Comparison of the effects of progesterone and 17 β-estradiol on Schwann cell markers expression in rat adipose-derived stem cells

Steroids promote the myelination and regeneration in the peripheral nervous system. Whereas, little is known about the inducing effects by which the hormones exert their effects on Schwann cells differentiation. This could be revealed by the expression of Schwann cell markers in adipose-derived stem cells (ADSCs). The purpose of this study was to present the effects of progesterone and 17 β-estradiol on the Schwann cell markers in rat ADSCs. The mesenchymal stem cell markers (CD73, and CD90) were assayed by flow cytometry. Rat ADSCs were sequentially treated with β-mercaptoethanol, and all-trans-retinoic acid, followed by a mixture of basic fibrobroblast growth factor, platelet-derived growth factor, forskolin and heregulin. In experimental groups, forskolin and heregulin were substituted by progesterone and 17 β-estradiol. After induction, the expression of Schwann cell markers P0, and S-100 and the cellular immunocytochemical staining positive rate of anti-S100 and anti-glial fibrillary acidic protein (GFAP) antibodies were compared in the experimental and control groups. Progesterone and 17 β-estradiol triggered P0 and S-100 genes expression and induced a cellular immunocytochemical staining positive rate of S-100 and GFAP in rats ADSCs. Progesterone induced these changes stronger than 17 β-estradiol. Thus, progesterone may induce rat ADSCs toward Schwann-like cells by expression of Schwann cell markers and is more potent than 17 β-estradiol in the expression of these markers. © 2018 Urmia University. All rights reserved

Melatonin and cancer: From the promotion of genomic stability to use in cancer treatment

Cancer remains among the most challenging human diseases. Several lines of evidence suggest that carcinogenesis is a complex process that is initiated by DNA damage. Exposure to clastogenic agents such as heavy metals, ionizing radiation (IR), and chemotherapy drugs may cause chronic mutations in the genomic material, leading to a phenomenon named genomic instability. Evidence suggests that genomic instability is responsible for cancer incidence after exposure to carcinogenic agents, and increases the risk of secondary cancers following treatment with radiotherapy or chemotherapy. Melatonin as the main product of the pineal gland is a promising hormone for preventing cancer and improving cancer treatment. Melatonin can directly neutralize toxic free radicals more efficiently compared with other classical antioxidants. In addition, melatonin is able to regulate the reduction/oxidation (redox) system in stress conditions. Through regulation of mitochondrial nction and inhibition of pro-oxidant enzymes, melatonin suppresses chronic oxidative stress. Moreover, melatonin potently stimulates DNA damage responses that increase the tolerance of normal tissues to toxic effect of IR and may reduce the risk of genomic instability in patients who undergo radiotherapy. Through these mechanisms, melatonin attenuates several side effects of radiotherapy and chemotherapy. Interestingly, melatonin has shown some synergistic properties with IR and chemotherapy, which is distinct from classical antioxidants that are mainly used for the alleviation of adverse events of radiotherapy and chemotherapy. In this review, we describe the anticarcinogenic effects of melatonin and also its possible application in clinical oncology. © 2018 Wiley Periodicals, Inc

A systematic review of radiation-induced testicular toxicities following radiotherapy for prostate cancer

Background: Prostate cancer is the second most common malignancy in men in the world, and radiotherapy is used as a standard treatment modality for this cancer. Although this treatment modality effectively kills prostate cancerous cells, it unavoidably irradiates the organs/tissues that are away from the treatment site. In this regard, radiation-induced testicular toxicities following prostate radiotherapy can affect sexual function, reproduction, and quality of life in cancer survivors. This review summarizes the available data on testicular exposure to radiation during prostate radiotherapy and the consequences on testicular function. Methods: To illuminate the radiation-induced testicular toxicities following prostate radiotherapy, a systematic search was conducted based on the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guideline in PubMed, Web of Science, Scopus, Embase, and clinical trials electronic databases up to September 2018. According to a set of prespecified inclusion and exclusion criteria, 31 eligible articles providing data on testicular function following radiotherapy in patients with prostate cancer were included in the study. Results: According to the different radiotherapeutic techniques used for prostate cancer treatment, the total tumor dose and scattered testicular dose values were ranging from 36.25 to 78.00 Gy and 0.06 to 6.48 Gy, respectively. Luteinizing hormone and follicle-stimulating hormone levels after prostate radiotherapy were signi�cantly higher in comparison with the pretreatment levels. Around 60 of the studies showed that testosterone levels after prostate radiotherapy were signi�cantly lower than the pretreatment levels. Furthermore, erectile dysfunction (ED), as an adverse side effect resulting from prostate radiotherapy, was reported and this complication is signi�cantly correlated with lower satisfaction with sexual life. Testicular atrophy following prostate radiotherapy has also been observed and its frequency in patients with prior prostate radiotherapy is 2.5 times more than that in the patients without prior radiotherapy. Conclusion: The data revealed that the scattered dose to testicular tissues during prostate radiotherapy can lead to testicular atrophy, variation of the male sex hormones, and quality of sexual life. © 2019 Wiley Periodicals, Inc

Blooming gelatin: an individual additive for enhancing nanoapatite precipitation, physical properties, and osteoblastic responses of nanostructured macroporous calcium phosphate bone cements

