Lower weight gain after vaping cessation than after smoking quitting

Background: Smoking is frequently a way to control appetite and weight. The data concerning the body mass gain after quitting among the users of electronic cigarettes who have no prior history of smoking traditional cigarettes is inconsistent. Objective: In our study we have compared smoking and vaping impact on weight gain and glycaemia. Material and methods: 3 groups of rats were used. The group A was exposed to vapour and group B were exposed to smoke. Rats in the group C constituted the control group without nicotine exposition. Results: During 6 weeks of experiment weight gain of rats in the A and B groups was comparable, while animals from group C had gained signifi0cantly more. During 2 weeks after cessation of exposition to nicotine animals from group B gained more weight than rats of A and C group. Blood glucose was higher in group B than in groups A and C 24 h after last exposure to nicotine and 2 weeks after nicotine exposure cessation. Conclusion: Effects of vaping on weight increase is similar to smoking, but after vaping cassation weight gain is lower and comparable with nicotine nonusers.

CB2R agonist prevents nicotine induced lung fibrosis.

INTRODUCTION: Nicotine stimulates fibroblast proliferation while increasing inflammation and fibrosis of tissues. The cannabinoid receptor 1 (CB1R) is mainly located in the CNS, while cannabinoid receptor 2 (CB2R) is located in the immune cells within the body. CB2R regulates inflammatory processes and fibroblast function. PURPOSE: We investigated the impact of CB2R agonist, JWH 133 and the antagonist, AM630 on lung tissue, applied directly before nicotine application. MATERIAL AND METHODS: 40 mice were placed into 4 groups. The experimental groups received nicotine intraperitoneally at a dose of 0.05 mg/kg of body weight (BW) for 14 days. Group B also received AM630 (0.5mg/kg of BW), while Group A was administered with JWH133 (1 mg/kg of BW). Group N received nicotine alone. The Control group C received 0.9% NaCl. After decapitation, lung tissues were stained with H&E, Trichrome Masson's method, and IHC against CTGF and α-SMA. The digital image processing system Image J with the IHC profiler plugins was then employed, optical density and IHC optical density score were calculated. RESULTS: In the N group, an increase in the thickness of alveolar spaces (9.16 SD4.95µm vs. 4.77SD2.99µm in the C group), leukocytes infiltration and collagen deposition has been observed(OD: 0.20 SD0.0vs 0.07SD0.04 in the C group). In the B group, the alveolar space thickness has been the highest (11.57SD8.13µm). Furthermore, in this group, hyperaemia, destruction of lung structure, hyperplasia of II type pneumocyte and interstitial fibrosis has been observed (OD: 0.23 SD0.08). In contrast, the lung tissue of the A group has had normal structure and the thinnest alveolar septum (3.88 SD2.64µm). The expression of CTGF and α-SMA has been the highest in the B group. CONCLUSION: Nicotine induces interstitial lung fibrosis that is enhanced by the CB2R antagonist and diminished by the CB2R agonist. Therefore, the CB2R agonist may offer a protection against fibrosis.

Dietary supplements ­ consumer assessment based on questionnaire survey

INTRODUCTION: Dietary supplements (DS) are dietary products aiming only at diet complementation. Nevertheless, they are frequently used in treatment of various conditions since they are safer substitutes for medication. AIM OF THE STUDY: The aim of this study was to analyze the frequency of dietary supplements using by young people, their knowledge about the used substances, and the assessment of the effectiveness of DS by those who consumed these products. MATERIALS AND METHODS: The present study was conducted by the means of an anonymous questionnaire assessed the DS intake among subjects aged between 15 and 54. The questionnaire was performed both on-line among 611 subjects and in paper form among 242 1st year medical students of Medical University of Lublin. The average age of the participants was 22.02 ± 3.74 years. Women constituted 72.92% of all respondents. RESULTS: DS consumption was reported by most questionnaire participants, that is 77. 84%. The supplements were purchased mainly in pharmacies (81.63%). 47.87% of the respondents, declared to be aware of the undesirable side effects of DS, and 67.29% claimed to be able to distinguish between a medication and a supplement. 20.48% of the respondents reported a significant improvement of their condition resulting from DS usage, 51.05% reported a partial improvement, and 28.46% observed no difference. CONCLUSIONS: Dietary supplements are commonly consumed by young people regardless of the fact that many do not observe any DS intake-related improvement of their health. The knowledge about the effects of dietary supplements and their adverse effects is relatively high. Yet, many people do not know the difference between a medication and DS. The knowledge concerning the risks of DS misuse should be promoted among young people in particular.

