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Mood Disorders Psychopharmacology Unit, University Health Network, Departments of Psychiatry and Pharmacology, University of Toronto, Toronto, Ontario, Canada
Youth Bipolar Disorders Program, Sunnybrook Health Sciences Centre, Department of Psychiatry, University of Toronto, Toronto, Ontario, Canada
Department of Psychiatry, University of Toronto, Toronto, Ontario, Canada
Mood and Anxiety Disorders Program, Sunnybrook Health Sciences Centre, Department of Psychiatry, University of Toronto, Toronto, Ontario, Canada
Douglas Mental Health University Institute, Department of Psychiatry, McGill University, Montréal, Québec, Canada
Mood and Metabolic Clinic, University Hospitals Case Medical Center, Case Western Reserve University, Cleveland, Ohio, USA
BACKGROUND: One goal of the Canadian Network for Mood and Anxiety Treatments (CANMAT) is to develop evidence-based and best practice educational programs and recommendations. Our group conducted a comprehensive literature review to provide evidence-based recommendations for treating metabolic comorbidity in individuals with major depressive disorder (MDD) and bipolar disorder (BD).
METHODS: We searched PubMed for all English-language articles published January 1966 to November 2010 using BD and MDD cross-referenced with metabolic syndrome, obesity, diabetes mellitus, hypertension, and dyslipidemia. That search was augmented by a review of articles reporting outcomes of an intervention targeting components of metabolic syndrome in individuals with MDD or BD.
RESULTS: Consensus exists for the recommendation that individuals with MDD and BD should be routinely screened for risk factors that increase risk for metabolic syndrome. For excess weight, the best-studied pharmacologic approaches are metformin and topiramate, with emerging evidence for liraglutide and modafinil. For binge eating disorder, the best evidence in mood disorders was for cognitive-behavioral therapy as well as topiramate, zonisamide, and in select cases selective serotonin reuptake inhibitors. For dysglycemia, dyslipidemia, and hypertension, evidence supports cognitive-behavioral interventions and anti-diabetic, antilipidemic, and antihypertensive treatments.
CONCLUSIONS: Comprehensive care of individuals with mood disorders should include routine evaluation of the risk and presence of metabolic syndrome and its components. Systematic evaluation of preventative and targeted treatments of metabolic syndrome in mood disorder populations is insufficient.
KEYWORDS: bipolar disorder, diabetes mellitus, major depressive disorder, obesity, cardiovascular disease, hypertension, dyslipidemia
Metabolic illness—including obesity, metabolic syndrome, and insulin resistance—has been amply documented during the past decade to differentially affect individuals with major depressive disorder (MDD) and bipolar disorder (BD).1,2 The co-occurrence of metabolic syndrome in the mood disorder population is associated with a more complex affective presentation and less favorable course and outcome.3,4 The considerable phenotypic overlap between mood disorders and metabolic syndrome provides the framework for hypothesizing that these conditions, albeit discrete, may have overlapping pathophysiology.5-7
Practitioners often encounter individuals with mood disorders who are overweight/obese and/or have evidence of dyslipidemia, dysglycemia, and/or hypertension. Prevention, screening, timely detection, treatment, and management of co-occurring metabolic abnormalities is a widely accepted recommendation for individuals with mood disorders.8 Emerging evidence also suggests that components of metabolic syndrome (eg, hypertension, obesity) are associated with negative effects on memory function in individuals with psychotic disorders.9,10 Moreover, mortality studies indicate that excess death in the mood disorder population is largely the result of excess cardiovascular disease, a consequence of the metabolic syndrome.11 Notwithstanding the salience and hazards posed by metabolic comorbidity in mood disorder populations, relatively few resources are available to inform treatment decisions in individuals with mood disorders when co-occurring metabolic syndrome or its components are present.
Relatively few studies have aimed primarily to evaluate the effect of metabolic syndrome or its components on the treatment of individuals with mood disorders (and vice versa). As in other sections of these treatment recommendations, we aim to synthesize and summarize extant study results pertaining to this topic. The tabular presentation of data is intended to foster accessibility and organizational clarity, as well as highlight gaps in the evidentiary base. This paper is organized into 3 sections: introduction, evidence review, and conclusions.
We conducted a PubMed search of all English-language articles published between January 1966 and November 2010. Search terms were bipolar disorder and major depressive disorder cross-referenced with: metabolic syndrome, obesity, diabetes mellitus, hypertension, and dyslipidemia. The search was augmented with a manual review of article reference lists and conference proceedings; the overarching aim was to identify all original articles reporting on the outcomes of an intervention targeting metabolic syndrome or its components in individuals with MDD or BD.
Metabolic syndrome in MDD and BD. Metabolic syndrome comprises a cluster of clinical and biochemical risk factors for cardiovascular disease, diabetes mellitus, and premature mortality.12 Although several definitions have been proposed for metabolic syndrome, the most often cited is the Third Report of the U.S. National Cholesterol Education Program Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (ATP-III).13 All schemas for defining metabolic syndrome emphasize obesity and insulin resistance as primary pathophysiologic processes. According to ATP-III, the clinical features defining metabolic syndrome are abdominal adiposity, hypertension, impaired fasting glucose or diabetes mellitus, and atherogenic dyslipidemia.
The age-adjusted prevalence of ATP-III-defined metabolic syndrome in American adults is 23.7%, according to data from the Third National Health and Nutrition Examination Survey.14 The risk for metabolic syndrome increases with age and is highest among women and Hispanic populations.2 The age-adjusted prevalence of World Health Organization (WHO)-defined metabolic syndrome in Europe is relatively lower (15.7% for men, 14.2% for women).15,16
The major underlying risk factors for metabolic syndrome are abdominal obesity and insulin resistance.17 Habitual inactivity, aging, and hormonal imbalances also are considered to be pathogenic factors.18 Metabolic syndrome predisposes an affected individual to type 2 diabetes mellitus and is considered to be a multidimensional risk factor for atherosclerotic cardiovascular disease. Other conditions associated with metabolic syndrome are fatty liver, polycystic ovarian syndrome, sleep apnea, and lipodystrophies.19
Before the widespread use of modern psychotropic agents, individuals with mood and psychotic disorders were documented to be at increased risk for obesity, hypertension, and diabetes mellitus when compared with unaffected populations.20 During the past decade, replicated evidence indicates that individuals with MDD and BD are differentially affected by metabolic syndrome. Interpretations and inferences that can be drawn from the existing data are limited by heterogeneity in study design (longitudinal vs cross-sectional), sample composition (epidemiologic vs clinical), treatment, diagnostic criteria for mood disorder and metabolic syndrome, and measurement of affective symptoms. Nevertheless, the reported rate of metabolic syndrome in MDD and BD ranges between 20% and 65%.22
In a clinical trial population, a similar prevalence of metabolic syndrome was reported in 125 stabilized outpatients with bipolar I disorder, where the rate of metabolic syndrome was 36%. Elevated waist circumference was identified as the most commonly encountered criterion (>60% of the population).22
Several factors predispose and portend mood disorder populations to metabolic syndrome (FIGURE 1). Medication-associated adverse events are the most replicated causative factor. Other evidence supports habitual inactivity, insufficient access to primary and preventative health care, and low socioeconomic status as contributing variables. The psychobiology of mood disorders (eg, hypothalamic-pituitary-adrenal [HPA] axis dysregulation, inflammatory cytokines, oxidative stress) may be a pathophysiologic nexus with metabolic syndrome and its components.5 Relatively few studies have reported on contributing effects of early childhood adversity on metabolic syndrome in mood disorders. Environmental insults are associated with several components of metabolic syndrome in nonpsychiatric samples and are more likely to occur in individuals with MDD or BD when compared with the general population.21
For clinicians, identifying metabolic syndrome in persons with mood disorders is important because of the complex interrelationship between metabolic syndrome and mood disorders.22 Comorbidity with metabolic syndrome is associated with a more complex illness presentation, lower probability of recovery, and more frequent episodes and suicide attempts. For example, the first report describing an association between metabolic syndrome and BD evaluated 171 individuals enrolled in the Bipolar Disorder Center for Pennsylvanians.23 Fagiolini et al. reported that 30% of their sample met ATP-III criteria for metabolic syndrome. They also reported that abdominal obesity was associated with suicidality.
The only study to include euthymic patients also reported an increased rate of metabolic syndrome. Data from 99 euthymic BD patients (51 female, 48 male) were included for the analysis. The sample mean age (SD) was 38 years (11.2). Thirty-one patients (32.6%) met criteria for metabolic syndrome, with no significant differences as a function of sex. Thirty-seven (41.1%) met the waist circumference criterion; 26 (27.6%) and 28 (29.7%) met diastolic and systolic blood pressure criteria; 31 (36.4%) met the high-density lipoprotein (HDL) criterion; and 33 (38.8%) met the triglyceride criterion. Five (6.1%) met the criterion for elevated fasting glucose, even though diabetes mellitus or glucose/insulin dysregulation were exclusion criteria at screening.24
Other studies in BD have observed an inverse correlation between cardiometabolic illnesses and the probability of achieving remission from depressive symptoms.25 Overweight and obese patients receiving conventional mood stabilizers such as lithium and valproate have been reported consistently to exhibit greater chronicity and severity of depression as well as lower psychosocial functioning.25,26
Mortality studies in mood disorders indicate that cardiometabolic disorders are the most common causes of premature death.27 In addition, individuals with BD have an increased prevalence of diabetes mellitus and higher rate of early mortality subsequent to the diagnosis of diabetes.28 Identifying risk factors (eg, metabolic syndrome) that increase risk for cardiovascular disease and diabetes therefore is a priority research objective in the mood disorder population.
