Pub Date : 2020-04-30DOI: 10.31435/rsglobal_ws/30042020/7018
T. Nagai, Noriyuki Ogawa, O. Ishizuka
Overactive bladder (OAB) is a storage symptom complex that includes urinary urgency with or without urge incontinence, urinary frequency and nocturia. OAB is common symp- tom complex and its morbidity is high and increased with age. Although many factors cause OAB, we can classify them as neurogenic or non-neurogenic. To diagnose OAB, we need to ask a patient about his condition using Overactive Bladder Symptom Score (OABSS), exam- ine physical findings and urinalysis. And we also need to exclude other urinary tract diseases that make bladder irritation. Pharmacotherapy and behavior therapy are useful for improving OAB symptoms. Anticholinergic agents are utilized for OAB treatment but we need to pay attention to the adverse effects.
{"title":"Overactive bladder.","authors":"T. Nagai, Noriyuki Ogawa, O. Ishizuka","doi":"10.31435/rsglobal_ws/30042020/7018","DOIUrl":"https://doi.org/10.31435/rsglobal_ws/30042020/7018","url":null,"abstract":"Overactive bladder (OAB) is a storage symptom complex that includes urinary urgency with or without urge incontinence, urinary frequency and nocturia. OAB is common symp- tom complex and its morbidity is high and increased with age. Although many factors cause OAB, we can classify them as neurogenic or non-neurogenic. To diagnose OAB, we need to ask a patient about his condition using Overactive Bladder Symptom Score (OABSS), exam- ine physical findings and urinalysis. And we also need to exclude other urinary tract diseases that make bladder irritation. Pharmacotherapy and behavior therapy are useful for improving OAB symptoms. Anticholinergic agents are utilized for OAB treatment but we need to pay attention to the adverse effects.","PeriodicalId":19307,"journal":{"name":"Nihon rinsho. Japanese journal of clinical medicine","volume":"18 1","pages":"573-578"},"PeriodicalIF":0.0,"publicationDate":"2020-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76937275","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}
Recently, unstable angina, acute myocardial infarction and sudden cardiac death have often been put together under the name 'acute coronary syndromes', because almost all of these conditions have been shown to be caused by thrombotic occlusion of a coronary artery following atherosclerotic plaque disruption. Acute coronary syndromes occur more frequently in the coronary arteries with no significant organic stenosis than in those with a higher degree of stenosis. A plaque prone to disruption has a thin fibrous cap, a large lipid core and increased infiltration of macrophages and T lymphocytes. The elimination or control of risk factors for atherosclerosis such as dyslipidemia, hypertension, smoking, diabetes mellitus, obesity and lack of exercise is essential for the prevention of acute coronary syndromes.
{"title":"[Acute coronary syndromes].","authors":"Hirofumi Yasue","doi":"10.1201/b14282-73","DOIUrl":"https://doi.org/10.1201/b14282-73","url":null,"abstract":"Recently, unstable angina, acute myocardial infarction and sudden cardiac death have often been put together under the name 'acute coronary syndromes', because almost all of these conditions have been shown to be caused by thrombotic occlusion of a coronary artery following atherosclerotic plaque disruption. Acute coronary syndromes occur more frequently in the coronary arteries with no significant organic stenosis than in those with a higher degree of stenosis. A plaque prone to disruption has a thin fibrous cap, a large lipid core and increased infiltration of macrophages and T lymphocytes. The elimination or control of risk factors for atherosclerosis such as dyslipidemia, hypertension, smoking, diabetes mellitus, obesity and lack of exercise is essential for the prevention of acute coronary syndromes.","PeriodicalId":19307,"journal":{"name":"Nihon rinsho. Japanese journal of clinical medicine","volume":"50 1","pages":"801-7"},"PeriodicalIF":0.0,"publicationDate":"2020-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90309817","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}
S. Kimata, S. Takahashi, H. Noda, N. Shibata, Y. Miyazaki, K. Hirosawa
{"title":"[Cardiogenic shock].","authors":"S. Kimata, S. Takahashi, H. Noda, N. Shibata, Y. Miyazaki, K. Hirosawa","doi":"10.1201/b14282-137","DOIUrl":"https://doi.org/10.1201/b14282-137","url":null,"abstract":"","PeriodicalId":19307,"journal":{"name":"Nihon rinsho. Japanese journal of clinical medicine","volume":"17 1","pages":"1937-45"},"PeriodicalIF":0.0,"publicationDate":"2020-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82552194","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}
Inherited or familial Creutzfeldt-Jakob disease (fCJD) is a very rare form of genetic prion disease (see this term) characterized by typical CJD features (rapidly progressive dementia, personality/behavioral changes, psychiatric disorders, myoclonus, and ataxia) with a genetic cause and sometimes a family history of dementia.
