Adherence to medication regimens among low-income patients with multiple comorbid chronic conditions.

This qualitative study sought to explore facilitators and barriers to adherence to multiple medications among low-income patients with comorbid chronic physical and mental health conditions. The 50 focus group participants identified personal/contextual and health system factors as major impediments to adherence to multiple medications. These factors included medication side effects, fear of harm from medication, fear of dependence on medication, complex instructions, suboptimal communications with doctor, suspicion about doctors' and pharmaceutical companies' motives in prescribing medication, and the high cost ofmedications. Participants also identified motivators, both internal (self-initiated) and external (initiated by family, doctor, support groups),to ensure adherence to multiple medications. These motivators included self-discipline, sense of personal responsibility, faith, support from family members and doctors, and focused health education and self-management support. Three themes emerged that enhanced understanding of the complexity of adherence to multiple medications: (1) reaching one's own threshold for medication adherence, (2) lack of shared information and decision making, and (3) taking less than the prescribed medication. Further analysis of the data revealed that the patients perceived a lack of shared decision making in the management of their comorbid chronic conditions and their medication regimen.

Delineation of multiple subpopulations of natural killer cells in rhesus macaques.

Natural killer (NK) cells in rhesus macaques have been variably defined as CD3- CD16+ or CD3- CD8+, although only limited efforts have been made to validate these definitions rigorously. To better understand the role of NK cells in macaque disease models, we undertook a multiparameter analysis of macaque NK cells employing four-colour flow cytometry and a panel of lineage-specific and non-lineage-specific lymphocyte markers. Using this approach, we identified two distinct populations of candidate NK cells: a major CD8bright CD16+ population and a minor CD8bright CD16- population. Further analysis of the major and minor NK cell populations revealed the expression of multiple markers characteristic of NK cells, including CD2, CD7, CD16, CD161, NKG2A and granzyme B. In addition, a CD56+ subset of cells within the minor rhesus NK population was identified which expressed chemokine and lymph node homing receptors similar to those expressed by the CD56bright NK cell population identified in humans. Cytolytic assays confirmed that the phenotypically defined rhesus NK cells lysed NK-susceptible target cells. Our observations support the existence of several distinct subpopulations of rhesus macaque NK cells, which have significant phenotypic and functional similarities to their human counterparts. These improved immunophenotypic definitions of macaque NK cells should facilitate future analysis of innate immune responses in rhesus macaques and the role of NK cells in AIDS pathogenesis in Simian immunodeficiency virus (SIV)-infected macaques.

Shedding of sabin poliovirus Type 3 containing the nucleotide 472 uracil-to-cytosine point mutation after administration of oral poliovirus vaccine.

A uracil-to-cytosine point mutation at nucleotide (nt) 472 of Sabin oral poliovirus vaccine (OPV) type 3 is found in conjunction with vaccine-associated paralytic poliomyelitis (VAPP). Direct RNA extraction and mutant analysis by polymerase chain reaction and restriction enzyme cleavage were used to identify this point mutation in clinical samples. A total of 238 stool samples were obtained from 28 healthy infants for 6 weeks after OPV vaccination. More than 25% of infants shed OPV3 in the week after vaccination, with a decrease on day 6. A second wave of OPV3 shedding occurred beginning the second week after vaccination and was maintained through the end of the study period. During the first week after vaccination, the proportion of nt 472 mutants in the shed OPV3 increased from undetectable to almost 100%. During the second shedding period, the proportion of nt 472 mutants remained close to 100%. These results suggest that selective mutation drives the VAPP-associated nt 472 point mutation for OPV3 in the human gastrointestinal tract.