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Pathophysiology
Kinds of Pathophysiology Selected AbstractsAPLASTIC ANEMIA , PATHOPHYSIOLOGY AND TREATMENT.HEMATOLOGICAL ONCOLOGY, Issue 3 20012000. No abstract is available for this article. [source] CARTILAGE IN BONE BIOLOGY AND PATHOPHYSIOLOGYINTERNATIONAL JOURNAL OF RHEUMATIC DISEASES, Issue 2006Article first published online: 6 JUL 200 No abstract is available for this article. [source] UNRAVELLING THE PATHOPHYSIOLOGY OF COMPLEX REGIONAL PAIN SYNDROME: FOCUS ON SYMPATHETICALLY MAINTAINED PAINCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 7 2008Gael F Gibbs SUMMARY 1In diseases such as complex regional pain syndrome (CRPS), where neuropathic pain is the primary concern, traditional pain classifications and lesion descriptors are of limited value. To obtain better treatment outcomes for patients, the underlying pathophysiological mechanisms of neuropathic pain need to be elucidated and analysed so that therapeutic targets can be identified and specific treatments developed. 2In the present review, we examine the current literature on sympathetically maintained pain (SMP), a subset of neuropathic pain, within the context of CRPS. Evidence from both human and animal studies is presented and discussed in terms of its support for the existence of SMP and the mechanistic information it provides. 3We discuss three current hypotheses that propose both a site and method for sympathetic,sensory coupling: (i) direct coupling between sympathetic and sensory neurons in the dorsal root ganglion; (ii) chemical coupling between sympathetic and nociceptive neuron terminals in skin; and (iii) the development of a-adrenoceptor-mediated supersensitivity in nociceptive fibres in skin in association with the release of inflammatory mediators. 4Finally, we propose a new hypothesis that integrates the mechanisms of chemical coupling and a-adrenoceptor-mediated supersensitivity. This hypothesis is based on previously unpublished data from our laboratory showing that a histological substrate suitable for sympathetic,sensory coupling exists in normal subjects. In the diseased state, the nociceptive fibres implicated in this substrate may be activated by both endogenous and exogenous noradrenaline. The mediating a-adrenoceptors may be expressed on the nociceptive fibres or on closely associated support cells. [source] Hypertrophic Scars and Keloids,A Review of Their Pathophysiology, Risk Factors, and Therapeutic ManagementDERMATOLOGIC SURGERY, Issue 2 2009DOLORES WOLFRAM MD BACKGROUND Hypertrophic scars and keloids result from an abnormal fibrous wound healing process in which tissue repair and regeneration-regulating mechanism control is lost. These abnormal fibrous growths present a major therapeutic dilemma and challenge to the plastic surgeon because they are disfiguring and frequently recur. OBJECTIVE To provide updated clinical and experimental information on hypertrophic scars and keloids so that physicians can better understand and properly treat such lesions. METHODS A Medline literature search was performed for relevant publications and for diverse strategies for management of hypertrophic scars and keloids. CONCLUSION The growing understanding of the molecular processes of normal and abnormal wound healing is promising for discovery of novel approaches for the management of hypertrophic scars and keloids. Although optimal treatment of these lesions remains undefined, successful healing can be achieved only with combined multidisciplinary therapeutic regimens. [source] Pathophysiology of ketoacidosis in Type 2 diabetes mellitusDIABETIC MEDICINE, Issue 10 2005P. Linfoot Abstract Aims Despite an increasing number of reports of ketoacidosis in populations with Type 2 diabetes mellitus, the pathophysiology of the ketoacidosis in these patients is unclear. We therefore tested the roles of three possible mechanisms: elevated stress hormones, increased free fatty acids (FFA), and suppressed insulin secretion. Methods Forty-six patients who presented to the Emergency Department with decompensated diabetes (serum glucose > 22.2 mmol/l and/or ketoacid concentrations , 5 mmol/l), had blood sampled prior to insulin therapy. Three groups of subjects were studied: ketosis-prone Type 2 diabetes (KPDM2, n = 13) with ketoacidosis, non-ketosis-prone subjects with Type 2 diabetes (DM2, n = 15), and ketotic Type 1 diabetes (n = 18). Results All three groups had similar mean plasma glucose concentrations. The degree of ketoacidosis (plasma ketoacids, bicarbonate and anion gap) in Type 1 and 2 subjects was similar. Mean levels of counterregulatory hormones (glucagon, growth hormone, cortisol, epinephrine, norepinephrine), and FFA were not significantly different in DM2 and KPDM2 patients. In contrast, plasma C-peptide concentrations were approximately three-fold lower in KPDM2 vs. non-ketotic DM2 subjects (P = 0.0001). Type 1 ketotic subjects had significantly higher growth hormone (P = 0.024) and FFA (P < 0.002) and lower glucagon levels (P < 0.02) than DM2. Conclusions At the time of hospital presentation, the predominant mechanism for ketosis in KPDM2 is likely to be greater insulinopenia. [source] Pathophysiology of KCNQ Channels: Neonatal Epilepsy and Progressive DeafnessEPILEPSIA, Issue 8 2000Thomas J. Jentsch No abstract is available for this article. [source] Pathophysiology of pruritus in atopic dermatitis: an overviewEXPERIMENTAL DERMATOLOGY, Issue 1 2002Sonja Ständer Abstract: Pruritus is an essential feature of atopic dermatitis (AD) and the diagnosis of active AD cannot be made without the history of itching. Because of the high impact on life quality, most of the patients measure the severity of eczema by the intensity of pruritus rather than appearance of skin lesions. However, although pruritus is a cardinal symptom of AD, its mechanism and association with the cutaneous nervous system is not completely understood. Recently, a considerable progress has been achieved in clarifying the complex pathophysiology of pruritus in AD. As a cutaneous sensory perception, itch requires excitation of neuropeptide-containing free nerve endings of unmyelinated nociceptor fibers. It is well known that histamine and acetylcholine provoke itch by direct binding to ,itch receptors' and several mediators such as neuropeptides, proteases or cytokines indirectly via histamine release. Interestingly, some variations of these complex mechanisms could be demonstrated in patients with AD. This review highlights the recent knowledge of different mechanisms which may be involved in regulating pruritus in patients with AD potentially leading to new therapeutic applications for the treatment of itch in AD. [source] Insights Into the Pathophysiology of Headache Provided by Recent Functional Imaging StudiesHEADACHE, Issue 9 2010Margarita Sanchez del Rio MD No abstract is available for this article. [source] Pediatric Short Bowel Syndrome: Pathophysiology, Nursing Care, and Management IssuesJOURNAL FOR SPECIALISTS IN PEDIATRIC NURSING, Issue 3 2000Louise D. Jakubik ISSUES AND PURPOSE. A comprehensive overview of the etiology, pathophysiology, nursing care, and medical and surgical management of the child with short bowel syndrome (SBS), which follows massive anatomical or functional loss of the small intestine. CONCLUSIONS. The outlook for children with SBS has improved due to recent advances in parenteral and enteral nutrition, pharmacologic interventions, and surgical options. PRACTICE IMPLICATIONS. Nurses whose practice reflects an in-depth knowledge of the etiology, pathophysiology, medical and surgical management, nursing interventions, and complications of SBS will be equipped to provide quality care for children and families affected by SBS. [source] Vitamin D Receptor: Key Roles in Bone Mineral Pathophysiology, Molecular Mechanism of Action, and Novel Nutritional Ligands,JOURNAL OF BONE AND MINERAL RESEARCH, Issue S2 2007Peter W Jurutka Abstract The vitamin D hormone, 1,25-dihydroxyvitamin D3 [1,25(OH)2D3], binds with high affinity to the nuclear vitamin D receptor (VDR), which recruits its retinoid X receptor (RXR) heterodimeric partner to recognize vitamin D responsive elements (VDREs) in target genes. 1,25(OH)2D3 is known primarily as a regulator of calcium, but it also controls phosphate (re)absorption at the intestine and kidney. Fibroblast growth factor 23 (FGF23) is a phosphaturic hormone produced in osteoblasts that, like PTH, lowers serum phosphate by inhibiting renal reabsorption through Npt2a/Npt2c. Real-time PCR and reporter gene transfection assays were used to probe VDR-mediated transcriptional control by 1,25(OH)2D3. Reporter gene and mammalian two-hybrid transfections, plus competitive receptor binding assays, were used to discover novel VDR ligands. 