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Kenuvis Romero

Journal of Cerebral Blood Flow & Metabolism - Multiple Microvascular and Astroglial 5-H... - 0 views

  • Physiologic and anatomic evidence suggest that 5-hydroxytryptamine (5-HT) neurons regulate local cerebral blood flow and blood-brain barrier permeability.
  • capillary endothelial cells exhibited mRNA for the h5-HT1D and for the 5-HT7 receptors whereas microvascular smooth muscle cells, in addition to h5-HT1D and 5-HT7, also showed polymerase chain reaction products for h5-HT1B receptors. Expression of 5-HT1F and 5-HT2A receptor mRNAs was never detected in any of the microvascular cell cultures. In contrast, messages for all 5-HT receptors tested were detected in human brain astrocytes with a predominance of the 5-HT2A and 5-HT7 subtypes. In all cultures, sumatriptan inhibited (35–58%, P < .05) the forskolin-stimulated production of cyclic AMP, an effect blocked by the 5-HT1B/1D receptor antagonists GR127935 and GR55562. In contrast, 5-carboxamidotryptamine induced strong increases (≥ 400%, P < .005) in basal cyclic AMP levels that were abolished by mesulergine, a nonselective 5-HT7 receptor antagonist. Only astroglial cells showed a ketanserin-sensitive increase (177%, P < .05) in IP3 formation when exposed to 5-HT. These results show that specific populations of functional 5-HT receptors are differentially distributed within the various cellular compartments of the human cortical microvascular bed, and that human brain astroglial cells are endowed with multiple 5-HT receptors. These findings emphasize the complex interactions between brain serotonergic pathways and non-neuronal cells within the CNS and, further, they raise the possibility that some of these receptors may be activated by antimigraine compounds such as brain penetrant triptan derivatives.
Kenuvis Romero

Psilocybin (magic mushrooms) - 0 views

  • The biosinthetic path that allow Psilocybin to be produced by mushrooms is as follow:
  • The several analogyes with triptophan aminoacid, with whom psilocybin has common origines are probably at the base of psilocybin ability to induced psychedelich alteration on humans.
  • Amino acids, including tryptophan, act as building blocks in protein biosynthesis. In addition, tryptophan functions as a biochemical precursor for many compounds like serotonin Serotonin (a neurotransmitter), synthesized via tryptophan hydroxylase. Serotonin, in turn, can be converted to melatonin (a neurohormone), via N-acetyltransferase and 5-hydroxyindole-O-methyltransferase activities
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  • it's been noticed that psilocyn can indirectly raise dopamine concentration withing the basal ganglia.
  • Almost 50% of oral psilocybin is absorbed by stomach and gut; from here is lead to liver, where it's converted in psilocin, pharmacologically active form, that can furtherly be glucoronated and escreted with urine or converted in other psilocinics metabolites.
  • In rats, the median lethal dose (LD50) when administered orally is 280 milligrams per kilogram (mg/kg), approximately one and a half times that of caffeine. When administered intravenously in rabbits, psilocybin's LD50 is approximately 12.5 mg/kg
  • traces of the compund can be detected in unine even after 7 days.
  • Clinical studies show that psilocin concentrations in the plasma of adults average about 8 µg/liter within 2 hours after ingestion of a single 15 mg oral psilocybin dose; psychological effects occur with a blood plasma concentration of 4–6 µg/liter. Psilocybin is about 100 times less potent than LSD on a weight per weight basis, and the physiological effects last about half as long.
  • Within 24 hours from administration 65% of the alucinogen is escreted by urine, while another 15-20% is excreted by bile and feces.
  • Monoamine oxidase inhibitors (MAOI) have been known to prolong and enhance the effects of psilocybin. Alcohol consumption may enhance the effects of psilocybin, because acetaldehyde, one of the primary breakdown metabolites of consumed alcohol, reacts with biogenic amines present in the body to produce MAOIs related to tetrahydroisoquinoline and β-carboline. Tobacco smokers can also experience more powerful effects with psilocybin, because tobacco smoke exposure decreases levels of MAO in the brain and peripheral organs.
  • This could lead to a lower usage o f glucose, but the same study admitted an increase glucose usage by the whole brain cell, meaning a differente use of this sugar while the drug is having effects.
  • use of MRI (functional magnetic resounance) showed that the decresed blood flow associate with decreasing in neural activity. A simple explanation for this unexpected situation could be the serotoning agonist action of psilocybin, action that seems to be focused more on 5-HT receptors than on 5-HT2A.
  • psilocibyn is able to act as a 5-HT agonist binding directly its receptors.
  • augmented glucose consumption in several brain regions; this lead to the conclusion that psilocybin is some way able to modify the physiological glucosal metabolic rate of our body
  • The strong inibition of the PCC is now thought to be most significant action of psilocybin on neural disaccoppiation
    • Kenuvis Romero
      Lower brain glucose metabolism is linked with increased capacity for working memory.
  • Psilocybin comprises approximately 1% of the weight of Psilocybe cubensis mushrooms, and so nearly 1.7 kilograms (3.7 lb) of dried mushrooms, or 17 kilograms (37 lb) of fresh mushrooms, would be required for a 60-kilogram (130 lb) person to reach the 280 mg/kg LD50 value.
  • psilocybin can cause anxiety and increased heart rate and BP which is very counter- productive for someone on metoprolol and micardis.
  • propose the possibility to use psilocybin as a palliative therapy for terminal illness like cancer but also as a real antidepressive active principle available for the family of the patient. The rational is foundable in the fact that we usually administer SSRI as antidepressive agents, so psilocibyn sholud be useful in this purpose for its selective agonist action on 5-HT2A receptors
Brandie Hayes

