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Drinking water bacteria are known to colonize commercial activated carbon block (ACB) point-of-use (PoU) drinking water filters. The breakthrough pattern of drinking water bacteria through these filters, however, is unclear. A manifold system was constructed with two of the most common filter brands in the U.S. and operated to simulate normal household diurnal use. The filters were fed tap water inoculated with two fluorescent-tagged bacterial species that were acclimated to drinking water conditions (GFP-Pseudomonas aeruginosa and mCherry-Escherichia coli). Separate breakthrough tests with abiotic fluorescent microspheres (1 μm) were also conducted. The fluorescent P. aeruginosa and E. coli strains were detected in filter effluent within the first 6 and 28 L processed, respectively. The fluorescent microspheres were also detected in the effluent within the first 6 L processed, indicating that preferential flow pathways with diameters larger than 1 μm allow influent particles to transit the entire thickness of the carbon block. P. aeruginosa broke through the filters more quickly than E. coli, possibly due to its smaller cell size. P. aeruginosa also displayed greater colonization advantages over E. coli, and its effluent cell number plateaued at levels two times the influent level. This study provides evidence that some bacteria, including species known to include opportunistic and enteric pathogenic strains, can be readily transmitted through solid block activated carbon filters and that these filters can elevate the levels of effective colonizers in drinking water.

Loss of ovarian hormones leads to increased adiposity and insulin resistance (IR), increasing the risk for cardiovascular and metabolic diseases. The purpose of this study was to investigate whether the molecular mechanism behind the adverse systemic and adipose tissue-specific metabolic effects of ovariectomy requires loss of signaling through estrogen receptor alpha (ERα) or estrogen receptor β (ERβ). We examined ovariectomized (OVX) and ovary-intactwild-type (WT), ERα-null (αKO), and ERβ-null (βKO) female mice (age ~49 weeks; n = 7–12/group). All mice were fed a phytoestrogen-free diet (P P

Prenatal overnutrition affects development into adulthood and influences risk of obesity. We assessed the transgenerational effect of maternal Western diet (WD) consumption on offspring physical activity. Voluntary wheel running was increased in juvenile (4-7 wk of age), but decreased in adult (16-19 wk of age), F1 female WD offspring In contrast, no wheel-running differences in F1 male offspring were observed. Increased wheel running in juvenile female WD offspring was associated with up-regulated dopamine receptor (DRD)-1 and -2 in the nucleus accumbens (NAc) and with down-regulated Lepr in the ventral tegmental area (VTA). Conversely, decreased wheel running by adult female WD offspring was associated with down-regulated DRD1 in the NAc and with up-regulated Lepr in the VTA. Body fat, leptin, and insulin were increased in male, but not in female, F1 WD offspring. Recombinant virus (rAAV) leptin antagonism in the VTA decreased wheel running in standard diet but not in WD F1 female offspring. Analysis of F2 offspring found no differences in wheel running or adiposity in male or female offspring, suggesting that changes in the F1 generation were related to in utero somatic reprogramming. Our findings indicate prenatal WD exposure leads to age-specific changes in voluntary physical activity in female offspring that are differentially influenced by VTA leptin antagonism.-Ruegsegger, G. N., Grigsby, K. B., Kelty, T. J., Zidon, T. M., Childs, T. E., Vieira-Potter, V. J., Klinkebiel, D. L., Matheny, M., Scarpace, P. J., Booth, F. W. Maternal Western diet age-specifically alters female offspring voluntary physical activity and dopamine- and leptin-related gene expression.

Disinfected wastewater effluent contains a complex mixture of biomolecules including DNA. If intact genes conveying antibiotic resistance survive the disinfection process, environmental bacteria may take them up. We treated plasmid pWH1266, which contains ampicillin resistance gene blaTEM-1 and tetracycline resistance gene tetA, with UV254 doses up to 430 mJ/cm2 and studied the ability of those genes to be acquired by Acinetobacter baylyi. The plasmids required approximately 20–25 mJ/cm2 per log10 loss of transformation efficiency. We monitored plasmid DNA degradation using gel electrophoresis and qPCR with both short amplicons (∼200 bps, representative of ARG amplicon lengths commonly used for environmental monitoring) and long amplicons (800–1200 bps, designed to cover the entire resistance genes). The rate of transformability loss due to UV254 treatment was approximately 20× and 2× larger than the rate of gene degradation measured with the short and long amplicons qPCR, respectively. When extrapolated ...

