An Open Group for Patients with Various Chronic Illnesses: A Qualitative Case Evaluation.

Many self-management and support groups for medical patients target a specific medical condition or diagnosis and are often time-limited. Presented is the Medical Issues Group (MIG), which is an integration of a self-management program and a therapist-led supportive psychotherapy group. This ongoing group is open to individuals with any significant chronic medical condition. Findings from our qualitative evaluation (n = 9) revealed that this group is positively received and can provide individuals who are experiencing challenges associated with living with medical illness a forum to receive high quality social support, address feelings of social isolation and loneliness, and develop adaptive coping strategies to adjust to medical illness. The inclusive structure of the group appears to provide enhanced access to high quality support and intervention for a vulnerable population. Limitations and implications are discussed.

Smoking by young women with restrained eating following a food prime in the context of an alternative distractor.

Female smokers with elevated dietary restraint (high restrainers) may smoke more than nonrestrained eaters after a disinhibiting food event. The current study aimed to determine whether high restrainers smoke merely to distract themselves from unplanned eating or whether the weight-control aspects of smoking play a role. Primary aims were to test the effect of restraint status and a food prime on smoking and eating behavior in the presence of an alternative distractor (a computer tablet) and to examine the role of expectancies. Utilizing a between-subject design, female smokers (N = 128) were randomized to receive a milkshake prime (Prime condition) or not (No-Prime). They then received access to tempting foods, cigarettes, and the computer tablet. As expected, higher dietary restraint predicted shorter latency to smoke and craving to smoke but not latency to use the tablet. Additionally, a pattern of proximal expectancy subscales associated with weight/appetite control predicted cigarette consumption. Neither restraint nor expectancies interacted with condition to predict smoking behavior. Findings suggest that dietary restrainers attempt to prevent food consumption by turning to cigarettes, beyond preference for other salient distracting stimuli. Thus, smoking appears to function as more than simply a distractor from eating, and it is also associated with strong beliefs about weight and appetite control. Results offer implications for assessment and intervention among individuals presenting for smoking cessation treatment, particularly young adult women. Specifically, assessment of dietary restraint and expectancies related to weight and appetite aspects of smoking may be important to consider for tailored interventions. (PsycINFO Database Record

A technique for lyopreservation of Clostridium ljungdahlii in a biocomposite matrix for CO absorption.

A system capable of biocatalytic conversion of distributed sources of single carbon gases such as carbon monoxide into hydrocarbons can be highly beneficial for developing commercially viable biotechnology applications in alternative energy. Several anaerobic bacterial strains can be used for such conversion. The anaerobic carbon monoxide-fixing bacteria Clostridium ljungdahlii OTA1 is a model CO assimilating microorganism that currently requires cryogenic temperature for storage of the viable strains. If these organisms can be stabilized and concentrated in thin films in advanced porous materials, it will enable development of high gas fraction, biocomposite absorbers with elevated carbon monoxide (CO) mass transfer rate, that require minimal power input and liquid, and demonstrate elevated substrate consumption rate compared to conventional suspended cell bioreactors. We report development of a technique for dry-stabilization of C. ljungdahlii OTA1 on a paper biocomposite. Bacterial samples coated onto paper were desiccated in the presence of trehalose using convective drying and stored at 4°C. Optimal dryness was ~1g H2O per gram of dry weight (gDW). CO uptake directly following biocomposite rehydration steadily increases over time indicating immediate cellular metabolic recovery. A high-resolution Raman microspectroscopic hyperspectral imaging technique was employed to spatially quantify the residual moisture content. We have demonstrated for the first time that convectively dried and stored C. ljungdahlii strains were stabilized in a desiccated state for over 38 days without a loss in CO absorbing reactivity. The Raman hyperspectral imaging technique described here is a non-invasive characterization tool to support development of dry-stabilization techniques for microorganisms on inexpensive porous support materials. The present study successfully extends and implements the principles of dry-stabilization for preservation of strictly anaerobic bacteria as an alternative to lyophilization or spray drying that could enable centralized biocomposite biocatalyst fabrication and decentralized bioprocessing of CO to liquid fuels or chemicals.

ß-arrestin-1 mediates nicotine-induced metastasis through E2F1 target genes that modulate epithelial-mesenchymal transition.

Cigarette smoking is a major risk factor in the development of non-small cell lung cancer (NSCLC), which accounts for 80% of all lung cancers. Nicotine, the major addictive component of tobacco smoke, can induce proliferation, invasion, and epithelial-to-mesenchymal transition (EMT) in NSCLC cell lines and promote metastasis of NSCLC in mice. Here, we demonstrate that the scaffolding protein ß-arrestin-1 is necessary for nicotine-mediated induction of mesenchymal genes vimentin and fibronectin as well as EMT regulators ZEB1 and ZEB2. Nicotine induced changes in cell morphology and ablate tight junctions consistent with EMT; ß-arrestin-1, but not ß-arrestin-2, was required for these changes. ß-Arrestin-1 promoted the expression of the mesenchymal genes, as well as ZEB1 and ZEB2, through the mediation of the E2F1 transcription factor; this required Src kinase activity. Stimulation of multiple NSCLC cell lines with nicotine led to enhanced recruitment of ß-arrestin-1 and E2F1 on vimentin, fibronectin, and ZEB1 and ZEB2 promoters. Furthermore, there was significantly more ß-arrestin-1 and E2F1 associated with these promoters in human NSCLC tumors, and ß-arrestin-1 levels correlated with vimentin and fibronectin levels in human NSCLC samples. A549-luciferase cells lacking ß-arrestin-1 showed a significantly reduced capacity for tumor growth and metastasis when orthotopically implanted into the lungs of SCID-beige mice. Taken together, these studies reveal a novel role for ß-arrestin-1 in the growth and metastasis of NSCLC.

