Comparing the quality of life of adolescent girls with and without polycystic ovary syndrome and identifying the predictor factors.

OBJECTIVES: Polycystic Ovary Syndrome (PCOS) is a complex hormonal disorder that affects the endocrine glands and reproductive processes in adolescent girls, potentially impacting their quality of life. This study aims to compare the quality of life between adolescent girls with PCOS and those without PCOS. METHODS: The present study is an analytical cross-sectional study. It involved 12-18-year-old girls who were diagnosed with PCOS based on the Rotterdam criteria for the case group. An ordinal logistic regression model was employed to assess the impact of the studied variables on different levels of quality of life, and Odds Ratio (OR) values were determined for predictor variables. RESULTS: The findings of the study revealed that the control group had a significantly higher percentage of individuals with excellent quality of life (score 209-260) compared to the group with polycystic ovary syndrome (p<0.05). The results of the ordinal logistic regression analysis indicated that age variables (OR=0.64, CI 95 %; 0.44-0.93), menstrual disorders (OR=0.07, CI 95 %; 0.01-0.38), and micromastia (OR=0.03, CI 95 %; 0.004-0.34) were identified as factors influencing the quality of life of girls with polycystic ovary syndrome. CONCLUSIONS: It was concluded that patients with PCOS had a lower quality of life score. The variables of age, menstrual disorders, and micromastia were determined as influencing factors the quality of life. The results of this study are significant and warrant further research in this area, particularly with regard to the financial resources of patients in the challenging economic circumstances facing the nation - the majority of which are brought on by economic sanctions.

The landscape of circRNAs in gliomas temozolomide resistance: Insights into molecular pathways.

As the deadliest type of primary brain tumor, gliomas represent a significant worldwide health concern. Circular RNA (circRNA), a unique non-coding RNA molecule, seems to be one of the most alluring target molecules involved in the pathophysiology of many kinds of cancers. CircRNAs have been identified as prospective targets and biomarkers for the diagnosis and treatment of numerous disorders, particularly malignancies. Recent research has established a clinical link between temozolomide (TMZ) resistance and certain circRNA dysregulations in glioma tumors. CircRNAs may play a therapeutic role in controlling or overcoming TMZ resistance in gliomas and may provide guidance for a novel kind of individualized glioma therapy. To address the biological characteristics of circRNAs and their potential to induce resistance to TMZ, this review has highlighted and summarized the possible roles that circRNAs may play in molecular pathways of drug resistance, including the Ras/Raf/ERK PI3K/Akt signaling pathway and metabolic processes in gliomas.

Ferroptosis contributes to the progression of female-specific neoplasms, from breast cancer to gynecological malignancies in a manner regulated by non-coding RNAs: Mechanistic implications.

Ferroptosis, a recently identified type of non-apoptotic cell death, triggers the elimination of cells in the presence of lipid peroxidation and in an iron-dependent manner. Indeed, ferroptosis-stimulating factors have the ability of suppressing antioxidant capacity, leading to the accumulation of reactive oxygen species (ROS) and the subsequent oxidative death of the cells. Ferroptosis is involved in the pathophysiological basis of different maladies, such as multiple cancers, among which female-oriented malignancies have attracted much attention in recent years. In this context, it has also been unveiled that non-coding RNA transcripts, including microRNAs, long non-coding RNAs, and circular RNAs have regulatory interconnections with the ferroptotic flux, which controls the pathogenic development of diseases. Furthermore, the potential of employing these RNA transcripts as therapeutic targets during the onset of female-specific neoplasms to modulate ferroptosis has become a research hotspot; however, the molecular mechanisms and functional alterations of ferroptosis still require further investigation. The current review comprehensively highlights ferroptosis and its association with non-coding RNAs with a focus on how this crosstalk affects the pathogenesis of female-oriented malignancies, from breast cancer to ovarian, cervical, and endometrial neoplasms, suggesting novel therapeutic targets to decelerate and even block the expansion and development of these tumors.

Comparison of effects of P-coumaric acid and coumarin on colorectal cancer cell line by inducing apoptosis and autophagy.

