Breaking down barriers: rationalisations and motivation to stop among Chinese male smokers under cigarette dependence.

BACKGROUND: Smoking rationalisation beliefs are a huge barrier to quitting smoking. What types of rationalisations should be emphasised in smoking cessation interventions? Although past literature has confirmed the negative relationship between those beliefs and motivation to stop smoking, little is known regarding the importance and performance of those beliefs on motivation with varying cigarette dependence. The study aimed to ascertain rationalisations that are highly important for motivation yet perform poorly in different cigarette dependence groups. METHODS: The cross-sectional study was conducted from November 19 to December 9, 2023 in Guiyang City, China. Adult male current smokers were enrolled. Partial least squares structural equation modelling was used to test the hypothesis. The multi-group analysis was used to determine the moderating effect of cigarette dependence, and the importance-performance map analysis was utilised to assess the importance and performance of rationalisations. RESULTS: A total of 616 adult male current smokers were analysed, and they were divided into the low cigarette dependence group (n = 297) and the high cigarette dependence group (n = 319). Except for risk generalisation beliefs, smoking functional beliefs (H1: -ß = 0.131, P < 0.01), social acceptability beliefs (H3: ß = -0.258, P < 0.001), safe smoking beliefs (H4: ß = -0.078, P < 0.05), self-exempting beliefs (H5: ß = -0.244, P < 0.001), and quitting is harmful beliefs (H6: ß = -0.148, P < 0.01) all had a significant positive influence on motivation. Cigarette dependence moderated the correlation between rationalisations and motivation. In the high-dependence group, the social acceptability beliefs and smoking functional beliefs were located in the "Concentrate Here" area. In the low-dependence group, the social acceptability beliefs were also situated in there. CONCLUSIONS: Social acceptability beliefs and smoking functional beliefs showed great potential and value for improvement among high-dependence smokers, while only social acceptability beliefs had great potential and value for improvement among low-dependence smokers. Addressing these beliefs will be helpful for smoking cessation. The multi-group analysis and the importance-performance map analysis technique have practical implications and can be expanded to other domains of health education and intervention practice.

[Study on the relationship between microsatellite alterations of RASSF1A gene and the development of cervical carcinoma].

OBJECTIVE: To explore the relationship between microsatellite alterations of RASSF1A gene and the development of cervical carcinoma, and HPV16 infection. METHODS: Two sites of microsatellite polymorphism of RASSF1A gene were selected, we used polymerase chain reaction (PCR) technique to detect the LOH and MSI of cervical tissues, and to detect the infection state of HPV16. RESULTS: There were significant differences of LOH rates at the two sites between clinical stage and pathological grade (P < 0.05). Significant differences were noted between the cervical carcinomas with lymph node metastasis and those without lymph node metastasis in regard to their LOH and MSI at the two sites ( P < 0.05). The incidence of LOH of RASSF1A gene was higher in HPV16(+) than that in HPV16(-) ( P < 0.05). CONCLUSION: The change of RASSF1A gene is a relatively late event in cervical carcinomas. The detection of the LOH and MSI of RASSF1A gene might be helpful to the early diagnosis and the screening of cervical carcinoma. It might also be useful for predicting the prognosis of cervical carcinoma. Infection of HPV16 and LOH of RASSF1A gene had reacted together in the development of cervical carcinoma.

The expression and functional role of nicotinic acetylcholine receptors in rat adipocytes.

To clarify whether nicotine has a direct effect on the function of adipocytes, we evaluated nicotinic acetylcholine receptor (nAChR) expression in adipocytes by reverse transcriptase-polymerase chain reaction (RT-PCR) and immunocytochemistry and the direct effects of nicotine on the production of adipocytokines by enzyme-linked immunosorbent assay and Western blot analysis. Receptor binding assays were performed using [3H]nicotine. RT-PCR studies revealed that alpha1-7, 9, 10, beta1-4, delta, and epsilon subunit mRNAs are expressed in adipocytes. Immunocytochemical experiments also suggested the presence of alpha7 and beta2 subunits. The receptor binding assay revealed a binding site for nicotine (Kd = 39.2 x 10(-9) M) on adipocytes. Adipocytes incubated with nicotine for 12 and 36 h released tumor necrosis factor-alpha (TNF-alpha), adiponectin, and free fatty acid (FFA) into the medium in a dose-dependent manner with increasing nicotine concentration from 6 x 10(-8) to 6 x 10(-4) M. However, TNF-alpha protein levels in adipocytes incubated for 12 and 36 h decreased in a dose-dependent manner with increasing nicotine concentration from 6 x 10(-8) to 6 x 10(-4) M. These results show that adipocytes have functional nAChRs and suggest that nicotine reduces TNF-alpha protein production in adipocytes through the activation of nAChRs. Nicotine may temporarily lower insulin sensitivity by stimulating the secretion of TNF-alpha and FFA, whereas long-term direct stimulation of nAChRs by nicotine in addition to autonomic nervous system stimulation may contribute to better insulin sensitivity in vivo through a modulated secretion of adipocytokines.

Long-term oral nicotine administration reduces insulin resistance in obese rats.

This study aimed to investigate the effect of long-term oral nicotine administration on insulin resistance in an animal model of obesity. Eight-week-old male Zucker fatty rats (ZFRs) were administered nicotine tartrate dihydrate (4.6 mg/kg/day) in the drinking water. The control group was pair-fed. The body weights and food intake over 8 weeks were similar in both groups. Plasma glucose levels at 3, 6, 9, 12, and 15 min after insulin administration (0.5 U/kg) in the nicotine group were significantly lower than those in the control group. The calculated K(ITT) value for the nicotine group was significantly higher than that for the control group. Wet weight of the liver in the nicotine group was significantly lower than that in the control group. Transaminases and histological examination of the liver revealed no alteration by nicotine administration. Glycogen, glycogen synthetase activity and gluconeogenesis in the liver in the nicotine group were significantly lower than those in the control group. Phosphorylase-a activity of the liver in the nicotine group was significantly higher than that in the control group. Glycogen, glycogen synthetase, and phosphorylase-a activity of skeletal muscle were similar in both groups. These results suggest that long-term oral nicotine administration may reduce insulin resistance in obese diabetic rats through a reduced hepatic glucose release and, in part, contribute to lowering blood glucose levels.