1,25(OH)2D3 induces FGF23 78-fold in osteoblasts, and because FGF23 in turn represses 1,25(OH)2D3 synthesis, a reciprocal relationship is established, with FGF23 indirectly curtailing 1,25(OH)2D3 -mediated intestinal absorption and counterbalancing renal reabsorption of phosphate, thereby reversing hyperphosphatemia and preventing ectopic calcification. Therefore, a 1,25(OH)2D3,FGF23 axis regulating phosphate is comparable in importance to the 1,25(OH)2D3,PTH axis that regulates calcium. 1,25(OH)2D3 also elicits regulation of LRP5, Runx2, PHEX, TRPV6, and Npt2c, all anabolic toward bone, and RANKL, which is catabolic. Regulation of mouse RANKL by 1,25(OH)2D3 supports a cloverleaf model, whereby VDR-RXR heterodimers bound to multiple VDREs are juxtapositioned through chromatin looping to form a supercomplex, potentially allowing simultaneous interactions with multiple co-modulators and chromatin remodeling enzymes. VDR also selectively binds certain ,3/,6 polyunsaturated fatty acids (PUFAs) with low affinity, leading to transcriptionally active VDR-RXR complexes. Moreover, the turmeric-derived polyphenol, curcumin, activates transcription of a VDRE reporter construct in human colon cancer cells. Activation of VDR by PUFAs and curcumin may elicit unique, 1,25(OH)2D3 -independent signaling pathways to orchestrate the bioeffects of these lipids in intestine, bone, skin/hair follicle, and other VDR-containing tissues. [source] Anatomy and Physiology of the Right Interganglionic Nerve: Implications for the Pathophysiology of Inappropriate Sinus TachycardiaJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 9 2008JING ZHOU M.D. Objective: To simulate inappropriate sinus tachycardia (IST) in experimental animals. Background: We recently found that epinephrine injected into the anterior right ganglionated plexi (ARGP) adjacent to the sinoatrial (SA) node induced an arrhythmia simulating IST. Methods: In 19 anesthetized dogs, via a right thoracotomy, the course of the interganglionic nerve (IGN) from the right stellate ganglion along the superior vena cava to the heart was delineated. High-frequency stimulation (HFS; 0.1 msec duration, 20 Hz, 4.5,9.3 V) was applied to IGN at the junction of innominate vein and SVC. Results: HFS of the IGN significantly increased the sinus rate (SR) (baseline: 156 ± 19 beats/minutes [bpm], 4.5 V: 191 ± 28 bpm*, 8.0 V: 207 ± 23 bpm*, 9.3 V: 216 ± 18 bpm*; *P < 0.01 compared to baseline) without significant changes in A-H interval or blood pressure. P-wave morphology, ice mapping, and noncontact mapping indicated that this tachycardia was sinus tachycardia. In 8 of 19 dogs, injecting hexamethonium (5 mg), a ganglionic blocker, into the ARGP attenuated the response elicited by IGN stimulation (baseline: 160 ± 21 bpm, 4.5 V: 172 ± 32 bpm, 8.0 V: 197 ± 32 bpm*, 9.3 V: 206 ± 26 bpm*; *P < 0.05 compared to baseline). In 19 of 19 animals, after formaldehyde injection into the ARGP, SR acceleration induced by IGN stimulation was markedly attenuated (baseline: 149 ± 17 bpm, 4.5 V: 151 ± 21 bpm, 8.0 V: 155 ± 23 bpm, 9.3 V: 167 ± 24 bpm*; *P < 0.05 compared to baseline). Conclusions: HFS of the IGN caused a selective and significant acceleration of the SR. A significant portion of IGN traverses the ARGP or synapses with the autonomic ganglia in the ARGP before en route to the SA node. Dysautonomia involving the IGN and/or ARGP may play an important role in IST. [source] Pathophysiology and Disease Progression of Atrial Fibrillation: Importance of Achieving and Maintaining Sinus RhythmJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 8 2008F.A.C.C., MARC COHEN M.D. Atrial fibrillation (AF) is a progressive disease in which arrhythmia-induced remodeling facilitates evolution from paroxysmal AF to persistent and permanent AF. Changes in electrical, structural, and contractile properties of cardiac tissue that are thought to underlie AF maintenance and progression are reviewed. Also examined is the negative impact of AF on clinical outcomes, as well as the potential