Objective: Autophagy, as a cellular pathway involved in removing damaged proteins and organelles, performs a vital function in the homeostasis and fate of cells. Natural compounds of coumarin (CO) are found in a variety of herbs. Due to their many medicinal properties, including antitumor and anti-proliferative activity, they are involved in apoptosis and autophagy processes. This investigation desired to analyze the apoptotic and autophagic effects of p-coumaric acid (PCA) and CO on HT-29 cells cultured in fibrin hydrogel. Materials and Methods: Cell viability and apoptotic and autophagic changes were evaluated by MTT assay, Acridine Orange, 4',6-diamidino-2-phenylindole (DAPI), and monodansylcadaverine (MDC) staining. The expression Bax, Bad, Bcl2, Lc3, Beclin-1, P53 and Atg5 was respectively measured by qRT-PCR and Western blotting. Results: CO (IC50=25 µM) and PCA (IC50=150 µM) had a dose- and time-dependent cytotoxic effect in HT-29 cells. So, the cytotoxic effects of CO were significantly higher than PCA and these differences were also evident in cell morphology investigations. The data illustrated a high expression of pro-apoptotic and pro-autophagic genes and a declined expression of anti-apoptotic and anti-autophagic genes. Conclusion: CO (that was more potent) and p-coumaric acid-induced autophagy via PI3K/Akt/mTOR and AMPK/mTOR signaling on HT-29 cells.

The emerging role of circular RNAs in cisplatin resistance in ovarian cancer: From molecular mechanism to future potential.

Ovarian cancer (OC) is the most common cause of death in female cancers. The prognosis of OC is very poor due to delayed diagnosis and identification of most patients in advanced stages, metastasis, recurrence, and resistance to chemotherapy. As chemotherapy with platinum-based drugs such as cisplatin (DDP) is the main treatment in most OC cases, resistance to DDP is an important obstacle to achieving satisfactory therapeutic efficacy. Consequently, knowing the different molecular mechanisms involved in resistance to DDP is necessary to achieve new therapeutic approaches. According to numerous recent studies, non-coding RNAs (ncRNAs) could regulate proliferation, differentiation, apoptosis, and chemoresistance in many cancers, including OC. Most of these ncRNAs are released by tumor cells into human fluid, allowing them to be used as tools for diagnosis. CircRNAs are ncRNA family members that have a role in the initiation, progression, and chemoresistance regulation of various cancers. In the current study, we investigated the roles of several circRNAs and their signaling pathways on OC progression and also on DDP resistance during chemotherapy.

BDNF-TrkB Signaling Pathway in Spinal Cord Injury: Insights and Implications.

Spinal cord injury (SCI) is a neurodegenerative disorder that has critical impact on patient's life expectance and life span, and this disorder also leads to negative socioeconomic features. SCI is defined as a firm collision to the spinal cord which leads to the fracture and the dislocation of vertebrae. The current available treatment is surgery. However, it cannot fully treat SCI, and many consequences remain after the surgery. Accordingly, finding new therapeutics is critical. BDNF-TrkB signaling is a vital signaling in neuronal differentiation, survival, overgrowth, synaptic plasticity, etc. Hence, many studies evaluate its impact on various neurodegenerative disorders. There are several studies evaluating this signaling in SCI, and they show promising outcomes. It was shown that various exercises, chemical interventions, etc. had significant positive impact on SCI by affecting BDNF-TrkB signaling pathway. This study aims to accumulate and evaluate these data and inspect whether this signaling is effective or not.

Nanoliposomes as nonviral vectors in cancer gene therapy.

Nonviral vectors, such as liposomes, offer potential for targeted gene delivery in cancer therapy. Liposomes, composed of phospholipid vesicles, have demonstrated efficacy as nanocarriers for genetic tools, addressing the limitations of off-targeting and degradation commonly associated with traditional gene therapy approaches. Due to their biocompatibility, stability, and tunable physicochemical properties, they offer potential in overcoming the challenges associated with gene therapy, such as low transfection efficiency and poor stability in biological fluids. Despite these advancements, there remains a gap in understanding the optimal utilization of nanoliposomes for enhanced gene delivery in cancer treatment. This review delves into the present state of nanoliposomes as carriers for genetic tools in cancer therapy, sheds light on their potential to safeguard genetic payloads and facilitate cell internalization alongside the evolution of smart nanocarriers for targeted delivery. The challenges linked to their biocompatibility and the factors that restrict their effectiveness in gene delivery are also discussed along with exploring the potential of nanoliposomes in cancer gene therapy strategies by analyzing recent advancements and offering future directions.

