Radioprotective effect of Cerebrolysin in the Rat's Brain Tissues.

AIM: The aim of this study is to evaluate radioprotective effects of Cerebrolysin (CBL) in rats' brain tissues after local irradiation. BACKGROUND: CBL has demonstrated antioxidant, anti-inflammatory, and tissue repair properties. In this study, the radioprotective effects of CBL in the brain tissues of rats after Irradiation (IR) (50 mg/ kg) were evaluated. OBJECTIVE: The levels of different oxidative stress markers, including malondialdehyde (MDA), nitric oxide (NO), glutathione peroxidase (GPx), catalase (CAT), and superoxide dismutase (SOD) were examined after treatment with radiation and CBL. METHODS: First, 20 male adult Wistar rats weighing 180-200 g were used. The animals were exposed to a single fraction of 15Gy using a linear accelerator unit at a dose rate of 200 cGy/mine. In this study, to check the amount of oxidative stress following the IR, the level of four markers MDA, NO, GPx, CAT, and SOD were examined and measured using the spectrophotometric method and purchased kits. RESULTS: The results showed that compared to the IR group, the administration of CBL increases the levels of GPX and SOD significantly (p < 0.05). CONCLUSION: Our finding suggests that CBL has radioprotective effects on the brain by enhancing antioxidant defense mechanisms.

Radiation-induced Testicular Damage in Mice: Protective Effects of Apigenin Revealed by Histopathological Evaluation.

BACKGROUND: Radiation exposure poses a significant threat to reproductive health, particularly the male reproductive system. The testes, being highly sensitive to radiation, are susceptible to damage that can impair fertility and overall reproductive function. The study aims to investigate the radioprotective effects of apigenin on the testis through histopathological evaluation. MATERIALS AND METHODS: This research involved utilizing a total of 40 mice, which were randomly divided into eight groups of five mice each. The groups were categorized as follows: A) negative control group, B, C, and D) administration of apigenin at three different doses (0.3 mg/kg, 0.6 mg/kg, and 1.2 mg/kg) respectively, E) irradiation group, and F, H, and I) administration of apigenin at three different doses (0.3 mg/kg, 0.6 mg/kg, and 1.2 mg/kg) in combination with irradiation. The irradiation procedure involved exposing the mice to a 2Gy X-ray throughout their entire bodies. Subsequently, histopathological assessments were conducted seven days after the irradiation process. RESULTS: The findings indicated that radiation exposure significantly impacted the spermatogenesis system. This research provides evidence that administering apigenin to mice before ionizing radiation effectively mitigated the harmful effects on the testes. Apigenin demonstrated radioprotective properties, positively influencing various parameters, including the spermatogenesis process and the presence of inflammatory cells within the tubular spaces. CONCLUSION: Apigenin can provide effective protection for spermatogenesis, minimize the adverse effects of ionizing radiation, and safeguard normal tissues.

Exploring the Potential of Metformin in Mitigating Radiation-Induced Gastrointestinal and Hematopoietic System Injury in Rats after wholebody X-ray Radiation: An Experimental Study.

BACKGROUND: The modern world faces a growing concern about the possibility of accidental radiation events. The Hematopoietic system is particularly vulnerable to radiationinduced apoptosis, which can lead to death. Metformin, a drug used to treat diabetes, has been shown to protect normal cells and tissues from the toxic effects of radiation. This study aimed to evaluate the effectiveness of metformin in mitigating radiation injury to the gastrointestinal and hematological systems of rats. MATERIALS AND METHODS: The study involved 73 male rats. After total body irradiation with 7.5 Gy of X-rays, rats were treated with metformin. Seven days later, the rats were sacrificed and blood samples were taken for evaluation. RESULTS: The study found that metformin was not effective in mitigating radiation injury. The histopathological assessment showed no significant changes in goblet cell injury, villi shortening, inflammation, or mucous layer thickness. In terms of biochemical evaluation, metformin did not significantly affect oxidative stress markers, but irradiation increased the mean MDA level in the radiation group. The complete blood count revealed a significant decrease in WBC and platelet, counts in the radiation group compared to the control group, but no significant difference was found between the radiation and radiation + metformin groups. CONCLUSION: In conclusion, metformin may not be a good option for reducing radiation toxicity after accidental exposure. Despite treatment, there was no improvement in platelet, white blood cell, and lymphocyte counts, nor was there any decrease in oxidative stress. Further research is needed to explore other potential treatments for radiation injury.