Smoking as alternative to eating among restrained eaters: effect of food prime on young adult female smokers.

OBJECTIVE: Restrained eaters attempt to employ cognitive control over decisions to eat, which leaves them prone to eat in a disinhibited manner. This eating style is associated with elevated rates of smoking compared to the general population. The current study merged smoking and eating research methodology to investigate a mechanism that may underlie this association by testing whether a food prime, which has been found to elicit disinhibited eating in restrained eaters, could also motivate smoking as an alternative to eating. METHOD: Using a randomized, 2-arm (Prime/No-Prime) between-subjects design, it was hypothesized that young adult female smokers who endorsed elevated dietary restraint and received a food prime would smoke more when given the option, compared to smokers who did not receive the food prime. RESULTS: As predicted, restraint score moderated the effect of the food prime upon smoking behavior (latency to first puff, ß = 1, t = 3.8, df = 123, p < .001) and cigarette craving (ß = -.79, t = -2.9, df = 127, p < .005), suggesting that after a food prime, restrained-eating smokers may opt to smoke to prevent further food intake. CONCLUSION: This study identified a pathway, namely violation of dietary restraint, linking eating and smoking behaviors that may contribute to the population-based covariance between disordered eating and tobacco use.

Influence of affective manipulations on cigarette craving: a meta-analysis.

BACKGROUND AND AIMS: Retrospective self-report and observational studies have yielded inconsistent findings regarding the capacity of negative affect (NA) to increase smoking motivation among dependent samples. Controlled laboratory studies offer an alternative paradigm for testing the role of affective state upon smoking motivation. The aim of the current study was to quantify cue-provoked cravings produced by affective manipulations in the published literature, and to identify theoretical and methodological moderators. METHODS: We conducted a systematic literature search to identify experimental studies that manipulated NA or positive affect (PA), and assessed post-manipulation craving. Separate random-effects meta-analyses examined NA and PA cues as predictors of self-reported craving. Self-reported affect (NA and PA), nicotine deprivation, gender, nicotine dependence, order of cue presentation, single versus multi-item craving assessment and affect induction method were tested as moderators of affective cue-induced craving. RESULTS: NA manipulations produced a medium effect [g = 0.47; confidence interval (CI) = 0.31-0.63] on craving, but no main effects were found for PA manipulations (g = 0.05; CI = -0.09 to 0.20) on craving. Self-reported NA moderated the extent to which NA and PA manipulations elicited craving (P < 0.02 for each). That is, more effective NA manipulations produced greater cravings, and PA manipulations reduced cravings when they reduced NA. CONCLUSIONS: Laboratory studies indicate that negative, but not positive, affect is a situational determinant of cravings to smoke among dependent smokers. Adverse emotional states increase craving to smoke among dependent smokers, but positive emotional states do not consistently reduce craving to smoke.

Responding to tobacco craving: experimental test of acceptance versus suppression.

Acceptance and Commitment Therapy (ACT) provides a theoretical rationale for "acceptance" of thoughts and feelings, and proscribes suppression, a more intuitive and commonly used coping strategy. Suppression is theorized to have negative consequences not applicable to acceptance, including depletion in self-control and ironic postsuppression rebound effects. However, it remains largely unknown whether these strategies differentially affect frequency of drug-related thoughts, craving intensity, drug use behavior, or other relevant outcomes. Adult smokers (N = 162) were randomly assigned to receive a brief laboratory-based coping intervention (acceptance or suppression) or were not given coping instructions (control group) and then were exposed to smoking cues. Results indicated that the suppression group was successful at suppressing thoughts of smoking, as they reported fewer thoughts of smoking than the other two groups. Also, both coping strategies were associated with benefits with respect to craving and affect. However, there were no group differences in depletion, and rebound effects did not occur when coping was discontinued. Following the laboratory session, all participants attempted to quit or at least reduce their smoking for 3 days; the acceptance and suppression groups resumed use of their strategy. At 3-day follow-up, the acceptance and suppression groups reported greater self-efficacy for avoiding smoking when experiencing craving compared to the control group. However, there were no group differences in the number of cigarettes smoked during the 3 days. This study provides support for the value of acceptance-based coping, but it also suggests that more research is needed to differentiate its benefits compared to suppression.

Regulation of vascular endothelial growth factor receptors by Rb and E2F1: role of acetylation.

