antibody rise to whole viral antigen was observed in 17 of 19 patients, that to gE: gI was not increased in 7 patients, and antibody to gE: gI in severe cases was significantly lower compared with mild cases in the convalescent phase than in the acute phase (p<0.05 Fisher's exact test). Antibody rise to gE: gI was well correlated with limited development of zoster lesions and, in contrast, antibody titer without rise was associated with increased severity and wider development of zoster lesions. As gE is the most abundant glycoprotein in the infected cells, the antibodies may be consumed in severe and widespread lesions, resulting in an antibody response to gE: gI without a rise. When the ratio of neutralizing antibody to anti-gE: gI antibody titers in the acute phase was compared with that in the recovery phase, the former was significantly lower in the severe cases than the latter (p=0.0082 Student t-test). This suggested that neutralizing antibody was specifically consumed in the acute phase of zoster among the anti-VZV antibodies. The role of humoral immunity in the pathogenesis of zoster might have been reflected in the antibody response to the neutralizing antibody in the acute phase and antibody to gE: gI in the severe cases.

Adult↗

PubMed1996

Renal and systemic hemodynamics, in falciparum malaria.

Renal and systemic hemodynamics, plasma arginine vasopressin, plasma renin activity, plasma norepinephrine, blood volume and water loading test were studied in 10 patients with falciparum malaria without renal failure. Six patients responded to water load normally, while 4 patients had a decreased response to water load. The patients with a normal water load response had normal renal and systemic hemodynamics and a normal hormonal profile. The patients with a decreased response to water load had hyponatremia, hypervolemia, high cardiac index, low systemic vascular resistance, high plasma arginine vasopressin, high plasma renin activity, high plasma norepinephrine, low creatinine and p-aminohippurate clearances, low urine sodium and high urine osmolality. They had a lower mean arterial pressure during the acute phase of the disease than during the recovery phase. The findings suggest that a decreased response to water load is due to peripheral vasodilatation which results in a decreased effective blood volume leading to the release of vasopressin and norepinephrine, increased renin activity and decreased renal hemodynamics.

Adult↗

PubMed1981

[Renin-angiotensin system in acute hepatitis (author's transl)].

Plasma renin activity (PRA) and plasma concentrations of angiotensin II (A.II) were measured radioimmunologically in 31 patients suffering from acute virus hepatitis during the course of the disease. Average PRA and A II values did not differ from values of normal persons, neither during the acute phase of the disease nor during the recovery phase though there were deviations from the normal in single cases. PRA and A II were correlated significantly (r = 0,86, p < 0,001), but there was no correlation to the levels of transaminases. There was no indication, that A II plasma levels were lowered because of increased activity of angiotensinases. In some cases PRA and A II were elevated; this however was probably due to increased renin secretion following changes in water and electrolyte balance rather than to decreased hepatic metabolism of renin.

Adolescent↗

PubMed1995

Effect of an abdominal binder during wheelchair exercise.

The purpose of this study was to determine whether use of an abdominal binder would affect oxygen uptake, trunk range of motion, and duration of the stroke phase during wheelchair propulsion. The subjects were six paraplegic wheelchair athletes with T1-T6 injuries and no abdominal muscle function. Each subject performed two trials, one while wearing the binder and one without the binder. Each trial consisted of submaximal and maximal exercise tests conducted on wheelchair rollers. Oxygen uptake was determined by open circuit spirometry while heart rate was determined by telemetry. Max VO2 values averaged 2.51 l.min-1 while average maximum heart rate values were 190 b.min-1. A 3-D video-based motion analysis system was used to obtain kinematic parameters of wheelchair propulsion. In general, 30% of the cycle time was comprised of the stroke phase, while 70% was comprised of the recovery phase across speeds. There were no statistically significant effects of the abdominal binder on any of the cardiovascular or kinematic variables at submaximal or maximal levels of exercise. Under the conditions of this laboratory investigation, it appears that an abdominal binder does not alter physiological or selected biomechanical measures in highly trained athletes.

Abdomen↗

PubMed1976

Effect of chronic pentobarbital treatment on the sleep patterns of squirrel monkeys.

Following a 30-day baseline, 60 days of sodium pentobarbital treatment (5 mg/kg) were given to squirrel monkeys 2 h prior to the start of a 12-h recording of EEG and EOG. Following the drug-treatment phase, an additional 30-day period was used to determine the rate of recovery. Repeated pentobarbital treatment significantly reduced awake time and slow wave sleep while it elevated the time spent in drowsy and light sleep. The recovery phase indicated a brief recovery of rapid eye movement sleep while the other stages failed to return to baseline levels. The cyclical nature of the changes observed with chronic pentobarbital suggest the importance of circadian fluctuations in the study of chronic drug treatment and the sleep-wakefulness process.

Animals↗

PubMed1996

Dynamics of TGF-beta 3 peptide activity during rat alveolar epithelial cell proliferative recovery from acute hyperoxia.

