Biomedical subjects

P G Wilcox

Publications and source records attributed to P G Wilcox.

At least 19 recordsLinked to original sources

PubMed2001

Infection with Burkholderia cepacia complex genomovars in patients with cystic fibrosis: virulent transmissible strains of genomovar III can replace Burkholderia multivorans.

Infection with Burkholderia cepacia complex in patients with cystic fibrosis (CF) results in highly variable clinical outcomes. The purpose of this study was to determine if there are genomovar-specific disparities in transmission and disease severity. B. cepacia complex was recovered from 62 patients with CF on > or =1 occasions (genomovar III, 46 patients; genomovar II [B. multivorans], 19 patients; genomovar IV [B. stabilis], 1 patient; genomovar V [B. vietnamiensis], 1 patient; and an unclassified B. cepacia complex strain, 1 patient). Patient-to-patient spread was observed with B. cepacia genomovar III, but not with B. multivorans. Genomovar III strains replaced B. multivorans in 6 patients. Genomovar III strains were also associated with a poor clinical course and high mortality. Infection control practices should be designed with knowledge about B. cepacia complex genomovar status; patients infected with transmissible genomovar III strains should not be cohorted with patients infected with B. multivorans and other B. cepacia genomovars.

Adolescent↗

PubMed2001

Predictability of oxygen desaturation during sleep in patients with cystic fibrosis : clinical, spirometric, and exercise parameters.

BACKGROUND: The purpose of this study was to determine how common sleep-related desaturation with preserved awake resting pulse oximetric saturation (SpO(2)) was in a large cohort of adult cystic fibrosis (CF) patients with variable degrees of pulmonary disease. We then determined whether nocturnal desaturation could reliably be predicted from standard clinical and exercise parameters. METHODS: Seventy CF patients participated in the study (mean [SD] age, 27.3 [8.7] years; women, 54%; percent predicted FEV(1) [%predFEV(1)], 55.7% [23.9%]). Nocturnal, resting, and exercise SpO(2) were measured. Nocturnal oximetry was measured in the patient's home. Maximal oxygen capacity (Vo(2)max) was determined from a graded exercise test on a stationary bicycle ergometer. The Shwachman-Kulczycki (S-K) illness severity score was calculated incorporating categories of functional capacity, physical examination, nutrition, and chest radiograph. RESULTS: Multivariate analysis reported significant differences (p < 0.0001) between pulmonary disease severity and overall distribution of nocturnal SpO(2), with the main difference being for patients with severe pulmonary disease (%predFEV(1) of < 50%) compared to patients with mild or moderate disease in the SpO(2) intervals of 100 to 96% (p < 0.0001) and 90 to 86% (p = 0.0001). Pulmonary function, S-K clinical scores, f1.gif" BORDER="0">O(2)max, and resting and maximal SpO(2) correlated significantly (p < 0.05) with nocturnal SpO(2) levels. Stepwise discriminant analysis identified %predFEV(1) (or S-K scores) and resting SpO(2) as the parameters that could best discriminate patients not likely to experience nocturnal desaturation. Specifically, our equation could predict 91% of cases less likely to nocturnally desaturate, but could only modestly predict those more likely to desaturate (i.e., 26% of cases). CONCLUSIONS: Spirometric parameters and measurements of awake resting oxygenation are of limited utility in predicting nocturnal desaturation. Nocturnal oximetry should be considered in patients with moderate to severe lung disease even with preserved awake resting SpO(2).

Adolescent↗

PubMed1999

Burkholderia cepacia in cystic fibrosis. Variable disease course.

