Calorimeters for precision power dissipation measurements on controlled-temperature superconducting radiofrequency samples.

Two calorimeters, with stainless steel and Cu as the thermal path material for high precision and high power versions, respectively, have been designed and commissioned for the 7.5 GHz surface impedance characterization system at Jefferson Lab to provide low temperature control and measurement for CW power up to 22 W on a 5 cm diameter disk sample which is thermally isolated from the radiofrequency (RF) portion of the system. A power compensation method has been developed to measure the RF induced power on the sample. Simulation and experimental results show that with these two calorimeters, the whole thermal range of interest for superconducting radiofrequency materials has been covered. The power measurement error in the interested power range is within 1.2% and 2.7% for the high precision and high power versions, respectively. Temperature distributions on the sample surface for both versions have been simulated and the accuracy of sample temperature measurements have been analyzed. Both versions have the ability to accept bulk superconductors and thin film superconducting samples with a variety of substrate materials such as Al, Al(2)O(3), Cu, MgO, Nb, and Si.

Note: Radio frequency surface impedance characterization system for superconducting samples at 7.5 GHz.

A radio frequency (RF) surface impedance characterization (SIC) system that uses a novel sapphire-loaded niobium cavity operating at 7.5 GHz has been developed as a tool to measure the RF surface impedance of flat superconducting material samples. The SIC system can presently make direct calorimetric RF surface impedance measurements on the central 0.8 cm(2) area of 5 cm diameter disk samples from 2 to 20 K exposed to RF magnetic fields up to 14 mT. To illustrate system utility, we present first measurement results for a bulk niobium sample.

Stem cells in the trabecular meshwork: present and future promises.

Primary open-angle glaucoma is recognized as a disease of aging, and studies show a relationship between aging and trabecular meshwork (TM) cell density. Human TM cell division occurs primarily in the anterior, non-filtering region. A commonly used glaucoma treatment, laser trabeculoplasty (LTP), triggers and increases cell division, as well as cell migration of these anterior TM cells. These freshly-divided migrating cells repopulate the burned laser sites, suggesting that they are stem cells. Several studies concerning this putative TM stem cell will be discussed.

Hepatitis C seroprevalence among newly incarcerated inmates in the Texas correctional system.

The seroprevalence of hepatitis C (HCV) infection was examined among a sample of incoming inmates in the Texas Department of Criminal Justice (TDCJ) prison system. Rates were compared across demographic factors and three types of prison facilities: substance abuse felony punishment units (SAFPs), state jails and prisons. The study sample consisted of 3712 incoming inmates incarcerated for any duration, dating from 1 November 1998 to 31 May 1999. Among males, inmates entering SAFPs and state jails had comparable HCV infection rates (29.7 and 27.0%, respectively) to those entering prisons (27.3%). Among females, inmates entering prisons had a higher rate of infection (48.6%) than those entering state jails (35.1%) or SAFPs (38.3%). For both genders, blacks exhibited a lower overall infection rate than whites and Hispanics, and HCV seroprevalence increased in a stepwise fashion with age. All subgroups of TDCJ inmates, including those held in alternative correctional facilities, exhibited HCV infection rates that were comparable with previous reports of inmate populations, but dramatically higher than general community samples. Given that most inmates held in alternative facilities will return to the general community in a short period of time, understanding the HCV infection rates in these subgroups holds particular public health relevance.

Familial chordoma, a tumor of notochordal remnants, is linked to chromosome 7q33.

Chordoma is a rare tumor originating from notochordal remnants that is usually diagnosed during midlife. We performed a genomewide analysis for linkage in a family with 10 individuals affected by chordoma. The maximum two-point LOD score based on only the affected individuals was 2.21, at recombination fraction 0, at marker D7S2195 on chromosome 7q. Combined analysis of additional members of this family (11 affected individuals) and of two unrelated families (one with 2 affected individuals and the other with 3 affected individuals), with 20 markers on 7q, showed a maximum two-point LOD score of 4.05 at marker D7S500. Multipoint analysis based on only the affected individuals gave a maximum LOD score of 4.78, with an approximate 2-LOD support interval from marker D7S512 to marker D7S684. Haplotype analysis of the three families showed a minimal disease-gene region from D7S512 to D7S684, a distance of 11.1 cM and approximately 7.1 Mb. No loss of heterozygosity was found at markers D7S1804, D7S1824, and D7S2195 in four tumor samples from affected family members. These results map a locus for familial chordoma to 7q33. Further analysis of this region, to identify this gene, is ongoing.

Guidewire incidents with inferior vena cava filters.

Several authors have demonstrated that prophylactically inserted inferior vena cava filters have decreased pulmonary thromboembolic complications in selected high-risk trauma patients. Guidewire-related mishaps are potential complications of inferior vena cava filters and are likely underreported. The authors present two cases and review strategies to prevent these complications.

Effects of mechanical stretching on trabecular matrix metalloproteinases.

