Fat Distribution and Lipid Profile of Young Adults with Congenital Adrenal Hyperplasia Due to 21-Hydroxylase Enzyme Deficiency

We aimed to compare detailed fat distribution and lipid profile between young adults with congenital adrenal hyperplasia due to 21-hydroxylase enzyme deficiency and a control group. We also verified independent associations of treatment duration and daily hydrocortisone dose equivalent (HDE) with lipid profile within patients. This case–control study included 23 patients (7 male and 16 female) matched by an age range of young adults (18–31 years) with 20 control subjects (8 male and 12 female). Dual energy X-ray absorptiometry was used to measure the fat distribution. Male patients demonstrated elevated indices of fat mass for total (7.7 ± 2.1 vs. 4.5 ± 1.3 kg/m², p = 0.003), trunk (4.0 ± 1.2 vs. 2.2 ± 0.8 kg/m², p = 0.005), android (0.63 ± 0.24 vs. 0.32 ± 0.15 kg/m², p = 0.008), gynoid (1.34 ± 0.43 vs. 0.74 ± 0.24 kg/m², p = 0.005), arm (0.65 ± 0.16 vs. 0.39 ± 0.10 kg/m², p = 0.009), and leg regions (2.7 ± 0.8 vs. 1.6 ± 0.4 kg/m², p = 0.005) than the control group, but not in females. However, female patients demonstrated elevated ratio of low-density lipoprotein cholesterol to high-density lipoprotein cholesterol (1.90 ± 0.46 vs. 1.39 ± 0.47, p = 0.009) than the control group, but not in males. Total fat mass was inversely correlated with total testosterone (r = −0.64, p = 0.014) and positively correlated with leptin in males (r = 0.75, p = 0.002). An elevated daily HDE (β = 0.43, p = 0.038 and β = 0.47, p = 0.033) and trunk to total fat mass ratio (β = 0.46, p = 0.025, and β = 0.45, p = 0.037) were independently correlated with impaired lipid profile markers. Although there is no altered lipid profile, male patients demonstrated an increased fat distribution. However, female patients presented with an impaired lipid profile marker but demonstrated close values of normal fat distribution. Interestingly, the dose of glucocorticoid therapy can have some role in the lipid mechanisms.     

Study of a BGO calorimeter using electron and hadron beams from 1 to 50 GeV

A calorimeter of 25 bismuth germanate (BGO) crystals equipped with silicon photodiode readout has been tested at the CERN SPS in the energy range 1–50 GeV. The response for electrons has been shown to be linear in this energy range and the rms resolution obtained ( ) is approximately 1%, for E > 4 GeV. The electron/pion separation was found to be better than 1:500 in the energy range 1–20 GeV. Data on lateral and longitudinal shower development were compared with the results of a Monte Carlo simulation using the SLAC-EGS program and found to be in good agreement.     

Combined time and wavelength multiplexing technique of optical fiber grating sensor arrays using commercial OTDR equipment

The use of a commercial optical time domain reflectometry device for simultaneous wavelength and time domain multiplexing of fiber-optic Bragg grating sensors is proposed and demonstrated. The realization of such systems provides an inexpensive way of interrogating several hundreds of sensors in a single fiber. Strain resolution of 30 /spl mu/m/m over a strain measuring range of 0.5% was obtained.     

Tensile and flexural creep rupture tests on partially-damaged concrete specimens

Three series of novel tensile and flexural creep tests on partially-damaged concrete specimens were carried out in order to gain some insight into creep crack growth and failure of strain-softening materials. In the tests, each specimen was initially loaded to a given point in the descending branch and thus had a lower load-carrying capacity than that at the peak-point. Then, the specimen was unloaded and reloaded to sustain a load which was from 70% to 95% of its current load-carrying capacity. Experimental creep curves display a three-stage process, consisting of primary, secondary and tertiary stages, with a decreasing, constant and increasing creep rate, respectively. The secondary stage dominates the whole failure lifetime, whereas both the secondary and tertiary stages are important in terms of creep deformation. Failure life-time seems to be more sensitive to the change of load level in flexural tests rather than in tensile tests. The decrease in load-carrying capacity due to damage tends to result in a shorter failure lifetime and a lower critical load level for creep rupture. The descending branch of the static load-deflection or load-CMOD curve may be used as an envelope criterion for creep fracture.     

Gag rules and trade secrets in managed care contracts. Ethical and legal concerns

Gag rules-clauses in managed care contracts that prevent physicians from disclosing information that the plan may find disparaging, but that could relate directly to the patient's health-have recently been the subject of ethical condemnation and legislative prohibition. Another serious problem in managed care contracts, trade secrets, or guidelines and quality assurance mechanisms that are imposed on physicians while their origins are shrouded in proprietary secrecy, have by contrast received little attention. Responses to these ethical challenges to the physician's integrity must involve individual physicians, managed care organizations, professional organizations, and public policymakers.     