Implications of c-Myc in the pathogenesis and treatment efficacy of urological cancers.

Urological cancers, including prostate, bladder, and renal cancers, are significant causes of death and negatively impact the quality of life for patients. The development and progression of these cancers are linked to the dysregulation of molecular pathways. c-Myc, recognized as an oncogene, exhibits abnormal levels in various types of tumors, and current evidence supports the therapeutic targeting of c-Myc in cancer treatment. This review aims to elucidate the role of c-Myc in driving the progression of urological cancers. c-Myc functions to enhance tumorigenesis and has been documented to increase growth and metastasis in prostate, bladder, and renal cancers. Furthermore, the dysregulation of c-Myc can result in a diminished response to therapy in these cancers. Non-coding RNAs, ß-catenin, and XIAP are among the regulators of c-Myc in urological cancers. Targeting and suppressing c-Myc therapeutically for the treatment of these cancers has been explored. Additionally, the expression level of c-Myc may serve as a prognostic factor in clinical settings.

The science of exosomes: Understanding their formation, capture, and role in cellular communication.

Extracellular vesicles (EVs) serve as a crucial method for transferring information among cells, which is vital in multicellular organisms. Among these vesicles, exosomes are notable for their small size, ranging from 20 to 150 nm, and their role in cell-to-cell communication. They carry lipids, proteins, and nucleic acids between cells. The creation of exosomes begins with the inward budding of the cell membrane, which then encapsulates various macromolecules as cargo. Once filled, exosomes are released into the extracellular space and taken up by target cells via endocytosis and similar processes. The composition of exosomal cargo varies, encompassing diverse macromolecules with specific functions. Because of their significant roles, exosomes have been isolated from various cell types, including cancer cells, endothelial cells, macrophages, and mesenchymal cells, with the aim of harnessing them for therapeutic applications. Exosomes influence cellular metabolism, and regulate lipid, glucose, and glutamine pathways. Their role in pathogenesis is determined by their cargo, which can manipulate processes such as apoptosis, proliferation, inflammation, migration, and other molecular pathways in recipient cells. Non-coding RNA transcripts, a common type of cargo, play a pivotal role in regulating disease progression. Exosomes are implicated in numerous biological and pathological processes, including inflammation, cancer, cardiovascular diseases, diabetes, wound healing, and ischemic-reperfusion injury. As a result, they hold significant potential in the treatment of both cancerous and non-cancerous conditions.

The multifaceted role of SOX2 in breast and lung cancer dynamics.

Breast and lung cancers are leading causes of death among patients, with their global mortality and morbidity rates increasing. Conventional treatments often prove inadequate due to resistance development. The alteration of molecular interactions may accelerate cancer progression and treatment resistance. SOX2, known for its abnormal expression in various human cancers, can either accelerate or impede cancer progression. This review focuses on examining the role of SOX2 in breast and lung cancer development. An imbalance in SOX2 expression can promote the growth and dissemination of these cancers. SOX2 can also block programmed cell death, affecting autophagy and other cell death mechanisms. It plays a significant role in cancer metastasis, mainly by regulating the epithelial-to-mesenchymal transition (EMT). Additionally, an imbalanced SOX2 expression can cause resistance to chemotherapy and radiation therapy in these cancers. Genetic and epigenetic factors may affect SOX2 levels. Pharmacologically targeting SOX2 could improve the effectiveness of breast and lung cancer treatments.

NF-ĸB axis in diabetic neuropathy, cardiomyopathy and nephropathy: A roadmap from molecular intervention to therapeutic strategies.

Diabetes mellitus (DM) is a metabolic illness defined by elevated blood glucose levels, mediating various tissue alterations, including the dysfunction of vital organs. Diabetes mellitus (DM) can lead to many consequences that specifically affect the brain, heart, and kidneys. These issues are known as neuropathy, cardiomyopathy, and nephropathy, respectively. Inflammation is acknowledged as a pivotal biological mechanism that contributes to the development of various diabetes consequences. NF-κB modulates inflammation and the immune system at the cellular level. Its abnormal regulation has been identified in several clinical situations, including cancer, inflammatory bowel illnesses, cardiovascular diseases, and Diabetes Mellitus (DM). The purpose of this review is to evaluate the potential impact of NF-κB on complications associated with DM. Enhanced NF-κB activity promotes inflammation, resulting in cellular harm and compromised organ performance. Phytochemicals, which are therapeutic molecules, can potentially decline the NF-κB level, therefore alleviating inflammation and the progression of problems correlated with DM. More importantly, the regulation of NF-κB can be influenced by various factors, such as TLR4 in DM. Highlighting these factors can facilitate the development of novel therapies in the future.