Hyperoxia causes a reproducible pattern of lung injury and recovery, characterized by proliferation of type II alveolar epithelial cells (AEC2) during the recovery phase. We measured TGF-beta peptide production by AEC2 and macrophages from lungs of adult male rats exposed to 100% oxygen for 48 h and then allowed to recover for up to 72 h in room air. TGF-beta peptide activity levels were measured using the PAI-1 promoter-luciferase mink lung epithelial cell assay and characterized with peptide specific inhibitory antibodies. Control AEC2 produced 997 +/- 54 pg active TGF-beta x 10(6) cells-1.24h-1 (mean +/- SD), of which > 70% was TGF-beta 3, while cultured macrophages produced 58 +/- 17 pg active TGF-beta x 10(6) macrophages-1.24 h-1, > 80% of which was TGF-beta 1. During hyperoxia and recovery, active TGF-beta 3 production by AEC2 decreased by 75%, with a nadir at 24 h recovery (P < 0.005). In contrast, TGF-beta peptide activity increased from undetectable levels in lung lavage from control rats to a peak of 1,470 +/- 743 pg/rat after 48 h oxygen exposure and 24 h recovery, while lavaged macrophage TGF-beta production in culture also increased threefold to a peak of 150 +/- 5 pg. 10(6) cells-1. 24 h-1 after 48 h oxygen exposure (P < 0.005). The nadir of active TGF-beta 3 production by AEC2 coincided with the peak of the AEC2 proliferative phase of repair as determined by BrdU incorporation and FACS analysis of freshly isolated AEC2. We conclude that active TGF-beta 3 production by AEC2 is dynamically downregulated during the proliferative phase of recovery from acute hyperoxic injury in rat. We speculate that decreased autocrine negative regulation of AEC2 proliferation by TGF-beta 3 may facilitate AEC2 proliferation during recovery from acute hyperoxic injury.

Acute Disease↗

PubMed1997

Predominant T-helper 1 cytokine profile of hepatitis B virus nucleocapsid-specific T cells in acute self-limited hepatitis B.

The cytokine pattern secreted by T cells on viral antigen recognition is believed to exert a profound influence on both the type of disease caused by the infecting agent and the final outcome of the viral infection. To characterize the cytokine pattern associated with spontaneous resolution of acute hepatitis B, we analyzed interferon gamma (IFN-gamma), interleukin (IL)-4, and IL-5 production by a wide series of hepatitis B virus (HBV) nucleocapsid-specific T-cell lines (34 lines) and T-cell clones (71 clones) derived from the peripheral blood of 13 patients during the acute or recovery phase of hepatitis B (2 and 7 of them were studied only in the recovery or the acute phase, respectively, and 4 during both). Most T-cell lines (67%) and clones (77%) isolated during the acute phase of infection expressed a T-helper (Th) 1 cytokine profile dominated by the production of IFN-gamma. A larger proportion (74%) of T-cell lines produced several years after resolution of hepatitis was able to secrete not only IFN-gamma, but also IL-4 and IL-5 (Th0-like cells). Results indicate that the antigen-specific fraction of peripheral blood T cells in acute self-limited hepatitis B selectively secrete Th1-type eytokines, suggesting that Th1-mediated effects may contribute not only to liver cell injury, but probably also to recovery from disease and successful control of infection.

Acute Disease↗

PubMed1999

Role of Kupffer cells in the ethanol-induced oxidative stress in the liver.

These studies test the hypothesis that acute and chronic alcohol intoxication stimulate the release of oxygen-derived radicals in the liver. Male Sprague-Dawley rats received an intravenous bolus followed by continuous infusion of ethanol to maintain blood alcohol level at about 175 mg/dl for 0-18 hr. They were then allowed to recover from this "alcohol binge" and the release of free radicals during the recovery phase was monitored. In the chronic alcohol intoxication model, rats were fed with 40% ethanol in agar blocks for 16 weeks. Acute ethanol intoxication induced two phases of hepatic superoxide release. The first phase peaked during the first 3 hr of alcohol intoxication, while the second phase reached its maximum at 6 hr of recovery following a 12 hr binge. The recovery period was also associated with elevated serum transaminase activity. Kupffer cells were largely responsible for hepatic superoxide release during the first phase, while both Kupffer and hepatic sinusoidal endothelial cells contributed to the second phase of free radical formation. Acute ethanol intoxication did not induce endotoxemia. During chronic alcohol intoxication, increased levels of serum endotoxin, TNF, IL-1, and transaminase were observed and hepatic superoxide anion release was present. Superoxide release by isolated Kupffer cells, blood and hepatic PMNs of alcoholic rats was also significantly enhanced in the chronic alcoholic rats. These data indicate that acute alcohol intoxication may directly stimulate the release of reactive oxygen intermediates, whereas chronic alcohol may elicit free radical generation through enhanced endotoxin influx and cytokine release. These studies further demonstrate that free radicals produced by hepatic non-parenchymal cells are likely to play an important role in the pathogenesis of hepatic injury in susceptible individuals with alcohol-related liver disorders.

