NORML’s Russ Belville vs. former ONDCP’s Dr. Kevin Sabet on Marijuana Legalization at James A. Baker Institute (VIDEO)

DFW NORML’s “Truth Enforcement Vehicle” was parked out front of the Baker Institute flashing the green lights to lead people to the event.

My undying thanks go out to The James A. Baker Institute for Public Policy for the invitation to participate in this illustrious event. I learned so much from the incredible presentations of Rev. Edwin Sanders, Sen. Larry Campbell, Prof. Alex Stevens, Dr. Ethan Nadelmann, Prof. Michelle Alexander, and everyone who participated.

I also thank the crews from DFW NORML, Houston NORML, and NORML of Waco Inc. for showing up with the Truth Enforcement Vehicle, putting on a great fundraiser, and showing me a NORML (if a little traffic-laden) good time in H-town.  (Once again, like last year, wherever I go, Portland-like rain follows me, leading Professor Bluntston to exclaim, “Russ ‘Break It Down’ Belville done brought the rain!”)

Debating Kevin Sabet was fun.  Before we went up, he thanked me for devoting half of my show to him (it was only a quarter, but whatever) and suggested that maybe it isn’t a good idea for me to give up my whole debate strategy before the debate.  I told him that when you have truth, facts, logic, and reason on your side, you don’t have to have much of a strategy.

Please take the time to watch the other videos from presenters at the Baker Institute.  I’m flattered by all the hits my video is getting, but you’ll learn a whole lot more from the learned people on the other videos.

160 thoughts

  1. Limbic regulation From Wikipedia, the free encyclopediaJump to: navigation, search It has been suggested that Limbic resonance be merged into this article or section. (Discuss) Proposed since April 2011.

    Limbic regulation, mood contagion or emotional contagion is the effect of contact with other people upon the development and stability of personality and mood.

    The concept was advanced in the book A General Theory of Love (2000), and is one of three interrelated concepts central to the book’s premise: that our brain chemistry and nervous systems are measurably affected by those closest to us (limbic resonance); that our systems synchronize with one another in a way that has profound implications for personality and lifelong emotional health (limbic regulation); and that these set patterns can be modified through therapeutic practice (limbic revision).

    Contents [hide]
    1 Definition
    2 Importance and history
    3 Subsequent use and definitions of the term
    4 References

    [edit] DefinitionAs the authors poetically frame it: “Human physiology finds a hub … in the harmonizing activity of nearby limbic brains. Our neural architecture places relationships at the crux of our lives, where, blazing and warm, they have the power to stabilize [italics in original]. When people are hurting and out of balance, they turn to regulating affiliations: groups, clubs, pets, marriages, friendships, masseuses, chiropractors, the Internet. All carry at least the potential for emotional connection.”[1]:170

    [edit] Importance and historyLewis, Amini and Lannon make a compelling case for the centrality of limbic regulation to our physiological as well as emotional well-being. They begin with a story from the dawn of scientific experimentation in human development—albeit heinously misguided—when in the thirteenth century Frederick II raised a group of infants to be completely cut off from human interaction, other than the most basic care and feeding, so as to discover what language would spontaneously arise absence of any communication prompts. The result of this notorious experiment was that the infants, deprived of any human discourse or affection, all died.[1]:68,69

    The authors find the hegemony of Freudian theory in the early days of psychology and psychiatry to be almost as harmful as the ideas of Frederick the Great. They condemn the focus on cerebral insight, and the ideal of a cold, emotionless analyst, as negating the very benefit that psychotherapy can confer by virtue of the empathetic bond and neurological reconditioning that can occur in the course of sustained therapeutic sessions. “Freud’s enviable advantage is that he never seriously undertook to follow his own advice. Many promising young therapists have their responsiveness expunged, as they are taught to be dutifully neutral observers, avoiding emotional contact….But since therapy is limbic relatedness, emotional neutrality drains life out of the process…” [1]:184

    A General Theory of Love is scarcely more sympathetic to Dr. Benjamin Spock and his “monumentally influential volume” Baby and Child Care, especially given Spock’s role in promoting the movement against co-sleeping, or allowing infants to sleep in the same bed as their parents. Lewis, Amini and Lannon cite the research of sleep scientist James McKenna, which seems to suggest that the limbic regulation between sleeping parents and infants is essential to the neurological development of the latter and a major factor in preventing Sudden Infant Death Syndrome (SIDS). “The temporal unfolding of particular sleep stages and awake periods of the mother and infant become entwined….on a minute to minute basis, throughout the night, much sensory communication is occurring between them.”[1]:195

    [edit] Subsequent use and definitions of the termIn Living a connected life (2003), Dr. Kathleen Brehony looks at recent brain research which shows the importance of proximity of others in our development. “Especially in infancy, but throughout our lives, our physical bodies are influencing and being influenced by others with whom we feel a connection. Scientists call this limbic regulation.” [2]

    Brehony goes on to describe the parallels between the “protest/despair” cycles of an abandoned puppy and human development. Mammals have developed a tendency to experience distraction, anxiety and measurable levels of stress in response to separation from their care-givers and companions, precisely because such separation has historically constituted a threat to their survival. As anyone who has owned a puppy can attest, when left alone it will cry, bark, howl, and seek to rejoin its human or canine companions. If these efforts are unsuccessful and the isolation is prolonged, it will sink into a state of dejection and despair. The marginal effectiveness of placing a ticking clock in the puppy’s bed is based on a universal need in mammals to synchronize to the rhythms of their fellow creatures.