Evaluating the Necessity and Radiation Risk of Brain CT Scans Requested by the Trauma Emergency Department.

Background: Numerous Computed Tomography (CT) scan requests for trauma patients have raised serious concern about the impacts of radiation such as radiation-induced cancers. Objective: This study aimed to evaluate the necessity rate of requested head CT scans for traumatic patients and to ultimately estimate the risk of radiation-induced brain cancer. Material and Methods: In this retrospective analytical study, traumatic patients, who had undergone a head CT scan in a two-month period from August 23 to October 22, 2018, were considered as the study population. Two radiologists reviewed each patient individually to evaluate the rate of normal and abnormal cases. Dose length product in milligrays (mGy) was utilized to calculate the effective dose (ED) in millisieverts (mSv), resulting in an assessment of the risk of radiation-induced brain cancer using ICRP 103. Results: Among 523 scans, 460 patients (88%) received normal reviews, while only 47 patients (9%) had findings related to their current trauma. The mean effective dose value was 1.05±0.36 mSv. Risk of the radiation induced brain cancer was calculated to be 0.037 and 0.030 new cancer cases in 10000 males and females per Gy, respectively. Conclusion: Final results demonstrated that a significant number of traumatic patients undergoing a CT scan are in fact, healthy. Such reckless usage of CT and consequently the excess exposure could result in a dramatic rise in cancer rates. The need to limit unnecessary CT scan usage and keeping the radiation given to patients as low as reasonably achievable (ALARA) when collecting essential diagnostic data is more critical than ever.

Protective Effects of Alpha-lipoic Acid, Resveratrol, and Apigenin against Oxidative Damages, Histopathological Changes, and Mortality Induced by Lung Irradiation in Rats.

AIM: This study investigated the protective effects of three antioxidants on radiationinduced lung injury. BACKGROUND: Oxidative stress is one of the key outcomes of radiotherapy in normal tissues. It can induce severe injuries in lung tissue, which may lead to pneumonitis and fibrosis. Recently, interest in natural chemicals as possible radioprotectors has increased due to their reduced toxicity, cheaper price, and other advantages. OBJECTIVE: The present study was undertaken to evaluate the radioprotective effect of Alpha-lipoic Acid (LA), Resveratrol (RVT), and Apigenin (APG) against histopathological changes and oxidative damage and survival induced by ionizing radiation (IR) in the lung tissues of rats. METHODS: First, the lung tissue of 50 mature male Wistar rats underwent an 18 Gy gamma irradiation. Next, the rats were sacrificed and transverse sections were obtained from the lung tissues and stained with hematoxylin and eosin (H and E) and Mason trichrome (MTC) for histopathological evaluation. Then, the activity of Glutathione peroxidase (GPx), Superoxide Dismutase (SOD), and Malondialdehyde (MDA) was measured by an ELISA reader at 340, 405, and 550 nm. RESULTS: Based on the results of this study, IR led to a remarkable increase in morphological changes in the lung. However, APG, RVT, and LA could ameliorate the deleterious effects of IR in lung tissue. IR causes an increase in GPX level, and APG+IR administration causes a decrease in the level of GPX compared to the control group. Also, the results of this study showed that RVT has significant effects in reducing MDA levels in the short term. In addition, compared to the control group, IR and RVT+IR decrease the activity of SOD in the long term in the lung tissues of rats. Also, the analysis of results showed that weight changes in IR, LA+IR, APG+IR, and control groups were statistically significant. CONCLUSION: APG and RVT could prevent tissue damage induced by radiation effects in rat lung tissues. Hence, APG, LA, and RVT could provide a novel preventive action with their potential antioxidant anti-inflammatory properties, as well as their great safety characteristic.

The metformin immunoregulatory actions in tumor suppression and normal tissues protection.

