Effect of opium dependency on secondary intention wound healing in a rat model: an experimental study

Opium dependency is a social and health problem in some middle eastern countries like Iran. Many of these people may require surgery. This study investigates the effects of opium dependency on histological parameters of secondary intention wound healing in rat. A full‐thickness wound (2 × 2 cm in diameters) was created on the dorsum of two groups of rats, a normal control group and a second group of rat depended to opium (Badawy's method). Several times during 14 days postwounding, the wound was excised with peripheral margins of normal skin and was evaluated for cellular population, reepithelialisation and revascularisation. Results are presented as the mean ± standard error. Data were compared by an unpaired t‐test or analysis of variance. Histological examination of the wound tissue showed evidence of increased population of fibroblasts, decreased recruitment of neutrophile and plateau of macrophage cells in opium depended animals comparing with control group. In the depended animals, reepithelialisation was seen to be enhanced significantly, while prohibiting progression of revascularisation. This study shows that opium dependency enhances reepitheliazation as well as tissue recruitment of fibroblasts; thereby probable enhancement of secondary intention wound healing.     

Dietary patterns and anthropometric indices among Iranian women with major depressive disorder

Major depression is a common mental disorder among women. A number of studies have demonstrated the association between some nutrients and food items with depression, but the studies on the association of dietary patterns with depression, especially in the Middle East, are rare. Further, the literature examining the relationship between anthropometric status and depression are inconsistent. In this study, 45 women with major depression and 90 patients with no mental disorder participated. We collected dietary intakes by a semi-quantitative food frequency questionnaire, and measured anthropometric indices (weight, height, waist and hip circumferences). Using factor analysis, two major dietary patterns were extracted: Healthy and Unhealthy. After adjusting for confounders, individuals who gained higher scores in healthy dietary pattern, had 84% lower odds of major depression; while the odds of major depression in participants who gained higher scores in unhealthy dietary pattern showed no significant association. No significant association was found between anthropometric indices and major depression. These results suggest that the healthy dietary pattern is significantly associated with lower odds of major depression in adult women. Further researches are needed to confirm these findings.     

Gemfibrozil Pretreatment Affecting Antioxidant Defense System and Inflammatory, but not Nrf-2 Signaling Pathways Resulted in Female Neuroprotection and Male Neurotoxicity in the Rat Models of Global Cerebral Ischemia–Reperfusion

Two important pathophysiological mechanisms involved during cerebral ischemia are oxidative stress and inflammation. In pathological conditions such as brain ischemia the ability of free radicals production is greater than that of elimination by endogenous antioxidative systems, so brain is highly injured due to oxidation and neuroinflammation. Fibrates as peroxisome proliferator-activated receptor (PPAR)-α ligands, are reported to have antioxidant and anti-inflammatory actions. In this study, gemfibrozil, a fibrate is investigated for its therapeutic potential against global cerebral ischemia–reperfusion (I/R) injury of male and female rats. This study particularly has focused on inflammatory and antioxidant signaling pathways, such as nuclear factor erythroid-related factor (Nrf)-2, as well as the activity of some endogenous antioxidant agents. It was found that pretreatment of animals with gemfibrozil prior to I/R resulted in a sexually dimorphic outcome. Within females it proved to be protective, modulating inflammatory factors and inducing antioxidant defense system including superoxide dismutase (SOD), catalase, as well as glutathione level. However, Nrf-2 signaling pathway was not affected. It also decreased malondialdehyde level as an index of lipid peroxidation. In contrast, gemfibrozil pretreatment was toxic to males, enhancing the expression of inflammatory factors such as tumor necrosis factor-α, nuclear factor-κB, and cyclooxygenase-2, and decreasing Nrf-2 expression and SOD activity, leading to hippocampal neurodegeneration. Considering that gemfibrozil is a commonly used anti-hyperlipidemic agent in clinic, undoubtedly more investigations are crucial to exactly unravel its sex-dependent neuroprotective/neurodegenerative potential.     

