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Perception of pain in males and females
ORAL PRESENTATIONS
tions for pain-related behaviors. The roles of h o r m o n a l status and c h r o n o b i o l o g y in clinical pain conditions in w o m e n (eg, clinical pain changes across the menstrual cycle, pain during pregnancy, and associations of pain conditions with puberty, menopause, and exogenous h o r m o n e use) deserve further investigation. There is growing evidence that h o r m o n e s influence migraine headache and temporomandibular pain. The evidence for h o r m o n a l influences o n other chronic pain conditions is less convincing. Future research should address these gaps in knowledge, with the aim of understanding mechanisms.
F1.15 18:00-18:30, Friday, February 24, 2006 Perception of Pain in Males and Females Farook A1-Azzawi
Gynaecology Research Unit, UniversityHospitals of Leiceste~ Leiceste~ UK Sexual dimorphism in nociceptive processing and pain responses involves the interactions of a multitude of biological, psychological, and socio-cultural factors. Among these factors are the influences of gonadal steroids that modulate the integration of nociceptive input in the central nervous system. They are to some extent linked to organizational as well as activational processes of gonadal steroids in influencing pattern of neurotransmission. Experimental pain models in animal studies demonstrate these sex-based differences, and in h u m a n clinical and experimental settings the data agree to a large extent that w o m e n report more severe levels of pain, more frequent pain, and pain of longer duration t h a n m e n do. Data also suggest female predominance in experiencing pain related to non-sex organs such as irritable bowel syndrome, fibromyalgia, rheumatoid arthritis, and temporomandibular disorders. Equally importantly, the evidence exists for a different response to opioid analgesia between sexes. Different pattern of respective receptors expression and/or binding of ligands, as well as differences in collateral association pathways may be responsible. Understanding these basic processes is fundamental to further develop an effective strategy for pain control in men and women.
F1.16 08:30-09:00, Friday, February 24, 2006 The Impact of Gender on the Mosaic of Autoimmunity Yehuda S h o e n f e l d
Sheba Medical Center, Dept. of Medicine B, Research Center for Autoimmunity; and Incumbent of the Laura Schwartz Kip/) Chair for Autoimmune, Tel Aviv University, Israel Autoimmune diseases are conditions in which the i m m u n e system damages normal c o m p o n e n t s of the individual. Autoimmune diseases were found to be multifactorial in their etiology. For practical reasons these factors are classified into four categories-Genetic: which entail the MHC class I, II, and III. A case in p o i n t will be the haplotypes of HLADR3, B8 which are prevalent in m a n y classical diseases. In addition, Gm allotype, idiotypes, and some c o m p l e m e n t deficiencies may have a genetic background. Immune deftciencies: C l q C2, C4 and IgA deficiencies are a m o n g the most c o m m o n defects associated with diverse autoimmune conditions. Hormonal state: Most autoimmune diseases are detected in females at the child bearing ages. The role of estrogens will be delineated. Some diseases, such as SLE, thyroid AID
diseases, and PBC are prevalent in females in a ratio of 10:1 to males. Estrogen receptors are found on lymphocytes and they activate them. Androgens are applied for therapy. Castration of males and Kleinfelter's syndrome, lead to AIDs, while androgens can ameliorate the manifestations. AIDs of the ThI-type improve in pregnancy, while type II cause exacerbations. Contraceptives and IVF therapies may also exacerbate type II. The intricate relationships between estrogen and autoimmunity will be detailed. In addition other hormones play a role, ie, prolactin. Environmental causes: Those are the most important as a trigger factors. Conclusion: The type of disease in an individual, in an autoimmune prone family, will be determined by the specific combination of the different factors m e n t i o n e d above.