Ovariectomy and high-fat diet (HFD) worsen obesity and metabolic dysfunction associated with low aerobic fitness. Exercise training mitigates metabolic abnormalities induced by low aerobic fitness, but whether the protective effect is maintained after ovariectomy and HFD is unknown.This study determined whether, after ovariectomy and HFD, exercise training improves metabolic function in rats bred for low intrinsic aerobic capacity.Female rats selectively bred for low (LCR) and high (HCR) intrinsic aerobic capacity (n = 30) were ovariectomized, fed HFD, and randomized to either a sedentary (SED) or voluntary wheel running (EX) group. Resting energy expenditure, glucose tolerance, and spontaneous physical activity were determined midway through the experiment, whereas body weight, wheel running volume, and food intake were assessed throughout the study. Body composition, circulating metabolic markers, and skeletal muscle gene and protein expression were measured at sacrifice.EX reduced body weight and adiposity in LCR rats (-10% and -50%, respectively; P0.05) and, unexpectedly, increased these variables in HCR rats (+7% and +37%, respectively; P0.05) compared with their respective SED controls, likely because of dietary overcompensation. Wheel running volume was approximately fivefold greater in HCR than LCR rats, yet EX enhanced insulin sensitivity equally in LCR and HCR rats (P0.05). This EX-mediated improvement in metabolic function was associated with thee gene upregulation of skeletal muscle interleukin-6 and interleukin-10. EX also increased resting energy expenditure, skeletal muscle mitochondrial content (oxidative phosphorylation complexes and citrate synthase activity), and adenosine monophosphate-activated protein kinase activation similarly in both lines (all P0.05).Despite a fivefold difference in running volume between rat lines, EX similarly improved systemic insulin sensitivity, resting energy expenditure, and skeletal muscle mitochondrial content and adenosine monophosphate-activated protein kinase activation in ovariectomized LCR and HCR rats fed HFD compared with their respective SED controls.

Activated carbon block (ACB)-based point-of-use (PoU) drinking water filters are widely used to remove residual disinfectant, heavy metals, and disinfection by-products (DBPs) from household tap water. The filters are not designed to remove bacteria, which can grow in the filter. Based on previous research, we hypothesized that more biofilm would form in PoU filters due to the presence of chlorinated phenolic DBPs, resulting in higher bacterial concentrations in filtered water. Therefore, studies were conducted by operating a manifold system with three sets of ACB PoU filters that received chloraminated tap water spiked with (50 and 100 ng L−1 added) and without (0 ng L−1 added) pentachlorophenol (PCP) as a surrogate chlorinated phenolic DBP. After processing 85% of the manufacturer's recommended water volume, effluent heterotrophic plate counts plateaued at levels up to 100 times greater than influent counts. The upstream filter fabric developed a significant biofilm that lightened with increasing PCP concentration; however, the overall biofilm mass was not different between treatments. Influent, effluent, and fabric samples had distinct bacterial community structures, and the structure of effluent communities was more similar to that of fabric communities than that of influent communities. The bacterial community structure changed across the filter primarily due to the filter environment itself, while PCP effects were subtle yet significant. The relative abundance of Mycobacterium increased within fabric biofilms when PCP was added, and the absolute abundance was estimated to increase in the effluent relative to the influent. In conclusion, ACB PoU filters significantly alter the bacterial abundance and composition of drinking water.

Rats selectively bred for high (HCR) and low (LCR) aerobic capacity show a stark divergence in wheel running behavior, which may be associated with the dopamine (DA) system in the brain. HCR possess greater motivation for voluntary running along with greater brain DA activity compared to LCR. We recently demonstrated that HCR are not immune to ovariectomy (OVX)-associated reductions in spontaneous cage (i.e. locomotor) activity. Whether HCR and LCR rats differ in their OVX-mediated voluntary wheel running response is unknown.To determine whether HCR are protected from OVX-associated reduction in voluntary wheel running.Forty female HCR and LCR rats (age ~27weeks) had either SHM or OVX operations, and given access to a running wheel for 11weeks. Weekly wheel running distance was monitored throughout the intervention. Nucleus accumbens (NAc) was assessed for mRNA expression of DA receptors at sacrifice.Compared to LCR, HCR ran greater distance and had greater ratio of excitatory/inhibitory DA mRNA expression (both line main effects, P

AB Introduction: In the absence of exercise training, rats selectively bred for high intrinsic aerobic capacity (high-capacity running (HCR)) are protected against ovariectomy (OVX)-induced insulin resistance (IR) and obesity compared with those bred for low intrinsic aerobic capacity (low-capacity running (LCR)). Purpose: This study determined whether OVX HCR rats remain protected with exposure to high-fat diet (HFD) compared with OVX LCR rats. Methods: Female HCR and LCR rats (n = 36; age, 27-33 wk) underwent OVX and were randomized to a standard chow diet (NC, 5% kcal fat) or HFD (45% kcal fat) ad libitum for 11 wk. Total energy expenditure, resting energy expenditure, spontaneous physical activity (SPA), and glucose tolerance were assessed midway, whereas fasting circulating metabolic markers, body composition, adipose tissue distribution, and skeletal muscle adenosine monophosphate-activated protein kinase (AMPK), and mitochondrial markers were assessed at sacrifice. Results: Both HCR and LCR rats experienced HFD-induced increases in total and visceral adiposity after OVX. Despite similar gains in adiposity, HCR rats were protected from HFD-induced IR and reduced total energy expenditure observed in LCR rats (P < 0.05). This metabolic protection was likely attributed to a compensatory increase in SPA and associated preservation of skeletal muscle AMPK activity in HCR; however, HFD significantly reduced SPA and AMPK activity in LCR (P < 0.05). In both lines, HFD reduced citrate synthase activity, gene expression of markers of mitochondrial biogenesis (tFAM, NRF1, and PGC-1[alpha]), and protein levels of mitochondrial oxidative phosphorylation complexes I, II, IV, and V in skeletal muscle (all P < 0.05). Conclusion: After OVX, HCR and LCR rats differentially respond to HFD such that HCR increase while LCR decrease SPA. This "physical activity compensation" likely confers protection from HFD-induced IR and reduced energy expenditure in HCR rats. (C) 2016 American College of Sports Medicine