FIGURE 1 Factors that predispose and portend mood disorder populations to metabolic syndrome
Treating the obese patient with MDD or BD. Overweight and obesity are the most common nutritional disorders in the United States.29 In adults, an epidemic rise in the prevalence of self-reported overweight (body mass index [BMI] >25 kg/m2) and obesity (BMI >30 kg/m2) has occurred in the past 2 decades.30,31 Moreover, the prevalence of obesity in child and adolescent populations has almost tripled since 1970.32 The medical complications of overweight and obesity are well-established: osteoarthritis, type 2 diabetes mellitus, cardiovascular disease, and some forms of cancer.33 All of these maladies are relatively more common in the mood disorder population.27,34-36 Many of the causes of overweight and obesity are potentially modifiable with behavioral and preventative treatment, which is recommended as first-line treatment (TABLE 1).37
No approved pharmacologic agent for MDD or BD has been purposefully studied in overweight/obese individuals. When selecting and sequencing pharmacotherapy in the overweight/obese mood disorder patient, the clinician needs to consider both short- and long-term weight-gain potential and the psychotropic agent's effect on adipose tissue distribution. Most atypical antipsychotics cause varying degrees of weight gain, as shown in acute and continuation studies. Weight gain with some antidepressants (eg, mirtazapine, paroxetine) often is slow but inexorable. The only approved agent for MDD or BD that is associated with weight loss is bupropion.38 Lamotrigine also has been associated with moderate weight loss in patients with bipolar I disorder and obesity but does not appear to be associated with weight loss in nonobese patients.39
Pharmacokinetics need to be considered when prescribing and monitoring the effects of psychotropic agents for overweight/obese individuals. Nonalcoholic steatohepatitis (NASH), a common cause of liver inflammation, is associated with obesity, insulin resistance, and hyperlipidemia. An estimated 10% to 15% of patients with histologically proven NASH progress to cirrhosis and its complications, such as liver failure and hepatocellular carcinoma.40 The effect of fatty infiltration of the liver on psychotropic agents' pharmacokinetics has not been sufficiently evaluated. Moreover, drug development programs do not require sponsors to report on the pharmacokinetics of agents as a function of percentage of adipose tissue. Whether NASH represents a form of pharmacokinetic variability in overweight patients remains a testable hypothesis.
The initial approach to managing overweight/obese affective disorder patients is to prevent further weight gain, increase in BMI (kg/m2), or visceral adipose tissue. Behavioral strategies, dietary modification, and increased aerobic activity are considered general recommendations for persons with mood disorders. Although a rationale for aerobic exercise as salutary in mood disorders is available for both MDD and BD, much of the available evidence has reported a modest beneficial effect of exercise in MDD.41-43
Symptomatic remission and functional recovery are the therapeutic objectives in managing the mood disorder patient. Replacing a weight-gain offending agent with a weight-neutral/favorable medication is recommended if the index agent's overall therapeutic value is unfavorable or equivocal. In many circumstances, however, psychotropic agents associated with weight gain should be continued if the clinician judges that the index agent provides optimal illness control. If behavioral strategies or substitution for a psychotropic agent associated with less weight gain prove unsuccessful, clinicians may consider using bariatric medicine.
The WHO recommends using bariatric medicine to control weight in an individual with a BMI of ≥27 with weight-related morbidity (eg, diabetes mellitus) or a BMI of ≥30 without weight-related morbidity.44 FDA-approved agents for weight loss are phentermine and orlistat. Phentermine, a sympathomimetic agent, has not been studied in mood disorder populations and has the potential to induce hypomania/mania.45 Although phentermine may help alleviate depressive symptoms in binge eating disorder, it has not been established as safe or efficacious in mood disorder populations.46 The elevated rate of cardiovascular disorders in mood disorder populations is an additional concern with sympathomimetics in this population.47
Orlistat is a pancreatic lipase inhibitor and is not known to alter the pharmacokinetics of psychotropic agents. This medication has no central activity, so the potential for drug-drug interaction with centrally acting psychotropic medications is small. Orlistat often is not acceptable to patients, however, because of adverse abdominal effects such as loose stools, possible uncontrolled bowel movements, flatulence with discharge, and abdominal pain.48
A naltrexone-bupropion combination also has been studied in individuals with obesity. The hypothesized mechanism of this agent's weight-loss effect is the hypothalamic melanocortin system, which integrates input related to energy balance and produces anorexigenic signalling.49 Moreover, both naltrexone and bupropion modulate the mesolimbic reward system implicated in reward value and goal-oriented behavior. The rationale for combining naltrexone with bupropion was based on observations that bupropion stimulates hypothalamic pro-opiomelanocortin neurons, whereas naltrexone blocks opioid-mediated pro-opiomelanocortin auto-inhibition. Contemporary models of obesity have implicated excess food intake as a behavioral consequence of addiction.49-51
Results from the largest of 4 Phase III studies with bupropion 360 mg/naltrexone 32 mg reported on 2 primary efficacy endpoints at 56 weeks: percent change in body weight and proportion of participants who achieved a ≥5% decrease in body weight.49 Mean change in body weight was –1.3% with placebo, and –6.1% with the naltrexone/bupropion combination. Sixteen percent of participants assigned to placebo had a decrease in body weight of ≥5% compared with 48% assigned to naltrexone/bupropion. The most frequent adverse event in participants assigned to combination treatment was nausea. A transient increase of approximately 1.5 mm Hg in mean systolic and diastolic blood pressure was followed by a reduction of approximately 1 mm Hg below baseline in the naltrexone/bupropion group. (The naltrexone-bupropion combination is not FDA-approved for weight loss; January 2012).
Modafinil is a stimulant-like wake-promoting agent that has shown utility as an adjunctive agent in treating bipolar depression.52 Emerging evidence indicates it also may promote weight loss through reduced food intake.53 Further studies will be needed to confirm this property.
Other agents have been used off-label for managing obesity in patients with mood disorders, often as a secondary prevention strategy for psychotropic-associated weight gain. These include topiramate, metformin, reboxetine, zonisamide, nizatidine, and amantadine.54-56 Liraglutide, a glucose lowering agent and glucagon-like peptide-1 (GLP-1) analogue, also has been evaluated as a weight loss agent in patients with obesity.57 The mechanisms that mediate liraglutide's weight reduction effects include appetite suppression and delayed gastric emptying.58 In a double-blind, placebo-controlled, 20-week trial, with open-label orlistat as an active comparator, participants taking liraglutide lost significantly more weight than did those taking placebo or orlistat. Seventy participants (76%) receiving liraglutide, 3 mg/d, lost >5% of baseline body weight compared with 29 (30%) receiving placebo and 42 (44%) receiving orlistat.57 To our knowledge, liraglutide has not been studied specifically in individuals with mood disorders.
Taken together, available evidence provides the greatest support for metformin as a pharmacologic treatment of weight gain. Most studies of metformin have attempted to mitigate antipsychotic-associated weight gain. A substantive body of evidence also exists in support of topiramate. The naltrexone/bupropion combination, although insufficiently studied, may be applicable particularly to individuals with mood disorders. A meta-analysis of pharmacologic treatments for obesity concluded that sibutramine, orlistat, phentermine, and probably diethylpropion, fluoxetine, bupropion, and topiramate promote weight loss for at least 6 months when given along with recommendations for diet and exercise. The additional weight loss attributable to these medications is modest (>5 kg at 1 year) but clinically significant.59
Bariatric surgery is recommended for individuals with BMI of 35 to 39 with ≥1 obesity-associated comorbidity requiring medical treatment or BMI ≥40 with or without obesity-associated comorbidity.60 The 3 most common bariatric procedures are Roux-en-Y gastric bypass, adjustable gastric banding, and sleeve gastrectomy.61 The effects of bariatric surgery on the pharmacokinetics of psychotropic medications have not been sufficiently evaluated. Because these procedures change the GI tract's surface area and transit time, postsurgical serum level monitoring and dosage adjustments may be warranted for many patients, notably those taking controlled-release or long-acting medications.
The impact of bariatric surgery on mood disorder outcomes also is understudied.62 Nevertheless, a 6-year follow-up analysis suggests that BMI reductions are associated with stable improvement in employment, reduced severity of anxiety and depressive symptoms, and improved health-related quality of life.63 Patients with actively treated depression likely could expect gastric bypass surgery outcomes equivalent to those of individuals without identifiable psychiatric illness or treatment.64 Available evidence suggests that a current diagnosis of an Axis I or II condition was not associated with gastric bypass outcomes at 6 months, but the presence of a lifetime mood or anxiety disorder was associated with a smaller decrease in BMI over 6 months.65,66 Most trials of gastric bypass in psychiatric populations are limited by short follow-up and small sample size.
Levels of evidence supporting treatments for overweight/obesity in patients with bipolar disorder or major depressive disorder
Binge eating disorder. Eating disorders are more likely to co-occur in BD than in MDD,67 and individuals with BD I and II are affected similarly by eating disorders. In the BD population, the presence of a comorbid eating disorder is associated with female sex, younger age, early age at onset of BD, mixed episodes, rapid cycling, suicide attempts, severe obesity, alcoholism, and drug abuse.68 The high frequency of binge eating as a separate diagnosable disorder (ie, binge eating disorder [BED]) or as part of bulimia nervosa warrants special consideration in the mood disorder population.
BED may compound the risk of metabolic syndrome over and above the risk attributable to obesity alone.69 Anticonvulsants and antidepressants have been the most studied agents in treating eating disorders (TABLE 2). Topiramate has the broadest spectrum of action, demonstrating anti-binge eating, anti-purging, and weight-loss effects, as demonstrated in 2 placebo-controlled trials in bulimia nervosa and 3 placebo-controlled trials in BED with obesity.70 Topiramate also has shown beneficial effects in night-eating syndrome and in sleep-related eating disorder.70
Zonisamide has demonstrated efficacy in treating BED and obesity. Topiramate and zonisamide are limited by GI- and CNS-related adverse events.70 Contrasting results are available for phenytoin in compulsive or binge-eating behavior, and for the few studies of carbamazepine or valproate. Lithium has been evaluated as an augmentation of topiramate in individuals with BD and comorbid BED and obesity.71 Negative data exist for lamotrigine in BED with obesity.69 Positive controlled data exist for escitalopram, citalopram, and atomoxetine across variable measures such as binge episodes, binge days, weight, BMI, and global severity of illness scores.72-74 Open-label data are available for sodium oxybate.75 No existing pharmacologic treatment strategy has been primarily examined in individuals with bulimia nervosa/BED in BD or MDD.
