Comparison of the performance of rapid HIV tests using samples collected for surveillance in Mozambique

Mozambique had low HIV prevalence until the mid‐1990s, but recent data indicate increasing rates. There is little information on HIV‐2. Therefore, HIV seroprevalence was assessed among pregnant women and field‐ready HIV diagnostic strategies were evaluated. A total of 6,930 samples collected by three health centers from 2002 to 2005 were tested on site by nurses with two simple/rapid tests, Determine HIV‐1/2 (Abbott Laboratories; screening) and Uni‐Gold HIV (Trinity Biotech; confirmation), which is the national HIV testing strategy. The prevalence of HIV was 14.0% (2002), 17.8% (2003), 16.5% (2004), and 20.2% (2005). A subset of 888 samples collected 2003 was sent to the Central Microbiology Laboratory, Maputo for evaluation of tests and testing strategies. The assays included for comparison were Capillus HIV‐1/HIV‐2 (Trinity Biotech), DoubleCheckGold HIV‐1&2 (Orgenics) and Enzygnost Anti‐HIV‐1/2 Plus (Behringwerke, reference ELISA). Confirmation of reactive samples was done by Uni‐Gold HIV and ImmunoComb II HIV‐1&2 BiSpot (for HIV type differentiation). The Capillus HIV‐1/ HIV‐2 + ImmunoComb II HIV‐1&2 BiSpot combination was the gold standard. The sensitivity of the rapid/simple screening assays (Determine HIV‐1/2, DoubleCheckGold HIV‐1&2) was 100% (N = 160) and their (initial) specificities were 99.6% and 99.7%, respectively. Repeated testing and combinations of assays increased the specificity. Four suspected cases of recent seroconversion were found. Together with the increasing prevalence rates, this may indicate that Mozambique is a high‐incidence area, although further studies are needed to confirm this. Testing strategies for on‐site screening and confirmation based on the combination of Determine HIV‐1/2, Uni‐Gold HIV and DoubleCheckGold HIV‐1&2 are well suited for local field use. J. Med. Virol. 81:1991–1998, 2009. © 2009 Wiley‐Liss, Inc.     

Elevated serotonin is involved in hyperactivity but not in the paradoxical effect of amphetamine in mice neonatally lesioned with 6-hydroxydopamine

The neonatal lesion with 6-hydroxydopamine (6-OHDA) in rodents induces juvenile hyperactivity and paradoxical hypolocomotor response to psychostimulants, in striking contrast to what is observed when similar lesions are carried out in adults. The early disruption of central dopaminergic pathways is followed by increased striatal serotonin (5-HT) contents although the functional role of this neurodevelopmental adaptation remains unclear. The aim of the present study is to investigate the participation of this neurochemical imbalance in the main behavioral phenotypes of this model. To this end, mice received a neonatal administration of 6-OHDA that induced an 80% striatal dopamine depletion together with 70% increase in 5-HT. Serotoninergic hyperinnervation was evidenced further by increased [(3)H] citalopram autoradiographic binding and 5-HT transporter immunohistochemistry in striatal sections. To investigate whether elevated 5-HT was implicated in hyperactivity, we treated control and 6-OHDA neonatally lesioned mice with the selective irreversible tryptophan hydroxylase inhibitor p-chlorophenylalanine (PCPA) to induce 5-HT depletion. Normalization of striatal 5-HT in 6-OHDA neonatally lesioned mice to control levels reversed hyperactivity to normal locomotor scores, whereas the same extent of 5-HT depletion did not affect spontaneous locomotor activity of control mice. In turn, the paradoxical response to amphetamine in neonatal DA-depleted mice was not prevented by PCPA treatment. Taken together, our results suggest that the increased striatal 5-HT that follows neonatal DA depletion is involved in hyperlocomotor behavior but not in the paradoxical calming response to amphetamine observed in this mouse model.     

Expression of a catalytically inactive transmembrane protein tyrosine phosphatase epsilon (tm-PTP epsilon) delays optic nerve myelination

