Neurocognitive markers of suicidal ideation in patients with anxiety and mood disorders

Abstract

Objective: This study aims at identifying associations between cognitive function and suicidal ideation in the sample of patients with anxiety and mood disorders (AMD).

Methods: In sum, 186 (age = 39?±?12.3 years; 142 [76.3%] females) patients with AMD were enrolled in the study. Assessment included evaluation of socio-demographic information, medication use, anxiety and depression symptoms. Cognitive tests included measures of psychomotor performance and incidental learning using the Digit Symbol Test. Trail Making Tests respectively measured perceptual speed, task-switching and executive control. Additionally, 21 patients completed tests from the Cambridge Automated Neuropsychological Test Battery measuring set shifting (Interdimensional/extradimensional set-shift), executive planning (Stockings of Cambridge), and decision making (Cambridge Gamble Task [CGT]).

Results: Almost half (45.0%, n?=?86) of the study sample patients had experienced suicidal ideations. In multivariable regression analysis, suicidal ideation was associated with a greater overall proportion of bet and risk taking on the CGT task (β?=?0.726, p?=?.010 and β?=?0.634, p?=?.019), when controlling for socio-demographic characteristics, medication use, anxiety and depression symptoms.

Conclusions: Outpatients with AMD and suicidal ideation could be distinguished by the presence of cognitive deficits in the executive function domain, particularly in impulse-control and risk taking.     

Parental Communication Not to Smoke and Adolescent Cigarette Smokers' Readiness to Quit: Differences by Age

There is limited information on the relationship between parental practices that specifically discourage current cigarette smoking and adolescent cessation, and how this relationship varies by age. Among 1629 adolescent smokers, self-reported receipt of parental communication not to smoke was significantly and positively associated with readiness to quit. The strength and significance of this association decreased from early to middle adolescence and was not significant in late adolescence.     

Causes of B chromosome variant substitution in the grasshopper Eyprepocnemis plorans

We have analysed B chromosome frequency for three consecutive years, B transmission rate at population and individual levels, clutch size, egg fertility and embryo–adult viability in a natural population of the grasshopper Eyprepocnemis plorans containing two different B chromosome variants, i.e. B₂ and B₂₄, the second being derived from the first and having replaced it in nearby populations. From 2002 to 2003 the relative frequency of both variants changed, although the differences did not reach significance. A mother–offspring analysis showed no significant effect of any of the two B variants on clutch size, egg fertility or embryo–adult viability, but B₂₄ was more efficiently transmitted than B₂ through males from the 2002 season, which explains the observed frequency change. Controlled crosses, at individual level, showed significant drive through some females for B₂₄ but not for B₂, suggesting that this difference in transmission rate might also be important for the substitution process. The analysis of relative fitness for B₂ and B₂₄ carriers for all fitness components, as a whole, showed a significantly better performance of B₂₄-carrying individuals, suggesting that the cumulative effect of these slight differences might contribute to the replacement of B₂ by B₂₄. Electronic Supplementary Material Supplementary material is available for this article at .     

Relative weight of glucose, insulin and parathyroid hormone in the urinary loss of phosphate by chronically diabetic rats

This report deals with the relationships between glucose (G) and insulin on the tubular transport of phosphate (P) in chronically diabetic rats with high plasma levels of parathyroid hormone (PTH). Alloxan-induced diabetes leads to phosphorus depletion of the soft tissues. This phenomenon appears associated with weight loss and negative P balances caused by the increased urinary P excretion. Administration of 2 IU of insulin/100 g body weight (bw) to diabetic rats normalized their P balance and body weight. The effect of parathyroid function on the P metabolism of diabetic rats was investigated with balance experiments. Diabetic rats, intact or thyroparathyroidectomized (TPTX), have a greater urinary excretion of P than their controls. However, in control rats, the ratio intact:TPTX for urinary P is 1.0:0.76, showing the antiphosphaturic effect of parathyroid ablation. For diabetic animals, on the other hand, the ratio is 1.0:1.44. The simultaneous deficit of insulin and PTH thus quadruples the urinary P loss, instead of compensating for each other. The contribution of insulin deficit and hyperglycemia to the defect in tubular reabsorption (TRP) was investigated with clearance experiments (done on anesthetized, perfused rats). Five experimental groups were used: Controls (C), diabetics (D), controls+glucose (C+G), diabetics+insulin (D+I) and diabetics+insulin+glucose (D+I+G). All experimental groups showed a linear relationship between the TRP of P and G. The regression equation for C is significantly different (F=40.1, P<0.001) from that of D animals. The slope value measure the number of μmoles of P per μmol of G reabsorbed. For C and D rats, the ratio P:G approximates 1:4 and 1:20, respectively. The increase in P:G ratios represents the competition between both substrates for tubular resorption. Glycemias up to 11 mM (C and D+I) exist concurrent with the P:G ratio 1:4. Glycemias above 25 mM (D, C+G and D+I+G) produce a P:G ratio of 1:20. Fractional excretion of P (FEP) increased significantly in untreated, chronically diabetic rats (0.47± 0.12 vs controls=0.05±0.01, P<0.001). After a single intramuscular injection of insulin, the FEP decreased as a function of insulin levels. To normalize the FEP of diabetic rats in short-term experiments, insulin had to be administered in doses that produce plasma insulin levels 25 times greater than normal. The general information afforded by the present experiments shows that in untreated, chronically diabetic rats, insulin deficit plays an indirect role. The absence of PTH enhances the effect of hyperglycemia. The latter and the concurrent tubular overload of glucose are the cause of hyperphosphaturia in these animals. Received: 10 September 1996 / Accepted in revised form: 18 April 1997     

