Evaluation of the Selfitis Behavior Scale Across Two Persian-Speaking Countries,Iran and Afghanistan: Advanced Psychometric Testing in a Large-Scale Sample

International Journal of Mental Health and Addiction - Selfitis—which started off as a hoax but has now been investigated empirically—has been defined as the obsessive–compulsive...     

Croatian population data for the C677T polymorphism in methylenetetrahydrofolate reductase: frequencies in healthy and atherosclerotic study groups

BACKGROUND: The aim of this study was to investigate the frequency of C677T methylenetetrahydrofolate reductase (MTHFR) mutation in healthy Croatian volunteers and in patients with atherosclerosis. METHODS: The C677T MTHFR gene mutation was determined by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) in 640 subjects, residents of the Zagreb city or Zagreb surroundings. Control group (n=298) was healthy blood donors. Patients (n=342) were divided into two groups of those with coronary heart disease, CAD (n=247) and those with >60% carotid stenosis, CS (n=95). RESULTS: CC genotype was recorded in 45% of healthy volunteers and 46% of patients (46.3% with CS and 46.2% with CAD). TC genotype was found in 49% of healthy volunteers and 45% of patients (46.3% with CS and 44.9% with CAD). There was no significant difference (p>0.05) from the control group in the genotype or allele frequency either for the overall group of patients with atherosclerosis or for the patient subgroups. CONCLUSION: The preliminary study of MTHFR polymorphism in control subjects and cardiovascular disease/carotid stenosis patients revealed that in Croats there was a low frequency of TT genotype (6% in controls vs. 9% in patients) and T allele (31% for cases and controls). Additionally, our results did not show significantly higher frequency of MTHFR mutation in CAD and CS studied groups.     

Executive function late effects in survivors of pediatric brain tumors and acute lymphoblastic leukemia

Background: Survivors of pediatric brain tumors (BT) and acute lymphoblastic leukemia (ALL) are at risk for neurocognitive late effects related to executive function. Procedure: Survivors of BT (48) and ALL (50) completed neurocognitive assessment. Executive function was compared to estimated IQ and population norms by diagnostic group. Results: Both BT and ALL demonstrated relative executive function weaknesses. As a group, BT survivors demonstrated weaker executive functioning than expected for age. Those BT survivors with deficits exhibited a profile suggestive of global executive dysfunction, while affected ALL survivors tended to demonstrate specific rapid naming deficits. Conclusion: Findings suggest that pediatric BT and ALL survivors may exhibit different profiles of executive function late effects, which may necessitate distinct intervention plans.     

The kisspeptin system of the human hypothalamus: sexual dimorphism and relationship with gonadotropin‐releasing hormone and neurokinin B neurons

Kisspeptin signaling via the kisspeptin receptor G‐protein‐coupled receptor‐54 plays a fundamental role in the onset of puberty and the regulation of mammalian reproduction. In this immunocytochemical study we addressed the (i) topography, (ii) sexual dimorphism, (iii) relationship to gonadotropin‐releasing hormone (GnRH) neurons and (iv) neurokinin B content of kisspeptin‐immunoreactive hypothalamic neurons in human autopsy samples. In females, kisspeptin‐immunoreactive axons formed a dense periventricular plexus and profusely innervated capillary vessels in the infundibular stalk. Most immunolabeled somata occurred in the infundibular nucleus. Many cells were also embedded in the periventricular fiber plexus. Rostrally, they formed a prominent periventricular cell mass (magnocellular paraventricular nucleus). Robust sex differences were noticed in that fibers and somata were significantly less numerous in male individuals. In dual‐immunolabeled specimens, fine kisspeptin‐immunoreactive axon varicosities formed axo‐somatic, axo‐dendritic and axo‐axonal contacts with GnRH neurons. Dual‐immunofluorescent studies established that 77% of kisspeptin‐immunoreactive cells in the infundibular nucleus synthesize the tachykinin peptide neurokinin B, which is known to play crucial role in human fertility; 56 and 17% of kisspeptin fibers in the infundibular and periventricular nuclei, respectively, contained neurokinin B immunoreactivity. Site‐specific co‐localization patterns implied that kisspeptin neurons in the infundibular nucleus and elsewhere contributed differentially to these plexuses. This study describes the distribution and robust sexual dimorphism of kisspeptin‐immunoreactive elements in human hypothalami, reveals neuronal contacts between kisspeptin‐immunoreactive fibers and GnRH cells, and demonstrates co‐synthesis of kisspeptins and neurokinin B in the infundibular nucleus. The neuroanatomical information will contribute to our understanding of central mechanisms whereby kisspeptins regulate human fertility.     

Interferon α and Tat involvement in the immunosuppression of uninfected T cells and C-C chemokine decline in AIDS

HIV type 1 (HIV-1) not only directly kills infected CD4⁺ T cells but also induces immunosuppression of uninfected T cells. Two immunosuppressive proteins, interferon α (IFNα) and extracellular Tat, mediate this process because specific antibodies against these proteins prevent generation of suppressor cells in HIV-1-infected peripheral blood mononuclear cell cultures. Furthermore, the production of C-C chemokines in response to immune cell activation, initially enhanced by IFNα and Tat, ultimately is inhibited by these proteins in parallel with their induction of immunosuppression. The clinical corollary is the immunosuppression of uninfected T cells and the decline in C-C chemokine release found at advanced stages of HIV-1 infection paralleling rising levels of IFNα and extracellular Tat. We, therefore, suggest that IFNα and Tat may be critical targets for anti-AIDS strategies.     

