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Type and type-founding -- Great Britain -- History -- 20th century : The skilled compositor, 1850-1914 : an aristocrat among working men / Patrick Duffy  2017 1
Type and type-founding -- Handbooks, manuals, etc.   2
Type and type-founding -- Historiography.   2
Type and type-founding -- History.   6
Type and type-founding -- History -- 20th century.   6
Type and type-founding in art -- Pictorial works. : Type player 2 : type as experiment, type as image / [chief editor, Wang Shaoqiang]  2011 1
Type and type-founding -- Italy -- Parma -- History -- 19th century. : Manual of typography = Manuale tipografico : 1818 / Giambattista Bodoni ; with an essay on Bodoni's Typography in Historical Perspective by Stephan Fussel  2016 1
 

Type and type-founding Music type -- See Music printing


  1
 

Type and type-founding Old English type -- See Gothic type


  1
Type and type-founding -- Periodicals. : "Emigre" No. 70 : the Look Back Issue : selections from "Emigre" Magazine #1 - #69, 1984-2009 / [designed and edited by Rudy Vanderlans]  2009 1
Type and type-founding -- Pictorial works.   2
Type and type-founding -- Problems, exercises, etc. : Lessons in typography : must-know typographic principles presented through lessons, exercises, and examples / Jim Krause  2016 1
 

Type and type-founding Script type -- See Script type


  1
Type and type-founding -- Specimens.   9
 

Type and type-founding Wood type -- See Wood types (Printing)


  1
 

Type B encephalitis -- See Japanese B encephalitis


  1
 

Type B 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
  1
 

Type-B Natriuretic Peptide -- See Natriuretic Peptide, Brain


A PEPTIDE that is secreted by the BRAIN and the HEART ATRIA, stored mainly in cardiac ventricular MYOCARDIUM. It can cause NATRIURESIS; DIURESIS; VASODILATION; and inhibits secretion of RENIN and ALDOSTERONE. It improves heart function. It contains 32 AMINO ACIDS
  1
 

Type, Body -- See Somatotypes


Particular categories of body build, determined on the basis of certain physical characteristics. The three basic body types are ectomorph (thin physique), endomorph (rounded physique), and mesomorph (athletic physique)
  1
 

Type c, Cytochromes -- See Cytochrome c Group


A group of cytochromes with covalent thioether linkages between either or both of the vinyl side chains of protoheme and the protein. (Enzyme Nomenclature, 1992, p539)
  1
 

Type C Oncovirus -- See Retroviridae


Family of RNA viruses that infects birds and mammals and encodes the enzyme reverse transcriptase. The family contains seven genera: DELTARETROVIRUS; LENTIVIRUS; RETROVIRUSES TYPE B, MAMMALIAN; ALPHARETROVIRUS; GAMMARETROVIRUS; RETROVIRUSES TYPE D; and SPUMAVIRUS. A key feature of retrovirus biology is the synthesis of a DNA copy of the genome which is integrated into cellular DNA. After integration it is sometimes not expressed but maintained in a latent state (PROVIRUSES)
  1
 

Type C Oncoviruses -- See Retroviridae


Family of RNA viruses that infects birds and mammals and encodes the enzyme reverse transcriptase. The family contains seven genera: DELTARETROVIRUS; LENTIVIRUS; RETROVIRUSES TYPE B, MAMMALIAN; ALPHARETROVIRUS; GAMMARETROVIRUS; RETROVIRUSES TYPE D; and SPUMAVIRUS. A key feature of retrovirus biology is the synthesis of a DNA copy of the genome which is integrated into cellular DNA. After integration it is sometimes not expressed but maintained in a latent state (PROVIRUSES)
  1
Type C Phospholipases. : Phospholipase C Gamma / Graham Carpenter, Cornelia Crooke  2007 1
 

Type C Retroviruses, Mammalian -- See Gammaretrovirus


A genus of RETROVIRIDAE comprising endogenous sequences in mammals, related RETICULOENDOTHELIOSIS VIRUSES, AVIAN, and a reptilian virus. Many species contain oncogenes and cause leukemias and sarcomas
  1
Type designers -- Awards. : Best of Graphis. Typography  1993 1
Type designers -- Biography. : Twentieth century type designers / Sebastian Carter  1995 1
Type designers -- France -- History -- 16th century. : The palaeotypography of the French Renaissance : selected papers on sixteenth-century typefaces / Hendrik D.L. Vervliet  2008 1
Type designers -- History.   2
Type designers -- Switzerland -- Biography. : The Adrian Frutiger, typefaces : the complete works / Heidran Osterer, Philipp Stamm ; edited by the Swiss Foundation Type and Typography  2014 1
 