Levels of evidence supporting treatments for bulimia nervosa/binge eating disorder in patients with bipolar disorder or major depressive disorder
Treating the hypertensive patient with MDD or BD. MDD and depressive symptoms are well-established risk factors for incident and recurrent coronary artery disease (CAD), decreased quality of life, and all-cause mortality in individuals with pre-existing heart disease.76 The risk attributable to depressive symptoms is independent of other known prognostic markers of CAD.76 Moreover, epidemiologic studies indicate that MDD is a risk factor for incident heart disease in populations initially free of heart disease.77 The association between mood disorders and cardiovascular disease is moderated and mediated by economic, behavioral, physiological, and iatrogenic factors.78 Results from cross-sectional and prospective studies have reported an association between depression and transient increases in blood pressure, as well as hypertension and hypotension.79
Available evidence also indicates that depressive symptoms may be more difficult to treat in patients with comorbid CAD. For example, in the Sertraline Anti-Depressant Heart Attack Trial, which evaluated sertraline in patients with acute myocardial infarction or unstable angina, the overall effect size of sertraline on the depression endpoint was small and only significant in the subset of patients with recurrent depression.80 Likewise, treatment with sertraline did not provide greater reduction in depression or improved cardiovascular status compared with placebo among patients with heart failure and depression (this may be due to a low event rate).81
Nevertheless, SSRIs may be tried as a therapeutic modality and are generally considered "blood pressure neutral" despite reports of hypo- and hypertension associated with their use (TABLE 3). Serotonin-norepinephrine reuptake inhibitors (SNRIs) such as venlafaxine, desvenlafaxine, and duloxetine are associated with dose-dependent elevations in systolic/diastolic blood pressure and sustained diastolic hypertension in a relatively small number of treated individuals. Hypertension has been reported with bupropion, although randomized, placebo-controlled, dose-dependent studies of bupropion's vasopressor effects have reported neutral and/or minimal effects on blood pressure.
Mirtazapine, nefazodone, and trazodone exhibit minimal effect on blood pressure, although orthostatic hypotension has been reported. Taken together, the tricyclic antidepressants and monoamine oxidase inhibitors (MAOIs) are associated with orthostatic hypotension. The possibility for malignant hypertension is increased when MAOIs or moclobemide are coadministered with other monoaminergic-based agents or tyramine-rich foods. Vasopressor effects are not noted with atypical antipsychotics, lithium, or anticonvulsant mood stabilizers.
Levels of evidence supporting treatments for hypertension, dyslipidemia, and dysglycemia in patients with bipolar disorder or major depressive disorder
Treating the dyslipidemic patient with MDD or BD. Dyslipidemia is an independent risk factor for incident and recurrent CAD.13 ATP-III indicates that low-density lipoprotein cholesterol (LDL-C) is the primary factor predicting CAD risk.13 A direct association between LDL-C (and total cholesterol) and new-onset CAD or recurrent coronary events has been reported in population-based studies.82 The CAD risk associated with atherogenic LDL-C levels (>100 mg/dl; 2.59 mmol/L) is greater in the presence of other established CAD risk factors.13,83 Recent meta-analyses indicate that elevated triglyceride levels are an independent risk factor for CAD.84,85
Broadly sketched, some (notably weight-gain promoting) antidepressants exert a clinically significant effect on lipid homeostasis that is yoked to alterations in body weight. Compelling evidence is lacking that some antidepressants significantly alter lipid levels independent of their effects on body weight, BMI, nutrition, and energy expenditure. On the other hand, antidepressants' effect on glucose-insulin homeostasis has been documented. Antidepressants directly affect tissue sensitivity to insulin (with increased insulin and glucose levels), and antipsychotics exert a variety of adverse effects on body anthropometrics and metabolic parameters.86-88 The effect of anticonvulsant mood stabilizers on lipid levels is more variable. For example, a neutral effect on lipid homeostasis has been reported for lamotrigine. In patients taking divalproex, observations of circulating lipid levels have been mixed: increased, no change, and decreased.
Abnormal lipid homeostasis in individuals receiving atypical antipsychotics most often is associated with weight gain. Although atypical antipsychotics as a class have been consistently implicated in promoting weight gain and cardiometabolic complications, recent evidence suggests a differential risk profile in the long-term treatment of BD. Maintenance studies in BD have reported clinically significant weight gain with most atypical antipsychotics, notably clozapine and olanzapine, with less weight gain and consequently metabolic abnormalities, in individuals receiving asenapine, aripiprazole, lurasidone, and ziprasidone.89-92
Aripiprazole and ziprasidone generally are regarded as having more favorable metabolic profiles compared with other atypical antipsychotics, although longer-term data have become available only recently. Aripiprazole can be used both short- and long-term without compromising patients' metabolic status, as no significant difference was observed between aripiprazole and placebo during 26 weeks of treatment. However, clinically significant weight gain occurred in a higher proportion of patients receiving aripiprazole (13%) compared with individuals receiving placebo (0%).93 In a randomized, double-blind, placebo-controlled maintenance trial of ziprasidone adjunctive to a mood stabilizer (lithium or valproate), overall changes in weight, lipids, or other metabolic parameters were relatively small and similar to those seen with placebo. This lack of significant change may reflect a continuing neutral and/or minimal effect of ziprasidone over time on these parameters (asenapine and aripiprazole also exert minimal effect on these parameters in long-term BD studies).94
Even though dyslipidemia is the second-most commonly encountered metabolic syndrome criterion, no studies have evaluated the effect of an antilipidemic therapy in mood disorder populations. Behavioral and dietary strategies for weight management are encouraged as first-line approaches.
Medications for dyslipidemia are HMG-CoA reductase inhibitors ("statins"), fibrates, niacin, and resins. All can reduce hypercholesterolemia. The statins (eg, atorvastatin, simvastatin, rosuvastatin, pravastatin) exert a robust effect on lowering LDL-C and also reduce very low-density lipoprotein cholesterol production. Statins' benefits include salutary effects on endothelial function, inflammatory signalling, foam cell formation/cholesterol accumulation, plaque stabilization, thrombosis formation, and antioxidation.
Adverse events associated with statins are largely GI-related. Increases in liver function tests commensurate with Hy's rule (ie, aspartate aminotransferase/alanine aminotransferase >3 times upper limits of normal [ULN] and bilirubin >2 times ULN) occur in approximately 2% of statin-treated patients. In addition, myopathy and rhabdomyolysis have been associated with statin therapy. Coadministration of agents that inhibit the 3A4 family of cytochrome P450 enzymes may increase the risk for liver and/or muscle toxicity with statin therapy. The use of statins and other lipid-lowering drugs does not appear to be associated with an increased risk of depression or suicide. In a nested case-control analysis, individuals with current statin use had a lower risk of developing depression, perhaps reflecting an improved quality of life because of decreased risk of cardiovascular events or greater attention to health maintenance.95
Some studies suggest an association between mood symptoms and abnormally low levels of cholesterol, although definitive evidence does not exist as to whether this represents a state or trait phenomenon. In one small study, lower cholesterol levels appeared to predispose individuals with BD to greater manic (but not depressive) symptomatology.96 Some studies also have found that individuals who use more violent methods to attempt suicide have lower cholesterol levels than those who use less violent methods.97
Treating the dysglycemic patient with MDD or BD. Diabetes mellitus is a group of metabolic diseases characterized by chronic hyperglycemia resulting from defects in insulin secretion, insulin action, or both.98 The estimated prevalence of diabetes mellitus in adults in the United States is 8%, with higher rates in older populations and some racial and ethnic groups (eg, African-Americans, Hispanics, and Southeast Asians).99 Persons with diabetes mellitus are at risk for acute life-threatening consequences such as hyperglycemia associated with ketoacidosis and nonketotic hyperosmolar syndrome.98,99 Long-term medical complications of diabetes mellitus include blindness, cardiovascular disease, end-stage renal disease, nontraumatic limb amputation, cognitive impairment, and peripheral and autonomic neuropathy.
Available evidence suggests that diabetic disorders and dysglycemia are more commonly encountered in individuals with MDD and BD than in general populations. Evidence is growing that conditions caused by abnormalities in insulin regulation, such as insulin resistance and type 2 diabetes mellitus, may increase the risk of age-related cognitive decline.100,101 Recently, a 4- and 10-year prospective study determined that metabolic syndrome and its individual components (ie, hyperlipidemia, hyperglycemia, hypertension, and abdominal obesity) significantly increased the risk of developing dementia, mild cognitive impairment, and decreased performance on global cognitive test scores.102,103 Moreover, the link between depression and dementia may be mediated in part by disturbances in insulin/ glucose homeostasis. Insulin is a regulatory peptide and is hypothesized to play a critical role in both physiologic (eg, neurotrophism, neuroplasticity, neuromodulation, neuroprotection) and pathophysiologic CNS processes (eg, Alzheimer's disease [AD]).104 A derivative of these observations is the hypothesis that the prevention and comprehensive treatment of depressive symptoms and insulin/glucose abnormalities would have the largest impact on reducing the incidence of dementia, possibly outweighing the effect of removing the ApoE4 genotype, which represents the best known risk factor for AD.105
Taken together, evidence indicates that successful treatment outcomes can be expected for both diabetes and mood disorders. A recent meta-analysis indicated that the combined effect of all antidepressant therapies in individuals with diabetes mellitus is moderate; a large effect is noted for psychotherapeutic interventions combined with diabetes self-management and moderate for pharmacologic treatment.106 No controlled trials have evaluated the effect of antidiabetic treatment in individuals with BD.
Psychotropic medications commonly disrupt glucose homeostasis; the most replicated evidence exists for weight-gain promoting antidepressants and atypical antipsychotics. Abnormal glucose homeostasis often is associated with decreased kidney function, which may affect the clearance of several psychotropic agents (eg, lithium). The commonly employed antidiabetic agents are insulin, sulfonylureas (eg, glipizide), biguanides (eg, metformin), thiazolidinediones (eg, pioglitazone), GLP-1 (eg, exenatide), and dipeptidyl peptidase-4 inhibitors (eg, sitagliptin).
Given the pathophysiologic overlap between metabolic syndrome and depressive disorders, a small pilot study evaluated the use of pioglitazone, an insulin sensitizer of the thiazolidinedione class, as monotherapy or adjunctive therapy for the treatment of major depressive episodes that co-occurred with abdominal obesity or metabolic syndrome.107 The study's primary objective was to test whether improving insulin sensitivity with pioglitazone would be accompanied by an antidepressant response.