The immune system is the key player in a wide range of responses in normal tissues and tumors to anticancer therapy. Inflammatory and fibrotic responses in normal tissues are the main limitations of chemotherapy, radiotherapy, and also some newer anticancer drugs such as immune checkpoint inhibitors (ICIs). Immune system responses within solid tumors including anti-tumor and tumor-promoting responses can suppress or help tumor growth. Thus, modulation of immune cells and their secretions such as cytokines, growth factors and epigenetic modulators, pro-apoptosis molecules, and some other molecules can be suggested to alleviate side effects in normal tissues and drug-resistance mechanisms in the tumor. Metformin as an anti-diabetes drug has shown intriguing properties such as anti-inflammation, anti-fibrosis, and anticancer effects. Some investigations have uncovered that metformin can ameliorate radiation/chemotherapy toxicity in normal cells and tissues through the modulation of several targets in cells and tissues. These effects of metformin may ameliorate severe inflammatory responses and fibrosis after exposure to ionizing radiation or following treatment with highly toxic chemotherapy drugs. Metformin can suppress the activity of immunosuppressive cells in the tumor through the phosphorylation of AMP-activated protein kinase (AMPK). In addition, metformin may stimulate antigen presentation and maturation of anticancer immune cells, which lead to the induction of anticancer immunity in the tumor. This review aims to explain the detailed mechanisms of normal tissue sparing and tumor suppression during cancer therapy using adjuvant metformin with an emphasis on immune system responses.

Investigating the effectiveness of intraoperative rapid parathyroid hormone assay in parathyroidectomy surgery in patients with secondary hyperparathyroidism.

INTRODUCTION: The use of Rapid Intraoperative parathyroid hormone (Io-PTH) assay during surgery in the management of parathyroid tissue in cases of primary hyperparathyroidism has been proven to be effective, while its utilization in secondary hyperparathyroidism (SHPT) has been rarely reported. In the present study, we aim to demonstrate the application of rapid Io-PTH assay in patients with SHPT following chronic kidney disease undergoing parathyroidectomy surgery. METHOD: In this prospective study, five blood samples were taken from patients undergoing parathyroidectomy and upper thymectomy. Among the samples, two were pre-excision, including prior to the first incision, after exploration, and before parathyroids resection. Two additional samples were taken 10 and 20 min after the excision of the parathyroid glands. Another sample was collected twenty-four hours after the operation. Serum Calcium levels and PTH levels were evaluated and analyzed. RESULTS: We successfully managed SHPT in all 36 patients in our study. The patients included 24 males (66.7%) with a mean age of 49.97 ± 14.92. The mean PTH decreased significantly at 10 min, 20 min, one day, and six months after surgery (P < 0.001). The highest reduction occurred 10 min after removal of the parathyroid glands so the mean PTH compared to time zero was reduced from 1737 to 439, and in 100% of cases, more than 50% reduction was seen in PTH. CONCLUSION: A 60% or more reduction in PTH Rapid at 10 min after parathyroidectomy has an accuracy of 94.4% and a positive predictive value of 100%. Thus, if the PTH level does not decrease by more than 60% at 10 min or more than 80% at 20 min, tissue exploration is continued with the aim of finding the ectopic parathyroid gland.

Nobiletin in Cancer Therapy; Mechanisms and Therapy Perspectives.

Cancer has remained to be one of the major challenges in medicine and regarded as the second leading cause of death worldwide. Different types of cancer may resist anti-cancer drugs following certain mutations such as those in tumor suppressor genes, exhaustion of the immune system, and overexpression of drug resistance mediators, which increase the required concentration of anticancer drugs so as to overcome drug resistance. Moreover, treatment with a high dose of such drugs is highly associated with severe normal tissue toxicity. Administration of low-toxic agents has long been an intriguing idea to enhance tumor suppression. Naturally occurring agents e.g., herb-derived molecules have shown a dual effect on normal and malignant cells. On the one hand, these agents may induce cell death in malignant cells, while on the other hand reduce normal cell toxicity. Nobiletin, one of the well-known polymethoxyflavones (PMFs), has reportedly shown various beneficial effects on the suppression of cancer and the protection of normal cells against different toxic agents. Our review aims to explain the main mechanisms underlying nobiletin as an inhibitor of cancer. We have reviewed the mechanisms of cancer cell death caused by nobiletin, such as stimulation of reactive oxygen species (ROS), modulation of immune evasion mechanisms, targeting tumor suppressor genes, and modulation of epigenetic modulators, among others; the inhibitory mechanisms of nobiletin affecting tumor resistance properties such as modulation of hypoxia, multidrug resistance, angiogenesis, epithelial-mesenchymal transition (EMT) have been fully investigated. Also, the inhibition of anti-apoptotic and invasive mechanisms induced by nobiletin will later be discussed. In the end, protective mechanisms of nobiletin on normal cells/tissue, clinical trial results, and future perspectives are reviewed.

