Does stress cause posttraumatic stress disorder?
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Humans↗
Biomedical subjects
J Paris
Publications and source records attributed to J Paris.
Is psychopharmacological treatment effective for the symptoms of borderline personality disorder (BPD)?
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Adult↗
Neuropsychological factors associated with borderline pathology in children.
OBJECTIVE: To determine whether children with borderline pathology have a specific pattern of neuropsychological risk factors. METHOD: The subjects were 94 school-age children in day treatment, divided into borderline (n = 41) and nonborderline (n = 53) groups according to results of the Child version of the Diagnostic Interview for Borderlines. All children were assessed with the Child Behavior Checklist, the Schedule for Affective Disorders and Schizophrenia for School-Age Children, and a neuropsychological battery. RESULTS: Children with borderline pathology had abnormal scores on the Wisconsin Card Sorting Test and on the Continuous Performance Test, both of which suggested problems with executive function. Although borderline pathology was highly comorbid with conduct disorder, most results were independent of this comorbidity. CONCLUSIONS: Borderline pathology in children has a unique pattern of neuropsychological risk factors that may reflect a diathesis for this syndrome.
Analysis of Variance↗
[Imaging of the adult sinusitis: indications for using conventional techniques, CT scan and MRI].
CT scanning has become the major investigation for sinusitis which is not acute, but chronic. It is a good diagnostic tool, but also allows follow-up assessment of progress, and preoperative evaluation of particular problems related to abnormalities or anatomical variations. MRI scanning has a lesser place, and is most useful in evaluating certain types of pseudo-tumorous sinus conditions, or excluding local complications (in the anterior cranial fossa or orbit).
Adult↗
[Extramedullary plasmocytoma of the nasal cavity: a case report].
PURPOSE OF STUDY: To establish a diagnosis and therapeutic management in patients with extramedullar plasmocytomas. METHOD: There is no consensus concerning extramedullar plasmocytoma treatment. One patient with a nasal cavity tumor location and a review of literature are reported. RESULTS: Extramedullar plasmocytoma is a rare tumor that occurs most frequently in the upper respiratory tract. The most common location is the nasal cavity. Diagnosis can only be made after histological and immunohistochemical examinations. Localized tumors are treated by radiation therapy, combined or not with surgery. Disseminated diseases are treated by chemotherapy. CONCLUSION: Diagnosis can only be confirmed after the exclusion of a systemic disease (multiple myeloma).
Adult↗
Coadministration of nomegestrol acetate does not diminish the beneficial effects of estradiol on coronary artery dilator responses in nonhuman primates (Macaca fascicularis).
OBJECTIVE: Our purpose was to examine the effect of coadministered nomegestrol acetate on estradiol-induced dilator responses of coronary arteries. STUDY DESIGN: In this prospective randomized trial, ovariectomized monkeys were fed a moderately atherogenic diet for 3 months while being treated with (1) no hormone replacement (control, n = 12), (2) estradiol (1.5 mg/d equivalent) added to the diet (n = 12), or (3) estradiol (1.5 mg/d equivalent) plus nomegestrol acetate (3.75 mg/d equivalent) (n = 12) added to the diet. Effects of treatment were measured with analysis of variance. Post hoc analyses were done by multiple comparison tests with Bonferroni corrections. RESULTS: Constrictor responses of epicardial coronary arteries (measured with quantitative angiography) and decreased coronary blood velocity (measured with Doppler ultrasonography) to acetylcholine (10(-6) mol/L) were less in the estradiol-treated monkeys (with or without cotreatment with nomegestrol acetate) than in the untreated monkeys (P <.05). Typical estrogenic responses were induced by estradiol in the endometrium (ie, increased proliferation [Ki-67 expression] [P <.04] and increased hormone receptor expression). These effects were antagonized by nomegestrol acetate. CONCLUSIONS: Although nomegestrol acetate has typical progestin-like effects on the uterus, it does not diminish the beneficial effects of estrogen on acetylcholine-induced dilator responses of coronary arteries.
Acetylcholine↗
An accessory peptide binding site with allosteric effect on the formation of peptide-MHC-II complexes?
MHC-II molecules bind a single peptide in their groove. Here, the authors summarise evidence that a second peptide could bind transiently to MHC-II molecules outside the groove and have an allosteric effect on peptide-MHC-II complex formation. This effect could modulate, after the antigen processing, the selection of the peptide subset presented by MHC-II molecules to the helper CD4 T cells, which regulate the specific immune response.
Allosteric Regulation↗
Estrogens, progestins, and coronary artery reactivity in atherosclerotic monkeys.
