Health care providers' perspectives of an intervention designed to improve colorectal cancer screening rates in family medicine residency clinics : a qualitative study.

The purpose of this study was to obtain feedback from family medicine residents and clinic nurses regarding a colorectal cancer screening (CRCS) intervention. Focus groups were used to ask participants three questions about their perceptions of the intervention and subsequent patient screening behaviors. Content analysis and constant comparison were used to yield two meaningful themes from the participant responses: patient-specific issues and study design issues.

Treatment of females convicted of molesting children.

The purpose of this study was to determine what kind of treatment women convicted of molesting children thought they should receive and what they hoped to achieve in treatment. Data were collected from 14 offenders in individual and focused group interviews. The data were analyzed by constant comparison.

Abnormal hematopoiesis in Gab2 mutant mice.

Gab2 is an important adapter molecule for cytokine signaling. Despite its major role in signaling by receptors associated with hematopoiesis, the role of Gab2 in hematopoiesis has not been addressed. We report that despite normal numbers of peripheral blood cells, bone marrow cells, and c-Kit(+)Lin(-)Sca-1(+) (KLS) cells, Gab2-deficient hematopoietic cells are deficient in cytokine responsiveness.

Germline KRAS mutations cause Noonan syndrome.

Noonan syndrome (MIM 163950) is characterized by short stature, facial dysmorphism and cardiac defects. Heterozygous mutations in PTPN11, which encodes SHP-2, cause approximately 50% of cases of Noonan syndrome. The SHP-2 phosphatase relays signals from activated receptor complexes to downstream effectors, including Ras.

Functional analysis of leukemia-associated PTPN11 mutations in primary hematopoietic cells.

PTPN11 encodes the protein tyrosine phosphatase SHP-2, which relays signals from growth factor receptors to Ras and other effectors. Germline PTPN11 mutations underlie about 50% of Noonan syndrome (NS), a developmental disorder that is associated with an elevated risk of juvenile myelomonocytic leukemia (JMML). Somatic PTPN11 mutations were recently identified in about 35% of patients with JMML; these mutations introduce amino acid substitutions that are largely distinct from those found in NS.