Pub Date : 2018-05-30DOI: 10.5772/INTECHOPEN.76446
P. Soler, C. Ferreira, J. Novaes, H. M. Fernandes
Body dysmorphic disorder (BDD) is defined by a recurring and persistent concern char - acterized by psychic suffering caused by a possible physical imperfection in appearance. It is a severe psychiatric condition, duly confirmed by neuroanatomical findings, very peculiar repetitive behaviors, and specific personalities. The prevalence of BDD is increas ing around the world and differs between countries, because of cultural differences and different health-care systems. This increase is worrying because BDD is a pathology that presents comorbidity like severe depression, suicidal ideation, and functional and social impairment. However, BDD is an unrecognized and often not diagnosed in our soci -ety. Many patients are ashamed of their complaints and do not usually seek psychiatric help with ease, and unfortunately, they seek help in cosmetic and surgical treatments to improve their appearance, and these professionals are not yet prepared to assist in the diagnosis of this disorder. Therefore, this chapter presents not only the psychopathology of BDD but also its associations with other pathologies and their main factors of influ - ence. Finally, we present a clinical experience with a detailed description of a clinical case. The aim is to contribute to the diagnosis and treatment of this pathology and also to future research that may benefit society and these patients.
{"title":"Body Dysmorphic Disorder: Characteristics, Psychopathology, Clinical Associations, and Influencing Factors","authors":"P. Soler, C. Ferreira, J. Novaes, H. M. Fernandes","doi":"10.5772/INTECHOPEN.76446","DOIUrl":"https://doi.org/10.5772/INTECHOPEN.76446","url":null,"abstract":"Body dysmorphic disorder (BDD) is defined by a recurring and persistent concern char - acterized by psychic suffering caused by a possible physical imperfection in appearance. It is a severe psychiatric condition, duly confirmed by neuroanatomical findings, very peculiar repetitive behaviors, and specific personalities. The prevalence of BDD is increas ing around the world and differs between countries, because of cultural differences and different health-care systems. This increase is worrying because BDD is a pathology that presents comorbidity like severe depression, suicidal ideation, and functional and social impairment. However, BDD is an unrecognized and often not diagnosed in our soci -ety. Many patients are ashamed of their complaints and do not usually seek psychiatric help with ease, and unfortunately, they seek help in cosmetic and surgical treatments to improve their appearance, and these professionals are not yet prepared to assist in the diagnosis of this disorder. Therefore, this chapter presents not only the psychopathology of BDD but also its associations with other pathologies and their main factors of influ - ence. Finally, we present a clinical experience with a detailed description of a clinical case. The aim is to contribute to the diagnosis and treatment of this pathology and also to future research that may benefit society and these patients.","PeriodicalId":272705,"journal":{"name":"Pathophysiology - Altered Physiological States","volume":"55 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2018-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"125056872","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2018-05-30DOI: 10.5772/INTECHOPEN.70848
Bassim Alsadi
Polycystic ovary syndrome (PCOS) is one of the most common endocrine disorders in women of reproductive age. The clinical picture characterized by both endocrine disorders (hyperandrogenism, menstrual cycle disorders, obesity) and metabolic alteration with implications for women’s health and reproductive and metabolic consequences. Leventhal described for the first time a syndrome characterized by polycystic ovaries associated with menstrual cycle disorders, hirsutism, and obesity. The pathophysiology and other metabolic disorders that make the PCOS more complex than originally described are the most common cause of infertility linked to chronic anovulation. In fact, this is a multifactorial disorder that involves the hypothalamus, pituitary, ovary, adrenal, and peripheral adipose tissues, which are simultaneously involved in the pathogenesis of the syndrome.