{"title":"[Inherited Creutzfeldt-Jakob disease].","authors":"H. Toda, H. Kishida, Y. Kuroiwa","doi":"10.32388/1c8w9w","DOIUrl":"https://doi.org/10.32388/1c8w9w","url":null,"abstract":"Inherited or familial Creutzfeldt-Jakob disease (fCJD) is a very rare form of genetic prion disease (see this term) characterized by typical CJD features (rapidly progressive dementia, personality/behavioral changes, psychiatric disorders, myoclonus, and ataxia) with a genetic cause and sometimes a family history of dementia.","PeriodicalId":19307,"journal":{"name":"Nihon rinsho. Japanese journal of clinical medicine","volume":"11 1","pages":"261-5"},"PeriodicalIF":0.0,"publicationDate":"2020-02-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88676390","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}
Xeroderma pigmentosum (XP), an autosomal recessive disorder, is characterized by extreme sensitivity to sun exposure, a high incidence of skin cancer and frequent neurological abnormalities. Cells from XP patients of seven complementation groups (A-G) have defects in the nucleotide excision repair of UV damage, whereas the defect of another type, the XP variant, is not yet known. Recent discoveries of causative genes of XP have uncovered the molecular mechanisms of nucleotide excision repair. The analysis of gene mutation in XPA gene made a diagnosis of patients and carriers quicker and easier. Further, a relationship between the type of XPA gene mutation and clinical severity has also been uncovered. By analysing skin cancers developed on XP patients, the representative of UV-induced skin cancers, the molecular bases of UV skin carcinogenesis have also been rapidly discovered.
{"title":"[Xeroderma pigmentosum].","authors":"M. Ueda, M. Ichihashi","doi":"10.32388/0dmdr1","DOIUrl":"https://doi.org/10.32388/0dmdr1","url":null,"abstract":"Xeroderma pigmentosum (XP), an autosomal recessive disorder, is characterized by extreme sensitivity to sun exposure, a high incidence of skin cancer and frequent neurological abnormalities. Cells from XP patients of seven complementation groups (A-G) have defects in the nucleotide excision repair of UV damage, whereas the defect of another type, the XP variant, is not yet known. Recent discoveries of causative genes of XP have uncovered the molecular mechanisms of nucleotide excision repair. The analysis of gene mutation in XPA gene made a diagnosis of patients and carriers quicker and easier. Further, a relationship between the type of XPA gene mutation and clinical severity has also been uncovered. By analysing skin cancers developed on XP patients, the representative of UV-induced skin cancers, the molecular bases of UV skin carcinogenesis have also been rapidly discovered.","PeriodicalId":19307,"journal":{"name":"Nihon rinsho. Japanese journal of clinical medicine","volume":"1 1","pages":"2815-20"},"PeriodicalIF":0.0,"publicationDate":"2020-02-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90100034","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}
The present paper reviews the recent progress of analysis of nephrogenic diabetes insipidus (NDI). NDI has been considered as a X-linked recessive inheritance. Arginine vasopressin (AVP) V2 receptors were cloned and characterized its structural and functional properties. The gene of AVP V2 receptors is localized in X chromosome q27-28. The mutations of AVP V2 receptor gene have been clarified in patients with NDI. They accounted for approximately 30 kinds of mutations, including deletion and insertion of nucleotide, and point mutation of nucleotides. The mutant receptors have an inability to bind to AVP ligand or activate adenylate cyclase, a post-receptor signal transduction. Also, there are patients with NDI, who were considered as an autosomal dominant or autosomal recessive inheritance. Water channel aquaporin of collecting duct (AQP-2) was cloned and characterized, which is localized in chromosome 12q13. Recent studies elucidated the mutations of AQP-2 gene in several families with autosomal recessive NDI. Also, the mutations of AQP-2 gene were found in patients with NDI, who were thought as autosomal dominant inheritance. Therefore, both mutations of AVP V2 receptors and AQP-2 are involved in pathogenesis of NDI.
{"title":"[Nephrogenic diabetes insipidus].","authors":"S. Ishikawa","doi":"10.32388/cy6nny","DOIUrl":"https://doi.org/10.32388/cy6nny","url":null,"abstract":"The present paper reviews the recent progress of analysis of nephrogenic diabetes insipidus (NDI). NDI has been considered as a X-linked recessive inheritance. Arginine vasopressin (AVP) V2 receptors were cloned and characterized its structural and functional properties. The gene of AVP V2 receptors is localized in X chromosome q27-28. The mutations of AVP V2 receptor gene have been clarified in patients with NDI. They accounted for approximately 30 kinds of mutations, including deletion and insertion of nucleotide, and point mutation of nucleotides. The mutant receptors have an inability to bind to AVP ligand or activate adenylate cyclase, a post-receptor signal transduction. Also, there are patients with NDI, who were considered as an autosomal dominant or autosomal recessive inheritance. Water channel aquaporin of collecting duct (AQP-2) was cloned and characterized, which is localized in chromosome 12q13. Recent studies elucidated the mutations of AQP-2 gene in several families with autosomal recessive NDI. Also, the mutations of AQP-2 gene were found in patients with NDI, who were thought as autosomal dominant inheritance. Therefore, both mutations of AVP V2 receptors and AQP-2 are involved in pathogenesis of NDI.","PeriodicalId":19307,"journal":{"name":"Nihon rinsho. Japanese journal of clinical medicine","volume":"53 1","pages":"819-24"},"PeriodicalIF":0.0,"publicationDate":"2020-02-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"73364737","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}
What is the thyroid gland? The thyroid is a butterfly-shaped gland in the front of the neck. The cells in a normal, healthy thyroid send out hormones, thyroxine (T4) and triiodothyronine (T3). The brain sends a message to the thyroid (thyroid stimulating hormone, TSH) that controls production of these two hormones. The thyroid sends them into the bloodstream. The blood carries these hormones everywhere in your child’s body.
