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.

The aim of the report was to evaluate the impact of soy protein containing isoflavones and soy isoflavones extract on lipid profile in postmenopausal women, as compared with placebo or protein of milk, casein or isolated soy protein with or without trace isoflavone content. We used the following databases: MEDLINE (PubMed), EMBASE and the Cochrane Library. Quantitative data synthesis was performed by applying a random-effects model. Subgroup analysis and meta-regression were performed to assess the modifiers of treatment response. In total, in the analysis studies, 2305 postmenopausal women took part. Changes in the lipid profile showed statistically significant decreases of total cholesterol by −0.12 (95% CI: −0.21, −0.03) mmol/L, −4.64 (95% CI: −8.12, −1.16) mg/dL, p = 0.01 and increased HDL-cholesterol by 0.03 (95% CI: 0.00, 0.06) mmol/L, 1.15 (95% CI: 0.00, 1.93) mg/dL, p = 0.05, as well as in LDL-cholesterol −0.05 (95% CI: −0.11, 0.01) mmol/L, −1.93 (95% CI: −4.25, 0.39) mg/dL, p = 0.08 and triacylglycerols −0.07 (95% CI: −0.14, 0.00) mmol/L, −6.123 (95% CI: −12.25, 0.00) mg/dL, p = 0.06. Our results suggests that soy and its isoflavones can be effective in correction changes in lipid metabolism in postmenopausal women and may favorably influence in preventing cardiovascular events.

A minor subset (approximately 5%) of peripheral T cells has their TCR build up from γ and δ chains instead of α and β—those are the γδ T lymphocytes. They can be functionally divided into subsets, e.g., Th1-, Th2-, Th9-, Th17-, Tfh-, and Treg-like γδ T cells. They share some specifics of both innate and adaptive immunity, and are capable of rapid response to a range of stimuli, including some viral and bacterial infections. Atopic diseases, including asthma, are one of major health-related problems of modern western societies. Asthma is one of the most common airway diseases, affecting people of all ages and having potential life-threatening consequences. In this paper, we review the current knowledge about the involvement of γδ T cells in the pathogenesis of asthma and its exacerbations. We summarize both the studies performed on human subjects as well as on the murine model of asthma. γδ T cells seem to be involved in the pathogenesis of asthma, different subsets probably perform opposite functions, e.g., symptom-exacerbating Vγ1 and symptom-suppressing Vγ4 in mice model of asthma.

Background: The role of probiotics, prebiotics, and synbiotics in preventing asthma and other allergic diseases has been widely explored via many randomized controlled trials. However, the results on the effect of their supplementation during infancy to the incidence of allergic rhinitis or asthma, are conflicting.The study was designed to bring to light the potential effects of pro-, pre-, and synbiotics supplementation in early childhood with regard to the future occurrence of allergic diseases.Method: The results of randomized controlled trials were searched for in several medical data bases. The study protocol was prepared in accordance with PRISMA guidelines and applied a Revised Cochrane risk-of-bias tool for randomized trials. Two writers were designed to perform studies selection.Results: Eleven randomized controlled trials, among 1659 children (525 in the probiotic group, 342 in prebiotic group, 128 in synbiotic group and 833 in control groups) were analyzed. There was no difference in asthma risk development between the groups that received probiotics or placebo. We observed lower risk of asthma in children receiving prebiotic and synbiotic than in control groups.Conclusion: The current study indicates that probiotics supplementation in the first months after birth does not decrease the risk of asthma development in the first years of life in high-risk children, although prebiotics and synbiotics may be the potential preventive factors that reduce the incidence of asthma in children.

The discovery of an effective airway inflammation marker which correctly identifies the condition and phenotype of asthma still constitutes a significant challenge. The determination of NLR, that is, the ratio of neutrophils to lymphocytes, would overcome this challenge. The role of the neutrophil–lymphocytic index in the diagnosis of specific types of asthma is investigated in the present study. The results of laboratory tests of 482 pediatric patients were used for the analysis. The results of 107 children without allergic disease symptoms were selected for the control group. The mean NLR in patients with asthma was 3.42 ± 4.05, and in the control group it was 1.94 ± 1.91. The difference between the NLR in allergic and non-allergic asthma was statistically significant in the allergic asthma and control groups. There was no statistically significant difference between NLR and body temperature, BMI, and gender. The value of NLR was significantly higher in the blood of patients suffering from asthma compared to the control group. The NLR was the highest among patients with allergic asthma. The use of this blood test in daily practice may facilitate the diagnosis of asthma and differentiation between asthma types, especially when the results of other tests are inconclusive.

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.