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With crude oil hitting a record high this week, gas prices here in the U.S. are soaring. According to CNN.com, the $100 fill-up has arrived in the United States.

Want to reduce your stress level, spend less money at the pump and do your part to help save the planet? Here’s one of the most simple yet effective tips that will accomplish all three: Slow Down.

Improve Your Financial Health: Use Less Gas

At highway speeds, wind resistance increases exponentially and fuel economy is reduced by approximately 4 miles per gallon for every 10 mile per hour increase [1]. Thus, the faster you drive, the more it will cost you. Consider this [1].

In a typical family sedan, every 10 miles per hour you drive over 60 is like the price of gasoline going up about 54 cents a gallon. That figure will be even higher for less fuel-efficient vehicles that go fewer miles on a gallon to start with.

That’s based on a $3.25 price per gallon, which is less than the current price of gas. So we’re talking more than 54 cents a gallon.

Additionally, if you do the math, speeding doesn’t save you anywhere near the time you might think it does. An average 30 mile commute traveling at 65 miles/hour takes 28 minutes, while that same trip at 80 miles/hour takes 23 minutes. You save a whole 5 minutes by driving 15 MPH faster.

How much money is that 5 minutes worth?

Reduce Stress and Stay Safe

Moderate levels of stress from a variety of sources, including other motorists, traffic congestion and roadway conditions, are common in everyday driving. However, driver stress has been shown to also be influenced by a combination of situational and personal factors, including factors external to the driving context [2].

Not surprisingly, studies have found that life stress is associated with higher rates of accidents and disease [3]. It’s been estimated that drivers who have experienced a recent stressful event are five times more likely to cause fatal accidents than unstressed drivers [4].

If you’re running late, remember that no matter how fast you drive, you’re still going to be late. If you’re under a great deal of personal stress, it’s probably best to avoid driving altogether.

Statistically, people who drive too fast cause or contribute to almost one-third of all fatal crashes. In 2006,13,543 lives were lost in speeding-related crashes [5]. Excessive speed does a number of things:

• it increases the distance a vehicle travels when a driver reacts to a dangerous situation
• it reduces a driver’s ability to steer safely around objects in the road
• it extends the distance necessary to stop

Want to reduce your stress level, spend less money on gas and do your part to help save the planet?

      Just Slow Down!

David over at The Good Human has some additional tips on saving money, saving fuel and saving the environment.

References

1. Slow down a little, save a lot of gas. Issue #1: America’s Money. CNN Money. 2008 Mar 27.
2. Hennessy et al. The Influence of Traffic Congestion, Daily Hassles, and Trait Stress Susceptibility on State Driver Stress: An Interactive Perspective. Journal of Applied Biobehavioral Research 5(2);162–179
   doi: 10.1111/j.1751-9861.2000.tb00072.x
3. Stuart and Brown. The relationship of stress and coping ability to incidence of diseases and accidents. Journal of Psychosomatic Research, 25(4), 255-260. 1981.
   View abstract
4. Brenner and Selzer. Risk of causing a fatal accident associated with alcoholism, psychopathology, and stress: further analysis of previous data. Behav Sci. 1969 Nov;14(6):490-5.
   View abstract
5. Traffic Safety Facts 2006 Data. National Highway Traffic Safety Administration National Center for Statistics and Analysis. 2006.

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A study published earlier this year in the American Journal of Medical Genetics suggests that lymphoblast gene expression may be used to identify biomarkers for panic disorder. Researchers at the University of Iowa evaluated gene expression profiles in lymphoblasts (immature white blood cells) cultured from patients with and without panic disorder and found specific disorder- and sex-related differences [1]. A blood test for panic disorder and other mental health conditions based on the study results is being developed. However, a commercial diagnostic test may be premature as the study results are far from conclusive.

Panic attacks and panic disorder

Panic attacks are episodes of acute, intense anxiety, characterized by a variety of physical symptoms that may include numbness in the hands and feet, shortness of breath, chest pain, heart palipitations, dizziness and a feeling of loss of control or dying. The onset of a panic attack is sudden and may have no obvious trigger. A panic attack is a response of the sympathetic nervous system, a branch of the autonomic nervous system that maintains homeostasis in the body, which becomes active during periods of stress.

