COPD burden on sexual well-being.

BACKGROUND: Sexual function is often affected in patients suffering from chronic diseases especially chronic obstructive pulmonary disease (COPD). However, the effect of COPD on sexual satisfaction is underappreciated in clinical practice. The aim of this study is to evaluate the impact of COPD on patient's sexuality and the explanatory variables of sexual dissatisfaction. METHODS: Questionnaires were emailed to participants and they submitted their responses on the Santé Respiratoire France website. Data about sexual well-being (Arizona Sexual Experience Scale, ASEX), Quality of life (VQ11), anxiety, depression (Hospitalized anxiety and depression, HAD) and self-declared COPD grade were collected. RESULTS: Seven hundred and fifty one subjects were included and were characterized as follows: women-51%, mean age-61 years, in a couple-62% and 70%-retired. Every grade of COPD was represented. Out of 751 participants, 301 participants (40%) had no sexual activity and 450 (60%) had sexual activity. From the 450 participants, 60% needed to change their sexual life because of their disease (rhythm, frequency and position). Subjects often used medications to improve sexual performance (43% used short-acting bronchodilator and 13% -specific erectile dysfunction drugs). ASEX questionnaire confirmed patients' dissatisfaction (diminution of sexual appetite for 68% and sexual desire for 60%) because of breathlessness and fatigue. Eighty one percent of the responders had an altered quality of life (VQ11 mean score 35) and frequent suspected anxiety or depression (HAD mean score 10.8). Ninety percent declared that sexual dysfunction had never been discussed by their doctors, while 36% of patients would have preferred to undergo a specialized consultation. CONCLUSION: Sexual dysfunction is frequent among COPD patients and leads to an altered well-being, however being a cultural taboo, it remains frequently neglected. Sexual guidance should be a part of patient's consultations improve quality of sexual life.

Recombinant anti-botulinum neurotoxin A single-chain variable fragment antibody generated using a phage display system.

A recombinant single-chain fragment variable antibody (scFv) to botulinum A neurotoxin (BoNT/A) was developed. BALB/C mice were immunized with BoNT/A. Splenomic RNA was isolated from the hyperimmune mice and used to prepare a cDNA library, from which the variable regions of the heavy and light chain antibody genes were generated and connected by a DNA linker. The resulting scFv genes were cloned into the phagemid vector pCANTAB5 in order to construct phage display scFv libraries. Individual anti-BoNT/A phage clones were isolated from the phage display libraries by immunoaffinity selection using immobilized BoNT/A and further evaluated by enzyme-linked immunosorbant assay, immunoprecipitation and Western blotting. Forty-eight clones were found to be BoNT/A-reactive. The most reactive clone, designated D12, was selected for further study. The scFv gene of D12 was subcloned into a Pichia pastoris vector, and expression in yeast was evaluated.

Capsulolabral augmentation increases glenohumeral stability in the cadaver shoulder.

Multidirectional instability is not clearly understood. Excessive capsular laxity has been proposed as the key component. However, because ligaments fail to resist humeral head translation until they are tensioned, glenohumeral instability in the mid range of motion cannot be explained by capsuloligamentous pathology alone. Capsulolabral augmentation is designed to increase glenohumeral stability by 2 separate mechanisms: deepening the glenoid concavity and reducing capsular laxity. This is accomplished by shifting the capsule to buttress the glenoid labrum. Hence, the glenolabral concavity in which the humeral head is stabilized by compression throughout the entire range is enhanced. The purposes of this study were to examine glenolabral depth and glenohumeral stability before and after labral augmentation and to measure the effect of diminished capsular laxity on motion in clinically important positions. We compared glenolabral depth, resistance to humeral head displacement, and glenohumeral range of motion before and after capsulolabral augmentation. Glenolabral depth was measured as the lateral displacement of the center of the humeral head translating from the glenoid fossa. We recorded a mean increase in glenoid depth of 1.9 mm inferiorly, 2.0 mm posteroinferiorly, and 0.9 mm posteriorly (P <.02). Resistance to humeral head displacement was measured by use of the stability ratio, defined as the translatory force required to displace the humeral head divided by the force compressing the humeral head into the glenoid fossa. The mean stability ratio was increased by 0.24 inferiorly and 0.24 posteroinferiorly (P <.02). Motion was measured by achieving 30 degrees and 60 degrees elevation in the 0 degrees, 30 degrees, 60 degrees, and 90 degrees planes of elevation and measuring the extent of possible internal rotation for each of these 8 positions when the capsule was tensioned to exert 1000 N-mm of torque. Reduction of internal rotation in these positions was a mean of 15 degrees at 1000 N-mm of torque. This study demonstrates that humeral head stability within the glenolabral fossa is increased by local capsular augmentation. A simultaneous reduction in capsular laxity is achieved, which partially limits glenohumeral motion. Understanding the biomechanical effect of this procedure helps the physician to establish surgical goals and to explain to patients the rationale of why this procedure may be clinically efficacious.

Cultured lung epithelium: A cellular model for lung preservation.

