God-Science-Universe

Wednesday, April 10, 2013

Rumination is defined as the compulsively focused attention on the symptoms of one's distress, and on its possible causes and consequences, as opposed to its solutions. Rumination is similar to worry except rumination focuses on bad feelings and experiences from the past, whereas worry is concerned with potential bad events in the future. Both rumination and worry are associated with anxiety and other negative emotional states. There is a difference between rumination and introspection. Anyone spending a lot of time in one’s own head is at risk of digging into rumination holes. One has to be mindful to prevent healthy self-examination from degenerating into unproductive rumination. Introspection is examination of thoughts, desires and conducts and is productive, rumination is not. Rumination is repetitive, negativistic, and often self-flagellating and a major risk factor for anxiety and depression.

Time spent alone in thought can be positive; a rich environment for personal growth and creativity, but it can also be dangerous when it is negatively turned against one’s self. Introspection is a process of healthy self-reflection, examination, and exploration, which is good for well-being of brain.

Neuroscientist and mindfulness experts describe time reflecting on oneself as “time in;” a period in which a person checks in with himself to see where one is emotionally. This “time in” is one of seven suggested activities on healthy mind platter. The problem is that mind is not always a safe place. Every person is divided between a healthy attitude toward self that is goal-directed and life-affirming, and a destructive side that can be self-critical, self-denying, paranoid, and suspicious. This inner critic or anti-self or critical inner voice can take over thinking and lead to rumination. Rumination occurs when one becomes trapped in negative cycle of circular thinking. This kind of thinking has a strong link to depression and suicide.

When one is in the realistic point of view of real self, one can have positive self-reflection. When one is in the point of view of anti-self, experiencing thoughts that focus on self as bad, one must avoid ruminating. When introspecting, one must adopt an attitude of curiosity, openness, acceptance and love and think about what one wants to challenge in self and how to differentiate from negative past influences. This gives life a meaning and direction without falling victim to inner critic that confiscates back and prevents one from achieving goals.

Another definition of rumination is repeated and passive thinking about the consequences of problems rather than getting into problem solving. For example, thinking about, "Why can’t I stop binge eating?" instead of chopping up a salad to take to work for lunch. Also, people often ruminate about comments other people have made. The trap of rumination sometimes thinking in-depth does lead to useful insights. When anything works intermittently such as a child asking parents for chocolate, those behaviors tend to be very resistant to change. It is the intermittent reinforcement trap.

Introverts needs silence to think about thoughts, because they often are more sensitive to everything around them, they need that down time, without interruption and input from the outside world, to process the stuff of the day, the interactions, their reactions to them, and simply to think their thoughts.

Introspection is about growth, we look inward in order to learn. Rumination is about getting stuck; the wheels are turning, but not getting anywhere other than to frustration, depression and anger. I don't think we'd worry about spending too much time being introspective, but when it comes to ruminating; if someone showed us the exit, we'd take it!

Instead of rehearsing, regurgitating, replaying experience, start making action plans. Explore, what can be done about the situation one cannot stop thinking about, and then face up to the conflict. Write out action plan. Even if not ready to take action, seeing action plan in writing will be part of the "getting ready" process. Set a time limit on rethinking, make five-minute appointments with yourself a couple of times during the day where you can ruminate if you like, but between the appointments, refuse to take worry's call: say, “You are too busy.”

The point that differentiates rumination from introspection is a great one. That point in some form often comes up in therapy. One often just knows when one is going over old ground or problem solving. There is a difference. The feeling that comes along is different with each one. With introspection, there is a sense of exploring something, considering new perspectives, and is more aware of feelings. Rumination feels like not just going in circles, but also digging in to oneself further into distressed feelings. So, being aware of thoughts, feelings, and reasons are essential for knowing the difference; and being compassionate to the struggle is essential in working ways through it. For this reason, one has to develop compassionate self-awareness, that is to say, a combination of self-compassion and self-awareness. Compassionate self-awareness provides a helpful perspective for many struggles.

Mindfulness comes up in anything we imagine to achieve in life. Wherever you go, there you are, so practice living a quiet life in this noisy world.

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It is hard to take pleasure in life when you don't care for yourself. People who haven't learned to accept and get along with themselves tend to have more difficulty accepting and getting along with others. I personally had a hard time getting along with people, until I finally realized how my difficulty with other people was rooted in my difficulty with myself.

The produce of life comes from the root within us. If you are rooted in humiliation, guilt, inferiority, rejection, lack of love and acceptance; the fruit of your relationships will suffer. However, once you are exposed to unconditional love and begin to accept yourself and others, these new roots will produce good fruit, and your relationship will flourish.