The interactions of docetaxel with tumor microenvironment.

There are several interactions within the tumor microenvironment (TME) that affect the response of cancer cells to therapy. There are also a large number of cells and secretions in TME that increase resistance to therapy. Following the release of immunosuppressive, pro-angiogenic, and metastatic molecules by certain cells such as tumor-associated macrophages (TAMs), cancer-associated fibroblasts (CAFs), and cancer cells, immune evasion, angiogenesis, and metastasis may be induced. However, natural killer (NK) cells and cytotoxic CD8 + T lymphocytes (CTLs) can responsively release anticancer molecules. In addition, anticancer drugs can modulate these cells and their interactions in favor of either cancer resistance or therapy. Docetaxel belongs to taxanes, a class of anti-tumor drugs, which acts through the polymerization of tubulin and the induction of cell cycle arrest. Also, it has been revealed that taxanes including docetaxel affect cancer cells and the other cells within TME through some other mechanisms such as modulation of immune system responses, angiogenesis, and metastasis. In this paper, we explain the basic mechanisms of docetaxel interactions with malignant cells. Besides, we review the diverse effects of docetaxel on TME and cancer cells in consequence. Lastly, the modulatory effects of docetaxel alone or in conjunction with other anticancer agents on anti-tumor immunity, cancer cell resistance, angiogenesis, and metastasis will be discussed.

Mechanisms of cancer cell death induction by triptolide.

Drug resistance is a hot topic issue in cancer research and therapy. Although cancer therapy including radiotherapy and anti-cancer drugs can kill malignant cells within the tumor, cancer cells can develop a wide range of mechanisms to resist the toxic effects of anti-cancer agents. Cancer cells may provide some mechanisms to resist oxidative stress and escape from apoptosis and attack by the immune system. Furthermore, cancer cells may resist senescence, pyroptosis, ferroptosis, necroptosis, and autophagic cell death by modulating several critical genes. The development of these mechanisms leads to resistance to anti-cancer drugs and also radiotherapy. Resistance to therapy can increase mortality and reduce survival following cancer therapy. Thus, overcoming mechanisms of resistance to cell death in malignant cells can facilitate tumor elimination and increase the efficiency of anti-cancer therapy. Natural-derived molecules are intriguing agents that may be suggested to be used as an adjuvant in combination with other anticancer drugs or radiotherapy to sensitize cancer cells to therapy with at least side effects. This paper aims to review the potential of triptolide for inducing various types of cell death in cancer cells. We review the induction or resistance to different cell death mechanisms such as apoptosis, autophagic cell death, senescence, pyroptosis, ferroptosis, and necrosis following the administration of triptolide. We also review the safety and future perspectives for triptolide and its derivatives in experimental and human studies. The anticancer potential of triptolide and its derivatives may make them effective adjuvants for enhancing tumor suppression in combination with anticancer therapy.

Critical parameters to translate gold nanoparticles as radiosensitizing agents into the clinic.

Radiotherapy is an inevitable choice for cancer treatment that is applied as combinatorial therapy along with surgery and chemotherapy. Nevertheless, radiotherapy at high doses kills normal and tumor cells at the same time. In addition, some tumor cells are resistant to radiotherapy. Recently, many researchers have focused on high-Z nanomaterials as radiosensitizers for radiotherapy. Among them, gold nanoparticles (GNPs) have shown remarkable potential due to their promising physical, chemical, and biological properties. Although few clinical trial studies have been performed on drug delivery and photosensitization with lasers, GNPs have not yet received Food and Drug Administration approval for use in radiotherapy. The sensitization effects of GNPs are dependent on their concentration in cells and x-ray energy deposition during radiotherapy. Notably, some limitations related to the properties of the GNPs, including their size, shape, surface charge, and ligands, and the radiation source energy should be resolved. At the first, this review focuses on some of the challenges of using GNPs as radiosensitizers and some biases among in vitro/in vivo, Monte Carlo, and clinical studies. Then, we discuss the challenges in the clinical translation of GNPs as radiosensitizers for radiotherapy and proposes feasible solutions. And finally, we suggest that certain areas be considered in future research. This article is categorized under: Therapeutic Approaches and Drug Discovery > NA.