Type directors -- See Typographers


Here are entered works on designers who select type and determine typesetting specifications for typesetting projects. Works on designers of typefaces or fonts are entered under Type designers
  1
 

Type faces -- See Type and type-founding


  1
 

Type, Fungal Mating -- See Genes, Mating Type, Fungal


Fungal genes that mostly encode TRANSCRIPTION FACTORS. In some FUNGI they also encode PHEROMONES and PHEROMONE RECEPTORS. The transcription factors control expression of specific proteins that give a cell its mating identity. Opposite mating type identities are required for mating
  1
 

Type I Arnold-Chiari Malformation -- See Arnold-Chiari Malformation


A group of congenital malformations involving the brainstem, cerebellum, upper spinal cord, and surrounding bony structures. Type II is the most common, and features compression of the medulla and cerebellar tonsils into the upper cervical spinal canal and an associated MENINGOMYELOCELE. Type I features similar, but less severe malformations and is without an associated meningomyelocele. Type III has the features of type II with an additional herniation of the entire cerebellum through the bony defect involving the foramen magnum, forming an ENCEPHALOCELE. Type IV is a form a cerebellar hypoplasia. Clinical manifestations of types I-III include TORTICOLLIS; opisthotonus; HEADACHE; VERTIGO; VOCAL CORD PARALYSIS; APNEA; NYSTAGMUS, CONGENITAL; swallowing difficulties; and ATAXIA. (From Menkes, Textbook of Child Neurology, 5th ed, p261; Davis, Textbook of Neuropathology, 2nd ed, pp236-46)
  1
 

Type I 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 I GM2-Gangliosidosis -- See Tay-Sachs Disease


An autosomal recessive neurodegenerative disorder characterized by the onset in infancy of an exaggerated startle response, followed by paralysis, dementia, and blindness. It is caused by mutation in the alpha subunit of the HEXOSAMINIDASE A resulting in lipid-laden ganglion cells. It is also known as the B variant (with increased HEXOSAMINIDASE B but absence of hexosaminidase A) and is strongly associated with Ashkenazic Jewish ancestry
  1
 

Type I, HSAN -- See Hereditary Sensory and Autonomic Neuropathies


A group of inherited disorders characterized by degeneration of dorsal root and autonomic ganglion cells, and clinically by loss of sensation and autonomic dysfunction. There are five subtypes. Type I features autosomal dominant inheritance and distal sensory involvement. Type II is characterized by autosomal inheritance and distal and proximal sensory loss. Type III is DYSAUTONOMIA, FAMILIAL. Type IV features insensitivity to pain, heat intolerance, and mental deficiency. Type V is characterized by a selective loss of pain with intact light touch and vibratory sensation. (From Joynt, Clinical Neurology, 1995, Ch51, pp142-4)
  1
 

Type I, HSN -- See Hereditary Sensory and Autonomic Neuropathies


A group of inherited disorders characterized by degeneration of dorsal root and autonomic ganglion cells, and clinically by loss of sensation and autonomic dysfunction. There are five subtypes. Type I features autosomal dominant inheritance and distal sensory involvement. Type II is characterized by autosomal inheritance and distal and proximal sensory loss. Type III is DYSAUTONOMIA, FAMILIAL. Type IV features insensitivity to pain, heat intolerance, and mental deficiency. Type V is characterized by a selective loss of pain with intact light touch and vibratory sensation. (From Joynt, Clinical Neurology, 1995, Ch51, pp142-4)
  1
 

Type I Interferon -- See Interferon Type I


Interferon secreted by leukocytes, fibroblasts, or lymphoblasts in response to viruses or interferon inducers other than mitogens, antigens, or allo-antigens. They include alpha- and beta-interferons (INTERFERON-ALPHA and INTERFERON-BETA)
  1
 

Type I Interferons -- See Interferon Type I


Interferon secreted by leukocytes, fibroblasts, or lymphoblasts in response to viruses or interferon inducers other than mitogens, antigens, or allo-antigens. They include alpha- and beta-interferons (INTERFERON-ALPHA and INTERFERON-BETA)
  1
 