{"title":"Polycystic Ovary Syndrome, Pathophysiology, and Reproductive Health Implications","authors":"Bassim Alsadi","doi":"10.5772/INTECHOPEN.70848","DOIUrl":"https://doi.org/10.5772/INTECHOPEN.70848","url":null,"abstract":"Polycystic ovary syndrome (PCOS) is one of the most common endocrine disorders in women of reproductive age. The clinical picture characterized by both endocrine disorders (hyperandrogenism, menstrual cycle disorders, obesity) and metabolic alteration with implications for women’s health and reproductive and metabolic consequences. Leventhal described for the first time a syndrome characterized by polycystic ovaries associated with menstrual cycle disorders, hirsutism, and obesity. The pathophysiology and other metabolic disorders that make the PCOS more complex than originally described are the most common cause of infertility linked to chronic anovulation. In fact, this is a multifactorial disorder that involves the hypothalamus, pituitary, ovary, adrenal, and peripheral adipose tissues, which are simultaneously involved in the pathogenesis of the syndrome.","PeriodicalId":272705,"journal":{"name":"Pathophysiology - Altered Physiological States","volume":"3 2 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2018-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"115636342","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2018-03-20DOI: 10.5772/INTECHOPEN.74269
G. F. Simões, Paula Sakuramoto, C. DosSantos, N. Furlan, T. M. Augusto
Additional information the Abstract The prostate is an accessory gland of the male reproductive tract, and its presence is universal in mammals. It is committed to the prostatic fluid production and storage, which is released with other semen components during ejaculation. Such fluid contributes to increasing motility and fertility of the spermatozoa, and the neutralization of the vagina, thus playing an important role in fertilization. Few pathological complications, often progressively aggravated with age, can affect this gland (i.e. benign and malignant proliferative changes; all to be described next in this chapter). Nowadays, the neoplastic expansion is the main motivator and contributor for studies on enlightening of growth regulation mechanisms and physiology of the prostate.
{"title":"An Overview on Prostate Pathophysiology: New Insights into Prostate Cancer Clinical Diagnosis","authors":"G. F. Simões, Paula Sakuramoto, C. DosSantos, N. Furlan, T. M. Augusto","doi":"10.5772/INTECHOPEN.74269","DOIUrl":"https://doi.org/10.5772/INTECHOPEN.74269","url":null,"abstract":"Additional information the Abstract The prostate is an accessory gland of the male reproductive tract, and its presence is universal in mammals. It is committed to the prostatic fluid production and storage, which is released with other semen components during ejaculation. Such fluid contributes to increasing motility and fertility of the spermatozoa, and the neutralization of the vagina, thus playing an important role in fertilization. Few pathological complications, often progressively aggravated with age, can affect this gland (i.e. benign and malignant proliferative changes; all to be described next in this chapter). Nowadays, the neoplastic expansion is the main motivator and contributor for studies on enlightening of growth regulation mechanisms and physiology of the prostate.","PeriodicalId":272705,"journal":{"name":"Pathophysiology - Altered Physiological States","volume":"126 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2018-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"123114596","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2017-12-20DOI: 10.5772/INTECHOPEN.70596
Zesergio Melo, J. A. Ruiz-Pacheco, C. Mendoza-Cerpa, R. Echavarria
Renal transplantation is currently the best alternative for patients with end-stage renal disease. Immune responses activated against the allograft are a decisive factor in transplantation outcomes and patient survival. Although short-term graft and patient survival have improved significantly as a result of better donor matching systems, novel immunosuppressive agents and enhanced care, long-term outcomes remain unfavorable and reflect sub-clinical injury caused by chronic rejection. The immune system lies at the intersection of immunogenic tolerance and graft failure; thus, it is a major determinant of pathology in the context of renal transplantation. During the early stages of transplantation increased expression of cytokines has been observed in addition to increased expression of adhesion proteins and immune cells. This early inflammatory response does not necessarily end in graft rejection, although this will depend on the severity of the inflammation. Activation of Toll-like Receptors (TLRs), damaging molecular patterns (DAMPs), and other components of innate immunity is key to the formation of atherosclerotic plaques and the development of autoimmune diseases. Initially the donor antigens are presented to the T lymphocytes of the recipient. This activation induces their proliferation, differentiation and cytokine production. Successful kidney transplant recipients need to develop immunologic tolerance against donor antigens. In this chapter, we address some of the innate and adaptive immune mechanisms associated with kidney transplantation; emphasizing their role in allograft rejection.
