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2 edition of Studies on glycogen in the nervous systems of Haemopis Sanguisuga and Planorbis Corneus. found in the catalog.

Studies on glycogen in the nervous systems of Haemopis Sanguisuga and Planorbis Corneus.

Leonard Henry Seal

Studies on glycogen in the nervous systems of Haemopis Sanguisuga and Planorbis Corneus.

by Leonard Henry Seal

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  • 31 Currently reading

Published by University of Salford in Salford .
Written in English


Edition Notes

PhD thesis, Biological Sciences.

SeriesD69645/86
ID Numbers
Open LibraryOL21685073M

- Explore tsetsi_com's board "Nice, Large leeches", followed by people on Pinterest. See more ideas about Arm numbness, This or that questions and How to remove.9 pins. (Forbe-debranching enzyme(s)) Erythrocyte glycogen elevated andenzymedefect in muscle and/or liver, andusually in bloodcells andfibroblasts Glycogen structure abnormal in fasted state (short outer chains) IV SLiver biopsy showscirrhosis and t glycogen ofabnormalstructure Lethal (Andersen-branching(Lackenzyme) i (CL22 instead of12).

Glycogenin is a protein that can act as an enzyme and initiate glycogen synthesis. It uses UDP-glucose and links it to its tyrosine residue. After elongation to a short alpha 1,4-glycosidic chain, the enzyme glycogen synthase can elongate further on. Glycogenin is found in the core of the glycogen granule. Type I glycogen storage disease (GSD I), also known as von Gierke’s disease, is the most common form of glycogen storage disease, accounting for 25% of all cases. It is an inherited disorder that affects the metabolism – the way the body breaks food down into energy.

Purpose: Glycogen Storage Disease Type III, glycogen debranching enzyme deficiency, causes accumulation of glycogen in liver, skeletal, and cardiac muscle. Some patients develop increased left ventricular thickness by echocardiography, but the rate of increase and its significance remain s: We evaluated 33 patients with Glycogen Storage Disease Type III, 23 with IIIa and . The introduction of 13C magnetic resonance spectroscopy (MRS) has enabled noninvasive measurement of muscle glycogen synthesis in humans. Conclusions based on measurements by the MRS technique assume that glucose metabolism in gastrocnemius muscle is representative for all skeletal muscles and thus can be extrapolated to whole-body muscle glucose metabolism.


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Studies on glycogen in the nervous systems of Haemopis Sanguisuga and Planorbis Corneus by Leonard Henry Seal Download PDF EPUB FB2

Studies on glycogen in the nervous systems of Haemopis sanguisuga (L) and Planorbis corneus (L) Author: Seal, L. ISNI: Awarding Body: University of Salford Current Institution: University of Salford Date of Award:   The data provide direct evidence that the label is partially incorporated into glycogen in nervous tissue.

Pentreath, L. Seal and M. Kai-Kai EXPERIMENTAL PROCEDURES Specimens of Planorbis corneus and Haemopis sanguisuga were collected locally and Cited by:   An- other preparation is the buccal ganglion of the snail, where the neurons are also large, though the sur- rounding glial cells are smaller in size (Pentreath et aL, ).

We have studied the effects of 5-HT on glycogen in the leech and, to a lesser extent, snail nervous systems, using chemical extraction and light- microscope by: Fischer E () Experimentally induced changes of the glycogen contents in the muscular and nervous system of the horse leech Haemopis sanguisuga L.

A histochemical study. A histochemical study. Acta Biol Acad Sci Hung –Cited by: 5. Some glycogen storage disorders, particularly type Ib, can affect your immune system and make you more susceptible to infections. Glycogen storage disorder type II can affect your heart, muscles, liver, nervous system and blood vessels.

In babies, this can lead to breathing problems, muscle weakness and abnormal enlargement of the heart. Glycogen storage disease type 2, also known as Pompe disease or acid maltase deficiency disease, is an inherited metabolic disorder. While glycogen storage disease type 2 is a single disease, it may be classified in 2 forms according to the rates of disease progression, its severity and the age at which symptoms start.