Investigating the trend of demographic changes, mortality, clinical and paraclinical findings of patients hospitalized in the Corona ward, before and after the start of general vaccination of COVID-19.

BACKGROUND: Prioritizing prevention over treatment has been a longstanding principle in the world health system. This study aims to compare the demographic changes, mortality, clinical, and paraclinical findings of patients hospitalized in the Corona ward before and after the start of general vaccination. METHODS: This cross-sectional study utilized the simple random sampling method in 2022, analyzing 300 medical records of patients admitted to the Corona ward at 22 Bahman Khaf Hospital. Data were collected using a checklist with the help of the Medical Care Monitoring System and analyzed using SPSS-22 statistical software and Chi-square statistical test at a significance level of p < 0.05. RESULTS: Before the start of general vaccination for COVID-19, the majority of patients were hospitalized in the Corona Intensive Care Unit (59.3%), aged between 51 and 65 years (47.3%), hospitalized for more than 3 days (54%), required intubation (49.3%), had SPO2 < 93% (60.7%), and exhibited common symptoms such as cough, shortness of breath, and loss of consciousness. Paraclinical findings included positive CRP, decreased lymphocytes, and ground glass opacity (GGO). After the start of general vaccination for COVID-19, most patients were hospitalized in the general care department of Corona (68%), aged between 36 and 50 years (47.3%), hospitalized for less than three days (66%), required intubation (20%), had SPO2 ≥ 93% (77.3%), and exhibited common symptoms such as weakness, headache, and body pain. Paraclinical findings were within the normal range. CONCLUSIONS: General vaccination for COVID-19 has significantly reduced patient mortality and morbidity. Health policymakers should prioritize general vaccination to achieve herd immunity and improve public health.

Amino acid transporters within the solute carrier superfamily: Underappreciated proteins and novel opportunities for cancer therapy.

BACKGROUND: Solute carrier (SLC) transporters, a diverse family of membrane proteins, are instrumental in orchestrating the intake and efflux of nutrients including amino acids, vitamins, ions, nutrients, etc, across cell membranes. This dynamic process is critical for sustaining the metabolic demands of cancer cells, promoting their survival, proliferation, and adaptation to the tumor microenvironment (TME). Amino acids are fundamental building blocks of cells and play essential roles in protein synthesis, nutrient sensing, and oncogenic signaling pathways. As key transporters of amino acids, SLCs have emerged as crucial players in maintaining cellular amino acid homeostasis, and their dysregulation is implicated in various cancer types. Thus, understanding the intricate connections between amino acids, SLCs, and cancer is pivotal for unraveling novel therapeutic targets and strategies. SCOPE OF REVIEW: In this review, we delve into the significant impact of amino acid carriers of the SLCs family on the growth and progression of cancer and explore the current state of knowledge in this field, shedding light on the molecular mechanisms that underlie these relationships and highlighting potential avenues for future research and clinical interventions. MAJOR CONCLUSIONS: Amino acids transportation by SLCs plays a critical role in tumor progression. However, some studies revealed the tumor suppressor function of SLCs. Although several studies evaluated the function of SLC7A11 and SLC1A5, the role of some SLC proteins in cancer is not studied well. To exert their functions, SLCs mediate metabolic rewiring, regulate the maintenance of redox balance, affect main oncogenic pathways, regulate amino acids bioavailability within the TME, and alter the sensitivity of cancer cells to therapeutics. However, different therapeutic methods that prevent the function of SLCs were able to inhibit tumor progression. This comprehensive review provides insights into a rapidly evolving area of cancer biology by focusing on amino acids and their transporters within the SLC superfamily.

Shedding light on function of long non-coding RNAs (lncRNAs) in glioblastoma.