    Limbic resonance and limbic regulation are also referred to as “mood contagion” or “emotional contagion” as in the work of Sigal Barsade. Barsade and colleagues at the Yale School of Management build on research in social cognition, and find that some emotions, especially positive ones, are spread more easily than others through such “interpersonal limbic regulation”.[3]

    Author Daniel Goleman has explored similar terrain across several works: in Emotional Intelligence (1995), an international best seller, The Joy Of Living, coauthored with Yongey Mingyur Rinpoche, and the Harvard Business Review on Breakthrough Leadership. In the latter book, Goleman considers the “open loop nature of the brain’s limbic system” which depends on external sources to manage itself, and examines the implications of interpersonal limbic regulation and the science of moods on leadership.[4]

    In Mindfully Green: A Personal and Spiritual Guide to Whole Earth Thinking (2003) author Staphine Kaza defines the term as follows: “Limbic regulation is a mutual simultaneous exchange of body signals that unfolds between people who are deeply involved with each other, especially parents and children.” She goes on to correlate love with limbic engagement and asserts that children raised with love learn and remember better than those who are abused. Kaza then proposes to “take this work a step further from a systems perspective, and imagine that a child learns through some sort of limbic regulation with nature”.[5]

    [edit] References1.^ a b c d Lewis, Thomas L.; Amini, Fari; Lannon, Richard (2000). A general theory of love. New York: Random House. ISBN 0-375-50389-7.
    2.^ Brehony, Kathleen A. PhD (2003). Living a connected life: creating and maintaining relationships that last. New York: Henry Holt & Co.. p. 26. ISBN 0-8050-7023-0.
    3.^ Barsade, Sigal (December 2002). “The Ripple Effect: Emotional Contagion and Its Influence on Group Behavior”. Administrative Science Quarterly (Johnson Graduate School of Management, Cornell University.): 644–675. JSTOR 3094912.
    4.^ Goleman, Dan; Peace, William J.; Pagonis, William G.; Peters, Tom F.; Jones, Gareth Stedman; Collingwood, Harris. Harvard Business Review on Breakthrough Leadership. Harvard Business School Press. pp. 31. ISBN 1-57851-805-9.
    5.^ Kaza, Stephanie (2008). Mindfully Green: A Personal and Spiritual Guide to Whole Earth Thinking. Shambhala. pp. 45, 46. ISBN 1-59030-583-3.

  2. Psychology is the study of the mind, occurring partly via the study of behavior.[1][2] Grounded in scientific method,[1][2] psychology has the immediate goal of understanding individuals and groups by both establishing general principles and researching specific cases,[3][4] and for many it ultimately aims to benefit society.[5][6] In this field, a professional practitioner or researcher is called a psychologist, and can be classified as a social scientist, behavioral scientist, or cognitive scientist. Psychologists attempt to understand the role of mental functions in individual and social behavior, while also exploring the physiological and neurobiological processes that underlie certain cognitive functions and behaviors

  3. The high lipid-solubility of cannabinoids results in their persisting in the body for long periods of time. Even after a single administration of THC, detectable levels of THC can be found in the body for weeks or longer (depending on the amount administered and the sensitivity of the assessment method). A number of investigators have suggested that this is an important factor in marijuana’s effects, perhaps because cannabinoids may accumulate in the body, particularly in the lipid membranes of neurons.[39]

    Until recently, little was known about the specific mechanisms of action of THC at the neuronal level. However, researchers have now confirmed that THC exerts its most prominent effects via its actions on two types of cannabinoid receptors, the CB1 receptor and the CB2 receptor, both of which are G-Protein coupled receptors. The CB1 receptor is found primarily in the brain as well as in some peripheral tissues, and the CB2 receptor is found exclusively in peripheral tissues.[40] THC appears to alter mood and cognition through its agonist actions on the CB1 receptors, which inhibit a secondary messenger system (adenylate cyclase) in a dose dependent manner. These actions can be blocked by the selective CB1 receptor antagonist SR141716A (rimonabant), which has been shown in clinical trials to be an effective treatment for smoking cessation, weight loss, and as a means of controlling or reducing metabolic syndrome risk factors.[41]

