Some topics for qualitative research in psychology are unsuitable for or cannot be adapted to the traditional qualitative designs such as case study, ethnography, grounded theory, or phenomenology. This paper explores reasons for this, and proposes that psychological researchers can use a generic qualitative design in such situations. After discussing the types of topics most suitable for a generic qualitative design, the paper differentiates generic qualitative designs from the more traditional qualitative designs, with particular attention to how generic qualitative inquiry differs from phenomenological psychological research. Finally, appropriate procedures for data collection and for thematic data analysis in a generic model are discussed and described in detail.

Extraintestinal manifestations of inflammatory bowel disease are numerous. This study examined the effects of two models of acute colitis on cerebral blood flow (CBF) and permeability of the blood-brain barrier in rabbits. CBF (measured with radiolabeled microspheres), or the extraction ratio or permeability-surface area (PS) product of the blood-brain barrier to fluorescein and FITC-dextran, was measured 48 h after colitis induction with acetic acid (HAc) or trinitrobenzene sulfonic acid (TNBS). PS product for fluorescein increased ( P < 0.05) in TNBS colitis (1.33 × 10−5 ± 0.52 × 10−5 ml/s and 0.48 × 10−5 ± 0.13 × 10−5ml/s (mean ± SE) for treated ( n = 14) and untreated ( n = 10) animals, respectively. PS product for the larger FITC-dextran was not different in TNBS colitis (0.24 × 10−5 ± 0.09 × 10−5ml/s, n = 7) compared with untreated controls (0.19 × 10−5 ± 0.04 × 10−5 ml/s, n = 8). PS product for fluorescein increased ( P < 0.01) in HAc colitis compared with vehicle (2.66 × 10−5 ± 1.46 × 10−5 ml/s and 0.33 × 10−5 ± 0.05 × 10−5ml/s, respectively; n = 6 in each group). The extraction of fluorescein from the blood to the brain increased by 75% during TNBS colitis when compared with vehicle ( P < 0.05). CBF and cerebrovascular resistance did not change from the untreated control after TNBS colitis. Our data suggest that, irrespective of induction method, acute colitis increases the permeability of the blood-brain barrier to small molecules without changing CBF.

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