Adipose tissue (AT) inflammation is a hallmark characteristic of obesity and an important determinant of insulin resistance and cardiovascular disease; therefore, a better understanding of factors regulating AT inflammation is critical. It is well established that reduced vascular endothelial nitric oxide (NO) bioavailability promotes arterial inflammation; however, the role of NO in modulating inflammation in AT remains disputed. In the present study, 10-wk-old C57BL6 wild-type and endothelial nitric oxide synthase (eNOS) knockout male mice were randomized to either a control diet (10% kcal from fat) or a Western diet (44.9% kcal from fat, 17% sucrose, and 1% cholesterol) for 18 wk ( n = 7 or 8/group). In wild-type mice, Western diet-induced obesity led to increased visceral white AT expression of inflammatory genes (e.g., MCP1, TNF-α, and CCL5 mRNAs) and markers of macrophage infiltration (e.g., CD68, ITGAM, EMR1, CD11C mRNAs, and Mac-2 protein), as well as reduced markers of mitochondrial content (e.g., OXPHOS complex I and IV protein). Unexpectedly, these effects of Western diet on visceral white AT were not accompanied by decreases in eNOS phosphorylation at Ser-1177 or increases in eNOS phosphorylation at Thr-495. Also counter to expectations, eNOS knockout mice, independent of the diet, were leaner and did not exhibit greater white or brown AT inflammation compared with wild-type mice. Collectively, these findings do not support the hypothesis that reduced NO production from eNOS contributes to obesity-related AT inflammation.

Premenopausal females are protected against adipose tissue inflammation and insulin resistance, until loss of ovarian hormone production (e.g., menopause). There is some evidence that females have greater brown adipose tissue (BAT) thermogenic capacity. Because BAT mass correlates inversely with insulin resistance, we hypothesized that increased uncoupling protein 1 (UCP1) expression contributes to the superior metabolic health of females. Given that UCP1 transiently increases in BAT following ovariectomy (OVX), we hypothesized that UCP1 may ‘buffer’ OVX-mediated metabolic dysfunction. Accordingly, female UCP1-knockout (KO) and WT mice received OVX or sham (SHM) surgeries at 12 weeks of age creating four groups (n = 10/group), which were followed for 14 weeks and compared for body weight and adiposity, food intake, energy expenditure and spontaneous physical activity (metabolic chambers), insulin resistance (HOMA-IR, ADIPO-IR and glucose tolerance testing) and adipose tissue phenotype (histology, gene and protein expression). Two-way ANOVA was used to assess the main effects of genotype (G), OVX treatment (O) and genotype by treatment (GxO) interactions, which were considered significant when P ≤ 0.05. UCP1KO mice experienced a more adverse metabolic response to OVX than WT. Whereas OVX-induced weight gain was not synergistically greater for KO compared to WT (GxO, NS), OVX-induced insulin resistance was significantly exacerbated in KO compared to WT (GxO for HOMA-IR, P

Phytoestrogen-rich soy is known to ameliorate menopause-associated obesity and metabolic dysfunction for reasons that are unclear. The gut microbiota have been linked with the development of obesity and metabolic dysfunction. We aimed to determine the impact of soy on cardiometabolic health, adipose tissue inflammation, and the cecal microbiota in ovariectomized (OVX) rats bred for low-running capacity (LCR), a model that has been previously shown to mimic human menopause compared to sham-operated (SHM) intact control LCR rats. In this study, soy consumption, without affecting energy intake or physical activity, significantly improved insulin sensitivity and body composition of OVX rats bred for low-running capacity. Furthermore, soy significantly improved blood lipid profile, adipose tissue inflammation, and aortic stiffness of LCR rats. Compared to a soy-free control diet, soy significantly shifted the cecal microbial community of LCR rats, resulting in a lower Firmicutes:Bacteroidetes ratio. Correlations among metabolic parameters and cecal bacterial taxa identified in this study suggest that taxa Prevotella, Dorea, and Phascolarctobacterium may be taxa of interest. Our results suggest that dietary soy ameliorates adiposity, insulin sensitivity, adipose tissue inflammation, and arterial stiffness and exerts a beneficial shift in gut microbial communities in a rat model that mimics human menopause.

