Skeletal muscle vascular responses in human limbs to isometric handgrip

Studies of whole limb blood flow have shown that static handgrip elicits a vasodilatation in the resting forearm and vasoconstriction in the resting leg. We asked if these responses occur in the skeletal muscle vascular bed, and if so, what is the relative contribution of local metabolic versus other mechanisms to these vascular responses. Blood flow recordings were made simultaneously in the skeletal muscle of the resting arm and leg using the Xenon-washout method in ten subjects during 3 min of isometric handgrip at 30% of maximal voluntary contraction. In the arm, skeletal muscle vascular resistance (SMVR) decreased transiently at the onset of exercise followed by a return to baseline levels at the end of exercise. In the leg SMVR remained unchanged during the 1st min of handgrip, but had increased to exceed baseline levels by the end of exercise. During exercise electromyography (EMG) recordings from nonexercising limbs demonstrated a progressive 20-fold increase in activity in the arm, but remained at baseline in the leg. During EMG-signal modelled exercise performed to mimic the inadvertent muscle activity, decreases in forearm SMVR amounted to 57% of the decrease seen with controlateral handgrip. The present study would seem to indicate that vascular tone in nonexercising skeletal muscle in the arm and leg are controlled differently during the early stages of static handgrip. Metabolic vasodilatation due to involuntary contraction could significantly modulate forearm skeletal muscle vascular responses, but other factors, most likely neural vasodilator mechanisms, must make major contributions. During the later stages of contralateral sustained handgrip, vascular adjustments in resting forearm skeletal muscle would seem to be the final result of reflex sympathetic vasoconstrictor drive, local metabolic vasodilator forces and possibly neurogenic vasodilator mechanisms.     

Detection of focal infection by 111In-human polyclonal IgG

Eleven patients with suspected foci of inflammation and/or infection were scanned with 111In-labeled polyclonal human IgG. Seven patients were suspected of having the source of their infection in the abdomen, three in the musculoskeletal system and one in the thoracic aorta. The test was truly positive in seven patients, truly negative in three and falsely negative in one. All the true positive cases showed abnormally increased radiopharmaceutical uptake at the site of infection by six hours, suggesting the diagnosis, although the intensity of uptake increased progressively 24 hours later. There were no untoward effects noted in this series. This examination is potentially useful in the early depiction of focal sources of infection/inflammation.     

EGF receptor signaling in prostate morphogenesis and tumorigenesis.

The growth and differentiation of the prostate gland are largely dependent on extracellular signaling factors. In addition to androgens, many polypeptide growth factors function through autocrine or paracrine networks. The paracrine interaction between stromal and epithelial cells is critical for androgen regulation, morphogenesis, epithelial cell proliferation, and secretory differentiation. Efforts to identify the essential growth factors and studies on their effects have been prompted by the fact that prostate cells in culture need substances other than androgens for proliferation. In this context, transforming growth factor-alpha and epidermal growth factor, among others, have been studied extensively. Recent advances have suggested that these EGF receptor (EGFR) ligands play roles not only during glandular development but also during neoplastic transformation and tumor progression. The cell responses most relevant to the role of this receptor signaling are both mitogenesis and cell motility. The aim of the review is to provide an overview of current knowledge about EGFR and its ligands in the organogenesis and tumorigenesis of the prostate gland.     

The role of complement in hydatid disease: In vitro studies

Kassis A. I. and Tanner C. E. 1976. The role of complement in hydatid disease: in vitro studies. International Journal for Parasitology6: 25–35. Fresh sera from normal humans, guinea pigs, sheep, cotton rats, B10.D2/n Sn mice or infected cotton rats lyse viable protoscoleces of Echinococcus granulosus and E. multilocularis in vitro. This protoscolecidal activity can be abolished by heating at 56°C, EDTA or incubating with cobra venom factor, suggesting that complement proteins participate in this lytic process. Crude unfiltered hydatid fluid, as well as complement-lysed dead protoscoleces, are anticomplementary in vitro and, as such, probably protect viable protoscoleces in vivo against the action of complement. This anticomplementary activity was found to be associated with the calcareous corpuscles. A hypothesis is presented which relates these in vitro findings to the development of the parasite in vivo. It is suggested that the use of formalin during surgery to kill the parasite should be replaced by fresh serum.