What are questions? by Jason Fried of 37signals - 43 views

  • “Questions are places in your mind where answers fit. If you haven’t asked the question, the answer has nowhere to go. It hits your mind and bounces right off. You have to ask the question – you have to want to know – in order to open up the space for the answer to fit.”
  • “Questions are places in your mind where answers fit. If you haven’t asked the question, the answer has nowhere to go. It hits your mind and bounces right off. You have to ask the question – you have to want to know – in order to open up the space for the answer to fit.”
    • Eric Nentrup
      I really like this acknowledgement of the role questions play in our cognitive process. They aren't just the knowledge equivalent of a meal ticket...they're our dinner date!
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  • Questions are your mind’s receptors for answers. If you aren’t curious enough to want to know why, to want to ask questions, then you’re not making the room in your mind for answers. If you stop asking questions, your mind can’t grow.
    Interesting statement about the role of questionging in acquiring new infomation. Your mind has to ask the question in order for your brain to have a place to hold onto the information.....interesting perspective. 
    I frequently say a similar thing when I talk about having students share their questions after a first reading. Their questions are such a great diagnostic of what they are ready to learn! Having students ask and answer their own questions not only gives them the info. they need now, but teaches them to be self-directed learners for a lifetime.
rmollap Rafa - 0 views


(PDF) A Systematic Review of Treatments for Music Performance Anxiety - 2 views

  • Four other studies (three of which are dissertations) assessed behavioral treatments forMPA on music students. Grishman (1989) and Mansberger (1988) used standard musclerelaxation techniques, Wardle (1969) compared insight/relaxation and systematic desensi-tisation techniques, and Deen (1999) used awareness and breathing techniques
  • A systematic review of all available treatment studies for music performance anxiety was undertaken.
  • reported that 24% of musicians frequently suffered stage fright, defined in this study as themost severe form of MPA, 13% experienced acute anxiety and 17% experienceddepression.
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  • 59% of musicians in symphony orchestras reported performance anxiety severe enough toimpair their professional and/or personal functioning.
  • A recent study indicated that MPA is not limited to orchestralmusicians, showing that opera chorus artists are also prone to high levels of performanceanxiety
  • However, since not allperformers suffer the same degree of MPA, or indeed report the same levels of occupationalstress, individual differences in a range of psychological characteristics are likely to accountfor variations in the degree to which musicians experience symptoms
  • A large number of treatment modalities (e.g., behavioral, cognitive, pharmacological andcomplementary) has been developed for music performance anxiety (MPA)
  • However, areview of this literature indicates that the field is still in its infancy with respect to theconceptual and theoretical formulations of the nature of MPA and its empiricalinvestigation.
  • Anxiety may be triggered by conscious,rational concerns or by cues that trigger, unconsciously, earlier anxiety producingexperiences or somatic sensations.
  • These findings suggest that multi-modal interventions are needed toaddress the multiple difficulties experienced by test anxious individuals.
  • with some focusing on behavioral change, some on cognitivechange, others on reduction of physiological symptoms through the use of pharmacotherapy,and some on idiosyncratic formulations
