Protocols psicològics d’actuació en situacions de crisi en el medi penitenciari

Una de les qüestions que ens preocupen com a psicòlegs i psicòlogues en l'àmbit penitenciari és saber fer front d’una manera vàlida i efectiva a les diverses situacions de crisi o emergència que es produeixen en aquest medi, encara que sigui puntualment, no per això deixen de ser significatives i a vegades traumàtiques, tant per a les persones preses com per al seu context. Tanmateix, som conscients que els professionals que assisteixen les persones o grups en crisi a la presó no són necessàriament psicòlegs, sinó que sovint són els funcionaris de vigilància o els mateixos membres de la direcció del centre els que han d’assumir aquestes funcions. És com a tècnics especialistes en el comportament i la personalitat humana i en la solució dels problemes relacionals que podem col·laborar i assessorar els responsables en la gestió d’aquests conflictes en procediments i estratègies del tractament més efectius a l’hora de negociar i assolir un equilibri adaptatiu entre les diverses parts que conformen els escenaris en crisi. Un dels objectius que ens plantejarem la comunitat de pràctiques en aquest curs 2009 és identificar les diverses situacions de crisi que es poden produir a la presó i elaborar un conjunt de protocols d’actuació psicològica que orientin el professional (el psicòleg inicialment però també d’altres agents del canvi dels comportaments antisocials) sobre quina és la millor manera d’intervenir-hi. No obstant això, es considera que més enllà de l'elaboració de guies o manuals d’intervenció (al cap i a la fi això es pot consultar en la literatura especialitzada sobre aquest tema), es tractava de ser el més pràctics possible i recollir en un tríptic aquella informació pertinent (allò imprescindible que s’ha de saber per actuar de manera efectiva i quins són els errors que cal evitar encara que només sigui per no complicar encara més les coses) que fos fàcil d’utilitzar per part del professional, és a dir, un recordatori esquematitzat però rigorós del pla d’acció que cal seguir per fer front a la crisi. També es pretén que sigui obert a les experiències i coneixements resolutius de qui intervé en aquestes situacions d’emergència i que permeti el feedback amb el grup de la comunitat de pràctiques, qui ho validaria, per tal d’anar incrementat progressivament la validesa i fiabilitat de l'instrument. Aquest curs presentem dos protocols/tríptics d’actuació: 1) notificació de males noticies/acompanyament en el dol; 2) intervenció en el risc de suïcidi o en conductes de autòlisi. La idea és elaborar-ne més en pròximes edicions. A més a més, com a protocol en format audiovisual, es presenta un curtmetratge on es desenvolupa una actuació psicològica per tal de desactivar una conducta violenta/ amenaçant.

Let's (not) talk about sex: The effect of information provision on gender differences in performance under competition

We study how gender differences in performance under competition areaffected by the provision of information regarding rival s gender and/ordifferences in relative ability. In a laboratory experiment, we use two tasks thatdiffer regarding perceptions about which gender outperforms the other. Weobserve women s underperformance only under two conditions: 1) tasks areperceived as favoring men and 2) rivals gender is explicitly mentioned. Thisresult can be explained by stereotype-threat being reinforced when explicitlymentioning gender in tasks in which women already consider they are inferior.Omitting information about gender is a safe alternative to avoid women sunderperformance in competition.

Signaling cross-talk between peroxisome proliferator-activated receptor/retinoid X receptor and estrogen receptor through estrogen response elements.

Peroxisome proliferator-activated receptors (PPARs) and retinoid X receptors (RXRs) are nuclear hormone receptors that are activated by fatty acids and 9-cis-retinoic acid, respectively. PPARs and RXRs form heterodimers that activate transcription by binding to PPAR response elements (PPREs) in the promoter of target genes. The PPREs described thus far consist of a direct tandem repeat of the AGGTCA core element with one intervening nucleotide. We show here that the vitellogenin A2 estrogen response element (ERE) can also function as a PPRE and is bound by a PPAR/RXR heterodimer. Although this heterodimer can bind to several other ERE-related palindromic response elements containing AGGTCA half-sites, only the ERE is able to confer transactivation of test reporter plasmids, when the ERE is placed either close to or at a distance from the transcription initiation site. Examination of natural ERE-containing promoters, including the pS2, very-low-density apolipoprotein II and vitellogenin A2 genes, revealed considerable differences in the binding of PPAR/RXR heterodimers to these EREs. In their natural promoter context, these EREs did not allow transcriptional activation by PPARs/RXRs. Analysis of this lack of stimulation of the vitellogenin A2 promoter demonstrated that PPARs/RXRs bind to the ERE but cannot transactivate due to a nonpermissive promoter structure. As a consequence, PPARs/RXRs inhibit transactivation by the estrogen receptor through competition for ERE binding. This is the first example of signaling cross-talk between PPAR/RXR and estrogen receptor.

Retribution in a cheap-talk experiment

We use a two-person 3-stage game to investigate whether people chooseto punish or reward another player by sacrificing money to increase or decrease the other person's payoff. One player sends a message indicating an intended play, which is either favorable or unfavorable to the other player in the game. After the message, the sender and the receiver play a simultaneous 2x2 game. A deceptive message may be made, in an effort to induce the receiver to make a play favorable to the sender. Our focus is on whether receivers' rates of monetary sacrifice depend on the process and the perceived sender's intention,as is suggested by the literature on deception and proceduralsatisfaction. Models such as Rabin (1993), Sen (1997), and Charnessand Rabin (1999) also permit rates of sacrifice to be sensitive to the sender's perceived intention, while outcome-based models such as Fehr and Schmidt (1999) and Bolton and Ockenfels (1997) predict otherwise. We find that deception substantially increases the punishment rate as a response to an action that is unfavorable to the receiver. We also find that a small but significant percentage of subjects choose to reward a favorable action choice made by the sender.

