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Acta Dermatovenerologica Alpina,... Jun 2008There are two main processes that induce skin aging: intrinsic and extrinsic. A stochastic process that implies random cell damage as a result of mutations during... (Review)
Review
There are two main processes that induce skin aging: intrinsic and extrinsic. A stochastic process that implies random cell damage as a result of mutations during metabolic processes due to the production of free radicals is also implicated. Extrinsic aging is caused by environmental factors such as sun exposure, air pollution, smoking, alcohol abuse, and poor nutrition. Intrinsic aging reflects the genetic background and depends on time. Various expressions of intrinsic aging include smooth, thinning skin with exaggerated expression lines. Extrinsically aged skin is characterized by photo damage as wrinkles, pigmented lesions, patchy hypopigmentations, and actinic keratoses. Timely protection including physical and chemical sunscreens, as well as avoiding exposure to intense UV irradiation, is most important. A network of antioxidants such as vitamins E and C, coenzyme Q10, alpha-lipoic acid, glutathione, and others can reduce signs of aging. Further anti-aging products are three generations of retinoids, among which the first generation is broadly accepted. A diet with lot of fruits and vegetables containing antioxidants is recommended as well as exercise two or three times a week.
Topics: Humans; Skin Aging
PubMed: 18709289
DOI: No ID Found -
Psychological Medicine Jul 2022Motivational processes underlie behaviors that enrich the human experience, and impairments in motivation are commonly observed in psychiatric illness. While motivated... (Review)
Review
Motivational processes underlie behaviors that enrich the human experience, and impairments in motivation are commonly observed in psychiatric illness. While motivated behavior is often examined with respect to extrinsic reinforcers, not all actions are driven by reactions to external stimuli; some are driven by 'intrinsic' motivation. Intrinsically motivated behaviors are computationally similar to extrinsically motivated behaviors, in that they strive to maximize reward value and minimize punishment. However, our understanding of the neurocognitive mechanisms that underlie intrinsically motivated behavior remains limited. Dysfunction in intrinsic motivation represents an important trans-diagnostic facet of psychiatric symptomology, but due to a lack of clear consensus, the contribution of intrinsic motivation to psychopathology remains poorly understood. This review aims to provide an overview of the conceptualization, measurement, and neurobiology of intrinsic motivation, providing a framework for understanding its potential contributions to psychopathology and its treatment. Distinctions between intrinsic and extrinsic motivation are discussed, including divergence in the types of associated rewards or outcomes that drive behavioral action and choice. A useful framework for understanding intrinsic motivation, and thus separating it from extrinsic motivation, is developed and suggestions for optimization of paradigms to measure intrinsic motivation are proposed.
Topics: Humans; Motivation; Reward; Punishment; Mental Disorders
PubMed: 35796023
DOI: 10.1017/S0033291722001611 -
Journal of Musculoskeletal & Neuronal... 2006Tendon disorders are frequent, and are responsible for much morbidity both in sport and the workplace. Although the presence of degenerative changes does not always lead... (Review)
Review
Tendon disorders are frequent, and are responsible for much morbidity both in sport and the workplace. Although the presence of degenerative changes does not always lead to symptoms, pre-existing degeneration has been implicated as a risk factor for acute tendon rupture. The term tendinopathy is a generic descriptor of the clinical conditions in and around tendons arising from overuse. The terms "tendinosis" and "tendinitis/tendonitis" should only be used after histopathological examination. Disordered healing is seen in tendinopathy, and inflammation is not typically seen. In acute injuries, the process of tendon healing is an indivisible process that can be categorized into three overlapping phases for descriptive purposes. Tendon healing can occur intrinsically, via proliferation of epitenon and endotenon tenocytes, or extrinsically, by invasion of cells from the surrounding sheath and synovium. Despite remodeling, the biochemical and mechanical properties of healed tendon tissue never match those of intact tendon. Tendon injuries account for considerable morbidity, and often prove disabling for several months, despite what is considered appropriate management. Chronic problems caused by overuse of tendons probably account for 30% of all running-related injuries, and the prevalence of elbow tendinopathy in tennis players can be as high as 40%. The basic cell biology of tendons is still not fully understood, and the management of tendon injury poses a considerable challenge for clinicians. This article describes the structure of tendons, and reviews the pathophysiology of tendon injury and healing.
