Hasil untuk "Physiology"

S. Wolf, H. Boddeke, H. Kettenmann

T. Panciera, L. Azzolin, M. Cordenonsi et al.

Sang-Min Jeon

5′-adenosine monophosphate (AMP)-activated protein kinase (AMPK) is an evolutionarily conserved serine/threonine kinase that was originally identified as the key player in maintaining cellular energy homeostasis. Intensive research over the last decade has identified diverse molecular mechanisms and physiological conditions that regulate the AMPK activity. AMPK regulates diverse metabolic and physiological processes and is dysregulated in major chronic diseases, such as obesity, inflammation, diabetes and cancer. On the basis of its critical roles in physiology and pathology, AMPK is emerging as one of the most promising targets for both the prevention and treatment of these diseases. In this review, we discuss the current understanding of the molecular and physiological regulation of AMPK and its metabolic and physiological functions. In addition, we discuss the mechanisms underlying the versatile roles of AMPK in diabetes and cancer. Therapies based on an enzyme involved in cellular energy balance may help prevent and treat cancer, obesity and diabetes. Sang-Min Jeon at Ajou University in Suwon, South Korea, reviewed current understanding of the enzyme ‘5’-AMP-activated protein kinase' (AMPK), and its potential to treat chronic diseases. Among other tasks, AMPK maintains energy balance in cells by regulating glucose levels and oxidizing fatty acids. Research indicates that AMPK levels are suppressed by over-eating, triggering insulin resistance and hence diabetes. Reducing AMPK levels can also induce chronic inflammation, a critical component of diseases like diabetes and cancer. Jeon's review finds evidence that activating AMPK in patients could prevent the progression of obesity and diabetes. A similar technique may help prevent and fight early-stage of carcinogenesis. However, Jeon warns that AMPK can exacerbate later-stage of carcinogenesis and established cancer tumors.

Yi-peng Wang, E. Mandelkow

J. Hall

E. Barka, P. Vatsa, L. Sanchez et al.

Satchidananda Panda

Maria Almeida, M. Laurent, V. Dubois et al.

S. Mathôt

Pupils respond to three distinct kinds of stimuli: they constrict in response to brightness (the pupil light response), constrict in response to near fixation (the pupil near response), and dilate in response to increases in arousal and mental effort, either triggered by an external stimulus or spontaneously. In this review, I describe these three pupil responses, how they are related to high-level cognition, and the neural pathways that control them. I also discuss the functional relevance of pupil responses, that is, how pupil responses help us to better see the world. Although pupil responses likely serve many functions, not all of which are fully understood, one important function is to optimize vision either for acuity (small pupils see sharper) and depth of field (small pupils see sharply at a wider range of distances), or for sensitivity (large pupils are better able to detect faint stimuli); that is, pupils change their size to optimize vision for a particular situation. In many ways, pupil responses are similar to other eye movements, such as saccades and smooth pursuit: like these other eye movements, pupil responses have properties of both reflexive and voluntary action, and are part of active visual exploration.

J. Lundberg, E. Weitzberg, M. Gladwin

Johanna Andrae, R. Gallini, C. Betsholtz

Platelet-derived growth factors (PDGFs) and their receptors (PDGFRs) have served as prototypes for growth factor and receptor tyrosine kinase function for more than 25 years. Studies of PDGFs and PDGFRs in animal development have revealed roles for PDGFR-alpha signaling in gastrulation and in the development of the cranial and cardiac neural crest, gonads, lung, intestine, skin, CNS, and skeleton. Similarly, roles for PDGFR-beta signaling have been established in blood vessel formation and early hematopoiesis. PDGF signaling is implicated in a range of diseases. Autocrine activation of PDGF signaling pathways is involved in certain gliomas, sarcomas, and leukemias. Paracrine PDGF signaling is commonly observed in epithelial cancers, where it triggers stromal recruitment and may be involved in epithelial-mesenchymal transition, thereby affecting tumor growth, angiogenesis, invasion, and metastasis. PDGFs drive pathological mesenchymal responses in vascular disorders such as atherosclerosis, restenosis, pulmonary hypertension, and retinal diseases, as well as in fibrotic diseases, including pulmonary fibrosis, liver cirrhosis, scleroderma, glomerulosclerosis, and cardiac fibrosis. We review basic aspects of the PDGF ligands and receptors, their developmental and pathological functions, principles of their pharmacological inhibition, and results using PDGF pathway-inhibitory or stimulatory drugs in preclinical and clinical contexts.

