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The beneficial and well-being effects of human sexual arousal induced by coitus or masturbation are reviewed. Greater sexual satisfaction and some health rewards are given by coitally obtained orgasms even though those from masturbation may be more physiologically intense. The functionality of the circulatory, neural and muscular systems of the male and female genitalia are maintained by arousal and orgasm (maintenance functions) both in the conscious state and when asleep. Prophylactic actions (preventative functions) occur in relation to prostate cancer, implantation and dysmenorrhoea. In the male, ejaculations keep sperm morphology and semen volume within normal ranges while leukocyte numbers are increased. In the female, with coital vaginal deposition of semen mood enhancement occurs, menstrual cycles are more often of the ovulatory (fertile) type and postmenopausal vaginal atrophy is counteracted. [ABSTRACT FROM AUTHOR]

A fundamental issue in T cell development is what controls whether a thymocyte differentiates into a γδ T cell or an αβ T cell, each defined by their distinct T cell receptor. Most likely, lessons learned in studying that issue will also provide insight into how the thymus produces T cell subsets with distinct functional and regulatory potentials. Here we review recent experiments, focusing on three factors that regulate thymocyte differentiation up to and including the expression of the first products of antigen receptor gene rearrangements. Those factors are the archetypal developmental regulator Notch, intrinsic signals emanating from antigen-receptor complexes, and trans conditioning, which reflects communication between different subsets of thymocytes. We also review new findings on the positive selection of γδ T cells and on extrathymic T cell development. [ABSTRACT FROM AUTHOR]

Recent studies examining the neuroendocrine response pattern underlying the human sexual response cycle revealed transient activation of the sympathoadrenal system and a substantial, long-lasting increase in plasma prolactin concentrations following orgasm in men and women. Prolactin has been discussed as being part of a feedback mechanism that signals centers in the central nervous system, such as the dopaminergic system controlling sexual arousal. To further elucidate the central role of neuropeptides, biogenic monoamines and neurotransmitters in human sexual behavior, a serial cerebrospinal fluid (CSF)-sampling technique was implemented using a previously established experimental paradigm for sexual activity in a laboratory setting. In parallel with peripheral endocrine measures, lumbar CSF was drawn via an indwelling spinal catheter during the sexual response cycle in 10 healthy males and 10 age-matched controls, and analysed for prolactin, oxytocin, biogenic monoamines and/or their metabolites as well as inhibitory and excitatory neurotransmitter concentrations. Parallel to raised peripheral sympathetic activity, norepinephrine also increased in CSF during audiovisual, masturbation-induced sexual arousal and orgasm, and remained elevated for the remainder of the session ( F4,72 = 8.79, P = 0.000). In contrast, none of the other measures, in particular prolactin and dopamine or its metabolites, reflected significant alteration. In conclusion, the human sexual response cycle is characterized by an increase in sympathetic activity in plasma and CSF, and by pronounced secretion of plasma prolactin after orgasm. However, alterations in dopaminergic or peptidergic activity are not found in lumbar CSF, possibly due to local and restricted release in diencephalic and mesencephalic brain regions. [ABSTRACT FROM AUTHOR]

There is a severe lack of knowledge regarding the brain regions involved in human sexual performance in general, and female orgasm in particular. We used [15O]-H2O positron emission tomography to measure regional cerebral blood flow (rCBF) in 12 healthy women during a nonsexual resting state, clitorally induced orgasm, sexual clitoral stimulation (sexual arousal control) and imitation of orgasm (motor output control). Extracerebral markers of sexual performance and orgasm were rectal pressure variability (RPstd) and perceived level of sexual arousal (PSA). Sexual stimulation of the clitoris (compared to rest) significantly increased rCBF in the left secondary and right dorsal primary somatosensory cortex, providing the first account of neocortical processing of sexual clitoral information. In contrast, orgasm was mainly associated with profound rCBF decreases in the neocortex when compared with the control conditions (clitoral stimulation and imitation of orgasm), particularly in the left lateral orbitofrontal cortex, inferior temporal gyrus and anterior temporal pole. Significant positive correlations were found between RPstd and rCBF in the left deep cerebellar nuclei, and between PSA and rCBF in the ventral midbrain and right caudate nucleus. We propose that decreased blood flow in the left lateral orbitofrontal cortex signifies behavioural disinhibition during orgasm in women, and that deactivation of the temporal lobe is directly related to high sexual arousal. In addition, the deep cerebellar nuclei may be involved in orgasm-specific muscle contractions while the involvement of the ventral midbrain and right caudate nucleus suggests a role for dopamine in female sexual arousal and orgasm. [ABSTRACT FROM AUTHOR]