  4. HistoryJohn W. Huffman, an organic chemist at Clemson University, synthesized analogues and metabolites of ?9-tetrahydrocannabinol (THC), the principal active component of cannabis. JWH-018 is one of these analogues, with studies showing an affinity for the cannabinoid (CB1) receptor five times greater than that of THC. Cannabinoid receptors are found in mammalian brain and spleen tissue; however, the structural details of the active sites are currently unknown.[7][8]

    On December 15, 2008, it was reported by the German pharmaceutical company THC Pharm that JWH-018 was found as one of the active components in at least three versions of the herbal blend Spice, which has been sold as an incense in a number of countries around the world since 2002.[9][10][11] An analysis of samples acquired four weeks after the German prohibition of JWH-018 took place found that the compound had been replaced with JWH-073.[12

  5. HistoryJohn W. Huffman, an organic chemist at Clemson University, synthesized analogues and metabolites of ?9-tetrahydrocannabinol (THC), the principal active component of cannabis. JWH-018 is one of these analogues, with studies showing an affinity for the cannabinoid (CB1) receptor five times greater than that of THC. Cannabinoid receptors are found in mammalian brain and spleen tissue; however, the structural details of the active sites are currently unknown.[7][8]

    On December 15, 2008, it was reported by the German pharmaceutical company THC Pharm that JWH-018 was found as one of the active components in at least three versions of the herbal blend Spice, which has been sold as an incense in a number of countries around the world since 2002.[9][10][11] An analysis of samples acquired four weeks after the German prohibition of JWH-018 took place found that the compound had been replaced with JWH-073.[12

  6. JWH-018 (1-pentyl-3-(1-naphthoyl)indole) or AM-678[1] is an analgesic chemical from the naphthoylindole family that acts as a full agonist at both the CB1 and CB2 cannabinoid receptors, with some selectivity for CB2. It produces effects in animals similar to those of THC, a cannabinoid naturally present in cannabis, leading to its use in synthetic cannabis products such as “legal cannabis herbal incense blends”, including Spice, Relaxinol, and Mr. Nice Guy, which are ‘legally’ sold as “incense” and labeled as “not for human consumption.

  7. A GABA agonist is a drug which acts to stimulate or increase the action at the GABA receptor, producing typically sedative effects, and may also cause other effects such as anxiolytic and muscle relaxant effects.

  8. ethanol (C2H5OH) is the type of alcohol found in alcoholic beverages, and in common speech the word alcohol refers specifically to ethanol.

  9. Applications
    Total recorded alcohol per capita consumption (15+), in litres of pure alcohol[6]Alcohols can be used as a beverage (ethanol only), as fuel and for many scientific, medical, and industrial utilities. Ethanol in the form of alcoholic beverages has been consumed by humans since pre-historic times. A 50% v/v solution of ethylene glycol in water is commonly used as an antifreeze.

    Some alcohols, mainly ethanol and methanol, can be used as an alcohol fuel. Fuel performance can be increased in forced induction internal combustion engines by injecting alcohol into the air intake after the turbocharger or supercharger has pressurized the air. This cools the pressurized air, providing a denser air charge, which allows for more fuel, and therefore more power.

    Alcohols have applications in industry and science as reagents or solvents. Because of its relatively low toxicity compared with other alcohols and ability to dissolve non-polar substances, ethanol can be used as a solvent in medical drugs, perfumes, and vegetable essences such as vanilla. In organic synthesis, alcohols serve as versatile intermediates.

    Ethanol can be used as an antiseptic to disinfect the skin before injections are given, often along with iodine. Ethanol-based soaps are becoming common in restaurants and are convenient because they do not require drying due to the volatility of the compound. Alcohol is also used as a preservative for specimens.

    Alcohol gels have become common as hand sanitizers.

  10. ProductionIn industry, alcohols are produced in several ways:

    By fermentation using glucose produced from sugar from the hydrolysis of starch, in the presence of yeast and temperature of less than 37 °C to produce ethanol, for instance, the conversion of invertase to glucose and fructose or the conversion of glucose to zymase and ethanol.
    By direct hydration using ethylene (ethylene hydration)[7] or other alkenes from cracking of fractions of distilled crude oil.

  11. Nucleophilic substitutionThe OH group is not a good leaving group in nucleophilic substitution reactions, so neutral alcohols do not react in such reactions. However, if the oxygen is first protonated to give R?OH2+, the leaving group (water) is much more stable, and the nucleophilic substitution can take place. For instance, tertiary alcohols react with hydrochloric acid to produce tertiary alkyl halides, where the hydroxyl group is replaced by a chlorine atom by unimolecular nucleophilic substitution. If primary or secondary alcohols are to be reacted with hydrochloric acid, an activator such as zinc chloride is needed. In alternative fashion, the conversion may be performed directly using thionyl chloride.[1]

    Alcohols may, likewise, be converted to alkyl bromides using hydrobromic acid or phosphorus tribromide, for example:

    3 R-OH + PBr3 ? 3 RBr + H3PO3
    In the Barton-McCombie deoxygenation an alcohol is deoxygenated to an alkane with tributyltin hydride or a trimethylborane-water complex in a radical substitution reaction.

