Olfaction: a potential cognitive marker of psychiatric disorders

Cognitive deficits are well documented in psychiatric disorders, particularly in schizophrenia and depression. Cognitive activity roots in perceptions. However, research on sensorial alterations in psychiatric conditions has mainly focused on visual or auditory processes and less on olfaction. Here, we examine data on olfactory deficits in psychiatric patients using a systematic review of recent publications. Schizophrenic patients are mainly characterized by no reliable change in odour sensitivity and by a deficit in odour identification, recognition and discrimination. Depressed patients principally exhibit a deficit in the hedonic aspects of this perception, even if, in some case, alterations in sensitivity or identification are also found. Changes in odour perception are also found in dementia and in some neurodegenerative disease, but in this case alterations concern all aspects of the sensorial experience (detection threshold, identification and recognition). Taken together, these data indicate that olfactory abnormalities might be a marker of psychiatric conditions, with a specific pattern for each disease.     

Reply to Comments on Staessen et al. (2004)

Sir, We appreciate the interest of Mastenbroek and colleagues andof Cohen and Munné in our randomized controlled trial(RCT) studying preimplantation genetic screening (PGS). We startedthis randomized study in order to evaluate the difference inoutcome between blastocyst transfer with or without PGS. Mastenbroek et al. raise the issue of using implantation rateper embryo as the main outcome measure. We certainly agree thatongoing pregnancy should be the primary outcome of assistedreproduction technology (ART) trials; however,     

Stereoselective metabolism of (-)-benzo[a]pyrene-7,8-diol by human lung microsomes and peripheral blood lymphocytes: effect of smoking.

Benzo[a]pyrene (B[a]P)-tetrols formed after stereoselective cytochrome P450-dependent metabolism from (-)-trans-7,8-dihydroxy-7,8- dihydrobenzo[a]pyrene [(-)-B[a]P-7, 8-diol] by lung microsomes (n = 19) and peripheral blood lymphocytes (n = 13) from lung cancer patients were measured, and the effect of smoking explored. B[a]P-tetrols were quantified by an HPLC/fluorescence assay with a detection limit of approximately 300 attomol, after incubation with peripheral blood lymphocytes or microsomes from lung cancer patients who were current cigarette smokers, ex-smokers and non-smokers. In lymphocytes from these subjects, high, medium and low metabolic activities respectively for (-)-B[a]P-7,8-diol to tetrol conversion were found, but there was no statistically significant difference between smokers, ex-smokers and non-smokers. When the B[a]P-tetrol formation by human lung microsomes was measured, recent smokers had 4- to 7-fold higher (P = 0.04) metabolic activity than ex-smokers and non-smokers. The mean lung microsomal arylhydrocarbon hydroxylase (AHH) activity was three times higher in smokers than in non-smokers and was undetectable in ex-smokers. AHH activity was correlated with tetrol formation in the same lung microsomal samples (r = 0.62, P less than 0.01 in smokers; and r = 0.67, P less than 0.01 in all subjects). When subjects were grouped according to smoking habits, however, no correlation was detected between mean tetrol formation by lung microsomes and that of lymphocytes. Thus, lymphocytes cannot serve as a surrogate for lung microsomes concerning the pulmonary metabolism of (-)-B[a]P-7,8-diol. The much higher B[a]P-tetrol formation observed in lung microsomes from smokers is in accord with a reported higher pulmonary AHH activity, cytochrome P450IA level, and CYP1A1 gene expression in recent tobacco smokers.     

Oxygen uptake during recovery following naloxone. Relationship with intraoperative heat loss.

