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1.
The purpose of the study was to attempt to replicate a finding of Persky et al. (1978) that midcycle peak values of testosterone (T) in women predicted differences in frequency of intercourse among married couples. Luteinizing hormone (LH), total testosterone (TT), and free testosterone (FT) values from 10 to 14 daily midcycle blood samples donated by 43 volunteering wives were analyzed against sexual activity patterns reported by the couples over a longer period of time. All couples were contracepting by means other than exogenous hormones or the rhythm method. Each morning through three menstrual cycles husbands and wives recorded independently and on separate forms answers to a series of questions concerning sexual activity in the previous 24 hr. Wives also recorded basal body temperatures (BBT). We designated midcycle values of TT and FT according to several definitions of midcycle. Total testosterone levels at the day of the BBT nadir and the day before the nadir correlated significantly with average intercourse frequency. Correlations with FT were statistically significant regardless of which midcycle measure was used; the day before the BBT nadir gave the highest correlation, 0.618, p = 0.01. Mean testosterone (TT or FT) values were not significantly related. We conclude that female midcycle total testosterone or free testosterone is indexing some unobserved event that affects the frequency of intercourse of couples. We speculate that this event affects the motivation of females, which influences the set point of the compromise frequency characteristic of couples.Research supported in part by NICHD Grant No. 1-R01-HDO7454-01.  相似文献   
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The prototypical cutaneous manifestations of human parvovirus B19 (B19) infection include a petechial eruption in a glove and stocking distribution, reticular truncal erythema, and the "slapped cheek" sign. An association with connective tissue disease (CTD) stigmata has recently been made. The clinical and dermatopathologic findings in 14 patients whose skin lesions were accompanied by serological evidence of B19 infection or documentation of B19 genome in lesional skin are presented. The authors encountered skin biopsy specimens from 14 patients who presented with skin eruptions accompanied by clinical signs or serology suggestive of antecedent B19 infection. Clinical findings were correlated to the light microscopic appearance of the lesions and the presence of B19 genome in lesional skin. The study group comprised 9 women, 3 men, and 2 boys. Eruptions characteristic of fifth disease, including the slapped cheek sign, reticulated truncal erythema, and acral petechiae, were present in 3 patients, 1 of whom later developed granuloma annulare. The other patients had atypical clinical presentations comprising an asymptomatic papular eruption (2), an eruption clinically resembling Sweet's syndrome (3), myopathic dermatomyositis (DM) (2), lupus erythematosus (LE)-like syndromes (2), and lower-extremity palpable purpura (2). Skin biopsy specimens in 12 cases showed interstitial histiocytic infiltrates with piecemeal fragmentation of collagen and a mononuclear cell-predominant vascular injury pattern. Other features included an interface dermatitis, eczematous alterations, and papillary dermal edema. Lesions with features of DM or LE also showed mesenchymal mucinosis, whereas a biopsied lesion of palpable purpura showed leukocytoclastic vasculitis (LCV). Immunofluorescent testing showed a positive lupus band test (LBT) with epidermal IgG and C5b-9 decoration in 1 patient with a systemic LE-like illness, whereas the DM patients had negative LBTs and vascular C5b-9 deposition typical for DM. Skin biopsy specimens from 11 patients, including those whose presentations resembled LE and DM, were positive for B19 genome. The dermatopathology of B19 infection suggests tissue injury mediated by delayed-type hypersensitivity, by antibody-dependent cellular immunity directed at microbial antigenic targets in the epidermis and endothelium, and by circulating immune complexes in the setting of LCV. These mechanisms appear to generate a clinical and histopathological picture that recapitulates that of CTD.  相似文献   
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In order to identify T cell epitopes within the Mycobacterium leprae 45-kD serine-rich antigen, we analysed responses to overlapping 17-mer peptides encompassing the whole antigen in non-exposed UK controls, Pakistani leprosy patients and tuberculosis patients in both the United Kingdom and Pakistan. This antigen has been described as M. leprae-specific, although it has a hypothetical homologue in M. tuberculosis. Human peripheral blood mononuclear cells were stimulated with peptide for 5 days and IFN-gamma measured in supernatants by ELISA. Some peptides were recognized more frequently by T cells from tuberculoid leprosy patients than those from UK controls, suggesting that such T cell epitopes might have diagnostic potential, while other peptides induced greater responses among UK control subjects. Short-term cell lines confirmed that these assays detected specific T cell recognition of these peptides. However, many tuberculosis patients also recognized these potentially specific peptides suggesting that there could be a true homologue present in M. tuberculosis.  相似文献   
5.