Glycogen storage disease-like phenotype with central nervous system involvement in a PGM1-CDG patient Article (PDF Available) in Neuro endocrinology letters 35(2) May with Reads. The isolated segmental ganglia of the horse leech Haemopis sanguisuga were used as a model system to study the utilization and control of glycogen stores within nervous tissue.

The glycogen in the. Wolfe, D. and Nicholls, J. Uptake of radioactive glucose and its conversion to glycogen by neurons and glial cells in the leech central nervous system. Glycogen metabolism. Glycogen is the storage form of glucose in cells and is essential for energy supply and glucose homeostasis.

The discovery of glycogen in liver in is attributed to Claude Bernard [].The general mechanism of glycogen synthesis and degradation is the same in all tissues, whilst the regulation of glycogen metabolism differs.

Glycogen storage disease type I (also known as GSDI or von Gierke disease) is an inherited disorder caused by the buildup of a complex sugar called glycogen in the body's cells. The accumulation of glycogen in certain organs and tissues, especially the liver, kidneys, and small intestines, impairs their ability to function normally.

Whereas, in muscle, where glycogen is the primary energy source, glycogen accumulates and muscle weakness and cramping occurs, exercise intolerance is present, and myoglobinuria is detectable.

Glycogen storage disease (GSD) type I, also known as von Gierke disease, is a group of inherited autosomal recessive metabolic disorders of the glucose phosphatase system which helps maintain glucose homeostasis. Von Gierke described the first patient with GSD type I in under the name hepatonephromegalia glycogenica.

Purpose: Glycogen storage disease type III is a rare disease of variable clinical severity affecting primarily the liver, heart, and skeletal muscle. It is caused by deficient activity of glycogen.

Glycogen storage disease type II, also called Pompe disease, is an autosomal recessive metabolic disorder which damages muscle and nerve cells throughout the body. It is caused by an accumulation of glycogen in the lysosome due to deficiency of the lysosomal acid alpha-glucosidase enzyme.

It is the only glycogen storage disease with a defect in lysosomal metabolism, and the first glycogen. Glycogen in the central nervous system of adults and developing anamnia.

Benedetti I, Marini M. The distribution of glycogen in the central nervous system of the viviparous teleost Gambusia affinis and of the oviparous teleost Jordanella floridae during development and in the adults, was examined.

Glycogen metabolism is further influenced by AMP-activated protein kinase, which associates with glycogen and regulates glucose uptake, and by lysosome activity. Glycogen content has been detected under different stress conditions, including starvation, cold hardness, over-winter or seasonal acclimation, and diapauses in previous studies (Koštál et al.

; Heydari and Izadi ; Ren et al. ; Keshan et al. ; Wang et al. a,b), but few studies reported GP and GS expression levels and. Yes, activation of the sympathetic nervous system increases blood glucose levels. Sympathetic activation stimulates increased glycogenolysis which is the break down of a polymer called glycogen.

How is glycogen storage disease (GSD) treated. Treatment varies depending on the type of GSD. For types of GSD that involve the liver, treatment is aimed at keeping the right level of glucose in the blood.

This is often enough to maintain the cells fuel needs and prevent long-term complications associated with poorly controlled GSD. Central nervous system may be affected in GSD type 1a even in patients with normal neurologic examination. Accumulation of abnormal results in patients with poor metabolic control supports the importance of metabolic control in GSD type 1a.

Key words: glycogen storage disease type 1a, central nervous system, hypoglycemia, intellectual disability.Campbell 9th edition, based on Mastering Biology Learn with flashcards, games, and more — for free.Glycogen storage disease type VI (also known as GSDVI or Hers disease) is an inherited disorder caused by an inability to break down a complex sugar called glycogen in liver cells.

A lack of glycogen breakdown interferes with the normal function of the liver. The signs and symptoms of GSDVI typically begin in infancy to early childhood.