Stress can alter immunological, neurochemical and endocrinological functions, but its role in cancer progression is not well understood. Here, we show that chronic behavioral stress results in higher levels of tissue catecholamines, greater tumor burden and more invasive growth of ovarian carcinoma cells in an orthotopic mouse model. These effects are mediated primarily through activation of the tumor cell cyclic AMP (cAMP)–protein kinase A (PKA) signaling pathway by the β2 adrenergic receptor (encoded by ADRB2). Tumors in stressed animals showed markedly increased vascularization and enhanced expression of VEGF, MMP2 and MMP9, and we found that angiogenic processes mediated the effects of stress on tumor growth in vivo. These data identify β-adrenergic activation of the cAMP–PKA signaling pathway as a major mechanism by which behavioral stress can enhance tumor angiogenesis in vivo and thereby promote malignant cell growth. These data also suggest that blocking ADRB-mediated angiogenesis could have therapeutic implications for the management of ovarian cancer. [ABSTRACT FROM AUTHOR]

On the basis of literature that suggests that child sexual abuse (CSA) survivors with post traumatic stress disorder (PTSD) have higher baseline sympathetic nervous system (SNS) activity than healthy controls and research that suggests that the SNS plays a critical role in female physiological sexual arousal, we examined the impact of SNS activation through intense exercise on sexual arousal in women with CSA and PTSD. We measured physiological and subjective sexual arousal in women with CSA ( n = 8), women with CSA and PTSD ( n = 10), and healthy controls ( n = 10) during exposure to nonerotic and erotic videos. After exercise, women with CSA and women with CSA and PTSD showed no significant differences in the physiological sexual response compared with no exercise, which was different from the increased physiological sexual response after exercise observed in control women. [ABSTRACT FROM AUTHOR]

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This study was designed to assess potential differences between sexually functional and dysfunctional women in dopamine (DA) and norepinephrine (NE) responses to erotic stimuli. Blood levels of homovanillic acid (HVA; the major metabolite of DA) and NE were taken during the showing of a nonsexual and a sexual film from 9 women with female sexual arousal disorder and hypoactive sexual desire disorder and from 13 sexually functional women. We assessed sexual arousal subjectively using a self-report scale and physiologically using a vaginal photoplethysmograph. HVA levels significantly decreased in sexually functional and dysfunctional women during the erotic versus during the neutral film. NE levels were not significantly different for either group of women during the neutral and erotic films. Sexually dysfunctional women had significantly higher levels of NE during both the neutral and erotic films compared with functional women. Subjective or physiological arousal differences between neutral and erotic films were not significantly different between functional and dysfunctional women. [ABSTRACT FROM AUTHOR]

This paper addresses the links between subjective experiences and physiological responses during sexual activity, by exploring the neurobiology of the feelings and emotions that are associated with peripheral bodily changes. Although women and men differ in the brain structures and chemical pathways that govern sexuality, human sexual behaviour is part of interpersonal relationships and is cognitively mediated. Nevertheless comparisons can be made with other mammals whose subcortical systems are similar. Research into the neurophysiology of attachment, love and sexual bonding in rodents is reviewed, indicating that the neuropeptides oxytocin and vasopressin, which are secreted from the pituitary gland, have a vital role in partner preference and copulation. Laboratory investigations into hormonal release during human sexual activity show that oxytocin is necessary for subjective pleasure during arousal and orgasm in both sexes, while vasopressin is released only during male arousal. Vasopressin is suggested to have the opposite effect on female sexuality, and to impair women's interest in sexual contact. As oxytocin and vasopressin are regulated by oestrogen and testosterone respectively, and are sensitive to developmental hormonal experiences, they could provide a link between biology and culture. It is also postulated that neuropeptide secretion in the human brain could account for some of the observed gender differences, such as the impact of puberty; aggressive and protective feelings; and consistency of sexual interest in committed relationships. Psychological approaches for relationships where negative emotional states inhibit responding, are considered more appropriate than pharmacological interventions at this stage, in view of the uniquely human need to regulate relationships and sex through awareness of mood states and feelings. [ABSTRACT FROM AUTHOR]

Focuses on link between the secretion of the pituitary hormone prolactin and discontinuation of sexual arousal in humans. Refractory period in erection and ejaculation; Secretion of hormones oxytocin and prolactin during orgasm; Role of prolactin in the regulation of peripheral and central mechanisms of sexual respite.