Pioglitazone treatment over an acute 12-week period was found to significantly reduce depression severity. Pioglitazone also was associated with improvement in measures of glucose homeostasis and dyslipidemia, including a significant reduction in fasting glucose, triglycerides, LDL-C, and HDL-C. Levels of highly sensitive C-reactive protein, a biomarker of inflammation implicated in the risk of first incident and recurrent cardiovascular events, also decreased during pioglitazone treatment. Similar to metformin, pioglitazone may represent a treatment strategy to help prevent diabetes from developing in high-risk patients, such as those receiving atypical antipsychotics.107
Among the glucose-lowering agents, the largest quantity of evidence exists for metformin as an adjunctive agent to mitigate weight gain. Most metformin studies are short-term and have focused on nonwhite populations (ie, Han Chinese) or patients receiving concomitant olanzapine therapy. The drug appears to be effective as a weight prevention or reduction agent among individuals with psychiatric disorders taking antipsychotics when used in combination with a lifestyle program.108 The effect of metformin on anthropometrics and insulin sensitivity are beneficial but modest, with one meta-analysis finding a mean weight difference of 3.16 kg.109
A comprehensive evaluation of patients with mood disorders includes assessing medical and behavioral factors associated with metabolic syndrome. Screen all patients for exercise habits, eating patterns, comorbid BED, bulimia nervosa, caffeine dependence, smoking, and thyroid dysfunction. Obtain baseline weight and BMI measurements; waist-to-hip ratio is an optional measure but a reliable proxy of visceral adipose tissue. Measure fasting blood glucose and lipid fractionation at baseline, and provide ongoing surveillance of anthropometrics and metabolic parameters. Despite consensus on the need for baseline and systematic monitoring, evidence indicates that most individuals with mood (and psychotic) disorders are not monitored on a regular basis.
Individuals with a mood disorder and metabolic syndrome ideally should receive care from a multidisciplinary coordinated team, with patients assuming an active role in their care. In patients with pre-diabetes (impaired fasting glucose/impaired glucose tolerance) lifestyle modification is strongly recommended.98
American Diabetes Association guidelines on the treatment of diabetes mellitus recommend earlier screening and more frequent monitoring of high-risk patients.110 The basic principles of managing metabolic syndrome in diabetic individuals are similar in mood disorder and non-psychiatrically affected populations. Unique, however, to diabetic individuals with mood disorders is their vulnerability to depression (ie, associated with poor diabetes compliance), propensity for impulsivity and suicidal behavior, comorbidity with alcohol and substance use disorders, higher prevalence of cardiovascular disease and smoking, frequent overeating and inactivity, and exposure to weight-gain promoting psychotropic agents.
DISCLOSURES: Dr. McIntyre is on advisory boards for AstraZeneca, Bristol-Myers Squibb, Eli Lilly and Company, Janssen-Ortho, Lundbeck, Merck, Pfizer, and Shire; is on speakers bureaus for AstraZeneca, Eli Lilly and Company, Janssen-Ortho, Lundbeck, Merck, Otsuka, and Pfizer; is involved in CME activities with AstraZeneca, Bristol-Myers Squibb, CME Outfitters, Eli Lilly and Company, Lundbeck, Merck, Otsuka, Pfizer, and the Physicians' Postgraduate Press; and receives research grants from AstraZeneca, Eli Lilly and Company, Forest, Janssen-Ortho, Lundbeck, Pfizer, Sepracor, and Shire. Dr. Alsuwaidan reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products. Dr. Goldstein receives grant/research support from Pfizer and is a speaker for Purdue Pharma. Dr. Taylor receives grant/research support from Bristol-Myers Squibb and Novartis, is a consultant to Bristol-Myers Squibb and Eli Lilly and Company, and is a speaker for Bristol-Myers Squibb, Eli Lilly and Company, Lundbeck, and Pfizer. Dr. Schaffer receives grant/research support from Pfizer Canada and the Canadian Institutes of Health Research (CIHR); is a consultant to AstraZeneca, Bristol-Myers Squibb, Eli Lilly and Company, and Lundbeck; and is a speaker for AstraZeneca, Bristol-Myers Squibb, and Eli Lilly and Company. Dr. Beaulieu receives grant/research support from AstraZeneca, Biovail, Bristol-Myers Squibb, the CIHR, Eli Lilly and Company, Fonds de recherche du Québec, Janssen-Ortho, Lundbeck, Merck-Frosst, Novartis, the National Alliance for Research on Schizophrenia and Depression, Pfizer Servier, Revue Santé mentale au Québec, and the Stanley Foundation; is a consultant to AstraZeneca, Bristol-Myers Squibb, Eli Lilly and Company, GlaxoSmithKline, Janssen-Ortho, Lundbeck, Oryx, Schering-Plough Merck, Wyeth Pfizer; and is a speaker for AstraZeneca, Biovail, Bristol-Myers Squibb, Eli Lilly and Company, GlaxoSmithKline, Janssen-Ortho, Lundbeck, Organon, Oryx, and Wyeth Pfizer. Dr. Kemp is a consultant to Bristol-Myers Squibb and Janssen; is a speaker for AstraZeneca and Pfizer; and his spouse has been a minor shareholder of sanofi-aventis and Abbott Laboratories within the last 12 months.
Annals of Clinical Psychiatry ©2012 Quadrant HealthCom Inc.
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Aloo Gobi
What the hell is that word? I don't even know. I definitely did not spell that right earlier. Thank god for Google. Or is Google actually God? Oh… Read More »
Sweet Curried Cauliflower Soup
Yep, jinxed myself on my car. She's laughing at me. I don't get her humor. It's expensive. So I have a problem. If you haven't noticed, I don't… Read More »
Smoky Bacon Chili
You know what I hate? Well, it seems like a lot of things by sound of my posts at times, but that's not totally true. I do hate… Read More »
Butternut Squash Curry Chili
I went to the Martin Solveig show the other night. It was at Beta nightclub. If you have never been there before, you can prob here a cops… Read More »
Garlic Chicken Butternut Squash Lasagna
I know some pretty rad bloggers out there. Know, meaning I read their blogs. Read, meaning I look at their pictures. And then I sometimes steal their ideas…. Read More »
Roasted Garlic Cauliflower Mashed Potatoes
I really liked this weekend. I did….ummmm….nothing. I slept 20+ hours, ate A LOT of food, and watched Disney movies. And movies about love. Terrible idea. I hate… Read More »
Pumpkin Cream Chicken Casserole
Let's chat. Laura and I are sitting on the couch right now, watching 'What Happens in Vegas' while she sings a random tune and makes random noises. She's… Read More »
Breakfast Pizza
I really did want to go out this past weekend, I swear I did. But alas, thinking about trying on outfits that don't fit, while trying to look… Read More »
Roasted Garlic Red Pepper Pesto Tilapia
As you may have noticed from previous posts, I really like my roommate Laura. She's super good looking, so I hang around her to look cooler. She also… Read More »
Coconut Ginger Mushroom Chicken
Oh so you know what's one of my favorite feelings in the world? My ass burning when I get in the shower. No, it's not what you may… Read More »
Pork Hatch Chile Breakfast Patties
I think I have an addictive personality. I'll find something I really like and can't get my mind off of it. Like Americanos with heavy cream, dear lord,… Read More »
Spinach and Artichoke Chicken Carbonara Pasta
People are obsessed with bacon. I mean, OBSESSED. Have you seen some of the blogs out there, dedicated strictly to bacon? It's unreal the heart felt love and… Read More »
Spicy Mexican Stuffed Poblanos
If you are under the age of 18 or have morals, you probably should not read this. I, as you may have figured out, lack those. That is… Read More »
Garlic Chicken Pasta
Hey boo. You like when I call you that, don't you? Will you call me that too? Well if you did, it really wouldn't matter, I can't even… Read More »
Indian Chicken and Rice
I just need to talk about something. It has nothing to do with this recipe so you can jump to the bottom if you just want to get… Read More »
Blueberry Maple BBQ Chicken
This idea sounds genius doesn't it!? I'm just so damn creative, right?! Wrong. The Domster came up with this idea. A while back, he mentioned that he wanted… Read More »
Moroccan Meatballs in Cumin Coriander Tomato Sauce
I ate a burger last night. Shocker. It was freaking delicious. Wednesday nights are Power Hour Crew nights. Don't know what the hell i'm talking about? Shame on… Read More »
Thai Coconut Lime Shrimp
Have you noticed how I rarely post any meals with fish or seafood in it? Yeah, that's because that sh*t is overpriced. It's stupid. I'd rather eat canned… Read More »
Chicken Pesto Pasta
Pasta? Say wha??? Do you even know what pasta tastes like anymore? I sure don't. I don't even crave pasta anymore. Chocolate cake, now that is a whole… Read More »
Korean Short Ribs over Homemade Slaw
So I really have no idea how to make Korean shorts ribs. Like, really NO idea. I don't even know the spices and sauces that make up Korean… Read More »
Loaded Turkey Stuffed-Twice Baked Sweet Potatoes
Do you like carbs? Hell yes you do. If you don't, you're either 1.) a liar, or 2.) a liar. Carbs make meals more delicious. The only problem… Read More »
Chicken Cattiatore with Grilled Veggies
I love anything with tomatoes/tomato sauce/tomato paste/tomato puree, etc. etc. in it. You know why? Because I always have a can of one of the many in my… Read More »
Salisbury Steak Burgers with Mushroom Gravy
I had literally never even heard of salisbury steaks before. It doesn't even look like a steak. It's name makes no sense to me. Would you call a… Read More »
Bacon and Currant Pork Burgers with Spicy Orange Dressing
I suck at inspiring myself at times. I'm really not that creative. I try. I try really hard, but I just don't make the cut sometimes. So when… Read More »
Stuffed Peppers with Spanish Sticky Rice
I know. I'm incredibly original. You are blown away by my originality with this recipe, aren't you? I sometimes have these genius ideas that just come to me… Read More »
Chicken Mole
No, that's not pronounced mole. It's mole-A! Give it a Mexican flare at the end, come on, try it!! TRY IT!!! Shout it at the roof tops. "Mole-A,… Read More »
So when I need a quick lunch, Chipotle is my go-to for something delicious and crazy satisfying. Have you seen the amount of guacamole they give you there?… Read More »

subset: commoncrawl


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Radisson Blu Hotel Dortmund
A stay at Radisson Blu Hotel Dortmund places you in the heart of Dortmund, steps from Westfalenpark Dortmund and close to Florian Tower. This 4.5-star hotel is within close proximity of German Cookbook Museum and Helmut-Koernig-Halle. Read More About Radisson Blu Hotel Dortmund
Radisson Blu Hotel Dortmund Deals & Specials
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The alt rockers fill up our airwaves with thoughts on some of their favorite films. "Apocalypto" apparently is not one of them. Sorry, Mel.