Ziba Orshesh, Saeed Hesaraki, Ali Khanlarkhani Biomaterials Group, Nanotechnology and Advanced Materials Department, Materials and Energy Research Center, Alborz, Iran Abstract: In recent years, there has been a great interest in using natural polymers in the composition of calcium phosphate bone cements to enhance their physical, mechanical, and biological performance. Gelatin is a partially hydrolyzed form of collagen, a natural component of bone matrix. In this study, the effect of blooming gelatin on the nanohydroxyapatite precipitation, physical and mechanical properties, and cellular responses of a calcium phosphate bone cement (CPC) was investigated. Various concentrations of blooming gelatin (2, 5, and 8 wt.%) were used as the cement liquid and an equimolar mixture of tetracalcium phosphate and dicalcium phosphate was used as solid phase. The CPC without any gelatin additive was also evaluated as a control group. The results showed that gelatin accelerated hydraulic reactions of the cement paste, in which the reactants were immediately converted into nanostructured apatite precipitates after hardening. Gelatin molecules induced 4%–10% macropores (10–300 µm) into the cement structure, decreased initial setting time by ~190%, and improved mechanical strength of the as-set cement. Variation in the above-mentioned properties was influenced by the gelatin concentration and progressed with increasing the gelatin content. The numbers of the G-292 osteoblastic cells on gelatin-containing CPCs were higher than the control group at entire culture times (1–14 days), meanwhile better alkaline phosphatase (ALP) activity was determined using blooming gelatin additive. The observation of cell morphologies on the cement surfaces revealed an appropriate cell attachment with extended cell membranes on the cements. Overall, adding gelatin to the composition of CPC improved the handling characteristics such as setting time and mechanical properties, enhanced nanoapatite precipitation, and augmented the early cell proliferation rate and ALP activity. Keywords: calcium phosphate cement, nanoapatite, cell studies, macroporosity, bone substitute, blooming gelati

A systematic review of radiation-induced testicular toxicities following radiotherapy for prostate cancer

Background: Prostate cancer is the second most common malignancy in men in the world, and radiotherapy is used as a standard treatment modality for this cancer. Although this treatment modality effectively kills prostate cancerous cells, it unavoidably irradiates the organs/tissues that are away from the treatment site. In this regard, radiation-induced testicular toxicities following prostate radiotherapy can affect sexual function, reproduction, and quality of life in cancer survivors. This review summarizes the available data on testicular exposure to radiation during prostate radiotherapy and the consequences on testicular function. Methods: To illuminate the radiation-induced testicular toxicities following prostate radiotherapy, a systematic search was conducted based on the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guideline in PubMed, Web of Science, Scopus, Embase, and clinical trials electronic databases up to September 2018. According to a set of prespecified inclusion and exclusion criteria, 31 eligible articles providing data on testicular function following radiotherapy in patients with prostate cancer were included in the study. Results: According to the different radiotherapeutic techniques used for prostate cancer treatment, the total tumor dose and scattered testicular dose values were ranging from 36.25 to 78.00 Gy and 0.06 to 6.48 Gy, respectively. Luteinizing hormone and follicle-stimulating hormone levels after prostate radiotherapy were signi�cantly higher in comparison with the pretreatment levels. Around 60 of the studies showed that testosterone levels after prostate radiotherapy were signi�cantly lower than the pretreatment levels. Furthermore, erectile dysfunction (ED), as an adverse side effect resulting from prostate radiotherapy, was reported and this complication is signi�cantly correlated with lower satisfaction with sexual life. Testicular atrophy following prostate radiotherapy has also been observed and its frequency in patients with prior prostate radiotherapy is 2.5 times more than that in the patients without prior radiotherapy. Conclusion: The data revealed that the scattered dose to testicular tissues during prostate radiotherapy can lead to testicular atrophy, variation of the male sex hormones, and quality of sexual life. © 2019 Wiley Periodicals, Inc

Thyroid function following breast cancer chemotherapy: A systematic review

Background: Chemotherapy, as a systemic therapy, is one of the most effective modalities for cancer treatment. However, the use of chemotherapeutic drugs in patients with breast cancer can lead to thyroid dysfunction. This systematic review summarizes the available data on thyroid function following breast cancer chemotherapy. Methods: To illuminate the thyroid toxicities induced by different chemotherapy regimens in patients with breast cancer, a systematic search was done in accordance with Preferred Reporting Items for Systematic Reviews and Meta-Analyses guideline in Scopus, Embase, PubMed and Web of Science electronic databases up to December 2018. On the basis of a set of prespecified inclusion and exclusion criteria, eight eligible articles providing data on thyroid function following chemotherapy in patients with breast cancer were included in the study. Results: According to the obtained results, it was found that for most cases, the levels of triiodothyronine (T3), free T3 (FT3), thyroxin (T4) and free T4 (FT4) hormones decrease following breast cancer chemotherapy regimens used in these eligible studies. However, alteration of thyroid-stimulating hormone (TSH) level after breast cancer chemotherapy was not clear. Conclusion: The findings showed that thyroid function and TSH hormone level can change in patients with breast cancer receiving different chemotherapy regimens. © 2019 Wiley Periodicals, Inc