Never say or think negative things about yourself, such as, "I never do anything right." "I'll never change." "I'm ugly." "I look terrible." "I'm dumb." "Who could ever love me?" By your words you will be justified, and by your words you will be condemned, as we think in our mind, so we are. The way we think about ourselves reveal how we feel about ourselves.

Talk good things about yourself in line with what the word says about you. I like starting the day making good declaration of my guilt. You can do this while you're driving to work or cleaning house. Never compare yourself with other people. Variety is the spice of life or we wouldn't have been all different even down to our fingerprints. You'll never succeed at being yourself if you're trying to be like someone else. Other people can be a good example to you, but photocopying even their good traits will look different through your individual personality.

Zoom in on your potential instead of your limitations. Refuse to concentrate on the supposed limitation and decide to concentrate on your potential. Hit upon things you like to do that you do well, and do it over and over. If you spend your time doing things you're not good at, it will frustrate you and cause you to feel defeated and ineffective.

Dare to be different and deal with disapproval. Be a God-pleaser, not a man-pleaser. If you dare to be different, you'll have to expect some criticism. Going along with the crowd when we know in our heart we must be going in a different direction is one reason we don't succeed at being ourselves. You won't like yourself very much if you go against your own convictions.

Don't let the way another person treats you determine your worth. Keep your flaws in perspective. People with a high level of confidence have just as many weaknesses as people without confidence, but they concentrate on their strengths, not their flaws or weaknesses.

To finish, let me remind you of my opening declaration: It is tough to take pleasure in life, when you don't like yourself. When you learn to succeed at being yourself, you will be on your way to enjoy life fully.

Friday, February 15, 2013

Common Chemicals Causes Osteoarthritis

Exposure to two common perfluorinated chemicals leads to osteoarthritis. Perfluorinated chemicals are used in more than 200 industrial processes and consumer products including certain stain and water-resistant fabrics, grease-proof paper food containers, personal care products, and other items. Because of their persistence, perfluorinated chemicals have become ubiquitous contaminants of humans and wildlife. The study, published in Environmental Health Perspectives, is the first to look at the associations between perfluorooctanoic acid and perfluorooctanesulfonic acid, and osteoarthritis, in a study population representative of the United States.

Perfluorooctanoic acid and perfluorooctanesulfonic acid exposures are associated with higher prevalence of osteoarthritis, particularly in women, a group that is disproportionately impacted by this chronic disease, says Sarah Uhl, who authored the study along with Yale Professor Michelle L. Bell and Tamarra James-Todd, an epidemiologist at the Harvard Medical School and Brigham and Women's Hospital. The research was the focus of Uhl's Master's of Environmental Science Program at the Yale School of Forestry and Environmental Studies.

Scientists analyzed data from six years of the National Health and Nutrition Examination Survey, which enabled them to account for factors such as age, income, and race/ethnicity. When the scientists looked at men and women separately, they found clear, strong associations for women, but not men. Women in the highest 25% of exposure to perfluorooctanoic acid had about two times the odds of having osteoarthritis compared to those in the lowest 25% of exposure.

Although production and usage of perfluorooctanoic acid and perfluorooctanesulfonic acid have declined due to safety concerns, human and environmental exposure to these chemicals remains widespread. Future studies are needed to establish temporality and shed light on possible biological mechanisms. Reasons for differences in these associations between men and women, if confirmed, also need further exploration. Better understanding the health effects of these chemicals and identifying any susceptible subpopulations could help to inform public health policies aimed at reducing exposures or associated health impacts.

Wednesday, January 23, 2013

Heuristics Used In Identify Disease Mechanisms And Treatments

Current views of human disease are based on simple correlation between clinical syndromes and pathological analysis dating from the late 19th century. Although, this approach to disease diagnosis, prognosis, and treatment has served the medical establishment and society well for many years, it has serious shortcomings for the modern era of the genomic medicine that stem from its reliance on reductionist principles of experimentation and analysis. Quantitative, holistic systems biology applied to human disease offers a unique approach for diagnosing established disease, defining disease predilection, and developing personalized treatment strategies that can take full advantage of modern molecular pathobiology and the comprehensive data sets that are rapidly becoming available for populations and individuals. In this way, systems pathobiology offers the promise of redefining our approach to disease and the field of medicine.