Simultaneous Inhibition of COX-2 and Activation of PPAR-γ Resulted in the Same Level and Pattern of Neuroprotection as They were Targeted Separately

The inflammatory response is an immune response of the body when exposed to internal and external stimuli. Cyclooxygenases (COX) are major inflammatory mediators implicated in inflammation. COX-2 is reported to be involved in neuroinflammation. Moreover, 15-Deoxy-d ^12,14-prostaglandin J2 (15d-PGJ2), an endogenous ligand of peroxisome proliferator-activated receptor gamma (PPAR-γ), has been demonstrated to have anti-inflammatory actions. In this study, we investigated whether co-therapy of a selective COX-2 inhibitor NS-398 and 15d-PGJ2 as a PPAR-γ ligand could exert additional neuroprotective effects in rat pheochromocytoma (PC12) cells. Our findings showed that 15d-PGJ2 and NS-398 suppress the apoptotic pathway in PC12 cells exposed to H₂O₂ by attenuation of the Bax/Bcl-2 ratio. This effect was mediated through PPAR-γ, as it was reversed by GW9662 (a PPAR-γ inhibitor). Also, 15d-PGJ2 and NS-398 induced the Nrf2 signaling pathway and decreased NF-κB level in a PPAR-γ-dependent manner. We found that coadministration of a selective COX-2 inhibitor and a PPAR-γ ligand in PC12 cells has equal neuroprotective effect compared to their effects when used separately. Considering the higher affinity of 15d-PGJ2 for PPAR-γ than NS-398, it seems that the observed neuroprotection of this combination therapy was from 15d-PGJ2.     

Reversal of Prenatal Morphine Exposure-Induced Memory Deficit in Male But Not Female Rats

Impaired memory performance in offspring is one of the long-lasting neurobehavioral consequences of prenatal opiate exposure. Here, we studied the effects of prenatal morphine exposure on inhibitory avoidance memory performance in male and female offspring and also investigated whether these deficits are reversible during the postnatal development. Pregnant Wistar rats received morphine sulfate through drinking water, from the first day of gestation up to the day 13, M_1–13, or to the time of delivery, M_1–21. Four- and ten-week-old (adolescent and adult, respectively) male and female offspring were subjected to behavioral assays and then analysis of proteins involved in apoptosis or in synaptic plasticity. Results revealed that adolescent and adult female rats failed in passive avoidance retention task in both M_1–13 and M_1–21 groups. Adolescent and adult male offspring were similar to control animals in M_1–13 group. However M_1–21 impaired retention task in prepubertal male offspring, and this memory loss was repaired in postpubertal stage. Consistently, Bax/Bcl-2 ratio and cleaved caspase-3 were significantly increased in both M_1–13 and M_1–21 adolescent and adult female rats, but only in M_1–21 adolescent male rats. Furthermore, prenatal morphine exposure reduced the expression of brain-derived neurotrophic factor precursor protein in adolescent and adult female offspring and also decreased p-ca(2+)/calmodulin-dependent kinase II/ca(2+)/calmodulin-dependent kinase II ratio in adolescent male and female rats. Altogether, the results show that prenatal morphine exposure, depending on the time or duration of exposure, has distinct effects on male and female rats, and postnatal development may reverse these deficits more likely in males.     

Long-term effects of sprint interval training on expression of cardiac genes involved in energy efficiency

Purpose

The real mechanisms of intensive exercise training-induced energy efficiency have not yet been well examined. Therefore, the aim of the present study was to investigate the effects of sprint interval training (SIT) on gene expression of uncoupling proteins (UCPs) and endothelial nitric oxide synthase (eNOS).