Topics: Animals; Biomechanical Phenomena; Humans; Tendon Injuries; Tendons
PubMed: 16849830
DOI: No ID Found -
Molecular Cancer Mar 2022N-methyladenosine (mA) is the most abundant epigenetic modification of RNA, and its dysregulation drives aberrant transcription and translation programs that promote... (Review)
Review
N-methyladenosine (mA) is the most abundant epigenetic modification of RNA, and its dysregulation drives aberrant transcription and translation programs that promote cancer occurrence and progression. Although defective gene regulation resulting from mA often affects oncogenic and tumor-suppressing networks, mA can also modulate tumor immunogenicity and immune cells involved in anti-tumor responses. Understanding this counterintuitive concept can aid the design of new drugs that target mA to potentially improve the outcomes of cancer immunotherapies. Here, we provide an up-to-date and comprehensive overview of how mA modifications intrinsically affect immune cells and how alterations in tumor cell mA modifications extrinsically affect immune cell responses in the tumor microenvironment (TME). We also review strategies for modulating endogenous anti-tumor immunity and discuss the challenge of reshaping the TME. Strategies include: combining specific and efficient inhibitors against mA regulators with immune checkpoint blockers; generating an effective programmable mA gene-editing system that enables efficient manipulation of individual mA sites; establishing an effective mA modification system to enhance anti-tumor immune responses in T cells or natural killer cells; and using nanoparticles that specifically target tumor-associated macrophages (TAMs) to deliver messenger RNA or small interfering RNA of mA-related molecules that repolarize TAMs, enabling them to remodel the TME. The goal of this review is to help the field understand how mA modifications intrinsically and extrinsically shape immune responses in the TME so that better cancer immunotherapy can be designed and developed.
Topics: Adenosine; Humans; Immunotherapy; Neoplasms; RNA; Tumor Microenvironment
PubMed: 35296338
DOI: 10.1186/s12943-022-01558-0 -
Journal of Hematology & Oncology May 2023Dysregulation of the Notch signaling pathway, which is highly conserved across species, can drive aberrant epigenetic modification, transcription, and translation.... (Review)
Review
Dysregulation of the Notch signaling pathway, which is highly conserved across species, can drive aberrant epigenetic modification, transcription, and translation. Defective gene regulation caused by dysregulated Notch signaling often affects networks controlling oncogenesis and tumor progression. Meanwhile, Notch signaling can modulate immune cells involved in anti- or pro-tumor responses and tumor immunogenicity. A comprehensive understanding of these processes can help with designing new drugs that target Notch signaling, thereby enhancing the effects of cancer immunotherapy. Here, we provide an up-to-date and comprehensive overview of how Notch signaling intrinsically regulates immune cells and how alterations in Notch signaling in tumor cells or stromal cells extrinsically regulate immune responses in the tumor microenvironment (TME). We also discuss the potential role of Notch signaling in tumor immunity mediated by gut microbiota. Finally, we propose strategies for targeting Notch signaling in cancer immunotherapy. These include oncolytic virotherapy combined with inhibition of Notch signaling, nanoparticles (NPs) loaded with Notch signaling regulators to specifically target tumor-associated macrophages (TAMs) to repolarize their functions and remodel the TME, combining specific and efficient inhibitors or activators of Notch signaling with immune checkpoint blockers (ICBs) for synergistic anti-tumor therapy, and implementing a customized and effective synNotch circuit system to enhance safety of chimeric antigen receptor (CAR) immune cells. Collectively, this review aims to summarize how Notch signaling intrinsically and extrinsically shapes immune responses to improve immunotherapy.
