{"title":"[Hemorrhoid].","authors":"Y. Tsuji, M. Takano, I. Kubota","doi":"10.32388/kzj06w","DOIUrl":"https://doi.org/10.32388/kzj06w","url":null,"abstract":"","PeriodicalId":79374,"journal":{"name":"Ryoikibetsu shokogun shirizu","volume":"109 1","pages":"855-7"},"PeriodicalIF":0.0,"publicationDate":"2020-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80621942","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":"[Biclonal gammopathy].","authors":"N. Maseki","doi":"10.32388/96udhi","DOIUrl":"https://doi.org/10.32388/96udhi","url":null,"abstract":"A primary disturbance in immunoglobulin synthesis characterized by the presence of two distinct monoclonal immunoglobulins in the serum or urine.","PeriodicalId":79374,"journal":{"name":"Ryoikibetsu shokogun shirizu","volume":"1 1","pages":"540-2"},"PeriodicalIF":0.0,"publicationDate":"2020-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82977945","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":"[Argininemia].","authors":"T. Matsuura","doi":"10.1201/b13564-32","DOIUrl":"https://doi.org/10.1201/b13564-32","url":null,"abstract":"The clinical features of argininemia in two cousins included hyperactivity, spasticity, ataxia, retardation, and repeated attacks of hyperammonemia. Study of a large kindred suggests that arginase-deficiency is transmitted as a Mendelian recessive. Treatment with an essential amino acid mixture with the total nitrogen intake limited to the requirement, controlled the hyperammonemia, reduced the plasma arginine level, and permitted a marked clinical improvement. There has been a significant increase in intelligence levels; the previously retarded children are now approaching the normal range of function.","PeriodicalId":79374,"journal":{"name":"Ryoikibetsu shokogun shirizu","volume":"297 1","pages":"219-20"},"PeriodicalIF":0.0,"publicationDate":"2020-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79627639","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":"[Neurofibromatosis type 1].","authors":"H. Naito","doi":"10.32388/8eauv3","DOIUrl":"https://doi.org/10.32388/8eauv3","url":null,"abstract":"Most adults with neurofibromatosis type 1 develop neurofibromas, which are noncancerous (benign) tumors that are usually located on or just under the skin. These tumors may also occur in nerves near the spinal cord or along nerves elsewhere in the body. Some people with neurofibromatosis type 1 develop cancerous tumors that grow along nerves. These tumors, which usually develop in adolescence or adulthood, are called malignant peripheral nerve sheath tumors. People with neurofibromatosis type 1 also have an increased risk of developing other cancers, including brain tumors and cancer of blood-forming tissue (leukemia).","PeriodicalId":79374,"journal":{"name":"Ryoikibetsu shokogun shirizu","volume":"21 1","pages":"488-91"},"PeriodicalIF":0.0,"publicationDate":"2020-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84108781","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":"[Histiocytic necrotizing lymphadenitis].","authors":"M. Abe","doi":"10.32388/0almhl","DOIUrl":"https://doi.org/10.32388/0almhl","url":null,"abstract":"Kikuchi-Fujimoto disease (histiocytic necrotizing lymphadenitis) was described in 1972 as a process which tends to heal spontaneously, characterized by cervical adenopathy, fever, and leukopenia. We present the case of a female patient, age 43 years, who presented manifestations of parotitis, cervical adenopathies, fever, and leukopenia. Observations were made by ultrasound, tomography, magnetic resonance, and positron emission tomography combined with simple tomography. A biopsy of lymph nodes in the neck was taken. Conclusion: diagnosis is always histopathological and with immunohistochemical studies.","PeriodicalId":79374,"journal":{"name":"Ryoikibetsu shokogun shirizu","volume":"16 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2020-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75508844","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":"[Mediastinal yolk sac tumor].","authors":"K. Kawakami, K. Kuno","doi":"10.32388/1op1on","DOIUrl":"https://doi.org/10.32388/1op1on","url":null,"abstract":"An extragonadal non-seminomatous malignant germ cell tumor that arises from the mediastinum. It is characterized by the presence of small pale cells with small amount of cytoplasm and round to oval nuclei with small nucleoli forming a variety of