    DehydrationAlcohols are themselves nucleophilic, so R?OH2+ can react with ROH to produce ethers and water in a dehydration reaction, although this reaction is rarely used except in the manufacture of diethyl ether.

    More useful is the E1 elimination reaction of alcohols to produce alkenes. The reaction, in general, obeys Zaitsev’s Rule, which states that the most stable (usually the most substituted) alkene is formed. Tertiary alcohols eliminate easily at just above room temperature, but primary alcohols require a higher temperature.

    This is a diagram of acid catalysed dehydration of ethanol to produce ethene:

    A more controlled elimination reaction is the Chugaev elimination with carbon disulfide and iodomethane.

    EsterificationTo form an ester from an alcohol and a carboxylic acid the reaction, known as Fischer esterification, is usually performed at reflux with a catalyst of concentrated sulfuric acid:

    R-OH + R’-COOH ? R’-COOR + H2O
    In order to drive the equilibrium to the right and produce a good yield of ester, water is usually removed, either by an excess of H2SO4 or by using a Dean-Stark apparatus. Esters may also be prepared by reaction of the alcohol with an acid chloride in the presence of a base such as pyridine.

    Other types of ester are prepared in a similar manner — for example, tosyl (tosylate) esters are made by reaction of the alcohol with p-toluenesulfonyl chloride in pyridine.

    OxidationMain article: Alcohol oxidation
    Primary alcohols (R-CH2-OH) can be oxidized either to aldehydes (R-CHO) or to carboxylic acids (R-CO2H), while the oxidation of secondary alcohols (R1R2CH-OH) normally terminates at the ketone (R1R2C=O) stage. Tertiary alcohols (R1R2R3C-OH) are resistant to oxidation.

    The direct oxidation of primary alcohols to carboxylic acids normally proceeds via the corresponding aldehyde, which is transformed via an aldehyde hydrate (R-CH(OH)2) by reaction with water before it can be further oxidized to the carboxylic acid.

    Mechanism of oxidation of primary alcohols to carboxylic acids via aldehydes and aldehyde hydratesReagents useful for the transformation of primary alcohols to aldehydes are normally also suitable for the oxidation of secondary alcohols to ketones. These include Collins reagent and Dess-Martin periodinane. The direct oxidation of primary alcohols to carboxylic acids can be carried out using potassium permanganate or the Jones reagent.

    ToxicityMain articles: Short-term effects of alcohol and Long-term effects of alcohol

    Most significant of the possible long-term effects of ethanol. In addition, in pregnant women, it causes fetal alcohol syndrome.Ethanol in alcoholic beverages has been consumed by humans since prehistoric times for a variety of hygienic, dietary, medicinal, religious, and recreational reasons. The consumption of large doses of ethanol causes drunkenness (intoxication), which may lead to a hangover as its effects wear off. Depending upon the dose and the regularity of its consumption, ethanol can cause acute respiratory failure or death. Because ethanol impairs judgment in humans, it can be a catalyst for reckless or irresponsible behavior. The LD50 of ethanol in rats is 10.3 g/kg.[8]

    Ethanol’s toxicity is largely caused by its primary metabolite; acetaldehyde[9] and secondary metabolite; acetic acid.[10][11][12][13] All primary alcohols are broken down into aldehydes then to carboxylic acids, and whose toxicities are similar to acetaldehyde and acetic acid.

    Some secondary and tertiary alcohols are less poisonous than ethanol because the liver is unable to metabolise them into these toxic by-products. This makes them more suitable for recreational[14][15] and medicinal[16] use as the chronic harms are lower. Ethchlorvynol is a good example of a tertiary alcohol which saw both medicinal and recreational use.

    Other alcohols are substantially more poisonous than ethanol, partly because they take much longer to be metabolized and partly because their metabolism produces substances that are even more toxic. Methanol (wood alcohol), for instance, is oxidized to formaldehyde and then to the poisonous formic acid in the liver by alcohol dehydrogenase and formaldehyde dehydrogenase enzymes, respectively; accumulation of formic acid can lead to blindness or death.[17] Likewise, poisoning due to other alcohols such as ethylene glycol or diethylene glycol are due to their metabolites, which are also produced by alcohol dehydrogenase.[18][19] An effective treatment to prevent toxicity after methanol or ethylene glycol ingestion is to administer ethanol. Alcohol dehydrogenase has a higher affinity for ethanol, thus preventing methanol from binding and acting as a substrate. Any remaining methanol will then have time to be excreted through the kidneys.[17][20][21]

