United States and Polish scientists confer on health effects of the micro-environments of housing: BCEM-PZITB symposium report.
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Biomedical subjects
Publications and source records attributed to R C Lee.
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Muscularity, or the proportion of adipose tissue-free body mass (ATFM) as skeletal muscle (SM), provides valuable body composition information, especially for age-related SM loss (i.e., sarcopenia). Limited data from elderly cadavers suggest a relatively constant SM/ATFM ratio, 0.540 +/- 0.046 for men (mean +/- SD, n = 6) and 0.489 +/- 0.049 for women (n = 7). The aim of the present study was to examine the magnitude and constancy of the SM/ATFM ratio in healthy adults. Whole-body SM and ATFM were measured using multi-scan magnetic resonance imaging. The SM/ATFM ratio was 0.528 +/- 0.036 for men (n = 139) and 0.473 +/- 0.037 for women (n = 165). Multiple regression analysis indicated that the SM/ATFM ratio was significantly influenced by sex, age, body weight, and race. The four factors explained 50% of the observed between individual variation in the SM/ATFM ratio. After adjusting for age, body weight, and race, men had a larger SM/ATFM ratio than women. Both older men and women had a lower SM/ATFM ratio than younger subjects, although the relative reduction was greater in men. After adjustment for sex, age, and body weight, there were no significant differences in the SM/ATFM ratios between Asian, Caucasian, and Hispanic subjects. In contrast, African-American subjects had a significantly greater SM/ATFM ratio than subjects in the other three groups. In addition, the SM/ATFM ratio was significantly lower in AIDS patients than corresponding values in healthy subjects.
We have measured the dynamics of extracellular matrix consolidation and strengthening by human dermal fibroblasts in hydrated collagen gels. Constraining matrix consolidation between two porous polyethylene posts held rigidly apart set up the mechanical stress which led to the formation of uniaxially oriented fibroblast-populated collagen matrices with a histology resembling a ligament. We measured the mechanical stiffness and tensile strength of these ligament equivalents (LEs) as a function of age at biweekly intervals up to 12 weeks in culture using a mechanical spectrometer customized for performing experiments under physiologic conditions. The LE load-strain curve changed as a function of LE age, increasing in stiffness and exhibiting less plastic-like behavior. At 12 weeks, LEs had acquired up to 30 times the breaking strength of 1-week-old LEs. Matrix strengthening occurred primarily through the formation of BAPN-sensitive, lysyl oxidase catalyzed crosslinks. Sulfated glycosaminoglycan (GAG) content increased monotonically with LE age, reaching levels that are characteristic of ligaments. Cells in the LEs actively incorporated [3H]proline and [35S]sulfate into the extracellular matrix. Over the first three weeks, DNA content increased rapidly but thereafter remained constant. This data represent the first documentation of strengthening kinetics for cell-assembled biopolymer gels and the results suggest that this LE tissue may be a valuable model for studying the cellular processes responsible for tissue growth, repair, and remodeling.
BACKGROUND: To report the dynamic magnetic resonance (MR) imaging findings of hepatolithiasis. METHODS: Dynamic MR images (fast spoiled gradient echo sequence with intravenous injection of gadopentate dimeglumine) and computed tomography, cholangiography, or angiography of nine patients with hepatolithiasis are analyzed. RESULTS: All affected hepatic segments showed atrophic changes and contained dilated intrahepatic ducts. These segments showed either iso- or hypointensity on T1-weighted imaging and hyperintensity on T2-weighted imaging. Preferential enhancement was noted throughout all phases of the dynamic study and persisted to delayed T1-weighted imaging in seven patients. In the last two patients, severe atrophic changes made evaluating signal intensity differences and enhancement patterns difficult. CONCLUSION: In addition to intrahepatic stones and biliary dilatation, segmental atrophy, signal intensity differences, and preferential and persistent enhancement are important MR findings of hepatolithiasis.
The renin-secreting tumor is a rare benign tumor of the kidney. It is usually detected in young hypertensive patients with high plasma renin activity and hypokalemia. We describe the magnetic resonance findings of a case of renin-secreting tumor of the kidney.