Type I Neurofibromatoses -- 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)
  1
 

Type I, 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)
  1
 

Type II Arnold-Chiari Malformation -- See Arnold-Chiari Malformation


A group of congenital malformations involving the brainstem, cerebellum, upper spinal cord, and surrounding bony structures. Type II is the most common, and features compression of the medulla and cerebellar tonsils into the upper cervical spinal canal and an associated MENINGOMYELOCELE. Type I features similar, but less severe malformations and is without an associated meningomyelocele. Type III has the features of type II with an additional herniation of the entire cerebellum through the bony defect involving the foramen magnum, forming an ENCEPHALOCELE. Type IV is a form a cerebellar hypoplasia. Clinical manifestations of types I-III include TORTICOLLIS; opisthotonus; HEADACHE; VERTIGO; VOCAL CORD PARALYSIS; APNEA; NYSTAGMUS, CONGENITAL; swallowing difficulties; and ATAXIA. (From Menkes, Textbook of Child Neurology, 5th ed, p261; Davis, Textbook of Neuropathology, 2nd ed, pp236-46)
  1
 

Type II 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 II diabetes -- See Non-insulin-dependent diabetes


  1
 

Type III Arnold-Chiari Malformation -- See Arnold-Chiari Malformation


A group of congenital malformations involving the brainstem, cerebellum, upper spinal cord, and surrounding bony structures. Type II is the most common, and features compression of the medulla and cerebellar tonsils into the upper cervical spinal canal and an associated MENINGOMYELOCELE. Type I features similar, but less severe malformations and is without an associated meningomyelocele. Type III has the features of type II with an additional herniation of the entire cerebellum through the bony defect involving the foramen magnum, forming an ENCEPHALOCELE. Type IV is a form a cerebellar hypoplasia. Clinical manifestations of types I-III include TORTICOLLIS; opisthotonus; HEADACHE; VERTIGO; VOCAL CORD PARALYSIS; APNEA; NYSTAGMUS, CONGENITAL; swallowing difficulties; and ATAXIA. (From Menkes, Textbook of Child Neurology, 5th ed, p261; Davis, Textbook of Neuropathology, 2nd ed, pp236-46)
  1
 

Type III 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 III 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)
  1
 

Type III Hyperlipoproteinemia -- See Hyperlipoproteinemia Type III


An autosomal recessively inherited disorder characterized by the accumulation of intermediate-density lipoprotein (IDL or broad-beta-lipoprotein). IDL has a CHOLESTEROL to TRIGLYCERIDES ratio greater than that of VERY-LOW-DENSITY LIPOPROTEINS. This disorder is due to mutation of APOLIPOPROTEINS E, a receptor-binding component of VLDL and CHYLOMICRONS, resulting in their reduced clearance and high plasma levels of both cholesterol and triglycerides
  1
 

Type III Hyperlipoproteinemias -- See Hyperlipoproteinemia Type III


An autosomal recessively inherited disorder characterized by the accumulation of intermediate-density lipoprotein (IDL or broad-beta-lipoprotein). IDL has a CHOLESTEROL to TRIGLYCERIDES ratio greater than that of VERY-LOW-DENSITY LIPOPROTEINS. This disorder is due to mutation of APOLIPOPROTEINS E, a receptor-binding component of VLDL and CHYLOMICRONS, resulting in their reduced clearance and high plasma levels of both cholesterol and triglycerides
  1
 

Type IV Arnold-Chiari Malformation -- See Arnold-Chiari Malformation


A group of congenital malformations involving the brainstem, cerebellum, upper spinal cord, and surrounding bony structures. Type II is the most common, and features compression of the medulla and cerebellar tonsils into the upper cervical spinal canal and an associated MENINGOMYELOCELE. Type I features similar, but less severe malformations and is without an associated meningomyelocele. Type III has the features of type II with an additional herniation of the entire cerebellum through the bony defect involving the foramen magnum, forming an ENCEPHALOCELE. Type IV is a form a cerebellar hypoplasia. Clinical manifestations of types I-III include TORTICOLLIS; opisthotonus; HEADACHE; VERTIGO; VOCAL CORD PARALYSIS; APNEA; NYSTAGMUS, CONGENITAL; swallowing difficulties; and ATAXIA. (From Menkes, Textbook of Child Neurology, 5th ed, p261; Davis, Textbook of Neuropathology, 2nd ed, pp236-46)
  1
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