The translation of new knowledge about mechanisms that govern human pathobiology into effective preventive, diagnostic, and therapeutic strategies is a slow and cumbersome process. A major contributor to this translational delay is the use of the traditional characterization and definition of human disease, which dates to the 19th century and is largely based on Oslerian clinicopathological correlation. The Oslerian formalism for human disease links clinical presentation with pathological findings. As a result, disease is defined on the basis of the principal organ system in which symptoms and signs are manifest, and in which gross anatomic pathology and histopathology are correlated. This approach has held sway for over a century, and although there has been continual refinement of the pathological markers used for correlation, for example, biochemical measurements, immunohistochemistry, flow cytometry, and, more recently, molecular pathological analyses of expressed genes, the general principles remain the same as when the approach was first proposed. Current classification of disease pathophenotype is, then, the result of inductive generalization from clinicopathological evidence predicated on the law of reductive parsimony. This paradigm has been helpful to clinicians as it establishes syndromic patterns that limit the number of potential pathophenotypes they may need to consider. Although quite useful in an earlier era, classifying disease in this way vastly over generalizes pathophenotypes, does not usually take into consideration susceptibility states or preclinical disease manifestations, and cannot be used to individualize disease diagnosis or therapy.

Based on this history, it is hardly surprising that these conventional pathophenotypes are far too limited to be useful in the postgenomic era. A simple example illustrates this shortcoming. The classic Mendelian disorder, sickle cell disease, is caused by a single point mutation at position 6 of the β-chain of hemoglobin, which changes hemoglobin’s oxygen affinity and promotes polymerization under hypoxic conditions. Notwithstanding Mendelian predictions to the contrary, this simple biochemical phenotype and its corresponding monogenotype do not yield a single pathophenotype. Individuals with sickle cell disease can present with painful crisis, osteonecrosis, acute chest syndrome, stroke, profound anemia, or mild anemia. There are many reasons for these different clinical pathophenotypes, ranging from the presence of disease modifying genes, for example, hemoglobin F to environmental influences; for example, hypoxia. Clearly, even the simplest genetically determined disease is manifestly complex in its expression, a fundamental observation that emphasizes the importance of the genomic and environmental contexts within which disease evolves.

Although conventional reductionist pathophenotyping has guided steady progress in diagnostics and therapeutics for many years, it is fraught with shortcomings, some of which are highlighted by this example, that are particularly problematic for contemporary molecular and genomic analyses. Put another way, in using this sorely outdated approach to defining human disease, one can construct nosological silos that focus exclusively on end-stage pathological processes in a single organ largely driven by late-appearing, generic end-stage mechanisms rather than true disease-specific susceptibility determinants viewed in their holistic, systems-based complexity.

With this background, one can rationally catalog the limitations of traditional disease definition as disease is typically defined by late-appearing manifestations in a dysfunctional organ system, without regard for or knowledge of preclinical pathophenotype or susceptibility factors that precede overt abnormalities. Thus, the focus is not on the specific genetic or environmental susceptibility determinants of the disease phenotype, but, rather, on the late-appearing, intermediate pathophenotypes like generic endopathophenotypes, including inflammation, immunity, fibrosis, thrombosis, hemorrhage, cell proliferation, apoptosis, and necrosis within a given organ system. As a result, typical therapeutic strategies do not focus on truly unique, targeted disease determinants, but on these same intermediate pathophenotypes, for example, anti-inflammatory or antithrombotic therapies for acute myocardial infarction.

Conventional disease paradigms generally neglect underlying pathobiological mechanisms that may extend beyond the disease-defining organ system, and do not typically consider the molecular (deterministic) and environmental (stochastic) factors that govern disease evolution from susceptibility state to preclinical pathophenotype to overt pathophenotype.

Conventional definitions of disease are excessively inclusive of the range of pathophenotypes and are based on the pathophysiological characterizations largely of the premolecular era. These inclusive definitions of disease not only obscure subtle, but potentially important, differences among individuals with common clinical presentations, but also neglect underlying disease mechanisms that cross organ systems and may yield more appropriate and specific therapeutic targets.

Yet another dimension to this problem stems from the reductionist approach we use to identify disease mechanisms or therapeutic targets. Disease is rarely, if ever, a simple consequence of

an abnormality in a single effector gene product, but, rather, is a reflection of pathobiological processes (deterministic and stochastic) that interact in a complex network to yield pathophenotype, which may be viewed as an emergent property, that is to say, discernible only by appreciating the behavior of the network as a whole rather than of its component parts in reductionist isolation of a pathobiological system.

These shortcomings of conventional disease definition account for many limitations of major recent genomebased efforts to define disease determinants, for example, the weak effect size of linked alleles observed in genomewide association studies of complex disease and to design rational therapies, for example, the failure of >90% of drug candidates. Thus, solving this problem is not simply an exercise in nosology, but is essential for moving the entire health care enterprise forward to reduce the burden of human disease and suffering.