Interest in the role of electrical interactions as epigenetic regulators of wound healing had its beginnings nearly 40 years ago. Because the mechanisms of action are not understood (which obviates rational therapy), the empiric application of fields to wounds has produced mixed results. However, taken collectively, clinical trials have demonstrated some beneficial effects. Tests on soft tissues of animals have shown that electric stimulation can influence the rate of wound healing and scar strength. Natural epithelial-derived sodium currents have been discovered in the wounds of invertebrates and mammals. It is theorized that these currents may be a normal controlling factor in wound healing. Therefore, perturbation of these signals is important to understand. The purpose of this review is to put into proper perspective the biophysical, physiological, and clinical data pertaining to use of electricity to control wound healing, with the goal of minimizing much of the prevailing confusion.
Electroporation of skeletal muscle cell membranes has been postulated to cause myonecrosis in victims of major electrical trauma. To evaluate this concept we carried out a series of experiments to measure the transmembrane potential (delta Vm) threshold for skeletal muscle membrane electroporation using isolated mammalian skeletal muscle cells and compared this threshold with the expected range of delta Vm in victims of electrical trauma. Alterations in membrane Mg2+ or Ca2+ permeability in response to applied extracellular field pulses were quantified by measuring the kinetics of influx before and after field exposure. To avoid heating effects, 4-msec duration field pulses were used. The resting intracellular [Mg2+] was 0.86 +/- 0.01 mmol/l, and [Ca2+] was 0.1 +/- 0.01 microns. The delta Vm threshold for transient or stable electropore formation was determined by performing experiments over a wide range of applied fields. A delta Vm of 340 mV produced no significant change in intracellular [Mg2+]. Delta Vms ranging between 340 to 480 mV caused only a transient influx of Mg2+, indicating that spontaneous sealing of the membrane electropores occurred. A delta Vm of greater than 540 mV caused stable electropore formation. In addition, the efficacy of two surface active polymers as membrane sealing agents was tested. Either 1 mmol/L Poloxamer-188 (8.1 kDa) or 1 mmol/L neutral dextran (10.1 kDa) prevented Mg2+ influx after delta Vms greater than 540 mV (p < 0.001, n = 7). These results suggest that the fields produced in victims of electric shock are sufficient to damage cell membranes by a nonthermal mechanism and that nonionic surfactants may rapidly seal electropores.
Tuberculosis of the prostate is uncommon. Here we present a case of tuberculosis of the prostate with its MR findings.
A direct competitive enzyme-linked immunosorbent assay (ELISA) for determination of total T-2 toxin metabolites in urine was developed. The assay involves coating anti-3-acetyl-neosolaniol-hemisuccinate-bovine serum albumin conjugate (anti-3-Ac-NEOS-HS-BSA) antibody to the ELISA plate and using 3-Ac-NEOS-HS-peroxidase as the enzyme marker. Competitive ELISA revealed that the antibody had good cross-reactivity with acetyldiacetoxyscirpenol (Ac-DAS), T-2 tetraol tetraacetate, 3'-OH-Ac-T-2, 3-Ac-NEOS, and 3,4,15-triacetyl-12,13-epoxytrichothec-9-en-8-one (Ac-T-2-8-one), but less cross-reactivity with Ac-T-2 toxin and T-2 toxin. All metabolites of T-2 toxin in urine were converted to T-2 tetraol tetraacetate (T-2-4ol-4Ac) by acetylation of the sample extract before ELISA. To test the ELISA accuracy, a radioimmunoassay (RIA) was performed simultaneously. The linear portion of the standard curve of this direct ELISA for T-2-4ol-4Ac was 0.2-2.0 ng/mL, which was 10 times more sensitive than RIA. The minimum detection level for T-2-4ol-4Ac was 0.02 ng/mL (0.4 pg/assay) in the absence of urine sample. The overall analytical recoveries for T-2 toxin, HT-2, T-2-4ol, 3'-OH-HT-2, NEOS, and a mixture of these 5 toxins added to the urine samples in the ELISA at concentrations of 0.05 and 0.2 ng/mL were 87 and 94%, respectively.
