À propos du post-partum blues

Since postpartum blues was described by Savage in 1875, the controversy regarding its nature and cause has been sustained. In a first part, the author reviews the conventional clinical assessment of the blues as described in international medical literature. Its constitutive symptoms are mundane, of an affective, emotional, cognitive or psychosomatic nature. On the other hand, their originality resides in the mildness, unusual nature and progressive profile of their expression. Some elements speak in favour of the normality of this phenomenon, such as its mildness and great frequency. But others give indication of a pathological process, notably its links with various entities or illnesses such as the premenstrual syndrome, acute psychoses and postpartum depressive moods. This aspect has moreover led to search for shared causes to these different co-morbidities, such as a constitutional predisposition, somatobiological disorders, a psychosocial condition or psychodynamic mechanisms. This debate, however, is far from being settled. In a second part - and in continuity with a previous work - the author adds three other symptoms to this classical approach: drop in intrinsic weight, decrease of activity and positivity to the dexamethasone test. In order to do so, he defines the notion of “gross prepartal weight” (weight as measured before delivery) and “neat prepartal weight” (resulting from the substraction of the foeto-annexial package from the gross prepartal weight). At the same time, he compares these data with those resulting from a questioning of twenty-one new mothers out of a university hospital ward on obstetrical difficulties, end-of-pregnancy psychic disorders or PMS case history. These analyses establish no specific link between the appearance of blues, the average age of the parturients, the notion of previous blues, lacteal inhibition under bromocryptine. On the other hand, as stated in the literature, the appearance of postpartum blues is closely connected to previous PMS history, a painful delivery, or a psychologically difficult end of pregnancy. The originality of these results consists of two elements: (1) the correlation between the intensity of the blues and the weight gain during pregnancy; (2) a probable increase of neat weight, as the author has defined it, in the first days following postpartum. In a more general way, the role of weight variation stands out distinctly if the weight curves during gestation and the aggravation of psychiatric morbidity are observed in parallel. In the analysis of surgical blues by Illes, the severity of cluster scores of decrease of activity and of vigilance is noted, along with a culmination of the pathology on the second day (and not on the fifth day as in postpartum), which can justifiably be attributed to the suddenness and precocity of weight drop. Also related to the role of weight, numerous quasi-experimental, historical or clinical situations of weight loss and their psychiatric impact can be quoted. On another level, one should consider the decrease of activity in the approached situations. While basic metabolism increases during pregnancy progressively to 20%, delivery occurs through short but intense efforts. Postpartum implies a sudden deceleration in the course of which a physiological bradycardian phase around the fifth day can be underlined, as Magnin well described it. Some authors have positively correlated the blues to the intensity of labour, which corresponds to the degree of deceleration. In the same way, symptoms of sleep apnea syndrome have been linked to its fragmentation and to O₂ desaturation induced intellectual lapses, but an involvment of diurnal fits of sleepiness cannot be rejected. In the same spirit, the activating role, prior to their mood stabilizing effect, of antidepressants is well known and the role of the musculorespiratory peak of the convulsive crisis in sismotherapies can be looked into. Finally, the nearly constant positivity to the dexamethasone suppression test (DST) is a symptom devoid of causal participation. Since Carrol's study, the frequent positivity of this test has been observed in depressed subjects. But there are multiple causes for positivity, starting with immediate postpartum, to such an extent that some authors have considered the test as more characteristic of the postnatal period than of any psychic disorder. However, the frequency of denutrition complications in DST - positive cases (insufficiently controlled diabetics, alcoholics, the aged and postpartum of course) is to be underlined. Numerous Anglo-Saxon authors have moreover put the emphasis on the link between weight loss and DST positivity, although they underlined the limits of this explanation. This is how the variations of activity may constitute an additional etiology. Actually, even if Weitzman has privileged the level of hypnic inhibition in regulating plasma cortisol, the inverted correlation between the latter's variations and those of activity is indeed striking. In this hypothesis, depressed subjects’ curves would diverge mostly in the daytime to the extent of a difference in activity or a lack of activity more distinct than at night. To support this thesis, we will also point out the lower sensitivity of the test in ambulatory care, which may reflect a relative mildness of these cases but also a better activity, the standardization of the test when a depressive phase changes to excitement, the early standardization of the DST before the improvement of the mental state during sismotherapy or sleep deprivation. Weight loss and decrease in activity, which are of a physiological nature, would thus have a causal value, and the DST would only reflect these two elements. In the last part, the author engages in various physiopathological hypotheses and some commentaries. In his physiopathological hypotheses, he takes up Delay's idea of a regulating centre of mood, potentially subjected to variations of weight and activity. He mentions in particular that these variations may compensate each other, as with anorectics, or increase each other, as in postpartum blues. In his commentaries, he expands the previous ideas into his favourite theme, the deep motive for his research, which is the consubstantiality of acting and of being as the cornerstone of the holistic unity of the living, this concept being otherwise developed in an additional work quoted in reference.     