    Methanol itself, while poisonous, has a much weaker sedative effect than ethanol. Some longer-chain alcohols such as n-propanol, isopropanol, n-butanol and t-butanol do, however, have stronger sedative effects, but also have higher toxicity than ethanol.[22][23] These longer chain alcohols are found as contaminants in some alcoholic beverages and are known as fusel alcohols,[24][25] and are reputed to cause severe hangovers although it is unclear if the fusel alcohols are actually responsible.[26] Many longer chain alcohols are used in industry as solvents and are occasionally abused by alcoholics,[27][28] leading to a range of adverse health effects.[29]

  12. ToxicityMain articles: Short-term effects of alcohol and Long-term effects of alcohol

    Most significant of the possible long-term effects of ethanol. In addition, in pregnant women, it causes fetal alcohol syndrome.Ethanol in alcoholic beverages has been consumed by humans since prehistoric times for a variety of hygienic, dietary, medicinal, religious, and recreational reasons. The consumption of large doses of ethanol causes drunkenness (intoxication), which may lead to a hangover as its effects wear off. Depending upon the dose and the regularity of its consumption, ethanol can cause acute respiratory failure or death. Because ethanol impairs judgment in humans, it can be a catalyst for reckless or irresponsible behavior. The LD50 of ethanol in rats is 10.3 g/kg.[8]

    Ethanol’s toxicity is largely caused by its primary metabolite; acetaldehyde[9] and secondary metabolite; acetic acid.[10][11][12][13] All primary alcohols are broken down into aldehydes then to carboxylic acids, and whose toxicities are similar to acetaldehyde and acetic acid.

    Some secondary and tertiary alcohols are less poisonous than ethanol because the liver is unable to metabolise them into these toxic by-products. This makes them more suitable for recreational[14][15] and medicinal[16] use as the chronic harms are lower. Ethchlorvynol is a good example of a tertiary alcohol which saw both medicinal and recreational use.

    Other alcohols are substantially more poisonous than ethanol, partly because they take much longer to be metabolized and partly because their metabolism produces substances that are even more toxic. Methanol (wood alcohol), for instance, is oxidized to formaldehyde and then to the poisonous formic acid in the liver by alcohol dehydrogenase and formaldehyde dehydrogenase enzymes, respectively; accumulation of formic acid can lead to blindness or death.[17] Likewise, poisoning due to other alcohols such as ethylene glycol or diethylene glycol are due to their metabolites, which are also produced by alcohol dehydrogenase.[18][19] An effective treatment to prevent toxicity after methanol or ethylene glycol ingestion is to administer ethanol. Alcohol dehydrogenase has a higher affinity for ethanol, thus preventing methanol from binding and acting as a substrate. Any remaining methanol will then have time to be excreted through the kidneys.[17][20][21]

    Methanol itself, while poisonous, has a much weaker sedative effect than ethanol. Some longer-chain alcohols such as n-propanol, isopropanol, n-butanol and t-butanol do, however, have stronger sedative effects, but also have higher toxicity than ethanol.[22][23] These longer chain alcohols are found as contaminants in some alcoholic beverages and are known as fusel alcohols,[24][25] and are reputed to cause severe hangovers although it is unclear if the fusel alcohols are actually responsible.[26] Many longer chain alcohols are used in industry as solvents and are occasionally abused by alcoholics,[27][28] leading to a range of adverse health effects.[29]

  13. Metastasis, or metastatic disease (sometimes abbreviated mets), is the spread of a disease from one organ or part to another non-adjacent organ or part.[1][2] It was previously thought that only malignant tumor cells and infections have the capacity to metastasize; however, this is being reconsidered due to new research.[3] The word metastasis means “displacement” in Greek, from ????, meta, “next”, and ??????, stasis, “placement”. The plural is metastases.

    Cancer occurs after a single cell in a tissue is progressively genetically damaged to produce a cancer stem cell possessing a malignant phenotype. These cancer stem cells are able to undergo uncontrolled abnormal mitosis, which serves to increase the total number of cancer cells at that location. When the area of cancer cells at the originating site becomes clinically detectable, it is called a primary tumor. Some cancer cells also acquire the ability to penetrate and infiltrate surrounding normal tissues in the local area, forming a new tumor. The newly formed “daughter” tumor in the adjacent site within the tissue is called a local metastasis.

    Some cancer cells acquire the ability to penetrate the walls of lymphatic and/or blood vessels, after which they are able to circulate through the bloodstream (circulating tumor cells) to other sites and tissues in the body. This process is known (respectively) as lymphatic or hematogeneous spread.

