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Peripheral neuropathies have many nonspecific features that are shared by various neurologic disorders. These disorders include atypical peripheral neuropathies along with neurologic disorders outside of the peripheral nervous system. An understanding of clinical fundamentals and a measured approach to laboratory work-up can assist the provider in achieving diagnostic confidence.It is increasingly recognized that diabetic neuropathy is associated with early diabetes, prediabetes, and the metabolic syndrome. Early detection and diagnosis are important to slow progression and prevent complications. Although strict glucose control is an effective treatment in type 1 diabetes, it is less effective in type 2 diabetes. There is a growing body of literature that lifestyle interventions may be able to prevent or slow progression of neuropathy in type 2 diabetes. In addition to the typical distal symmetric polyneuropathy, there are many types of "atypical" diabetic neuropathies that are important to recognize.Compression neuropathies, also known as entrapment neuropathies, are common neurologic conditions seen in medicine. These often are due to mechanical injury, either compression or stretch of the affected nerve, and initially result in focal demyelinating changes. If left untreated, secondary axonal injury and lasting disability can result. Patients typically present with pain, sensory changes, and potentially weakness in the distribution of the affected nerve; therefore, a basic knowledge of neuromuscular anatomy is necessary to identify these conditions. Initial treatment of mild to moderate cases often is conservative. In severe cases or those refractory to conservative therapy, surgery should be considered.Peripheral nerve imaging is a helpful and sometimes essential adjunct to clinical history, physical examination, and electrodiagnostic studies. Advances in imaging technology have allowed the visualization of nerve structures and their surrounding tissues. The clinical applications of ultrasound and magnetic resonance imaging (MRI) in the evaluation of peripheral nerve disorders are growing exponentially. This article reviews basics of ultrasound and MRI as they relate to nerve imaging, reviews advantages and limitations of each imaging modality, reviews the applications of ultrasound and MRI in disorders of peripheral nerve, and discusses emerging advances in the field.Nerve conduction studies and electromyography are useful diagnostic tools that neurologists use to diagnose diseases of the peripheral nerves, neuromuscular junction, and muscles. These tests are considered an extension of clinical history and examination, and their results should always be interpreted with the clinical context. Neuromuscular diseases are common and affect a large proportion of the elderly population. With an aging population in expansion, these diseases are expected to become even more prevalent. It is important to highlight the basics of electrophysiology and provide a reference for providers who are planning to send their patients to electromyographers for these studies.V.Peripheral neuropathy is one of the most prevalent neurologic conditions encountered by neurologists and nonneurologists. Geriatricians and primary care physicians often face the task of screening patients for early neuropathy when they have underlying conditions such as diabetes mellitus and evaluating patients who report new symptoms that suggest neuropathy. An understanding about different forms of neuropathies based on anatomic pattern and type of nerve fiber involvement and ability to perform basic neurologic examination reliably can help determine how to pursue further investigations and identify those patients who are likely to benefit from early specialist referral.Autophagy and cellular senescence are two potent tumor suppressive mechanisms activated by various cellular stresses, including the expression of activated oncogenes. However, emerging evidence has also indicated their pro-tumorigenic activities, strengthening the case for the complexity of tumorigenesis. More specifically, tumorigenesis is a systemic process emanating from the combined accumulation of changes in the tumor support pathways, many of which cannot cause cancer on their own but might still provide excellent therapeutic targets for cancer treatment. In this review, we discuss the dual roles of autophagy and senescence during tumorigenesis, with a specific focus on the stress support networks in cancer cells modulated by these processes. A deeper understanding of such context-dependent roles may help to enhance the effectiveness of cancer therapies targeting autophagy and senescence, while limiting their potential side effects. This will steer and accelerate the pace of research and drug development for cancer treatment.Cellular senescence, cancer and aging are highly interconnected. Among many important molecular machines that lie at the intersection of this triad, the mechanistic (formerly mammalian) target of rapamycin (mTOR) is a central regulator of cell metabolism, proliferation, and survival. The mTOR signaling cascade is essential to maintain cellular homeostasis in normal biological processes or in response to stress, and its dysregulation is implicated in the progression of many disorders, including age-associated diseases. Accordingly, the pharmacological implications of mTOR inhibition using rapamycin or others rapalogs span the treatment of various human diseases from immune disorders to cancer. Importantly, rapamycin is one of the only known pan-species drugs that can extend lifespan. The molecular and cellular mechanisms explaining the phenotypic consequences of mTOR are vast and heavily studied. In this review, we will focus on the potential role of mTOR in the context of cellular senescence, a tumor suppressor mechanism and a pillar of aging. selleck products We will explore the link between senescence, autophagy and mTOR and discuss the opportunities to exploit senescence-associated mTOR functions to manipulate senescence phenotypes in age-associated diseases and cancer treatment.Senescence is a cellular state which can be viewed as a stress response phenotype implicated in various physiological and pathological processes, including cancer. Therefore, it is of fundamental importance to understand why and how a cell acquires and maintains a senescent phenotype. Direct evidence has pointed to the homeostasis of the endoplasmic reticulum whose control appears strikingly affected during senescence. The endoplasmic reticulum is one of the sensing organelles that transduce signals between different pathways in order to adapt a functional proteome upon intrinsic or extrinsic challenges. One of these signaling pathways is the Unfolded Protein Response (UPR), which has been shown to be activated during senescence. Its exact contribution to senescence onset, maintenance, and escape, however, is still poorly understood. In this article, we review the mechanisms through which the UPR contributes to the appearance and maintenance of characteristic senescent features. We also discuss whether the perturbation of the endoplasmic reticulum proteostasis or accumulation of misfolded proteins could be possible causes of senescence, and-as a consequence-to what extent the UPR components could be considered as therapeutic targets allowing for the elimination of senescent cells or altering their secretome to prevent neoplastic transformation.
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