Think J.K. Rowling will buy a solid gold Roomba with all the bank "Harry Potter and the Deathly Hallows - Part 2" made this weekend? Plus, "Captain America" is getting cocky, but that's A-OK by us.
"Captain America" director Joe Johnston is trying to talk George Lucas into letting him do a movie on "Star Wars" character Boba Fett. Also -- spoiler alert! -- Team NextMovie will be at San Diego Comic-Con.


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Remember Me
Neon Indian :: 03.26.10 :: Mezzanine :: San Francisco, CA
The common denominator of the entire performance was a fuzzy, droning hum that was introduced before the full band even made it onstage. Like warm waves washing over all bodies present, the sound would persist in slightly altered incarnations and served as the segue glue that linked each selection together. After ample time was allowed for this hum to run its scene-setting course, business in the form of an actual song was addressed, and it was immediately apparent what type of direction this Texas-based collective was taking. What followed was a vivid array of neo-psychedelia-meets-retro-synth-pop that was weird enough to get lost in but bouncy enough to boogie to. Careful attention was paid to introducing and constructing each piece, and nearly every song featured some additives not found on the studio version that only enhanced the already-solid base.
"Mind, Drips," one of Chasms' standout tracks, saw some striking additions that made it soar notably higher than the rest. With a foundation of spacey synth arpeggios and an electronic bass-kick that together denoted cosmic sailing of some sort, lead singer Alan Palomo's distant, echoed vocals on top of the 'oohs' and 'aahs' of the backup singing helped further convey the notion of passing through the atmosphere into the ether. As if visual components were needed to complete the interplanetary picture, vibrant green and red lasers ran patterned courses overhead in sequence with the divine sounds below.
The only disappointment, albeit a minor one, came in the form of "Should Have Taken Acid With You," considered one of their two major hit singles. Though extended like every other number they put forth, nothing supplemental or innovative stood out with this one, and for the only time all show, Palomo's vocals sounded weak and inferior. Trippy little drips and drops still pushed through and twisted things up a bit, compliments of Leanne Macomber's tweaked-out keyboard work, but as a whole it left something to be desired. Fortunately, the other hit, "Deadbeat Summer," did more than enough to redeem the brief sleeper. The quintessential jam that characterizes Neon Indian's sound more than any other, "Summer" had everything that makes them such a satisfying listen - basic drum beat, well-placed distorted guitar jabs, a dancing, high-pitched key progression with some phaser and flanger effects, and Palomo's caressing vocals issued while he glided back and forth across the stage. A very distinctive form of dancing - something like toned-down hippie flailing spliced with some left-to-right foot shimmying and casual head nods - accompanied this tune and was a unique sight to behold.
To cap off a stellar presentation of onstage skills and commanding presence, they encored with one straight from the annals of the early '80s: Yazoo's "Situation." Given the fact that most of their tracks contain direct underpinnings that can be traced back to '80s greats like Depeche Mode and The Cure, it made sense that they'd pull out this sometimes-forgotten gem to close things out. The familiar refrain and identifiable chord progression did plenty to stir things up one final time and turn the place into a Miami Vice-like nightclub.
For such a young band out of a pool of unproven, hyped-up acts to already be putting on bangers such as this, it's a safe to raise the bar of expectations just a smidgeon and spread the word about what this troop is capable of.
Neon Indian Tour Dates :: Neon Indian News :: Neon Indian Concert Reviews
JamBase | Illuminated
Go See Live Music!
To read comments and participate in this story, please visit the Articles forum »


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Athol (GNIS FID: 972181) is a populated place located in Warren County at latitude 43.493 and longitude -73.843.
The elevation is 787 feet. Athol appears on the Warrensburg U.S. Geological Survey Map. Warren County is in the Eastern Time Zone (UTC -5 hours).
Warren County: Cities & Towns | ZIP Codes | Schools | Features (airports, churches, hospitals, etc.)
BIG Map |
Driving Directions |
Data Source - USGS GNIS FID: 972181
BOUNDARY MAPS: Town of Thurman | Warren County
Warrensburg, NY
(3.4 miles E)
Lake George, NY (8 miles SE)
Bolton Landing, NY (10.4 miles ENE)
Chestertown, NY
(11.3 miles N)
Hadley, NY (12.2 miles S)
Glens Falls North CDP, NY (13.5 miles SE)
Thurman, NY
(4.5 miles NW)
Big Hollow, NY (6 miles SE)
The Glen, NY (6.4 miles N)
Stony Creek, NY
(6.4 miles SW)
Diamond Point, NY (7.9 miles E)
Darrowsville, NY (8.3 miles NNE)


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[Editor's Note: Portions of the following article should have been attributed to "Rethinking mandatory sentencing," an article written by Dan Stewart that appeared in The Week on Sept. 14, 2013.]
If I told you that in America almost 1 million black Americans were forever forbidden from voting, you might think I was talking about Jim Crow 50 years ago, but you would be wrong. According to the Sentencing Project, a staggering number of nonviolent individuals who have been released from prison, are not on probation or parole and who have committed no further crimes, are forever prohibited from voting.
Many black Americans are prevented from ever voting because of the war on drugs.
On Wednesday, I testified before the Senate Judiciary Committee and described the injustice and effects of mandatory-minimum sentences.
These sentences are disproportionally affecting minorities and low-income communities. A recent report from the American Civil Liberties Union reports that blacks are four to five times more likely to be convicted for drug possession. Some dismiss this because they think blacks are committing more drug crimes, but in June, The New York Times reported that although black Americans were four times more likely to be arrested than whites for marijuana possession, both groups used the drug at similar rates.
Why are the arrest rates so lopsided? One widely cited study by The San Jose Mercury News reviewed 700,000 criminal cases that were matched by crime and criminal history of the defendant. The analysis revealed that similarly situated whites were far more successful than blacks and Hispanics in the plea-bargaining process.
Today, the United States incarcerates more people than any other country in the world, and the racial disparity in arrest rates has been absolutely devastating to the black community. Professor Michelle Alexander has even called the war on drugs "the New Jim Crow."
It's not just black Americans. Regardless of the color of your skin, the war on drugs has ruined the lives of thousands of young people.
I know a man about my age in Kentucky who grew marijuana plants in his apartment closet in college. Thirty years later, he still can't vote, can't own a gun, and when he looks for work, he must check the box that basically says: "I'm a convicted felon, and I guess I'll always be one." Getting a job is nearly impossible for him.
John Horner was a 46-year-old father of three when he sold some of his prescription painkillers to a friend. His friend turned out to be a police informant, and he was charged with dealing drugs. Horner pleaded guilty and was later sentenced to the mandatory minimum of 25 years in prison.
John will be 72 years old by the time he is released, and his three young children will have grown up without him. The informant, who had a long history of drug offenses, was more fortunate — he received a reduced sentence of just 18 months, and is now free.
So many judges oppose mandatory-minimum sentencing precisely because such an arbitrary law does not take into account that each case is different.
I want to be clear: I am not advocating for any type of get-out-of-jail-free passes for individuals who break the law. I am simply arguing that the federal government should get out of the way, and allow local and state judges to do their jobs.
Mandatory-minimum sentences automatically impose a minimum number of years in prison for specific crimes — usually related to drugs. By design, mandatory-sentencing laws take discretion away from prosecutors and judges so as to impose harsh sentences, regardless of circumstances.
Since mandatory sentencing began in the 1970s in response to a growing drug-and-crime epidemic, America's prison population has quadrupled, to 2.4 million. America now jails a higher percentage of its citizens than any other country, including China and Iran, at the staggering cost of $80 billion a year. Drug offenders in the United States spend more time under the criminal justice system's formal control than drug offenders anywhere else in the world.


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Cherokee Uniforms recognizes healthcare professionals for service,
sacrifice and innovation
LOS ANGELES, Oct. 3 /PRNewswire/ -- Now celebrating five years of honoring the nation's healthcare heroes, Cherokee Uniforms announced today 10 winners of the 2007 Cherokee Inspired Comfort Award. Selected from over 1,000 nominations nationwide, the winners represent a cross-section of healthcare facilities, from VA medical centers and regional cancer centers to community hospitals and home hospice providers. Although each winner has their own distinct story about caring for others, all of them share the same mission day after day -- to provide the best care possible to those in need.
"Cherokee Uniforms is proud to honor these 10 outstanding individuals for their dedication, skill, compassion and devotion. This award was created to acknowledge healthcare professionals who often sacrifice their own desires to fulfill the needs of others," said Michael Singer, president and CEO of Cherokee Uniforms. "We hope the winners' stories will inspire all healthcare workers to continue giving their best. We also hope they encourage others to consider careers in this rewarding industry."
A panel of nurse leaders, former Cherokee Inspired Comfort Award recipients and Cherokee Uniforms professionals selected the honorees who were nominated for their exceptional service, sacrifice and innovation by colleagues, friends and family. Nominations were received in five categories: Advanced Practice Nurse, Registered Nurse, Licensed Practical Nurse/Licensed Vocational Nurse, Student Nurse and Non-Physician Healthcare Professional.
This year's Grand Prize, Top National and National Winners are:
Advanced Practice Nurses (APNs)
Grand Prize Winner -- Margaret Talley, RN, CNS, CWCN-AP -- Palomar
Pomerado Health, Escondido, California
Upon discovering a much higher rate of pressure ulcer prevalence than
the national ben
|SOURCE Cherokee Uniforms
Copyright©2007 PR Newswire.
All rights reserved


text:
We've encountered a number of schools bearing stately namesakes thus far in our mid-major melange, from Oral Roberts, to Robert Morris, Austin Peay to St. Peter's, it seems as if everyone has their own school these days. It's even more prevalent in the lower divisions. Here, take a gander at a this sample DIII conference tournament bracket and see for yourself:
(1) Grover Cleveland St.
(6) Saint Pete Beach
(3) Rube L. Goldberg
(4) Ernest P. Worrell
(2) Soulja Boy Military Institute
(5) Hall & Oats
I know what you're thinking, and yes, Ernest P. Worrell is indeed a sleeper, but allow me to direct your attention to the Southland Conference Tournament and this year's most intriguing namesake, Sam Houston State.