{"title":"Immunopathology of Kidney Transplantation","authors":"Zesergio Melo, J. A. Ruiz-Pacheco, C. Mendoza-Cerpa, R. Echavarria","doi":"10.5772/INTECHOPEN.70596","DOIUrl":"https://doi.org/10.5772/INTECHOPEN.70596","url":null,"abstract":"Renal transplantation is currently the best alternative for patients with end-stage renal disease. Immune responses activated against the allograft are a decisive factor in transplantation outcomes and patient survival. Although short-term graft and patient survival have improved significantly as a result of better donor matching systems, novel immunosuppressive agents and enhanced care, long-term outcomes remain unfavorable and reflect sub-clinical injury caused by chronic rejection. The immune system lies at the intersection of immunogenic tolerance and graft failure; thus, it is a major determinant of pathology in the context of renal transplantation. During the early stages of transplantation increased expression of cytokines has been observed in addition to increased expression of adhesion proteins and immune cells. This early inflammatory response does not necessarily end in graft rejection, although this will depend on the severity of the inflammation. Activation of Toll-like Receptors (TLRs), damaging molecular patterns (DAMPs), and other components of innate immunity is key to the formation of atherosclerotic plaques and the development of autoimmune diseases. Initially the donor antigens are presented to the T lymphocytes of the recipient. This activation induces their proliferation, differentiation and cytokine production. Successful kidney transplant recipients need to develop immunologic tolerance against donor antigens. In this chapter, we address some of the innate and adaptive immune mechanisms associated with kidney transplantation; emphasizing their role in allograft rejection.","PeriodicalId":272705,"journal":{"name":"Pathophysiology - Altered Physiological States","volume":"70 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2017-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"124614830","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2017-12-20DOI: 10.5772/INTECHOPEN.68725
C. Tóthová, O. Nagy
Transthyretin (also known as prealbumin) is an important transport protein, which plays an essential role in the binding of thyroid hormones and retinol with varying affinities in mammalian, as well as avian species. The determination of transthyretin concentrations may be used as a diagnostic tool for some disease conditions in humans, but is more often used as a nutritional marker to assess protein-calorie malnutrition and as prognostic indicator in critically ill patients. Transthyretin has shorter half-life (2–3 days) than that of albumin and belongs to negative acute phase proteins. This may complicate the use of transthyre- tin as a nutritional marker and the interpretation of results in the diagnosis of diseases. Although some studies have been carried out to determine the usefulness of transthyretin in selected disease conditions and disorders also in animals, it is a relatively rarely used parameter to evaluate health state and illness in veterinary medicine. The usefulness of transthyretin in the diagnosis of diseases and evaluation of nutritional status in humans and animals are reviewed in this article, including the laboratory assays available to mea- sure its concentrations and the possible clinical application of the results, as well as its usefulness as a prognostic indicator in some disease conditions.