B. Clarke

H. Pörtner, A. Farrell

J. Schimel, T. Balser, M. Wallenstein

P. S. Nobel

This is the fourth edition of an established and successful reference for plant scientists. The author has taken into consideration extensive reviews performed by colleagues and students who have touted this book as the ultimate reference for research and learning. The original structure and philosophy of the book continue in this new edition, providing a genuine synthesis of modern physicochemical and physiological thinking, while entirely updating the detailed content. Key concepts in plant physiology are developed with the use of chemistry, physics, and mathematics fundamentals. The figures and illustrations have been improved and the list of references has been expanded to reflect the author's continuing commitment to providing the most valuable learning tool in the field. This revision will ensure the reputation of Park Nobel's work as a leader in the field.It includes more than 40 per cent new coverage. It incorporates student-recommended changes from the previous edition. It also includes: five brand new equations and four new tables, with updates to 24 equations and six tables; and, 30 new figures added with more than three-quarters of figures and legends improved . It is organized so that a student has easy access to locate any biophysical phenomenon in which he or she is interested. It features: per-chapter key equation tables; problems with solutions presented in the back of the book; appendices with conversion factors, constants/coefficients, abbreviations and symbols.

B. Vallée, K. Falchuk

S. Alfonso, M. Gesto, B. Sadoul

The capacity of fishes to cope with environmental variation is considered to be a main determinant of their fitness and is partly determined by their stress physiology. By 2100, global ocean temperature is expected to rise by 1-4°C, with potential consequences for stress physiology. Global warming is affecting animal populations worldwide, through chronic temperature increases and an increase in the frequency of extreme heatwave events. As ectotherms, fishes are expected to be particularly vulnerable to global warming. Although little information is available about the effects of global warming on stress physiology in nature, multiple studies describe the consequences of temperature increases on stress physiology in controlled laboratory conditions, providing insight into what can be expected in the wild. Chronic temperature increase constitutes a physiological load than can alter the ability of fishes to cope with additional stressors, which might compromise their fitness. Besides, rapid temperature increases are known to induce acute stress responses in fishes and might be of ecological relevance in particular situations. This review summarizes knowledge about effects of temperature increases on the stress physiology of fishes, and discusses these in a context of global warming. This article is protected by copyright. All rights reserved.

J., Bussemaker, M. J.H.G. et al.

H. Critchley, J. Maybin, Gregory M. Armstrong et al.

The physiological functions of the uterine endometrium (uterine lining) are preparation for implantation, maintenance of pregnancy if implantation occurs, and menstruation in the absence of pregnancy. The endometrium thus plays a pivotal role in reproduction and continuation of our species. Menstruation is a steroid regulated event and there are alternatives for a progesterone-primed endometrium, i.e. pregnancy or menstruation. Progesterone withdrawal is the trigger for menstruation. The menstruating endometrium is a physiological example of an injured or "wounded" surface that is required to rapidly repair each month. The physiological events of menstruation and endometrial repair provide an accessible in vivo human model of inflammation and tissue repair. Progress in our understanding of endometrial patho-physiology has been facilitated by modern cellular and molecular discovery tools, along with animal models of simulated menses. Abnormal uterine bleeding (AUB), including heavy menstrual bleeding (HMB) imposes a massive burden on society, affecting one in four women of reproductive age. Understanding structural and non-structural causes underpinning AUB is essential to optimise and provide precision in patient management. This is facilitated by careful classification of causes of bleeding. We highlight the crucial need for understanding mechanisms underpinning menstruation and its aberrations. The endometrium is a prime target tissue for selective progesterone receptor modulators (SPRMs). This class of compounds has therapeutic potential for the clinical unmet need of HMB. SPRMs reduce menstrual bleeding by mechanisms still largely unknown. Human menstruation remains a taboo topic and many questions concerning endometrial physiology that pertain to menstrual bleeding are yet to be answered.

Dakota R. Kamm, K. McCommis

Hepatic stellate cells (HSCs) comprise a minor cell population in the liver but serve numerous critical functions in the normal liver and in response to injury. HSCs are primarily known for their activation upon liver injury and for producing the collagen‐rich extracellular matrix in liver fibrosis. In the absence of liver injury, HSCs reside in a quiescent state, in which their main function appears to be the storage of retinoids or vitamin A‐containing metabolites. Less appreciated functions of HSCs include amplifying the hepatic inflammatory response and expressing growth factors that are critical for liver development and both the initiation and termination of liver regeneration. Recent single‐cell RNA sequencing studies have corroborated earlier studies indictaing that HSC activation involves a diverse array of phenotypic alterations and identified unique HSC populations. This review serves to highlight these many functions of HSCs, and to briefly describe the recent genetic tools that will help to thoroughly investigate the role of HSCs in hepatic physiology and pathology.