Sam Houston, the man, is the only gent in our nation's history to govern two states (TN, TX) and a hell of a model american. His team, Southland Conference regular season champs, begin their post-season trek this evening with the hopes of earning just their second trip to the tournament in school history.
My interest in the Bearkats began way back in November, when I was on hand to watch them play in Rupp Arena. They left with a 10 point loss, but not before setting an arena record by draining 18 of 38 3-pointers and scaring the hell out of everyone in the Bluegrass. 11 of those 3's came off the finger-tips of one Cory Allmond, who was an astounding 11-16 from long range to finish with 38 points, and got his name in the arena's hallowed record books as well.
Well, 18-38 is impossible to top, but the Bearkats have maintained their hot shooting and prolific offense for the entire season, ranking 8th nationally in 3's per game and scoring average. They also average an NCAA leading 20 assists per game and even though Kentucky's defense in November was nothing more than dribbling cones, Sam Houston St. showed what they're capable of.
With their reliance on the 3 ball, the Bearkats are always one off-night from having their season come to an end, but man when they're hot, look out big conference under-performer (see: Kentucky, 18 point win @ Auburn).
The Southland tournament is already under way in Katy, TX, with Sam Houston set to tip-off against Nicholls St. at 7. Keep an eye on Southland and see if the Bearkats indeed packed their tournament touch.
Southland Conference Tournament
Katy, TX
Today's Scores:
(2) Stephen F. Austin 77
(7) UT-Arlington 54
(3)Texas A&M-Corpus Christi 78
(6) UT-San Antonio 66
Blog Entry
Pride of the Southland
Posted on: March 10, 2010 6:47 pm
Category: NCAAB


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The work by Witte and his colleagues was prompted by the desire to add to a short list of probes now used in PET scanning and to develop new probes that monitor different molecular functions than the current probes.
"What we wanted to do was to develop new ways to look inside a living organism and gather as much information as we can about the immune system," said Caius Radu, an assistant professor of molecular and medical pharmacology, a Jonsson Cancer Center researcher and the first author of the study. "We wanted to know how cells move from one site in the body to another and find a way to trace them to tumors."
In previous studies, Witte and other UCLA researchers were able to track the immune system as it recognized and responded to cancer. But in those studies, the cells had to be modified with "reporter" genes that sequestered a specifically designed PET probe that allowed scientists to monitor them. The new probe doesn't require modified cells, making it easier and less expensive to use and giving it far broader applications than existing probes. In addition to modeling and measuring the immune system, those applications include stratifying different types of cancers and their response to therapy, defining the level of immune response in both normal and pathological situations and helping to determine whether new drugs prompt an immune response to cancer and other diseases.
"This probe will tell us things about the immune system that existing probes can't," said Radu, who also is a member of the Crump Institute for Molecular Imaging.
|Contact: Kim Irwin
University of California - Los Angeles


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Hello, I've been flipping through the topics on this board and they look pretty interesting and potantially useful! I'm starting up riding again after a summer off (had an accident last summer that kept me out of riding). I tend to go for low-impact rides locally on side roads, maybe for an a hour or so. I use a road bike with mountain tires that was assembled from a kit.
I initially came here to find advice about getting a new saddle, but it seems I'll need to form my own opinion. Has anyone been able to buy a saddle locally and return it for another one until you find the right saddle?


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Alaska from North to South
|June 13
|Arrive in Anchorage
|June 14
|Fly to Prudhoe Bay to meet Hugh
|June 15
|Search for Prudhoe Bay birds and Arctic wildlife
|June 16
|Drive the stunning Dalton Highway (Haul Road)
|June 17
|Wiseman and the Brooks Range
|June 18
|Drive to Fairbanks past the Arctic Circle and over the Yukon River
|June 19 - 21
|Famous Denali National Park, including flight-seeing
|June 22
|Drive to Anchorage with stops along the way
|June 23 - 26
|Prince William Sound on the MV Discovery
|June 27
|More Prince William Sound then back to Anchorage
|June 28
|Fly to Katmai National Park
|June 29 - 30
|Bears at Katmai National Park
|July 1
|Fly to Anchorage for an overnight
|July 2
|Flights and arrive home
Return to top
June 13, Wednesday Arrive in Anchorage
Choose the best route to Anchorage, Alaska, to arrive in time to connect with the early afternoon flight to Prudhoe Bay on June 14. See flight schedule details. We strongly suggest that you arrive in Anchorage on June 13 and book your own hotel room. If you arrive on June 13 for one night, then we recommend a lodge near the airport with free airport shuttle, such as the Courtyard. If you plan to arrive a few days early, we recommend the Susitna Place Bed and Breakfast, which is in a quiet location for a very pleasant stay in downtown Anchorage. Arrange your own taxi ride to the Susitna Place, which is reasonably priced. Arriving early will allow time to explore downtown Anchorage and its fine museums, especially the Alaska Public Lands Information Center, which contains exhibits of Alaskan history, culture, geology, flora and fauna. Anchorage has an amazing diversity of wildlife. Loons, ducks and Red-necked Grebes are frequently observed on lagoons in parks within the city limits, such as at Westchester Lagoon. Anchorage is the largest community in North America with a population of breeding loons. The loud resonant yodeling call of a loon late in the evening across a still lake is an unforgettable experience, especially in an urban setting. Other avifauna found in the local area include Hudsonian Godwits, Alder Flycatchers, Common Redpolls, Rusty Blackbirds, Boreal and Black-capped chickadees, and several species of warblers.
Lodging: Your own arrangements
June 14, Thursday Fly to Prudhoe Bay to meet Hugh
Hugh will meet you at the Prudhoe airport upon arrival in the afternoon to begin this amazing Alaskan adventure. Check in at the lodge before heading out into the field to seek the mammals and birds that make their home on the Arctic coastal plain during the brief summer season. Muskoxen, Caribou, Grizzly Bears, Gray Wolves and other wildlife all are present at this season along the Arctic Ocean on the magnificent coastal plain. After a welcome dinner we will either drive to a location to walk amongst Arctic birds or walk directly from the hotel and watch the midnight sun dip towards the horizon, but never set.
Lodging: Prudhoe Bay Hotel
Common Eider © Hugh Rose
June 15, Friday Search for Prudhoe Bay birds and Arctic wildlife
After an early breakfast, we will spend our day searching for birds and mammals in the unlikely environment of the Prudhoe Bay oilfields. Birding and bird photography are spectacular here with Pacific Loons, Common Loons and Red-throated loons all in breeding plumage and regularly seen in this area. Other species, such as Common Eiders, Baird Sandpipers and 125 other species of birds are seen in this birding paradise. Arctic Fox and the native Red Fox are common visitors. A short drive down the Dalton Highway (Haul Road) in the afternoon may afford us looks at Long-tailed Jaeger, Arctic Warbler, Muskoxen, Grizzly Bear, Caribou, possible Bluethroat and maybe wolves.
Lodging: Prudhoe Bay Hotel
June 16, Saturday Drive the stunning Dalton Highway (Haul Road)
After breakfast in Prudhoe Bay, drive south down the Dalton Highway, the 500-mile long road that stretches from Fairbanks to Deadhorse. Travel half way, to arrive at Wiseman for a two-night stay. We drive south across the Arctic coastal plain to the distant foothills of the Brooks Range. This first 130 miles is wildlife rich, taking us through an alien landscape of flats and low rolling hills devoid of any trees, but covered with a brilliant green carpet of tundra vegetation. Wildlife flocks to the coastal plain in the summer to partake of the brief, but intense bloom of life that feeds on the tundra vegetation. Caribou, Moose and Muskoxen are often seen browsing on willows and sedges, while predators, such as wolves, fox, bear, Golden Eagle, Snowy Owl, and Gyrfalcon, search the tundra for a meal.
Next we ascend the foothills of the Brooks Range and over the Atigun Pass at 5,000 feet, the highest mountain pass on any road in Alaska. We will stop along the way for a small hike and picnic lunch. Wildflowers carpet the tundra here at this time of year, and it we can count as many as fifty species of wildflowers in the high alpine of the Brooks Range. We descend from Atigun Pass onto the south side of the Brooks Range and enter the scenic Koyukuk River Valley and the northern edge of the boreal forest. The drive for the next 75 miles is through the spectacular Koyukuk Valley, past craggy peaks of 400 million year old limestone and dense spruce forest. Here we may see Grizzlies, Grey (Timber) Wolves, Moose and even Lynx. At the end of an unforgettable 250-mile drive, arrive in the historic gold mining town of Wiseman to overnight at the Arctic Get-away Bed & Breakfast commonly known as "Igloo #8." The Igloo Club, similar to the Elks Club, originally built this historic bed and breakfast lodge. It is a real log cabin where get a feel of the true Alaskan wilderness. Many of the historic log cabins still stand today, housing residents or small businesses such as Igloo #8 and the Wiseman Museum.
Lodging: Igloo #8
June 17, Sunday Wiseman and the Brooks Range
After breakfast in the comfortable kitchen of Igloo #8, set out for a day of exploring and photography on the south side of the Brooks Range. Take a picnic lunch and stop to eat on a carpet of wildflowers that should be stretching in all directions. This afternoon will be an excellent opportunity to explore the town of Wiseman. Settled in 1903, most of the buildings are older than the oldest surviving buildings in Fairbanks. Several old log cabins, a general store, and lots of historic gold mining artifacts can be found within a short walk of Igloo #8.
Lodging: Igloo #8
June 18, Monday Drive to Fairbanks past the Arctic Circle and over the Yukon River
After an early breakfast we depart for Fairbanks, located 250 miles south of Wiseman. The drive traverses boreal forest and ascends mountain peaks of windswept tundra. A crossing of the Arctic Circle sixty miles south of Wiseman will be celebrated with good cheer. Sixty miles further south we cross the mighty Yukon River and continue through the White Mountains to Fairbanks. An afternoon arrival in Fairbanks allows us a chance to relax and enjoy Fairbanks in the summer. Well known for warm summers and cold winters, high temperatures can be in the 90s this time of year, but average 65 to 70°F. Dinner is on our own this evening. A choice of dining is available in Fairbanks to allow you to try the cuisine that appeals most to you. Finish this exciting day with the night at River's Edge Resort.
