Adonis Diaries

Archive for December 26th, 2017

Becoming too complicated acting the usual male?

The recurring past, of males taking advantages of new females starting their carrier, has shed a heavy shadow on how to deal with the other gender.

The 7 reasons why Males don’t understand sexual consent.

« C’est devenu compliqué d’être un homme »

« Harvey Weinstein a un peu salopé l’image de ma jeunesse » : notre grand reporter assiste, désemparé, au chavirement du monde dans lequel il a grandi.

M le magazine du Monde |  Par Philippe Ridet

Un père, un grand-père, un compagnon.

Quelques jours après le début de l’affaire Weinstein, mon fils aîné, bientôt 32 ans, m’a adressé, ainsi qu’à son jeune frère, bientôt 15, un lien vers un article de l’écrivain américain David Wong, 43 ans.

Les âges, ici, ont leur importance. J’y ajoute le mien : 62 ans. Le texte, très habile, s’intitule Sept raisons pour lesquelles tant d’hommes ne comprennent pas le consentement sexuel.

L’auteur écrit ceci :

« Longtemps avant que j’aie l’âge de sortir avec des filles ou même que j’aie des amies, les choses ont été rendues très claires : dans toutes les relations, les hommes sont des prédateurs et les femmes sont des proies. Leurs expressions de peur et de rejet sont un jeu de dupes qu’il faut vaincre comme le fermoir difficile d’un soutien-gorge»

Sur la route du festival de jazz-rock Riviera 76, sorte de Woodstock français, au Castellet, dans le Var, en 1976.
Sur la route du festival de jazz-rock Riviera 76, sorte de Woodstock français, au Castellet, dans le Var, en 1976. | BRUNO BARBEY / MAGNUM PHOTOS

David Wong se rappelle tous les films qu’il a vus dans son adolescence où les héros, James Bond ou Han Solo dans La Guerre des étoiles, ne s’embarrassaient pas des rebuffades de leurs conquêtes, les embrassant, jusqu’à ce que consentement s’ensuive, comme si leur refus initial n’était qu’une minauderie.

J’ai vu tous les James Bond, je n’avais rien remarqué. Je me suis senti un peu coupable.

« Blow-Up », caricature de la domination masculine

La même semaine, je lis dans Le Monde le témoignage d’une manifestante anti-Polanski – accusé d’agressions sexuelles sur des mineures – devant la Cinémathèque française qui lui rendait hommage.

Directrice artistique free-lance de 41 ans, elle déclare : « J’avais adoré Le Bal des vampires quand j’étais petite. J’ai montré récemment le film à ma fille de 13 ans, elle a trouvé ça dégoûtant, plein de sous-entendus, les filles n’y sont représentées que comme des amusements et les mecs y sont de gros débiles queutards. (…) Il y a un truc qui s’est passé. Les générations qui viennent sont moins soumises à la séduction, à la domination. On les a éduquées…

How Anti-Depression Drugs Work?

New insights into how selective serotonin re-uptake inhibitors work suggest they reverse inhibited nerve regeneration and connectivity that may underlie depression

Rather than a shortage of serotonin, a lack of synaptogenesis (the growth of new synapses, or nerve contacts) and neurogenesis (the generation and migration of new neurons) could cause depression?

Research shows that people with depression often have lower than normal levels of serotonin.

The types of medications most commonly prescribed to treat depression act by blocking the recycling, or re-uptake, of serotonin by the sending neuron. Image: NIMH

Jeanene Swanson published in Scientific American this Dec. 10, 2013

Unraveling the Mystery of How Antidepression Drugs Work

Depression strikes some 35 million people worldwide, according to the World Health Organization, contributing to lowered quality of life as well as an increased risk of heart disease and suicide.

Treatments typically include psychotherapy, support groups and education as well as psychiatric medications. SSRIs, or selective serotonin reuptake inhibitors, currently are the most commonly prescribed category of antidepressant drugs in the U.S., and have become a household name in treating depression.

The action of these compounds is fairly familiar.

SSRIs increase available levels of serotonin, sometimes referred to as the feel-good neurotransmitter, in our brains. Neurons communicate via neurotransmitters, chemicals which pass from one nerve cell to another. A transporter molecule recycles unused transmitter and carries it back to the pre-synaptic cell.

For serotonin, that shuttle is called SERT (short for “serotonin transporter”). An SSRI binds to SERT and blocks its activity, allowing more serotonin to remain in the spaces between neurons. Yet, exactly how this biochemistry then works against depression remains a scientific mystery.

In fact, SSRIs fail to work for mild cases of depression, suggesting that regulating serotonin might be an indirect treatment only. “There’s really no evidence that depression is a serotonin-deficiency syndrome,” says Alan Gelenberg, a depression and psychiatric researcher at The Pennsylvania State University. “It’s like saying that a headache is an aspirin-deficiency syndrome.”

SSRIs work insofar as they reduce the symptoms of depression, but “they’re pretty nonspecific,” he adds.

Now, research headed up by neuroscientists David Gurwitz and Noam Shomron of Tel Aviv University in Israel supports recent thinking that rather than a shortage of serotonin, a lack of synaptogenesis (the growth of new synapses, or nerve contacts) and neurogenesis (the generation and migration of new neurons) could cause depression.

In this model lower serotonin levels would merely result when cells stopped making new connections among neurons or the brain stopped making new neurons.

So, directly treating the cause of this diminished neuronal activity could prove to be a more effective therapy for depression than simply relying on drugs to increase serotonin levels.

Evidence for this line of thought came when their team found that cells in culture exposed to a 21-day course of the common SSRI paroxetine (Paxil is one of the brand names) expressed significantly more of the gene for an integrin protein called ITGB3 (integrin beta-3).

Integrins are known to play a role in cell adhesion and connectivity and therefore are essential for synaptogenesis.

The scientists think SSRIs might promote synaptogenesis and neurogenesis by turning on genes that make ITGB3 as well as other proteins that are involved in these processes.

A microarray, which can house an entire genome on one laboratory slide, was used to pinpoint the involved genes.

Of the 14 genes that showed increased activity in the paroxetine-treated cells, the gene that expresses ITGB3 showed the greatest increase in activity.

That gene,ITGB3, is also crucial for the activity of SERT. Intriguingly, none of the 14 genes are related to serotonin signaling or metabolism, and, ITGB3 has never before been implicated in depression or an SSRI mode of action.

These results, published October 15 in Translational Psychiatry, suggest that SSRIs do indeed work by blocking SERT. But, the bigger picture lies in the fact that in order to make up for the lull in SERT, more ITGB3 is produced, which goes to work in bolstering synaptogenesis and neurogenesis, the true culprits behind depression.

“There are many studies proposing that anti-depressants act by promoting synaptogenesis and neurogenesis,” Gurwitz says. “Our work takes one big step on the road for validating such suggestions.”


adonis49

adonis49

adonis49

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