{"title":"Transthyretin in the Evaluation of Health and Disease in Human and Veterinary Medicine","authors":"C. Tóthová, O. Nagy","doi":"10.5772/INTECHOPEN.68725","DOIUrl":"https://doi.org/10.5772/INTECHOPEN.68725","url":null,"abstract":"Transthyretin (also known as prealbumin) is an important transport protein, which plays an essential role in the binding of thyroid hormones and retinol with varying affinities in mammalian, as well as avian species. The determination of transthyretin concentrations may be used as a diagnostic tool for some disease conditions in humans, but is more often used as a nutritional marker to assess protein-calorie malnutrition and as prognostic indicator in critically ill patients. Transthyretin has shorter half-life (2–3 days) than that of albumin and belongs to negative acute phase proteins. This may complicate the use of transthyre- tin as a nutritional marker and the interpretation of results in the diagnosis of diseases. Although some studies have been carried out to determine the usefulness of transthyretin in selected disease conditions and disorders also in animals, it is a relatively rarely used parameter to evaluate health state and illness in veterinary medicine. The usefulness of transthyretin in the diagnosis of diseases and evaluation of nutritional status in humans and animals are reviewed in this article, including the laboratory assays available to mea- sure its concentrations and the possible clinical application of the results, as well as its usefulness as a prognostic indicator in some disease conditions.","PeriodicalId":272705,"journal":{"name":"Pathophysiology - Altered Physiological States","volume":"48 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2017-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"122723405","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2017-12-20DOI: 10.5772/INTECHOPEN.70602
G. Pîrcălăbioru, Ariana Picu, Laura Petcu, M. Popa, M. Chifiriuc
The most recent World Health Organization report revealed that the number of adults suffering from diabetes has almost quadrupled since 1980 to 422 million, thus drawing attention to the urgent need to step up prevention and treatment of this disease. This chronic ailment is often associated with serious complications such as increased risk of heart disease, stroke and kidney failure. In 2012 alone, diabetes lead to 1.5 million deaths. This dramatic rise is mainly due to the increased prevalence of type 2 diabetes and fac tors driving it include overweight and obesity. Novel studies in this area have advanced our understanding regarding the complex relationship between diet, gut microbiota and diabetes. Despite no clear microbiota signature is associated with diabetes, patients harbour a reduction of butyrate-producing species ( Faecalibacterium prausnitzii, Roseburia intestinalis) as well as an increase in opportunistic pathogens. Furthermore, the func tions of the gut microbiome (i.e., vitamin metabolism, transport of sugars, carbohydrate metabolism, short chain fatty acid (SCFA) synthesis, etc.) are also different in patients with type 2 diabetes, a fact that may significantly alter the course of disease. Diet is one of the most decisive factors that have an impact on the gut microbiome. Nutritional interventions using prebiotics (i.e., inulin-type fructans), polyphenols and arabinox - ylans have been employed for the treatment of diabetes. Besides the shifts produced by these dietary components in the microbiome composition, it is worth mentioning their impact on host physiology through modulation of gut peptide production and glucose metabolism. The information presented within this chapter summarizes the most recent advances in the study of the microbiome-diet-diabetes interplay and analyses how these novel findings can be used in order to establish new therapeutic approaches for those with diabetes. humans.
{"title":"The Intricate Relationship between Diabetes, Diet and the Gut Microbiota","authors":"G. Pîrcălăbioru, Ariana Picu, Laura Petcu, M. Popa, M. Chifiriuc","doi":"10.5772/INTECHOPEN.70602","DOIUrl":"https://doi.org/10.5772/INTECHOPEN.70602","url":null,"abstract":"The most recent World Health Organization report revealed that the number of adults suffering from diabetes has almost quadrupled since 1980 to 422 million, thus drawing attention to the urgent need to step up prevention and treatment of this disease. This chronic ailment is often associated with serious complications such as increased risk of heart disease, stroke and kidney failure. In 2012 alone, diabetes lead to 1.5 million deaths. This dramatic rise is mainly due to the increased prevalence of type 2 diabetes