Exercise enhances insulin sensitivity; it also improves adipocyte metabolism and reduces adipose tissue inflammation through poorly defined mechanisms. Fibroblast growth factor 21 (FGF21) is a pleiotropic hormone-like protein whose insulin-sensitizing properties are predominantly mediated via receptor signaling in adipose tissue (AT). Recently, FGF21 has also been demonstrated to have anti-inflammatory properties. Meanwhile, an association between exercise and increased circulating FGF21 levels has been reported in some, but not all studies. Thus, the role that FGF21 plays in mediating the positive metabolic effects of exercise in AT are unclear. In this study, FGF21-knockout (KO) mice were used to directly assess the role of FGF21 in mediating the metabolic and anti-inflammatory effects of exercise on white AT (WAT) and brown AT (BAT). Male FGF21KO and wild-type mice were provided running wheels or remained sedentary for 8 weeks (n = 9–15/group) and compared for adiposity, insulin sensitivity (i.e., HOMA-IR, Adipo-IR) and AT inflammation and metabolic function (e.g., mitochondrial enzyme activity, subunit content). Adiposity and Adipo-IR were increased in FGF21KO mice and decreased by EX. The BAT of FGF21KO animals had reduced mitochondrial content and decreased relative mass, both normalized by EX. WAT and BAT inflammation was elevated in FGF21KO mice, reduced in both genotypes by EX. EX increased WAT Pgc1alpha gene expression, citrate synthase activity, COX I content and total AMPK content in WT but not FGF21KO mice. Collectively, these findings reveal a previously unappreciated anti-inflammatory role for FGF21 in WAT and BAT, but do not support that FGF21 is necessary for EX-mediated anti-inflammatory effects.

We tested the hypothesis that female mice null for uncoupling protein 1 (UCP1) would have increased susceptibility to Western diet-induced “whitening” of brown adipose tissue (AT) and glucose intolerance. Six-week-old C57BL/6J wild-type (WT) and UCP1 knockout (UCP1−/−) mice, housed at 25°C, were randomized to either a control diet (10% kcal from fat) or Western diet (45% kcal from fat and 1% cholesterol) for 28 wk. Loss of UCP1 had no effect on energy intake, energy expenditure, spontaneous physical activity, weight gain, or visceral white AT mass. Despite similar susceptibility to weight gain compared with WT, UCP1−/− exhibited whitening of brown AT evidenced by a striking ~500% increase in mass and appearance of large unilocular adipocytes, increased expression of genes related to inflammation, immune cell infiltration, and endoplasmic reticulum/oxidative stress ( P < 0.05), and decreased mitochondrial subunit protein (COX I, II, III, and IV, P < 0.05), all of which were exacerbated by Western diet ( P < 0.05). UCP1−/− mice also developed liver steatosis and glucose intolerance, which was worsened by Western diet. Collectively, these findings demonstrate that loss of UCP1 exacerbates Western diet-induced whitening of brown AT, glucose intolerance, and induces liver steatosis. Notably, the adverse metabolic manifestations of UCP1−/− were independent of changes in body weight, visceral adiposity, and energy expenditure. These novel findings uncover a previously unrecognized metabolic protective role of UCP1 that is independent of its already established role in energy homeostasis.

Cardiometabolic impairments that begin early in life are particularly critical, because they often predict metabolic dysfunction in adulthood. Obesity, high-fat diet (HFD), and inactivity are all associated with adipose tissue (AT) inflammation and insulin resistance (IR), major predictors of metabolic dysfunction. Recent evidence has also associated the gut microbiome with cardiometabolic health.The objective of this study is to compare equal energy deficits induced by exercise and caloric reduction on cardiometabolic disease risk parameters including AT inflammation, IR, and gut microbiota changes during HFD consumption.Obesity-prone rats fed HFD were exercise trained (Ex, n = 10) or weight matched to Ex via caloric reduction although kept sedentary (WM, n = 10), and compared with ad libitum HFD-fed (Sed, n = 10) rats for IR, systemic energetics and spontaneous physical activity (SPA), adiposity, and fasting metabolic parameters. Visceral, subcutaneous, periaortic, and brown AT (BAT), liver, aorta, and cecal digesta were examined.Despite identical reductions in adiposity, Ex, but not WM, improved IR, increased SPA by approximately 26% (P0.05 compared with WM and Sed), and reduced LDL cholesterol (P0.05 compared with Sed). WM and Ex both reduced inflammatory markers in all AT depots and aorta, whereas only Ex increased indicators of mitochondrial function in BAT. Ex significantly increased the relative abundance of cecal Streptococcaceae and decreased S24-7 and one undefined genus in Rikenellaceae; WM induced similar changes but did not reach statistical significance.Both Ex and WM reduced AT inflammation across depots, whereas Ex caused more robust changes to gut microbial communities, improved IR, increased fat oxidation, increased SPA, and increased indices of BAT mitochondrial function. Our findings add to the growing body of literature indicating that there are weight-loss-independent metabolic benefits of exercise.

High-capacity running (HCR) rats are protected against the early (i.e., ∼11 wk postsurgery) development of ovariectomy (OVX)-induced insulin resistance (IR) compared with low-capacity running (LCR) rats. The purpose of this study was to utilize the hyperinsulinemic euglycemic clamp to determine whether 1) HCR rats remain protected from OVX-induced IR when the time following OVX is extended to 27 wk and 2) tissue-specific glucose uptake differences are responsible for the protection in HCR rats under sedentary conditions. Female HCR and LCR rats ( n = 40; aged ∼22 wk) randomly received either OVX or sham (SHM) surgeries and then underwent the clamp 27 wk following surgeries. [3-3H]glucose was used to determine glucose clearance, whereas 2-[14C]deoxyglucose (2-DG) was used to assess glucose uptake in skeletal muscle, brown adipose tissue (BAT), subcutaneous white adipose tissue (WAT), and visceral WAT. OVX decreased the glucose infusion rate and glucose clearance in both lines, but HCR had better insulin sensitivity than LCR ( P < 0.05). In both lines, OVX significantly reduced glucose uptake in soleus and gastrocnemius muscles; however, HCR showed ∼40% greater gastrocnemius glucose uptake compared with LCR ( P < 0.05). HCR also exhibited greater glucose uptake in BAT and visceral WAT compared with LCR ( P < 0.05), yet these tissues were not affected by OVX in either line. In conclusion, OVX impairs insulin sensitivity in both HCR and LCR rats, likely driven by impairments in insulin-mediated skeletal muscle glucose uptake. HCR rats have greater skeletal muscle, BAT, and WAT insulin-mediated glucose uptake, which may aid in protection against OVX-associated insulin resistance.