Summary 1 Increasing evidence indicates the occurrence of functional interconnections between immune and nervous systems, although data available on the mechanisms of this bi-directional cross-talking are frequently incomplete and not always focussed on their relevance for neuroimmune modulation. 2 Primary (bone marrow and thymus) and secondary (spleen and lymph nodes) lymphoid organs are supplied with an autonomic (mainly sympathetic) efferent innervation and with an afferent sensory innervation. Anatomical studies have revealed origin, pattern of distribution and targets of nerve fibre populations supplying lymphoid organs. 3 Classic (catecholamines and acetylcholine) and peptide transmitters of neural and non-neural origin are released in the lymphoid microenvironment and contribute to neuroimmune modulation. Neuropeptide Y, substance P, calcitonin gene-related peptide, and vasoactive intestinal peptide represent the neuropeptides most involved in neuroimmune modulation. 4 Immune cells and immune organs express specific receptors for (neuro)transmitters. These receptors have been shown to respond in vivo and/or in vitro to the neural substances and their manipulation can alter immune responses. Changes in immune function can also influence the distribution of nerves and the expression of neural receptors in lymphoid organs. 5 Data on different populations of nerve fibres supplying immune organs and their role in providing a link between nervous and immune systems are reviewed. Anatomical connections between nervous and immune systems represent the structural support of the complex network of immune responses. A detailed knowledge of interactions between nervous and immune systems may represent an important basis for the development of strategies for treating pathologies in which altered neuroimmune cross-talking may be involved. [ABSTRACT FROM AUTHOR]

Fibrosis is a pathophysiological process of wound repair that leads to the deposit of connective tissue in the extracellular matrix. This complication is mainly associated with different pathologies affecting several organs such as lung, liver, heart, kidney, and intestine. In this fibrotic process, macrophages play an important role since they can modulate fibrosis due to their high plasticity, being able to adopt different phenotypes depending on the microenvironment in which they are found. In this review, we will try to discuss whether the macrophage phenotype exerts a pivotal role in the fibrosis development in the most important fibrotic scenarios. [ABSTRACT FROM AUTHOR]

Presents the author index for volume 31, supplement 1, 1999 of the journal "European Surgical Research".

I Introduction II Pharmacological modulation of food intake and forestomach motility II 1. Orexigenic agents 1.1 glutamate 1.2 benzodiazepines 1.3 opioid receptor agonists and antagonists 4 neuropepetides Y (NPY) II 2. Anorectic agents 2.1 cholecystokinin (CCK) agonists and antagonists 2.2 serotonin receptor agonists and antagonists 2.3 dopamine receptor agonists and antagonists 2.4 alpha-2 adrenoceptor agonists and antagonists III Anorexia and ruminal stasis during the Acute Phase Response to infections 1. cytokines 2. prostaglandins 3. hormones 4. nitric oxide IV Conclusions V References. [ABSTRACT FROM AUTHOR]

Cardiorenal syndrome is a term that defines the complex bidirectional nature of the interaction between cardiac and renal disease. It is well established that patients with kidney disease have higher incidence of cardiovascular comorbidities and that renal dysfunction is a significant threat to the prognosis of patients with cardiac disease. Fibrosis is a common characteristic of organ injury progression that has been proposed not only as a marker but also as an important driver of the pathophysiology of cardiorenal syndromes. Due to the relevance of fibrosis, its study might give insight into the mechanisms and targets that could potentially be modulated to prevent fibrosis development. The aim of this review was to summarize some of the pathophysiological pathways involved in the fibrotic damage seen in cardiorenal syndromes, such as inflammation, oxidative stress and endoplasmic reticulum stress, which are known to be triggers and mediators of fibrosis. [ABSTRACT FROM AUTHOR]