Reversible tyrosine phosphorylation is integral to the process of oligodendrocyte differentiation. To interfere with the subset of the phosphorylation cycle overseen by protein tyrosine phosphatase epsilon (PTP epsilon) in oligodendrocytes, we applied a substrate-trapping approach in the development of transgenic mice overexpressing a catalytically inactive, transmembrane PTP epsilon-hemaglutinin (tm-PTP epsilon-HA) from the dual promoter element of the gene encoding the myelin protein 2',3'-cyclic nucleotide 3'-phosphodiesterase (CNP). Transgene expression peaked during the active myelinating period, at 2-3 weeks postnatal. Two tyrosine phosphoproteins, alpha-enolase and beta-actin, were phosphorylated to a greater degree in transgenic mice. Despite a high degree of tm-PTP epsilon-HA expression, myelin was grossly normal in nearly all axonal tracts. Phenotypic abnormalities were limited to optic nerve, where a decrease in the degree of myelination was reflected by reduced levels of myelin proteins on postnatal day 21 (PND21), as well as a decrease in the density of differentiated oligodendrocytes. The optic chiasm was reduced in thickness in transgenic mice; optic nerves similarly exhibited a reduction in transverse width. Further analyses of the optic pathway demonstrated that transgenic protein was unexpectedly present in retinal ganglion cells, whose axons are the targets of myelination by optic nerve oligodendrocytes. On PND28, transgenic protein declined dramatically in both oligodendrocytes and retinal ganglion cells contributing to the recovery of optic nerve myelination. Thus, delayed myelination arises only when tm-PTP epsilon-HA is simultaneously expressed in myelin-forming glia and their neuronal targets. While tm-PTP epsilon related signaling pathways may figure in axon-glial interactions, interfering with tm-PTP epsilon activity does not perceptibly affect the development or myelinating capacity of most oligodendrocytes.     

Motor neuron disease and optic neuropathy after acute exposure to a methanol-containing solvent mixture.

A 34-years-old floor-layer developed optic neuropathy and motor neuron disease after being accidentally exposed to a solvent mixture containing methanol and other substances. Optic neuropathy is a complication of methanol poisoning, but the onset of a motor neuron disorder resembling amyotrophic lateral sclerosis after the exposure to these substances has not been previously described. The temporal onset of the clinical symptoms, biological plausibility, young age of the patient and absence of neurological disorders in the family history raises suspicion of a possible causative relationship.     

The Relationship Between Temperament and Impulsive Behaviors in Eating Disordered Subjects

To date, few studies have examined the personality characteristics and clinical predictors of impulsive behaviors in eating disorders (ED). The aim of this work was to study the prevalence of a wide range of impulsive behaviors in a sample of 554 ED subjects and to examine the predictors of these behaviors. Subjects were diagnosed according to DSM-IV criteria as having anorexia nervosa restricting type (ANR; n = 183), anorexia nervosa binge eating/purging type (ANBP; n = 65), bulimia nervosa purging type (BNP; n = 244), and bulimia nervosa nonpurging type (BNNP; n = 62). Nine different types of impulsive behaviors were assessed in these groups. About 55% of the whole sample reported at least one type of impulsive behavior, 35% more than one, and about 13% more than three. According to findings, impulsive and multi-impulsive subjects are characterized by the presence of purging behavior and by specific temperamental features such as high levels of novelty seeking and low persistence. The prediction of impulsive behavior is further improved by considering the presence of a history of childhood abuse, maternal psychiatric morbidity, and some specific psychological symptoms such as maturity fears, perfectionism, depression, and obsessive-compulsive symptoms. The presence of impulsive behavior appears to be associated with overall higher levels of psychiatric symptomatology and eating psychopathology, thus indicating that they are an important feature to be considered in the assessment and treatment of ED.     

Risk factors for hypochondriacal concerns in a sample of military veterans

OBJECTIVE: The aim was to examine the influence of combat exposure and other risk factors on the development of hypochondriacal concerns among veterans of the Gulf War and to learn whether these concerns might be a source of increased symptom reporting among them. METHOD: Six hundred two veterans who were deployed to the Gulf or elsewhere during the 1991 war took part in a two-phase study of symptoms and illnesses occurring among these veterans. Hypochondriacal beliefs and attitudes were assessed by the Whiteley Index and somatic symptoms by a factor-analytically derived measure. Multiple regression models were developed for these outcomes. RESULTS: Hypochondriacal concerns were significantly associated with level of education, personal history of depression, number of prewar physical conditions, family history of functional syndromes, negative and positive temperament and disinhibition, military combat, level of military preparedness, social support, and perceived life stress. Somatic symptoms were associated with these same variables, as well as branch of service, family history of physical conditions, combat, and level of combat exposure. A regression model for hypochondriacal concerns included the number of prewar physical conditions, negative temperament, lack of social support, and perceived life stress. CONCLUSIONS: Hypochondriacal concerns were not strongly related to combat exposure. Consequently, it is not likely that such concerns account for increased symptom reporting among the veterans studied. Hypochondriacal concerns appeared to arise in response to threats posed by physical illness. Vulnerability to such threats appeared to center on the personality dimension of negative temperament. This model may serve as a guide to future investigations.