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Aim: Current treatments for obsessive‐compulsive disorder (OCD) encounter resistance and limiting adverse events, necessitating novel therapeutic strategies. This study aimed to investigate the benefits of naproxen, a medication with effects on inflammation and neuronal function, on OCD. Methods: One hundred and four OCD outpatients with a Yale‐Brown Obsessive‐Compulsive Scale (Y‐BOCS) score of >21 were equally assigned to receive fluoxetine plus either naproxen 250 mg or matched placebo q12hr. Patients were assessed using the Y‐BOCS by recording the subscale scores at baseline and weeks 5 and 10 to evaluate efficacy. They were also assessed in terms of tolerability. Results: Data from 96 patients were analyzed. The baseline characteristics were comparable between the groups. There were significant time‐treatment interaction effects on the obsession subscale (ηP2 = 0.055) and total (ηP2 = 0.043) scores of Y‐BOCS. Reductions in the obsession subscale and total scores of Y‐BOCS were significantly greater in the fluoxetine plus naproxen group until the endpoint (Cohen's d = 0.560 and Cohen's d = 0.477, respectively). However, the difference in compulsion subscale score changes between the groups was not significant. Respondents with a reduction of ≥35% in Y‐BOCS total scores were significantly more in the fluoxetine plus naproxen group (80.0% versus 47.8%). The side effect frequencies were comparable between the groups. Conclusion: Naproxen, adjunct to fluoxetine, outperformed adjunctive placebo in treating obsession and total symptoms of OCD patients in a safe and tolerable manner. Clinical trial registration: The study protocol was registered and published in the Iranian Registry of Clinical Trials (http://www.irct.ir; registration number IRCT20090117001556N139). [ABSTRACT FROM AUTHOR]

Background: Environmental risk factors are significant contributors to cancer mortality, which are neglected. Purpose: This study aimed to estimate the population attributable fraction of cancer mortality due to the environmental risk factors. Methods: Golestan cohort study is a population-base cohort on 50045 participants between 40–75 with about 18 years of follow up. We detected 2,196 cancer mortality and applied a multiple Cox model to compute the hazard ratio of environmental risk factor on all cancer and cancer-specific mortality. The population attributable fraction was calculated, accordingly. Results: Biomass fuels for cooking, as an indoor air pollution, increased the risk of colorectal, esophageal, gastric cancer, and all-cancer mortality by 84%, 66%, 37%, and 17% respectively. Using gas for cooking, particularly in rural areas, could save 6% [Population Attributable Fraction: 6.36(95%CI: 1.82, 10.70)] of esophageal cancer, 3% [Population Attributable Fraction: 3.43 (0, 7.33)] of gastric cancer, and 6% [Population Attributable Fraction: 6.25 (1.76, 13.63)] of colorectal cancer mortality. Using a healthy tap water source could save 5% [Population Attributable Fraction:5.50(0, 10.93)] of esophageal cancer mortality, particularly in rural areas. There was no significant association between indoor air pollution for heating purposes and animal contact with cancer mortality. Conclusion: Considering the results of this study, eliminating solid fuel for most daily usage, among the population with specific cancer types, is required to successfully reduce cancer related mortality. Adopting appropriate strategies and interventions by policymakers such as educating the population, allocating resources for improving the healthy environment of the community, and cancer screening policies among susceptible populations could reduce cancer related mortalities. [ABSTRACT FROM AUTHOR]

A major factor in long‐term impairment is stroke. Patients with persistent stroke and severe functional disabilities have few therapy choices. Long noncoding RNAs (lncRNAs) may contribute to the regulation of the pathophysiologic processes of ischemic stroke as shown by altered expression of lncRNAs and microRNA (miRNAs) in blood samples of acute ischemic stroke patients. On the other hand, multipotent mesenchymal stem cells (MSCs) increase neurogenesis, and angiogenesis, dampen neuroinflammation, and boost brain plasticity to improve functional recovery in experimental stroke models. MSCs can be procured from various sources such as the bone marrow, adipose tissue, and peripheral blood. Under the proper circumstances, MSCs can differentiate into a variety of mature cells, including neurons, astrocytes, and oligodendrocytes. Accordingly, the capability of MSCs to exert neuroprotection and also neurogenesis has recently attracted more attention. Nowadays, lncRNAs and miRNAs derived from MSCs have opened new avenues to alleviate stroke symptoms. Accordingly, in this review article, we examined various studies concerning the lncRNAs and miRNAs' role in stroke pathogenesis and delivered an overview of the therapeutic role of MSC‐derived miRNAs and lncRNAs in stroke conditions. Significance Statement: The potential for using mesenchymal stem cells (MSCs) to treat a variety of human disorders, including stroke recovery, is substantial. Some of the qualities that make MSC particularly appealing as a therapeutic candidate are immune privileged status, availability from a variety of potential sources, inherent multipotency, and the ability to promote repair through numerous channels concurrently, including immunoregulation, neurogenesis, and angiogenesis. In the end, we came to the conclusion that MSC‐extracellular vesicles, like microRNAs and long noncoding RNAs, improved neurological function and prevented neuronal death, which in turn decreased brain damage following stroke. This research adds to our understanding of MSC‐based stroke therapy and provides support for a novel restorative treatment for stroke patients who may be at risk for cognitive impairments. [ABSTRACT FROM AUTHOR]