Body implants and implantable medical devices have dramatically improved and prolonged the life of countless patients. However, our body repair mechanisms have evolved to isolate, reject, or destroy any object that is recognized as foreign to the organism and inevitably mounts a foreign body reaction (FBR). Depending on its severity and chronicity, the FBR can impair implant performance or create severe clinical complications that will require surgical removal and/or replacement of the faulty device. The number of review articles discussing the FBR seems to be proportional to the number of different implant materials and clinical applications and one wonders, what else is there to tell? We will here take the position of a fibrosis researcher (which, coincidentally, we are) to elaborate similarities and differences between the FBR, normal wound healing, and chronic healing conditions that result in the development of peri-implant fibrosis. After giving credit to macrophages in the inflammatory phase of the FBR, we will mainly focus on the activation of fibroblastic cells into matrix-producing and highly contractile myofibroblasts. While fibrosis has been discussed to be a consequence of the disturbed and chronic inflammatory milieu in the FBR, direct activation of myofibroblasts at the implant surface is less commonly considered. Thus, we will provide a perspective how physical properties of the implant surface control myofibroblast actions and accumulation of stiff scar tissue. Because formation of scar tissue at the surface and around implant materials is a major reason for device failure and extraction surgeries, providing implant surfaces with myofibroblast-suppressing features is a first step to enhance implant acceptance and functional lifetime. Alternative therapeutic targets are elements of the myofibroblast mechanotransduction and contractile machinery and we will end with a brief overview on such targets that are considered for the treatment of other organ fibroses. [ABSTRACT FROM AUTHOR]

Stress belongs to the most frequent negative feelings people are confronted with in daily life. Strategies against acute stress include, e.g., relaxation techniques or medications, but it is also known that placebos can successfully reduce negative emotional stress. While it is widely held that placebos require deception to provoke a response, recent studies demonstrate intriguing evidence that placebos may work even without concealment (e.g., against anxiety or pain). Most of these studies are based on self-report questionnaires and do not include physiological measures. Here we report results of a study examining whether placebos without deception reduce acute stress. A total of 53 healthy individuals received either placebos without deception or no pills before participating in a laboratory stress test (Maastricht Acute Stress Test, MAST). We recorded self-report stress measures and cortisol responses before and after the MAST. Results showed no significant differences between the placebo and the control group, but when comparing participants with high relative to low beliefs in the power of placebos we found significant lower anxiety and cortisol responses for the placebo believers. These results show that non-deceptive placebos may successfully reduce acute anxiety and stress, but only in participants who had a strong belief in placebos. We discuss the results by suggesting that open-label placebos might be a possible treatment to reduce stress at least for some individuals. [ABSTRACT FROM AUTHOR]

Heart disease is the number one mortality disease in the world. In particular, cardiac fibrosis is considered as a major factor causing myocardial infarction and heart failure. In particular, oxidative stress is a major cause of heart fibrosis. In order to control such oxidative stress, the importance of nuclear factor erythropoietin 2 related factor 2 (NRF2) has recently been highlighted. In this review, we will discuss the activation of NRF2 by docosahexanoic acid (DHA), eicosapentaenoic acid (EPA), and the specialized pro-resolving lipid mediators (SPMs) derived from polyunsaturated lipids, including DHA and EPA. Additionally, we will discuss their effects on cardiac fibrosis via NRF2 activation. [ABSTRACT FROM AUTHOR]

Sarcoidosis is a systemic inflammatory disease characterized by development of granulomas in the affected organs. Sarcoidosis is often a diagnosis of exclusion, and traditionally used tests for sarcoidosis demonstrate low sensitivity and specificity. We propose that accuracy of diagnosis can be improved if biomarkers of altered lymphocyte populations and levels of signaling molecules involved in disease pathogenesis are measured for patterns suggestive of sarcoidosis. These distinctive biomarkers can also be used to determine disease progression, predict prognosis, and make treatment decisions. Many subsets of T lymphocytes, including CD8+ T-cells and regulatory T-cells, have been shown to be dysfunctional in sarcoidosis, and the predominant CD4+ T helper cell subset in granulomas appears to be a strong indicator of disease phenotype and outcome. Studies of altered B cell populations, B cell signaling molecules, and immune complexes in sarcoidosis patients reveal promising biomarkers as well as possible explanations of disease etiology. Furthermore, examined biomarkers raise questions about new treatment methods and sarcoidosis antigens. [ABSTRACT FROM AUTHOR]