benefits of restoration and maintenance of sinus rhythm. Because of the limited efficacy and adverse effects of current antiarrhythmics, new antiarrhythmic drugs need to be developed that provide safer and more effective rhythm control in AF. [source] Pathogenesis and Pathophysiology of the Cardiometabolic SyndromeJOURNAL OF CLINICAL HYPERTENSION, Issue 12 2009Erik P. Kirk PhD The cardiometabolic syndrome represents a cluster of metabolic abnormalities that are risk factors for cardiovascular disease. The mechanism(s) responsible for developing the cardiometabolic syndrome is not known, but it is likely that multi-organ insulin resistance, which is a common feature of the cardiometabolic syndrome, is involved. Insulin resistance is an important risk factor for type 2 diabetes and can cause vasoconstriction and renal sodium reabsorption, leading to increased blood pressure. Alterations in adipose tissue fatty acid and adipokine metabolism are involved in the pathogenesis of insulin resistance. Excessive rates of fatty acid release into the bloodstream can impair the ability of insulin to stimulate muscle glucose uptake and suppress hepatic glucose production. Noninfectious systemic inflammation associated with adipocyte and adipose tissue macrophage cytokine production can also cause insulin resistance. In addition, increased free fatty acid delivery to the liver can stimulate hepatic very low-density lipoprotein triglyceride production, leading to dyslipidemia. [source] Pathophysiology of Target-Organ Disease: Does Angiotensin II Remain the Key?JOURNAL OF CLINICAL HYPERTENSION, Issue 2007Ronald G. Victor MD Basic research provides an increasingly compelling rationale for renin-angiotensin system (RAS) blockade in hypertension treatment and cardiovascular risk reduction. Clinical trials addressing blood pressure-independent effects of angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers, however, have yielded mixed results, in part because of incomplete RAS blockade. Animal studies have shed new light on the complexity of RAS pathways involved in the induction of target-organ damage. New outcomes trials are under way to explore the full potential of more complete RAS blockade with regard to cardiovascular target-organ protection. [source] Hepatobiliary Diseases: Pathophysiology and ImagingJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 6 2002GEOFF MCCAUGHAN No abstract is available for this article. [source] Roles for Imaging in Understanding the Pathophysiology, Clinical Evaluation, and Management of Patients with Mitochondrial DiseaseJOURNAL OF NEUROIMAGING, Issue 4 2003A. Parry MRCP ABSTRACT Primary mitochondrial disorders remain uncommon, but they enter into the differential diagnosis for a broad range of syndromes. Functional and structural imaging methods offer important clinical tools for patient assessment when these diseases are suspected. Although the findings are not specific, in the appropriate clinical context, these tests can guide the use of more specific or invasive investigations. They have provided considerable information concerning the underlying pathophysiology of this heterogeneous range of disorders. Monitoring these changes potentially facilitates the identification of new therapies and their individualization. [source] Pathophysiology of the antiphospholipid syndromeJOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 8 2005P. G. DE GROOT Summary., Antiphospholipid syndrome is a distinct disorder with the clinical features of recurrent thrombosis in the venous or arterial circulation and fetal losses. Its serological marker is the presence of antiphospholipid antibodies in the blood of these patients. The relation between the presence of antibodies against anionic phospholipids and thromboembolic complications is well established over the last 25 years but the pathophysiology of the syndrome is largely unclear. Even after all these years, there is a persisting debate about the specificity and sensitivity of the assays for the detection of antiphospholipid antibodies. We now accept that antibodies to ,2-glycoprotein I rather than to anionic phospholipids are the major pathological antibodies, although there is no clear consensus on how the presence of these antibodies correlates with