Taller staff occupationally exposed to less radiation to the temple in cardiac procedures, but risk higher doses during vascular cases.

This study aimed to evaluate the effect of nurse and doctor height on occupational dose to the temple during fluoroscopically guided cardiovascular procedures. Additionally, an evaluation of the relationship between doctor height and table height was performed. Staff exposed during fluoroscopic procedures may be at elevated risk of cardiovascular damage or oncogenesis and have demonstrated a higher incidence of subscapular cataracts. The heads of taller staff may be exposed to reduced levels of radiation due to the increased distance from the area of highest intensity X-ray scatter. Limited research has been performed investigating height as a predictor of head dose to nursing staff. The level of radiation dose at the level of the temple to the doctor (n = 25), scrub (n = 28), and scout nurse (n = 29) was measured in a prospective single-center, observational study using Philips DoseAware badges. Procedural characteristics were recorded for vascular and cardiac cases performed in three dedicated angiography suites. Data were also collected to investigate relationships between doctor height and table height. Data were collected for 1585 cardiac and 294 vascular procedures. Staff height was a statistically significant predictor of temple dose for doctors, scrub, and scout nurses when considering the full data sample. The log temple dose demonstrated an inverse relationship to staff height during cardiac procedures, but a positive relationship for scrub and scout nurses during vascular studies. This observational study has demonstrated that taller staff are exposed to less cranial exposure dose during fluoroscopically guided cardiac examinations but has revealed a positive correlation between height and temple dose during vascular procedures. It was also determined that doctor height was correlated with average procedural table height and that vascular access point influences the choice of table elevation.

Transient upregulation of GRP and its receptor critically regulate colon cancer cell motility during remodeling.

Gastrin-releasing peptide (GRP) is typically viewed as a growth factor in cancer. However, we have suggested that in colon cancer, GRP acts primarily as a morphogen when it and its receptor (GRP-R) are aberrantly upregulated. As such, GRP/GRP-R act(s) primarily to modulate processes contributing to the assumption or maintenance of tumor differentiation. One of the most important such processes is the ability of tumor cells to achieve directed motility in the context of tissue remodeling. Yet the cellular conditions affecting GRP/GRP-R expression, and the biochemical pathways involved in mediating its morphogenic properties, remain to be established. To study this, we evaluated the human colon cancer cell lines Caco-2 and HT-29 cells. We found that confluent cells do not express GRP/GRP-R. In contrast, disaggreation and plating at subconfluent densities results in rapid GRP/GRP-R upregulation followed by their progressive decrease as confluence is achieved. GRP/GRP-R coexpression correlated with that of focal adhesion kinase (FAK) phosphorylation of Tyr(397), Tyr(407), Tyr(861), and Tyr(925) but not Tyr(576) or Tyr(577). To more specifically evaluate the kinetics of GRP/GRP-R upregulation, we wounded confluent cell monolayers. At t = 0 h GRP/GRP-R were not expressed, yet cells immediately began migrating into the gap created by the wound. GRP/GRP-R were first detected at approximately 2 h, and maximal levels were observed at approximately 6 h postwounding. The GRP-specific antagonist [d-Phe(6)]-labeled bombesin methyl ester had no effect on cell motility before GRP-R expression. In contrast, this agent increasingly attenuated cell motility with increasing GRP-R expression such that from t = 6 h onward no further cell migration into the gap was observed. Overall, these findings indicate the existence of GRP-independent and -dependent phases of tumor cell remodeling with the latter mediating colon cancer cell motility during remodeling via FAK.

Capillarization and vascular endothelial growth factor expression in hypertrophying anterior latissimus dorsi muscle of the Japanese quail.

Hypertrophy may increase the diffusion distances from capillaries to the interior of the muscle fibers. We hypothesized that capillary proliferation occurs during hypertrophy, which is accompanied by an up-regulation of vascular endothelial growth factor (VEGF). Hypertrophy of the left anterior latissimus dorsi muscle of Japanese quail (2-3 months old) was induced by 1-4 week stretch-overload. Capillarization was analyzed in cross-sections stained for ATPase. VEGF expression was determined with RT-PCR. Initially, hypertrophy was not accompanied by increases in fiber cross-sectional area (FCSA), but after 1 week the average FCSA did increase. The capillary to fiber ratio was decreased after 1 week, but returned to control values in subsequent weeks. This indicates that capillary proliferation occurred, because this model is characterized by extensive fiber proliferation. The absence of any significant change in VEGF mRNA levels indicates that increased levels of VEGF mRNA are not crucial for capillary proliferation during muscle hypertrophy.

Capillarization in skeletal muscle of rats with cardiac hypertrophy.

PURPOSE: Exercise intolerance during chronic heart failure (CHF) is localized mainly in skeletal muscle. A decreased capillarization may impair exchange of oxygen between capillaries and muscle tissue and in this way contribute to exercise intolerance. We assessed changes in capillary supply in plantaris and diaphragm muscles of a rat aorta-caval fistula (ACF) preparation, a volume overload model for CHF. METHODS: An ACF was created under equithesin anesthesia. Plantaris and diaphragm muscles were removed 6 wk postsurgery and examined for myosin heavy chain (MyHC) content and capillary supply. RESULTS: Cardiac hypertrophy was 96% (P < 0.002) after ACF. The Type IIb MyHC content of the plantaris muscles increased (33.9 +/- 3.3 vs 49.8 +/- 3.8%; mean +/- SEM) at the expense of Type IIa MyHC (17.6 +/- 1.8 vs 11.2 +/- 1.7%) in ACF rats (P < 0.05). In the diaphragm, the number of Type I (32.1 +/- 2.3 vs 40.6 +/- 2.7%) and IIb fibers (40.6 +/- 1.9 vs 49.6 +/- 3.6%) increased at the expense of Type IIa fibers (26.8 +/- 2.5 vs 9.4 +/- 0.9%) (P < 0.05). The capillary number per fiber did not change, and this indicated that no capillary loss occurred with ACF. Also, the capillary density was maintained in the diaphragm and plantaris muscles of ACF rats. Furthermore, the coupling between fiber type, size, and metabolic type of surrounding fibers, with the capillary supply to a fiber, was maintained in rats with an ACF. CONCLUSION: The cardiac hypertrophy induced by volume overload seems adequate to prevent atrophy and changes in the microcirculation of limb and diaphragm muscles.