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Työmarkkinat -- See SVT. Työmarkkinat


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Työmies Kustannusyhtiö -- See Työmies Publishing Company


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Työmies Publishing Company -- History : Challenge accepted : a Finnish immigrant response to industrial America in Michigan's copper country / Gary Kaunonen  2010 1
Diabetes mellitus -- Typ 1 -- Jugend -- Aufsatzsammlung. : Diabetes in childhood and adolescence / volume editors, F. Chiarelli, K. Dahl-Jørgensen, W. Kiess  2005 1
Diabetes mellitus -- Typ 1 -- Kind -- Aufsatzsammlung. : Diabetes in childhood and adolescence / volume editors, F. Chiarelli, K. Dahl-Jørgensen, W. Kiess  2005 1
Jugend -- Diabetes mellitus -- Typ 1 -- Aufsatzsammlung. : Diabetes in childhood and adolescence / volume editors, F. Chiarelli, K. Dahl-Jørgensen, W. Kiess  2005 1
Kind -- Diabetes mellitus -- Typ 1 -- Aufsatzsammlung. : Diabetes in childhood and adolescence / volume editors, F. Chiarelli, K. Dahl-Jørgensen, W. Kiess  2005 1
 

Type 1 Craniosynostoses -- See Craniosynostoses


Premature closure of one or more CRANIAL SUTURES. It often results in plagiocephaly. Craniosynostoses that involve multiple sutures are sometimes associated with congenital syndromes such as ACROCEPHALOSYNDACTYLIA; and CRANIOFACIAL DYSOSTOSIS
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Type 1 Craniosynostosis -- See Craniosynostoses


Premature closure of one or more CRANIAL SUTURES. It often results in plagiocephaly. Craniosynostoses that involve multiple sutures are sometimes associated with congenital syndromes such as ACROCEPHALOSYNDACTYLIA; and CRANIOFACIAL DYSOSTOSIS
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Type 1 Cystatins -- See Cystatins


A homologous group of endogenous CYSTEINE PROTEINASE INHIBITORS. The cystatins inhibit most CYSTEINE ENDOPEPTIDASES such as PAPAIN, and other peptidases which have a sulfhydryl group at the active site
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  Type 1 diabetes -- 2 Related Subjects   2
 

Type 1 Diabetes Mellitus -- See Diabetes Mellitus, Type 1


A subtype of DIABETES MELLITUS that is characterized by INSULIN deficiency. It is manifested by the sudden onset of severe HYPERGLYCEMIA, rapid progression to DIABETIC KETOACIDOSIS, and DEATH unless treated with insulin. The disease may occur at any age, but is most common in childhood or adolescence
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Type 1 Gaucher Disease -- See Gaucher Disease


An autosomal recessive disorder caused by a deficiency of acid beta-glucosidase (GLUCOSYLCERAMIDASE) leading to intralysosomal accumulation of glycosylceramide mainly in cells of the MONONUCLEAR PHAGOCYTE SYSTEM. The characteristic Gaucher cells, glycosphingolipid-filled HISTIOCYTES, displace normal cells in BONE MARROW and visceral organs causing skeletal deterioration, hepatosplenomegaly, and organ dysfunction. There are several subtypes based on the presence and severity of neurological involvement
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Type 1 GM2 gangliosidosis -- See Tay-Sachs disease


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Type 1 Inositol 1,4,5-trisphosphate Receptor -- See Inositol 1,4,5-Trisphosphate Receptors


Intracellular receptors that bind to INOSITOL 1,4,5-TRISPHOSPHATE and play an important role in its intracellular signaling. Inositol 1,4,5-trisphosphate receptors are calcium channels that release CALCIUM in response to increased levels of inositol 1,4,5-trisphosphate in the CYTOPLASM
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Type 1 Neurofibromatosis -- See Neurofibromatosis 1


