Total colpocleisis for vaginal eversion

OBJECTIVE: This report describes a technique for total colpocleisis performed on women with posthysterectomy vaginal eversion and presents the outcome of this surgery. STUDY DESIGN: Thirty-three women, aged 51 to 94 years (78.1 +/- 8.8, average +/- SD) with vaginal eversion were treated with total colpocleisis. Twenty-four women had previously undergone a total of 40 operations for prolapse, and many had a massive prolapse with scarring and ulceration. Five women had stress incontinence, and an additional 12 had poor urethral support without stress incontinence. In association with colpocleisis, 14 had suburethral plication of the endopelvic fascia; two, needle suspensions; and one, a pubovaginal sling. Three had a perineorrhaphy. RESULTS: Operations lasted from 30 to 205 minutes (101 +/- 33.4, average +/- SD), and the estimated blood loss ranged from 20 to 750 ml (206 +/- 171, average +/- SD). No operative complications occurred. Postoperatively, congestive heart failure developed in two women and one had pneumonia; all illnesses resolved with appropriate therapy. There were no complications at the operative site. Average follow-up was 35 (+/-48) months. All women were initially cured of the vaginal eversion. Recurrent eversion developed in one woman 1 year after surgery and was successfully treated with repeat colpocleisis. Of five women with preoperative stress incontinence, four were cured and one lost to follow-up. No new stress incontinence occurred. CONCLUSION: Total colpocleisis is an effective operation for the treatment of vaginal eversion in selected situations. When defective urethral support is corrected at the time of the operation, postoperative incontinence is not usually a problem.     

Noise, physiology, and human performance: the potential role of effort

The equine fetlock joint cavity shows ten pouches. The dorsal recess, which is oriented to the proximal side, is separated from those three pouches, which show to the distal direction, by several capsular folds. These folds are documented by means of sagittal sections through the fetlock joint. A medial/lateral recess is covered by the deep part of the collateral ligament of the fetlock joint. The collateral ligaments as well as the sesamoidean collateral ligaments are closely connected with the joint capsule, from which two capsular folds are separated. Between the part of the sesamoidean collateral ligament, that inserts to the metacarpus/metatarsus and the part that inserts to the proximal phalanx, the fetlock joint cavity pouches as Recessus palmaris/plantaris distalis medialis/lateralis. The palmar/plantar distal pouch, which lies in the median line, is covered by the Ligamentum sesamoideum rectum. This recess is narrowed down by the cruciated sesamoidean ligaments. The dominant palmar/plantar proximal recess is subdivided into several small pouches by strings or bands of the joint capsule, which can already be seen with an unaided eye.     

The effect of attentional spread on spatial resolution

The effects of attentional spread were studied by having subjects detect a luminance increment along a row of evenly spaced dots. The increment could occur for the central, fixated dot (Narrow Attention) or for either the fixation dot or one of the four dots to its left or right (Broad Attention). Narrow Attention enhanced the detection of luminance increments for the fixated dot, and also enhanced spatial resolution near the fixation dot for judgments of vernier alignment and separation. This indicated that the sensitivity of small spatial filters in the fovea was increased more by narrowly focused than broadly spread attention. Effects of attentional spread on spatial resolution were not obtained for judgments of the separation between two peripherally located targets, perhaps because of their dependence on eccentricity (position) rather than separation.     

Endothelin-1 levels in induced sputum samples from asthmatic and normal subjects

BACKGROUND: Endothelin-1 (ET-1) is a potent bronchoconstrictor which may have a role in the pathogenesis of asthma. The levels of ET-1 in saliva, induced sputum, and plasma from asthmatic and non-asthmatic subjects were compared. METHODS: Sputum induction was performed on 28 asthmatic subjects and nine normal volunteers. ET-1 levels were measured in plasma, saliva, and sputum samples and reversed phase high performance liquid chromatography (RP-HPLC) was performed on saliva and sputum samples. RESULTS: ET-1 was present in the following order of concentration in both normal and asthmatic subjects: saliva > sputum > plasma (saliva, median 30.1 and 23.9 pg/ ml, respectively; sputum, median 15.5 and 11.2 pg/ml; plasma, median 3.1 and 3.6 pg/ ml). There were no differences between asthmatic and normal subjects in the levels of ET-1 in each fluid. The levels of ET-1 in asthmatic subjects were not influenced by whether or not they were taking inhaled steroids. RP-HPLC of sputum and saliva confirmed the presence of ET-1 in these fluids. CONCLUSIONS: Levels of ET-1 can be measured in saliva and sputum obtained by sputum induction in asthmatic and healthy subjects and, although no difference was found in basal levels of ET-1 in sputum, saliva and plasma between normal subjects and asthmatics without bronchoconstriction, it is apparent that ET-1 is produced or released locally within the respiratory tract in concentrations higher than those in plasma.     