    After the tumor cells come to rest at another site, they re-penetrate through the vessel or walls, continue to multiply, and eventually another clinically detectable tumor is formed. This new tumor is known as a metastatic (or secondary) tumor. Metastasis is one of three hallmarks of malignancy (contrast benign tumors).[4] Most tumors and other neoplasms can metastasize, although in varying degrees (e.g. basal cell carcinoma) rarely metastasize.[4]

    When tumor cells metastasize, the new tumor is called a secondary or metastatic tumor, and its cells are like those in the original tumor. This means, for example, that, if breast cancer metastasizes to the lungs, the secondary tumor is made up of abnormal breast cells, not of abnormal lung cells. The tumor in the lung is then called metastatic breast cancer, not lung cancer.

  14. Treatment and survival is determined by whether or not a cancer is local or has spread to other locations. If the cancer spreads to other tissues and organs, it may decrease a patient’s likelihood of survival. However, there are some cancers (i.e., some forms of leukemia, a cancer of the blood) that can kill without spreading at all.

    When cancer has metastasized, it may be treated with radiosurgery, chemotherapy, radiation therapy, biological therapy, hormone therapy, surgery or a combination of these. The choice of treatment generally depends on the type of primary cancer, the size and location of the metastasis, the patient’s age and general health, and the types of treatments used previously. In patients diagnosed with CUP, it is still possible to treat the disease even when the primary tumor cannot be located.

    The treatment options currently available are rarely able to cure metastatic cancer, though some tumors, such as testicular cancer and thyroid cancer, are usually still curable.

  15. Apoptosis ( /?æp??to?s?s/)[1][2] is the process of programmed cell death (PCD) that may occur in multicellular organisms.[3] Biochemical events lead to characteristic cell changes (morphology) and death. These changes include blebbing, cell shrinkage, nuclear fragmentation, chromatin condensation, and chromosomal DNA fragmentation. (See also apoptotic DNA fragmentation.) Unlike necrosis, apoptosis produces cell fragments called apoptotic bodies that phagocytic cells are able to engulf and quickly remove before the contents of the cell can spill out onto surrounding cells and cause damage.[4]

    In contrast to necrosis, which is a form of traumatic cell death that results from acute cellular injury, apoptosis, in general, confers advantages during an organism’s life cycle. For example, the differentiation of fingers and toes in a developing human embryo occurs because cells between the fingers apoptose; the result is that the digits are separate. Between 50 and 70 billion cells die each day due to apoptosis in the average human adult. For an average child between the ages of 8 and 14, approximately 20 billion to 30 billion cells die a day.[5]

    Research in and around apoptosis has increased substantially since the early 1990s. In addition to its importance as a biological phenomenon, defective apoptotic processes have been implicated in an extensive variety of diseases. Excessive apoptosis causes atrophy, whereas an insufficient amount results in uncontrolled cell proliferation, such as cancer.

  16. Atrophy
    Classification and external resources

    Mice with spinal muscular atrophy
    MeSH D001284

    Atrophy is the partial or complete wasting away of a part of the body. Causes of atrophy include mutations (which can destroy the gene to build up the organ), poor nourishment, poor circulation, loss of hormonal support, loss of nerve supply to the target organ, excessive amount of apoptosis of cells, and disuse or lack of exercise or disease intrinsic to the tissue itself. Hormonal and nerve inputs that maintain an organ or body part are referred to as trophic [noun] in medical practice (‘trophic” is an adjective that can be paired with various nouns). Trophic describes the trophic condition of tissue. A diminished muscular trophic is designated as atrophy.

    Atrophy is the general physiological process of reabsorption and breakdown of tissues, involving apoptosis on a cellular level. When it occurs as a result of disease or loss of trophic support due to other disease, it is termed pathological atrophy, although it can be a part of normal body development and homeostasis as well.

  17. Homeostasis (from Greek: ??????, hómoios, “similar”[1], and ??????, stásis, “standing still”[2]) is the property of a system that regulates its internal environment and tends to maintain a stable, constant condition of properties like temperature or pH. It can be either an open or closed system.

  18. Positive feedback
    Positive feedback is a mechanism by which an output is enhanced, such as protein levels. However, in order to avoid any fluctuation in the protein level, the mechanism is inhibited stochastically (I), therefore when the concentration of the activated protein (A) is past the threshold ([I]), the loop mechanism is activated and the concentration of A increases exponentially if d[A]=k [A]Positive feedback mechanisms are designed to accelerate or enhance the output created by a stimulus that has already been activated.

    Unlike negative feedback mechanisms that initiate to maintain or regulate physiological functions within a set and narrow range, the positive feedback mechanisms are designed to push levels out of normal ranges. To achieve this purpose, a series of events initiates a cascading process that builds to increase the effect of the stimulus. This process can be beneficial but is rarely used by the body due to risks of the acceleration’s becoming uncontrollable.

