A domain wall is created halfway the thickness of a permalloy film (dimensions
ℓ
×
b
×
d
=
120
×
30
mm
2
×
9
μ
m
) by passing a 16
A current in the direction of the width
b through the film. The ...equilibrium position of this wall is varied by an in-plane magnetic field and determined from 3D polarisation analysis after transmitting a polarised neutron beam
(
λ
=
0.2
nm
)
through the film (at
8
∘
to the beam). Over a small field interval the net precession of the polarisation vector ranges from
-
π
to
+
π
with little depolarisation, implying that the domain wall moves from
1
4
to
3
4
of the thickness. If the wall approaches closer to either surface, the beam is fully depolarised. These observations apply also to AC fields up to 1
kHz. This suggests that the film can be used as wavelength adaptable flipper.
Circulating endothelial cells (CEC) are considered a promising marker to determine the extent of vascular damage. However, currently available and validated CEC enumeration assays are laborious, time ...consuming and costly, which limits their clinical utility. Here, we evaluated the feasibility of quantifying mRNA levels of the endothelium-associated markers CD31, CD144, CD146 and von Willebrand factor (vWf) in peripheral blood (PB) of healthy donors, patients, and human umbilical veins by real-time reverse transcriptase polymerase chain reaction (RT-PCR) and their use as surrogate markers for CEC. Whole blood samples and CD146+ cell-enriched fractions were assessed for mRNA and protein expression of CD31, CD144, CD146 and vWf by RT-PCR and flow cytometry, respectively. We showed the feasibility to detect endothelial mRNA isolated from HUVEC numbers as low as 10. However, no endothelial mRNA could be measure in whole blood samples, and only low levels of CD31 and CD146 mRNA were detected in suspensions of isolated CEC with numbers up to 4,450 CEC per sample. We conclude that mRNA levels of CD31, CD144, CD146 and vWf in whole blood as detected by real time RT-PCR cannot be used as biomarkers for end-stage endothelial cells such as CEC.
Summary Objective To develop an animal experimental model for the induction and assessment of joint damage caused by haemarthrosis in the temporomandibular joint (TMJ) in rats. Methods Both TMJs of ...10 young mature male Wistar rats were injected with autologous blood with additional heparin and Gd-DTPA. Two rats served as controls and were injected with physiological saline solution with additional heparin and Gd-DTPA. All rats were subsequently scanned with magnetic resonance imaging (MRI) to verify the accuracy of the intra-articular injection. The experimental rats were sacrificed after 6 and 24 h, and 2, 3 and 4 days, respectively. The rats of the control group were sacrificed after 6 and 24 h. Histopathological analysis was performed. Results MRI showed that all TMJs, except one were correctly injected. One injection site was considered doubtful but after renewed injection proved to be correct. Histopathological examination showed a correct injection of blood in all joints, but showed no signs of inflammation or intra-articular damage. Conclusion We have established a reproducible animal model for the induction of haemarthrosis in the TMJ of rats. Histopathological analysis showed neither signs of intra-articular damage nor inflammation.
Two mutations of the ATM gene were recently suggested to confer breast cancer risks similar to mutations of BRCA1 or BRCA2. Here, we set out to confirm these findings in 961 families with ...non-BRCA1/BRCA2 breast cancer from diverse geographical regions. We did not detect the ATM 7271T-->G mutation in any family. The ATM IVS10-6T-->G mutation was detected in eight families, which was similar to its frequency among population-matched control individuals (pooled Mantel-Haenszel odds ratio = 1.60; 95% confidence interval = 0.48 to 5.35; P = 0.44). Bayesian analysis of linkage in the ATM IVS10-6T-->G-positive families showed an overall posterior probability of causality for this mutation of 0.008. We conclude that the ATM IVS10-6T-->G mutation does not confer a significantly elevated breast cancer risk and that ATM 7271T-->G is a rare event in familial breast cancer.
The data processing model for the CDF experiment is described. Data processing reconstructs events from parallel data streams taken with different combinations of physics event triggers and further ...splits the events into datasets of specialised physics interests. The design of the processing control system makes strict requirements on bookkeeping records, which trace the status of data files and event contents during processing and storage. The computing architecture was updated to meet the mass data flow of the Run II data collection, recently upgraded to a maximum rate of 40 MByte/sec. The data processing facility consists of a large cluster of Linux computers with data movement managed by the CDF data handling system to a multi-petaByte Enstore tape library. The latest processing cycle has achieved a stable speed of 35 MByte/sec (3 TByte/day). It can be readily scaled by increasing CPU and data-handling capacity as required
Objective
The p53 tumor suppressor gene is overexpressed in synovial tissue (ST) from patients with longstanding rheumatoid arthritis (RA), and may contain somatic mutations. The aim of this study ...was to determine p53 expression in ST from RA patients in different stages of the disease, compared with disease controls.
Methods
ST biopsy specimens were obtained from the knee joints of 31 RA patients in varying disease phases, 8 patients with reactive arthritis (ReA), 10 patients with inflammatory osteoarthritis (OA), and 6 control patients (4 with meniscus pathology, 2 with vascular insufficiency). ST was also obtained from the clinically uninvolved knee joints of 9 RA patients. Expression of p53 was determined by immunohistology with DO1 monoclonal antibody (mAb) in all patients and by Western blot analysis with DO7 mAb in a subgroup of the patients.
Results
The p53 protein was detected by immunohistology in 10 of the 13 patients with early RA (duration <6 months) and in 12 of the 14 patients with longstanding RA (duration >5 years). The p53 protein was also demonstrated in clinically uninvolved knee joints. Western blots revealed immunoreactive p53 in ST extracts from all RA patients. Expression of p53 was about twice as high in ST from patients with longstanding RA as in early RA samples, but the difference did not reach statistical significance. Small amounts of p53 were also detected in ST from ReA and OA patients, although the expression in RA synovium was significantly higher. Immunohistologic analysis of normal ST gave negative results for p53.
Conclusion
This study shows that p53 overexpression is specific for RA, compared with OA and ReA. This phenomenon is probably secondary to increased production of wild‐type p53 protein in response to DNA damage and secondary to somatic mutations caused by the genotoxic local environment in inflamed ST. Of interest, p53 overexpression can also be found in the earliest stages of RA and in clinically uninvolved joints.
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