and fac tors driving it include overweight and obesity. Novel studies in this area have advanced our understanding regarding the complex relationship between diet, gut microbiota and diabetes. Despite no clear microbiota signature is associated with diabetes, patients harbour a reduction of butyrate-producing species ( Faecalibacterium prausnitzii, Roseburia intestinalis) as well as an increase in opportunistic pathogens. Furthermore, the func tions of the gut microbiome (i.e., vitamin metabolism, transport of sugars, carbohydrate metabolism, short chain fatty acid (SCFA) synthesis, etc.) are also different in patients with type 2 diabetes, a fact that may significantly alter the course of disease. Diet is one of the most decisive factors that have an impact on the gut microbiome. Nutritional interventions using prebiotics (i.e., inulin-type fructans), polyphenols and arabinox - ylans have been employed for the treatment of diabetes. Besides the shifts produced by these dietary components in the microbiome composition, it is worth mentioning their impact on host physiology through modulation of gut peptide production and glucose metabolism. The information presented within this chapter summarizes the most recent advances in the study of the microbiome-diet-diabetes interplay and analyses how these novel findings can be used in order to establish new therapeutic approaches for those with diabetes. humans.","PeriodicalId":272705,"journal":{"name":"Pathophysiology - Altered Physiological States","volume":"29 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2017-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"128668767","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2017-12-20DOI: 10.5772/INTECHOPEN.70598
J. Baumann
The formation of calcium (Ca) stones occurs in an initial phase by fixed growth on kidney calcifications consisting either of intratubular crystal accumulations protruding in renal calices (Randall’s plugs) or of interstitial hydroxyapatite deposits (Randall’s plaques) broken through the covering epithelial layers. Crystal aggregation (AGN) seems to be responsible for stone growth during crystalluria. This chapter reports on new aspects of the AGN of calcium oxalate being the most frequent stone compound and tries to explain why despite the widespread occurrence of kidney calcifications and crystallu - ria not everybody forms stones. Urinary crystals normally are protected from AGN by coats of urinary macromolecules (UMs) which by their identical electronegative charge create zones of electrostatic repulsion. At high urinary concentration or ionic strength respectively, these zones are compressed and can be bridged by self-aggregated UMs. Self-AGN occurs in concentrated urine by the adsorption of UMs on free surfaces like Randall’s plugs or plaques. High oxalate excretion and high urine concentration favor - ing intratubular crystal accumulation, breaking of epithelial layers on Randall’s plaques and self-AGN of UMs are most deleterious factors in Ca stone formation and have to be avoided by stone metaphylaxis.
{"title":"The Way from Renal Calcifications and Urinary Crystals to Kidney Stones: An Important Aspect in the Pathogenesis of Calcium Nephrolithiasis","authors":"J. Baumann","doi":"10.5772/INTECHOPEN.70598","DOIUrl":"https://doi.org/10.5772/INTECHOPEN.70598","url":null,"abstract":"The formation of calcium (Ca) stones occurs in an initial phase by fixed growth on kidney calcifications consisting either of intratubular crystal accumulations protruding in renal calices (Randall’s plugs) or of interstitial hydroxyapatite deposits (Randall’s plaques) broken through the covering epithelial layers. Crystal aggregation (AGN) seems to be responsible for stone growth during crystalluria. This chapter reports on new aspects of the AGN of calcium oxalate being the most frequent stone compound and tries to explain why despite the widespread occurrence of kidney calcifications and crystallu - ria not everybody forms stones. Urinary crystals normally are protected from AGN by coats of urinary macromolecules (UMs) which by their identical electronegative charge create zones of electrostatic repulsion. At high urinary concentration or ionic strength respectively, these zones are compressed and can be bridged by self-aggregated UMs. Self-AGN occurs in concentrated urine by the adsorption of UMs on free surfaces like Randall’s plugs or plaques. High oxalate excretion and high urine concentration favor - ing intratubular crystal accumulation, breaking of epithelial layers on Randall’s plaques and self-AGN of UMs are most deleterious factors in Ca stone formation and have to be avoided by stone metaphylaxis.","PeriodicalId":272705,"journal":{"name":"Pathophysiology - Altered Physiological States","volume":"52 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2017-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"127956020","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2017-12-20DOI: 10.5772/INTECHOPEN.70597