Researchers aren’t sure what causes panic attacks. A variety of biological and pharmacological factors can trigger them, including stress, stimulants, hyperventilation, vitamin b deficiency and heredity. According to the American Psychological Association:

Many people experience occasional panic attacks, and if you have had one or two such attacks, there probably isn’t any reason to worry. The key symptom of panic disorder is the persistent fear of having future panic attacks. If you suffer from repeated (four or more) panic attacks, and especially if you have had a panic attack and are in continued fear of having another, these are signs that you should consider finding a mental health professional who specializes in panic or anxiety disorders.

Indeed, repeated attacks can become very debilitating. Increased phobias and anxiety can lead to the development of panic disorder, which affects about 6 million American adults [2] and is twice as common in women as in men [3]. Panic disorder is characterized as an anxiety disorder, which involves having recurrent, unexpected panic attacks followed by at least one month of persistent concern about having another attack, worry about the consequences of panic attacks and a change in behavior as a result of the attacks [4]. Patients with panic disorder have an increased risk of developing other psychiatric disorders. Panic disorder is further associated with other medical conditions such as migraines, fibromyalgia and irritable bowel syndrome [5].

Genetics

Studies of twins and families suggest that genetics plays a role in the development of panic disorder. First-degree biological relatives of people with panic disorder are 4 to 7 times more likely to develop panic disorder [4]. Children of parents who have panic disorder are up to 8 times more likely to develop the condition [4]. Additionally, children of parents who have either depression or bipolar disorder are also at a higher risk of developing panic disorder [6-7].

A large number of candidate gene studies and several genome-wide studies have been conducted to identify genetic factors associated with increased susceptibility to panic disorder. These studies have failed to clearly describe the biology of panic disorder. Indeed, the phenotypic and genetic complexity of panic disorder has made biological studies challenging [8]. Obstacles defining the molecular mechanisms involved in panic disorder arise, in part, from the inherent difficulties accessing brain tissue in quantities and qualities necessary for scientific study.

To overcome these issues, University of Iowa researchers recently used lymphocytes and their derived lymphoblast cell lines as an alternative tissue source, citing a number of studies that have demonstrated that gene expression differences found in either lymphoblasts or lymphoblast cell lines are predictive of complex “medical” illnesses including hyperlipidemia, hypertension and arthritis [9]. They suggest that peripheral blood cells could serve as a biosensor if environmental or gene-environmental interactions are important in the etiology of panic disorder, since nearly 82% of the genes expressed in the central nervous system are expressed in peripheral blood and the expression of genes in peripheral blood is affected by “environmental conditions.”

Cultured lymphoblast gene expression was compared from 16 patients with panic disorder and 17 without the disorder. Patients with panic disorder were found to have significantly different patterns of lymphoblast gene expression compared to patients without. Interestingly, almost 7 times more genes were found to be activated than repressed in patients with panic disorder. Researchers also identified a number of sex-specific differences in gene expression; that is, increased or decreased gene expression in cell lines from women with panic disorder as compared to female control lines, and from men with panic disorder as compared to male control lines. However, the study has a number of problems, some of which are troubling given that the data is being used to develop a costly predictive test [10].

First, although panic disorder is a disease of brain cells, the study evaluated the expression of genes from lymphoblasts. The principle assumption is that environmental or gene-environmental interactions are causal factors for panic disorder and gene expression differences in lymphoblasts will be predictive of panic disorder. However, this has yet to be shown. Second, all but 2 of the 16 patients with panic disorder were on psychiatric medications, which may confound the results. Third, there was discrepancies in the age of cell lines between patients with and without panic disorder. Fourth, only 5 genes were selected for confirmation by qRT-PCR, and only 3 of the 5 passed. Lastly, functional cluster analysis, which attempts to ascribe biological function to clusters of genes displaying similar expression patterns by identifying statistical over-representation of genes associated with biological pathways or processes, failed to identify any significant enrichment.