  • For drug studies, the keywords were beta-blocker [Beta blockers block the effect ofadrenaline (the hormone norepinephrine) on the body’s beta receptors. This slows downthe nerve impulses that travel through the heart. As a result, the resting heart rate is lower,the heart does not have to work as hard and requires less blood and oxygen
  • Brodsky (1996) and Nube´(1991) were most useful.
  • The interventionsassessed included systematic desensitization, progressive muscle relaxation, awareness andbreathing and behavioural rehearsal
  • In summary, behavioral treatments do appear to be at least minimally effective in thetreatment of MPA, although the heterogeneity of the treatment approaches employedmakes it difficult to isolate consistent evidence for the superiority of any one type ofbehavioral intervention
  • Two studies (see Tables II and IV) assessed the therapeutic effect of cognitive techniquesalone on MPA.
  • A dissertation by Patston (1996) reported a comparison of cognitive (e.g.positive self-talk, etc.) and physiological strategies in the treatment of MPA. No significantimprovements on vocal and visual manifestations of performance anxiety were found foreither treatment or control groups. However, the sample consisted of only 17 operastudents who were not specifically selected on the basis of their MPA severity, and theintervention was conducted by the author, a singer and teacher, who had no training inpsychology.
  • Three studies (see Table III) assessed the therapeutic effect of cognitive-behavioralstrategies on MPA. Harris (1987), Roland (1993), and Kendrick et al. (1982) all reportedthat standard CBT techniques were effective in the treatment of MPA in studentsspecifically selected for study because of the severity of their MPA.
  • Harris (1987) and Roland(1993) reported that CBT led to reductions in state anxiety as measured by the STAI,although Kendrick et al. (1982) failed to find a significant difference between treatment andcontrol groups on this measure.
  • The evidence for improvements in MPA following CBT is quite consistent, althoughfurther studies with larger samples are needed to confirm this evidence.
  • Beta-blockers have become increasingly popular among performers in recent years. Forexample, Lockwood (1989), in a survey of 2,122 orchestral musicians, found that 27% usedpropranolol to manage their anxiety prior to a performance; 19% of this group used thedrug on a daily basis.
  • Nube´ (1991) identified nine studies examining the effects of various beta-blockers(Atenolol, Metopolol, Nadolol, Oxprenolol, Propranolol, Pindolol) on MPA.
  • The findings regarding the effects of beta blockers on otheroutcome measures were less conclusive.
  • A rigorous definition of MPA is needed to advance treatment. However, defining MPA as asocial anxiety (social phobia) using criteria set out in DSM-IV-TR (APA, 2000) as theinclusion criteria may be too restrictive, particularly if the musician presenting for treatmentexperiences MPA as a focal anxiety (ie does not meet other criteria for social anxiety).
  • Few ofthe intervention studies reviewed acknowledged that performers need a certain amount ofarousal or anxiety to maximise their performance.
  • None of the studies could be pooled in a meta-analysis primarily because too fewprovided sufficient data to calculate effect sizes, use of diverse subject groups andtreatments, duration and intensity of treatment, and use of disparate outcome measures
  • In conclusion, the literature on treatment approaches for MPA is fragmented, incon-sistent, and methodologically weak. These limitations make it difficult to reach any firmconclusions about the effectiveness of the various treatment approaches reviewed. Forsignificant progress to be made, future research will require a clear definition of MPA,consistency and strength in methodology, and the development of robust and appropriateoutcome measures.
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