MicroRNAs (miRNAs) play critical roles in cancer pathobiology, acting as regulators of gene expression and pivotal drivers of tumorigenesis. It is believed that miRNAs act through canonical mechanisms, involving the binding of mature miRNAs to target messenger RNAs (mRNAs) and subsequent repression of protein translation or degradation of target mRNAs. miR‐142‐3p/5p has been extensively studied and established as a key regulator in various malignancies. Recent discoveries have revealed miR‐142‐3p/5p serve as either oncogene or tumor suppressor in cancer. By targeting epigenetic factor and cancer‐related signaling pathway, miR‐142‐3p/5p can regulate wide range of downstream genes. The immune modulatory role of miR‐142‐3p/5p has been shown in various cancers, which provides significant insight into immunosuppression and tumor escape from the immune response. Exosomes with miR‐142‐3p/5p facilitate cell communication and can affect cancer cell behavior, offering potential therapeutic, and diagnosis applications in cancer therapy. In this review, for the first time, we comprehensively summarize the current knowledge regarding mentioned functions of miR‐142‐3p/5p in cancer pathobiology. Significance statement: Targeting the cancer‐related signaling pathway and epigenetic factor, miR‐142‐3p/5p can control a large number of downstream genes. Numerous cancers have demonstrated the immune‐modulatory function of miR‐142‐3p/5p, which offers important new understanding of immunosuppression and tumor resistance to the immune system. Exosomes containing miR‐142‐3p/5p have the ability to influence cancer cell behavior and enhance cell‐to‐cell communication, potentially providing therapeutic and diagnostic applications in cancer therapy. For the first time, we provide a thorough summary of the state of knowledge regarding the roles that miR‐142‐3p/5p have been mentioned in cancer pathobiology in this review. [ABSTRACT FROM AUTHOR]

Pancreatic cancer is the fourth most common malignant tumor in the world, which has a high mortality rate due to high invasiveness, early metastases, lack of specific symptoms, and high invasiveness. Recent studies have shown that exosomes can be essential sources of biomarkers in pancreatic cancer. Over the past ten years, exosomes have been implicated in multiple trials to prevent the growth and metastasis of many cancers, including pancreatic cancer. Exosomes also play essential roles in immune evasion, invasion, metastasis, proliferation, apoptosis, drug resistance, and cancer stemness. Exosomes help cells communicate by carrying proteins and genetic material, such as non-coding RNAs, including mRNAs and microRNAs. This review examines the biological significance of exosomes in pancreatic cancer and their functions in tumor invasion, metastasis, treatment resistance, proliferation, stemness, and immune evasion. We also emphasize recent advances in our understanding of the main functions of exosomes in diagnosing and treating pancreatic cancer. [ABSTRACT FROM AUTHOR]

Lysosomal-driven autophagy is a tightly controlled cellular catabolic process that breaks down and recycles broken or superfluous cell parts. It is involved in several illnesses, including cancer, and is essential in preserving cellular homeostasis. Autophagy prevents DNA mutation and cancer development by actively eliminating pro-oxidative mitochondria and protein aggregates from healthy cells. Oncosuppressor and oncogene gene mutations cause dysregulation of autophagy. Increased autophagy may offer cancer cells a pro-survival advantage when oxygen and nutrients are scarce and resistance to chemotherapy and radiation. This finding justifies the use of autophagy inhibitors in addition to anti-neoplastic treatments. Excessive autophagy levels can potentially kill cells. The diagnosis and treatment of ovarian cancer present many difficulties due to its complexity and heterogeneity. Understanding the role of autophagy, a cellular process involved in the breakdown and recycling of cellular components, in ovarian cancer has garnered increasing attention in recent years. Of particular note is the increasing amount of data indicating a close relationship between autophagy and ovarian cancer. Autophagy either promotes or restricts tumor growth in ovarian cancer. Dysregulation of autophagy signaling pathways in ovarian cancers can affect the development, metastasis, and response to tumor treatment. The precise mechanism underlying autophagy concerning ovarian cancer remains unclear, as does the role autophagy plays in ovarian carcinoma. In this review, we tried to encapsulate and evaluate current findings in investigating autophagy in ovarian cancer. [ABSTRACT FROM AUTHOR]