Variable clinical course has been reported with the acquisition of Burkholderia cepacia in patients who have cystic fibrosis (CF). We hypothesized that the perceived worsening with B. cepacia may reflect the underlying severity of pulmonary disease at the time of acquisition. To test this hypothesis, we matched CF patients colonized with B. cepacia with CF patients not colonized with the organism. Two-year pre- and postacquisition data and long-term data were compared. Patients were matched for gender, age (+/- 1 yr), height (+/- 5 cm), weight (+/- 8 kg), percent predicted forced expiratory volume in one second (% pred FEV(1)) (+/- 10%), and pancreatic sufficiency status. Differences in rates of change pre- and postacquisition for FEV(1), FVC, weight, and frequency of intravenous courses were compared within pairs with the Wilcoxon signed rank test. Two-year and long-term survival was compared within pairs with the McNemar test. No significant differences were observed in mean annual rates of change in weight (0.33 and -0.28 kg/yr), % pred FEV(1) (-0.36 and -1.74%/yr), and percent predicted forced vital capacity (% pred FVC) (-3.80 and -2.32%/yr) between B. cepacia and control pairs in 2-yr and long-term postacquisition interval, respectively. Similar rates of change were noted for pre- to postacquisition intervals within pairs for weight (0.17 kg/yr), % pred FEV(1) (-0.16%/yr), % pred FVC (5.02 %/yr). There was a significantly higher rate of intravenous antibiotic courses in B. cepacia cases in the 2-yr and long-term postacquisition interval. Higher mortality was observed in the B. cepacia cases in the long term (p < 0.05). We conclude that colonization with B. cepacia does not necessarily adversely affect pulmonary status, but is associated with reduced long term survival. Whereas previous associations may be attributed to a propensity to colonize those who had more advanced disease, specific strain types of B. cepacia may have enhanced pathogenicity.

Adolescent↗

PubMed1997

Noninvasive positive pressure ventilation in acute respiratory failure of chronic obstructive pulmonary disease.

Noninvasive positive pressure ventilation (NPPV) has reemerged as an effective strategy for reducing morbidity and mortality associated with acute exacerbations of chronic obstructive pulmonary disease (COPD). During acute respiratory failure, dynamic hyperinflation, intrinsic PEEP, and increased airway resistance result in a mechanical workload that exceeds inspiratory muscle capacity. NPPV provides augmentation of alveolar ventilation and respiratory muscle rest. Observational, cohort, and more recently, randomized controlled trials have demonstrated the ability of NPPV to increase the need for endotracheal intubation and decrease complications and mortality. NPPV performs better in COPD patients without significant comorbid illness. It should be initiated during COPD exacerbations if arterial pH is less than 7.35 or if the patient is severely distressed. Pressure support ventilation (10-20 cmH2O) via face mask is likely the optimal technique and, when successful, results in rapid clinical improvement.

Acute Disease↗

PubMed1997

Pregnancy and cystic fibrosis: a case-controlled study.

STUDY OBJECTIVES: Changes in cardiorespiratory and pulmonary function that occur with normal pregnancy along with increased maternal and fetal demands related to cystic fibrosis (CF) may augment morbidity for the woman with CF. Status prior to pregnancy is implicated in pregnancy outcome and maternal life expectancy postpartum. The purpose of this study was to investigate the effect of pregnancy on these patients' course during pregnancy and document prepregnancy status and 2-year postpregnancy survival. DESIGN: Patients with documented pregnancies were matched to nonpregnant CF patients of similar age (+/-2 years), severity of airflow obstruction (percent predicted forced expiratory volume in 1 min [+/-15%]), weight (+/-10 kg), height (+/-5 cm), and pancreatic sufficiency status at 1 year preconception. PATIENTS: Using their 1-year preconception data, seven women with CF and with documented pregnancies were matched to nonpregnant control subjects. All patients were pancreatic insufficient. INTERVENTIONS: Weight, forced expiratory volume in 1 min (% FEV1), FVC, Schwachman-Kulczycki (S-K) and Brasfield scores, sputum cultures, pregnancy outcome, and pulmonary exacerbations were followed from 1 year preconception, during pregnancy, and 2 years postpregnancy. MEASUREMENTS AND RESULTS: Mean weight gain during pregnancy was 5.2 kg. There were no differences between the groups in the rate of decline for pulmonary function or S-K scores over time. Greater rate of decline was noted in the pregnancy group, however, for body weight and Brasfield scores in the postpartum interval. One patient in the pregnancy group died 6 months postpartum. CONCLUSIONS: Pregnancy has little adverse effect on patients with stable CF, but poor outcomes can occur in individuals with more advanced disease.

Adult↗

PubMed1996

Effect of the beta-agonist clenbuterol on dexamethasone-induced diaphragm dysfunction in rabbits.