Tumor-associated Macrophages (TAMs) in Cancer Resistance; Modulation by Natural Products.

Tumor-associated macrophages (TAMs) play a pivotal role in the progression and resistance of tumors to different anticancer drugs. TAMs can modulate the tumor microenvironment (TME) in favor of immune system exhaustion. The interactions of TAMs with TME can affect the function of cytotoxic CD8+ T lymphocytes (CTLs) and natural killer (NK) cells. Furthermore, TAMs can induce cancer cell proliferation by releasing some growth factors, such as transforming growth factor (TGF)-ß. TAMs have several positive cross-talks with other immune suppressive cells such as regulatory T cells (Tregs), myeloid-derived suppressor cells (MDSCs), cancerassociated fibroblasts (CAFs), and cancer cells, leading to the release of growth factors, the proliferation of cancer cells and tumor growth. These interactions also can induce invasion and migration of cancer cells, angiogenesis, and metastasis. The inhibition of TAMs is an intriguing strategy for overcoming tumor resistance and suppression of cancer cells. Some natural-derived agents such as melatonin, curcumin, resveratrol, apigenin, and other flavonoids have shown the ability to modulate TME, including TAMs. These adjuvants may be able to boost antitumor immunity through the modulation of TAMs. This review explains the modulatory effects of some well-known naturally derived agents on the activity of TAMs. The modulation of TAMs by these agents may be useful in suppressing tumor growth and invasion.

Cardiac Injury Following Chemo/Radiation Therapy: An Updated Review on Mechanisms and Therapeutic Approaches.

Cardiovascular disorders are among the critical side effects of cancer therapy. Damage to the function and normal structure of the heart can cause serious threats to patients that are being treated for cancer. Cardiovascular complications may be induced by various types of chemotherapy drugs and also radiation therapy. The severity of cardiovascular toxicity depends on several factors, such as types of drugs, tumor location for radiotherapy, the presence of cardiac disease history, the dose of drugs or ionizing radiation, etc. Radiotherapy and chemotherapy can cause heart diseases through various mechanisms, such as oxidative stress, inflammation, cell death, fibrosis, endothelial to mesenchymal transition (EndMT), etc. Chronic inflammation following damage to a huge number of cells can trigger more accumulation of inflammatory cells and chronic release of reactive oxygen species (ROS) and nitric oxide (NO). Oxidative stress can induce more cell death and cardiac remodeling through damage to vessels and valvular and disruption of the normal structure of the extracellular matrix. These changes may lead to cardiomyopathy, myocarditis, pericarditis, and vascular disorders that may lead to heart attack and death. This review provides basic information on cellular and molecular mechanisms of different types of cardiovascular disorders following cancer therapy by radiation or chemotherapy. We also recommend some adjuvants and targets to reduce the risk of heart toxicity by radiation/chemotherapy.

Immunoregulation by resveratrol; implications for normal tissue protection and tumour suppression.

Immune reactions are involved in both tumour and normal tissue in response to therapy. Elevated secretion of certain chemokines, exosomes and cytokines triggers inflammation, pain, fibrosis and ulceration among other normal tissue side effects. On the other hand, secretion of tumour-promoting molecules suppresses activity of anticancer immune cells and facilitates the proliferation of malignant cells. Novel anticancer drugs such as immune checkpoint inhibitors (ICIs) boost anticancer immunity via inducing the proliferation of anticancer cells such as natural killer (NK) cells and CD8+ T lymphocytes. Certain chemotherapy drugs and radiotherapy may induce anticancer immunity in the tumour, however, both have severe side effects for normal tissues through stimulation of several immune responses. Thus, administration of natural products with low side effects may be a promising approach to modulate the immune system in both tumour and normal organs. Resveratrol is a well-known phenol with diverse effects on normal tissues and tumours. To date, a large number of experiments have confirmed the potential of resveratrol as an anticancer adjuvant. This review focuses on ensuing stimulation or suppression of immune responses in both tumour and normal tissue after radiotherapy or anticancer drugs. Later on, the immunoregulatory effects of resveratrol in both tumour and normal tissue following exposure to anticancer agents will be discussed.

Cavernous mediastinal hemangioma presenting with persistent cough: a rare case report and review of literature.