Adipose tissue inflammation links obesity and metabolic disease. Both exercise and estrogen improve metabolic health, enhance mitochondrial function, and have anti-inflammatory effects. We hypothesize that there is an inverse relationship between mitochondrial function and inflammation in adipose tissue and that exercise acts as an estrogen “mimetic”. Explicitly, exercise may improve adipose tissue “immunometabolism” by improving mitochondrial function and reducing inflammation.

Fibroblast growth factor 21 (FGF21) is an endocrine hormone known to enhance adipocyte metabolism via "browning" of white adipose tissue (WAT) and activation of brown adipose tissue (BAT). Exercise...

Regular physical activity is effective in reducing visceral white adipose tissue (AT) inflammation and oxidative stress, and these changes are commonly associated with reduced adiposity. However, the impact of multiple periods of physical activity, intercalated by periods of inactivity, i.e., intermittent physical activity, on markers of AT inflammation and oxidative stress is unknown. In the present study, 5-wk-old male C57BL/6 mice were randomized into three groups ( n = 10/group): sedentary, regular physical activity, and intermittent physical activity, for 24 wk. All animals were singly housed and fed a diet containing 45% kcal from fat. Regularly active mice had access to voluntary running wheels throughout the study period, whereas intermittently active mice had access to running wheels for 3-wk intervals (i.e., 3 wk on/3 wk off) throughout the study. At death, regular and intermittent physical activity was associated with similar reductions in visceral AT mass (approximately −24%, P < 0.05) relative to sedentary. However, regularly, but not intermittently, active mice exhibited decreased expression of visceral AT genes related to inflammation (e.g., monocyte chemoattractant protein 1), immune cell infiltration (e.g., CD68, CD11c, F4/80, CD11b/CD18), oxidative stress (e.g., p47 phagocyte oxidase), and endoplasmic reticulum stress (e.g., CCAAT enhancer-binding protein homologous protein; all P < 0.05). Furthermore, regular, but not intermittent, physical activity was associated with a trend toward improvement in glucose tolerance ( P = 0.059). Collectively, these findings suggest that intermittent physical activity over a prolonged period of time may lead to a reduction in adiposity but with retention of a sedentary obese white AT and metabolic phenotype.

Ovariectomized rodents model human menopause in that they rapidly gain weight, reduce spontaneous physical activity (SPA), and develop metabolic dysfunction, including insulin resistance. How contrasting aerobic fitness levels impacts ovariectomy (OVX)-associated metabolic dysfunction is not known. Female rats selectively bred for high and low intrinsic aerobic fitness [high-capacity runners (HCR) and low-capacity runners (LCR), respectively] were maintained under sedentary conditions for 39 wk. Midway through the observation period, OVX or sham (SHM) operations were performed providing HCR-SHM, HCR-OVX, LCR-SHM, and LCR-OVX groups. Glucose tolerance, energy expenditure, and SPA were measured before and 4 wk after surgery, while body composition via dual-energy X-ray absorptiometry and adipose tissue distribution, brown adipose tissue (BAT), and skeletal muscle phenotype, hepatic lipid content, insulin resistance via homeostatic assessment model of insulin resistance and AdipoIR, and blood lipids were assessed at death. Remarkably, HCR were protected from OVX-associated increases in adiposity and insulin resistance, observed only in LCR. HCR rats were ∼30% smaller, had ∼70% greater spontaneous physical activity (SPA), consumed ∼10% more relative energy, had greater skeletal muscle proliferator-activated receptor coactivator 1-alpha, and ∼40% more BAT. OVX did not increase energy intake and reduced SPA to the same extent in both HCR and LCR. LCR were particularly affected by an OVX-associated reduction in resting energy expenditure and experienced a reduction in relative BAT; resting energy expenditure correlated positively with BAT across all animals ( r = 0.6; P < 0.001). In conclusion, despite reduced SPA following OVX, high intrinsic aerobic fitness protects against OVX-associated increases in adiposity and insulin resistance. The mechanism may involve preservation of resting energy expenditure.