The researchers mention several calcium channel genes that were dysregulated in patients with panic disorder. The role of calcium in anxiety disorders has been proposed for decades. However, the limited analysis and failure to identify functional enrichment leaves little to be derived from the study. Nevertheless, the identification of lymphoblast gene expression differences in patients with and without panic disorder is promising for future investigation.

Treatment

There is no way to prevent panic disorder. However, if you have been diagnosed with panic disorder, avoiding caffeine, alcohol and some over-the-counter cold medications may help prevent panic attacks. Many people with anxiety disorder benefit from self-help and/or support groups.

A number of health-focused social networks that offer mental health support groups are listed in the Highlight HEALTH Web Directory - Health 2.0 - Patient Social Networks, including:

• MD Junction
• DailyStrength
• Revolution Health

Additional information on “Panic Attacks” and “Panic Disorder” can be found at Organized Wisdom, iMedix and TauMed.

Effective treatment for panic attacks and panic disorder is available and may involve cognitive behavior therapy to better understand panic attacks, the triggers, and how to deal with them, as well as medications, including an antidepressant, such as sertraline (Zoloft), paroxetine (Paxil) or fluoxetine (Prozac, Sarafem), and a benzodiazepine, such as clonazepam (Klonopin) or alprazolam (Xanax). Anxiety disorders also include obsessive-compulsive disorder (OCD), post-traumatic stress disorder (PTSD), social and specific phobias, and generalized anxiety disorder.

References

1. Blood Tests May Be Possible For Mental Health Conditions. University of Iowa News Services. 2007 Mar 6.
2. Kessler et al. Prevalence, severity, and comorbidity of twelve-month DSM-IV disorders in the National Comorbidity Survey Replication (NCS-R). Archives of General Psychiatry, 2005 Jun;62(6):617-27.
   View abstract
3. Psychiatric Disorders in America: the Epidemiologic Catchment Area Study. Robins LN and Regier DA, eds. New York: The Free Press, 1991.
4. Diagnostic and Statistical Manual of Mental Disorders (DSM-IV), Fourth Edition. Washington, DC: American Psychiatric Association, 2000.
5. Hudson et al. Comorbidity of fibromyalgia with medical and psychiatric disorders. Am J Med. 1992 Apr;92(4):363-7.
   View abstract
6. MacKinnon et al. Comorbid bipolar disorder and panic disorder in families with a high prevalence of bipolar disorder. Am J Psychiatry. 2002 Jan;159(1):30-5.
   View abstract
7. Biederman et al. Patterns of psychopathology and dysfunction in high-risk children of parents with panic disorder and major depression. Am J Psychiatry. 2001 Jan;158(1):49-57.
   View abstract
8. Finn and Smoller. The genetics of panic disorder. Curr Psychiatry Rep. 2001 Apr;3(2):131-7.
   View abstract
9. Philibert et al. Transcriptional profiling of lymphoblast lines from subjects with panic disorder. Am J Med Genet B Neuropsychiatr Genet. 2007 Jul 5;144(5):674-82. DOI: 10.1002/ajmg.b.30502
   View abstract
10. Panic Disorder Blood Test May Aid Treatment. ABC News. 2007 Sep 21.

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A novel gene was discovered recently that suppresses the growth of human tumors in a number of different cancers. The study, published in the journal Nature Medicine, found that the gene HACE1, an acronym for HECT domain and ankyrin repeat containing, E3 ubiquitin protein ligase 1, is able to help cells deal with various forms of stress that cause tumor formation [1].

What is a ubiquitin protein ligase?

Ubiquitin is a small protein consisting of only 76 amino acids. It is attached to other proteins by an enzyme called a protein ubiquitin ligase in a process known as ubiquitination. Ubiquitin acts as a marker that targets proteins for proteolysis (meaning cleavage of proteins by proteases, enzymes that degrade protein molecules). Ubiquitin is appropriately named since it is ubiquitious and present in essentially all cell types.