BACKGROUND: Cavernous hemangioma is a rare benign tumor which can sometimes mimic the clinical presentation and radiological findings of malignant tumors. Here we present a rare presentation of cavernous hemangioma in the mediastinum (CHM), along with a literature review among the main databases. CASE PRESENTATION: We present a 48-year-old male who had suffered from persistent cough as the sole symptom of an anterior CHM. Computed tomography scan demonstrated a 12.5 × 10.8 cm mass in the anterior mediastinum. The mass was surgically resected, and histopathological evaluation established the diagnosis of CHM. The patient was discharged in good condition, in which during his four-month follow-up period, no recurrence of the tumor has been observed. CONCLUSION: Although cavernous hemangioma rarely present in the mediastinum, it should be considered in the differential diagnosis of mediastinal tumors. However, our review of literature demonstrated a female dominance and average age of 40 years, with a 52% mortality rate based on previous reports.

Mechanisms of Cancer-killing by Quercetin; A Review on Cell Death Mechanisms.

Cancer drug resistance has always been a serious issue regarding cancer research and therapy. Different cancers undergo different mutations, which may cause suppression of tumor suppressor genes, inhibition of apoptosis, stimulation of drug resistance mediators, and exhaustion of the immune system. The modulation of pro-death and survival-related mediators is an intriguing strategy for cancer therapy. Several nature-derived molecules, e.g., quercetin, have shown interesting properties against cancer through the modulation of apoptosis and autophagy mediators. Such molecules, e.g., quercetin, have been shown to stimulate apoptosis and other types of cell death pathways in cancers via the modulation of ROS metabolism. Quercetin may affect immune system function and trigger the expression and activity of tumor suppressor genes. Furthermore, it may suppress certain multidrug resistance mechanisms in cancer cells. This paper aims to review the effects of quercetin on various cell death mechanisms such as apoptosis, autophagic cell death, senescence, ferroptosis, and others.

Induction of Cancer Cell Death by Apigenin: A Review on Different Cell Death Pathways.

Induction of cell death and inhibition of cell proliferation in cancer have been set as some of the main goals in anti-tumor therapy. Cancer cell resistance leads to less efficient cancer therapy, and consequently, to higher doses of anticancer drugs, which may eventually increase the risk of serious side effects in normal tissues. Apigenin, a nature-derived and herbal agent, which has shown anticancer properties in several types of cancer, can induce cell death directly and/or amplify the induction of cell death through other anti-tumor modalities. Although the main mechanism of apigenin in order to induce cell death is apoptosis, other cell death pathways, such as autophagic cell death, senescence, anoikis, necroptosis, and ferroptosis, have been reported to be induced by apigenin. It seems that apigenin enhances apoptosis by inducing anticancer immunity and tumor suppressor genes, like p53 and PTEN, and also by inhibiting STAT3 and NF-κB signaling pathways. Furthermore, it may induce autophagic cell death and ferroptosis by inducing endogenous ROS generation. Stimulation of ROS production and tumor suppressor genes, as well as downregulation of drug-resistance mediators, may induce other mechanisms of cell death, such as senescence, anoikis, and necroptosis. It seems that the induction of each type of cell death is highly dependent on the type of cancer. These modulatory actions of apigenin have been shown to enhance anticancer effects by other agents, such as ionizing radiation and chemotherapy drugs. This review explains how cancer cell death may be induced by apigenin at the cellular and molecular levels.

Efficacy of drug regimen with and without oseltamivir in hospitalized patients with COVID-19: A retrospective study.

Introduction: Coronavirus disease 2019 (COVID-19) is the most critical issue in nowadays medicine. We aimed to evaluate the use and therapeutic outcomes of oseltamivir, an antiviral drug for patients with COVID-19. Materials and method: In an observational study conducted at Imam Khomeini Hospital in Amol, Iran, data for 544 patients with laboratory and CT scan result confirmed COVID-19 were retrospectively collected between February 24th and April 13th 2020. To compare the characteristics of patients based on gender, the chi-square test was used. Logistic regression was used to evaluate the effect of oseltamivir on the outcome of treatment. Logrank test were used to compare the length of hospital stay in people treated with oseltamivir and drugs other than oseltamivir. Results: Kaplan-Meier and logrank test showed no significant reduction in hospitalization time and survival rate following treatment with oseltamivir. However, a significant increase in lymphocytes count and reduction of C-reactive protein (CRP) level detected. Conclusion: Administration of oseltamivir for patients with COVID-19 didn't show any improvement in hospitalization duration and survival rate.

