Hollisfuentes6874
Acquired immunodeficiency syndrome (AIDS) emerged as an epidemic in Africa in 1981, and now it has become a most destructive global pandemic. Human immunodeficiency virus (HIV) is responsible for the pathogenesis of AIDS, and it is usually transmitted through unsafe sexual activities. HIV is a lentivirus that can remain latent in the host cells for a long period, and it has various mechanisms to establish latency. The HIV genome encodes several microRNAs (miRNA-TAR, miRNA-H1, miRNA-H3, and miRNA-Nef-367) that act as posttranscriptional control by targeting mRNA sequences. The miRNA-TAR, miRNA-Nef-367, and miRNA-H1 have established roles in HIV latency, whereas miRNA-H3 can activate the latent reservoirs of HIV. The human genome also encodes several miRNAs that have defensive roles against infections. Cellular miRNAs (miRNA-29a, miRNA-146a, miRNA-34c-5'p, miRNA-186, miRNA-210 and miRNA-222) also contribute to viral latency. The most challenging hurdle in the development of effective HIV therapeutics is viral latency. A complete understanding of latency will enable us to develop efficient therapeutics and to eradicate HIV from the globe.Induction of highly pathogenic hepatitis C virus (HCV) causes chronic hepatitis round the world. This virus is easily prone to developing resistance against antiviral drugs because of two viral polymerases that do not possess the proofreading and overlapping reading frame abilities. There is more than one explanation for how this virus builds up resistance against antiviral drug treatments. Assays are now available to detect HCV-resistant variants, based on phenotypic and genotypic assays, and next generation sequencing. But these assays are of a little value at baseline, because they are not influential enough for making therapeutic decisions in HCV patients. Moreover, HCV monitoring is now an essential part of clinical practice. Special patients, such as those with thalassemia, renal transplant due to renal failure, and the patients undergoing hemodialysis, are at higher risk for acquiring this infection. Management of HCV infection in these patient groups is complicated by multiple side effects, including flu-like symptoms, neutropenia, fever, and neuropsychiatric disorders, thus limiting the use of ribavirin and coexisting iron overload. In HCV patients suffering from depression, the treatment may be discontinued because of some defects in neurochemical pathways caused by interferon, which can enhance the level of depression in these patients. In addition, obesity has been found to be a marker of failure of HCV treatment. There will be many resistance tolerant HCV treatment options available in the near future.Oxidative stress is caused by an imbalance in a redox system. It may involve either excessive production of reactive oxygen species or dysfunction of the antioxidant defense system. Unlike other viscera, the brain is especially highly susceptible to oxidative damage because of it requires a high oxygen level and contains an abundance of peroxida-tion-susceptible lipid cells. Oxidative stress is among the common etiological factors involved in neurodegeneration. To measure The extent of oxidative stress is measured with several indicators or biomarkers that are known to arise from oxidation of major biomolecules, including lipids, proteins, carbohydrates, and nucleic acids. In this review, we will discuss oxidative stress biomarkers associated with neurodegenerative diseases, for instance, Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, and Huntington's disease. We will also highlight the biomarkers of antioxidant defense mechanisms that are impaired in these diseases.Deregulation of AKT (protein kinase B) is frequently observed in human malignancies including gastrointestinal (GI) cancers. Liraglutide Here we have reviewed the association between AKT phosphorylation (activation) and clinical and pathological characteristics of patients with GI cancer. Articles in the EMBASE, PubMed, Cochrane Library, and Web of Science databases were searched up to July 2018. Eighteen studies comprising 1,698 patients with 5 different cancer types were included in the meta-analysis. In the pooled analysis, AKT phosphorylation was positively correlated with tumor size (r = 0.14, 95% CI 0.06-0.22; P less then 0.001), tumor grade (r = 0.08, 95% CI 0.02-0.14; P less then 0.009), tumor stage (r = 0.19, 95% CI 0.13-0.24; P less then 0.001), lymph node status (r = 0.18, 95% CI 0.09-0.25; P less then 0.001) and the presence of distant metastasis (r = 0.14, 95% CI 0.06-0.22; P less then 0.001) in the patients with GI cancer. These findings support the potential clinical value of AKT as a prognostic marker and therapeutic target in patients with GI carcinomas.Melanoma is a skin cancer caused by a malignancy of melanocytes. Incidence of melanoma is rapidly increasing worldwide, which results in public health problems. Primary extracutaneous melanomas can be ocular, gastrointestinal, mucosal, leptomeningeal, genitourinary, and lymphatic. The relationship between exposure to ultraviolet (UV) light and development of melanoma is intensively acute and complex, and intermittent sun exposure greatly increases the risk of melanoma. It is the fifth most common type of cancer in men number and the sixth most common in women. The diagnosis of melanoma is made through clinical assessment of the pigmented by health care professionals. Architectural features of malignant melanoma including asymmetry, confluence of growth, marked cellularity, and poor circumscription. The cytological feature of malignant melanoma include an irregular and thick nuclear membrane and prominent nucleoli. The preventive measures include reducing exposure to UV light and the sun. The early detection of skin cancer greatly reduces both short- and long-term morbidity and mortality. The treatment and follow-up with the doctor for melanoma patients may differ because of the stage of the tumor and the primary lesion. The typical therapy for malignant melanoma is surgical excision, immunotherapy such as interleukin 2 (IL-2), gene therapy, and biochemotherapy.