The Association of Iron Intake and Hypertension, Does Iron Intake Decrease Blood Pressure?

Previous studies reported that iron may have an indispensable role in the risk of hypertension (HTN). However, the result of the studies on the relationship between iron and risk of HTN is inconsistent. This study aimed to assess the association between the association of dietary iron intake and HTN in the Iranian population. This case-control study was conducted on 4184 people aged 35 to 70, including 1239 people with HTN and 2945 people with normal blood pressure (BP) in Sabzevar, Iran. Dietary intake was assessed using a food frequency questionnaire (FFQ). The Nutritionist IV software was used in terms of the assessment of dietary intake of iron. An inverse association was found between iron intake and HTN (OR = 0.97, CI 95%: 0.94-0.99, P = 0.04). The association remained significant after adjustment for age, gender, smoking, drinking alcohol, calorie intake, and BMI (OR = 0.94, CI 95%: 0.89-0.98, P = 0.01). As a conclusion, iron intake was inversely associated with HTN. Further longitudinal studies on the effect of iron intake on BP are required to confirm this finding.

Thymoquinone ameliorates acrylamide-induced reproductive toxicity in female rats: An experimental study.

Background: Acrylamide (AA) is a carcinogenic compound that causes severe reproductive impairments and represents a high environmental risk factor. Thymoquinone (TQ) has a unique antioxidant activity and has been widely used as a protective agent against various types of toxicity. Objective: To evaluate the protective effects of TQ against AA-induced reproductive toxicity in female rats. Materials and Methods: In this experimental study, 40 female albino rats (120-150 gr, 8-10 wk) were sorted into 4 groups, (n = 10/each), vehicle group (received a daily oral administration of 0.5 ml saline [9%]); AA group (received a daily oral administration with freshly prepared AA, 20 mg/kg body weight) for 21 days which is less than the lethal dose LD 50 of AA in rats (20 mg/kg body weight); AA+TQ group (received a daily oral administration of TQ, 10 mg/kg body weight) after AA intoxication for 21 days, and TQ group (received a daily oral administration of TQ only, 10 mg/kg body weight) for 21 consecutive days. Reproductive hormones, carcinogenic biomarkers, and oxidative stress markers were measured. The histological assessment showed the protective effect of TQ against AA-induced ovarian injury. Network pharmacology analysis and molecular docking approach were carried out to determine the binding affinity of TQ with cyclooxygenase 2. Results: TQ administration significantly enhanced the functional capacity of the ovary at hormones, oxidative biomarkers, and tumor markers at a significant level of p < 0.001. Besides, TQ protects the ovary of AA-treated rats from the severe degeneration effect. Conclusion: TQ showed a promising protective effect against AA-induced reproductive toxicity in female rats.

Antibacterial and Biocompatible Hydrogel Dressing Based on Gelatin- and Castor-Oil-Derived Biocidal Agent.

Favored antibacterial activity associated with excellent biocompatibility, mechanical durability, and exudate handling needs to be addressed by modern dressing to achieve the desired wound healing. This paper deals with developing a new green and facile approach to manufacturing nonleachable antibacterial gelatin-based films for wound dressing. Therefore, a reactive methoxy-silane-functionalized quaternary ammonium compound bearing a fatty amide residue originating from castor oil (Si-CAQ) was initially synthesized. The antibacterial dressings were then fabricated via sol-gel and condensation reactions of the mixture containing gelatin, Si-CAQ, (3-glycidyloxypropyl) trimethoxysilane, and poly(vinyl alcohol). By utilizing bioactive polymers as starting materials and eliminating organic solvents during the dressing preparation, desirable clinical safety could be ensured. The gelatin-based films presented appropriate mechanical properties, such as flexibility and strength, in both dried and hydrated states (tensile strength >6 MPa and elongation >100). It is due to the in situ generations of the inorganic silicon domain in the organic framework via the sol-gel cross-linking process. The prepared dressings exhibited desirable features, including excellent biocompatibility (cell viability >95%), proper wound-exudate-managing characteristics (equilibrium water contact (EWA) 280-350% and water vapor transmission rate (WVTR) 2040-2200 g/m2/day), fluid handling capacity (FHC) (3-3.35 g), as well as commendable hemocompatibility. The promising bactericidal activity of the dressing against Bacillus subtilis, methicillin-resistant Staphylococcus aureus, and Escherichia coli strains with a contact-killing efficacy of 100% could prevent infection development at the wounded area. As evaluated by the wound scratch assay, the desired fibroblast cell growth, migration, and proliferation indicated the capability of the dressing to facilitate the healing process by encouraging fibroblast cell migration to the damaged area. In vivo wound-healing results showed that the prepared biocidal dressing stimulates wound healing and enhances epithelialization, collagen maturation, and vascularization of wounds due to their antibacterial effects and accelerated cellular functions.

Effects of different routes of nicotine administration on gastric morphology and hormonal secretion in rats.

NEW FINDINGS: What is the central question of this study? Does chronic administration of nicotine by different routes affect gastric hormonal secretions and morphology in rats? What is the main finding and its importance? Chronic nicotine administration increased levels of gastrin, ghrelin and histamine but decreased prostaglandin E2 . Nicotine administered orally and by inhalation had a marked negative impact on the histological structure of the gastric mucosa compared with intraperitoneal administration. The negative impact of nicotine administration on gastric structure was associated with an increased concentration of gastrin and decreased prostaglandin E2 , which might be the cause of gastric/peptic ulcers in heavy smokers. The increase in ghrelin concentration and its effect following chronic nicotine administration needs further investigation. The aim was to assess the effects of different routes of chronic nicotine administration on gastric morphology and hormonal secretion; mainly gastrin, ghrelin, histamine and prostaglandin E2 (PGE2 ). Forty adult male albino rats were randomly assigned into four groups (10 rats per group), treated for 21 days as follows: control group (given standard rat pellets and water only); oral nicotine-treated group [50 µg (ml drinking water)(-1) ]; intraperitoneal nicotine-treated group [0.5 mg (kg body weight)(-1) ]; and inhaled nicotine-treated group [0.5 mg (kg body weight)(-1) ]. Concentrations of gastrin, ghrelin, PGE2 and histamine in serum and gastric tissue homogenates were assessed using ELISA kits. Stomach fundus was processed for histopathology and immunohistochemistry using light and electron microscopy. Different routes of chronic nicotine administration resulted in a significant increase in serum and gastric homogenate gastrin and ghrelin concentrations and a significant decrease in serum and homogenate PGE2 concentrations compared with the control group. Moreover, nicotine administration via oral and inhalation routes caused gastric erosion, transformation of peptic cells into the mucous variety, a significant increase in parietal cell numbers and an increase in expression of gastrin. In conclusion, the negative impact of nicotine administration on gastric structure that is associated with an increased concentration of gastrin and decreased concentration PGE2 might be the leading cause of gastric/peptic ulcers in heavy smokers. The increased ghrelin concentration and its effect following nicotine chronic administration needs further investigation. Based on these findings, we suggest that the alteration in gastric structure following chronic administration of nicotine can be prevented by reducing gastrin secretion and/or targeting its receptors.