11 research outputs found

    Human disease on stage

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    Theater, being in most cases a representation of real life, can refer to anyone of its aspects, including disease. Human disease is a specific condition associated with several effects in the behavior of both, the patient and his environment, as well as their interrelationship. Several play writers, even from the ancient years, have tried to present these effects. Furthermore, another topic for the theater can be the way Medicine is practiced, usually with a critical approach. Of course play writers have not in general studied Medicine and so their references to disease may not be always absolutely right, especially if they represent aspects of past time. Furthermore, if we refer to poetic or symbolic drama it may express unrealistic situations only to serve the main idea of the author

    A LETTER FROM THE EDITOR: LETTER

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    Hypocholesterolemia: a blessing or a problem?

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    We are all accustomed to face serum cholesterol as a potential threat for our health and so wish and try to have its levels as low as possible. So, in clinical practice we are rather indifferent or even satisfied when we find very low serum cholesterol levels -what we can call “hypocholesterolemia- in a certain individual. Is this practice right or it should be reevaluated? Since cholesterol is an important component of all cell membranes and its concentrations affect membrane permeability and fluidity it is highly probable that very low levels of it may disturb some cell functions and participate in the pathogenesis of diseases. Let’s start with a definition of the term, although this is not generally accepted. It can be described as a serum total cholesterol level under the fifth percentile of a general population adjusted for sex and age.1 In a less complicated manner it can be defined as less than 115 mg/dl.  In a study of 7,000 healthy blood donors, a percentage of 7,8% were found to meet the criteria for hypocholesterolemia. Hypocholesterolemia may be congenital or acquired. Congenital conditions are either combined with low LDL- (low density lipoprotein) or low HDL- (high density lipoprotein) cholesterol levels

    Artificial Intelligence: Are we creating a new Frankenstein?

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    Mary Shelley (1797-1851) is an English novelist best known for her Gothic novel[1] Frankenstein or The Modern Prometheus, written in 1818. In this novel, Victor Frankenstein, an excellent young scientist specialized in chemistry but also connoisseur of other sciences, develops a genius technique to impart life in a huge humanoid that he constructed using parts of dead human bodies. However, when he sees his creature come into life he abandons it terrified. As the creature wanders without an aim or help, it faces human enmity and that transforms it to a maniac for vengeance, extremely directed against its creator. It does not hesitate to murder the persons who are most precious to Victor, including his younger brother and even his bride at the night of their wedding. Victor starts a desperate chase of his creature that leads him to the North Pole, where he dies of exhaustion. The Creature, seeing him dead, mourns for him and, having decided to die too, drifts away on an ice raft and is  soon "lost in darkness and distance", never to be seen again.1 Although the “Creature†remains nameless in the novel, it is usually referred in every-day practice with the name of its creator. That’s why the name “Frankenstein†is often used metaphorically to describe an evil existence that causes death and destruction (fig. 1)

    Sustained serotonin syndrome in a treatment-resistant depressed patient during maintenance treatment with combination of three serotonergic agents

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    Serotonin syndrome (SS) is a relatively rare but potentially life-threatening  condition caused by agents affecting serotonin (5-Hydroxytryptamine; 5-HT) metabolism or acting as direct 5-HT receptor agonists or both.15-HT is a monoamine neurotransmitter synthesized from the amino acid tryptophan. In the central nervous system,it regulates functions such as mood, appetite, sexual activity, sleep and some cognitive functions. Peripherally, 5-HT promotes  platelet  aggregation and also affects peristalsis and vascular tone2,3. A large number of agents, such as antidepressants (monoamine oxidase inhibitors-MAOIs, tricyclic antidepressants-TCAs, selective serotonin reuptake inhibitors-SSRIs, serotonin-norepinephrine reuptake inhibitors-SNRIs, buspirone, St. John’s wort),antibiotics (linezolid), antiemetics (ondansetron) antimigraine medications (sumatriptan), drugs of abuse (amphetamine, cocaine, LSD, ecstasy), herbal supplements and others have been associated with SS1.The vast majority of antidepressants can cause SS either by direct receptor agonism (buspirone), through decreased reuptake of 5-HT(SSRIs, SNRIs, TCAs) or  decreased  5-HT breakdown(MAOIs)1. Lithium is used in combination with other antidepressants and has also been implicated in the development of SS4,5

    Erythrocyte and Liver Porphobilinogen Deaminase in Cirrhosis and Clinical or Experimental Cholestasis

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    BACKGROUND? ? Porphobilinogen deaminase, the third enzyme in the haem synthetic process -mainly expressed in the erythrocytes and liver - has a key role in the pathogenesis of the acute porphyrias.DESIGN AND RESULTS We studied the effect of cirrhosis or cholestasis on this enzyme activity and found that:1. Erythrocyte porphobilinogen deaminase was significantly increased (p=0.0003) in 27 patients with non-alcoholic liver cirrhosis (19.89?±6.65 ??moles/h.l) and 24 patients with extrahepatic cholestasis (20.69?±11.17 ??moles/h.l) as compared to 30 controls (12.77?±4.76 ??moles/h.l). Its activity was positively correlated to the prothrombin time in both patient groups and negatively to the alkaline phosphatase in the cholestasis group.2. Erythrocyte porphobilinogen deaminase of controls significantly increased when their plasma was substituted by that of patients with cholestasis (p lt; 0.001) or cirrhosis (p=0.05), although it remained lower than that of the latter. No change was observed in samples from patients with cirrhosis or cholestasis when their plasma was substituted by that of controls.3. In 8 rabbits, cholestasis produced by ligation of the common bile duct significantly increased porphobilinogen deaminase both in the erythrocytes (from 30.26?±10.33 to 48.87?±15.82 nmoles/h.l, p=0.002) and the liver (from 13.27?±4.79 to 17.68?±5.42 nmoles/h.g, p=0.035). In 8 sham-operated rabbits erythrocyte porphobilinogen deaminase also increased (from 29.60?±9.85 to 33.32?±12.23 nmoles/h.l, p=0.016), but to a significantly lower degree than that of the ???cholestatic?? group (111.10?±10.95 % versus 167.96?±41.64% p=0.006) while the hepatic enzyme remained unchanged (from 13.40?±3.85 to 13.83?±7.21 nmoles/h.g, p=0.80).4. In 5 patients with cholestasis the mean hepatic PBG-D activity was higher than in the 5 controls (12.63?±3.24 versus 9.64?±1.17 nmoles/h.g), although not significantly higher (p=0.11).CONCLUSION PBG-D activity is considerably increased in liver cirrhosis and clinical or experimental cholestasis. It seems probable that plasma factors may play a role in this effect by inducing PBG-D activity
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