Addiction Mindsets and Psychological Processes of Quitting Smoking

Background: Lay belief systems about the malleability of human attributes have been shown to impact behavior change in multiple domains. Addiction mindset—i.e., beliefs about the permanence (vs. malleability) of addiction — may affect cigarette smokers’ ability to quit, but this has never been examined. Objectives: The aims of the present research were to develop a measure of addiction mindset (study 1) and examine its associations with various psychological aspects of quitting smoking (study 2). Methods: In Study 1, using factor analysis of current smokers’ and nonsmokers’ (n?=?600) responses to 22 items designed to measure addiction mindset, we developed a reliable six-item Addiction Mindset Scale (AMS). In Study 2, adult smokers (n?=?200) completed the AMS, and measures of a number of psychological processes related to smoking. Results: Higher scores on the AMS, indicative of the belief that addiction is malleable (referred to as a growth mindset), were positively and significantly associated with greater motivation to quit, greater commitment to quitting, greater self-efficacy to abstain, less attribution of failure to lack of ability to change addiction, and fewer self-reported barriers to cessation (all p’s < .05). Conclusions: The results of this study show a relationship between the beliefs about the permanence of addiction and psychological processes relevant to quitting smoking. The findings underscore the potential of future research exploring how addiction mindsets relate to successful smoking cessation as well as other types of addictive behavior and how they can be applied to change people’s behavior.     

HPLC-MS Method for Simultaneous Quantitative Determination of an Innovative Russian Gestagen and its Metabolites in Rat and Rabbit Blood Sera

Pharmaceutical Chemistry Journal - An HPLC-MS method for simultaneous quantitative determination of a novel gestagenic pharmaceutical and two of its metabolites in rat and rabbit blood sera was...     

Sacituzumab govitecan: breakthrough targeted therapy for triple-negative breast cancer

Introduction: Triple negative breast cancer (TNBC) is an aggressive breast cancer subtype associated with an increased risk of recurrence and cancer-related death. Unlike hormone receptor-positive or HER2-positive breast cancers, there are limited targeted therapies available to treat TNBC and cytotoxic chemotherapy remains the mainstay of treatment. Sacituzumab govitecan (IMMU-132) is an antibody-drug conjugate targeting Trop-2 expressing cells and selectively delivering SN-38, an active metabolite of irinotecan.

Areas covered: This review covers the mechanism of action, safety and efficacy of sacituzumab govitecan in patients with previously treated, metastatic TNBC. Additionally, efficacy data in other epithelial malignancies is included based on a PubMed search for ‘sacituzumab govitecan’ and ‘clinical trial’.

Expert opinion: Sacituzumab govitecan has promising anti-cancer activity in patients with metastatic TNBC previously treated with at least two prior lines of systemic therapy based on a single arm Phase I/II clinical trial. A confirmatory Phase III randomized clinical trial is ongoing. Sacituzumab govitecan has a manageable side effect profile, with the most common adverse events being nausea, neutropenia, and diarrhea. The activity of sacituzumab govitecan likely extends beyond TNBC with promising early efficacy data in many other epithelial cancers, including hormone receptor-positive breast cancer.     

Klinische Notfall- und Akutmedizin als hochqualitative Weiterbildung nach internationalem Vorbild: die Perspektive der Weiterzubildenden

Notfall + Rettungsmedizin -     

Sorsby fundus dystrophy: Insights from the past and looking to the future

Sorsby fundus dystrophy (SFD), an autosomal dominant, fully penetrant, degenerative disease of the macula, is manifested by symptoms of night blindness or sudden loss of visual acuity, usually in the third to fourth decades of life due to choroidal neovascularization (CNV). SFD is caused by specific mutations in the Tissue Inhibitor of Metalloproteinase-3, (TIMP3) gene. The predominant histo-pathological feature in the eyes of patients with SFD are confluent 20–30 m thick, amorphous deposits found between the basement membrane of the retinal pigment epithelium (RPE) and the inner collagenous layer of Bruch's membrane. SFD is a rare disease but it has generated significant interest because it closely resembles the exudative or “wet” form of the more common age-related macular degeneration (AMD). In addition, in both SFD and AMD donor eyes, sub-retinal deposits have been shown to accumulate TIMP3 protein. Understanding the molecular functions of wild-type and mutant TIMP3 will provide significant insights into the patho-physiology of SFD and perhaps AMD. This review summarizes the current knowledge on TIMP3 and how mutations in TIMP3 cause SFD to provide insights into how we can study this disease going forward. Findings from these studies could have potential therapeutic implications for both SFD and AMD.