The increased metabolic and respiratory demand during naloxone recovery from opioid-based anesthesia could be related to the return of thermoregulation in hypothermic patients and thus be avoided by preventing intraoperative hypothermia. In this study, we measured O2 uptake (VO2) during naloxone-induced recovery in two groups of patients to determine the effect of intraoperative heat loss on postoperative VO2 changes. In seven patients, intraoperative hypothermia was prevented (normothermic group), whereas hypothermia was allowed to develop in seven other patients (hypothermic group). Core and skin temperatures were measured throughout the study to calculate changes in body heat content. Before naloxone antagonism of fentanyl-supplemented anesthesia, core temperature (mean +/- SEM) was 36.8 +/- 0.1 degrees C in the normothermic group and 34.2 +/- 0.2 degrees C in the hypothermic group (P less than 0.001). After titrated administration of naloxone during recovery, VO2 and minute ventilation (VE) increased in the hypothermic group, by 114 +/- 37% and 97 +/- 52% respectively (P less than 0.05), with a three-fold increase in four patients. In the normothermic group, VO2 increased significantly less (25 +/- 5%), without any significant change in VE. The change in VO2 and VE was significantly greater in patients who were hypothermic. VO2 was integrated throughout the recovery period to calculate recovery energy expenditure. Recovery energy expenditure and intraoperative heat loss were highly correlated (r = 0.88; P less than 0.01). This study demonstrates that the metabolic and respiratory stresses associated with naloxone-induced recovery from opioid-based anesthesia depend on the intraoperative heat loss and can therefore be reduced by preventing intraoperative hypothermia.     

Limb body wall complex and amniotic band sequence in sibs

We report on a woman who gave birth consecutively to an infant with limb body wall complex (LBWC) and then to an infant with amniotic band sequence (ABS). This paper reviews the different etiological hypotheses and the classification problems for the amniotic band diseases. No maternal factors were found, but this clinical report suggests further research in this direction, as well as the need to look more closely at the relation between LBWC and ABS.     

The effect of in vitro human immunodeficiency virus infection on dendritic-cell differentiation and function

CD1a+ dendritic cells (DC) differentiate from a major population of nonadherent CD13(hi)lin- cells that appear when human cord blood CD34+ hematopoietic progenitor cells are cultured with stem-cell factor, granulocyte/macrophage (MA) colony-stimulating factor, and tumor necrosis factor-alpha (TNF-alpha) for 5 days. CD13hilin- cells, which also comprise MA and granulocyte precursors, are CD4+ and can thus be targets of human immunodeficiency virus (HIV). Low replication was noted when these day 5 cells were infected with lymphotropic HIV-1LA1 (p24: < or = 4 ng/mL on day 8 postinfection [PI]), while high virus production occurred with MA-tropic HIV-1Ba-L, HIV-1Ada, or HIV-1-m-n. (p24: 50 to > or = 1,000 ng/mL). Strong cytopathicity (CPE) was then observed in nonadherent cells as in adherent MA. However, FACS analysis on day 7 PI showed that HIV did not affect differentiation of DC that survived CPE: apart from CD4 downmodulation related to HIV production, overall expression of CD40, CD80, and CD86 costimulatory molecules, and of HLA-DR, was unchanged relative to controls. At that time, the capacity of DC from HIV-infected cultures to stimulate the mixed leukocyte reaction was only altered less than 10-fold. Immunocytochemistry on day 7 PI showed that most HIV-infected cells were included in syncytia that were stained by anti-CD1a, anti-S100, and anti-CD14 antibodies, indicating that syncytia consisted of DC and cells of the MA lineage. Polymerase chain reaction analysis of FACS- sorted CD1a+ cells confirmed that they harbored then HIV DNA. Viral DNA was also detected in CD1a+ DC from noninfected cultures that had been exposed to HIV only after sorting. Therefore, we examined whether in infected cultures DC precursors were infected at the onset or if virus spread later from other infected cells to differentiated DC. This was answered by showing that, 24 hours postexposure to HIV, viral DNA was preferentially detected in day 5 sorted CD13hilin- versus CD13hilin- cells, and that it was found in the CD1a+ progeny of CD13(hi)lin- cells 48 hours later. In addition, HIV replication did not affect myeloid clonogenic progenitors in day 0 to day 7 PI cultures, although viral DNA was detected in colony-forming unit-granulocyte/macrophage (CFU- GM)/CFU-M colonies derived from day 3 and 7 PI cultures. Thus, precursors of DC and their progeny are susceptible to HIV in vitro, but, apart from CPE, the effect of virus production on DC differentiation or function is limited.