Despite relevant advances made in therapies for cardiovascular diseases (CVDs), they still represent the first cause of death worldwide. Cardiac fibrosis and excessive extracellular matrix (ECM) remodeling are common end-organ features in diseased hearts, leading to tissue stiffness, impaired myocardial functional, and progression to heart failure. Although fibrosis has been largely recognized to accompany and complicate various CVDs, events and mechanisms driving and governing fibrosis are still not entirely elucidated, and clinical interventions targeting cardiac fibrosis are not yet available. Immune cell types, both from innate and adaptive immunity, are involved not just in the classical response to pathogens, but they take an active part in "sterile" inflammation, in response to ischemia and other forms of injury. In this context, different cell types infiltrate the injured heart and release distinct pro-inflammatory cytokines that initiate the fibrotic response by triggering myofibroblast activation. The complex interplay between immune cells, fibroblasts, and other non-immune/host-derived cells is now considered as the major driving force of cardiac fibrosis. Here, we review and discuss the contribution of inflammatory cells of innate immunity, including neutrophils, macrophages, natural killer cells, eosinophils and mast cells, in modulating the myocardial microenvironment, by orchestrating the fibrogenic process in response to tissue injury. A better understanding of the time frame, sequences of events during immune cells infiltration, and their action in the injured inflammatory heart environment, may provide a rationale to design new and more efficacious therapeutic interventions to reduce cardiac fibrosis. [ABSTRACT FROM AUTHOR]

Although the treatment of multiple-injured patients has been improved during the last decades, sepsis and multiple organ failure (MOF) still remain the major cause of death. Following trauma, profound alterations of a large number of physiological systems can be observed that may potentially contribute to the development of sepsis and MOF. This includes alterations of the neuroendocrine and the immune system. A large number of studies focused on posttraumatic changes of the immune system, but the cause of posttraumatic immune disturbance remains to be established. However, an increasing number of data indicate that the bidirectional interaction between the neuroendocrine and the immune system may be an important mechanism involved in the development of sepsis and MOF. The aim of this article is to highlight the current knowledge of the neuroendocrine modulation of the immune system during trauma and sepsis. [ABSTRACT FROM AUTHOR]

The article presents an author index to the November 01, 2004 issue of the periodical "European Surgical Research." Some of the authors are: Z. Acun; G. Enders; O. Ince; R. Oberbeck; K. Pamuk; etc.

Presents a table of contents for the November 01, 2004, issue of the periodical "European Surgical Research."

Radiation therapy is one of the most important treatment modalities for thoracic tumors. Despite significant advances in radiation techniques, radiation-induced lung injury (RILI) still occurs in up to 30% of patients undergoing thoracic radiotherapy, and therefore remains the main dose-limiting obstacle. RILI is a potentially lethal clinical complication of radiotherapy that has 2 main stages: an acute stage defined as radiation pneumonitis, and a late stage defined as radiation-induced lung fibrosis. Patients who develop lung fibrosis have a reduced quality of life with progressive and irreversible organ malfunction. Currently, the most effective intervention for the treatment of lung fibrosis is lung transplantation, but the lack of available lungs and transplantation-related complications severely limits the success of this procedure. Over the last few decades, advances have been reported in the use of mesenchymal stem cells (MSCs) for lung tissue repair and regeneration. MSCs not only replace damaged lung epithelial cells but also promote tissue repair through the secretion of anti-inflammatory and anti-fibrotic factors. Here, we present an overview of MSC-based therapy for radiation-induced lung fibrosis, focusing in particular on the molecular mechanisms involved and describing the most recent preclinical and clinical studies carried out in the field. [ABSTRACT FROM AUTHOR]