The brain tumors and especially glioblastoma, are affecting life of many people worldwide and due to their high mortality and morbidity, their treatment is of importance and has gained attention in recent years. The abnormal expression of genes is commonly observed in GBM and long non-coding RNAs (lncRNAs) have demonstrated dysregulation in this tumor. LncRNAs have length more than 200 nucleotides and they have been located in cytoplasm and nucleus. The current review focuses on the role of lncRNAs in GBM. There two types of lncRNAs in GBM including tumor-promoting and tumor-suppressor lncRNAs and overexpression of oncogenic lncRNAs increases progression of GBM. LncRNAs can regulate proliferation, cell cycle arrest and metastasis of GBM cells. Wnt, STAT3 and EZH2 are among the molecular pathways affected by lncRNAs in GBM and for regulating metastasis of GBM cells, these RNA molecules mainly affect EMT mechanism. LncRNAs are involved in drug resistance and can induce resistance of GBM cells to temozolomide chemotherapy. Furthermore, lncRNAs stimulate radio-resistance in GBM cells. LncRNAs increase PD-1 expression to mediate immune evasion. LncRNAs can be considered as diagnostic and prognostic tools in GBM and researchers have developed signature from lncRNAs in GBM.

Nanostructures for site-specific delivery of oxaliplatin cancer therapy: Versatile nanoplatforms in synergistic cancer therapy.

As a clinically approved treatment strategy, chemotherapy-mediated tumor suppression has been compromised, and in spite of introducing various kinds of anticancer drugs, cancer eradication with chemotherapy is still impossible. Chemotherapy drugs have been beneficial in improving the prognosis of cancer patients, but after resistance emerged, their potential disappeared. Oxaliplatin (OXA) efficacy in tumor suppression has been compromised by resistance. Due to the dysregulation of pathways and mechanisms in OXA resistance, it is suggested to develop novel strategies for overcoming drug resistance. The targeted delivery of OXA by nanostructures is described here. The targeted delivery of OXA in cancer can be mediated by polymeric, metal, lipid and carbon nanostructures. The advantageous of these nanocarriers is that they enhance the accumulation of OXA in tumor and promote its cytotoxicity. Moreover, (nano)platforms mediate the co-delivery of OXA with drugs and genes in synergistic cancer therapy, overcoming OXA resistance and improving insights in cancer patient treatment in the future. Moreover, smart nanostructures, including pH-, redox-, light-, and thermo-sensitive nanostructures, have been designed for OXA delivery and cancer therapy. The application of nanoparticle-mediated phototherapy can increase OXA's potential in cancer suppression. All of these subjects and their clinical implications are discussed in the current review.

The protective impact of curcumin, vitamin D and E along with manganese oxide and Iron (III) oxide nanoparticles in rats with scrotal hyperthermia: Role of apoptotic genes, miRNA and circRNA.

BACKGROUND: Infertility is one of the major factors affecting most people around the world. Short-term exposure to high temperatures can cause hyperthermia, which is one of the causes of male infertility. The aim of this study was to investigate the protective effect of curcumin, vitamins D and E along with Iron (III) oxide nanoparticles (Fe2O3-NPs) and manganese oxide nanoparticles (MnO2-NPs) on semen parameters and its effect on miRNA21 and circRNA0001518 expression. MATERIAL AND METHODS: In this study, the lower part of the rat was exposed to 43 °C for 5 weeks every other day for 5 weeks. Then the animals were killed. Tissue samples were collected for sperm parameters analysis, and tissue samples were taken for evaluation of apoptosis levels in germ cells, and RNA extraction in order to examine the expression of Bax, Bcl-2, miRNA, and CircRNA genes. RESULTS: The results of this study showed that administration of curcumin, vitamin D, and vitamin E with Fe2O3-NPs and MnO2-NPs can improve the parameters of semen, Bax gene expression, Bcl-2 as well as miRNA and CircRNA in rats with testicular hyperthermia. In addition, curcumin by reducing the toxicity of Fe2O3 nanoparticles was able to reduce its negative effects and also reduce apoptosis in germ cells. This decrease in apoptosis was attributed to decreased Bcl-2 gene expression and increased expression of Bax, miRNA-21, and circRNA0001518. CONCLUSION: All the results of this study confirmed that Fe2O3-NPs and Mno2-NPs containing antioxidants or vitamins are useful in improving fertility in rats due to scrotal hyperthermia. Although Fe2O3-NPs and Mno2-NPs containing both antioxidants and vitamins had a greater effect on improving fertility and reducing the toxic effects of nanoparticles.