A simple, rapid enzyme-linked immunoassay (ELISA) was used to evaluate the performance of each step (extraction, filtration, solvent partition, and silica gel column chromatography) of a solvent-efficient thin-layer chromatographic (TLC) method which is undergoing interlaboratory collaborative study for the determination of aflatoxin B1 in corn, raw peanuts, and peanut butter. The apparent average recoveries using the ELISA method were about 30 to 50% higher than those using the TLC method if only the amount of B1 added to the samples was used in the calculations. After the cross-reaction of the antibody with other aflatoxins added to the samples was considered, the amounts recovered approached the levels of aflatoxins added in all 3 commodities tested. With no cleanup treatment, ELISA recoveries at aflatoxin B1 levels above 7.5 ng/g were 84, 79, and 103% for corn, raw peanuts, and peanut butter, respectively. The coefficients of variation were between 5.2 and 25.2%. With each cleanup step in the TLC method, ELISA detected a progressive decrease in recovery from 150.5 to 105.3% (before correction for the presence of other aflatoxins) or from 93.5 to 65.4% (after correction for other aflatoxins) of B1 added to the samples. The ELISA data support the conclusion obtained from previous studies that cleanup treatments were not necessary in the ELISA. When large amounts of other aflatoxins are present, an understanding of the cross-reactivity of antibody with other aflatoxins in the ELISA is essential for final interpretation of the data.
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Joule heating has long been considered the principal component of tissue damage in electrical injury. Recent studies suggest electroporation, a nonthermally mediated mechanism of cell membrane damage, is also a factor. We investigated whether electroporation-mediated muscle necrosis can occur in vivo without significant Joule heating. Pulsed electric fields approximately 150 V/cm were produced in the hind limbs of anesthetized rats. In shocked limbs core muscle temperature rose less than 1.8 degrees C, yet significant damage occurred as determined by technetium-99m pyrophosphate uptake, elevated serum creatine phosphokinase, and prominent hypercontraction band degeneration of myofibers on histopathologic examination. This study is significant because it directly addresses whether nonthermal mechanisms of cell damage can cause tissue necrosis. These results indicate that electroporation effects can mediate skeletal muscle necrosis without visible thermal changes. Thus the phenomenon of "progressive recognition" may be characteristically largely explained by the occurrence of nonthermally mediated tissue damage.
Fibroblast cytomorphology is tightly coupled to phenotypic expression, particularly as it relates to extracellular matrix protein synthesis and degradation. We have observed that calcium antagonists, such as verapamil and trifluoperazine, depolymerize actin filaments and alter fibroblast cell shape from bipolar to spherical. Characteristically, the depolymerization of actin filaments, which mediates the cell shape change, turns on procollagenase gene expression in normal human skin fibroblasts. We have found the same effects of calcium antagonists on cell shape, cytoskeletal components, and induction of procollagenase in the keloid fibroblasts of three cell lines, CB792, CW792, and WT949. Rounded cells were seen in 74.8% of verapamil-treated and 86.7% of trifluoperazine-treated cells, whereas only 1.1% of the control cells were spherical. The percentage of cells that synthesized collagenase in the control, verapamil-treated, and trifluoperazine-treated groups was 3.8%, 42.8%, and 53.4%, respectively. Approximately 60% of rounded cells exhibited increased collagenase synthesis when the cells were treated with a calcium antagonist. These results indicate considerable heterogeneity in the phenotypic response to morphologic change. The amount of procollagenase synthesized in a cell was estimated by the fluorescence intensity of the fluorescein-labeled antibody. The normalized fluorescence intensity of procollagenase in the control cells was about 2 to 2.6 times that of background. In contrast, the normalized fluorescence intensity of procollagenase in the calcium antagonist-treated cells was about 2.4 to 12 times that of background. This high intensity level indicates an increase in procollagenase production in the calcium antagonist-treated cells. Calcium green dye used to study cytosolic calcium revealed that after cells were treated with verapamil, the cytosolic calcium ion concentration first increased and then decreased. The change of cytosolic calcium ion concentration may be related to the depolymerization of actin filaments and the alteration of cell shape.