An autosomal dominant inherited disorder (with a high frequency of spontaneous mutations) that features developmental changes in the nervous system, muscles, bones, and skin, most notably in tissue derived from the embryonic NEURAL CREST. Multiple hyperpigmented skin lesions and subcutaneous tumors are the hallmark of this disease. Peripheral and central nervous system neoplasms occur frequently, especially OPTIC NERVE GLIOMA and NEUROFIBROSARCOMA. NF1 is caused by mutations which inactivate the NF1 gene (GENES, NEUROFIBROMATOSIS 1) on chromosome 17q. The incidence of learning disabilities is also elevated in this condition. (From Adams et al., Principles of Neurology, 6th ed, pp1014-18) There is overlap of clinical features with NOONAN SYNDROME in a syndrome called neurofibromatosis-Noonan syndrome. Both the PTPN11 and NF1 gene products are involved in the SIGNAL TRANSDUCTION pathway of Ras (RAS PROTEINS)
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Type 1 Spinocerebellar Ataxia -- See Spinocerebellar Ataxias


A group of dominantly inherited, predominately late-onset, cerebellar ataxias which have been divided into multiple subtypes based on clinical features and genetic mapping. Progressive ataxia is a central feature of these conditions, and in certain subtypes POLYNEUROPATHY; DYSARTHRIA; visual loss; and other disorders may develop. (From Joynt, Clinical Neurology, 1997, Ch65, pp 12-17; J Neuropathol Exp Neurol 1998 Jun;57(6):531-43)
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Type 2 Cystatins -- See Cystatins


A homologous group of endogenous CYSTEINE PROTEINASE INHIBITORS. The cystatins inhibit most CYSTEINE ENDOPEPTIDASES such as PAPAIN, and other peptidases which have a sulfhydryl group at the active site
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  Type 2 Diabetes -- 2 Related Subjects   2
Type 2 diabetes.   16
Type 2 diabetes -- Australia   3
Type 2 diabetes -- Chemotherapy   2
Type 2 diabetes -- Complications : Type-2 diabetic nephropathy in Japan : from bench to bedside / volume editor, Yasuhiko Tomino  2001 1
Type 2 diabetes -- Complications -- Pathophysiology : Molecular and cell biology of type 2 diabetes and its complications / volume editors, F. Belfiore [and others]  1998 1
Type 2 diabetes -- Congresses : Metabolic issues of clinical nutrition / editors, Simon P. Allison, Vay Liang W. Go  2004 1
 

Type 2 Diabetes Mellitus -- See Diabetes Mellitus, Type 2


A subclass of DIABETES MELLITUS that is not INSULIN-responsive or dependent (NIDDM). It is characterized initially by INSULIN RESISTANCE and HYPERINSULINEMIA; and eventually by GLUCOSE INTOLERANCE; HYPERGLYCEMIA; and overt diabetes. Type II diabetes mellitus is no longer considered a disease exclusively found in adults. Patients seldom develop KETOSIS but often exhibit OBESITY
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Type 2 diabetes -- Molecular aspects : Molecular and cell biology of type 2 diabetes and its complications / volume editors, F. Belfiore [and others]  1998 1
Type 2 diabetes -- Molecular aspects -- Complications : Molecular and cell biology of type 2 diabetes and its complications / volume editors, F. Belfiore [and others]  1998 1
Type 2 diabetes -- Molecular aspects -- Congresses : Molecular pathogenesis of MODYs / American Diabetes Association: Symposium, Scottsdale, AZ, USA, November 6-8, 1998 ; volume editors, F.M. Matschinsky, M.A. Magnuson  2000 1
Type 2 diabetes -- Pathophysiology : Molecular and cell biology of type 2 diabetes and its complications / volume editors, F. Belfiore [and others]  1998 1
Type 2 diabetes -- Prevention : Prevention of type 2 diabetes : from science to therapy / Derek LeRoith, editor  2012 1
Type 2 diabetes -- Treatment   2
 