This highlights the clear need to reconsider and redefine the determinants of human disease. All disease is complex, even simple Mendelian disorders. Pathophenotype reflects the action of a deterministic, defective molecular network within a stochastic environmental context that modulates network function. Defined in this way, disease is the result of the output of a complex modular network of –omic and environmental nodes linked mechanistically to yield pathophenotype. With this background and rationale, we can redefine all human disease using a combination of approaches to identify systems-based pathobiological mechanisms that render one susceptible to preclinical and overt pathophenotypes. This approach challenges the existing disease paradigm directly, and is justifiable owing to the largely heuristic strategies that have been used to identify disease mechanisms and treatments to date.

Systems Medicine A Reality

Systems medicine is the application of systems biology approaches to medical research and medical practice. Its objective is to integrate a variety of biological and medical data at all relevant levels of cellular organization using the power of computational and mathematical modeling, to enable understanding of the pathophysiological mechanisms, prognosis, diagnosis and treatment of disease.

The clinical needs should be the driver for the applications of systems biology methods in medicine and for the evolution of the essential new technologies. The possible actions required are, systems biology approaches could guide clinical trial design, shortening times and costs. Re-defining clinical phenotypes based on molecular and dynamic parameters, discovering effective biomarkers of multiple nature for disease progression; clinically useful for risk, prognosis, diagnosis. Combinatorial therapy approach would be useful to find out a combination and lower doses of effective drugs, in particular in the case of co-morbidity, where more than one disease is affecting the patient, upgrading of drug development; optimizing drug efficacy, safety and delivery, timing and dosage of therapy. Finally, healthy individual are to be addressed in the long term.

Scientific areas for partnership in Systems Medicine includes understanding the pathophysiology of chronic diseases, multifactorial diseases like cancer, diabetes, obesity, metabolic disorders, aging through network analysis of disease processes, and the recognition of biomarkers for early diagnosis and prognosis and personalized treatment, combinatorial therapies and combinatorial drug screening and mixing of personalized genomics with personalized metabolomics, endocrinomics, proteomics and clinical phenotyping.

The major confrontation is for systems biology to furnish a change in the medical model in order to build the foundation for a prospective medicine that will be predictive, personalized, preventive and participatory. In order for systems medicine to become a reality, one needs coordinated vision of all relevant stakeholders and a field guide at the same level of ambition as the Human Genome project. In addition, the creation of a strong networking effort among funded systems biology projects is essential, in order to share information and resources on successful methodological approaches and tools with the broader systems biology and clinical community.

Recent years have seen the rapid emergence of systems biology as a new discipline. In the biomedical sciences, this trend is very apparent as research moves from a reductionist approach to a systems understanding model that attempts to understand biology and pathophysiology in an integrative manner, making use of the rapidly increasing amounts of novel (-omics) data and other relevant quantitative biological and medical data that are becoming available.

However, despite the spectacular advances in the post-genomic era, there exists a hiatus between experimental data and medical knowledge, and even a greater gap exists when we evaluate new knowledge in terms of clinical utility and benefit to patients. As a result, despite major technological advances, there are still obstacles that separate systems biology from medical applications. Systems medicine, a newly emerging area should aim the bridging of this gap.

Experts in a wide range of relevant disciplines from clinical, diagnostics and pharmaceutical areas, to high throughput –omics technologies, and computational and systems biology, including representatives from academia, industry, and funding agencies should get together to explore opportunities and challenges for the development of systems medicine. The aims are to analyze the state-of-the-art of systems biology for medical applications, identify key opportunities and bottlenecks for the translation of systems biology to medicine and the clinic, and identifying key research and policy areas for joint research in the short, medium and long term in order to make systems medicine a reality.

Thursday, January 17, 2013

Strange&Piercing Celestial&Dreamlike

While these stunning images look like still shots, they’re actually the handiwork of “amateur” French photographer David Keochkerian. David’s style of infrared photography is achieved by using a special camera or lens filter to block out all light but the infrared waves. The result is another-worldly effect where the color is strange and piercing and the quality is celestial and dreamlike. By taking advantage of nature’s inherent beauty; from trees in bloom to a pond’s reflective properties, vivid tones and striking contrasts come together to produce the sort of magical surrealism that movies are made of. But as any behind-the-scenes creative talent knows, these shots required way more than the wave of a wand to materialize. Starting off with a D70 infrared and an external infrared filter and ultimately moving to a 590 nm internal filter for the D700; the photographer captures the images displayed below and perfect them in post-production.

Tips for those inclined to give infrared photography a spin; lush green foliage and the sunny skies of spring and summer are I feel ideal conditions for infrared photography; a tripod and remote is a must due to extended exposure times; shoot RAW images and adjust the white balance to your preference in post-production. Now, let’s take a peek at David Keochkerian’s compositions for inspiration, his treatments and styles.