H. Orimo
Hypophosphatasia (HPP) is an inherited systemic bone disease caused by the deficiency of tissue-nonspecific alkaline phosphatase (TNAP). HPP is classified into six forms and the symptoms of HPP vary depending on the form. The pathophysiology of HPP is basi - cally due to a defect of bone mineralization. TNAP is encoded by the ALPL gene, and the TNAP protein expressed in bone, kidney, liver, and neuronal cells and is linked to the cell membrane via a glycosylphosphatidylinositol anchor. TNAP is an ectoenzyme hydrolyzing phosphate compound such as inorganic pyrophosphate. TNAP plays an important role in mineralization of hard tissues. Defect of mineralization process causes hypomineralization of hard tissues, which leads to rickets or osteomalacia and dental manifestations. In addition, hypomineralization of the ribs results in respiratory failure in the severe forms, which is the main cause of death. Inheritance of HPP is autosomal recessive, but autosomal dominant cases have been reported in the milder forms. To date, a total of 335 mutations in the ALPL gene have been reported, and mutation sites are scattered throughout the gene. Recent development of enzyme replacement therapy has opened up a new vista on the treatment of this previously untreatable
{"title":"Hypophosphatasia: A Systemic Skeletal Disorder Caused by Alkaline Phosphatase Deficiency","authors":"H. Orimo","doi":"10.5772/INTECHOPEN.70597","DOIUrl":"https://doi.org/10.5772/INTECHOPEN.70597","url":null,"abstract":"Hypophosphatasia (HPP) is an inherited systemic bone disease caused by the deficiency of tissue-nonspecific alkaline phosphatase (TNAP). HPP is classified into six forms and the symptoms of HPP vary depending on the form. The pathophysiology of HPP is basi - cally due to a defect of bone mineralization. TNAP is encoded by the ALPL gene, and the TNAP protein expressed in bone, kidney, liver, and neuronal cells and is linked to the cell membrane via a glycosylphosphatidylinositol anchor. TNAP is an ectoenzyme hydrolyzing phosphate compound such as inorganic pyrophosphate. TNAP plays an important role in mineralization of hard tissues. Defect of mineralization process causes hypomineralization of hard tissues, which leads to rickets or osteomalacia and dental manifestations. In addition, hypomineralization of the ribs results in respiratory failure in the severe forms, which is the main cause of death. Inheritance of HPP is autosomal recessive, but autosomal dominant cases have been reported in the milder forms. To date, a total of 335 mutations in the ALPL gene have been reported, and mutation sites are scattered throughout the gene. Recent development of enzyme replacement therapy has opened up a new vista on the treatment of this previously untreatable","PeriodicalId":272705,"journal":{"name":"Pathophysiology - Altered Physiological States","volume":"1 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2017-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"128087504","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2017-12-20DOI: 10.5772/INTECHOPEN.70601
Jesús E. Pérez-Ortega, J. Bargas
In Parkinson’s disease, there is a loss of dopaminergic innervation in the basal ganglia. The lack of dopamine produces substantial changes in neural plasticity and generates pathological activity patterns between basal ganglia nuclei. The treatment to relieve Parkinsonism is the administration of levodopa . However, the treatment produces dys -kinesia. The question to answer is how the interactions between neurons change in the brain microcircuits under these pathological conditions. Calcium imaging is a way to record the activity of dozens of neurons simultaneously with single-cell resolution in brain slices from rodents. We studied these interactions in the striatum, since it is the nucleus of the basal ganglia that receives the major dopaminergic innervation. We used network analysis, where each active neuron is taken as a node and its coactivity with other neurons is taken as its functional connections. The network obtained represents the functional connectome of the striatal microcircuit, which can be characterized with a small set of parameters taken from graph theory. We then quantify the pathological changes at the functional histological scale and the differences between normal and path ological conditions.