{"title":"[Congenital hypothyroidism].","authors":"K. Onigata","doi":"10.32388/82bg19","DOIUrl":"https://doi.org/10.32388/82bg19","url":null,"abstract":"What is the thyroid gland? The thyroid is a butterfly-shaped gland in the front of the neck. The cells in a normal, healthy thyroid send out hormones, thyroxine (T4) and triiodothyronine (T3). The brain sends a message to the thyroid (thyroid stimulating hormone, TSH) that controls production of these two hormones. The thyroid sends them into the bloodstream. The blood carries these hormones everywhere in your child’s body.","PeriodicalId":19307,"journal":{"name":"Nihon rinsho. Japanese journal of clinical medicine","volume":"1 1","pages":"105-10"},"PeriodicalIF":0.0,"publicationDate":"2020-02-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82396261","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}
{"title":"[MODY].","authors":"Akihiko Sasaki, Y. Horikawa, Junichi Takeda","doi":"10.32388/qdq99y","DOIUrl":"https://doi.org/10.32388/qdq99y","url":null,"abstract":"","PeriodicalId":19307,"journal":{"name":"Nihon rinsho. Japanese journal of clinical medicine","volume":"1 1","pages":"54-8"},"PeriodicalIF":0.0,"publicationDate":"2020-02-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79919589","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}
Adult-onset Huntington disease, the most common form of this disorder, usually appears in a person's thirties or forties. Early signs and symptoms can include irritability, depression, small involuntary movements, poor coordination, and trouble learning new information or making decisions. Many people with Huntington disease develop involuntary jerking or twitching movements known as chorea. As the disease progresses, these movements become more pronounced. Affected individuals may have trouble walking, speaking, and swallowing. People with this disorder also experience changes in personality and a decline in thinking and reasoning abilities. Individuals with the adult-onset form of Huntington disease usually live about 15 to 20 years after signs and symptoms begin.
{"title":"[Huntington disease].","authors":"S. Kwak","doi":"10.32388/ecchjl","DOIUrl":"https://doi.org/10.32388/ecchjl","url":null,"abstract":"Adult-onset Huntington disease, the most common form of this disorder, usually appears in a person's thirties or forties. Early signs and symptoms can include irritability, depression, small involuntary movements, poor coordination, and trouble learning new information or making decisions. Many people with Huntington disease develop involuntary jerking or twitching movements known as chorea. As the disease progresses, these movements become more pronounced. Affected individuals may have trouble walking, speaking, and swallowing. People with this disorder also experience changes in personality and a decline in thinking and reasoning abilities. Individuals with the adult-onset form of Huntington disease usually live about 15 to 20 years after signs and symptoms begin.","PeriodicalId":19307,"journal":{"name":"Nihon rinsho. Japanese journal of clinical medicine","volume":"34 1","pages":"417-21"},"PeriodicalIF":0.0,"publicationDate":"2020-02-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72865942","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}
Wolfram syndrome is a condition that affects many of the body's systems. The hallmark features of Wolfram syndrome are high blood sugar levels resulting from a shortage of the hormone insulin (diabetes mellitus) and progressive vision loss due to degeneration of the nerves that carry information from the eyes to the brain (optic atrophy). People with Wolfram syndrome often also have pituitary gland dysfunction that results in the excretion of excessive amounts of urine (diabetes insipidus), hearing loss caused by changes in the inner ear (sensorineural deafness), urinary tract problems, reduced amounts of the sex hormone testosterone in males (hypogonadism), or neurological or psychiatric disorders.
{"title":"[Wolfram syndrome].","authors":"Y. Oka","doi":"10.32388/s04l5q","DOIUrl":"https://doi.org/10.32388/s04l5q","url":null,"abstract":"Wolfram syndrome is a condition that affects many of the body's systems. The hallmark features of Wolfram syndrome are high blood sugar levels resulting from a shortage of the hormone insulin (diabetes mellitus) and progressive vision loss due to degeneration of the nerves that carry information from the eyes to the brain (optic atrophy). People with Wolfram syndrome often also have pituitary gland dysfunction that results in the excretion of excessive amounts of urine (diabetes insipidus), hearing loss caused by changes in the inner ear (sensorineural deafness), urinary tract problems, reduced amounts of the sex hormone testosterone in males (hypogonadism), or neurological or psychiatric disorders.","PeriodicalId":19307,"journal":{"name":"Nihon rinsho. Japanese journal of clinical medicine","volume":"47 1","pages":"138-42"},"PeriodicalIF":0.0,"publicationDate":"2020-02-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75922370","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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