长期饮酒对大鼠睾丸睾酮合成和雄激素结合蛋白mRNA表达的影响

目的探讨饮酒对大鼠睾丸组织睾酮合成和雄激素结合蛋白（ABP）mRNA表达的影响。方法雄性Wistar大鼠40只，按体重随机分为4组，每组10只，即对照组（蒸馏水5g·kg^-1·d^-1）；大剂量饮酒组（酒精量5g·kg^-1·d^-1）；中剂量饮酒组（酒精量2．5g·kg^-1·d^-1）；小剂量饮酒组（酒精量0．5g·kg^-1·d^-1），喂养时间5个月。ELISA测定睾酮含量，RT—PCR测定睾丸组织外周型苯二氮革受体（PBR）、PPARα和ABP mRNA水平。结果与对照组相比，（1）大剂量饮酒组大鼠睾丸组织睾酮含量下降31．13％（P〈0．05），中剂量饮酒组下降26．8％（P〈0．05），小剂量饮酒组下降14．2％（P〉0．05）；（2）各饮酒组PBR mRNA水平明显降低（均P〈0．05），PPARα mRNA水平也明显降低（均P〈0．05）；（3）各饮酒组ABP mRNA水平明显下降（均P〈0．05）。结论长期饮酒可显著降低大鼠睾酮合成，PBR和PPARα表达降低是其可能机制之一；长期饮酒还可抑制大鼠ABP表达，影响睾酮生物学效应的发挥。     

Diplotypes of the human serotonin 1B receptor promoter predict growth hormone responses to sumatriptan in abstinent alcohol-dependent men.

BACKGROUND: Some studies have associated alcohol dependence (AD) with the human serotonin (5-HT)(1B) receptor (HTR1B). This investigation explored the functional responsivity of HTR1B in abstinent AD men using a sumatriptan challenge, while measuring genetic heterogeneity in the HTR1B promoter. METHODS: Abstinent AD men (n = 27) and abstinent men without any alcohol use disorder (n = 19) were administered 6 mg of sumatriptan succinate, subcutaneously. Plasma samples collected over the following 2 hours were assayed for growth hormone (GH) concentrations. His DNA was genotyped for the A-161T and T-261G polymorphisms of the HTR1B promoter and diplotypes determined. RESULTS: Integrated GH responses were predicted by interactions of AD and promoter diplotypes, as well as subject ethnicity. The final model accounted for nearly 35% of the variance in GH responses. Post hoc evaluation revealed that AD was associated with a blunting of GH secretion only among individuals with the most common HTR1B diplotype (TT/TT). CONCLUSIONS: A blunting of GH responses in abstinent AD men was observed only among those with the most common HTR1B promoter diplotype. Less common promoter diplotypes appeared protective. Controlling for genetic background is a useful augmentation of case-control pharmacological challenge strategies designed to elucidate the psychobiology of AD and other complex disorders.     

Increased NoGo-anteriorisation in first-episode schizophrenia patients during Continuous Performance Test