It has been known for many years that sex hormones modulate vasodilator responses of arteries supplying the uterus with blood. Recently, it has been shown that sex hormones such as estrogen modulate vasomotor responses of other arteries, including coronary arteries. It is thought that modulation of vasodilator and constrictor responses of coronary arteries may be one mechanism by which estrogen affects the risk of coronary heart disease. Although several studies have examined the effects (and potential mechanisms) of estrogen on vasodilator responses of nonatherosclerotic arteries, few have focused on estrogen's effects on atherosclerotic coronary arteries. In studies of ovariectomized atherosclerotic female cynomolgus monkeys, both long-term (2 years) and short-term (20 min) estradiol treatment augments dilator responses to acetylcholine, but not nitroglycerin. Presumably, this indicates an effect of estradiol on endothelium-mediated dilator responses of coronary arteries. Addition of the progestin medroxyprogesterone acetate diminishes the beneficial effect of conjugated equine estrogens on these dilator responses. This is significant because a progestin is usually added to estrogen replacement to reduce the risk of endometrial and breast cancer associated with unopposed estrogen therapy. However, it would seem that not all progestins act similarly on vascular reactivity. Studies in monkeys indicate that addition of progesterone or the progestin medroxyprogesterone acetate does not diminish the beneficial effects of estrogen on coronary dilator responses. Thus it would appear that different estrogen/progestin combinations may affect vascular reactivity in different manners, There is also an effort being made to examine the potential of different kinds of estrogens on cardiovascular risk. Studies in monkeys indicate that one of the estrogens found in conjugated equine estrogens (17 alpha-dihydroequilenin) has estrogen effects on vascular reactivity without having detrimental effects on uterine pathology. The isoflavones "plant estrogens" found in soy protein also have estrogenic effects on vascular reactivity and inhibition.
Acetylcholine↗
Progestins and breast cancer.
In the last years there has been an extraordinary development in the synthesis of new progestins. These compounds are classified, in agreement with their structure, in various groups which include progesterone, retroprogesterones, 17alpha-hydroxyprogesterones, 19-norprogesterones, 17alpha-hydroxyprogesterone derivatives, androstane and estrane derivatives. The action of progestins is a function of many factors: its structure, affinity to the progesterone receptor or to other steroid receptors, the target tissue considered, the biological response, the experimental conditions, dose, and metabolic transformation. The information on the action of progestins in breast cancer patients is very limited. Positive response with the progestins: medroxyprogesterone acetate and megestrol acetate was obtained in post-menopausal patients with advanced breast cancer. However, extensive information on the effect of progestins was obtained in in vitro studies using hormone-dependent and hormone-independent human mammary cancer cell lines. It was demonstrated that in the hormone-dependent breast cancer cells, various progestins (nomegestrol acetate, tibolone, medrogestone, promegestone) are potent sulfatase inhibitory agents. The progestins can also involve the inhibition of mRNA of this enzyme. In another series of studies it was also demonstrated that various progestins are very active in inhibiting the 17beta-hydroxysteroid dehydrogenase for the conversion of estrone to estradiol. More recently it was observed that the progestins promegestone or medrogestone stimulate the sulfotransferase for the formation of estrogen sulfates. Consequently, the blockage in the formation of estradiol via sulfatase, or the stimulatory effect on sulfotransferase activity, by progestins can open interesting and new possibilities in clinical applications in breast cancer.
17-Hydroxysteroid Dehydrogenases↗
Phenylalanine derivatives active against Toxoplasma gondii brain cysts in mice.
The action of phenylalanine derivatives against a cyst forming strain of Toxoplasma gondii was tested in vitro and in vivo in mice. These compounds were Phe-Phe-OMe (dipeptide methyl ester) 1 and its cyclized product, 3,6-dibenzyl-2,5-dioxopiperazine 2, Boc-L-Phe 3, L-Phe-OMe 4, Boc-L-Phe-L-Phe-OMe 5. After a 48 hr incubation in vitro, the compounds 3 and 5 induced a higher inhibition than the control molecule, pyrimethamine. In the in vivo studies, the compound 3 induced a 77% decrease in the number of cerebral cysts, comparable to pyrimethamine. Compounds 1, 5 and 4 induced a decrease of about 63% in the cyst number. A size reduction and an alteration of the wall of treated cysts were often noted. In a histological study, a reduction in cyst size without either inflammation or intervention of the nevroglial cells was observed. The present study provides evidence on the efficacy of phenylalanine derivatives and especially Boc-Phe 3, against T.gondii brain cysts in mice.
Animals↗
Genome-wide mapping of unselected transcripts from extraembryonic tissue of 7.5-day mouse embryos reveals enrichment in the t-complex and under-representation on the X chromosome.