    One positive feedback example event in the body is blood platelet accumulation, which, in turn, causes blood clotting in response to a break or tear in the lining of blood vessels. Another example is the release of oxytocin to intensify the contractions that take place during childbirth.[10]

    [edit] Negative feedbackNegative feedback mechanisms consist of reducing the output or activity of any organ or system back to its normal range of functioning. A good example of this is regulating blood pressure. Blood vessels can sense resistance of blood flow against the walls when blood pressure increases. The blood vessels act as the receptors and they relay this message to the brain. The brain then sends a message to the heart and blood vessels, both of which are the effectors. The heart rate would decrease as the blood vessels increase in diameter (known as vasodilation). This change would cause the blood pressure to fall back to its normal range. The opposite would happen when blood pressure decreases, and would cause vasoconstriction.

    Another important example is seen when the body is deprived of food. The body would then reset the metabolic set point to a lower than normal value. This would allow the body to continue to function, at a slower rate, even though the body is starving. Therefore, people who deprive themselves of food while trying to lose weight would find it easy to shed weight initially and much harder to lose more after. This is due to the body readjusting itself to a lower metabolic set point to allow the body to survive with its low supply of energy. Exercise can change this effect by increasing the metabolic demand.

    Another good example of negative feedback mechanism is temperature control. The hypothalamus, which monitors the body temperature, is capable of determining even the slightest variation of normal body temperature (37 degrees Celsius). Response to such variation could be stimulation of glands that produce sweat to reduce the temperature or signaling various muscles to shiver to increase body temperature.

    Both feedbacks are equally important for the healthy functioning of one’s body. Complications can arise if any of the two feedbacks are affected or altered in any way.

    [edit] Homeostatic imbalanceMany diseases are a result of disturbance of homeostasis, a condition known as homeostatic imbalance. As it ages, every organism will lose efficiency in its control systems. The inefficiencies gradually result in an unstable internal environment that increases the risk for illness. In addition, homeostatic imbalance is also responsible for the physical changes associated with aging. Even more serious than illness and other characteristics of aging is death. Heart failure has been seen where nominal negative feedback mechanisms become overwhelmed, and destructive positive feedback mechanisms then take over.[10]

    Diseases that result from a homeostatic imbalance include diabetes, dehydration, hypoglycemia, hyperglycemia, gout, and any disease caused by a toxin present in the bloodstream. All of these conditions result from the presence of an increased amount of a particular substance. In ideal circumstances, homeostatic control mechanisms should prevent this imbalance from occurring, but, in some people, the mechanisms do not work efficiently enough or the quantity of the substance exceeds the levels at which it can be managed. In these cases, medical intervention is necessary to restore the balance, or permanent damage to the organs may result.

    According to the following quote, every illness has aspects to it that are a result of lost homeostasis:

    “Just as we live in a constantly changing world, so do the cells and tissues survive in a constantly changing microenvironment. The ‘normal’ or ‘physiologic’ state then is achieved by adaptive responses to the ebb and flow of various stimuli permitting the cells and tissues to adapt and to live in harmony within their microenvironment. Thus, homeostasis is preserved. It is only when the stimuli become more severe, or the response of the organism breaks down, that disease results – a generalization as true for the whole organism as it is for the individual cell.” (Pathologic Basis of Disease, third edition, S.L. Robbins MD, R.S. Cotran MD, V.K. Kumar MD. 1984, W.P. Saunders Company)

  19. You may hear people ask, “If it’s dangerous, why do so many people have medical marijuana cards?”40 It’s true that scientists have determined that the cannabis plant has the potential for addressing a range of medical conditions. But it’s also true that when you’re young and your body is still growing, marijuana actually has the potential of inflicting a long-lasting, negative impact on your developing brain.

    Using marijuana at a young age can result in structural and functional deficits of the brain. This could cause you to develop weakened verbal and communication skills, lowered learning capabilities and a shortened attention span.40

    wonder why NIDA????

  20. LONG-TERM EFFECTS
    In addition to the possible effects on your brain, smoking marijuana may also be hazardous to your developing lungs. Marijuana smoke contains 50% to 70% more carcinogenic hydrocarbons than tobacco smoke.41

    You may have heard people argue that marijuana is a “gateway drug” to harder drug use. Some say this is a myth, others insist it is a fact. The truth is that there is a link. Research shows that the earlier you start using marijuana, the more likely you are to become dependent on it or other types of drugs later in life.42

    THE BOTTOM LINE
    Some movies and music make “stoner” culture seem cool, natural and like it’s not a big deal. But if being fit and getting good grades are some of your goals, using marijuana can become a big deal, fast. Marijuana limits your brain’s effectiveness, slows your thinking and impairs your coordination. A number of studies have also shown an association between chronic marijuana use and increased rates of anxiety, depression and schizophrenia. 41

    Is there a causal link NIDA?

  21. The menonites have a very primitive culture. They dont even believe in using the internet…is it a bad thing? exposure to anything can be pretty bad… The essence of the belief is to figure that out for yourself

  22. What did the NASA paper do? Scientists started out the project with extremophile bacteria from Mono Lake in California. This is not a pleasant place for most living creatures: it’s an alkali lake with a pH of close to 10, and it also has high concentrations of arsenic (high being about 200 µM) dissolved in it. The bacteria living there were already adapted to tolerate the presence of arsenic, and the mechanism of that would be really interesting to know…but this work didn’t address that.

