Integrative Therapies in Cancer Pain.

Integrative medicine is an approach to medical care that embraces all effective therapies including complementary treatments such as acupuncture and hypnosis. There is growing use of complementary therapies in the cancer patient population, making it important that health care providers be aware of both the risks and benefits of treatments that lie outside of the traditional allopathic medicine paradigm. This chapter will explore some of the most common and well-investigated complementary therapies for the treatment and prevention of cancer-related pain. This will include discussions of: acupuncture, dietary supplements, massage, guided imagery and cryotherapy among others. The goal of this is to provide a framework for discussions between medical providers and their patients to ensure safety, discussion of all available treatments, and to facilitate open lines of communication.

The product of SPO1 gene 56 inhibits host cell division during infection of Bacillus subtilis by bacteriophage SPO1.

Although cells of Bacillus subtilis continue to grow after being infected by bacteriophage SPO1, they do not undergo cell division. The product of SPO1 gene 56 is necessary and sufficient for this inhibition of cell division. GP56 inhibits cell division when expressed in uninfected B. subtilis, without preventing cell growth, DNA synthesis or chromosome segregation, ultimately causing filamentation and loss of viability. During infection, a gene 56 mutation prevents the inhibition of cell division that occurs in wild-type infection. Under the laboratory conditions used, the gene 56 mutation did not affect burst size, latent period, or other components of the host-takeover process.

Roles of genes 38, 39, and 40 in shutoff of host biosyntheses during infection of Bacillus subtilis by bacteriophage SPO1.

A nonsense mutation in SPO1 gene 40 prevented normal shutoff of both host DNA and host RNA synthesis, showing that gp40 is required for the normal occurrence of both shutoffs. A gene 39 nonsense mutation caused accelerated shutoff of both host DNA and host RNA synthesis (aided by a gene 38 nonsense mutation), showing that gp39 (aided by gp38) limits the rate at which both shutoffs occur. The 40(-) mutation suppressed the accelerative effects of the 39(-) and 38(-) mutations, showing that gp40 also plays an essential role in the accelerated shutoffs. To the best of our knowledge, proteins with the particular activities implied for gp39 and gp40 have not been identified in any other bacteriophage. SPO1 has at least three different mechanisms that have the effect of delaying the shutoff of host DNA and RNA synthesis.