Animals↗

PubMed2001

Feasibility of tidal volume-guided ventilation in newborn infants: a randomized, crossover trial using the volume guarantee modality.

BACKGROUND AND AIM: Volume guarantee (VG) is a new composite mode of pressure-limited ventilation, available on the Dräger Babylog 8000 ventilator, which allows the clinician to set a target mean tidal volume to be delivered while still maintaining control over peak airway pressures. This study aimed to investigate the feasibility and efficacy of this mode of ventilation in premature newborn infants with respiratory distress syndrome (RDS). METHODS: Two groups of infants were studied: those receiving synchronized intermittent positive pressure ventilation (SIPPV) in early phase of RDS (group 1) and those in recovery phase of RDS being weaned from artificial ventilation through synchronized intermittent mandatory ventilation (SIMV; group 2). Both groups of infants were studied over a 4-hour period. Before the start of the study, the infants were either receiving SIPPV (group 1) or SIMV (group 2). Infants in group 1 were randomized to either continue on SIPPV for the first hour of the study or to receive SIPPV plus VG for the first hour. Subsequently, the 2 modes were used alternately for the remaining three 1-hour periods. Similarly, infants in group 2 were randomized to either continue on SIMV for the first hour of the study or to receive SIMV plus VG for the first hour. Data on ventilation parameters and transcutaneous carbon dioxide and oxygen were collected continuously. RESULTS: Forty infants were studied, 20 in each group. The mean (standard error) gestational age was 27.9 (0.3) weeks; birth weight was 1064 (60) g. No adverse events were observed during the study. Fractional inspired oxygen during SIMV plus VG was 0.31 (0.3); during SIMV, 0.31 (0.3); during SIPPV plus VG, 0.41 (0.4); and during SIPPV, 0.40 (0.4). Transcutaneous carbon dioxide pressure during SIMV plus VG was 6.0 (2.2) kPa; during SIMV, 5.9 (2.2) kPa; during SIPPV plus VG, 6.4 (2.9) kPa; and during SIPPV, 6.4 (2.8) kPa. Transcutaneous partial pressure of oxygen during SIMV plus VG was 8.4 (8.7) kPa; during SIMV, 8.6 (8.8) kPa; during SIPPV plus VG, 7.6 (4.0) kPa; and during SIPPV, 7.7 (4.2) kPa. None of these differences was statistically significant. The mean (standard error) peak inspiratory pressure used during SIMV was 17.1 (3.4) cm of water; during SIMV plus VG, 15.0 (7.5) cm of water; during SIPPV plus VG, 17.1 (9.3) cm of water; and during SIPPV, 18.7 (8.3) cm of water. The mean airway pressure during SIMV plus VG was 6.5 (3.1) cm of water; during SIMV, 6.9 (2.8) cm of water; during SIPPV plus VG, 9.6 (4.5) cm of water; and during SIPPV, 9.8 (4.6) cm of water. CONCLUSION: VG seems to be a stable and feasible ventilation mode for neonatal patients and can achieve equivalent gas exchange using statistically significant lower peak airway pressures both during early and recovery stages of RDS.ventilation, airway pressure, volume guarantee, tidal volume.

Birth Weight↗

PubMed2003

Delayed introduction of G-CSF after chemotherapy does not affect peripheral blood stem cell yield and engraftment kinetics in children with high-risk malignancies: retrospective study of 45 cases.

We retrospectively compared the effects of two time points of G-CSF (Filgrastim) introduction for PBSC mobilization in 45 children with different malignancies. Seventeen patients received the first G-CSF dose on day 2 or 3 following chemotherapy (group 1). Twenty-eight patients received a "flexible" G-CSF injection schedule when the G-GSF was started at the time of the first platelet count rise during post-chemotherapy recovery phase (group 2). Leukapheresis was performed when WBC recovery reached >2.0 x 10(9)/l or if the peripheral blood CD34(+) cell level was >0.01 x 10(9)/l. A median of 2 (1-4) leukapheresis procedures was performed in both groups to yield a median of 4.2 and 6.1 x 10(6) CD34(+) cells/kg in groups 1 and 2, respectively, which was generally sufficient for auto-transplantation. The proportion of patients with a failure of PBSC collection was similar and G-CSF consumption estimated through the total cycle dose was 2.3 times less in group 2 without increasing infectious risks. The short-term hematological recovery and the early post-transplant course were similar in the two groups. Delayed introduction of G-CSF after chemotherapy allowed PBSC harvest equivalent to that obtained after early G-CSF introduction. This approach could be an interesting alternative in PBSC mobilization but should be assessed by a prospective controlled study.

Adolescent↗