F1.17 09:00-09:30, Friday, February 24, 2006 Neural Immune Interactions in Health and Disease: Relevance to Women's Health Esther Sternberg; Cherie Butts; a n d A l e x a n d r a TaiL
National Institute of Mental Health~National Institutes of Health, Bethesda, MD, USA H o r m o n a l factors regulate i m m u n i t y and affect susceptibility to a u t o i m m u n e / i n f l a m m a t o r y disease. Regulation of i m m u n i t y by and interactions between the hypothalamic pituitary adrenal (HPA) and hypothalamic pituitary gonadal (HPG) axes contribute to the two- to ten-fold higher incidence and severity of a u t o i m m u n e / i n f l a m m a t o r y diseases in females compared to males. Activation of the HPA axis generally inhibits inflammation through the i m m u n o s u p pressive effects of the glucocorticoids binding to glucocorticold receptors (GR). Hormones of the HPG axis, particularly estrogens, can directly affect i m m u n i t y at the cellular level and also interact with the HPA axis to alter glucocorticold regulation of immunity. Interruptions of the HPA or HPG axis through surgical or pharmacological means alter host susceptibility to inflammatory disease. Differences in receptor n u m b e r or sensitivity contribute to altered imm u n e cell responsiveness to hormones. Changes in i m m u n e cell GR and ER numbers during d e v e l o p m e n t may contribute to gender and developmental differences in autoimm u n e disease. We have recently s h o w n that dendritic cells express progesterone receptors (PR) and respond to progesterone differentially during maturation. Decreased GR sensitivity related to mutations or environmental factors may also induce glucocorticoid resistance and result in e n h a n c e d i m m u n e responses. We have recently shown that bacterial toxins selectively repress GR and other nuclear h o r m o n e receptor transactivation, including the PR and the ERr Understanding h o r m o n a l interactions with i m m u n e cells at multiple levels will shed light o n gender differences in i m m u n i t y and will lead to new avenues for therapy.
F1.18 09:30-10:00, Friday, February 24, 2006 Multiple Sclerosis as a Predominantly Female Immune-Mediated Disease Ariel Miller
Technion--Rappaport Faculty of Medicine & Research Institute, Haifla, Israel; and Multiple Sclerosis & Brain Research Center, Department of Neurology, Carmel Medical Center, Haifla, Israel Multiple sclerosis (MS), the most c o m m o n neurological disease afflicting young adults, is characterized by i m m u n e sys-
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tions for pain-related behaviors. The roles of h o r m o n a l status and c h r o n o b i o l o g y in clinical pain conditions in w o m e n (eg, clinical pain changes across the menstrual cycle, pain during pregnancy, and associations of pain conditions with puberty, menopause, and exogenous h o r m o n e use) deserve further investigation. There is growing evidence that h o r m o n e s influence migraine headache and temporomandibular pain. The evidence for h o r m o n a l influences o n other chronic pain conditions is less convincing. Future research should address these gaps in knowledge, with the aim of understanding mechanisms.
F1.15 18:00-18:30, Friday, February 24, 2006 Perception of Pain in Males and Females Farook A1-Azzawi
Gynaecology Research Unit, UniversityHospitals of Leiceste~ Leiceste~ UK Sexual dimorphism in nociceptive processing and pain responses involves the interactions of a multitude of biological, psychological, and socio-cultural factors. Among these factors are the influences of gonadal steroids that modulate the integration of nociceptive input in the central nervous system. They are to some extent linked to organizational as well as activational processes of gonadal steroids in influencing pattern of neurotransmission. Experimental pain models in animal studies demonstrate these sex-based differences, and in h u m a n clinical and experimental settings the data agree to a large extent that w o m e n report more severe levels of pain, more frequent pain, and pain of longer duration t h a n m e n do. Data also suggest female predominance in experiencing pain related to non-sex organs such as irritable bowel syndrome, fibromyalgia, rheumatoid arthritis, and temporomandibular disorders. Equally importantly, the evidence exists for a different response to opioid analgesia between sexes. Different pattern of respective receptors expression and/or binding of ligands, as well as differences in collateral association pathways may be responsible. Understanding these basic processes is fundamental to further develop an effective strategy for pain control in men and women.
