The relationship between women's subjective and physiological sexual arousal

Previous literature presents discordant results on the relationship between physiological and subjective sexual arousal in women. In this study, the use of hierarchical linear modeling (HLM) revealed a significant concordance between continuous measures of physiological and subjective sexual arousal as assessed during exposure to erotic stimuli in a laboratory setting. We propose that past studies that have found little or no association between the two measures may have been in part limited by the methodology and statistical analyses employed.     

Sequential Measurements of Chemokines in Urosepsis and Experimental Endotoxemia

Chemokines are a superfamily of small chemotactic proteins. While increased levels of interleukin-8 have been measured in serum and urine during urinary tract infection, little is known about other chemokines in this condition. Monocyte chemoattractant protein (MCP)–1, macrophage inflammatory protein (MIP)–1, MIP-1 and interferon- inducible protein (IP)–10 were measured in 30 patients with culture-proven urosepsis during a 3-day follow-up and in 11 healthy humans after intravenous injection of endotoxin (4 ng/kg). Urine and serum levels of MCP-1, MIP-1, and IP-10, but not of MIP-1, were elevated in patients on admission, and decreased after initiation of antibiotic treatment. Endotoxin administration to healthy subjects induced increases in plasma and urine concentrations of all four chemokines. These data indicate that clinical and experimental gram-negative infection in humans is associated with enhanced production of chemokines that act mainly on mononuclear cells and that these chemokines are at least in part locally produced.     

Temperature dependence of mutant mevalonate kinase activity as a pathogenic factor in hyper-IgD and periodic fever syndrome

Hyper-IgD and periodic fever syndrome (HIDS) and mevalonic aciduria are autosomal recessive disorders characterized by recurrent episodes of fever and generalized inflammation. Both syndromes are caused by specific mutations in the gene encoding mevalonate kinase (MK), resulting in a depressed enzymatic activity mainly due to reduced protein levels. We studied the effect of temperature on the activity of wild-type and several mutant MKs in fibroblasts. All fibroblast cell lines from HIDS patients and harbouring the common V377I MVK allele displayed substantially higher MK activities at 30 degrees C as compared to 37 degrees C. As shown by temperature inactivation experiments this resulted in a protein nearly as stable as in control cell lines, indicating that primarily the maturation of the protein is affected. Accordingly, when HIDS cell lines were cultured at 39 degrees C, MK activity decreased further. This triggered a compensatory increase in 3-hydroxy-3-methylglutaryl-CoA reductase activity, indicating that MK becomes progressively rate-limiting. A similar phenomenon occurs in vivo. MK activity in peripheral blood mononuclear cells drops 2-8-fold when HIDS patients experience febrile attacks. Our results suggest that minor elevations in temperature can set off a chain of events with MK becoming progressively rate-limiting, leading to a temporary deficiency of isoprenoid end-products, which induces inflammation and fever.     

Neurobehavioral phenotype in carriers of the fragile X premutation

There have been contradictory findings in the fragile X (fraX) literature about possible neurocognitive and psychological symptoms due to the fraX premutation (pM). The purpose of the present study was to investigate the relationship between CGG repeat length and neurobehavioral functioning in carriers of the fraX pM. Eighty‐five female carriers of the pM with allele sizes ranging from 59–166 were administered a comprehensive IQ test (WAIS‐III) and completed a questionnaire designed to measure psychopathology (Symptom Checklist (SCL)‐90‐R). No relationship between allele size and cognition was identified. A significant negative relationship between allele size and age was found, as well as a positive relationship between allele size and depression. Follow‐up analyses separating small and large allele sizes (below and above 100 CGG repeats) indicated that individuals with larger allele sizes scored significantly higher on the Interpersonal Sensitivity and Depression subscales of the SCL‐90‐R. Despite the limitation of few individuals with high CGG repeat lengths, our findings suggest that females with larger premutated alleles (≥ 100 repeats) display some clinical manifestations of fraX syndrome. © 2001 Wiley‐Liss, Inc.     

Multisensory integration mechanisms in haptic space perception

It has been argued that representations of peripersonal space based on haptic input are systematically distorted by egocentric reference frames. Interestingly, a recent study has shown that noninformative vision (i.e., freely viewing the region above the haptic workspace) improves performance on the so-called haptic parallel-setting task, in which participants are instructed to rotate a test bar until it is parallel to a reference bar. In the present study, we made a start at identifying the different sensory integration mechanisms involved in haptic space perception by distinguishing the possible effects of orienting mechanisms from those of noninformative vision. We found that both the orienting direction of head and eyes and the availability of noninformative vision affect parallel-setting performance and that they do so independently: orienting towards a reference bar facilitated the parallel-setting of a test bar in both no-vision and noninformative vision conditions, and noninformative vision improved performance irrespective of orienting direction. These results suggest the effects of orienting and noninformative vision on haptic space perception to depend on distinct neurocognitive mechanisms, likely to be expressed in different modulations of neural activation in the multimodal parietofrontal network, thought to be concerned with multimodal representations of peripersonal space.     