patterns, including microcystic, macrocystic, pseudopapillary, myxomatous, hepatoid, polyvesicular vitelline, and solid. It manifests with respiratory distress, thoracic pain, fever, and superior vena cava syndrome.","PeriodicalId":79374,"journal":{"name":"Ryoikibetsu shokogun shirizu","volume":"103 1","pages":"429-31"},"PeriodicalIF":0.0,"publicationDate":"2020-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"91038466","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":"[Alport syndrome].","authors":"R. Momota, T. Oohashi","doi":"10.32388/v26250","DOIUrl":"https://doi.org/10.32388/v26250","url":null,"abstract":"People with Alport syndrome experience progressive loss of kidney function. Almost all affected individuals have blood in their urine (hematuria), which indicates abnormal functioning of the kidneys. Many people with Alport syndrome also develop high levels of protein in their urine (proteinuria). The kidneys become less able to function as this condition progresses, resulting in end-stage renal disease (ESRD).","PeriodicalId":79374,"journal":{"name":"Ryoikibetsu shokogun shirizu","volume":"57 1","pages":"522-5"},"PeriodicalIF":0.0,"publicationDate":"2020-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89352659","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":"[Myelitis].","authors":"H. Shoji","doi":"10.32388/35casr","DOIUrl":"https://doi.org/10.32388/35casr","url":null,"abstract":"Acute transverse myelitis (ATM) with moderate symptomatology and smaller multiple magnetic resonance imaging lesions is often caused by multiple sclerosis. Severe ATM with extensive magnetic resonance imaging lesions with or without associated meningitis often has a viral cause, particularly in the younger age groups, whereas vascular disorders may prevail among older patients. Previously, one had to rely on indirect evidence such as viral serology or viral identification in throat washings to confirm a diagnosis of myelitis. Thus, mycoplasma myelitis may occur coincident with a mycoplasma pneumonia. Viral myelitis is now often diagnosed by specific polymerase chain reaction of the cerebrospinal fluid, for echovirus, Coxsackie virus, mumps virus, herpes simplex virus or varicella-zoster virus, but an autoimmune component may still be important. An anterior horn syndrome may be produced by the tick-borne encephalomyelitis virus. Severe ATM may also be a postinfectious or postvaccinal disorder [i.e. a partial acute disseminated encephalomyelitis (ADEM)]. Neuromyelitis optica, a combination of severe myelitis and optic neuritis, is often a manifestation of ADEM or systemic lupus erythematosus. Many of these disorders are potentially treatable with specific antiviral agents or immunosuppression. 'Idiopathic' ATM is probably a consequence of inadequate examination and follow up. The differential diagnoses-viral myelitis, multiple sclerosis, ADEM, neuromyelitis optica, spinal arteriovenous malformation and arteritis-should be considered and are usually identified by a rapid diagnostic work-up, leaving few ATM cases undiagnosed.","PeriodicalId":79374,"journal":{"name":"Ryoikibetsu shokogun shirizu","volume":"30 1","pages":"46-8"},"PeriodicalIF":0.0,"publicationDate":"2020-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75763220","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":"[Turner syndrome].","authors":"T. Ogata","doi":"10.32388/qqnt9w","DOIUrl":"https://doi.org/10.32388/qqnt9w","url":null,"abstract":"Turner syndrome is a chromosomal condition that affects development in females. The most common feature of Turner syndrome is short stature, which becomes evident by about age 5. An early loss of ovarian function (ovarian hypofunction or premature ovarian failure) is also very common. The ovaries develop normally at first, but egg cells (oocytes) usually die prematurely and most ovarian tissue degenerates before birth. Many affected girls do not undergo puberty unless they receive hormone therapy, and most are unable to conceive (infertile). A small percentage of females with Turner syndrome retain normal ovarian function through young adulthood.","PeriodicalId":79374,"journal":{"name":"Ryoikibetsu shokogun shirizu","volume":"13 1","pages":"767-70"},"PeriodicalIF":0.0,"publicationDate":"2020-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78340102","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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