Type 2 Gaucher Disease -- See Gaucher Disease


An autosomal recessive disorder caused by a deficiency of acid beta-glucosidase (GLUCOSYLCERAMIDASE) leading to intralysosomal accumulation of glycosylceramide mainly in cells of the MONONUCLEAR PHAGOCYTE SYSTEM. The characteristic Gaucher cells, glycosphingolipid-filled HISTIOCYTES, displace normal cells in BONE MARROW and visceral organs causing skeletal deterioration, hepatosplenomegaly, and organ dysfunction. There are several subtypes based on the presence and severity of neurological involvement
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Type 2 Histiocytoses -- See Histiocytosis, Langerhans-Cell


A group of disorders resulting from the abnormal proliferation of and tissue infiltration by LANGERHANS CELLS which can be detected by their characteristic Birbeck granules (X bodies), or by monoclonal antibody staining for their surface CD1 ANTIGENS. Langerhans-cell granulomatosis can involve a single organ, or can be a systemic disorder
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Type 2 Histiocytosis -- See Histiocytosis, Langerhans-Cell


A group of disorders resulting from the abnormal proliferation of and tissue infiltration by LANGERHANS CELLS which can be detected by their characteristic Birbeck granules (X bodies), or by monoclonal antibody staining for their surface CD1 ANTIGENS. Langerhans-cell granulomatosis can involve a single organ, or can be a systemic disorder
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Type 2 Spinocerebellar Ataxia -- See Spinocerebellar Ataxias


A group of dominantly inherited, predominately late-onset, cerebellar ataxias which have been divided into multiple subtypes based on clinical features and genetic mapping. Progressive ataxia is a central feature of these conditions, and in certain subtypes POLYNEUROPATHY; DYSARTHRIA; visual loss; and other disorders may develop. (From Joynt, Clinical Neurology, 1997, Ch65, pp 12-17; J Neuropathol Exp Neurol 1998 Jun;57(6):531-43)
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Type 3 Cystatins -- See Cystatins


A homologous group of endogenous CYSTEINE PROTEINASE INHIBITORS. The cystatins inhibit most CYSTEINE ENDOPEPTIDASES such as PAPAIN, and other peptidases which have a sulfhydryl group at the active site
  1
 

Type 3 Gaucher Disease -- See Gaucher Disease


An autosomal recessive disorder caused by a deficiency of acid beta-glucosidase (GLUCOSYLCERAMIDASE) leading to intralysosomal accumulation of glycosylceramide mainly in cells of the MONONUCLEAR PHAGOCYTE SYSTEM. The characteristic Gaucher cells, glycosphingolipid-filled HISTIOCYTES, displace normal cells in BONE MARROW and visceral organs causing skeletal deterioration, hepatosplenomegaly, and organ dysfunction. There are several subtypes based on the presence and severity of neurological involvement
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Type 3 Hereditary Sensory Neuropathy, Dominant -- See Dysautonomia, Familial


An autosomal disorder of the peripheral and autonomic nervous systems limited to individuals of Ashkenazic Jewish descent. Clinical manifestations are present at birth and include diminished lacrimation, defective thermoregulation, orthostatic hypotension (HYPOTENSION, ORTHOSTATIC), fixed pupils, excessive SWEATING, loss of pain and temperature sensation, and absent reflexes. Pathologic features include reduced numbers of small diameter peripheral nerve fibers and autonomic ganglion neurons. (From Adams et al., Principles of Neurology, 6th ed, p1348; Nat Genet 1993;4(2):160-4)
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Type 3 Inositol 1,4,5-trisphosphate Receptor -- See Inositol 1,4,5-Trisphosphate Receptors


Intracellular receptors that bind to INOSITOL 1,4,5-TRISPHOSPHATE and play an important role in its intracellular signaling. Inositol 1,4,5-trisphosphate receptors are calcium channels that release CALCIUM in response to increased levels of inositol 1,4,5-trisphosphate in the CYTOPLASM
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Type 3, Neurofibromatosis -- See Neurofibromatoses