Mammalian embryos can only survive if they attach to the uterus (implantation) and establish proper maternal-fetal interactions. To understand this complex implantation pathway, we have initiated genomic analysis with a systematic study of the cohort of genes expressed in extraembryonic cells that are derived from the conceptus and play a major role in this process. A total of 2103 cDNAs from the extraembryonic portion of 7.5-day post-conception mouse embryos yielded 3186 expressed sequence tags, approximately 40% of which were novel to the sequence databases. Furthermore, when 155 of the cDNA clones with no homology to previously detected genes were genetically mapped, apparent clustering of these expressed genes was detected in subregions of chromosomes 2, 7, 9 and 17, with 6.5% of the observed genes localized in the t-complex region of chromosome 17, which represents only approximately 1.5% of the mouse genome. In contrast, X-linked genes were under-represented. Semi-quantitative RT-PCR analyses of the mapped genes demonstrated that one third of the genes were expressed solely in extraembryonic tissue and an additional one third of the genes were expressed predominantly in the extraembryonic tissues. The over-representation of extraembryonic-expressed genes in dosage-sensitive autosomal imprinted regions and under-representation on the dosage-compensated X chromosome may reflect a need for tight quantitative control of expression during development.
Animals↗
Molecular modeling of hen egg lysozyme HEL[52-61] peptide binding to I-Ak MHC class II molecule.
A bound conformation of the antigenic decapeptide hen egg lysozyme HEL[52-61] associated to the mouse MHC class II (MHC II) I-Ak was modeled by homology with the three-dimensional structure of hemagglutinin HA[306-318]-HLA-DR1 complex. HEL peptide Tyr53 could not be aligned with the HA peptide Tyr308 because this resulted in a buried Tyr53 side chain within the I-Ak peptide-binding groove and this conflicted with this side chain being recognized by T cells. Therefore, Asp52 of HEL was fixed as the P1 anchor and aligned on Tyr308 of HA. After molecular dynamics, the modeled complex was stable even in the absence of any constraint. The peptide backbone adopted a polyproline II-like conformation with canonical hydrogen bonding between the peptide backbone and MHC II molecule. Asp52, IIe55, Gin57 and Ser60 were predicted to be deeply buried into P1, P4, P6 and P9 MHC II pockets, and Tyr53, Leu56, Asn59 and Arg61 as TCR contacting residues. The modeling of 15 complexes associating I-Ak with peptides derived from HEL[52-61] by single amino acid substitution proved stable with conserved hydrogen bonds and side chain orientation compatible with their recognition by two T cell hybridomas. Moreover, comparison with the recently solved crystal structure of the related HEL[50-62]-I-Ak complex revealed striking similarities.
Amino Acid Sequence↗
Twin study of dissociative experience.
The relative influence of genetic and environmental influences on measures of pathological and nonpathological dissociative experience was estimated using a classic twin-study design. Subjects were 177 monozygotic and 152 dizygotic volunteer general population twin pairs who completed two measures of dissociative capacity identified from the items comprising the Dissociative Experiences Scale (DES). Additive genetic influences accounted for 48% and 55% of the variance in scales measuring pathological and nonpathological dissociative experience, respectively. Heritability estimates did not differ by gender. The genetic correlation between these measures was estimated at .91, suggesting common genetic factors underlying pathological and nonpathological dissociative capacity. Genetic and environmental correlations between the DES scales and measures of personality disorder traits (Dimensional Assessment of Personality Pathology-Basic Questionnaire; DAPP-BQ) were also estimated. Significant genetic correlations (median = .38) were found between the DES scales and DAPP-BQ cognitive dysregulation, affective lability, and suspiciousness, suggesting that the genetic factors underlying particular aspects of personality disorder also influence dissociative capacity.
Adolescent↗
Personality disorders: psychiatry's stepchildren.
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Attitude of Health Personnel↗
Does childhood trauma cause personality disorders in adults?
OBJECTIVE: To examine the relationship between trauma in childhood and personality disorders in adulthood. METHOD: A review of the literature was conducted. RESULTS: The reported associations between trauma and personality pathology are illuminated by the following research findings: 1) personality is heritable; 2) only a minority of patients with severe personality disorders report childhood trauma; and 3) children are generally resilient, and traumatic experiences do not consistently lead to psychopathology. CONCLUSIONS: The role of trauma in the personality disorders is best understood in the context of gene-environment interactions.
Adult↗
Managing patients with personality disorders.
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Chronic Disease↗
Personality disorders in sociocultural perspective.
Personality disorders are shaped by a social and cultural context. This principle is supported by evidence that Axis II diagnoses have a different prevalence in different societies, and that some disorders demonstrate cohort effects. Transitions from traditional to modern social structures, accompanied by social disintegration and rapid social change, could account for these phenomena. The main mechanisms of action would involve interference with family functioning and with buffering from the social community.
Cross-Cultural Comparison↗