Isoenzyme variation of human salivary amylase

Skude, G.

doi:10.1007/bf00702777

Cited by 12 publications

(3 citation statements)

References 8 publications

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“…Skude (5) reported recently that the amylase clearances values in young healthy adults did not exhibit any significant differences in comparison with those found in healthy children (range 6-16 years). The sick children were admitted to the hospital with the.…”

Section: Subjectsmentioning

confidence: 82%

Urinary Isoamylases in Juvenile Diabetics

Kamarýt¹,

Stejskal²,

Osicková³

1978

Clinical Chemistry and Laboratory Medicine

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An anomalous ratio of salivary to pancreatic amylase activities has been observed in urine from juvenile diabetics. Decreased pancreatic amylase activity in urine from these subjects appears to be a characteristic trait. Isoamylasen im Harn bei juvenilen DiabetikernZusammenfassung: Im Harn juveniler Diabetiker wurde ein von Gesunden abweichendes Verhältnis von Speichelzu Pankreasamylase-Aktivität beobachtet. Die erniedrigte Pankreasamylase-Aktivität im Harn gesunder Diabetiker scheint ein für diese Patienten charakteristisches Merkmal zu sein.

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Section: Subjectsmentioning

confidence: 82%

Urinary Isoamylases in Juvenile Diabetics

Kamarýt¹,

Stejskal²,

Osicková³

1978

Clinical Chemistry and Laboratory Medicine

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“…However, they started from the erroneous assumption that parotid amylase was 'a stable monomer without isoenzymatic forms'. On the contrary, salivary amy lase consists of up to seven genetically determined isoenzymes in man (3,18,19,26,35,39) and of four isoamylases in the rat (31,32). When investigating those, we found that two of them were less active in senescent parotid glands whereas the activity of the other two remained unaffected (7).…”

Section: Effect Of Cytostatic Agentsmentioning

confidence: 88%

Effect of Cytostatic Agents on Salivary Gland Tissue of the Rat

Chilla¹,

Deltow²,

Arglebe³

1976

ORL

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“…A total of 60 polymorphic systems were studied with techniques, slightly modified, as described in the following papers: C3 (Teisberg 1970), BF (Alper et al 1972), PGP (Barker & Hopkinson 1978), F X l l l A (Board 1979), LP (Berg 1963), PI (van den Broek et al 1976), chromosome polymorphisms (Caspersson et al 1970), GPTl (Chen & Giblett 1971), BG (Cleve 1968), PON , PLG , ALADH ), AK1 (Fildes & Harris 1966), PGD (Fildes & Parr 1963), CHEl (Garry 1971, Garry et al 1972) UMPK (Giblett et al 1974), HP (Habib & Eiberg 1983), ESD (Hopkinson et al 1973), ORM (Johnson et al 1969), AMY2 (Kamaryt & Laxova 1965), PGMl and SOD1 (Kiihnl & Spielmann 1978a, Spencer et al 1964, TF (Kiihnl & Spielmann 1978b), GLOl (Kompf et al 1975), PTC (Mohr 1951), HLA-A,-B,-C and D ), C6 (Olving et al 1977), blood groups (Race & Sanger 1968), CHE2 (Simpson 1972), AMY1 (Skude 1971), ADA (Spencer et al 1968), ACPl (Smensen 1970), GC (Thymann 1981). The methods concerning systems A2HS, F"' "2 and FX111B are described in other papers submitted to the present journal.…”

Section: Methodsmentioning

confidence: 99%

Gentics and linkage relationships of the C3 polymorphism: discovery of C3‐Se linkage and assignment of LES‐C3‐DM‐Se‐PEPD‐Lu synteny to chromosome 19

et al. 1983

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The C3 complement system was examined in our Danish material of normal families, which had earlier been examined for 59 marker systems, and in a myotonic dystrophy family material. A total of 8 alleles were recognized, with allele frequencies as follows: C3*S = 0.7902, C3*F = 0.2018, C3*S rare (3 lumped together) = 0.0036, C3* F rare (2 lumped together) = 0.0024; a silent allele was recognized in three families and its frequency to C3*QO = 0.002. The distribution of unrelated inviduals did not deviate significantly from the Hardy‐ Weinberg expectation, it was not siginicantly different between the sexes, and the for none of the mating types was there any significant deviation from the expected ratios of children. As to linkage relationships of C3 with market systems and with myotonic dystrophy, there was evidence (most of it first presented at the 6th International Congress of Human Genetics, Jerusalem 1981) for synteny with ABH secretion (Se): C3‐Se (males) ẑ= 4.35, θC = 0.12 and with Lewis secretion (LES): C3‐LES (males ẑ= 3.63, θC = 0.04). There were indicative or suggestive lod scores for Se‐PEPD (males & females ẑ= 2.41, θC = 0.00), C3‐Lu (ẑ= 1.88, θC = 0.15), C3‐DM (ẑ= 1.69, θC = 0.06) and PEPD‐C3 (male ẑ= 0.95, θC = 0.17). The most likely sequence of these 6 systems would appear to be LES‐C3‐DM‐(Se‐PEPD)‐Lu and the synteny would reside on chromosome 19.

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Isoenzyme variation of human salivary amylase

Cited by 12 publications

References 8 publications

Urinary Isoamylases in Juvenile Diabetics

Urinary Isoamylases in Juvenile Diabetics

Effect of Cytostatic Agents on Salivary Gland Tissue of the Rat

Gentics and linkage relationships of the C3 polymorphism: discovery of C3‐Se linkage and assignment of LES‐C3‐DM‐Se‐PEPD‐Lu synteny to chromosome 19

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