Evidence for the existence of non-GABAergic, cholinergic interneurons in the rodent hippocampus

Previous studies have revealed a small number of hippocampal interneurons immunoreactive for choline acetyltransferase, the acetylcholine-synthesizing enzyme. It remained an open question, however, whether these neurons represented a subgroup of inhibitory GABAergic neurons co-localizing acetylcholine. In this study, we have combined immunocytochemistry for choline acetyltransferase and in situ hybridization for glutamate decarboxylase messenger RNA, the GABA-synthesizing enzyme. None of the choline acetyltransferase-immunoreactive neurons in the various layers of the hippocampus proper and fascia dentata were found to co-localize glutamate decarboxylase messenger RNA. The lack of an in situ hybridization signal in these neurons is unlikely to result from the combination of the two labeling techniques. When combining in situ hybridization for glutamate decarboxylase messenger RNA with immunostaining for parvalbumin, a calcium-binding protein expressed by many GABAergic hippocampal interneurons, numerous double-labeled cells were observed. These data provide neurochemical evidence for the existence of non-GABAergic, supposedly cholinergic non-principal cells in the hippocampus.     

The Hierarchical Clustering of Clinical Psychology Practicum Competencies: A Multisite Study of Supervisor Ratings

Competency evaluation rating forms are widely used to assess a range of global and specific psychology practitioner competencies during and at the end of clinical placements. Surprisingly, there is little research examining the dimensional structure or the hierarchical clustering of items on these ratings. The current, multisite study examined supervisor ratings of clinical psychology trainees (N = 204) on the Clinical Psychology Practicum Competencies Rating Scale (CΨPRS). Based on the proximity criterion chosen, hierarchical clustering yielded either nine clusters or four super clusters: Good Practitioner Attributes and Conduct, Scientist Practitioner and Professional Management, Assessment and Intervention, and Psychological Testing. The study also tracked the developmental trajectory of competency attainment. CΨPRS ratings differentiated groups between early but not between later stages of training. Measurement issues and implications for training and practice are discussed.     

Plasma levels of asymmetric dimethylarginine in premature neonates: its possible involvement in developmental programming of chronic diseases

Aim: The endothel dysfunction in early life may play a role in developmental programming of cardiovascular morbidity. The changes of dimethylarginines' plasma levels during the first month among preterm infants and their determinants had been investigated in our study.
Methods: Twenty preterm infants of healthy mothers were studied. Mean (±SD) birth weight and gestational age were 919.5 ± 235.5 g and 26.7 ± 1.6 weeks, respectively. Blood samples were taken by venipuncture at the 3rd, 7th, 14th, 21st and 28th days. Plasma concentrations of L-arginine, asymmetric and symmetric dimethylarginine (SDMA) were measured by liquid chromatography-mass spectrometry method, evaluated by multivariate linear regression analysis.
Results: L-arginine (p < 0.001) and asymmetric dimethylarginine (ADMA) levels (p < 0.001) were positively associated with postnatal age. ADMA levels were negatively correlated with gestational age (p = 0.007), dopamine-need on the 3rd day of life (p = 0.015) and late infection (p = 0.038). The higher birth weight was associated with higher L-arginine (p = 0.052) and ADMA (p = 0.002) concentrations. The dopamine-need on the 7th day of life had a significant effect on postnatal elevation of SDMA levels (p = 0.035).
Conclusion: The progressive increase of ADMA levels described by our study among preterm infants suggests that early endothel dysfunction may take part in developmental programming of chronic adult diseases.     

Aspirin acetylation of betaLys-82 of human hemoglobin. NMR study of acetylated hemoglobin Tsurumai

Acetylation of hemoglobin by aspirin and other compounds has been of interest for the development of agents useful for the treatment of sickle cell disease. In the present study, we have used 2D NMR methods in combination with [1-(13)C-acetyl]salicylic acid to probe the acetylation sites of hemoglobin A and hemoglobin Tsurumai, a mutant human hemoglobin characterized by a betaLys-82-Gln substitution. In contrast to earlier studies by Klotz and coworkers (e.g. Shamsuddin M, Mason RG, Ritchey JM, Honig GR and Klotz KM, Proc Natl Acad Sci USA 71: 4693-4697, 1974) in which it was concluded that betaLys-144 is the principal target residue acetylated by aspirin, the present study confirms our previous but less conclusive demonstration (Xu ASL, Macdonald JM, Labotka RJ and London RE, Biochim Biophys Acta 1432: 333-349, 1999) that betaLys-82 is the primary acetylation site of aspirin and related agents. The present studies also provide conclusive evidence that acetylation of betaLys-82 produces multiple resonances, probably as a consequence of additional acetylation of other sites, particularly betaLys-82' on the second beta chain. The present results also resolve the apparent discrepancy between the targets of modification by aspirin and double-headed aspirin analogs, and provide an explanation for the changes in oxygen affinity and aggregation threshold of aspirin-modified hemoglobin previously observed under in vitro conditions. In light of the present identification of the principal site of acetylation, the potential therapeutic benefit of aspirin in the treatment of sickle cell disease is discussed.