BackgroundWe compared cord blood antibody titers in unvaccinated pregnant women to those vaccinated with seasonal influenza vaccine during the 2nd and the 3rd trimesters.MethodsPregnant women had cord blood collected at delivery for hemagglutination inhibition assay against vaccine reference viruses: A/California/07/2009 (H1N1)pdm09, A/Switzerland/9715293/2013 (H3N2), and B/Phuket/3073/2013 (Yamagata lineage). Geometric mean titer (GMT) ratios were calculated comparing vaccinated versus unvaccinated pregnant women, and women vaccinated in the 2nd and the 3rd trimesters. Proportions of women achieving defined titers were compared using the χ2 test.ResultsOf 307 women, 190 (62%) were unvaccinated. Fifty and 67 were vaccinated during the 2nd and the 3rd trimesters, respectively. Median enrollment age was 29 years (interquartile range 24–34). Sixteen (5%) women had pre-existing conditions, but none were immunocompromised. GMT ratios comparing vaccinated and unvaccinated women were 5.90 (95% confidence interval [CI] 5.06–6.96) for influenza A/California, 5.39 (95% CI 4.18–6.08) for influenza A/Switzerland, and 5.05 (95% CI 4.43–5.85) for influenza B/Phuket. Similarly, the GMT ratios comparing the 3rd and the 2nd trimester vaccinated women were 2.90 (95% CI 2.54–3.39), 2.82 (95% CI 2.56–3.13), and 2.83 (95% CI 2.56–3.14), respectively. The proportions of women with defined titers for the three vaccine reference viruses did not differ between 2nd and 3rd trimester vaccinated women (titers ≥40: 68–92% versus 70–93%; ≥110: 32% versus 33–63%; and ≥330: 4–10% versus 3–21%).ConclusionsPregnant women vaccinated against influenza had more placental transfer of influenza antibodies to their infants than unvaccinated women. Placental transfer of antibodies was higher among those vaccinated in the 3rd trimester than in the 2nd trimester. There was no difference in the proportions of women achieving antibody titers corresponding to protection against influenza in children. Findings support the current World Health Organization’s recommendation that pregnant women may be vaccinated in either 2nd or 3rd trimester of pregnancy.  相似文献   
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Epstein-Barr virus (EBV)-associated gastric cancer (EBVaGC) cells originate from a single-cell clone infected with EBV. However, more than 95% of patients with gastric cancer have a history of Helicobacter pylori (H. pylori) infection, and H. pylori is a major causative agent of gastric cancer. Therefore, it has long been argued that H. pylori infection may affect the development of EBVaGC, a subtype of gastric cancer. Atrophic gastrointestinal inflammation, a symptom of H. pylori infection, is observed in the gastric mucosa of EBVaGC. Therefore, it remains unclear whether H. pylori infection is a cofactor for gastric carcinogenesis caused by EBV infection or whether H. pylori and EBV infections act independently on gastric cancer formation. It has been reported that EBV infection assists in the onco-genesis of gastric cancer caused by H. pylori infection. In contrast, several studies have reported that H. pylori infection accelerates tumorigenesis initiated by EBV infection. By reviewing both clinical epidemiological and experimental data, we reorganized the role of H. pylori and EBV infections in gastric cancer formation.  相似文献   
10.
Familial atrial fibrillation is a genetically heterogeneous disorder   总被引:14,自引:0,他引:14  
OBJECTIVES: The aims of this study were to identify and characterize familial cases of atrial fibrillation (AF) in our clinical practice and to determine whether AF is genetically heterogeneous. BACKGROUND: Atrial fibrillation is not generally regarded as a heritable disorder, yet a genetic locus for familial AF was previously mapped to chromosome 10. METHODS: Of 2,610 patients seen in our arrhythmia clinic during an 18-month study period, 914 (35%) were diagnosed with AF. Familial cases were identified by history and medical records review. Four multi-generation families with autosomal dominant AF (FAF 1 to 4) were tested for linkage to the chromosome 10 AF locus. RESULTS: Fifty probands (5% of all AF patients; 15% of lone AF patients) were identified with lone AF (age 41 +/- 9 years) and a positive family history (1 to 9 additional relatives affected). In FAF 1 to 3, AF was associated with rapid ventricular response. In contrast, AF in FAF-4 was associated with a slow ventricular response and, with progression of the disease, junctional rhythm and cardiomyopathy. Genotyping of FAF 1 to 4 with deoxyribonucleic acid markers spanning the chromosome 10q22-q24 region excluded linkage of AF to this locus. In FAF-4, linkage was also excluded to the chromosome 3p22-p25 and lamin A/C loci associated with familial AF, conduction system disease, and dilated cardiomyopathy. CONCLUSIONS: Familial AF is more common than previously recognized, highlighting the importance of genetics in disease pathogenesis. In four families with AF, we have excluded linkage to chromosome 10q22-q24, establishing that at least two disease genes are responsible for this disorder.  相似文献   
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