The process of ubiquitination occurs in three steps:

1. Ubiquitin is activated by an E1 ubiquitin-activating enzyme.
2. Activated ubiquitin is transferred from E1 to the ubiquitin-conjugating enzyme E2.
3. The E3 ubiquitin-ligating enzyme interacts with both the E2 enzyme and the substrate (meaning the molecule upon which an enzyme acts), and transfers ubiquitin to the substrate protein.
4. Frequently, the process is repeated to form a polyubiquitin chain.

The 2004 Nobel Prize in Chemistry was awarded to Aaron Ciechanover and Avram Hershko (Technion Israel Institute of Technology, Haifa, Israel), and Irwin Rose (University of California, Irvine, US) for the discovery of ubiuitin-mediated protein degredation.

Study results

The British Columbia Cancer Research Centre study, done in both mice and human tumor cells, demonstrated that HACE1 is a tumor suppressor. Researchers “knocked out” the gene in mice (meaning the gene was inactivated so that it wasn’t expressed) and found that as the mutant mice aged, they spontaneously developed a spectrum of tumors, including melanoma (the most serious form of skin cancer), hepatocellular carcinoma (primary liver cancer), spontaneous lung adenocarcinoma (lung cancer), angiosarcoma (tumors that develop from blood or lymphatic vessels), mammary carcinomas (breast cancer) and lymphomas (a family of cancers that develop from immune system cells called lymphocytes).

Additionally, loss of HACE1 expression also rendered the mice susceptible to environmental and genetic second hits for the development of multiple cancers. The mutant mice were subjected to various forms of stress, including ultraviolet radiation, lung carcinogens or other genetic alterations, and the result was a dramatic increase in cancer growth. The mice developed breast, lung, and liver cancers, as well as lymphomas, melanomas and sarcomas.

When HACE1 was expressed in human tumor cells, the cells lost their ability to form tumors. The tumor-suppressor function of HACE1 was shown to be dependent on its E3 ligase activity and the researchers suggest that HACE1 regulates cell cycle progression during cell stress by influencing degredation of the protein cyclin D1, which plays a key regulatory role during the G1 phase of the cell cycle.

What does all this mean? A distinctive feature of cancer is the subversion of normal growth signaling pathways and cell cycle regulators are natural targets during tumor development. Overexpression or amplification of cyclin D1, an oncogene, has been identified or associated with a range of human cancers, including B mantle cell lymphoma [2], non-small cell lung cancers [3], head and neck squamous cell carcinoma [4], pancreatic carcinomas [5], bladder cancer [6] and breast carcinoma [7]. If scientists can express HACE1 in human tumors or prevent HACE1 inactivation, it may be possible to improve cancer treatments.

References

1. Zhang et al. The E3 ligase HACE1 is a critical chromosome 6q21 tumor suppressor involved in multiple cancers. Nat Med. 2007 Oct;13(9):1060-1069. Epub 2007 Aug 12.
   View abstract
2. Williams et al. Chromosome t(11;14)(q13;q32) breakpoints in centrocytic lymphoma are highly localized at the bcl-1 major translocation cluster. Leukemia. 1993 Sep;7(9):1437-40.
   View abstract
3. Yamanouchi et al. Expression of cyclin E and cyclin D1 in non-small cell lung cancers. Lung Cancer. 2001 Jan;31(1):3-8.
   View abstract
4. Izzo et al. Dysregulated cyclin D1 early in head and neck tumorigenesis: in vivo evidence for an association with subsequent gene amplification. Oncogene. 1998;17:2113-22.
   View abstract
5. Gansauge et al. Overexpression of cyclin D1 in human pancreatic carcinoma is associated with poor prognosis. Cancer Res. 1997;57:1634-7.
   View abstract
6. Hall and Peters. Genetic alterations of cyclins, cyclin-dependent kinases, and cdk inhibitors in human cancer. Adv Cancer Res. 1996;68:67-108.
   View abstract
7. Barnes and Gillett. Cyclin D1 in breast cancer. Breast Cancer Res Treat. 1998;52(1-3):1-15.
   View abstract

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