    Next, what they did was culture the bacteria in the lab, and artificially jacked up the arsenic concentration, replacing all the phosphate (PO43-) with arsenate (AsO43-). The cells weren’t happy, growing at a much slower rate on arsenate than phosphate, but they still lived and they still grew. These are tough critters.

    They also look different in these conditions. Below, the bacteria in (C) were grown on arsenate with no phosphate, while those in (D) grew on phosphate with no arsenate. The arsenate bacteria are bigger, but thin sections through them reveal that they are actually bloated with large vacuoles. What are they doing building up these fluid-filled spaces inside them? We don’t know, but it may be because some arsenate-containing molecules are less stable in water than their phosphate analogs, so they’re coping by generating internal partitions that exclude water.

  23. HERE ARE THE FEDERAL PENALTIES:

    Any amount (first offense) misdemeanor 1 year $1,000
    Any amount (second offense) misdemeanor 15 days MMS* $2,500
    Any amount (subsequent offense) misdemeanor or felony 90 days MMS* – 3 years $5,000
    *Mandatory minimum sentence.

  24. Less than 50 plants/50 kg (first offense) felony not more than 5 years $250,000
    50-99 plants/50-99 kg (first offense) felony
    not more than 20 years
    $1,000,000
    100-999 plants/100-999 kg (first offense) felony 5 – 40 years $2M-$5M
    1000 plants/1000 kg or more (first offense) felony 10 years – life $4M-$10M
    To a minor felony double penalty double penalty
    Within 1,000 feet of a school, or other specified areas felony double penalty double penalty
    Gift of small amount
    see Possession

  25. we should have a national referendum on the issue of making the penalty of personal possession at the federal level a 150$ fine

  26. DETAIL:

    possession of marijuana is punishable by up to one year in jail and a minimum fine of $1,000 for a first conviction. For a second conviction, the penalties increase to a 15-day mandatory minimum sentence with a maximum of two years in prison and a fine of up to $2,500. Subsequent convictions carry a 90-day mandatory minimum sentence and a maximum of up to three years in prison and a fine of up to $5,000.

    Distribution of a small amount of marijuana, for no remuneration, is treated as possession. Manufacture or distribution of less than 50 plants or 50 kilograms of marijuana is punishable by up to five years in prison and a fine of up to $250,000. For 50-99 plants or 50-99 kilograms the penalty increases not more than 20 years in prison and a fine of up to $1 million if an individual, $5 million if other than an individual for the first offense. Manufacture or distribution of 100-999 plants or 100-999 kilograms carries a penalty of 5 – 40 years in prison and a fine of $2-$5 Million. For 1000 plants or 1000 kilograms or more, the penalty increases to 10 years – life in prison and a fine of $4-$10 Million.

    Distribution of greater than 5 grams of marijuana to a minor under the age of 21 doubles the possible penalties. Distribution within 1,000 feet of a school, playground, public housing or within 100 feet of a youth center, public pool or video arcade also doubles the possible penalties.

    The sale of paraphernalia is punishable by up to three years in prison.

    The sentence of death can be carried out on a defendant who has been found guilty of manufacturing, importing or distributing a controlled substance if the act was committed as part of a continuing criminal enterprise – but only if the defendant is (1) the principal administrator, organizer, or leader of the enterprise or is one of several such principal administrators, organizers, or leaders, and (2) the quantity of the controlled substance is 60,000 kilograms or more of a mixture or substance containing a detectable amount of marijuana, or 60,000 or more marijuana plants, or the if the enterprise received more than $20 million in gross receipts during any 12-month period of its existence.

    Applicable Statute:

  27. If the supreme court upholds 1000 dollar penalties for medical marijuana….i would like to see if pennsylvanians would uphold it

  28. golly we better… we organized the tea party that defeated the British. If tony doesnt believe marijuana is good for you… i guess you cant convince any can you?

  29. maybe i just need a little more alcohol psu… but i just dont get it… Lincoln said prohibition was an evil that should be fought… this man who freed slaves thought we shouldnt interfere with an individual’s right to put whatever they want into their body…I want to say something about addiction… any addiction stimulates dopamine… if an addict is to have anything…why not marijuana??? It seems completely reasonable to allow people to drink. No one should mix marijuana and alcohol though. there would be like a 1,000,000% chance there would be an accident. I don’t see any insurance liabilities there

  30. If i were to write the state referendum for medicinal use of marijuana, i would make the penalty a 150$ fine. Dont take up jail cells with people smoking marijuana… its that simple…if we want blood for smoking pot y dont we tar some people up good RENDELL?

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