Intrinsic apoptosis pathway in fallopian tube epithelial cells induced by cladribine.

Cladribine is a purine nucleoside analog which initiates the apoptotic mechanism within cells. Moreover, the available data confirms that cladribine, with the participation of the p53 protein, as well as the proapoptotic proteins from the Bcl-2 family, also induces the activation of the intrinsic apoptosis pathway. However, while there has been a lot of research devoted to the effect of cladribine on lymphatic system cells, little is known about the impact of cladribine on the reproductive system. The aim of our study was to evaluate apoptosis in oviduct epithelial cells sourced from 15 different female rats. In so doing, the sections were stained with caspases 3, 9, and 8. Results suggest that cladribine also induces apoptosis in the oviduct epithelial cells by way of the intrinsic pathway. Indeed, the discontinuing of the administration of cladribine leads to a reduction in the amount of apoptotic cells in the oviduct epithelium.

All That Glitters Is Not Gold: Assessment of Bee Pollen Supplementation Effects on Gastric Mucosa.

The aim of this study was to assess the influence of bee pollen supplementation on the levels of enzymes important for gastric mucosal homeostasis, namely cyclooxygenase-1 (COX-1), cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), and a biomarker-asymmetric dimethylarginine (ADMA)-in the gastric mucosa of Wistar rats. The experimental phase divided the rats into four groups: two control groups, sedentary and active, both not supplemented, and two experimental groups, sedentary and active, supplemented with bee pollen. The results indicated that bee pollen supplementation reduced the levels of COX-1 and elevated iNOS levels, while showing no significant impact on COX-2 levels. These findings do not conclusively support the gastroprotective and anti-inflammatory effects of bee pollen on gastric mucosa. However, the supplementation could have resulted in reduced ADMA levels in the physically active supplemented group. Our study does not unequivocally demonstrate the positive effects of bee pollen supplementation on the gastric mucosa, which may be attributed to the specific metabolism and bioavailability of substances within unprocessed, dried bee pollen. Further research should explore the topic of potential therapeutic applications of bee pollen in gastrointestinal health and its interactions with ADMA signaling pathways.

Lung histomorphological alterations in rats exposed to cigarette smoke and electronic cigarette vapour.

Electronic cigarettes are becoming increasingly common as a form of nicotine usage, known as vaping. Numerous studies have demonstrated that using electronic cigarettes may lead to nicotine dependence and has a potentially harmful impact on health. The present study compared the impact of electronic and conventional cigarettes on lung tissue. The experiment included 30 male Wistar rats. The animals were divided into three groups: Group A was exposed to electronic cigarette liquid vapour; group B to conventional smoke; and group C constituted the control group without exposition to the nicotine. In both experimental groups numerous alterations were observed, including a collapse of parenchyma, hyperhagia, hyperplasia of type II of pneumocytes, collagen deposition and an increased number of macrophages within thickened alveolar septa. Additionally, an initial elastolysis was observed. The elastic fibers were disrupted, sparse, irregular and thickened, whereas the numbers of α-SMA positive myofibroblasts and blood vessels were highest in the group exposed to conventional cigarette smoke. In conclusion, the usage of the electronic cigarettes leads to milder pathological alterations compared with traditional cigarette smoking. Nevertheless, the histopathological damage caused by vaping may lead to the development of alterations in the lung tissue which consequently hinder gas exchange.

Expression of caspase 1 and histomorphology of lung after cladribine treatment.