Methods

For this purpose, 16 Albino Wistar rats (250–300 g) were randomly divided into equal groups of control and sprint training. The animals run on treadmill for 10 weeks, 5 days per week at intensity corresponding to 90–95% maximal oxygen consumption. The gene expression of UCP2, UCP3 and eNOS was analyzed by RT-PCR method in hearts. The data were analyzed by independent samples T test at P?<?0.05 level.

Results

Sprint interval training significantly decreased mRNA expression of UCP2 (t₁₄?=?4.818, P?=?0.001) and UCP3 (t₁₄?=?4.620, P?=?0.001) in cardiac muscle of rats. In contrast, mRNA expression of eNOS in cardiac muscle significantly increased following sprint interval training (t₁₄?=?7.967, P?=?0.001).

Conclusion

This study elucidates that SIT through reduction in gene expression of uncoupling proteins can improve energy efficiency. But, more studies are needed to confirm this hypothesis.

     

Hospital-acquired infections in a tertiary hospital in Iran before and during the COVID-19 pandemic

Wiener Medizinische Wochenschrift - Infection prevention protocols are the accepted standard to control nosocomial infections. These protective measures intensified after the coronavirus 2019...     

The effects of low-level laser irradiation on breast tumor in mice and the expression of Let-7a,miR-155, miR-21, miR125, and miR376b

Low-level laser therapy (LLLT) is a form of photon therapy which can be a non-invasive therapeutic procedure in cancer therapy using low-intensity light in the range of 450–800 nm. One of the main functional features of laser therapy is the photobiostimulation effects of low-level lasers on various biological systems including altering DNA synthesis and modifying gene expression, and stopping cellular proliferation. This study investigated the effects of LLLT on mice mammary tumor and the expression of Let-7a, miR155, miR21, miR125, and miR376b in the plasma and tumor samples. Sixteen mice were equally divided into four groups including control, and blue, green, and red lasers at wavelengths of 405, 532, and 632 nm, respectively. Weber Medical Applied Laser irradiation was carried out with a low power of 1–3 mW and a series of 10 treatments at three times a week after tumor establishment. Tumor volume was weekly measured by a digital vernier caliper, and qRT-PCR assays were performed to accomplish the study. Depending on the number of groups and the p value of the Kolmogorov-Smirnov test of normality, a t test, a one-way ANOVA, or a non-parametric test was used for data analyses, and p?<?0.05 was considered to be statistically significant. The average tumor volume was significantly less in the treated blue group than the control group on at days 21, 28, and 35 after cancerous cell injection. Our data also showed an increase of Let-7a and miR125a expression and a decrease of miR155, miR21, and miR376b expression after LLLT with the blue laser both the plasma and tumor samples compared to other groups. It seems that the non-invasive nature of laser bio-stimulation can make LLLT an attractive alternative therapeutic tool.     

Hepatic Hemodynamic Changes Following Stepwise Liver Resection

Aim

Extended liver resection has increased during the last decades. However, hepatic hemodynamic changes after resection and the consequent complications like post hepatectomy liver failure are still a challenging issue. The aim of this study was to systematically evaluate the role of stepwise liver resection on hepatic hemodynamic changes.

Methods

To evaluate this effect we performed 25, 50, and 75 % sequential liver resections in 10 pigs. Before and after each resection, the hepatic artery flow and portal vein flow in relation to the remnant liver volume (RLV) as well as hepatic vascular pressures were measured and compared between the groups.

Results

Following sequential liver resection, the hepatic artery flow /100 g decreases and the portal vein flow increases up to 17 and 167 % following extended liver resection (75 %), respectively. Also, during stepwise liver resection, the portal vein pressure increases gradually up to 33 % following extended hepatectomy (75 %).

Conclusion

Sequential decrease in the RLV decreases the hepatic artery flow /100 g and increases the portal vein flow /100 g and portal vein pressure. As the consequence, the liver goes under more poor-oxygenated blood supply and higher pressure. This may be one of the most important mechanisms of the post hepatectomy liver failure in case of extended liver resection.