Attenuated fibroblast growth factor 21 response to acute aerobic exercise in obese individuals.

BACKGROUND AND AIM: Fibroblast growth factor 21 (FGF21) is positively associated with body mass index, potentially as a compensatory mechanism to mediate obesity related metabolic and inflammatory insult due to chronic low-grade elevations of the pro-inflammatory cytokines interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-α). Therefore, FGF21 response in obese subjects and the associations with increased pro-inflammatory cytokines, insulin resistance, and energy utilization warrants investigation. METHODS AND RESULTS: Twenty four untrained subjects (12 obese and 12 normal-weight) performed 30 min of continuous submaximal aerobic exercise. Following exercise, obese subjects exhibited a blunted FGF21 response to exercise compared to normal-weight subjects as indicated by area-under-the-curves "with respect to increase" (AUCi) analyses (p = 0.005). Furthermore, while exercise-induced plasma FGF21 was not associated with any inflammatory cytokine (IL-6 and TNF-α) response, FGF21 AUCi was positively correlated with glucose AUCi (r = 0.495, p = 0.014), total relative energy expenditure (r = 0.562, p = 0.004), and relative maximal oxygen consumption (VO2max; r = 0.646, p = 0.001) in all subjects. CONCLUSION: Impaired cardiorespiratory fitness may influence the sensitivity of FGF21 response to acute exercise in obese individuals, potentially contributing to the attenuated metabolic response (e.g., glucose) and total exercise energy expenditure. Therefore, exercise training aimed at improving cardiorespiratory fitness and/or body composition may augment cardioprotective properties against obesity-associated CVD through enhanced FGF21 flux.

Clinical analysis of the novel breast cancer serum assay BT1.

In an effort to define possible clinical relationships to the BT1 serum assay, a retrospective study population including both Caucasian and African American breast cancer patients was tested. Test results were compared to clinical information provided by the Virginia Cancer Registry. The 64 patients, ages 29 through 69, had a wide range of BT1 values which were not attributable to race or age. The majority of these patients had infiltrating duct carcinoma, with eight additional morphology of neoplasm diagnoses represented in the entire group. No morphology code was associated with either a reactive or non-reactive BT1 result. Staging information was available for 26 patients, diagnosed with stages I, II, and III breast cancer. Positive BT1 values were found throughout these diagnosis stages. In addition, multiple serum samples were available from some patients. Analysis of these longitudinal samples showed different patterns, with test values remaining unreactive in 4 patients, and reactive in 9 others. Interestingly, 5 patients showed values increasing from negative to positive while 3 patients went from positive to negative over time.

Evaluation of the BT-1 serum assay for breast cancer.

The BT-1 assay which identifies a novel breast tumor associated serum analyte was performed for 143 patients previously diagnosed with breast cancer. Mucin tumor markers CA15-3/CA27-29 values were available for 50 patients and there was very minor overlap between patients positive by both tests. Patients' follow-up clinical status at sample draw was compared to BT-1 assay results. 27% of patients originally diagnosed as Stage II and 20% patients originally diagnosed as Stage III who were evaluated 'no disease' had positive BT-1 values. 8% patients diagnosed as Stage II had negative BT-1 results in samples drawn within 90 days of chemotherapy initiation, whereas 23% of patients diagnosed as Stage III cancer were BT-1 test positive within 90 days of chemotherapy initiation. 50% of patients tested before initial breast cancer surgery had positive BT-1 values, suggesting that the BT-1 assay may be useful in identification women with more advanced disease at diagnosis.

A comparison of demand-valve and bag-valve ventilations in a swine pneumothorax model.

OBJECTIVE: Two means of delivering artificial ventilation readily available to out-of-hospital personnel are the bag-valve (BV) and the O2-powered demand-valve (OPDV). However, use of the OPDV has been limited because of concerns that it may worsen an underlying pneumothorax. This study compared the changes in size of pneumothorax in swine ventilated with the 2 devices. METHODS: Three swine were anesthetized, intubated, and instrumented with a femoral arterial line and a pediatric Swan-Ganz catheter. A chest tube was placed, the chest was opened, and the lung parenchyma was visualized. The lung was disrupted by a single stab with a #10 scalpel; the chest was then sealed; and a pneumothorax was created by injecting 30 mL of air through the chest tube. The animals were ventilated by 12 emergency medical technicians using either BV or OPDV. After 10 minutes of ventilation, the pneumothorax volume was measured. RESULTS: When comparing final pneumothorax volumes after 10 minutes of ventilation with the 2 devices, there was no significant difference (mean +/- SD = 40.8 +/- 28.2 mL vs 52.3 +/- 23.1 mL, p = 0.286). CONCLUSION: There is no difference in final pneumothorax volumes after OPDV or BV ventilation.

Ventilatory strategies affect gas exchange in a pig model of closed-chest cardiac compression.

STUDY OBJECTIVE: To identify the arterial and mixed venous blood gas changes caused by different ventilatory strategies during resuscitation from ventricular fibrillation in a pig model of closed-chest cardiac compression. METHODS: A prospective randomized animal study was performed using 27 domestic pigs (body weight, 30 to 35 kg). Pentobarbital-anesthetized pigs were assigned to receive one of three treatments: (1) chest compression without assisted ventilation (n = 8), (2) assisted ventilation with room air (n = 8), and (3) assisted ventilation with 100% oxygen (n = 8). A fourth group, with the airway completely blocked, was added at the end of the experiment (n = 3). After instrumentation, the ventricles were fibrillated, and chest compression was begun 30 seconds after fibrillation with the use of the Thumper Mechanical CPR system (Michigan Instruments). Arterial and mixed venous blood gas samples were collected at 1, 3, 10, and 20 minutes of resuscitation. Defibrillation was attempted after the 20-minute sample was taken. RESULTS: Fibrillation followed by chest compression alone caused a significant drop in arterial and mixed venous partial pressure of oxygen (PO2) and a significant increase in arterial and mixed venous partial pressure of carbon dioxide (PCO2). Compared with the chest compression only, ventilation with room air significantly increased arterial and mixed venous PO2 and decreased arterial and mixed venous PCO2. Ventilation with 100% oxygen further increased arterial and mixed venous PO2 but did not affect PCO2, when compared with room air ventilation. The only successful defibrillations (3 animals) occurred in the group receiving 100% oxygen. CONCLUSION: This study indicates that passive air movement during chest compression does not allow physiologically significant pulmonary gas exchange and that room air ventilation alone is not sufficient to maintain mixed venous PO2.

Transient increase in plasma catecholamines following hypertonic/hyperosmotic fluid administration in conscious rats

Plasma norepinephrine and epinephrine levels were monitored to determine possible alterations of the sympathetic nervous system caused by hypertonic fluid adeministration. Iv infusion (3.5 ml/Kg, 1 min) of 7.5% NaCl/6% Hespan transiently increased both plasma norepinephrine and epinehrine levels to 197 ñ 28% and 220 ñ 30% of control, respectively, at 1 min. These increases were no longer significant 5 or 15 min following infusion. A brief hypotension was also observed immediately following hypertonic fluid administration. This, prolonged sympathetic activation does not occur following hypertonic fluid infusion in normovolemic conscious rats