Background: Matrix metalloproteinase-9 is closely associated with the invasive and metastatic potential of most types of solid cancers. Our objective was to investigate the MMP-9 expression in lung cancer and to evaluate their relations to histopathologic types and prognosis. Methods: Bronchoscopic samples were obtained from tumor and normal bronchial mucosa in 25 patients with lung cancer. Total RNA was isolated from the tissues, and the relative expression as well as the activity of MMP-9 was evaluated. Results: Non–small cell lung cancer (NSCLC) and small cell lung cancer (SCLC) showed significantly higher MMP-9 expression (P<0.0001) compared with normal tissues. MMP-9 activity in tissue and serum samples from both cancer groups were significantly higher than normal tissue and serum controls (P<0.0001). Also, MMP-9 expression and tissue and serum activity were significantly higher in NSCLC than in SCLC (P=0.0167, 0.0454, and 0.004, respectively). As regards the pathologic types of NSCLC, similar results were found for the adenocarcinoma subgroup versus squamous cell lung cancer (P=0.0015, 0.0052, and 0.0011, respectively). MMP-9 expression and tissue activity were higher in stage III-IV NSCLC cases compared with early tumor stages (P=0.0120 and 0.0271, respectively). Conclusions: The expression and activity of MMP-9 are upregulated in NSCLC and are related to the pathologic type and clinical stage of NSCLC. Significantly higher expression and activity of MMP-9 in tumor tissue than in the surrounding tissue supports the important role of this metalloproteinase in the growth of lung cancer, and it could be used as a suggested therapeutic target.

Nutrition has a predominant and recognizable role in health management. Nutrigenetics is the science that identifies and characterizes gene variants associated with differential response to nutrients and relating this variation to variable disease states especially cancer. This arises from the epidemiological fact that cancer accounts for a high proportion of total morbidity and mortality in adults throughout the world. There is much evidence to support that genetic factors play a key role in the development of cancer; these genetic factors such as DNA instability and gene alterations are affected by nutrition. Nutrition may also lead to aberrant DNA methylation, which in turn contributes to carcinogenesis. The aim of this work is to clarify the basic knowledge about the vital role of nutrition-related genes in various disease states, especially cancer, and to identify nutrigenetics as a new concept that could highlight the relation between nutrition and gene expression. This may help to understand the mechanism and pathogenesis of cancer. The cause of cancer is a complex interplay mechanism of genetic and environmental factors. Dietary nutrient intake is an essential environmental factor and there is a marked variation in cancer development with the same dietary intake between individuals. This could be explained by the variation in their genetic polymorphisms, which leads to emergence of the concept of nutrigenomics and nutrigenetics.

Factors such as aging, an unhealthy lifestyle with decreased physical activity, snacking, a standard Western diet, and smoking contribute to raising blood pressure to a dangerous level, increasing the risk of coronary artery disease and heart failure. Atherosclerosis, or aging of the blood vessels, is a physiological process that has accelerated in the last decades by the overconsumption of carbohydrates as the primary sources of caloric intake, resulting in increased triglycerides and VLDL-cholesterol and insulin spikes. Classically, medications ranging from beta blockers to angiotensin II blockers and even calcium channel blockers were used alone or in combination with lifestyle modifications as management tools in modern medicine to control arterial blood pressure. However, it is not easy to control blood pressure or the associated complications. A low-carbohydrate, high-fat (LCHF) diet can reduce glucose and insulin spikes, improve insulin sensitivity, and lessen atherosclerosis risk factors. We reviewed articles describing the etiology of insulin resistance (IR) and its impact on arterial blood pressure from databases including PubMed, PubMed Central, and Google Scholar. We discuss how the LCHF diet is beneficial to maintaining arterial blood pressure at normal levels, slowing down the progression of atherosclerosis, and reducing the use of antihypertensive medications. The mechanisms involved in IR associated with hypertension are also highlighted.

The prevalence of insulin resistance syndrome increases during menopause with the overproduction of reactive oxygen species and impairment of the free radical scavenger function. Therefore, we investigated the effects of 17β-estradiol (E₂) and vitamin E, as an antioxidant, on lipid peroxidation and antioxidant levels in the brain cortex and liver of ovariectomized rats as well as on insulin resistance in those rats. Forty female Sprague–Dawley rats, 3 months of age and weighing 231.5 ± 9.4 g, were divided into 4 groups: sham, ovariectomized (OVX), OVX treated with E₂ (40 µg/kg subcutaneously), and OVX treated with E₂ and vitamin E (100 mg/kg intraperitoneally). The 4 groups received the appropriate treatment every day for 8 weeks. Levels of glutathione, glutathione peroxidase, superoxide dismutase , catalase, and malondialdehyde in the brain cortex and liver of ovariectomized rats were measured. Also, fasting plasma insulin, glucose, and homeostatis model assessment of insulin resistance (HOMA-IR) were determined. Malondialdehyde increased and antioxidants (glutathione, glutathione peroxidase, catalase, superoxide dismutase) decreased in the brain cortex and liver of OVX rats. Also, fasting glucose, insulin, and HOMA-IR increased in OVX rats. E₂ and E₂ plus vitamin E decreased malondialdehyde and increased antioxidants in the brain cortex and liver of OVX rats. Moreover, they decreased fasting glucose, insulin, and HOMA-IR in ovariectomized rats. This study demonstrates that E₂ and E₂ plus vitamin E supplementation to OVX rats may improve insulin resistance, strengthen the antioxidant system, and reduce lipid peroxidation.

This review article studies the complex field of noncoding RNAs (ncRNAs) in cancer biology, focusing on their potential use as biomarkers and therapeutic targets. NcRNAs include circular RNAs (circRNAs), long noncoding RNAs (lncRNAs), and microRNAs (miRNAs). We discuss how ncRNAs affect gene expression in cancerous cells, the spread of cancer, and metastasis. The article illustrates the complex pathways through which ncRNAs can affect oncogenesis, tumor suppression, and therapeutic resistance. It also assesses the potential clinical uses of non-coding RNAs (ncRNAs), including their utility in cancer diagnosis, and prognosis. Besides, their potential for personalized cancer therapy is documented. Finally, it is concluded that understanding the role of ncRNA is of clinical importance regarding carcinogenesis, cancer diagnosis, and personalized therapy.

Objective: To investigate the combined effect of both pioglitazone and methotrexate on disease activity of rheumatoid arthritis in a biphasic study; experimental and clinical. Methods: Experimentally: 50 rats were divided into 5 equal groups; controls, experimental arthritis, methorexate treated (0.1 mg/Kg daily), pioglitazone-treated (10 mg/kg daily), and methotrexate and pioglitazone treated. Clinically: forty-nine diabetic rheumatoid arthritis patients were included. Patients group consisted of 28 patients and they received pioglitazone 30 mg orally beside their usual treatment. Control group consisted of 21 patients and they continued their usual treatment plus placebo. Disease activity was assessed using DAS28 score. Patients were followed up for 3 months. Results: Pioglitazone produced a significant improvement of serum oxidative stress parameters ( P < 0.05), and inflammatory cytokines in the treated arthritic group ( P < 0.05). Clinically, the pioglitazone treated group showed significant improvement in DAS28 ( P = 0.001) and C-reactive protein ( P < 0.0001) compared to placebo group. Conclusion: The concomitant use of the PPAR γ agonist pioglitazone and methotrexate appears to be promising therapeutic strategy for rheumatoid arthritis patients.