{"title":"Changes in the Striatal Network Connectivity in Parkinsonian and Dyskinetic Rodent Models","authors":"Jesús E. Pérez-Ortega, J. Bargas","doi":"10.5772/INTECHOPEN.70601","DOIUrl":"https://doi.org/10.5772/INTECHOPEN.70601","url":null,"abstract":"In Parkinson’s disease, there is a loss of dopaminergic innervation in the basal ganglia. The lack of dopamine produces substantial changes in neural plasticity and generates pathological activity patterns between basal ganglia nuclei. The treatment to relieve Parkinsonism is the administration of levodopa . However, the treatment produces dys -kinesia. The question to answer is how the interactions between neurons change in the brain microcircuits under these pathological conditions. Calcium imaging is a way to record the activity of dozens of neurons simultaneously with single-cell resolution in brain slices from rodents. We studied these interactions in the striatum, since it is the nucleus of the basal ganglia that receives the major dopaminergic innervation. We used network analysis, where each active neuron is taken as a node and its coactivity with other neurons is taken as its functional connections. The network obtained represents the functional connectome of the striatal microcircuit, which can be characterized with a small set of parameters taken from graph theory. We then quantify the pathological changes at the functional histological scale and the differences between normal and path ological conditions.","PeriodicalId":272705,"journal":{"name":"Pathophysiology - Altered Physiological States","volume":"97 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2017-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"125761833","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2017-12-20DOI: 10.5772/INTECHOPEN.70599
E. M. Kumaran
Breathing is the vital function based on the conductance of air through a system of branch- ing tubes that taper off and eventually connect to the alveoli. Nose act as an interface between atmospheric air and lower respiratory system, constitute the moist respiratory epithelium, which performs various vital physiological functions like filtering the inspired air, warming, and humidifying. Several anatomical and physiological factors are responsi - ble for the passage of airflow in two nostrils, which are asymmetric in nature. The inequal ity airflow passage in both the nostrils exists for a specific duration. This phenomenon of altering asymmetrical airflow from one nasal passage to the other is called ‘nasal cycle’. For every regular interval of time period, the swap of predominant nasal airflow between two nostrils determines the nasal patency. This cycle is controlled by the central regulator located at hypothalamus by coordinating the autonomic nervous system that comprises sympathetic and parasympathetic nerves that clog the nasal mucosa. The nostril decongest when the sympathetic nerves in one nostril become active. In this biorhythm, if the sym - pathetic nerves of one nostril drop, immediately the parasympathetic nerves take over, so that the other nostril congests. It is unclear why these cycles exist but the total nasal airway resistance is almost unchanged. There are a range of activities and reflexes, which can affect the nasal airway. This biorhythm is categorized under ultradian cycle since the mean dura - tion of nasal cycle is about two and a half hours. In this study, it observed changes in nasal airflow duration, pattern, and rhythm that correspond to various disease states in human.
{"title":"Alteration in Nasal Cycle Rhythm as an Index of the Diseased Condition","authors":"E. M. Kumaran","doi":"10.5772/INTECHOPEN.70599","DOIUrl":"https://doi.org/10.5772/INTECHOPEN.70599","url":null,"abstract":"Breathing is the vital function based on the conductance of air through a system of branch- ing tubes that taper off and eventually connect to the alveoli. Nose act as an interface between atmospheric air and lower respiratory system, constitute the moist respiratory epithelium, which performs various vital physiological functions like filtering the inspired air, warming, and humidifying. Several anatomical and physiological factors are responsi - ble for the passage of airflow in two nostrils, which are asymmetric in nature. The inequal ity airflow passage in both the nostrils exists for a specific duration. This phenomenon of altering asymmetrical airflow from one nasal passage to the other is called ‘nasal cycle’. For every regular interval of time period, the swap of predominant nasal airflow between two nostrils determines the nasal patency. This cycle is controlled by the central regulator located at hypothalamus by coordinating the autonomic nervous system that comprises sympathetic and parasympathetic nerves that clog the nasal mucosa. The nostril decongest when the sympathetic nerves in one nostril become active. In this biorhythm, if the sym - pathetic nerves of one nostril drop, immediately the parasympathetic nerves take over, so that the other nostril congests. It is unclear why these cycles exist but the total nasal airway resistance is almost unchanged. There are a range of activities and reflexes, which can affect the nasal airway. This biorhythm is categorized under ultradian cycle since the mean dura - tion of nasal cycle is about two and a half hours. In this study, it observed changes in nasal airflow duration, pattern, and rhythm that correspond to various disease states in human.","PeriodicalId":272705,"journal":{"name":"Pathophysiology - Altered Physiological States","volume":"746 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2017-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"126936276","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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