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1.
Vet Rec ; 106(26): 547-51, 1980 Jun 28.
Article in English | MEDLINE | ID: mdl-7192026

ABSTRACT

A herd of lactating British Friesian cows was divided into two equal groups. After 14 days during which all the cows had free access to water one group (restricted) was allowed only 50 per cent of the voluntary water intake of the other group (control). After four days when the experiment was terminated, the milk yield of the restricted group had fallen to 74 per cent of that of the control group and their mean body-weight was reduced by 14 per cent. In the restricted group there were significant increases in the concentrations of urea, sodium, total protein and copper in serum, in the osmolality of serum, in the plasma activities of the enzymes creatine kinase and glutamate-oxaloacetate transaminase and in the packed cell volume of blood. The restricted cows behaved very aggressively around their water trough and spent more time in its vicinity. They spent less time lying down than the cows of the control group and some of them were not seen to drink and were withdrawn from the experiment before the end of four days. In a second experiment half the herd was allowed approximately 90 per cent of the water intake of the control group for 14 days. Decreases in milk yield and body-weight and changes in blood composition were much smaller and difficult to detect. However, changes in behaviour were still easily recognised although not as marked as in the first experiment.


Subject(s)
Behavior, Animal , Cattle/physiology , Lactation , Water Deprivation , Aggression , Animals , Body Weight , Cattle/blood , Drinking , Female , Humans , Milk/analysis , Pregnancy
2.
Am J Clin Pathol ; 65(2): 199-205, 1976 Feb.
Article in English | MEDLINE | ID: mdl-1251813

ABSTRACT

Telangiectasia, commonly called Rendu-Osler disease, in its uncomplicated state is a genetic trait, not a disease, which is transmitted as a dominant. It is difficult to diagnose because the identifying characteristics, which are collectively called telangiectases, are multiform. They often do not appear until adult life and frequently are secondary to extraneous or environmental factors such as alcohol, various drugs of which aspirin is an example, and, in a few subjects, exposure to sunlight. The tourniquet test is positive in a high percentage of cases. Eight patients have been selected for discussion to illustrate the application and helpfulness of this test in attaining a better evaluation of the clinical aspects of telangiectasia.


Subject(s)
Telangiectasia, Hereditary Hemorrhagic/diagnosis , Tourniquets , Adolescent , Adult , Aneurysm/etiology , Aspirin/adverse effects , Environment , Female , Humans , IgA Vasculitis/etiology , Male , Middle Aged , Photosensitivity Disorders/etiology , Physical Exertion , Telangiectasia, Hereditary Hemorrhagic/chemically induced , Telangiectasia, Hereditary Hemorrhagic/complications , Telangiectasia, Hereditary Hemorrhagic/genetics
3.
4.
N Engl J Med ; 293(10): 507-8, 1975 Sep 04.
Article in English | MEDLINE | ID: mdl-1152869
6.
Am J Clin Pathol ; 64(1): 87-94, 1975 Jul.
Article in English | MEDLINE | ID: mdl-1080353

ABSTRACT

The vascular component of hemostatis is determined by the bleeding time as designed by Duke or by the Ivy modification, which is a combined bleeding time-tourniquet test. A prolonged bleeding time is observed: (1) in thrombopathic thrombocytopenia, which may be (a) hereditary or (b) acquired, as in the immune types or from depression of bone marrow, and (2) athrombocytopenically, as in von Willebrand's disease, Glanzmann's thrombasthenia, or from aspirin intolerance. The role of a specific bleeding time determinant in the plasma (labile bleeding time factor of Perkins) is discussed and its possible relation to platelets suggested.


Subject(s)
Blood Coagulation Tests/methods , Hemorrhagic Disorders/diagnosis , Aspirin/adverse effects , Blood Coagulation/drug effects , Blood Coagulation Disorders/blood , Blood Coagulation Disorders/diagnosis , Blood Coagulation Disorders/physiopathology , Blood Coagulation Factors/physiology , Blood Platelet Disorders/blood , Blood Platelet Disorders/diet therapy , Blood Platelets/physiology , Hemophilia A/blood , Humans , Phospholipids/therapeutic use , Purpura, Thrombocytopenic/blood , Syndrome , Thrombocytopenia/blood , von Willebrand Diseases/blood
7.
Thromb Diath Haemorrh ; 33(2): 191-8, 1975 Apr 30.
Article in English | MEDLINE | ID: mdl-1138416

ABSTRACT

The physiological mechanism to prevent and control abnormal bleeding is dependent on three vitamins (C, K, and Q). Two of these are unequivocally established as essential for hemostasis while the existence of the third (Q) is supported by experimental evidence and by clinical and therapeutic observations (Quick 1972; Quick 1974). The interrelationship of these three vitamins has remained moot except for clue observations. Both vitamins C and K have a key structure in their molecules which supplies a redox mechanism, ascorbic acid and 2-methyl, 1,4-naphthoquinone, respectively. Both vitamins are concerned with growth. Lack of vitamin C, which clinically is the basic defect of scurvy, does not appear to cause a defect in blood coagulation while vitamin K affects the clotting mechanism by being essential for the production of four distinct clotting factors: prothrombin, factors VII, IX and X. In this presentation an attempt is made to correlate the action of the vitamin K-dependent clotting factors grouping them in a diagram to show how two systems of thrombin formation exist, one being essentially intrinsic, the second extrinsic requiring tissue thromboplastin and factor VII. The possible interlocking of vitamin Q in this mechanism is presented.


Subject(s)
Blood Coagulation , Vitamins/physiology , Animals , Ascorbic Acid/physiology , Ascorbic Acid Deficiency/physiopathology , Blood Coagulation Factors/biosynthesis , Factor VII/metabolism , Humans , Lampreys , Models, Biological , Oxidation-Reduction , Prothrombin Time , Thromboplastin/physiology , Vitamin K/physiology , Vitamins/metabolism
10.
JAMA ; 230(1): 37, 1974 Oct 07.
Article in English | MEDLINE | ID: mdl-4479215
13.
N Engl J Med ; 290(13): 751, 1974 Mar 28.
Article in English | MEDLINE | ID: mdl-4813756
14.
Science ; 182(4107): 87, 1973 Oct 05.
Article in English | MEDLINE | ID: mdl-4730060
17.
N Engl J Med ; 288(20): 1079, 1973 May 17.
Article in English | MEDLINE | ID: mdl-4696624
19.
Minn Med ; 55(8): 705-9, 1972 Aug.
Article in English | MEDLINE | ID: mdl-5053558
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