Introducción: la enfermedad por coronavirus 2019 (COVID-19) es el tema más crítico en la medicina actual. Nuestro objetivo fue evaluar el uso y los resultados terapéuticos de oseltamivir, un medicamento antiviral para pacientes con COVID-19. Materiales y método: en un estudio observacional realizado en el Hospital Imam Khomeini en Amol, Irán, los datos de 544 pacientes con resultados de laboratorio y tomografía computarizada confirmados de COVID-19 se recopilaron retrospectivamente entre el 24 de febrero y el 13 de abril de 2020. Para comparar las características de los pacientes en función del género se utilizó la prueba de chi-cuadrado. Se utilizó regresión logística para evaluar el efecto de oseltamivir en el resultado del tratamiento. Se utilizó la prueba de rango logarítmico para comparar la duración de la estancia hospitalaria en personas tratadas con oseltamivir y otros fármacos distintos del oseltamivir. Resultados: Kaplan­Meier y la prueba de rango logarítmico no mostraron una reducción significativa en el tiempo de hospitalización y la tasa de supervivencia después del tratamiento con oseltamivir. Sin embargo, se detectó un aumento significativo en el recuento de linfocitos y una reducción del nivel de proteína C reactiva (PCR). Conclusión: la administración de oseltamivir para pacientes con COVID-19 no mostró ninguna mejora en la duración de la hospitalización y la tasa de supervivencia.

Resveratrol in Cancer Therapy: From Stimulation of Genomic Stability to Adjuvant Cancer Therapy: A Comprehensive Review.

Cancer therapy through anticancer drugs and radiotherapy is associated with several side effects as well as tumor resistance to therapy. The genotoxic effects of chemotherapy and radiotherapy may lead to genomic instability and increased risk of second cancers. Furthermore, some responses in the tumor may induce the exhaustion of antitumor immunity and increase the resistance of cancer cells to therapy. Administration of low-toxicity adjuvants to protect normal tissues and improve therapy efficacy is an intriguing strategy. Several studies have focused on natural-derived agents for improving the antitumor efficiency of radiotherapy, chemotherapy, and novel anticancer drugs such as immunotherapy and targeted cancer therapy. Resveratrol is a naturally occurring substance with intriguing antioxidant, cardioprotective, anti-diabetes, and antitumor properties. Resveratrol has been demonstrated to modulate tumor resistance and mitigate normal tissue toxicity following exposure to various drugs and ionizing radiation. Compelling data suggest that resveratrol may be an appealing adjuvant in combination with various anticancer modalities. Although the natural form of resveratrol has some limitations, such as low absorption in the intestine and low bioavailability, several experiments have demonstrated that using certain carriers, such as nanoparticles, can increase the therapeutic efficacy of resveratrol in preclinical studies. This review highlights various effects of resveratrol that may be useful for cancer therapy. Consequently, we describe how resveratrol can protect normal tissue from genomic instability. In addition, the various mechanisms by which resveratrol exerts its antitumor effects are addressed. Moreover, the outcomes of combination therapy with resveratrol and other anticancer agents are reviewed.

Mechanisms of cancer cell killing by metformin: a review on different cell death pathways.

Cancer resistance to anti-tumour agents has been one of the serious challenges in different types of cancer treatment. Usually, an increase in the cell death markers can predict a higher rate of survival among patients diagnosed with cancer. By increasing the regulation of survival genes, cancer cells can display a higher resistance to therapy through the suppression of anti-tumour immunity and inhibition of cell death signalling pathways. Administration of certain adjuvants may be useful in order to increase the therapeutic efficiency of anti-cancer therapy through the stimulation of different cell death pathways. Several studies have demonstrated that metformin, an antidiabetic drug with anti-cancer properties, amplifies cell death mechanisms, especially apoptosis in a broad-spectrum of cancer cells. Stimulation of the immune system by metformin has been shown to play a key role in the induction of cell death. It seems that the induction or suppression of different cell death mechanisms has a pivotal role in either sensitization or resistance of cancer cells to therapy. This review explains the cellular and molecular mechanisms of cell death following anticancer therapy. Then, we discuss the modulatory roles of metformin on different cancer cell death pathways including apoptosis, mitotic catastrophe, senescence, autophagy, ferroptosis and pyroptosis.