Lodging: River's Edge Resort
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June 19, Tuesday Travel to Denali National Park
After a relaxing morning in Fairbanks with time to explore the "Golden Heart City of Interior Alaska", we'll drive south to the entrance of Denali National Park (formally Mount McKinley National Park) to enjoy the east side of the Park. We will arrive at the wonderful Earth Song Lodge, located on the edge of the park, in time for dinner.
Lodging: Earth Song Lodge
Brown Bear in
Denali National Park
©Hugh Rose
June 20, Wednesday Denali to Kantishna
Depart early to leisurely drive through the best part of Denali National Park to mile 95 at the end of the road. Hugh has a special vehicle permit, which is possible because we will be staying at the private Skyline Lodge in Kantishna. There are only 100 miles of gravel road within the 9,300 square mile park. In order to protect wildlife viewing opportunities, the use of non-permitted private vehicles is restricted to the first fifteen miles of road; only specially sanctioned park shuttle buses and those with special permits are allowed on the remaining road system. This is probably the best park in North America for viewing wildlife and wildflowers from early June through August. Moose, Grizzly Bear, Dall Sheep, Caribou, Red Fox, Arctic Ground Squirrel, Marmot, and Pika are all seen from this road. Even Wolverine and Wolves are occasionally found. A total of 37 species of mammals have been documented in the Park. Interesting birds include Golden Eagles, Gyrfalcon, Rough-legged Hawks, Long-tailed Jaegers, Rock and Willow ptarmigan, Northern Wheatear, Arctic Warbler, American Golden Plover and over 100 other species. One area of interest is the Stony Creek area where 132 species of wildflowers occur, as well as wheatears, nesting shorebirds, Long-tailed Jaeger, and other birds. Hugh knows this area very well from his employment as resident naturalist at Camp Denali.
Denali National Park and Preserve lies 250 miles south of the Arctic Circle and 237 highway miles north of Anchorage. Spend all day traversing the gravel spur road through the center of the park. Stop to observe and photograph both large and small wildlife and incredible scenery. Large mammals may be found feeding very close to the road, such as the Denali Grizzly Bear with their beautiful blond fur. We will explore on foot some of the best spots for photography and scenery, which Hugh knows so well. Enjoy a picnic lunch in the field and arrive at Skyline Lodge for dinner with an incredible view of Mount Denali, weather permitting. "Denali" is a local Indian word meaning "Great One" referring to North America's highest mountain, still often called Mount McKinley.
The Skyline Lodge consists of three large, clean and comfortable cabins: one dining cabin and two sleeping cabins. Each sleeping cabin contains one big sleeping room equipped with a sleeping loft, affording some privacy although not what we may normally be used to. The bathroom and toilet facilities are in the adjacent dining cabin. The privilege of exploring this remote area of Denali National Park on our own schedule makes this rustic accommodation well worth our two-night stay. The meals at Skyline Lodge are excellent. We have stayed at other lodges but found that the regimented activity schedule did not accommodate our desire to spend as much time in the field as possible.
Lodging: Skyline Lodge
Northern Hawk-Owl
©Hugh Rose
June 21, Thursday Flight-seeing, hiking and viewing at Wonder Lake
The Skyline Lodge owner offers "flight-seeing" excursions in a single engine aircraft operated from a small airstrip located at Kantishna. The flight is included in the cost of this trip. The north face of Denali's 20,320-foot summit is only 20 miles from Kantishna. The vertical relief of this impressive mountain from its base to its summit is 18,000 feet, even greater than that of Mt. Everest. Bring your wide-angle lens - Denali more than fills a picture window at the lodge on a clear day! The mountain makes its own weather and it can be cloud-hidden as much as 60% of the time. Winter temperatures on the mountain can dip to 85°F below zero and winds can gust to more than 150 miles per hour. Even summer temperatures on its summit can be severe. Permanent snowfields cover more than 50% of the mountain and feed the many glaciers that surround its base. Over 1,000 people now attempt to climb the mountain each year by a multitude of routes. The most popular route is not technically difficult, but low temperatures and awesome winds in upper reaches make this environment one of the harshest on earth, usually claiming the lives of some climbers every year. The park exemplifies interior Alaska's character as one of the world's last great frontiers offering an opportunity for wilderness adventure. Most of Denali remains largely wild and unspoiled, but there are many development pressures. Today we'll walk in the Kantishna Hills to look for birds, mammals and wildflowers. We'll enjoy a picnic lunch amid the magnificent scenery that surrounds this area. Also spend time at Wonder Lake, one of the best places to photograph Moose, if one comes to drink in the late afternoon. A delicious dinner awaits us at the lodge at the end of our day.
Lodging: Skyline Lodge
June 22, Friday Drive to Anchorage with stops along the way
After a hearty breakfast at Skyline Lodge, we depart early for more great wildlife experiences traversing slowly back across the park. Stop at the park entrance to explore this area and eat lunch. Depart on the George Parks Highway south to Anchorage. The trip will take us through fertile Matanuska Valley farmlands, across high bridges spanning several Susitna River tributaries, and will provide spectacular views of Denali, weather permitting. Make a stop halfway at Denali State Park for a short hike and a chance to photograph and sightsee on the south side of the Alaska Range. We will arrive in Anchorage and drive directly to the inn for the night. Dinner is on your own this evening.
Lodging: Susitna Place Bed and Breakfast
June 23, Saturday To the dock in Whittier and board the MV Discovery
After breakfast, we depart for the dock in Whittier, where we rendezvous with the MV Discovery. Meet the captain, Dean Rand, and crew at the harbor for a warm welcome. It is owned and operated by Dean, a long-time Alaskan, who expertly pilots boat through the Sound's narrow passages. The MV Discovery has six cabins with two baths and offers a comfortable means to explore this astoundingly rich wilderness seacoast. Relax in the cozy lounge and enjoy a specially prepared lunch. Then depart for Prince William Sound, where breath-taking glacial scenery, blue icebergs, spectacular birdlife, Orca and other marine mammals await.
Lodging: Aboard the MV Discovery
Sea Otter ©Hugh Rose
June 24 - 26, Sunday - Tuesday Prince William Sound aboard the MV Discovery
Weather and wildlife will dictate our destinations, but we will strike out on a route around Prince William Sound to maximize our marine wildlife and bird viewing, and will visit some of the most spectacular glacial scenery in the Northern Hemisphere, such as Icy Bay and Harriman Fjord. Prince William Sound is surrounded by the northern-most temperate rainforest in the world. Each day will consist of excursions on shore to hike and view wildlife and scenery up close. The MV Discovery is equipped with Zodiacs, which make shore excursions easy. Humpback Whale viewing should be outstanding, weather permitting.
Lodging: aboard the Discovery
June 27, Wednesday From Prince William Sound to Anchorage
Awake to some of the world's most spectacular scenery: corridors of breathtaking beauty, sprawling glaciers, and a panoramic skyline of mountain grandeur. Harbor Seals hauled out on the flotillas of icebergs watch closely as the MV Discovery navigates the icy, blue waters of Barry Arm. The enveloping mountains of this inlet stretch skyward to nearly 10,000 feet, with glacier after glacier descending the terraced mountain valleys. Alaska's lush rainforest vegetation drapes the hillsides in green as streaming waterfalls fall from the rocky cliffs. Listen to the cracks, pops, and thunderous roars of the Cascade, Barry, and Coxe glaciers while the MV Discovery, dwarfed by blue and white walls, drifts silently by these actively calving rivers of ice. Enjoy a buffet lunch while our boat exits this magical place back to the Whittier Harbor. After disembarking, return to Anchorage and check in at the Susitna Place Bed and Breakfast. Dinner is on our own this evening.
Lodging: Susitna Place Bed and Breakfast
June 28, Thursday From Anchorage to Katmai National Park
After breakfast depart for the Anchorage international airport and take the one hour flight (included in the trip cost) to King Salmon located in Bristol Bay. Many government resource agency offices (Alaska Department of Fish and Game, National Park Service, US Fish and Wildlife Service) are located here along with several sport fishing lodges. From King Salmon, take a 20-minute flight on a single-engine airplane equipped with pontoons to Brooks Lodge in Katmai National Park. The scenic, low-level flight and smooth water takeoff and landing will be a unique, exhilarating, and safe experience. Brooks Lodge is situated on a peninsula at the mouth of the Brooks River, which flows from Brooks Lake 1-1/2 miles before emptying into Naknek Lake. Naknek is the largest freshwater lake in the National Park system and is the fourth largest lake in Alaska. The lodge complex, operated by a concessionaire under Park service permit, consists of eight cabins, a main dining room and a small trading post. Adjacent Park Service facilities include a small campground and a visitors' center. Delicious family style meals are served.
With only eight very popular cabins at Brooks Lodge, the owners will allow us only two cabins. We make reservations over a year in advance. We will occupy all the available beds in the two cabins - each cabin has two bunk beds with four beds total. Each cabin has one bathroom. With wildlife this spectacular in this wonderful setting, we easily make do with less privacy, taking turns dressing if necessary. The porch outside each cabin is great for sitting and bears might even walk by, not to mention moose and Bald Eagles. There is also a set of bathrooms very close to the cabins.
The opportunity to observe concentrations of Brown Bears fishing for salmon is the primary attraction of this area. Alaska Brown and Grizzly Bears are considered one species (Ursus arctos), but the coastal Browns are larger due to their high protein salmon diet for a portion of the year. Mature males may weigh in excess of 1,000 pounds. Mating occurs from May to mid July, with cubs born in the dens in mid-winter. Up to four cubs are born weighing a mere one-pound each. Cubs stay with their mother for two or three years during which time she does not reproduce. Brown Bears dig a new den each year entering in November and emerging in April. About half of their life is spent in their dens.
Upon arrival at the Lodge we will receive orientation from Park Rangers about bear behavior. Hugh will provide additional information on safety precautions when in bear country. In late June as many as 30 bears may be present in the vicinity of Brooks Falls (located mid-way down the river), which acts as a partial migration barrier to salmon. Bears normally begin arriving by the third week of June and begin departing in August to feed on more accessible salmon in adjacent smaller streams. Special observation platforms are available for observing and photographing fishing bears at the river's mouth and the upstream falls, easily accessible from well-maintained trails. Lunch will be served at the lodge when we arrive and the rest of the day will be spent viewing bears and becoming familiar with the surroundings.