Double window multi-user detection for asynchronous DS-CDMA

One-shot (window) detection allows multi-user detection schemes to operate symbol by symbol in asynchronous systems and retain near-far resistance. A novel technique, double window detection, is presented, which significantly outperforms single window detection, especially for decorrelating receivers. Results for decorrelation and MMSE detection, using both windowing types are presented     

Heart transplant coronary artery disease detected by coronary angiography: a multiinstitutional study of preoperative donor and recipient risk factors. Cardiac Transplant Research Database

BACKGROUND: Controversy exists regarding donor and recipient factors that promote the development and progression of coronary artery disease after heart transplantation and the likelihood of coronary artery disease causing death or retransplantation. METHODS: To investigate this issue in a large cohort of patients, we analyzed 5963 postoperative angiograms performed in 2609 of the 3837 patients undergoing heart transplantation at 39 institutions between January 1990 and December 1994. Coronary artery disease was classified as mild, moderate, or severe on the basis of left main involvement, primary vessel stenoses, and branch stenoses. Coronary artery disease was considered severe if left main stenosis was > 70% or 2 or more primary vessels stenoses were > 70% or branch stenoses were > 70% in all 3 systems. RESULTS: By the end of 5 years after heart transplantation, coronary artery disease was present in 42% of the patients, mild in 27%, moderate in 8%, and severe in 7%. Coronary artery disease-related events (death or retransplantation) had an actuarial incidence of 7% at 5 years and occurred in 2 of 3 of the patients with development of angiographically severe coronary artery disease. By multivariable logistic analysis, risk factors for donor coronary artery disease included older donor age (P < .0001) and donor hypertension (P=.0002). By multivariable analysis in the hazard function domain, risk factors identified for the earlier onset of allograft coronary artery disease included older donor age (P < .0001 ), donor male sex (P=.0006), donor hypertension (P=.07), recipient male sex (P=.02), and recipient black race (P=.01). The actuarial incidence of severe coronary artery disease was 9% at 5 years. CONCLUSIONS: Angiographic coronary artery disease is very common after heart transplantation, occurring in approximately 42% of the patients by 5 years. Older donor age, donor hypertension, and male donor or recipient predict earlier onset of angiographic allograft coronary artery disease. Although severe angiographic allograft coronary artery disease occurs in only 7% of the patients at 5 years, its presence is highly predictive of subsequent coronary artery disease-related events or retransplantation.     

Atypical protein kinase C isozyme zeta mediates carbachol-stimulated insulin secretion in RINm5F cells

Carbachol-stimulated insulin release in the RINm5F cell is associated with elevation of the cytosolic Ca2+ concentration ([Ca2+]i) through mobilization of Ca2+ from thapsigargin-sensitive intracellular stores and with the generation of diacylglycerol (DAG). Thus carbachol activates phospholipase C, and this was thought to be the means by which it stimulates insulin secretion. However, when the elevation of [Ca2+]i was blocked by thapsigargin, the effect of carbachol to stimulate insulin release was unchanged. Thus the effect of carbachol to increase [Ca2+]i was dissociated from the stimulation of release. When the role of protein kinase C (PKC) was examined, carbachol-stimulated insulin release was found to be unaffected by phorbol ester-induced downregulation of PKC, using 12-O-tetradecanoylphorbol-13-acetate (TPA), and by the PKC inhibitors staurosporine, bisindolylmaleimide, and 1-O-hexadecyl-2-O-methylglycerol (AMG-C16). These treatments abolished the stimulation of release by TPA. Thus the carbachol activation of PKC appeared also to be dissociated from the stimulation of insulin release. However, when the activation of several different PKC isozymes was studied, an atypical PKC isozyme, zeta, was found to be translocated by carbachol. By Western blotting analysis, carbachol selectively translocated the conventional PKC isozymes alpha and beta (the activation of which is dependent on Ca2+ and DAG) from the cytosol to the membrane. Carbachol also translocated the atypical PKC isozyme zeta, which is insensitive to Ca2+, DAG, and phorbol esters. The PKC inhibitors staurosporine, bisindolylmaleimide, and AMG-C16 blocked the stimulated translocation of PKC-alpha and -beta, but not that of PKC-zeta. Prolonged treatment of the cells with TPA downregulated PKC-alpha and -beta, but not PKC-zeta. Under all these conditions, carbachol-stimulated insulin release was unaffected. However, a pseudosubstrate peptide inhibitor specific for PKC-zeta inhibited the translocation of PKC-zeta and 70% of the carbachol-stimulated insulin secretion. The data indicate that carbachol-stimulated insulin release in RINm5F cells is mediated to a large degree by the activation of the atypical PKC isozyme zeta.     

Method for reduction of inhibition in a Mycobacterium tuberculosis-specific ligase chain reaction DNA amplification assay

The present study describes the identification of inhibitors of a Mycobacterium tuberculosis-specific gap ligase chain reaction (LCR) DNA amplification assay as well as a method for their removal. A major contributor to inhibition was deduced to be a calcium phosphate precipitate, CaHPO4. The precipitate forms during N-acetyl-L-cysteine-sodium hydroxide (NALC-NaOH) decontamination, digestion, and concentration of respiratory specimens. The solubility product of CaHPO4 precipitate at pH 7.8, the pH at which gap LCR is optimized, indicates that the precipitate releases an amount of phosphate ions sufficient to inhibit amplification. A method for removal of the precipitate was identified. The precipitate is dissociated by exposing it to a mildly acidic (pH 4.1) buffer during the first of two centrifugation steps; the inhibitory phosphate ions are removed by the centrifugation steps. When 100 NALC-NaOH respiratory sediments were tested by gap LCR, none of the sediments were inhibitory when the acidic buffer was used while 24 samples were inhibitory when TE buffer, pH 7.8, was used. In another study, when the acidic buffer wash was applied to 1,440 NALC-NaOH respiratory sediments, only 10 sediments were found to be inhibitory. None of the inhibited sediments were culture positive for M. tuberculosis. This work demonstrates that when inhibition mechanisms are identified, relatively simple protocols can be used to obtain low inhibition rates and to allow the use of larger volume equivalents in amplification reactions.