The present study was designed to examine whether clenbuterol (CLEN) could reduce dexamethasone (DEX)-induced diaphragm dysfunction. We studied four groups of New Zealand white (NZW) rabbits, each receiving one of the following daily injections subcutaneously for 2 wk: saline (control), DEX 3 mg/kg, DEX 3 mg/kg + CLEN 2 mg/kg, and CLEN 2 mg/kg. Diaphragm fiber cross-sectional areas (CSA) were measured. Twitch transdiaphragmatic pressure (Pdi) and tetanic Pdi were measured during bilateral phrenic stimulation both before and after 60 min of inspiratory resistive loading (IRL). DEX produced a marked atrophy of type IIa and type IIb diaphragm fibers. This diaphragm atrophy was prevented by CLEN in the DEX plus CLEN group. CLEN alone increased CSAs of all three types of diaphragm fibers. Significant reductions in twitch Pdi and tetanic Pdi at all stimulation frequencies both before and after IRL were observed similarly in the DEX group as well as in the DEX plus CLEN group compared with the control animals. We conclude that DEX produces significant diaphragm atrophy and decreases diaphragmatic contractility. CLEN produces hypertrophy of the diaphragm and minimizes diaphragm atrophy induced by DEX, but it has no demonstrable protective effect on DEX-induced diaphragm dysfunction.

Adrenergic beta-Agonists↗

PubMed1995

Ventilatory muscle strength and endurance in myasthenia gravis.

Patients with generalized myasthenia gravis (MG) often have associated ventilatory muscle involvement. It is not known whether patients with isolated ocular muscle involvement have identifiable involvement of their ventilatory muscles. Most studies have assessed muscle involvement by measuring muscle strength; however, we hypothesized that measures of ventilatory muscle endurance may be more sensitive tests of ventilatory muscle involvement in myasthenia gravis. We studied 17 patients with myasthenia gravis (four with ocular involvement alone and 13 with varying degrees of generalized myasthenia gravis). Spirometry, ventilatory muscle strength (maximum inspiratory and expiratory pressures (MIP and MEP)) and endurance (2 min incremental threshold loading test) were measured before and 20 min after i.m. neostigmine. We compared the results with those of 10 normal controls. We found no difference between patients with isolated ocular involvement and controls. Ocular myasthenia gravis patients did not improve after neostigmine. The patients with generalized myasthenia gravis had reduced baseline ventilatory muscle strength (MIP 67 cmH2O (70% of predicted), MEP 86 cmH2O (50% of pred) and endurance (mean maximal load achieved = 246 g, mean pressure at highest load (P) = 19.4 cmH2O) compared with controls. After neostigmine, there was a significant increase in MIP in patients with generalized myasthenia gravis and a trend towards an increased MEP. As a group, the patients with generalized myasthenia gravis did not demonstrate a change in their ventilatory muscle endurance after neostigmine; however, there was considerable interpatient variability in response. We conclude that patients with isolated ocular MG have normal ventilatory muscle strength when tested conventionally.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1994

Decrease in left ventricular contractility after tumor necrosis factor-alpha infusion in dogs.

Whether systolic contractility or diastolic compliance changes soon after tumor necrosis factor-alpha (TNF-alpha) exposure is not known. Accordingly, we measured hemodynamics, left ventricular contractility using the slope of the end-systolic pressure-volume relationship, and diastolic pressure-volume relationships in six control dogs and in six dogs receiving 60 micrograms.kg-1.h-1 i.v. of TNF-alpha. Mean aortic pressure decreased by 22% 1 h after TNF-alpha infusion and remained decreased (P < 0.05). Cardiac output increased by 19% 1 h after TNF-alpha infusion and remained significantly greater than control values (P < 0.05). Left ventricular contractility decreased by 23% (P < 0.05) 1 h after TNF-alpha infusion and decreased by 52% (P < 0.01) 5 h after TNF-alpha infusion. The diastolic pressure-volume relationship did not change in the TNF-alpha group or the control group. Ejection fraction did not change after TNF-alpha infusion despite the decrease in contractility because afterload decreased. We conclude that TNF-alpha is important in causing the hypotensive, hyperdynamic circulation of sepsis. The new finding that left ventricular contractility is decreased shortly after TNF-alpha infusion suggests that TNF-alpha, or another mediator released very soon after TNF-alpha, is an important myocardial depressant factor.

Animals↗

PubMed1994

Tumor necrosis factor alpha decreases in vivo diaphragm contractility in dogs.