OBJECTIVE: NoGo-stimuli during a Continuous Performance Test (CPT) activate prefrontal brain structures such as the anterior cingulate gyrus and lead to an anteriorisation of the positive electrical field of the NoGo-P300 relative to the Go-P300, so-called NoGo-anteriorisation (NGA). NGA during CPT is regarded as a neurophysiological standard index for cognitive response control. While it is known that patients with chronic schizophrenia exhibit a significant reduction in NGA, it is unclear whether this also occurs in patients undergoing their first-episode. Thus, the aim of the present study was to determine NGA in a group of patients with first-episode schizophrenia by utilizing a CPT paradigm. METHODS: Eighteen patients with first-episode schizophrenia and 18 matched healthy subjects were investigated electrophysiologically during a cued CPT, and the parameters of the Go- and NoGo-P300 were determined using microstate analysis. Low resolution tomography analysis (LORETA) was used for source determination. RESULTS: Due to a more posterior Go- and a more anterior NoGo-centroid, NGA was greater in patients than in healthy controls. LORETA indicated the same sources for both groups after Go-stimuli, but a more anterior source in patients after NoGo-stimuli. In patients P300-amplitude responses to both Go- and NoGo-stimuli were decreased, and P300-latency to NoGo-stimuli was increased. After the Go-stimuli false reactions and reaction times were increased in patients. CONCLUSIONS: Attention was reduced in patients with first-episode schizophrenia, as indicated by more false reactions, prolongation of reaction time, P300-latencies and by a decrease in P300-amplitude. Significantly however, the NGA and prefrontal LORETA-sources indicate intact prefrontal brain structures in first-episode schizophrenia patients. Previously described changes in this indicator of prefrontal function may be related to a progressive decay in chronic schizophrenia. SIGNIFICANCE: The results support the idea of a possible new biological marker of first episode psychosis, which may be a useful parameter for the longitudinal measurement of changing prefrontal brain function in a single schizophrenia patient.     

食品中污染酵母菌的RAPD分类鉴定

目的探索采用RAPD技术对食品污染酵母进行分类鉴定的可行性。方法采用RAPD技术对从食品中分离到的22株污染酵母菌进行分子分型并以UPGMA法构建以上菌株的带型关系系统树状图。结果22株污染酵母菌总共扩增出11种不同的指纹图谱，经聚类分析可分为2个聚类群。结论RAPD技术可以作为一种有效、快速、简便的对污染酵母菌进行分类鉴定的手段。     

Effects of Hostility on Alcohol Stress-Response-Dampening

The purpose of this study was to compare the stress-response-dampening (SRD) effect of alcohol in hostile and nonhostile men based on a combined score of four subscales of the Cook-Medley Hostility Scale . Subjects were 72 male social drinkers. Subjects' cardiac interbeat-interval, and systolic and diastolic blood pressure reactivity to a situational stressor were measured following the consumption of either alcohol, no alcohol, or an active placebo beverage. Results demonstrated that hostile men evinced lower heart rate and systolic blood pressure (SBP) reactivity to the stressor when given alcohol, compared with intoxicated nonhostile subjects, and lower reactivity relative to all other groups, with the exception of SBP in the nonhostile controls. These results allow for speculation that hostile men may be more likely than controls to experience possible SRD effects of alcohol and thus, perhaps, be predisposed to increased alcohol consumption when under stress.     

Protein kinase C isozymes that mediate enhancement of neurite outgrowth by ethanol and phorbol esters in PC12 cells

Using PC12 cells to study ethanol's effects on growth of neural processes, we found that ethanol enhances NGF- and basic FGF-induced neurite outgrowth. Chronic ethanol exposure selectively up-regulates δ and ε protein kinase C (PKC) and increases PKC-mediated phosphorylation in PC12 cells. Since PKC regulates differentiation, we investigated the role of PKC in enhancement of neurite outgrowth by ethanol. Like ethanol, 0.3–10 nM phorbol 12-myristate, 13-acetate (PMA) increased NGF-induced neurite outgrowth. However, higher concentrations did not, and immunoblot analysis demonstrated that 100 nM PMA markedly depleted cells of β, δ and ε PKC. PMA (100 nM) also down-regulated β, δ and ε PKC in ethanol-treated cells and completely prevented enhancement of neurite outgrowth by ethanol. In contrast, the cAMP analogue 8-bromoadenosine cAMP did not completely mimic the effectsof ethanol on neurite outgrowth, and ethanol was able to enhance neurite formation in mutant PC12 cells deficient in protein kinase A (PKA). These findings implicate β, δ or εPKC, but not PKA, in the neurite-promoting effects of ethanol and PMA. Since chronic ethanol exposure up-regulates δ and ε, but not βPKC, these findings suggest that δ or εPKC regulate neurite outgrowth.     

