Funny Post: Frownies Facial Pads, 144 ea

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Product Features

Frownies are a simple method to reverse deep expression lines Frownies repair wrinkle-damaged skin without dangers of injections or toxic chemicals
Dramatically reduce lines and wrinkles safely and naturally
Trains the underlying facial muscles to regain the strength and tone they have lost
Use daily or nightly; leave on for a minimum of three hours
Please read all label information on delivery

Important Information

Indications Reduce Wrinkles Ingredients unbleached natural kraft paper with water-activated gum adhesive. Directions Apply moistened pads to frown lines and wrinkles on freshly cleansed face. Use daily or nightly.

Product Description

144 patches in a box Frownies Facial Patches are applied to the forehaed and between the eyses over lines and wrinkles caused by expressions.

Product Details

Product Dimensions: 6 x 5 x 4 inches ; 1.4 ounces
Shipping Weight: 1.6 ounces

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Many bacteria and higher eukaryotes live in harmony in a symbiotic relationship that benefits one or both of the partners. Indeed, we are colonised by bacterial cells which outnumber our own cells ten to one. This amicable bacterial lifestyle contrasts with a pathogenic one, in which the bacterium causes damage to its host. This is a potentially dangerous strategy for a bacterium, because the provoked host is capable of fighting back. A pathogenic lifestyle offers short-term gain. By outcompeting other bacteria within its host, the bacterium can achieve local dominance and, by more widespread colonisation, expand its territory more globally. However, evolution has to balance these advantages against the possibility that the bacterium is eliminated. The latter could occur if the bacterium is too weak to prevent its destruction by the strong host defences it has incited or if its potent virulence wipes out the host and, thus, its source of food. As pathogenicity appears to be such a risky business, it may be an abnormal condition. Evidence to support this view comes from several lines. First, many of the genes involved in virulence appear to be relatively new – that is, new to the organism made pathogenic by their presence. These genes are frequently found on mobile genetic elements such as plasmids, phage, and pathogenicity islands that have recently been acquired by the organism. Secondly, it is thought that many severe diseases begin with ferocious virulence which later abates – mainly as a result of reduced pathogenicity – thereby suggesting that pathogenicity is not such a good strategy after all. Several types of genes lead to pathogenicity. Bacterial adhesion, the topic of the first book in this series, is the first step a pathogen has to take. However, by itself adhesion does not promote disease: commensal bacteria adhere without causing tissue damage. The main route to bacterial disease is driven by bacterial toxins that specifically attack host cell function. Those toxins that act inside cells fall into two groups: the classical multidomain toxins and toxins that bacteria inject directly into cells. The latter are also called effector proteins. In each case, these toxins modify important cell functions. Because signalling mechanisms and the regulation of the cell cycle are key to a cell’s continued existence, it is not surprising that these components have been targeted by toxins. Equally, it is not surprising that perturbation of these cellular systems frequently leads to aberrant regulation of cell growth. This book describes toxins that interfere with the regulation of cell growth. Our perspective concerns not just the toxin, but also the cell and the whole organism. Several of the chapters describe the molecular interactions of toxins with their host target, whereas for other toxins these mechanisms are not yet clear. We have also included bacteria for which the precise effects on cell growth have not yet been ascribed to toxin action, on the premise that toxins are likely to be responsible. The relationship between the bacterial perturbation of cell growth and cancer is examined specifically for Helicobacter pylori, where various molecular mechanisms have been suggested and, generally, where the evidence is still at the epidemiological stage. We hope that the reader will gain an understanding of these potent molecules and appreciate how their study not only illuminates infectious disease but also opens doors into exciting aspects of cell biology.

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