The distribution of cardiac output between compliant vasculature (e.g., splanchnic organs and skin) and noncompliant vasculature (e.g., skeletal muscle) is proposed to constitute an important determinant of the amount of blood available to the heart (central blood volume and pressure). The aim here was to directly test the hypothesis that diversion of blood flow from a relatively noncompliant vasculature (muscle) to compliant vasculature (splanchnic organs and skin) acts to reduce right atrial pressure. The approach was to inflate an occluder cuff on the terminal aorta for 30 s in one of two modes of ventricular pacing in five awake dogs with atrioventricular block and autonomic blockade. In one trial, cardiac output was maintained constant, meaning cuff inflation caused a portion of terminal aortic flow (a noncompliant circulation) to be diverted to the splanchnic and skin circulations (compliant circulations). In the other trial, arterial pressure was maintained constant, meaning blood flow to these other regions did not change. The response of right atrial pressure (corrected for differences in arterial pressure between the two trials) fit our hypothesis, being lower when blood flow was diverted to compliant regions. We conclude that a small (4% of cardiac output) diversion of blood flow from a noncompliant region to a compliant region reduces right atrial pressure by 0.7 mmHg.

Previous studies examining the delay to the onset of vasodilation have primarily focused on the onset of exercise, a setting complicated by the fact that the muscle pump and the vasodilator systems are both activated, making it difficult to attribute changes in blood flow to one or both. The goal here was to determine the delay to the onset of vasodilation after changes in work rate imposed by changes in treadmill grade (work intensity) during locomotion at a steady speed. The rationale was that constant speed would help ensure constant muscle pump activity (contraction frequency) such that vasodilator responses could be examined in isolation. Seven Sprague-Dawley rats underwent three trials each in which treadmill incline was suddenly ( approximately 1 s) elevated from -10 degrees to +10 degrees. The delay to the onset of vasodilation averaged 5.0 +/- 1.8 s, and this delay was not altered by inhibition of nitric oxide synthase. Similar or longer delays were seen during sinusoidal exercise. Thus there is a significant delay before the onset of vasodilation after an increase in work intensity (muscle force) during locomotory exercise at constant speed.

Past studies have suggested that amlodipine, a dihydropyridine L-type Ca(2+) channel antagonist, may exert useful effects in congestive heart failure (CHF). The present study examined the effects of amlodipine or nifedipine treatment in a model of developing CHF on left ventricular (LV) pump function and myocyte contractility.Pigs (25 kg) were randomly assigned to 1 of 4 groups: 1) pacing-induced CHF (rapid atrial pacing at 240 bpm) for 3 weeks (n = 9), 2) concomitant Ca(2+) channel blockade with amlodipine (1.5 mg/kg/day) and rapid pacing (n = 7), 3) concomitant Ca(2+) channel blockade with nifedipine (0.7 mg/kg twice daily) and rapid pacing (n = 7), and 4) sham controls (n = 7). LV fractional shortening fell with pacing CHF from baseline values (17% +/- 1% v 42% +/- 1%, P.05). With rapid pacing and concomitant amlodipine treatment, LV fractional shortening increased from pacing CHF values (24% +/- 1%, P.05) but was unchanged with concomitant nifedipine treatment (20% +/- 2%, P =.2). LV myocyte velocity of shortening, as measured by high speed videomicroscopy, was reduced with pacing CHF compared with controls (42 +/- 2 microm/s v 87 +/- 9 microm/s, P.05), and increased from pacing CHF values with amlodipine or nifedipine treatment (62 +/- 8 microm/s, 64 +/- 4 microm/s, respectively; P.05). Inotropic response to extracellular Ca(2+) (8 mmol/L) was reduced with pacing CHF (94 +/- 5 microm/s v 160 +/- 15 microm/s, P.05) and increased from CHF values with amlodipine or nifedipine treatment (132 +/- 14 microm/s and 133 +/- 7 microm/s, respectively, P.05) CONCLUSIONS: These results suggest that the primary mechanism for the effects of amlodipine on myocyte contractility in developing CHF is because of direct Ca(2+) channel blockade.

Recent models of physician-patient communication emphasize information exchange in promoting partnership. Although considerable attention has been given to physicians' information exchange, little research has examined patients' communication contributions. The purpose of this research was to test the effectiveness of a training booklet designed to enhance patients' communication skills in information exchange. A nested design was used, such that 25 physicians each saw six patients, two patients in each of three communication skills interventions (i.e. trained, informed, control). The dependent variables included several discourse categories designed to assess patients' information seeking, provision, and verifying. Results indicate that trained patients engaged in more effective and efficient information seeking, provided physicians with more detailed information about their medical condition, and used more summarizing utterances to verify information they received from physicians. Additionally, dyads consisting of trained patients demonstrated a more patient-controlled style of communication than did dyads consisting of informed or untrained patients.

Objective To examine the relationship between communication skills training for patients and their compliance with recommended treatment. Design A randomized control design was used, with patients nested within physicians. Each physician was audiotaped with 6 patients, 2 patients in each of the 3 intervention conditions: (1) a trained group (n = 50) received a training booklet in the mail 2 to 3 days prior to the scheduled appointment, (2) an informed group (n = 49) received a brief written summary of the major points contained in the training booklet while in the waiting room prior to the scheduled appointment, and (3) an untrained group (n = 51) did not receive any form of communication skills intervention. Setting Participants included physicians and patients from 9 different primary care, family practice locations. Two locations were clinics associated with a large, university-based medical school and hospital, while 7 were private practice offices in the community. Participants The sample included 25 family physicians (averaging 11 years postresidency) and 150 patients. Patients were randomly selected from appointment records and randomly assigned to 1 of 3 intervention conditions. Intervention A training booklet designed to instruct patients in information seeking, provision, and verification. Main outcome measure Patients' compliance with medications, behavioral treatment (e.g., diet, exercise, smoking cessation), and/or follow-up appointments and referrals. Results Trained patients were more compliant overall than untrained or informed patients. Training positively influenced compliance with behavioral treatments and follow-up appointments and referrals. Conclusion Training patients in communication skills may be a cost-effective way of increasing compliance and improving the overall health of patients.