Towards cellular receptors for prions

Transmissible spongiform encephalopathies (TSE) are attributed to the conversion of the cellular prion protein (PrP(c)) into an abnormal isoform (PrP(sc)). This can be caused by the invasion of living organisms by infectious particles, or be inherited due to mutations on the PrP(c) gene. One of the most intriguing problems of prion biology is the inability to generate the infectious agent in vitro. This argues strongly that other cellular proteins besides those added in test tubes or found in cellular preparations are necessary for infection. Despite recent progress in the understanding of prion pathology, the subcellular compartments in which the interaction and conversion of PrP(c) into PrP(sc) take place are still controversial. PrP(c) interacts with various macromolecules at the cell membrane, in endocytic compartments and in the secretory pathway, all of which may play specific roles in the internalisation of PrP(sc) and conversion of PrP(c). A specific interacting protein required for the propagation of prions was originally proposed as a prion receptor, and later referred to as a ligand, a cofactor, protein X, or a partner. However, current studies indicate that PrP(c) associates with multi-molecular complexes, which mediate a variety of functions in distinct cellular compartments. It is proposed that a deeper understanding of the mechanics of such interactions, coupled to a better knowledge of the corresponding signalling pathways and ensuing cellular responses, will have a major impact on the prevention and treatment of TSE.     

Evidence that non-NMDA receptors are involved in the excitatory pathway from the pedunculopontine region to nigrostriatal dopaminergic neurons

Summary Extracellular single-neuron recordings were obtained from electrophysiologically identified nigrostriatal neurons in chloral hydrate anesthetized rats, in order to test the hypothesis that excitatory amino acid receptors are involved in responses of these neurons to electrical stimulation of the pontine region where the pedunculopontine nucleus (PPN) is located. The effects of iontophoretic application of excitatory amino acids and their antagonists as well as of cholinergic antagonists were tested on the fast orthodromic excitation of nigrostriatal neurons evoked by stimulation of the PPN region. The N-methyl-D-aspartate (NMDA) receptor antagonist D-a-aminoadipic acid as well as the cholinergic receptor antagonists mecamylamine and atropine failed to suppress the synaptic excitation of nigral neurons. The NMDA receptor antagonist DL-2-amino-5-phosphonovalerate exerted a weak depressant action on the synaptic response in a few neurons only. On the contrary, the broad spectrum antagonists of excitatory amino acid receptors kynurenic acid and gamma-Dglutamyl-amino-methyl-sulphonate were found to block simultaneously both the synaptic excitation and the neuronal responses to iontophoretic pulses of glutamate while leaving unaffected the neuronal responses to local application of acetylcholine or carbachol. The competitive antagonist of non-NMDA receptors 6-cyano-2,3-dihy-droxy-7-nitro-quinoxaline suppressed the synaptic excitation at ejection currents which antagonized neuronal responses to quisqualate and kainate. These results suggest that PPN excitatory fibers synapsing onto pars compacta nigrostriatal neurons utilize an excitatory amino acid as a synaptic transmitter acting preferentially on non-NMDA receptors.     

Antigenic and genomic relation between human influenza viruses that circulated in Argentina in the period 1995-1999 and the corresponding vaccine components.

BACKGROUND: The analysis of epidemic influenza virus has been focused on antigenic and genomic characterization of the hemagglutinin (HA) glycoprotein in order to detect new variants for the recommendation of the vaccine strains in each season. Since October 1998, WHO organized a second meeting to evaluate the vaccine formula for the southern hemisphere. OBJECTIVES: (a) Present the antigenic and genomic characterization of influenza strains obtained from the Argentina surveillance network, (b) compare between strains collected in Argentina and other countries with the vaccine formula strains used in each season. STUDY DESIGN: Influenza strains were collected during a 5-year period (1995-1999). Initially, laboratory diagnosis was done by immunofluorescence (IF) assay on clinical samples, followed by viral isolation in Madin-Darby canine kidney (MDCK) cells. The isolates were characterized antigenically by hemagglutination-inhibition (HI) assay with post-infection ferret antisera. The genomic characterization consisted on RT-PCR followed by sequencing of the HA1 portion of the HA gene. The comparison between reference and circulating strains was analyzed by the construction of phylogenetic trees. RESULTS: The H3N2 circulating strains matched the corresponding vaccine component only in 1999, the first year when a vaccine recommended specifically for the southern hemisphere was used. Besides, H1N1 circulating strains matched the corresponding vaccine component only in 1998. Regarding to influenza B, only in 1995, the circulating strains showed no match to the B vaccine component. CONCLUSIONS: The results showed the usefulness of an intensified influenza laboratory surveillance to access the correct vaccine and the importance of having the necessary tools to characterize the circulating strains.