Homelessness and smoking cessation: insights from focus groups.

Smoking prevalence among homeless persons is approximately 70%, yet little is known about tobacco use patterns or smoking cessation practices in this population. We assessed smoking attitudes and behaviors, psychosocial and environmental influences on smoking, barriers to and interest in quitting, and preferred methods for cessation among some homeless smokers. Six 90-min focus groups of current smokers (N = 62) were conducted at homeless service facilities. Participants had a mean age of 41.5 years (SD = 9.3), were predominantly male (69.4%) and African American (59%), and smoked an average of 18.3 cigarettes/day. Although most reported that they were motivated to quit, a number of barriers to quitting were identified. Participants reported that the pervasiveness and social acceptance of tobacco use in homeless settings contributed to smoking more cigarettes per day, adopting alternative smoking behaviors such as smoking cigarette butts and making their own cigarettes, and experiencing difficulty in quitting. High levels of boredom and stress also were cited as reasons for continued smoking. Smoking frequently occurred in combination with alcohol or illicit drug use or to achieve a substitute "high." Most participants (76%) reported that they planned to quit smoking in the next 6 months. Many were interested in using pharmacotherapy in combination with behavioral treatments. Results suggest that, although motivated to quit smoking, homeless smokers are faced with unique social and environmental barriers that make quitting more difficult. Interventions must be flexible and innovative to address the unique needs of homeless smokers. Smoking restrictions at homeless service facilities and funding for smoking cessation assistance in this underserved population may help to reduce prevalence.

Epithelial hedgehog signals pattern the intestinal crypt-villus axis.

Morphological development of the small intestinal mucosa involves the stepwise remodeling of a smooth-surfaced endodermal tube to form finger-like luminal projections (villi) and flask-shaped invaginations (crypts). These remodeling processes are orchestrated by instructive signals that pass bidirectionally between the epithelium and underlying mesenchyme. Sonic (Shh) and Indian (Ihh) hedgehog are expressed in the epithelium throughout these morphogenic events, and mice lacking either factor exhibit intestinal abnormalities. To examine the combined role of Shh and Ihh in intestinal morphogenesis, we generated transgenic mice expressing the pan-hedgehog inhibitor, Hhip (hedgehog interacting protein) in the epithelium. We demonstrate that hedgehog (Hh) signaling in the neonatal intestine is paracrine, from epithelium to Ptch1-expressing subepithelial myofibroblasts (ISEMFs) and smooth muscle cells (SMCs). Strong inhibition of this signal compromises epithelial remodeling and villus formation. Surprisingly, modest attenuation of Hh also perturbs villus patterning. Desmin-positive smooth muscle progenitors are expanded, and ISEMFs are mislocalized. This mesenchymal change secondarily affects the epithelium: Tcf4/beta-catenin target gene activity is enhanced, proliferation is increased, and ectopic precrypt structures form on villus tips. Thus, through a combined Hh signal to underlying ISEMFs, the epithelium patterns the crypt-villus axis, ensuring the proper size and location of the emerging precrypt compartment.

Cis elements of the villin gene control expression in restricted domains of the vertical (crypt) and horizontal (duodenum, cecum) axes of the intestine.

Villin, an actin bundling protein found in the apical brush border of absorptive tissues, is one of the first structural genes to be transcriptionally activated in the embryonic intestinal endoderm. In the adult, villin is broadly expressed in every cell of the intestinal epithelium on both the vertical axis (crypt to villus tip) and the horizontal axis (duodenum through colon) of the intestine. Here, we document that a 12.4-kilobase region of the mouse villin gene drives high level expression of two different reporter genes (LacZ and Cre recombinase) within the entire intestinal epithelium of transgenic mice. Deletion of a portion of this transgene results in reduction of beta-galactosidase activity in restricted domains of the small intestine (duodenum) and large intestine (cecum). In addition, expression is reduced in the crypt compartment throughout the intestine. Thus, the global expression pattern of villin in the intestine is apparently the consequence of an amalgam of distinct and individual domain-specific control processes. That is, expression of villin in the duodenum and cecum requires different regulatory sequences than the rest of the intestine, and the expression of villin in crypts is regulated by different circuitry than expression of villin on villus tips.