Cellular models have helped with the development of conditions needed for hypothermic preservation of kidney, liver, and heart. Recently, highly differentiated cultured lung epithelial cell lines grown with basolateral side feeding technique have become available that can mimic airspace, epithelium, and interstitium of lung parenchyma. Cultured lung epithelium coupled with Ussing's short-circuit current technique was used as a cellular model system for lung preservation. A parametric study was conducted to correlate the effects of luminal fluid composition (University of Wisconsin (UW) solution and phosphate-buffered saline) and storage gas (air vs nitrogen) at 4 degrees C for 24 h on postischemic electrogenic properties (transepithelial ion transport and resistance). The results showed that cells were better preserved with the UW solution on both sides as measured by their transepithelial resistance, an indicator of tight junction integrity (Rte approximately 65% of control values approximately 135 Omega cm2). In addition, they responded better to mediators that stimulate chloride secretion than cells preserved with other conditions. Cells preserved with no additional fluid on the apical side had substantially lowered Rte (<20%) than those preserved with an additional thin layer of fluid ( approximately 35-65%). This cellular model system is a realistic representation of lung epithelium and can provide an accurate assessment of preservation quality through the measurements of tight junction integrity and active ion transport.

Serological reactivity to a synthetic analog of phenolic glycolipid I and early detection of leprosy in an area of low endemicity.

A total of 23,863 individuals living in an area of low endemicity for leprosy were tested by enzyme-linked immunosorbent assay with a semisynthetic analogue of the phenolic glycolipid I antigen of Mycobacterium leprae. The proportion found positive was 3.86% which was significantly higher than that in a sample of a population known to be free of leprosy. Clinical examinations as well as Mitsuda and skin smear tests were organized for those defined as seropositive. The proportion of individuals with lepromin reactions of less than 3 mm increased 18.9% per serological interval as antibodies rose though it was not statistically significant. As a result of the clinical and bacteriological examinations, 2 cases with clinical signs and heavy bacillary load were found, whereas acid-fast bacilli were demonstrated in 2 other individuals without clinical manifestations of leprosy. The usefulness of the system for control purposes is discussed.

Radiotracer studies of cystic fibrosis transmembrane conductance regulator expressed in Xenopus oocytes.

We measured fluxes of radiotracers in Xenopus oocytes expressing the cystic fibrosis transmembrane conductance regulator (CFTR). Addition of adenosine 3',5'-cyclic monophosphate (cAMP)-elevating agents [forskolin and 3-isobutyl-1-methylxanthine (I/F)] led to large increases in uptake of 36Cl, 125I, and 82Br into oocytes expressing wild-type CFTR or delta F508 CFTR but not sham-injected oocytes. I/F also stimulated halide efflux from CFTR and delta F508 oocytes in the sequence Cl > Br > I. cAMP-induced increases in 36Cl efflux from delta F508 oocytes were approximately 20% of those in CFTR oocytes. Increases in halide efflux were blocked by diphenylamine-2-carboxylic acid but not by 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid. The phorbol ester, phorbol 12-myristate 13-acetate, also stimulated 36Cl efflux from CFTR oocytes. ATP uptakes into CFTR and sham oocytes were similar, and both were reduced by I/F. However, ATP uptake into I/F-treated CFTR oocytes was slightly greater (approximately 40%) than into I/F-treated sham oocytes. Urea uptake into CFTR and sham oocytes was similar and in both cases was increased by I/F. However, the I/F-induced increase in urea uptake into CFTR oocytes was significantly greater than for sham oocytes. I/F stimulated formate uptake into CFTR oocytes but not into sham oocytes. Fluxes of 22Na, 86Rb, 35SO4, 32PO4, and mannitol were unaltered by expression and activation of CFTR.

Hemophilia A carrier detection by restriction fragment length polymorphism analysis and discriminant analysis based on ELISA of factor VIII and vWf.

We performed carrier determination on female subjects from 32 hemophilia A kindreds with a combination of restriction fragment length polymorphism analysis and discriminant analysis of factor VIII antigen and von Willebrand factor antigen analyzed by enzyme-linked immunosorbent assay. Subjects included 25 obligate carriers, 30 at-risk female subjects from 19 kindreds each with two or more male subjects, with hemophilia and 28 at-risk female subjects from 13 kindreds each with a single sporadic case. Deoxyribonucleic acid (DNA) analysis with factor VIII intragenic probes clarified the carrier status of 15 female subjects, and extragenic probes classified an additional 14. Discriminant analysis, which identified 24 of 25 (96%) obligate carriers with carrier probabilities greater than or equal to 0.71 and 37 of 39 (95.0%) normal female subjects with probabilities less than or equal to 0.30, was useful for clarifying the carrier status of the female subjects who were not helped by DNA analysis and those that were classified by extragenic probes alone. Twenty-nine female subjects could not be categorized by restriction fragment length polymorphism analysis because DNA was unavailable from the subject or from key family members, key female subjects were noninformative, or carriership could not be excluded by restriction fragment length polymorphism in kindreds with sporadic cases. We studied 28 of these female subjects by discriminant analysis; 15 had carrier probabilities of greater than or equal to 0.71, 12 less than or equal to 0.30, and 1 = 0.35. All carriers by extragenic probes had carrier probability values greater than or equal to 0.71, whereas all noncarriers had values less than or equal to 0.30. In some families, particularly those in which gonadal mosaicism was a possibility, extensive family studies together with DNA and discriminant analyses were required for clarifying the source of the mutation, and hence the carrier status of the at-risk female subjects. Thus DNA and discriminant analyses complement each other, and when combined with careful pedigree analysis, the power of carrier determination is increased in some families.