Details the steps which were taken in the process of hiring a Director of Pastoral Care for a 274-bed acute care regional referral center in southern Alberta, Canada. Stresses the importance of anchoring the hiring process steps within a relevant context. Offers recommendations for hospitals and clergy faced with a similar project.

Posttraumatic stress disorder (PTSD) is a disabling and prevalent psychiatric disorder. Researchers and scientists have developed a neurobiological basis, which provides a framework for understanding the complexities of PTSD, for many symptoms of the disorder. The estimated lifetime prevalence of PTSD among adult Americans is 7.8%, with women twice as likely as men to have PTSD. Onset of symptoms can occur years after exposure to trauma, and the duration of the illness can last a lifetime. Patients with PTSD often encounter multiple psychosocial problems that result from the symptoms they experience, and their distorted perceptions can affect relationships within the family and the workplace. Nurses in various roles (e.g., educator, therapist, prescriber, case manager, staff nurse) may encounter individuals with PTSD. The nursing profession has traditionally sought to explain sophisticated language to patients in understandable terms, and nurses serve in encouraging, supporting, and evaluating roles, all of which will be increasingly important as science and technology discover more information about the neurobiological basis for mental illnesses.

Radiotherapy portal imaging is the process of producing images using a radiation treatment linear accelerator or cobalt 60 unit. Portal images are used to evaluate the position of the radiation treatment beam and placement of shielding blocks with respect to the patient's anatomy. This paper discusses types, characteristics and clinical use of radiation therapy portal imaging systems.© (1996) COPYRIGHT SPIE--The International Society for Optical Engineering. Downloading of the abstract is permitted for personal use only.

Within the past few years, considerable progress has been made in the understanding of the molecular genetics of methane and methanol oxidation. In order to summarize this progress and to illustrate the important genetic methods employed, this review will focus on several well-studied organisms. These organisms include the gram-negative faculative methylotrophs Methylobacterium extorquens, Methylobacterium organophilum and Paracoccus denitrificans. In addition, the obligate methanotrophs Methylococcus capsulatus and Methylosinus trichosporium are discussed. We have chosen not to discuss the genetics of methanol oxidation in the yeasts or in gram-positive bacteria. Likewise, the genetics of related topics (for example, methylamine oxidation and carbon assimilation pathways) are not reviewed here. Broad host range conjugatable plasmids have enabled researchers to complement mutations and clone genes from gram-negative methylotrophic bacteria. More recently, 'promoter probe' derivative plasmids have been used to elucidate aspects of gene regulation. Also, alternative gene-cloning techniques are proving useful in circumventing problems in the genetic studies of the obligate methanotrophs, the group of bacteria that is the most refractory to traditional methods.

Hyperglycemia has been identified as potent and independent risk factor for adverse outcomes for patients. An initiative was undertaken to reduce hyperglycemia hospitalwide in adults.In a multistep process, insulin protocols were implemented hospitalwide via an electronic provider order entry system. Education regarding basal bolus insulin delivery preceded implementation. Protocols were modified in an ongoing manner on the basis of clinical staff feedback and blood glucose monitoring. Key practice changes included intravenous insulin for initial management in ICU patients, insulin replacement based on the basal bolus approach, elimination of sliding-scale insulin, standardization of blood glucose monitoring before meals, adjustment of prandial dose insulin based on food consumed, administration of prandial dose after the meal, evening snacks ordered based on insulin type, and a glycosolated hemoglobin (A1C) determination for patients with admission glucose180 mg/dL. Median inpatient glucose levels in patients with diabetes were assessed using statistical process control methodology.Between January 2004 and September 2007, median glucose for all inpatients with diabetes decreased 15% from 159 mg/dL to135 mg/dL. The percentage of inpatients with diabetes who experienced a day with a glucose measurement above 180 mg/dl decreased from 66% to 53%. Frequency of hypoglycemia (60 mg/dL) did not change following protocol implementation.Major improvements in hospitalwide blood glucose control are feasible and safe, employing standard protocols based on the basal-bolus concept. Improvement was sustained during a four-year period with ongoing institutional support, multidisciplinary education, collaboration between clinical services, and monitoring of clinical outcomes on a quarterly basis.

Contemporary medicine depends on computers the way 19th century farming depended on horses. In hospitals, virtually every department relies on computing in one form or another. Health workers, from nurses to cooks, find data terminals indispensable to their jobs. Ironically, doctors have been among the last to employ computers in their care of patients. Or more precisely, most doctors have not made direct use of the information handling functions of computers.