the different clinical manifestations of the syndrome. In this review, we discuss the current methods of detection of the antibodies and our insight into the pathobiology of the syndrome. We propose a mechanism for describing how the presence of anti- ,2-glycoprotein I antibodies relates to the different clinical manifestations observed. [source] Pathophysiology of renal disease associated with liver disorders: Implications for liver transplantation.LIVER TRANSPLANTATION, Issue 2 2002Part I Renal and hepatic function are often intertwined through both the existence of associated primary organ diseases and hemodynamic interrelationships. This connection occasionally results in the chronic failure of both organs, necessitating combined liver-kidney transplantation (LKT). Since 1988, more than 850 patients in the United States have received such transplants, with patient survival somewhat less than that for patients receiving either organ alone. Patients with renal failure caused by acute injury or hepatorenal syndrome have classically not been included as candidates for combined transplantation because of the reversibility of renal dysfunction after liver transplantation. However, the rate and duration of renal failure before liver transplantation is increasing in association with prolonged waiting list times. Thus, the issue of acquired permanent renal damage in the setting of hepatic failure continues to confront the transplant community. The following article and its sequel (Part II, to be published in vol 8, no 3 of this journal) attempt to review the problem of primary and secondary renal disease in patients with end-stage liver disease, elements involved in renal disease progression and recovery, the impact of renal disease on liver transplant outcome, and results of combined LKT; outline the steps in the pretransplantation renal evaluation; and provide the beginnings of an algorithm for making the decision for combined LKT. [source] Pathophysiology and therapy of pruritus in allergic and atopic diseasesALLERGY, Issue 7 2010J. Buddenkotte To cite this article: Buddenkotte J, Steinhoff M. Pathophysiology and therapy of pruritus in allergic and atopic diseases. Allergy 2010; 65: 805,821. Abstract Pruritus (itch) is a major characteristic and one of the most debiliating symptoms in allergic and atopic diseases and the diagnostic hallmark of atopic dermatitis. Pruritus is regularly defined as an unpleasant sensation provoking the desire to scratch. Although we achieved rather good knowledge about certain inducers of itch such as neuropeptides, amines, ,-opioids, cytokines and proteases, for example, less is known about the pathophysiological specifities among the different diseases, and the therapeutic consequences which may derive thereoff. This review dissects the role of mediators, receptors and itch inhibitors on peripheral nerve endings, dorsal root ganglia, the spinal cord and the CNS leading to the amplification or , vice versa , suppression of pruritus. As the treatment of pruritus in allergic and atopic skin disease is still not satisfactory, knowing these pathways and mechanisms may lead to novel therapeutic approaches against this frequently encountered skin symptom. [source] Emerging Concepts in the Pathophysiology of Type 2 Diabetes MellitusMOUNT SINAI JOURNAL OF MEDICINE: A JOURNAL OF PERSONALIZED AND TRANSLATIONAL MEDICINE, Issue 3 2009Prasanth N. Surampudi MD Abstract Type 2 diabetes mellitus is a multifactorial metabolic disorder. It is characterized by chronic hyperglycemia, insulin resistance, and a relative insulin secretion defect. The prevalence of type 2 diabetes mellitus has risen worldwide in large part because of an increase in obesity and sedentary lifestyles. The underlying pathophysiology and complications of type 2 diabetes mellitus are still being elucidated. Recent advances in diabetes research have helped us to gain a better understanding about insulin resistance and insulin secretion defects. The evolving understanding about the influence of the incretin effect, insulin signal transduction, adipose tissue, intra,islet cell communication, and inflammation is changing the way in which we view type 2 diabetes mellitus. This new understanding will eventually provide us with new treatment