BACKGROUND: Cladribine is a useful immunosuppressive drug for the treatment of autoimmune diseases, leukemias and multiple sclerosis (MS). Despite the drug having low toxicity, side effects have been reported connected with myelosuppression, neutropenia and severe anemia. OBJECTIVES: The objective of this study was to investigate the influence of cladribine on lung pathomorphology and the expression of caspase 1 using immunohistochemistry method. MATERIAL AND METHODS: The study was conducted on Wistar rats, which were divided into a control group (C) and an experimental group (E). In group C, the rats were given a 0.9% NaCl solution by a subcutaneous injection, at the same dose as the dose of drug used in the experiment. In group E, the animals received cladribine at a dose of 0.07 mg/kg/24 h by a subcutaneous injection. The animals were decapitated 24 h following the last dose. To detect collagen deposition, we utilized Masson's trichrome staining. To evaluate the intensity of the inflammatory process in the lung, an immunohistochemistry reaction was carried out with the use of caspase 1. RESULTS: In group E, we observed an increase in the thickness of space between the alveoli. A statistically significant (p < 0.017243) difference between the thicknesses of the interalveolar septum was seen between the research groups. In E group, we observed regions with collagen deposition, alveolar epithelial cell hyperplasia, hyperemia and inflammatory cell infiltration. Caspase 1 activity was higher in group E. The immunohistochemical reaction with caspase 1 was positive in 49% of all the interalveolar cells in group E; however, in group C about 13% of the interalveolar cell showed positive immunohistochemistry (IHC) response. CONCLUSIONS: Cladribine-based therapy might have negative influence on lung morphology. The interstitial changes in the lung tissue suggest that cladribine is a drug that may be the cause of drug-induced lung disease and may lead to several respiratory disorders.

P53 protein in proliferation, repair and apoptosis of cells.

The p53 protein is an important factor of many intra- and extracellular processes. This protein regulates the repair of cellular DNA and induces apoptosis. It is also responsible for the regulation of the senescence and the cell entering the subsequent stages of the cellular cycle. The protein p53 is also involved in inhibiting angiogenesis and the induction of oxidative shock. In our study, we examined the activity of p53 protein in the uterine epithelial cells in rats treated with cladribine. Its action is mainly based on apoptosis induction. We compared the activity of p53 protein in cells with a high apoptosis index and in cells with active repair mechanisms and high proliferation index. We observed stronger p53 protein expression in the epithelial cells of the materials taken 24 h after the last dose of 2-CdA associated with the active process of apoptosis and inhibition of proliferation. After 4 weeks from the last dose of cladribine, the stronger expression of p53 protein was associated with both the existing changes in the cell's genome, the effects of the ongoing repair mechanisms, as well as the high proliferation activity.

Immunohistochemical evaluation of cell proliferation and apoptosis markers in ovarian surface epithelial cells of cladribine-treated rats.

Cladribine has been used in the treatment of hairy cell leukemia for about 30 years. In addition, the number of indications for the application of 2-CdA is constantly increasing. The treatment with cladribine, of younger persons and even children, appears to be a major factor stimulating the more exact recognition of its activities. However, till now, little has been known about the impact of cladribine on the reproductive system. The aim of the study was to evaluate the immunohistochemical expression of cell proliferation and apoptosis markers in ovarian surface epithelial (OSE) cells. In our study, ten rats were placed into two equal groups. The study group received daily subcutaneous injections of cladribine in a dose of 0.10 mg/kg of weight/day for one cycle lasting 7 days. The control group received only saline injections. The rats were sacrificed 24 h after the last injection, and their ovaries were extracted. The sections were immunohistochemically stained with cell proliferation marker Ki-67 and the apoptosis marker caspase 3. The expressions of the markers were evaluated using a light microscope. An analysis was made using an image analysis system and the CellAD software. The results were then statistically explored by way of the Mann-Whitney U test. The proliferative index (Ki-67) of ovarian surface epithelial cells was significantly lower in the study group than in the control group (p < 0.05). These results suggest that cladribine treatment has a potential to inhibit the OSE cell proliferation in rats. The apoptosis marker demonstrated a significant increase after the cladribine treatment. These suggest that cladribine induces apoptosis in OSE cells.