Electromechanical elongation of nematic elastomers for actuation

In classical electrostriction the Maxwell stress caused by the charging of electrodes attached to a solid’s surfaces causes contraction along the field direction and hence elongation in the two directions in the plane of the electrodes. We discuss the opposite possibility, that is where a nematic elastomer (the working solid) would shrink in the plane and lengthen along the field direction. The mechanism is by electrically induced rotation of the nematic director which determines the long dimension of the elastomer. Theory finds such a non-classical response only if the dielectric anisotropy exceeds the shape anisotropy, whereupon the Maxwell stress is overcome by the reduction in energy on redirecting the solid’s most polarisable direction along the applied field. We thereby suggest an alternative to the usual electrostrictive actuation paradigm in that in-plane contraction arises.     

Activation of protein kinase C modulates cell-cell and cell-substratum adhesion of a human colorectal carcinoma cell line and restores 'normal' epithelial morphology

Abnormal cell adhesion is an important contributing factor in invasion and metastasis. Here, we show that morphologically 'normal' cell-cell and cell-substratum adhesion can be restored to a poorly differentiated carcinoma cell line by activation of protein kinase C (PKC). This cell line, VACO 10MS, grows as multicellular aggregates loosely attached to the substratum. The phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA, 7.5 nM) induces rapid adhesive changes with 2 components. First, within 15 min of TPA the cells become closely apposed, an event resembling the 'compaction' seen in the mouse early embryo. Next, over 2 hr, the cells spread, forming a monolayer. We show that compaction depends on extracellular calcium, E-cadherin-mediated adhesion and F-actin but not on protein synthesis, microtubules or substratum adhesion. By contrast, cell spreading is independent of cadherin and extracellular Ca2+ but involves the formation of focal contacts containing alpkha(v) integrin. TPA treatment causes rapid translocation of PKC-alpha to the insoluble fraction. During compaction, actin- and PKC-alpha-containing lamellae form over the entire aggregate surface, those adjacent to the substratum appearing to initiate spreading. Compaction does not involve increased phosphorylation of the cadherin/catenin complex. We conclude that activation of PKC-alpha restores 'normal' morphology to these poorly differentiated cells. Our results are of general interest in relation to the regulation of cell adhesion and, through further investigation, may lead to identification of novel targets for therapeutic suppression of invasion and metastasis.     

Adult smoking intervention programmes in Massachusetts: a comprehensive approach with promising results

This paper provides a brief overview of the history of Massachusetts' opposition to smoking. It describes the current Massachusetts Tobacco Control Program and its smoking intervention programmes; changes in public opinion, perceptions and attitudes toward smoking; and programme impact. Massachusetts has been successful in developing a comprehensive intervention that has had encouraging results in changing public attitudes about smoking and in helping smokers to quit.     

Flucytosine monotherapy for cryptococcosis

Medullary carcinoma is a recently recognized tumor of the kidney with distinctive microscopic features; the most notable are diffuse and glandular growth patterns, inflammatory infiltrates, and rhabdoid/plasmacytoid cells. It is a clinically aggressive tumor that occurs in relatively young patients. Moreover, this tumor shows a peculiar clinical association: it occurs in patients with sickle cell hemoglobinopathy. The case presented is that of a 37-year-old black woman with a history of bronchial asthma who died suddenly. Autopsy showed a 4-cm renal mass with extension to the inferior vena cava and metastases to the liver. Histologic evaluation showed the characteristic findings of medullary carcinoma of the kidney. This diagnosis prompted the investigation and subsequent detection of sickle cell trait in the deceased, alerting the family to the genetic nature of her illness. This case is the first report of this entity since the original described series of patients and shows the unique nature of this cancer as a marker of a genetic medical disease.     

Flaujeac factor deficiency. Reconstitution with highly purified bovine high molecular weight-kininogen and delineation of a new permeability-enhancing peptide released by plasma kallikrein from bovine high molecular weight-kininogen

Flaujeac trait is the functional deficiency of a plasma protein of the intrinsic coagulation, kinin-forming, and plasma fibrinolytic pathways. The Flaujeac factor in man has been isolated and tentatively identified as a kininogen of high molecular weight (HMW). Highly purified bovine HMW-kininogen, but not bovine low molecular weight kininogen, repaired Flaujeac factor deficiency. The two subspecies of this molecule, HMW-kininogen a and HMW-kininogen b, also corrected Flaujeac factor deficiency. When bovine HMW-kininogen was incubated with bovine plasma kallikrein, kinin-free HMW-kininogen, bradykinin, and a glycopeptide fragment (peptide 1-2; 12,584 daltons) were rapidly released. None of these fragmentation products corrected Flaujeac factor deficiency alone or in mixtures. The function of HMW-kininogen appeared to depend upon the structural integrity of the native molecule. When injected in concentrations of 2 pmol-8 nmol/0.1 ml, peptide 1-2 caused increased vascular permeability in rabbits, rats, or guinea pigs. The enhanced permeability was maximal within 1-2 min and terminated in 5-10 min, differing from that of bradykinin or histamine. Injected together in equimolar amounts, peptide 1-2 and bradykinin produced a synergistic permeability response which was immediate in onset as well as prolonged in duration. Peptide 1-2 is a rapidly acting, highly basic glyco-peptide which mediates increased vascular permeability in a complementary and synergistic manner with bradykinin.     

Prostaglandin E2 induction of labor for fetal demise

Intrauterine fetal demise is a source of anxiety to both patient and physician. Heretofore, the standard treatment was either careful observation until the patient went into labor or attempt at induction of labor with oxytocin. Unfortunately, oxytocin stimulation has not proven to be uniformly successful for this problem. Prostaglandin E2 suppositories have been shown to be effective in inducing uterine evacuation after intrauterine fetal demise. In the opinion of the authors, this approach will in the future replace the sometimes dangerous and emotionally laden convention of watchful delayed therapy.