Pleiotropic Action of TGF-Beta in Physiological and Pathological Liver Conditions.

The aim of this study is to review and analyze the pleiotropic effects of TGF-β in physiological and pathological conditions of the liver, with particular emphasis on its role in immune suppression, wound healing, regulation of cell growth and differentiation, and liver cell apoptosis. A literature review was conducted, including 52 studies, comprising review articles, in vitro and in vivo studies, and meta-analyses. Only studies published in peer-reviewed scientific journals were included in the analysis.

Autoimmune Encephalitis with Antibodies: Anti-NMDAR, Anti-AMPAR, Anti-GQ1b, Anti-DPPX, Anti-CASPR2, Anti-LGI1, Anti-RI, Anti-Yo, Anti-Hu, Anti-CV2 and Anti-GABAAR, in the Course of Psychoses, Neoplastic Diseases, and Paraneoplastic Syndromes.

Encephalitis is a condition with a variety of etiologies, clinical presentations, and degrees of severity. The causes of these disorders include both neuroinfections and autoimmune diseases in which host antibodies are pathologically directed against self-antigens. In autoimmune encephalitis, autoantibodies are expressed in the central nervous system.

The index of the Prognosis Rural Landscape Preferences (IPRLP) as a tool of generalizing peoples' preferences on rural landscape.

Social preferences of visual landscape quality are commonly analysed based on diverse techniques, among which the assessment of landscape photographs are the most often applied. Such evaluation is affected by the presence, configuration, colour, texture, etc. of different landscape attributes combined with respondent characteristics such as level of education, gender, age and environmental attitudes.

Blockade of nitric oxide formation in the rat brain does not disturb development of endotoxin tolerance.

The involvement of nitric oxide (NO) in tolerance development to endotoxin has been proposed because peripherally administered NG-nitro-L-arginine methyl ester (L-NAME) (NO synthases inhibitor) delays the endotoxin tolerance formation. Since L-NAME is capable of crossing the blood-brain barrier, the question arises of where activity of NO synthases (inside or outside the blood-brain barrier) is crucial for development of endotoxin tolerance. To clarify the role of different NO synthases (NOS) isoforms, acting in the brain, on the tolerance development, effects of highly selective iNOS and nNOS inhibitors on stepwise attenuation of febrile response during tolerance formation were examined in freely moving biotelemetered rats.

Intracerebroventricular injection of neuronal and inducible nitric oxide synthase inhibitors does not influence febrile response in rats during turpentine abscess.

The purpose of this study was to investigate the role of neuronal nitric oxide synthase (nNOS) and inducible NOS (iNOS) in the brain during development of fever in response to localized tissue inflammation caused by injection of turpentine in freely moving biotelemetered rats. To determine the role of both NOSs in turpentineinduced fever, we injected vinyl-L-NIO (N(5) - (1-Imino-3-butenyl) - ornithine (vLNIO), a selective nNOS inhibitor, and aminoguanidine hydrochloride, a selective iNOS inhibitor, intracerebroventricularly (i.c.

Intracerebroventricular injection of neuronal and inducible nitric oxide synthase inhibitors attenuates fever due to LPS in rats.

Nitric oxide (NO) has been shown to be an important mediator of febrile response to lipopolisaccharide (LPS). To clarify the role of different isoforms of NO synthase (NOS) in febrile response to immune challenge, effects of selective iNOS and nNOS inhibitors on fever to LPS were examined in freely moving biotelemetered rats. Vinyl-L-NIO (N(5) - (1-Imino-3-butenyl) - ornithine (vL-NIO), a neuronal nitric oxide synthase (nNOS) inhibitor, and aminoguanidine hydrochloride, an inducible nitric oxide synthase (iNOS) inhibitor, were injected intracerebroventricularly at a dose of 10 microg/rat just before intraperitoneal injection of LPS at a dose of 50 microg/kg.

Molecular mechanism of emotional fever--the role of nitric oxide.

The purpose of these studies was to assess the involvement of nNOS and iNOS inhibitors on stress fever caused by exposure to an open field in freely moving biotelemetered rats. Vinyl-L-NIO (N(5) - (1-Imino-3-butenyl) - ornithine, a neural nitric oxide synthase (nNOS) inhibitor, and aminoguanidine, an inducible nitric oxide synthase (iNOS) inhibitor, were injected into the lateral ventricle (icv) at a dose of 5 microg and 10 microg, respectively, and then immediately exposed to open field for 30 min. After exposure to the open field, rats not treated with NOS inhibitors responded with a rapid rise in T(b) and it was accompanied with an increase of motor activity.

["Sickness behavior"--mechanisms of origin and significance].

Psychoneuroimmunology, a combination of immunology and neurobiology, is a new field that has emerged over the past 20 years. There is now overwhelming evidence suggesting that the central nervous system is capable of regulating the immune response via two pathways--the autonomic and the neuroendocrine. It is also well documented that the immune system can influence the central nervous system by regulatory molecules or cytokines produced by activated immune cells.

[The pathogenesis and the adaptive value of fever].

Fever is a part of the acute phase response to infection and inflammation. We now understand that fever is a complex physiological response that is aimed at facilitating survival of the host. The fever is induced by endogenous inflammatory mediators, such as prostaglandins and pyrogenic cytokines, that are released by immune cells activated by exogenous pyrogens.

Inhibition of nitric oxide synthase delays the development of tolerance to LPS in rats.

