Cardiovascular implications of anabolic steroid abuse.

Anabolic steroids are synthetic derivatives of the hormone testosterone. Anabolic effects such as anticatabolism, increased skeletal muscle mass, and increased aggressiveness are usually desired; however, androgenic effects also result. Decreases in high-density lipoprotein, increases in low-density lipoprotein, changes in total serum cholesterol, hematocrit, and clotting factors, and the development of hypertensive diseases have all been implicated as resulting from anabolic steroid use. Research does not directly link anabolic steroids with cardiovascular diseases, but steroid use can significantly increase risk factors for atherosclerotic cardiovascular disease.     

Retention of habituation in PC12 cells.

The time course of habituation and recovery of neurotransmitter release was measured in neuronally differentiated PC12 cells stimulated with either acetylcholine or ATP. The release of norepinephrine in response to either stimulant declined exponentially with repeated presentation of that stimulant. When the stimulus was withheld, the cells' ability to respond recovered to initial levels with an exponential time course. The rate of response recovery depended on the stimulant used and, in the case of stimulation with acetylcholine, on the number of previous stimuli. After habituation and recovery, or partial recovery, of norepinephrine release, the response to a second series of repetitive stimuli declined more rapidly than in the naive case. This increase in habituation rate was dependent on the number of previous stimuli and, in the case of stimulation with acetylcholine, was stable with time for at least 90 min after stimulation. These phenomena are analogous to characteristics of short- and long-term memories of habituative learning observed in behavioral studies. Kinetic equations based on a putative reversible stimulation-dependent inactivation of the cellular response mechanism were used to analyze the rates of habituation and response recovery.     

Twelve immunotherapy drugs that could cure cancers

Summary: Immune T cells can kill cancer cells. Cancer vaccines function by increasing the number of immune T cells. There are exceedingly strict biologic limits imposed on the immune system to prevent excessive T-cell activation and expansion. The same biological restrictions limit cancer vaccines. Immunotherapeutic agents that circumvent the biological restrictions have been invented and formulated, including (i) dendritic cell activators and growth factors, (ii) vaccine adjuvants, (iii) T-cell stimulators and growth factors, (iv) immune checkpoint inhibitors, and (v) agents to neutralize or inhibit suppressive cells, cytokines, and enzymes. Few of these agents are broadly available for the development of effective multiple component regimens. The major problem facing immunotherapy today is a lack of broad availability of agents already in existence. The National Cancer Institute has developed a well-vetted ranked list of agents with high potential to serve as immunotherapeutic drugs. This review focuses on 12 of the agents, all with proven ability to augment T-cell responses. Alone, each has little chance of making substantial inroads into cancer therapy. In combinations dictated by biology, the agents are overwhelmingly likely to have an impact. Future availability of these agents for development of innovative combination cancer therapy regimens will provide a benchmark for the resolve of the national cancer therapy translational research enterprise.