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Background: The newly emerged coronavirus disease 2019 (COVID-19) seems to involve different organs, including the cardiovascular system. We systematically reviewed COVID-19 cardiac complications and calculated their pooled incidences. Secondarily, we compared the cardiac troponin I (cTnI) level between the surviving and expired patients. Methods: A systematic search was conducted for manuscripts published from December 1, 2019 to April 16, 2020. Cardiovascular complications, along with the levels of cTnI, creatine kinase (CK), and creatine kinase MB (CK-MB) in hospitalized PCR-confirmed COVID-19 patients were extracted. The pooled incidences of the extracted data were calculated, and the unadjusted cTnI level was compared between the surviving and expired patients. Results: Out of 1094 obtained records, 22 studies on a total of 4,157 patients were included. The pooled incidence rate of arrhythmia was 10.11%. Furthermore, myocardial injury had a pooled incidence of 17.85%, and finally, the pooled incidence for heart failure was 22.34%. The pooled incidence rates of cTnI, CK-MB, and CK elevations were also reported at 15.16%, 10.92%, and 12.99%, respectively. Moreover, the pooled level of unadjusted cTnI was significantly higher in expired cases compared with the surviving (mean difference = 31.818, 95% CI = 17.923-45.713, P value <0.001). Conclusion: COVID-19 can affect different parts of the heart; however, the myocardium is more involved.

Lead (Pb) is one of the most important heavy metals that possess many applications in different kinds of industrial procedures and consumer products. The adverse effects of Pb on different parts of the immune system have been reported in various studies. Although it has been shown that high concentrations of Pb have low cytotoxicity on human lymphocytes, the effects of non-cytotoxic concentrations of Pb (detected in human blood) on cellular organelles and oxidative stress factors of human lymphocytes have yet to be determined. In this study, human lymphocytes were obtained from the blood of healthy male volunteers through the use of the Ficoll standard method. The intention of this paper was to determine the effects of non-cytotoxic concentrations of Pb on human lymphocytes using the accelerated cytotoxicity mechanism screening technique. For determination of cell viability, lymphocytes were treated with 0–1 m

Purpose: Unique physiochemical properties of Fe2O3 nanoparticles make them great agents to serve as therapeutic and diagnostic nanoparticles (NPs). In this study, we developed gold coated Fe2O3 nanoparticles for photothermal therapy of breast cancer cells.Methods: Fe2O3 nanoparticles was prepared via microemulsion method and their surface was modified via gold. Differential light scattering (DLS) and transmission electron microscopy (TEM) methods were applied to evaluate physicochemical properties of NPs. Gold coated NP was further modified with MUC-1 aptamer as a targeting agent to increase drug delivery into the desired tissue. To evaluate cytotoxicity of prepared cells, MTT assay was employed. Targeting ability of aptamer modified NPs was assessed through confocal microscopy and flow cytometry method. Subsequently, MCF-7 and CHO cells were treated with aptamer modified NPs and were then irradiated via near infrared light (NIR) to produce heat.Results: The morphology of NPs was spherical and monodisperse with the size of 16 nm, which was confirmed via DLS and TEM. Confocal microscopy and flow cytometry results indicated that aptamer modified NPs had higher uptake compared to bare NPs. Finally, NIR exposure results revealed that higher uptake of NPs and application of NIR led to significant death of MCF-7 cells compared to CHO cells.Conclusion: To sum up, aptamer modified Fe2O3 nanoparticles showed higher uptake by cancerous cells and led to eradication of cancerous cells after exposure to NIR light.

Today, despite significant progress in developing skin tissue engineering products, the fabrication of an ideal wound dressing that could meet the essential criteria, such as promoting angiogenesis -mainly in a diabetic wound- still remains a challenge. A diabetic wound is a chronic wound in which vascularization is low, and the wound healing process may stop. In this regard, Nitric oxide (NO) enhances the healing of diabetic wounds by promoting angiogenesis and providing antibacterial activity in wound sites. In this study, we produced a NO-releasing wound dressing (CMC-ALg-GSNO) composed of Carboxymethyl chitosan (CMC), sodium alginate (ALg), and Snitrosoglutathione (GSNO). The results obtained from the scanning electron microscopy (SEM) show that wound dressing has a porous structure. The water uptake and water vapor transmission for the wound dressing were obtained 4354.1 ± 179.3 % and 2753.8 ± 54.6 g/m2 per day, respectively. NO release study showed that NO release from CMC-ALg-GSNO continuously occurred within 168 hours. In vivo test, The CMC-ALg-GSNO wound dressing developed wound healing in a rat model of full-thickness diabetic wounds compared to the CMC-ALg and Gauze wound dressings. Thus, this study showed that CMC-ALg-GSNO wound dressing could lead to novel therapeutic invasions to treat diabetic wounds.

The present study shows interactive effects of bucladesine (db-cAMP) as a cyclic adenosine monophosphate (cAMP) agonist and H-89 as a protein kinase A (PKA) inhibitor on naloxone-induced withdrawal signs in morphine-dependent mice. Animals were treated subcutaneously with morphine thrice daily with doses progressively increased from 50 to 125 mg/kg. A last dose of morphine (50 mg/kg) was administered on the 4th day. Several withdrawal signs were precipitated by intraperitoneal (i.p.) administration of naloxone (5 mg/kg). Different doses of bucladesine (50, 100, 200 nm/mouse) and H-89 (0.05, 0.5, 1, 5 mg/kg) were administered (i.p.) 60 min before naloxone injection. In combination groups, bucladesine was injected 15 min before H-89 injection. Single administration of H-89 (0.5, 1, 5 mg/kg) and bucladesine (50, 100 nm/mouse) significantly attenuated prominent behavioral signs of morphine withdrawal. Lower doses of bucladesine (50, 100 nm/mouse) in combination with H-89 (0.05 mg/kg) increased the inhibitory effects of H-89 on withdrawal signs while in high dose (200 nm/mouse) decreased the ameliorative function of H-89 (0.05 mg/kg) in morphine-dependent animals. It is concluded that H-89 and bucladesine could affect morphine withdrawal syndrome via possible interaction with cyclic nucleotide messengering systems, protein kinase A signaling pathways, and modified related neurotransmitters.

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