In this study, we hypothesized that tumor necrosis factor alpha (TNF alpha) is an important mediator of sepsis-related impairment in diaphragm contractility (1-2). In 12 anesthetized, ventilated dogs, bipolar stimulating electrodes were placed on the phrenic nerves and diaphragm electromyographic activity (EMG) and shortening were recorded with needle electrodes and piezoelectric crystals, respectively. Transdiaphragmatic pressure (Pdi) was also recorded using esophageal (Pes) and abdominal balloon catheters (Pdi = Pab-Pes). Dogs were randomized to receive saline injection (n = 6), or TNF alpha 60 micrograms/kg (n = 6). All parameters were recorded hourly for 6 h. Mean arterial blood pressure decreased 1 h after infusion in TNF alpha animals (p < 0.05) with no significant change thereafter. Cardiac output increased early after TNF alpha infusion (p < 0.05) and remained at greater than baseline values at study termination. Diaphragm pressure generation and costal shortening decreased progressively from 3 to 6 h post TNF alpha infusion (p < 0.05) with no significant change in control animals. Compound diaphragm action potential in response to supramaximal phrenic stimulation decreased in TNF alpha animals (p < 0.01) with no significant change in control animals 3 and 6 h postinfusion. We conclude that TNF alpha infusion was associated with significant declines in isotonic and quasi-isometric diaphragm contraction and that this could be explained, at least in part, by impaired neuromuscular transmission.

Action Potentials↗

PubMed1994

Respiratory dysrhythmias in patients with tardive dyskinesia.

Tardive dyskinesia (TD) is a disorder characterized by abnormal involuntary movements and associated with neuroleptic therapy. To determine whether the respiratory muscles are involved in this condition, we compared the breathing pattern of ten patients with TD with ten patients with chronic schizophrenia receiving neuroleptic therapy without evidence of TD, and ten age-matched normal control subjects during resting tidal breathing, forearm pronation-supination (a maneuver designed to elicit the abnormal movements of TD), and breathing to a set frequency. Breathing patterns were also assessed in seven patients with TD during a progressive incremental exercise test and an overnight polysomnogram. Patients with TD had an irregular tidal breathing pattern, with a greater variability in both tidal volume and time of the total respiratory cycle (TTOT). Both groups of patients receiving neuroleptic therapy had a rapid shallow breathing pattern when performing forearm pronation-supination compared with control subjects. There were no differences between any of the subject groups when breathing to a set frequency. The patients with TD had a normal response to progressive exercise and inspiratory time and TTOT values were less variable during non-rapid eye movement sleep compared with wakefulness. We conclude that patients with TD have irregular rapid shallow breathing which is less variable during sleep and does not limit their exercise performance.

Adult↗

PubMed1991

Normal values and ranges for ventilation and breathing pattern at maximal exercise.

Assessment of the breathing pattern at maximal exercise in patients is limited because the range of ventilatory responses (minute ventilation; tidal volume; respiratory rate) at maximal exercise in normal humans is unknown. We studied 231 normal subjects (120 women; 111 men) equally distributed according to age from 20 to 80 years. Each subject performed a progressive incremental cycle ergometer exercise test to their symptom-limited maximum. Mean ventilation at the end of exercise (Vemax) was significantly higher in men (mean +/- SD, 97 +/- 25 L/min) than in women (69 +/- 22 L/min) (p less than 0.001). Minute ventilation at the end of exercise as a fraction of predicted maximal voluntary ventilation (Vemax/MVV) for all subjects was 0.61 +/- 0.14 (range, 0.28 to 1.02). There was no difference in Vemax/MVV between men (0.62 +/- 0.14) and women (0.59 +/- 0.14). Tidal volume at the end of exercise (Vtmax) was higher in men (2.70 +/- 0.48 L) than in women (1.92 +/- 0.41 L) (p less than 0.001). Any differences in Vtmax between men and women disappeared when Vtmax was corrected for baseline FVC. Respiratory rate at the end of exercise (RRmax) was 36.1 +/- 9.2 breaths per minute for all subjects. There was no difference in RRmax between men and women. The Vemax correlated best with carbon dioxide output at the end of exercise (r = 0.91; p less than 0.001) and with maximal oxygen uptake (r = 0.90; p less than 0.001) for all subjects. This study of a large group of subjects has demonstrated the wide range of possible breathing patterns which are adopted during exercise and has provided a wide range of "normal" responses which must be taken into consideration when maximal ventilatory data from exercise tests are analyzed.