Despite efforts to standardize therapies for high cost Diagnosis Related Groups, little data exists regarding experiences with critically ill infants. We hypothesized that use of a carepath for extremely low birthweight (ELBW) infants in the first 14 days of life would result in 1) decreased variability in care and 2) decreased unnecessary laboratory procedures. This multidisciplinary carepath contained guidelines for laboratory monitoring, nutritional management, medications, nursing activities and parent education. Resource utilization in this group of 32 infants was compared to data collected prospectively on a group of 25 infants who would have been eligible for the carepath in the 9 months immediately prior to implementation. * p < 0.01 ** p

The convalescent course of 55 infants transported from a Level III hospital back to the community hospitals from which they were originally transported was compared with the course of 58 infants who convalesced in the tertiary center nurseries. The events in their prenatal course and acute neonatal course were similar, thus making comparisons of their convalescent course possible. Weight gain was greater among the transported infants for infants with birth weights greater than or equal to 2,000 g and comparable if birth weight was less than 2,000 g. Transported infants received fewer transfusions than their nontransported counterparts. Tolerance of feedings, the occurrence of apnea and bradycardia, and use and discontinuance of supplemental oxygen were similar in both groups. Major new health problems occurred in 27% of all subjects, 20% of transported infants and 32% of nontransported infants. Readmission to the tertiary center or a change in status to more intensive care in the tertiary center occurred in 10% of all infants, 7% of transported and 14% of nontransported infants. It was concluded that convalescing infants often presented new clinical problems, in similar numbers and severity whether convalescing in the tertiary center or after back transport to community hospitals. Community hospital care givers were considered alert to these new problems and to have provided appropriate care, including retransfer to the tertiary center when necessary.

The amounts of creatinine, protein, carbohydrate and sialic acid in the urine of 19 patients with cystic fibrosis (CF), 12 normal controls and 11 pathological controls with chronic lung disease have been determined. The mean creatinine excretion levels of the total CF group as well as the CF subgroups are significantly decreased when compared to normal controls but comparable to pathological controls. Mean urinary protein levels appear to be increased in patients with CF compared to normal controls and pathological controls but the increased levels resulted from factors (e.g., presence of diabetes mellitus) other than CF. No significant differences were found in amounts of total carbohydrate and sialic acid in urine and fractionated urinary preparations for the total group of nondiabetic patients with CF when compared to both normal and pathological controls. HPLC fractionation of low Mr (less than 10,000 Daltons) urinary preparations indicated the presence of an unknown peak in all of the antibiotic-treated CF patients, 43% of CF patients on low or no medication, 17% of the normal controls and 9% of the pathological controls. The present results illustrate the importance of including appropriate pathological controls and dividing patients with CF into subgroups according to clinical factors and types of therapy employed.

Rhizobium leguminosarum bv. trifolii T24 is ineffective in symbiotic nitrogen fixation, produces a potent antibiotic (referred to here as trifolitoxin) that is bacteriostatic to certain Rhizobium strains, and is very competitive for clover root nodulation (EA Schwinghamer, RP Belkengren 1968 Arch Mikrobiol 64: 130-145). The primary objective of this work was to demonstrate the roles of nodulation and trifolitoxin production in the expression of nodulation competitiveness by T24. Unlike wildtype T24, transposon mutants of T24 lacking trifolitoxin production were unable to decrease clover nodulation by an effective, trifolitoxin-sensitive strain of R. leguminosarum bv. trifolii. A non-nodulating transposon mutant of T24 prevented clover nodulation by a trifolitoxin-sensitive R. leguminosarum bv. trifolii when co-inoculated with a T24 mutant lacking trifolitoxin production. Neither mutant alone prevented nodulation by the trifolitoxin-sensitive strain. These results demonstrate that trifolitoxin production and nodulation are required for the expression of nodulation competitiveness by strain T24. A trifolitoxin-sensitive strain of R. meliloti did not nodulate alfalfa when co-inoculated with T24 and a trifolitoxin-resistant strain of R. meliloti. Thus, a trifolitoxin-producing strain was useful in regulating nodule occupancy on a legume host other than clover. Trifolitoxin production was constitutive in both minimal and enriched media. Trifolitoxin was found to inhibit the growth of 95% of all strains of R. leguminosarum bvs. trifolii, viceae, and phaseoli tested. Strains of all 13 biotypes of R. leguminosarum bv. trifolii were inhibited by trifolitoxin. Three strains of R. fredii were also inhibited. Strain T24 ineffectively nodulated 46 clover species, did not nodulate Trifolium ambiguum, and induced partially effective nodules on Trifolium micranthum. Since T24 produced partially effective nodules on T. micranthum and since a trifolitoxin-minus mutant of T24 induced ineffective nodules, trifolitoxin production is not the cause of the symbiotic ineffectiveness of T24.

Calculations are presented which demonstrate that the kinetics of dehydration of methylene glycol (hydrated formaldehyde) must be considered in determining the rate of hydroxymethanesulfonic acid formation in weakly acidic or neutral solution.

The clinical course of 55 back-transported (BT) infants was compared with that of 49 infants who remained at a regional peri natal center for convalescent care (NT). Although the mean birth-weight and mean gestational age of the BT infants was significantly less than that of NT infants (BT = 1614±522 gms and 32±2.7 wks, NT = 1902±626 and 33.1±2.5; p