Counselor motivational interviewing skills and young adult change talk articulation during brief motivational interventions.

The process of eliciting client language toward change (change talk [CT]) is implicated as a causal mechanism in motivational interviewing (MI) and brief motivational interventions (BMI). We investigated the articulation of counselor behaviors and CT during BMI with young men. We coded 149 sessions using the Motivational Interviewing Skill Code and summarized these codes into three counselor categories (MI-consistent [MICO], MI-inconsistent [MIIN], other) and three client categories (CT, counter CT [CCT], follow/neutral [F/N]). We then computed immediate transition frequencies and odds ratios using sequential analysis software. CT was significantly more likely following MICO behaviors, whereas MIIN behaviors only led to CCT and F/N. This strongly supports the use of MI skills to elicit CT during BMI with young men, whose speech also predicted counselor behaviors (particularly CT to MICO and CCT to MIIN). Additional analyses showed that among MICO behaviors, reflective listening may be a particularly powerful technique to elicit CT.

Re-thinking cell cycle regulators: the cross-talk with metabolism.

Analysis of genetically engineered mice deficient in cell cycle regulators, including E2F1, cdk4, and pRB, showed that the major phenotypes are metabolic perturbations. These key cell cycle regulators contribute to lipid synthesis, glucose production, insulin secretion, and glycolytic metabolism. It has been shown that deregulation of these pathways can lead to metabolic perturbations and related metabolic diseases, such as obesity and type II diabetes. The cyclin-cdk-Rb-E2F1 pathway regulates adipogenesis in addition to its well-described roles in cell cycle regulation and cancer. It was also shown that E2F1 directly participates in the regulation of pancreatic growth and function. Similarly, cyclin D3, cdk4, and cdk9 are also adipogenic factors with strong effects on whole organism metabolism. These examples support the emerging notion that cell cycle regulatory proteins also modulate metabolic processes. These cell cycle regulators are activated by insulin and glucose, even in non-proliferating cells. Most importantly, these cell cycle regulators trigger the adaptive metabolic switch that normal and cancer cells require in order to proliferate. These changes include increased lipid synthesis, decreased oxidative metabolism, and increased glycolytic metabolism. In summary, these factors are essential regulators of anabolic biosynthetic processes, blocking at the same time oxidative and catabolic pathways, which is reminiscent of cancer cell metabolism.

The therapeutic potential of immune cross-talk in leishmaniasis.

Veterans of infection, Leishmania parasites have been plaguing mammals for centuries, causing a morbidity toll second only to that of malaria as the most devastating protozoan parasitic disease in the world. Cutaneous leishmaniasis (CL) is, by far, the most prevalent form of the disease, with symptoms ranging from a single self-healing lesion to chronic metastatic leishmaniasis (ML). In an increasingly immunocompromised population, complicated CL is becoming a more likely outcome, characterized by severely inflamed, destructive lesions that are often refractory to current treatment. This is perhaps because our ageing arsenal of variably effective antileishmanial drugs may be directly or indirectly immunomodulatory and may thus have variable effects in each type and stage of CL. Indeed, widely differing immune biases are created by the various species of Leishmania, and these immunological watersheds are further shifted by extrinsic disturbances in immune homeostasis. For example, we recently showed that a naturally occurring RNA virus (Leishmania RNA virus (LRV)) within some Leishmania parasites creates hyperinflammatory cross-talk, which can predispose to ML: a case of immunological misfire that may require a different approach to immunotherapy, whereby treatments are tailored to underlying immune biases. Understanding the intersecting immune pathways of leishmaniasis and its co-infections will enable us to identify new drug targets, and thereby design therapeutic strategies that work by untangling the immunological cross-wires of pathogenic cross-talk.

c-Jun N-terminal kinase binding domain-dependent phosphorylation of mitogen-activated protein kinase kinase 4 and mitogen-activated protein kinase kinase 7 and balancing cross-talk between c-Jun N-terminal kinase and extracellular signal-regulated kinase pathways in cortical neurons

The c-Jun N-terminal kinase (JNK) is a mitogen-activated protein kinase (MAPK) activated by stress-signals and involved in many different diseases. Previous results proved the powerful effect of the cell permeable peptide inhibitor d-JNKI1 (d-retro-inverso form of c-Jun N-terminal kinase-inhibitor) against neuronal death in CNS diseases, but the precise features of this neuroprotection remain unclear. We here performed cell-free and in vitro experiments for a deeper characterization of d-JNKI1 features in physiological conditions. This peptide works by preventing JNK interaction with its c-Jun N-terminal kinase-binding domain (JBD) dependent targets. We here focused on the two JNK upstream MAPKKs, mitogen-activated protein kinase kinase 4 (MKK4) and mitogen-activated protein kinase kinase 7 (MKK7), because they contain a JBD homology domain. We proved that d-JNKI1 prevents MKK4 and MKK7 activity in cell-free and in vitro experiments: these MAPKK could be considered not only activators but also substrates of JNK. This means that d-JNKI1 can interrupt downstream but also upstream events along the JNK cascade, highlighting a new remarkable feature of this peptide. We also showed the lack of any direct effect of the peptide on p38, MEK1, and extracellular signal-regulated kinase (ERK) in cell free, while in rat primary cortical neurons JNK inhibition activates the MEK1-ERK-Ets1/c-Fos cascade. JNK inhibition induces a compensatory effect and leads to ERK activation via MEK1, resulting in an activation of the survival pathway-(MEK1/ERK) as a consequence of the death pathway-(JNK) inhibition. This study should hold as an important step to clarify the strong neuroprotective effect of d-JNKI1.