approaches to help patients who have type 2 diabetes mellitus. This article gives a review of the current and emerging concepts of the pathophysiology of type 2 diabetes mellitus. Mt Sinai J Med 76: 216,226, 2009. © 2009 Mount Sinai School of Medicine [source] Pathophysiology of spastic paresis.MUSCLE AND NERVE, Issue 5 2005II: Emergence of muscle overactivity Abstract In the subacute and chronic stages of spastic paresis, stretch-sensitive (spastic) muscle overactivity emerges as a third fundamental mechanism of motor impairment, along with paresis and soft tissue contracture. Part II of this review primarily addresses the pathophysiology of the various forms of spastic overactivity. It is argued that muscle contracture is one of the factors that cause excessive responsiveness to stretch, which in turn aggravates contracture. Excessive responsiveness to stretch also impedes voluntary motor neuron recruitment, a concept termed stretch-sensitive paresis. None of the three mechanisms of impairment (paresis, contracture, and spastic overactivity) is symmetrically distributed between agonists and antagonists, which generates torque imbalance around joints and limb deformities. Thus, each may be best treated focally on an individual muscle-by-muscle basis. Intensive motor training of the less overactive muscles should disrupt the cycle of paresis,disuse,paresis, and concomitant use of aggressive stretch and focal weakening agents in their more overactive and shortened antagonists should break the cycle of overactivity,contracture,overactivity. Muscle Nerve, 2005 [source] Pathophysiology as a basis for understanding symptom complexes and therapeutic targetsNEUROGASTROENTEROLOGY & MOTILITY, Issue 2 2004M. Camilleri Abstract, Sensorimotor disorders of the stomach, small intestine and colon have a limited repertoire of clinical manifestations, and there is the potential for more than one mechanism to lead to symptoms. In many recent clinical trial programs of novel agents in neurogastroenterology, the emphasis has been primarily on symptom assessment of broad groups of patients identified by the Rome criteria. Drugs of potential value have fallen by the wayside with this approach. We propose the current paradigm is partly to blame; physiological testing should provide the basis for identifying more homogeneous populations and therapeutic targets within functional bowel disease, and this applies to the upper and lower gut. Here we summarize the evidence that certain biomarkers can, in a limited fashion, be used to predict the success of an experimental medicine in common disorders of gastrointestinal function, including the irritable bowel syndrome and functional dyspepsia. Although the current evidence is limited and is most convincingly demonstrated with examples of transit measurements (for loperamide, alosetron, tegaserod and piboserod), we perceive this paradigm that studies using validated and responsive biomarkers have an important role to play in drug development. [source] Pathophysiology of the Pulmonary Vein as an Atrial Fibrillation Initiator:PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 7p2 2003From Bench to Clinic The basic electrophysiologic studies have proved the arrhythmogenic mechanisms of the pulmonary vein as an atrial fibrillation initiator; the mechanisms include enhanced automaticity, triggered activity, and microreentry from myocardial sleeves inside pulmonary veins. Immunohistology study has proved the conduction characteristics of pulmonary vein myocardium, and further study of ionic currents are important for understanding atrial fibrillation initiation from the pulmonary vein. (PACE 2003; 26[Pt. II]:1576,1582) [source] Pathophysiology and treatment of arterial dissection and strokePROGRESS IN NEUROLOGY AND PSYCHIATRY, Issue 6 2007Kunal Khanna Arterial dissection is the commonest cause of stroke in younger people; however, the mechanisms involved and how it is treated remain controversial. In this article, the authors outline the possible pathophysiology of arterial dissection causing stroke, how it is currently diagnosed and treated and how further large trials are required to improve the prognosis of this condition. Copyright © 2007 Wiley Interface Ltd [source] Urinary Incontinence in Spayed Bitches: New Insights into the Pathophysiology and Options for Medical TreatmentREPRODUCTION IN DOMESTIC ANIMALS, Issue 2009S Arnold No abstract is available for this article. [source] Four faces of a parapneumonic effusion: Pathophysiology and varied radiographic presentationsRESPIROLOGY, Issue 4 2007Jay HEIDECKER Abstract: We report a patient methicillin-resistant Staphylococcus aureus pneumonia who developed fluid collections in three spaces in the thorax, the pleural space, the pericardial space, and a pre-existing bulla, in addition to mediastinal oedema. We discuss the universal pathogenesis for the development of these fluid collections and the explanation for the most common presentation being a parapneumonic effusion. [source] The Kappa-Opiate Receptor Impacts the Pathophysiology and Behavior of Substance UseTHE AMERICAN JOURNAL ON ADDICTIONS, Issue 4 2009David Mysels MD There is increasing evidence that the kappa-opiate receptor, in addition to the mu-opiate receptor, plays an important role in substance use pathophysiology and behavior. As dopamine activity is upregulated through chronic substance use, kappa receptor activity, mediated through the peptide dynorphin, is upregulated in parallel. Dynorphin causes dysphoria and decreased locomotion, and the upregulation of its activity on the kappa receptor likely dampens the excitation caused by increased dopaminergic activity. This feedback mechanism may have significant clinical implications for treating drug dependent patients in various stages of their pathology. [source] ORIGINAL ARTICLE: Role of Inflammatory Cytokines and eNOS Gene Polymorphism in Pathophysiology of Pre-EclampsiaAMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY, Issue 3 2010Archana Singh Citation Singh A, Sharma D, Raghunandan C, Bhattacharjee J. Role of inflammatory cytokines and eNOS gene polymorphism in pathophysiology of pre-eclampsia. Am J Reprod Immunol 2010; 63: 244,251 Problem, Pre-eclampsia involves endothelial vascular dysfunction. The aim of this study was to test the hypothesis that (i) endothelial nitric oxide (NO) synthase Glu298Asp gene polymorphism limits constitutive NO production causing endothelial dysfunction and (ii) inflammatory cytokines impairs endothelium dependent relaxation in pre-eclampsia. Method of study, This cross-sectional study included 50 women with pre-eclampsia and 50 healthy pregnant women. Their blood samples were analyzed for NO, inflammatory cytokines and endothelial NO synthase (eNOS) gene polymorphism. Result, Decreased NO levels whereas increased tumor necrosis factor-,, interleukin (IL)-6 and interleukin-2 were found in pre-eclampsia (P < 0.001). No significant differences were found in genotype/allele distribution between two groups. Significant negative correlation was observed between NO and IL-6 in pre-eclamptic group (P = 0.001). Conclusion, An IL-6-mediated endothelium dependent NO-cyclic guanine monophosphate-mediated relaxation pathway may be inhibited in systemic vessels in pre-eclampsia. As observed in this study Glu298Asp eNOS gene polymorphism did not showed significant association with pre-eclampsia. [source] ORIGINAL ARTICLE: Serum IL-6 Level May Have Role in the Pathophysiology of Unexplained InfertilityAMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY, Issue 4 2009Bulent Demir Problem, The aim of this study was to compare the serum levels of interleukin (IL)-6 of women with unexplained infertility with fertile subjects. Method of study, Serum IL-6, and tumor necrosis factor-, (TNF-,) levels of 45 infertile and 44 fertile women on day 3 of menstrual cycle were assessed and compared for this prospective controlled study. Results, The mean serum IL-6 level was significantly higher in women with unexplained infertility, compared with fertile women (5.71 ± 1.81 and 4.31 ± 1.79, P < 0.001, Student's t -test). There was no significant difference in TNF-, level among the groups. Conclusion, Significant difference in serum IL-6 levels between unexplained infertile and fertile women suggests that this cytokine may be involved in pathophysiology of unexplained infertility. [source] P-02 Pathophysiology of Sexual DysfunctionsTHE JOURNAL OF SEXUAL MEDICINE, Issue 2007Chairpersons J. Angulo [source] | |||||||||||||||||||||||||||||||||||||