The role of nitric oxide (NO) was investigated in endotoxin (lipopolysaccharide, LPS) tolerance in freely moving biotelemetered rats. We monitored changes in febrile response and feeding behavior (food intake, water intake) during the development of tolerance to repeated intraperitoneal injections of LPS (50 microg/kg) along with injections of N(omega)-nitro-L-arginine methyl ester (L-NAME; 50 mg/kg), an inhibitor of NO synthase. Rats were treated with LPS and L-NAME for three consecutive days.

Blockade of nitric oxide formation enhances thermal and behavioral responses in rats during turpentine abscess.

Objective: The purpose of this study was to investigate the role of nitric oxide (NO) during the development of fever and other symptoms of sickness behavior (i.e. anorexia, cachexia) in response to localized tissue inflammation caused by injection of turpentine in freely moving biotelemetered rats.

The inhibition of nitric oxide synthase suppresses LPS- and psychological-stress-induced fever in rats.

The purpose of this study was to assess the effects of a non-selective nitric oxide synthase (NOS) inhibitor on changes in fever response due to injection of lipopolysaccharide (LPS) or on stress fever caused by exposure to an open field in freely moving biotelemetered rats. N(omega)-nitro-L-arginine methyl ester (L-NAME), an inhibitor of all NOS-isoforms, was injected intraperitoneally (ip) at a dose of 50 mg/kg just before intraperitoneal injection of LPS at a dose of 50 microg/kg or exposure to open field. L-NAME at a dose of 50 mg/kg had no effect on normal day-time body temperature (T(b)) and normal night-time T(b).

[Mechanisms for development of tolerance to repeated injections of exogenous pyrogens].

Pyrogenic tolerance has been recognized for many years in a variety of species although the mechanisms that are responsible for its development are not well understood. The development of pyrogenic tolerance is associated with the stepwise diminution of pathophysiological and behavioral responses induced by exogenous pyrogens, such as fever, reduction in food and water intake. Several studies either in vivo or ex vivo have indicated the role of various proinflammatory cytokines in the development of pyrogenic tolerance.

[[Stressful increase in body temperature--hyperthermia or fever].

Psychological factors are recognized to influence immune responses and susceptibility to various disease processes. Exposure to psychological stress produces rise in body temperature in animals and human beings. Ther are considerable evidence that support the hypothesis that stress "hyperthermia" is actually a fever (i.

Beta-adrenergic receptor subtype effects on stress fever and thermoregulation.

Exposure to psychological stress increases body temperature (Tb). This stress fever may be immunologically beneficial in some patient populations but detrimental in others (e.g.

Role of fever in disease.

Infection, trauma, and injury result in a stereotypical response that includes loss of food appetite, increased sleepiness, muscle aches, and fever. For thousands of years fever was considered a protective response, and fevers were induced by physicians to combat certain infections. But with the advent of antipyretic drugs, physicians started to reduce fevers, and fever therapy was virtually abandoned.

IL-6 and IL-1 beta in fever. Studies using cytokine-deficient (knockout) mice.

Previous data support the hypothesis that during inflammation, interleukin (IL)-1 beta and IL-6 are involved in fever, in activation of the hypothalamic-pituitary-adrenal (HPA) axis, and in the induction of eicosanoids. Most of the pathophysiologic effects of IL-1 beta and Il-6 are mediated by prostaglandins (PGs), modulated by other cytokines, and antagonized by glucocorticoids (GC), a final product of the HPA axis. To further test these relationships, we measured changes in body temperature using biotelemetry in mice deficient in genes for IL-1 beta and/or IL-6 (IL-1 beta knockout [KO] and IL-6 KO) following injection with lipopolysaccharide (LPS) to induce systemic inflammation or turpentine to induce local abscess.

Effect of nicotine on the immune system: possible regulation of immune responses by central and peripheral mechanisms.

Nicotine (NT) treatment impairs T-cell receptor (TCR)-mediated signaling, leading to the arrest of T cells in the G1 phase of the cell cycle and inhibition of the antibody plaque-forming cell (AFC) response to sheep red blood cells (SRBC). This paper summarizes some of the previous findings related to cigarette smoke/NT and the immune response, and presents preliminary evidence suggesting that mice chronically treated with NT (0.5 mg/day/kg body weight) have a depressed inflammatory response in the turpentine-induced abscess model of inflammation.

Endotoxin tolerance does not alter open field-induced fever in rats.

Exposure to an open field has been shown to cause a rise in the body temperature of rats. In many respects, this rise in body temperature is similar to fevers caused by endotoxin and other inflammatory stimuli. Rats repeatedly injected with endotoxin develop tolerance to the fever-inducing action of endotoxin.

Effect of heat stress on LPS-induced fever and tumor necrosis factor.

Exposure to heat stress leads to both short-term and long-term effects on morbidity. Male rats were exposed to a high ambient temperature of 40 degrees C, which resulted in biotelemetered core body temperature rising to approximately 42 degrees C. This treatment led to a marked enhancement in lipopolysaccharide (LPS)-induced fever at 24 h after exposure to heat stress.

Dietary n-3 fatty acids differentially affect sickness behavior in mice during local and systemic inflammation.

We tested the hypothesis that increased dietary fish oil levels (via modulation of the production of inflammatory mediators) modulate sickness symptoms (i.e., anorexia, cachexia, fever, lethargy) of systemic and local inflammation.

Sickness behavior in mice deficient in interleukin-6 during turpentine abscess and influenza pneumonitis.

Interleukin-6 (IL-6), among other cytokines, is thought to be involved in the regulation of sickness behavior (e.g., anorexia, cachexia, fever, and lethargy) induced by infections bacterial and viral origin) and sterile tissue necrosis (burns and surgical traumas).