Adult↗

PubMed1990

Respiratory muscle weakness and dyspnea in thyrotoxic patients.

Dyspnea on exertion is a frequently reported symptom of thyrotoxicosis. In the majority of cases, there is no obvious cause of dyspnea, but as skeletal myopathy is also common in thyrotoxic patients, it has been postulated that increased dyspnea could be secondary to respiratory muscle weakness. We sought to determine whether thyrotoxic patients were in fact more dyspneic on exertion than age- and sex-matched controls, and if so, whether the increased dyspnea was secondary to respiratory muscle weakness. The study group consisted of 12 thyrotoxic patients and 12 control subjects matched for age and gender. We measured lung volumes, compliance, elastic recoil, respiratory muscle strength, maximal exercise performance, and the intensity of breathlessness (modified Borg scale) at various levels of exercise in all subjects. The respiratory muscles were weaker in patients than controls. This weakness improved in treated patients (p less than 0.05) with concomitant increases in VC, IC, and TLC (all p less than 0.05). Despite this, we found no differences in breathlessness intensity scores between patients and controls or in patients before and after successful antithyroid therapy.

Adult↗

PubMed1990

Respiratory muscle function during obstructive sleep apnea.

Obstructive sleep apnea (OSA) is characterized by recurrent upper airway obstruction during sleep. Inspiratory muscles may be subjected to potentially fatiguing loads during an obstructive apnea and this may be related to the termination of obstructive apnea. We have measured transdiaphragmatic pressure (Pdi) and breathing patterns in six male patients with OSA during sleep to characterize respiratory muscle function in OSA and determine whether apnea termination is consistently related to a pressure time index of the diaphragm (PTI) associated with respiratory muscle fatigue. There was a large intersubject variability in Pdi generation during apnea. No consistent level of PTI was associated with apnea termination. During prolonged apneas, the respiratory duty cycle plateaued, which is suggestive of an inhibitory reflex possibly mediated by chest wall afferents. There were intersubject differences in both inspiratory and expiratory muscle recruitment during apnea. In the majority of patients, the diaphragm appeared to be the primary inspiratory muscle during apnea, but in some it appeared to be the intercostal/accessory muscles. The majority of patients demonstrated an increase in gastric pressure and inward abdominal movement during the expiratory phases of an apnea, consistent with abdominal muscle recruitment stimulated by increased ventilatory drive.

Diaphragm↗

PubMed1990

Recovery of the ventilatory and upper airway muscles and exercise performance after type A botulism.

We studied six patients with type A botulism to determine the degree of initial respiratory compromise and to quantitate the time course and extent of recovery of the ventilatory and upper airway muscles and exercise performance. The VM weakness was identified in all patients early after botulism. Upper airway muscle weakness was also common, requiring intubation for airway protection in one patient. Recovery of VM and upper airway muscle strength occurred in all patients, predominantly over the first 12 weeks but continued up to one year in several. A similar time course of improvement was noted for exercise performance. Ventilatory limitation was an unusual cause for exercise limitation. By 12 months, lung function, VM and upper airway muscle strength and exercise performance had returned to normal in all but one patient. We conclude that VM and upper airway muscle weakness occurs in most patients with clinically significant type A botulism.

Adult↗

PubMed1990

Recovery after unilateral phrenic injury associated with coronary artery revascularization.

Hemidiaphragmatic paralysis occurs in some patients following CAB surgery, possibly related to an intraoperative stretch or cold-induced phrenic injury. To determine the time and extent of recovery of phrenic nerve function, we studied five patients with left phrenic paresis or paralysis after CAB. The FVC, FEV1, Pmax and PEmax pressures, latency of conduction and amplitude of CDAP with phrenic nerve stimulation, and diaphragmatic excursion during fluoroscopy were measured for 12 months after CAB. Left phrenic paralysis was substantiated in four of five patients, and paresis was present in the other patient. Recovery of the left phrenic nerve occurred in all patients, complete in one and partial in four, but was delayed and continued for up to 12 months. We conclude that phrenic nerve recovery is delayed after CAB-associated injury and may be incomplete up to 14 months later, in keeping with rates of regeneration of other peripheral nerves.

