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1.  Necroptosis induced by RIPK3 requires MLKL but not Drp1 
Cell Death & Disease  2014;5(2):e1086-.
Necroptosis is a mechanism by which cells can kill themselves that does not require caspase activity or the presence of the pro-apoptotic Bcl-2 family members Bax or Bak. It has been reported that RIPK3 (receptor interacting protein kinase 3) activates MLKL (mixed lineage kinase domain-like) to cause cell death that requires dynamin-related protein 1 (Drp1), because survival was increased in cells depleted of Drp1 or treated with the Drp1 inhibitor mdivi-1. To analyze necroptosis in a system that does not require addition of tumor necrosis factor (TNF), we used a construct that allows RIPK3 to be induced in cells, and then dimerized via an E. coli gyrase domain fused to its carboxyl-terminus, using the dimeric gyrase binding antibiotic coumermycin. We have previously shown elsewhere that RIPK3 dimerized in this manner not only induces necroptosis but also apoptosis, which can be inhibited by the broad-spectrum caspase inhibitor Q-VD-OPh (QVD). In response to RIPK3 dimerization, wild-type mouse embryonic fibroblasts (MEFs) underwent cell death that was reduced but not completely blocked by QVD. In contrast, death upon dimerization of RIPK3 in Mlkl−/− MEFs was completely inhibited with QVD, confirming that MLKL is required for necroptosis. Similar to wild-type MEFs, most Drp1−/− MEFs died when RIPK3 was activated, even in the presence of QVD. Furthermore, overexpression of wild-type MLKL or dominant active mutants of MLKL (Q343A or S345E/S347E) caused death of wild-type and Drp1−/− MEFs that was not inhibited with QVD. These results indicate that necroptosis caused by RIPK3 requires MLKL but not Drp1.
PMCID: PMC3944236  PMID: 24577084
necroptosis; receptor interacting protein kinases; MLKL; caspases
2.  Diet, Breakfast, and Academic Performance in Children 
Annals of nutrition & metabolism  2002;46(0 1):24-30.
To determine whether nutrient intake and academic and psychosocial functioning improve after the start of a universal-free school breakfast program (USBP).
Information was gathered from 97 inner city students prior to the start of a USBP and again after the program had been in place for 6 months. Students who had total energy intakes of <50% of the recommended daily allowance (RDA) and/or 2 or more micronutrients of <50% of RDA were considered to be at nutritional risk.
Prior to the USBP, 33% of all study children were classified as being at nutritional risk. Children who were at nutritional risk had significantly poorer attendance, punctuality, and grades at school, more behavior problems, and were less likely to eat breakfast at school than children who were not at nutritional risk. Six months after the start of the free school breakfast programs, students who decreased their nutritional risk showed significantly greater: improvements in attendance and school breakfast participation, decreases in hunger, and improvements in math grades and behavior than children who did not decrease their nutritional risk.
Participation in a school breakfast program enhanced daily nutrient intake and improvements in nutrient intake were associated with significant improvements in student academic performance and psychosocial functioning and decreases in hunger.
PMCID: PMC3275817  PMID: 12428078
School breakfast; Low-income children; Psychosocial functioning; Nutrition; Dietary intake
3.  The Role of 5-HT3 Receptors in Drug Abuse and as a Target for Pharmacotherapy 
Alcohol and drug abuse continue to be a major public health problem in the United States and other industrialized nations. Extensive preclinical research indicates the mesolimbic dopamine (DA) pathway and associated regions mediate the rewarding and reinforcing effects of drugs of abuse and natural rewards, such as food and sex. The serotonergic (5-HT) system, in concert with others neurotransmitter systems, plays a key role in modulating neuronal systems within the mesolimbic pathway. A substantial portion of this modulation is mediated by activity at the 5-HT3 receptor. The 5-HT3 receptor is unique among the 5-HT receptors in that it directly gates an ion channel inducing rapid depolarization that, in turn, causes the release of neurotransmitters and/or peptides. Preclinical findings indicate that antagonism of the 5-HT3 receptor in the ventral tegmental area, nucleus accumbens or amygdala reduces alcohol self-administration and/or alcohol-associated effects. Less is known about the effects of 5-HT3 receptor activity on the self-administration of other drugs of abuse or their associated effects. Clinical findings parallel the preclinical findings such that antagonism of the 5-HT3 receptor reduces alcohol consumption and some of its subjective effects. This review provides an overview of the structure, function, and pharmacology of 5-HT3 receptors, the role of these receptors in regulating DA neurotransmission in mesolimbic brain areas, and discusses data from animal and human studies implicating 5-HT3 receptors as targets for the development of new pharmacological agents to treat addictions.
PMCID: PMC2878195  PMID: 19128203
Serotonin; dopamine; ethanol; cocaine; nicotine; amphetamine; opiates; addictions
4.  Letter: Cello scrotum. 
British Medical Journal  1974;2(5914):335.
PMCID: PMC1610985  PMID: 4827125

Results 1-4 (4)