V antigen-polyhistidine fusion peptide: binding to LcrH and active immunity against plague

The structural gene for V antigen (lcrV) is known to be encoded within the lcrGVH-yopBD operon of the approximately 70-kb low-calcium-response or Lcr plasmid of Yersinia pestis. This 37-kDa monomeric peptide was reported to provide active immunity in mice, suppress inflammatory cytokines, and regulate expression of the low calcium response (Lcr+). Here we describe pVHB62, encoding a polyhistidine-V antigen fusion peptide (Vh) and linked LcrH. Vh underwent degradation from both the C terminus and N terminus during classical chromatographic fractionation but remained intact within two compartments during Ni2+ affinity chromatography. The first was homogeneous, capable of active immunization (mouse intravenous 50% lethal dose, > 10(7) bacteria), and stable at 4 degrees C. The second remained bound to the affinity column but could be eluted as a mixture of Vh, LcrH, and low-molecular-weight material by application of 6 M guanidine HCl. This mixture was dialyzed, denatured in 8 M urea, and again applied to the affinity column, which then hound Vh but not LcrH. The latter was recovered and renatured, and low-molecular-weight material was removed by biochemical fractionation. The resulting homogeneous LcrH bound protein AN antigen fusion peptide but not protein A in a sandwich enzyme-linked immunosorbent assay, and this reaction was inhibited by Vh. These observations indicate that LcrH normally binds V antigen in bacterial cytoplasm and suggest that only free LcrH down-regulates expression of the low calcium response.     

Microsatellite loci for stringless bees

What ethical concerns regarding the application of new antidementia compounds are pertinent to the best interests of patients with Alzheimer's disease and their caregivers? Based on collected preliminary anecdotal accounts, these concerns are important and should be considered carefully by clinicians, researchers, and families.     

Differential class III and glibenclamide effects on action potential duration in guinea-pig papillary muscle during normoxia and hypoxia/ischaemia

1. Microelectrode recording techniques were used to study the effects of several potassium channel blockers which are considered to be Class III antiarrhythmic compounds. The effects of (+)-sotalol, UK-66,914, UK-68,798 and E-4031 on action potential duration (APD) were determined in guinea-pig isolated papillary muscles. The compounds were evaluated under normoxic or hypoxic/ischaemic conditions at 36.5 degrees C and compared to glibenclamide, which is considered to be a blocker of ATP-dependent potassium channels. Prolongation of action potential duration at 90% repolarization (APD90) was taken as an indirect measure of potassium channel blockade. 2. Under normoxic conditions, the Class III compounds prolonged APD in a concentration-dependent manner. According to EC15 values, the order of potency of the Class III compounds was found to be UK-68,798 > E-4031 > UK-66,914 > (+)-sotalol. Glibenclamide did not significantly prolong APD90 under normoxic conditions. 3. Perfusion with an experimental hypoxic or ischaemic bathing solution produced qualitatively similar effects on action potentials. Over a period of 20-25 min in either of the experimental solutions, there was a small decrease in action potential amplitude (APA) and a prominent shortening of APD. The ischaemic solution also depolarized the resting membrane potential by about 15 mV. 4. (+)-Sotalol and UK-66,914 did not reverse the shortening of APD induced by perfusion with hypoxic Krebs solution. High concentrations of glibenclamide (10 microM) and UK-68,798 (30 and 60 microM) partially reversed the hypoxia-shortened APD. Glibenclamide was more potent and exhibited a greater time-dependent action than UK-68,798. 5. During experimental ischaemia, the Class III compound E-4031 (10 microM, n = 7) produced small, but significant, increases in the APD90 (11 +/-3 ms after 20 min) which were not clearly time-dependent(14 +/- 4 ms after 30 min). UK-68,798 (10 microM) also produced a small, but insignificant, increase in APD90(12 =/-6 ms at 20 min, n = 4). Higher concentrations of UK-68,798 (30 and 60 microM, n = 4) did not produce a consistently significant increase in APD90 during ischaemia: significance was only attained after 20 min in the presence of 60 microM UK-68,798 (24 +/- 12 ms). However, in marked contrast to the effects of the Class III compounds, glibenclamide (10 microM) produced large time-dependent increases in ischaemic APD90 (34 +/- 11 ms at 7 min, n = 9) which were significant 15 min or more after drug addition(52 +/- 12 ms at 20 min, n = 7; 74 +/- 5 ms at 30 min, n = 6).6. The present microelectrode data suggest that blockers of ATP-dependent potassium channels, such as glibenclamide, might prove to be more effective than Class III compounds against ischaemia-induced shortening of cardiac action potentials.     

The gene encoding human glutathione synthetase (GSS) maps to the long arm of chromosome 20 at band 11.2

Two forms of glutathione synthetase deficiency have been described. While one form is mild, causing hemolytic anemia, the other more severe form causes 5-oxo-prolinuria with secondary neurological involvement. Despite the existence of two deficiency phenotypes, Southern blots hybridized with a glutathione synthetase cDNA suggest that there is a single glutathione synthetase gene in the human genome. Analysis of somatic cell hybrids showed the human glutathione synthetase gene (GSS) to be located on chromosome 20, and this assignment has been refined to subband 20q11.2 using in situ hybridization.