Action Potentials↗

PubMed1989

Diaphragmatic weakness and paralysis.

Diaphragmatic weakness implies a decrease in the strength of the diaphragm. Diaphragmatic paralysis is an extreme form of diaphragmatic weakness. Diaphragmatic paralysis is an uncommon clinical problem while diaphragmatic weakness, although uncommon, is probably frequently unrecognized because appropriate tests to detect its presence are not performed. Weakness of the diaphragm can result from abnormalities at any site along its neuromuscular axis, although it most frequently arises from diseases in the phrenic nerves or from myopathies affecting the diaphragm itself. Presence of diaphragmatic weakness may be suspected from the complaint of dyspnea (particularly on exertion) or orthopnea; the presence of rapid, shallow breathing or, more importantly, paradoxical inward motion of the abdomen during inspiration on physical examination; a restrictive pattern on lung function testing; an elevated hemidiaphragm on chest radiograph; paradoxical upward movement of 1 hemidiaphragm during fluoroscopic imaging; or reductions in maximal static inspiratory pressure. The diagnosis of diaphragmatic weakness is confirmed, however, by a reduction in maximal static transdiaphragmatic pressure (Pdimax). The diagnosis of diaphragmatic paralysis is confirmed by the absence of a compound diaphragm action potential on phrenic nerve stimulation. There are many causes of diaphragmatic weakness and paralysis. In this review we outline an approach we have found useful in attempting to determine a specific cause. Most frequently the cause is either a phrenic neuropathy or diaphragmatic myopathy. Often the neuropathy or myopathy affects other nerves or muscles that can be more easily investigated to determine the specific pathologic basis, and, by association, it is presumed that the diaphragmatic weakness or paralysis is secondary to the same disease process.

Diaphragm↗

PubMed1989

Maximal static respiratory pressures in the normal elderly.

To determine if a relationship exists between maximal static respiratory pressures measured at the mouth and age greater than 55 yr, and if so, whether regression equations can be derived that accurately reflect this, we measured maximal inspiratory (Plmax) and expiratory (PEmax) pressures in 64 normal women and 40 normal men older than 55 yr of age. We found no relationship between PImax and PEmax and age greater than 55 yr (all r squared values less than 0.14). We tested the reproducibility of our measurements of PImax and PEmax in 13 and 12 subjects, respectively, on three separate occasions. Repeated measures analysis showed no significant differences in these measurements. Using the measurements obtained in this large study, we calculated 95% confidence limits for PImax and PEmax values in men and women older than 55 yr of age. The 95% confidence limits for PImax in men were 55 to 161 cm H2O, and 26 to 124 cm H2O in women. The 95% confidence limits for PEmax in men were 90 to 256 cm H2O, and 46 to 184 cm H2O in women. We conclude that given the large interindividual variation, a cross-sectional study such as this or other previous studies may not be able to reveal age-dependent changes unless very large numbers are used, and even then potential for bias exists. However, with the small intraindividual coefficients of variation in repeated measurements of PImax and PEmax, a longitudinal study may provide more pertinent information.

Aged↗

PubMed1989

Prediction of maximal oxygen uptake and power during cycle ergometry in subjects older than 55 years of age.

One hundred twenty-eight healthy volunteers (81 women, 47 men) older than 55 yr of age were studied with an incremental progressive cycle ergometer test to a symptom-limited, maximal tolerable work load. Mean (+/- SD) age was 66 +/- 6 yr in women and 66 +/- 5 years in men. Subjects with a history of ischemic heart disease, diabetes, pulmonary disease, or neuromuscular disease were excluded. Smokers were included, but all subjects had normal FEV1 and FVC. The objective of the study was to compare measured values of VO2max and Wmax in this older population with previously published predicted values based on subjects of all ages. We found that Wmax observed exceeded Wmax predicted by 9.5 +/- 22% (mean +/- SD) and that VO2max observed exceeded VO2max predicted by 17.5 +/- 22%. Because of this systematic underestimate of VO2max and Wmax by the previous prediction equations, we constructed new prediction equations for use in subjects older than 55 yr of age using height, weight, age, and sex as variables. We conclude that these new prediction equations more accurately predict Wmax and VO2max in subjects older than 55 yr of age because they are based solely on subjects in this age group.

Age Factors↗