Consequence of long-term exposure to corticosterone or dexamethasone on ethanol consumption in the adrenalectomized rat,and the effect of type I and type II corticosteroid receptor antagonists

The daily fluid intake of male Wistar rats with simultaneous access to 6% ethanol and water was determined during a baseline period (1 week), following adrenalectomy (1 week) and for 3 weeks following SC implantation of hormone pellets containing corticosterone (CORT) or dexamethasone (DEX). Ethanol consumption dropped during the first week of adrenalectomy (ADX) but increased again in the absence of hormone replacement to reach preoperative levels during the ensuing weeks. The CORT treatment, which produced plasma hormone levels similar to the 24-h mean concentration of adrenally intact rats, not only reversed the effect of ADX on alcohol consumption but also enhanced it to levels above those observed in intact rats. Water intake was not affected by the CORT treatment. DEX implants stimulated water intake, but did not enhance the drinking of ethanol. SC injections of RU 28318 (type I corticosterone receptor antagonist; 10 mg/kg) or mifepristone (RU 38486; type II receptor antagonist; 25 mg/kg) at the beginning and halfway through three daily, 6-h tests failed to affect ethanol drinking in adrenally intact rats or in ADX rats bearing CORT implants. Similarly, there was no effect of giving the two antagonists in combination. These results suggest that exogenous CORT can induce excessive alcohol intake in genetically unselected rats and that this facilitatory effect may be mediated by non-genomic cellular mechanisms.     

Reliability of a Store Observation Tool in Measuring Availability of Alcohol and Selected Foods

Alcohol and food items can compromise or contribute to health, depending on the quantity and frequency with which they are consumed. How much people consume may be influenced by product availability and promotion in local retail stores. We developed and tested an observational tool to objectively measure in-store availability and promotion of alcoholic beverages and selected food items that have an impact on health. Trained observers visited 51 alcohol outlets in Los Angeles and southeastern Louisiana. Using a standardized instrument, two independent observations were conducted documenting the type of outlet, the availability and shelf space for alcoholic beverages and selected food items, the purchase price of standard brands, the placement of beer and malt liquor, and the amount of in-store alcohol advertising. Reliability of the instrument was excellent for measures of item availability, shelf space, and placement of malt liquor. Reliability was lower for alcohol advertising, beer placement, and items that measured the “least price” of apples and oranges. The average kappa was 0.87 for categorical items and the average intraclass correlation coefficient was 0.83 for continuous items. Overall, systematic observation of the availability and promotion of alcoholic beverages and food items was feasible, acceptable, and reliable. Measurement tools such as the one we evaluated should be useful in studies of the impact of availability of food and beverages on consumption and on health outcomes.     

Flow Cytometric Analysis of Lymphocyte Subsets of Mice Maintained on an Ethanol-Containing Liquid Diet

Alcoholic patients often have impaired immune function, yet little is known about the precise mechanism(s) of this impairment. We have previously shown that ethanol consumption by mice alters copolymer-specific humoral and cellular immune responses. In this study, we asked whether alcohol consumption by mice would phenotypically alter lymphocyte populations. Female C57BL/6 mice were fed a nutritionally complete liquid diet containing 35% ethanol-derived calories for up to 8 days. As controls, mice either were fed a liquid control diet that isocalorically substitutes sucrose for ethanol or remained on a standard solid diet and water ad libitum. Although mice fed ethanol-containing liquid or pair-fed control liquid diets have decreased numbers of spleen cells compared with solid diet controls, only the ethanol-containing diet allowed normally nonresponder C57BL/6 spleen cells to make antibody responses to the poly(Glu⁵⁰Tyr⁵⁰) synthetic copolymer antigen. Flow cytometric analysis of splenic lymphocyte populations of mice on the ethanol-containing diet shows an increase in the relative proportion of T-lymphocytes as compared with mice on either solid or liquid control diets. No such change is seen for either B-cell or natural killer cell populations in these same mice. Both liquid control and liquid ethanol diets caused a slight decrease in the CD4:CD8 ratios of splenic T-lymphocytes. We see the relative percentage of T-cells bearing the αβ-cell receptor (TcR) increases in the spleens of liquid ethanol diet mice; a smaller increase TcRαβ usage is seen in the spleens of liquid control mice, compared with solid diet mice. Flow cytometric analysis shows that little, if any, difference exists in TcRγδ expression between the liquid ethanol and either the liquid control or solid diet groups. Preliminary analysis of TcRαβ subsets suggest that ethanol increases the percentage of T-cells expressing Vβ5 and Vβ8, and decreases the percentage of Vβ11 expressing cells. These findings suggest that, in addition to modifying the immune response, ethanol alters the phenotypic expression of lymphocyte subsets.