F1.16 08:30-09:00, Friday, February 24, 2006 The Impact of Gender on the Mosaic of Autoimmunity Yehuda S h o e n f e l d
Sheba Medical Center, Dept. of Medicine B, Research Center for Autoimmunity; and Incumbent of the Laura Schwartz Kip/) Chair for Autoimmune, Tel Aviv University, Israel Autoimmune diseases are conditions in which the i m m u n e system damages normal c o m p o n e n t s of the individual. Autoimmune diseases were found to be multifactorial in their etiology. For practical reasons these factors are classified into four categories-Genetic: which entail the MHC class I, II, and III. A case in p o i n t will be the haplotypes of HLADR3, B8 which are prevalent in m a n y classical diseases. In addition, Gm allotype, idiotypes, and some c o m p l e m e n t deficiencies may have a genetic background. Immune deftciencies: C l q C2, C4 and IgA deficiencies are a m o n g the most c o m m o n defects associated with diverse autoimmune conditions. Hormonal state: Most autoimmune diseases are detected in females at the child bearing ages. The role of estrogens will be delineated. Some diseases, such as SLE, thyroid AID
diseases, and PBC are prevalent in females in a ratio of 10:1 to males. Estrogen receptors are found on lymphocytes and they activate them. Androgens are applied for therapy. Castration of males and Kleinfelter's syndrome, lead to AIDs, while androgens can ameliorate the manifestations. AIDs of the ThI-type improve in pregnancy, while type II cause exacerbations. Contraceptives and IVF therapies may also exacerbate type II. The intricate relationships between estrogen and autoimmunity will be detailed. In addition other hormones play a role, ie, prolactin. Environmental causes: Those are the most important as a trigger factors. Conclusion: The type of disease in an individual, in an autoimmune prone family, will be determined by the specific combination of the different factors m e n t i o n e d above.
F1.17 09:00-09:30, Friday, February 24, 2006 Neural Immune Interactions in Health and Disease: Relevance to Women's Health Esther Sternberg; Cherie Butts; a n d A l e x a n d r a TaiL
National Institute of Mental Health~National Institutes of Health, Bethesda, MD, USA H o r m o n a l factors regulate i m m u n i t y and affect susceptibility to a u t o i m m u n e / i n f l a m m a t o r y disease. Regulation of i m m u n i t y by and interactions between the hypothalamic pituitary adrenal (HPA) and hypothalamic pituitary gonadal (HPG) axes contribute to the two- to ten-fold higher incidence and severity of a u t o i m m u n e / i n f l a m m a t o r y diseases in females compared to males. Activation of the HPA axis generally inhibits inflammation through the i m m u n o s u p pressive effects of the glucocorticoids binding to glucocorticold receptors (GR). Hormones of the HPG axis, particularly estrogens, can directly affect i m m u n i t y at the cellular level and also interact with the HPA axis to alter glucocorticold regulation of immunity. Interruptions of the HPA or HPG axis through surgical or pharmacological means alter host susceptibility to inflammatory disease. Differences in receptor n u m b e r or sensitivity contribute to altered imm u n e cell responsiveness to hormones. Changes in i m m u n e cell GR and ER numbers during d e v e l o p m e n t may contribute to gender and developmental differences in autoimm u n e disease. We have recently s h o w n that dendritic cells express progesterone receptors (PR) and respond to progesterone differentially during maturation. Decreased GR sensitivity related to mutations or environmental factors may also induce glucocorticoid resistance and result in e n h a n c e d i m m u n e responses. We have recently shown that bacterial toxins selectively repress GR and other nuclear h o r m o n e receptor transactivation, including the PR and the ERr Understanding h o r m o n a l interactions with i m m u n e cells at multiple levels will shed light o n gender differences in i m m u n i t y and will lead to new avenues for therapy.
F1.18 09:30-10:00, Friday, February 24, 2006 Multiple Sclerosis as a Predominantly Female Immune-Mediated Disease Ariel Miller
Technion--Rappaport Faculty of Medicine & Research Institute, Haifla, Israel; and Multiple Sclerosis & Brain Research Center, Department of Neurology, Carmel Medical Center, Haifla, Israel Multiple sclerosis (MS), the most c o m m o n neurological disease afflicting young adults, is characterized by i m m u n e sys-
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