E2F transcription factors regulate a variety of cellular processes, but their role in angiogenesis is not clear. We find that many genes involved in angiogenesis such as FLT-1, KDR, and angiopoietin 2 have potential E2F1 binding sites in their promoter. Chromatin immunoprecipitation (ChIP) assays showed that E2F1 can associate with these promoters and the recruitment of E2F1 was enhanced upon vascular endothelial growth factor (VEGF) stimulation with concomitant dissociation of Rb, leading to the transcriptional activation of these promoters. Transient transfection experiments showed that these promoters were induced by E2F1 and repressed by Rb, whereas depletion of E2F1 decreased their expression. The increased binding of E2F1 to these promoters upon VEGF stimulation correlated with the acetylation of histones and E2F1; this required VEGF receptor function, as seen in ChIP-re-ChIP experiments. This suggests the existence of a positive feedback loop regulating E2F1 acetylation and VEGF receptor expression. Acetylation associated with VEGF signaling seems to be predominantly mediated by P300/CBP-associated factor, and the depletion of histone acetyl transferases disrupted the formation of angiogenic tubules. These results suggest a novel role for E2F1 and acetylation in the angiogenic process.

Nicotine promotes tumor growth and metastasis in mouse models of lung cancer.

BACKGROUND: Nicotine is the major addictive component of tobacco smoke. Although nicotine is generally thought to have limited ability to initiate cancer, it can induce cell proliferation and angiogenesis in a variety of systems. These properties might enable nicotine to facilitate the growth of tumors already initiated. Here we show that nicotine significantly promotes the progression and metastasis of tumors in mouse models of lung cancer. This effect was observed when nicotine was administered through intraperitoneal injections, or through over-the-counter transdermal patches. METHODS AND FINDINGS: In the present study, Line1 mouse adenocarcinoma cells were implanted subcutaneously into syngenic BALB/c mice. Nicotine administration either by intraperitoneal (i.p.) injection or transdermal patches caused a remarkable increase in the size of implanted Line1 tumors. Once the tumors were surgically removed, nicotine treated mice had a markedly higher tumor recurrence (59.7%) as compared to the vehicle treated mice (19.5%). Nicotine also increased metastasis of dorsally implanted Line1 tumors to the lungs by 9 folds. These studies on transplanted tumors were extended to a mouse model where the tumors were induced by the tobacco carcinogen, NNK. Lung tumors were initiated in A/J mice by i.p. injection of NNK; administration of 1 mg/kg nicotine three times a week led to an increase in the size and the number of tumors formed in the lungs. In addition, nicotine significantly reduced the expression of epithelial markers, E-Cadherin and beta-Catenin as well as the tight junction protein ZO-1; these tumors also showed an increased expression of the alpha(7) nAChR subunit. We believe that exposure to nicotine either by tobacco smoke or nicotine supplements might facilitate increased tumor growth and metastasis. CONCLUSIONS: Our earlier results indicated that nicotine could induce invasion and epithelial-mesenchymal transition (EMT) in cultured lung, breast and pancreatic cancer cells. This study demonstrates for the first time that administration of nicotine either by i.p. injection or through over-the-counter dermal patches can promote tumor growth and metastasis in immunocompetent mice. These results suggest that while nicotine has only limited capacity to initiate tumor formation, it can facilitate the progression and metastasis of tumors pre-initiated by tobacco carcinogens.

Nicotine induces cell proliferation, invasion and epithelial-mesenchymal transition in a variety of human cancer cell lines.

Cigarette smoking is strongly correlated with the onset of nonsmall cell lung cancer (NSCLC). Nicotine, an active component of cigarettes, has been found to induce proliferation of lung cancer cell lines. In addition, nicotine can induce angiogenesis and confer resistance to apoptosis. All these events are mediated through the nicotinic acetylcholine receptors (nAChRs) on lung cancer cells. In this study, we demonstrate that nicotine can promote anchorage-independent growth in NSCLCs. In addition, nicotine also induces morphological changes characteristic of a migratory, invasive phenotype in NSCLCs on collagen gel. These morphological changes were similar to those induced by the promigratory growth factor VEGF. The proinvasive effects of nicotine were mediated by alpha7-nAChRs on NSCLCs. RT-PCR analysis showed that the alpha7-nAChRs were also expressed on human breast cancer and pancreatic cancer cell lines. Nicotine was found to promote proliferation and invasion in human breast cancer. The proinvasive effects of nicotine were mediated via a nAChR, Src and calcium-dependent signaling pathway in breast cancer cells. In a similar fashion, nicotine could also induce proliferation and invasion of Aspc1 pancreatic cancer cells. Most importantly, nicotine could induce changes in gene expression consistent with epithelial to mesenchymal transition (EMT), characterized by reduction of epithelial markers like E-cadherin expression, ZO-1 staining and concomitant increase in levels of mesenchymal proteins like vimentin and fibronectin in human breast and lung cancer cells. Therefore, it is probable that the ability of nicotine to induce invasion and EMT may contribute to the progression of breast and lung cancers.