Detection of Bartonella henselae DNA by two different PCR assays and determination of the genotypes of strains involved in histologically defined cat scratch disease

Cat scratch disease (CSD) is a common cause of subacute regional lymphadenopathy, not only in children but also in adults. Serological and molecular studies demonstrated that Bartonella henselae is the etiologic agent in most cases of CSD. Amplification of B. henselae DNA in affected tissue and detection of antibodies to B. henselae are the two mainstays in the laboratory diagnosis of CSD. We designed a retrospective study and investigated formalin-fixed, paraffin-embedded lymph nodes from 60 patients (25 female, 35 male) with histologically suspected CSD by PCR amplification. The sensitivities of two different PCR assays were compared. The first primer pair amplified a 296-bp fragment of the 16S rRNA gene in 36 of the 60 samples, corresponding to a sensitivity of 60%. The second primer pair amplified a 414-bp fragment of the htrA gene in 26 of the 60 lymph nodes, corresponding to a sensitivity of 43.3%. Bartonella DNA could be detected in a total of 39 (65%) of the 60 lymph nodes investigated. However, histopathologic findings are typical but not specific for CSD and cannot be considered as a "gold standard" for diagnosis of CSD. The sensitivity of the PCR assays increased from 65 to 87% if two criteria (histology and serology) were used in combination for diagnosis of CSD. Two genotypes (I and II) of B. henselae are described as being involved in CSD. Genotype I was found in 23 (59%) and genotype II was found in 9 (23%) of the 39 PCR-positive lymph nodes. Seven (18%) lymph nodes were negative in both type-specific PCR assays. Thirty (50%) of our 60 patients were younger than 20 years old (15 were younger than 10 years), 20 (33%) were between 21 and 40 years old, and 10 (17%) patients were between 41 and 84 years old. Our data suggest that detection of Bartonella DNA in patients' samples might confirm the histologically suspected diagnosis of CSD.     

A new method to bind allergens for the measurement of specific IgE antibodies

BACKGROUND: Detection of allergen-specific IgE antibodies in patients' sera plays a key role for the diagnosis of IgE-mediated allergy. If no validated test system is available, diagnostic tools must be developed, usually by coupling or binding the allergens to a solid phase. Streptavidin ImmunoCAP is a new solid phase for binding of allergens which can be used in the Pharmacia CAP system. OBJECTIVE: It was the aim of this study to assess the diagnostic validity of Streptavidin ImmunoCAP. METHODS: Biotinylation and allergen concentration for binding to Streptavidin ImmunoCAP were optimized and IgE obtained with natural rubber latex, obeche wood, wheat and rye flour Streptavidin ImmunoCAP were compared with the results of ImmunoCAP and Enzyme Allergo-Sorbent Test (EAST) using sera from patients complaining of workplace-related respiratory symptoms. RESULTS: While the relation of biotin-label and protein was critical (best results were obtained with a 5- fold molar excess), labelled protein for coupling to streptavidin ImmunoCAP was applicable in a wide concentration range. On average, IgE values with streptavidin ImmunoCAP were as high as with ImmunoCAP but considerably higher than values obtained by EAST. CONCLUSION: Streptavidin ImmunoCAP is a valuable tool for sensitive and specific measurement of IgE binding to new allergens superior to cellulose disk-based methods.     

Genomic screen for loci associated with alcohol dependence in Mission Indians.

Alcohol dependence is a leading cause of morbidity and mortality in Native Americans, yet biological factors underlying the disorder in this ethnic group remain elusive. This study's aims were to map susceptibility loci for DSM-III-R alcohol dependence and two narrower alcohol-related phenotypes in Mission Indian families. Each participant gave a blood sample and completed an interview using the Semi-Structured Assessment for the Genetics of Alcoholism (SSAGA) that was used to make alcohol dependence diagnoses and the narrower phenotypes of withdrawal, and drinking severity. Genotypes were determined for a panel 791 microsatellite polymorphisms. Analyses of multipoint variance component LOD scores for the dichotomous DSM-III-R phenotype revealed no peak LOD scores that exceeded 2.0 at any chromosome location. Two chromosomes, 4 and 12, had peak LOD scores that exceeded 2 for the alcohol use severity phenotype and three chromosomes 6, 15, 16 were found to have peaks with LOD scores that exceeded 2 for the withdrawal phenotype. Evidence for linkage to chromosomes 4 and 15, and 16 have been reported previously for alcohol related phenotypes whereas no evidence has as yet been reported for chromosomes 6 and 12. Combined linkage and association analysis suggest that alcohol dehydrogenase 1B gene polymorphisms are partially responsible for the linkage result on chromosome 4 in this population. These results corroborate the importance of several chromosomal regions highlighted in prior segregation studies in alcoholism and further identify new regions of the genome that may be unique to either the restricted phenotypes evaluated or this population of Mission Indians.