Lodging: Brooks Lodge in Katmai National Park
Brown Bear Fishing in Katmai National Park ©Hugh Rose
June 29 - 30, Friday - Saturday Katmai National for Park Bear Viewing
We'll spend time observing and photographing these phenomenal bears. It is also possible to see a wolf in the vicinity of the falls, as they have been seen scavenging for fish remains. Young bears not yet competing with adults for the live salmon will search downriver for floating fish carcasses.
Or you might choose to travel one day by bus on a 23-mile gravel road to the Valley of Ten Thousand Smokes (additional cost of about $100 paid at that time). Let Hugh know and he will make arrangements while at Katmai. This trip offers a view of wilderness sculptured by glaciers, stream erosion and volcanism. After a picnic lunch at the road's end, hike to the valley floor on a steep, but well maintained trail. This is the site of one of the most violent volcanic eruptions in recorded history. Novarupta Volcano, located near Mt. Katmai, exploded in June, 1912, with blasts of hot, glowing pumice and ash destroying all living things over a large area and covering 40 square miles of lush valley to a depth of 700 feet. The valley floor is composed of a myriad of subtle colors of pumice and ash. Return to the lodge for dinner. Take a short evening hike to observe bears and possibly attend the visitor center program.
Lodging: Brooks Lodge in Katmai National Park
July 1, Sunday Katmai then fly back to Anchorage for an overnight
Enjoy the last day bear viewing and depart mid-afternoon on the floatplane back to King Salmon, and then on to Anchorage. After arrival in the Anchorage airport, we will transfer to the Susitna Place Bed and Breakfast. A final dinner and going away party at a local restaurant will be planned.
Lodging: Susitna Place Bed and Breakfast
July 2, Monday Flights and arrive home or continue on your own
After breakfast, Hugh will make the drive to the Anchorage airport for your flight home. Transfers to the airport are included in the trip cost, but will only be offered after breakfast. A taxi is easily arranged for later transfers. See flight schedule details. Alternatively, stay longer to explore Alaska on your own.
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The Discovery in a cloud of
Black-legged Kittiwakes
in Prince William Sound
©Hugh Rose
MV Discovery is meticulously fitted to combine the finest blend of luxury, comfort and utility, the 65 foot classic working yacht gently sails you into one of the world's richest marine environments. Named after one of Captain Cook's ships, the Discovery's atmosphere is one of charm and style. The lower deck includes sleeping accommodations for up to 12 guests in 6 cabins, plus crew quarters, two bathrooms with hot showers, and stowage space. Guests can readily view and photograph the panoramic scenery and marine life from the ship's complete walk-around deck and expansive windows. Unlike the cumbersome cruise ship giants, the Discovery's size enables access to Alaska's lesser traveled, more intimate inside passages. Well equipped for travel in Alaska's wilderness, the Discovery safely charts the Sound's remote waterways. Review more ship details including the deckplan.
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Costs, Payments and Cancellations: Upon receiving your deposit, we will send trip materials and travel insurance information. Until the final payment date, payments are refundable except for a cancellation fee of $150 per person. This fee may go toward another tour if reserved within six months of the departure date of the cancelled trip.
|Cost per Person
|Trip cost, double occupancy
|Payment Schedule
|Deposit - to reserve your space
|October 1, 2011 - second payment
|March 1, 2012 - final payment
|remaining balance
|For reservations made after the second payment date, the deposit and second payment will be due with registration.
Not Included:
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To Make a Reservation: Please contact us to assure space availability and to let us answer your questions. Then, print our reservation form, fill it out, and post it to us in the mail with your deposit:
Cheesemans' Ecology Safaris
20800 Kittredge Road
Saratoga, CA 95070
Toll Free: (800) 527-5330
Local: (408) 741-5330
Fax: (408) 741-0358
Email: firstname.lastname@example.com
Hugh Rose
Leader: Hugh Rose is an outstanding resident naturalist. He has led Alaska tours since 1991 receiving unending praise for his broad knowledge, attention to details, and ability to fulfill everyone's needs. He has an excellent understanding of all aspects of Alaskan natural history from in-depth bird behavior to geology. Hugh is a professional photographer and is also on our Antarctica staff. Onboard the MV Discovery, Captain Dean Rand will lend his expertise. After more than 20 years of experience on Alaska's waters, Captain Rand really knows Prince William Sound and all its special places.
Flights: Please let us know if you would like help arranging your own flights. Fly from your home to Prudhoe Bay via Anchorage, and then back home from Anchorage. Alaska Air can help you with most, if not all parts of this route. The Alaska Air flight from Anchorage to Prudhoe Bay costs close to $400 if purchased separately, so it's best to purchase it along with your ticket to and from Anchorage. We will arrange the internal flights from Anchorage to Denali and back to Anchorage, included in your tour cost.
Arrival - Arrive in Prudhoe Bay (SCC), also known as Deadhorse, by the afternoon of June 14. Please book Alaska Air flight AS53 from Anchorage (ANC) to Prudhoe Bay (SCC), currently scheduled to depart ANC at 2:15 pm on June 14. This is the flight that Hugh will arrange transfer for. Please note: this flight time could change to the morning, so it is better to arrive in Anchorage on June 13 for an overnight. Please book your own room (see the suggestions mentioned earlier in the itinerary) for an overnight on June 13.
Departure - Fly home from Anchorage (ANC) on the morning of July 2, unless you wish to spend additional time there on your own.
Travel Insurance: Emergency Medical Insurance is optional, but encouraged, for this tour. Read about travel insurance and our recommendations and requirements.
Trip Materials
Detailed information about your specific tour will be sent to you after you make your reservation with us. These trip materials include information about flights, packing, entry and departure requirements, airport transfers, gratuities, etc. Please take a moment to read this important informtation upon receipt.
Mailing List
If you would like to be on our mailing list or request information, please use our online information request form or contact us to give us your name, address, email address and phone number. Please note we will never share your personal information with anybody!
Cheesemans' Ecology Safaris, Saratoga, California, act only as agents and shall not be responsible or become liable for any delay incurred by any person in connection with any means of transportation, nor for the loss, damage, or injury to person or property by reason of any event beyond the control of the agency or default of such agency suppliers. We reserve the right to cancel the tour prior to departure in which case full refund will constitute full settlement to the passenger. No refund will be made for any unused portion of the tour unless arrangements are made at the time of booking. All rates are based on current tariffs, exchange rates and fuel prices and are subject to adjustment in the event of any change therein. By sending your initial deposit, you agree to accept our payment schedule as a contract. If payments are still outstanding two weeks after the due date, your space may be forfeited. Baggage is at the owner's risk.
Cheesemans' Ecology Safaris is registered as California Seller of Travel #2063050-40. Registration as a seller of travel does not constitute approval by the State of California. Cheesemans' Ecology Safaris is a participant in the Travel Consumer Restitution Corporation (TCRC). In event of a client canceling where a refund is applicable in accordance with the schedule above, or in the event that CES needs to cancel the trip, all payments for transportation or travel service not provided to the client shall be promptly refunded, unless the client instructs us otherwise in writing. All client payments are deposited into a trust account in accordance with California law. If for any reason a valid refund is not forthcoming, the client may request reimbursement from the TCRC within six months of the scheduled end of the tour. Please feel free to ask us for more information.
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All material © Cheesemans' Ecology Safaris.
All photos © Doug or Ted Cheeseman, unless otherwise credited.
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text:
May 6, 1944 Feb. 1, 2007
WILLARD Virginia Lee Salyer, 62, of Willard, died Thursday night at Stein Hospice, Sandusky.
She was born May 6, 1944 in Prestonsburg, Ky. to the late Richard and Mae (Stevens) Gray.
She was a homemaker and a member of the Faith Builders Church of God. She enjoyed spending time at church and spending time with her grandchildren. She spent her evenings reading her Bible.
She is survived by her husband, Glenn Salyer, whom she married June 22, 1963; a son, Doyle Salyer of Willard; seven grandchildren; brothers, Richard (Betty) Gray of Texas and Timothy Gray of Kite, Ky.; sisters, Jeanette (Clarence) Mosley of Shelby, Janice Johnson of Fla., Margaret (Willie) Howell of Wheeling, Ky., Juanita (Ernie) Lafferty of Prestonsburg, Ky., Elizabeth (Boyd) Caudill of Sassafras, Ky. and Loretta Tenant of Stillwater, Minn.
She was preceded in death by a son, Earl Dean Salyer; daughter, Denise Ellen Salyer; and a grandson, Christopher Harrison.
Friends may call from noon Sunday until the time of the service at 11 a.m. Tuesday at Faith Builders Church of God on Main Street. Burial will be in Greenwood Cemetery, Willard.
Memorial gifts may be sent to the family.
Lindsey-Kocher Funeral Service, 323 Myrtle Ave., Willard, is handling arrangements.


text:
VANCOUVER, BRITISH COLUMBIA Women who smoke during pregnancy may be putting their newborns at risk for congenital heart defects, and the more they smoke, the higher the risk, according to a study to be presented Saturday, May 3, at the Pediatric Academic Societies (PAS) annual meeting in Vancouver, British Columbia, Canada.
Cigarette smoking during pregnancy has been linked to many birth defects, such as cleft lips and palates, and missing and deformed limbs. Some studies also suggest maternal smoking may be associated with heart defects.
The authors of this study used birth certificate data and hospital discharge records from Washington state to determine if maternal smoking during the first trimester of pregnancy is linked to heart defects and if so, what types of defects.
"I care for kids with complex congenital heart disease on a daily basis, and I see these kids and their families enduring long hospitalizations and often sustaining serious long-term complications as a result of their disease. Usually, the cause of a heart defect is unknown. I saw this research as an opportunity to study what might be a preventable cause of congenital heart defects," said lead author Patrick M. Sullivan, MD, FAAP, clinical fellow in pediatric cardiology at Seattle Children's Hospital and a master's student in epidemiology at the University of Washington School of Public Health.
Using hospital discharge records, researchers identified 14,128 children born with a variety of heart defects from 1989-2011. They matched these cases to 62,274 children without heart defects born in the same year. Then, they compared the proportion of children with heart defects whose mothers reported smoking during pregnancy to the proportion of children without heart defects whose mothers smoked. Mothers' smoking status, as well as how much they smoked daily, was available from birth certificates.
Results showed that children with heart defects were
|Contact: Debbie Jacobson
American Academy of Pediatrics