A group of disorders characterized by an autosomal dominant pattern of inheritance with high rates of spontaneous mutation and multiple neurofibromas or neurilemmomas. NEUROFIBROMATOSIS 1 (generalized neurofibromatosis) accounts for approximately 95% of cases, although multiple additional subtypes (e.g., NEUROFIBROMATOSIS 2, neurofibromatosis 3, etc.) have been described. (From Neurochirurgie 1998 Nov;44(4):267-72)
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Type 4 Spinocerebellar Ataxia -- See Spinocerebellar Ataxias


A group of dominantly inherited, predominately late-onset, cerebellar ataxias which have been divided into multiple subtypes based on clinical features and genetic mapping. Progressive ataxia is a central feature of these conditions, and in certain subtypes POLYNEUROPATHY; DYSARTHRIA; visual loss; and other disorders may develop. (From Joynt, Clinical Neurology, 1997, Ch65, pp 12-17; J Neuropathol Exp Neurol 1998 Jun;57(6):531-43)
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Type 5 Spinocerebellar Ataxia -- See Spinocerebellar Ataxias


A group of dominantly inherited, predominately late-onset, cerebellar ataxias which have been divided into multiple subtypes based on clinical features and genetic mapping. Progressive ataxia is a central feature of these conditions, and in certain subtypes POLYNEUROPATHY; DYSARTHRIA; visual loss; and other disorders may develop. (From Joynt, Clinical Neurology, 1997, Ch65, pp 12-17; J Neuropathol Exp Neurol 1998 Jun;57(6):531-43)
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Type 6 Spinocerebellar Ataxia -- See Spinocerebellar Ataxias


A group of dominantly inherited, predominately late-onset, cerebellar ataxias which have been divided into multiple subtypes based on clinical features and genetic mapping. Progressive ataxia is a central feature of these conditions, and in certain subtypes POLYNEUROPATHY; DYSARTHRIA; visual loss; and other disorders may develop. (From Joynt, Clinical Neurology, 1997, Ch65, pp 12-17; J Neuropathol Exp Neurol 1998 Jun;57(6):531-43)
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Type 7 Spinocerebellar Ataxia -- See Spinocerebellar Ataxias


A group of dominantly inherited, predominately late-onset, cerebellar ataxias which have been divided into multiple subtypes based on clinical features and genetic mapping. Progressive ataxia is a central feature of these conditions, and in certain subtypes POLYNEUROPATHY; DYSARTHRIA; visual loss; and other disorders may develop. (From Joynt, Clinical Neurology, 1997, Ch65, pp 12-17; J Neuropathol Exp Neurol 1998 Jun;57(6):531-43)
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  Type A behavior -- 2 Related Subjects   2
Type A behavior.   14
Type A behavior -- Congresses. : Type A behavior pattern : research, theory, and intervention / editors, B. Kent Houston and C.R. Snyder  1988 1
Type A behavior in children -- United States. : Raising your type A child : how to help your child make the most of an achievement-oriented personality / Steven Shelov and John Kelly  1991 1
 

Type A Monoamine Oxidase -- See Monoamine Oxidase


An enzyme that catalyzes the oxidative deamination of naturally occurring monoamines. It is a flavin-containing enzyme that is localized in mitochondrial membranes, whether in nerve terminals, the liver, or other organs. Monoamine oxidase is important in regulating the metabolic degradation of catecholamines and serotonin in neural or target tissues. Hepatic monoamine oxidase has a crucial defensive role in inactivating circulating monoamines or those, such as tyramine, that originate in the gut and are absorbed into the portal circulation. (From Goodman and Gilman's, The Pharmacological Basis of Therapeutics, 8th ed, p415) EC 1.4.3.4
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