Topics: Humans; Immunotherapy; Neoplasms; Antigens, Neoplasm; Nanoparticles; Signal Transduction; Tumor Microenvironment
PubMed: 37131214
DOI: 10.1186/s13045-023-01439-z -
Tuberkuloz Ve Toraks Mar 2023Hypersensitivity pneumonitis (HP) is an immunological lung disease that affects individuals who are sensitive and susceptible to occupational and environmental... (Review)
Review
Hypersensitivity pneumonitis (HP) is an immunological lung disease that affects individuals who are sensitive and susceptible to occupational and environmental exposures. While clinical and radiological findings may resemble other interstitial lung diseases, identifying the causative agents can aid in the differential diagnosis. However, this can be challenging and may result in delayed diagnosis and poor prognosis. A gold standard test for diagnosis is currently unavailable, and therefore, a multidisciplinary approach involving a clinician, radiologist, and pathologist is necessary. Avoiding exposure is the first step in treatment, with immunosuppressive therapeutics also being used. Antifibrotic agents show promise for future treatment approaches. Despite recent advancements in data and guidelines, knowledge about managing occupational HP remains limited. This review provides a summary of the epidemiological, clinical, and radiological findings, as well as diagnostic and treatment principles of occupational HP based on current literature.
Topics: Humans; Alveolitis, Extrinsic Allergic; Lung; Lung Diseases, Interstitial; Environmental Exposure; Pneumonia
PubMed: 36912413
DOI: 10.5578/tt.20239911 -
Radiologia Dec 2022The term inhalational lung disease comprises a group of entities that develop secondary to the active aspiration of particles. Most are occupational lung diseases....
The term inhalational lung disease comprises a group of entities that develop secondary to the active aspiration of particles. Most are occupational lung diseases. Inhalational lung diseases are classified as occupational diseases (pneumoconiosis, chemical pneumonitis), hypersensitivity pneumonitis, and electronic-cigarette-associated lung diseases. The radiologic findings often consist of nonspecific interstitial patterns that can be difficult to interpret. Therefore, radiologists' experience and multidisciplinary teamwork are key to ensure correct evaluation. The role of the radiologist is fundamental in preventive measures as well as in diagnosis and management, having an important impact on patients' overall health. It is crucial to take into account patients' possible exposure to particles both at work and at home.
Topics: Humans; Lung Diseases; Pneumoconiosis; Lung; Alveolitis, Extrinsic Allergic; Pneumonia
PubMed: 36737167
DOI: 10.1016/j.rxeng.2022.10.007 -
The Western Journal of Medicine Nov 1993Although the cause and development of most inflammatory and fibrotic interstitial lung diseases are unknown, both the antigenic stimuli and the immunopathogenic... (Review)
Review
Although the cause and development of most inflammatory and fibrotic interstitial lung diseases are unknown, both the antigenic stimuli and the immunopathogenic mechanisms that produce the syndrome of hypersensitivity pneumonitis have been well described. Hypersensitivity pneumonitis is a group of related inflammatory and fibrotic interstitial lung diseases that result from hypersensitivity immune reactions to the repeated inhalation of antigens derived from fungal, bacterial, animal protein, and reactive chemical sources. Immune complex-induced inflammatory reactions initiate acute lung injury; T cell-mediated hypersensitivity reactions perpetuate it and induce chronic inflammatory, granulomatous, and fibrotic responses in the interstitium of the lungs. Because the natural history of many interstitial lung diseases of unknown causes involves the progressive evolution through these same phases, knowledge about immune pathogenesis gained from studies of hypersensitivity pneumonitis may provide a way to understand the causes and development of other interstitial lung diseases.
Topics: Acute Disease; Alveolitis, Extrinsic Allergic; Antigens; Chronic Disease; Humans; Immunity, Cellular
PubMed: 8279154
DOI: No ID Found