Adipose-derived stem cells (ASCs) have been routinely used from several years in regenerative surgery without any definitive statement about their potential pro-oncogenic or anti-oncogenic role. ASCs has proven to favor tumor progression in several experimental cancer models, playing a central role in regulating tumor invasiveness and metastatic potential through several mechanisms, such as the paracrine release of exosomes containing pro-oncogenic molecules and the induction of epithelial-mesenchymal transition. However, the high secretory activity and the preferential tumor-targeting make also ASCs a potentially suitable vehicle for delivery of new anti-cancer molecules in tumor microenvironment. Nanotechnologies, viral vectors, drug-loaded exosomes, and micro-RNAs (MiR) represent additional new tools that can be applied for cell-mediated drug delivery in a tumor microenvironment. Recent studies revealed that the MiR play important roles in paracrine actions on adipose-resident macrophages, and their dysregulation has been implicated in the pathogenesis of obesity, diabetes, and diabetic complications as wounds. Numerous MiR are present in adipose tissues, actively participating in the regulation of adipogenesis, adipokine secretion, inflammation, and inter-cellular communications in the local tissues. These results provide important insights into Adipocyte-secreted exosomal microRNA (A-SE-MiR) function and they suggest evaluating the potential role of A-SE-MiR in tumor progression, the mechanisms underlying ASCs-cancer cell interplay and clinical safety of ASCs-based therapies. [ABSTRACT FROM AUTHOR]

The effect of bacterial sepsis on animal behavior and physiology is complex due to direct and indirect actions. The most common form of bacterial sepsis in humans is from gram-negative bacterial strains. The endotoxin (lipopolysaccharide, LPS) and/or associated peptidoglycans from the bacteria are the key agents to induce an immune response, which then produces a cascade of immunological consequences. However, there are direct actions of LPS and associated peptidoglycans on cells which are commonly overlooked. This study showed behavioral and neural changes in larval Drosophila fed commercially obtained LPS from Serratia marcescens. Locomotor behavior was not altered, but feeding behavior increased and responses to sensory tactile stimuli were decreased. In driving a sensory-central nervous system (CNS)-motor neural circuit in in-situ preparations, direct application of commercially obtained LPS initially increased evoked activity and then decreased and even stopped evoked responses in a dose-dependent manner. With acute LPS and associated peptidoglycans exposure (10 min), the depressed neural responses recovered within a few minutes after removal of LPS. Commercially obtained LPS induces a transitory hyperpolarization of the body wall muscles within seconds of exposure and alters activity within the CNS circuit. Thus, LPS and/or associated peptidoglycans have direct effects on body wall muscle without a secondary immune response. [ABSTRACT FROM AUTHOR]

Human sexual behavior is mediated by a complex interplay of cerebral and spinal centers, as well as hormonal, peripheral, and autonomic functions. Neuroimaging studies identified central neural signatures of human sexual responses comprising neural emotional, motivational, autonomic, and cognitive components. However, empirical evidence regarding the neuromodulation of these neural signatures of human sexual responses was scarce for decades. Pharmacological functional magnetic resonance imaging (fMRI) provides a valuable tool to examine the interaction between neuromodulator systems and functional network anatomy relevant for human sexual behavior. In addition, this approach enables the examination of potential neural mechanisms regarding treatment-related sexual dysfunction under psychopharmacological agents. In this article, we introduce common neurobiological concepts regarding cerebral sexual responses based on neuroimaging findings and we discuss challenges and findings regarding investigating the neuromodulation of neural sexual stimulus processing. In particular, we summarize findings from our research program investigating how neural correlates of sexual stimulus processing are modulated by serotonergic, dopaminergic, and noradrenergic antidepressant medication in healthy males. [ABSTRACT FROM AUTHOR]

Presents the author index of vol. 25, 2002 issue of the journal "Neuropsychobiology."

Presents the table of contents for volume 31, supplement 1, of the journal "European Surgical Research", covering abstracts presented at the 34th Congress of the European Society for Surgical Research (ESSR).

The post-orgasmic refractory period in men is characterized by penile sensitivity, detumescence, and reduced arousabilty. The literature suggests that a comparable phenomenon either does not occur in women or is [...]

In this paper we review the existing literature on the relationship between breastfeeding and postpartum maternal sexuality. Latency to resumption of sexual activity and frequency of sexual activity, sexual desire, [...]

This report investigates if a partial loss of immunity results in alterations of murine behaviors in the open field (ambulation, a correlate of exploration or extroversion, and defecation, a correlate [...]

This instalment of Sex Research Update summarizes recent research on an intervention to increase female condom use; an HIV risk behaviour change intervention for high school students; the epidemiological characteristics [...]