PURPOSE: The homeostatic mechanisms responsible for intraocular pressure (IOP) regulation are not understood. Studies were conducted to evaluate the hypothesis that trabecular meshwork (TM) cells sense increases in IOP as stretching or distortion of their extracellular matrix (ECM) and respond by increasing ECM turnover enzymes. METHODS: Flow rates were increased in perfused human anterior segment organ cultures and the matrix metalloproteinase (MMP) levels and IOP were evaluated. Human TMs in stationary anterior segment organ culture were mechanically stretched, and MMP levels were analyzed. TM cells were grown on membranes, which were then stretched, and MMP levels were evaluated. Western immunoblots, zymography, and confocal immunohistochemistry were used to evaluate changes in MMPs and their tissue inhibitors, the TIMPS: RESULTS: Doubling the flow rate in perfused human organ cultures increased gelatinase A levels in the perfusate by 30% to 50% without affecting gelatinase B or stromelysin levels. Immediately after doubling the flow rate, the measured IOP doubled. However, over the next few days the IOP gradually returned to the initial level, although the flow rate was maintained at double the initial value. Stretching stationary organ cultures or stretching TM cells grown on membranes resulted in similar increases in gelatinase A without changes in gelatinase B or stromelysin levels. The gelatinase A increases occurred between 24 and 72 hours and were approximately proportional to the degree of stretching. Although coating the membranes with different ECM molecule affected the gelatinase A response, the optimum response occurred when the cells had been grown long enough to produce their own ECM. By Western immunoblot and confocal immunohistochemistry, the stretch-induced increases in gelatinase A were accompanied by strong decreases in TIMP-2 levels and moderate increases in one membrane type MMP, MT1-MMP. After mechanical stretching of the membrane, gelatinase A, MT1-MMP and TIMP-2 all exhibited a similar punctate immunostaining pattern over the TM cell surface. CONCLUSIONS: These results are compatible with the hypothesis that elevations in IOP are sensed by TM cells as ECM stretch/distortion. TM cells respond by increasing gelatinase A and MT1-MMP, while decreasing TIMP-2 levels. This will increase ECM turnover rates, reduce the trabecular resistance to aqueous humor outflow, and restore normal IOP levels. This hypothesis provides a regulatory feedback mechanism for IOP homeostasis.

The Community Partnerships Experience: a report of institutional transition at East Tennessee State University.

The Community Partnerships Program, sponsored by the W. K. Kellogg Foundation, served as a catalyst for significant changes within East Tennessee State University (specifically its schools of medicine, nursing, and public and allied health) and the rural communities involved. The authors describe the development and implementation of the program and its effects on the students, faculty, communities, and the three participating schools over the period 1992-1999. They also review the changes the program fostered in health professions education and the resulting institutional changes at their university. The primary motivation for change at East Tennessee State University was the desire to develop primary care providers who could more effectively function in an interdisciplinary and interprofessional health care system and who would be sensitive to community needs in rural and underserved areas. The planning process, curricular transformation, implementation of inquiry-based learning, community collaboration, and interdisciplinary education involving students from the three health professions schools are described, including challenges and difficulties (e.g., student attrition; retention of volunteer community-based clinical preceptors; initial faculty resistance; a climate of competition rather than cooperation). Outcomes are described, including students' enrollment and attrition in the program over time, performances on the U.S. Medical Licensing Examination, program graduates' career choices, and the types and locations of their practices. The program's students performed as well on professional licensing examinations as did their peers enrolled in traditional programs. Program graduates have been much more likely to select primary care careers and to practice in rural locations than have their non-program peers. The development strategies and experience gained could give useful insights to other universities contemplating a community-based component for health professionals within their existing curricula.

Genetic changes in contralateral bronchioloalveolar carcinomas of the lung.

OBJECTIVE: The pattern of metastases and recurrence of bronchioloalveolar carcinoma (BAC) differs from adenocarcinoma of the lung, occurring more frequently within the lung without extrapulmonary involvement. Analyses of genetic differences of contralateral BACs may help to explain these clinical differences. METHODS: We compared paired tumors from 5 patients with contralateral metachronous BACs for loss of heterozygosity (LOH) on 6 chromosomal arms (2q, 3p, 5q, 9p, 13q and 17p) and mutational analysis of p53 and K-ras. RESULTS: Two patients, patients 1 and 2, had discordant patterns of LOH on 2 and 3 of the chromosome arms, respectively. In addition, patient 2 had a detectable K-ras mutation in his initial tumor but not in his second. These results suggest that in patients 1 and 2, the contralateral tumors were clonally unrelated. Patient 3 had no mutations in the K-ras or p53 gene and no LOH on any of the 5 informative chromosome arms. Patient 4 had LOH of 9p and mutated K-ras in both the first and the second tumor, with a mutation in the p53 gene in the first but not in the second tumor. Patient 5 had LOH of 17p and the same p53 mutations in both the first and the second tumor, with a mutation of K-ras in the first tumor but not in the second. CONCLUSIONS: The preponderance of evidence suggests that in patients 3, 4 and 5, the paired tumors were clonally related. The different patterns of LOH and mutations in clinically similar contralateral metachronous BACs provide evidence of genetic heterogeneity in the tumors of this patient group.

Human nonsyndromic hereditary deafness DFNA17 is due to a mutation in nonmuscle myosin MYH9.

The authors had previously mapped a new locus-DFNA17, for nonsyndromic hereditary hearing impairment-to chromosome 22q12.2-q13. 3. DFNA17 spans a 17- to 23-cM region, and MYH9, a nonmuscle-myosin heavy-chain gene, is located within the linked region. Because of the importance of myosins in hearing, MYH9 was tested as a candidate gene for DFNA17. Expression of MYH9 in the rat cochlea was confirmed using reverse transcriptase-PCR and immunohistochemistry. MYH9 was immunolocalized in the organ of Corti, the subcentral region of the spiral ligament, and the Reissner membrane. Sequence analysis of MYH9 in a family with DFNA17 identified, at nucleotide 2114, a G-->A transposition that cosegregated with the inherited autosomal dominant hearing impairment. This missense mutation changes codon 705 from an invariant arginine (R) to histidine (H), R705H, within a highly conserved SH1 linker region. Previous studies have shown that modification of amino acid residues within the SH1 helix causes dysfunction of the ATPase activity of the motor domain in myosin II. Both the precise role of MYH9 in the cochlea and the mechanism by which the R705H mutation leads to the DFNA17 phenotype (progressive hearing impairment and cochleosaccular degeneration) remain to be elucidated.