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A. Ainsworth Hagen

Texas A&M Health Science Center

Publishes on Hormonal and reproductive studies, Inflammatory mediators and NSAID effects, Estrogen and related hormone effects. 35 papers and 957 citations.

35Publications
957Total Citations

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Top publicationsby citations

Centralization of Low Back Pain and Perceived Functional Outcome
Aaron Sufka, Bruce Hauger, Michael Trenary et al.|Journal of Orthopaedic and Sports Physical Therapy|1998
Cited by 112

McKenzie's methods for evaluating and treating low back pain are used often but studied little. When using the McKenzie system, it is important to observe signs of symptom movement to a central location (centralization). This study investigated the relationships between centralization of low back pain and/or radiculopathy and the subjects' rating of functional outcome. Thirty-six subjects with low back pain volunteered to participate and were evaluated and treated by six researchers. Subjects were tested initially and again 14 days after initiation of treatment using the Oswestry Low Back Pain Disability Questionnaire and the Performance Assessment and Capacity Testing Spinal Function Sort (SFS). Symptoms were monitored for the occurrence of "complete centralization." Of the 36 subjects, 25 showed complete centralization within 14 days. The SFS score changes were significantly higher for subjects who completely centralized (p = 0.015). The results supported the hypothesis that subjects who centralize will have improved functional outcome and, thus, quality of life. However, shorter time to occurrence of complete centralization does not necessarily correlate with improved outcome.

Experimental Study on the Genesis of Cerebral Vasospasm
Cited by 102

The cerebral vasospasm produced by blood, fractions of blood, and blood-borne agents administered intracisternally was studied arteriographically to attain a better understanding of the genesis of vasospasm. The results indicate this phenomenon is multifarious in origin, involving a number of spasmogens. Whole blood, platelets, platelet extracts, some isolated components of platelets, plasma, thrombin, histamine, serotonin and prostaglandins F 1α , E 2 and F 2α produced a significant incidence and duration of spasm. Norepinephrine and prostaglandin E 1 were inactive. Spasm produced by arachidonic acid and red blood cells was of questionable significance. Compared to whole blood, thrombin usually produced spasm which was more delayed in onset while most other active substances produced a shorter-lived spasm. However, among the pure substances tested, serotonin, prostaglandin E 2 and prostaglandin F 2α induced spasm in small doses which most nearly resembled that observed with whole blood. The hypothesis that the course of spasm depends upon synthesis of spasmogens by brain and blood is advanced. Prostaglandin synthesis plays a major role in this concept.

METABOLISM OF 17-BETA-OESTRADIOL-4-14-C IN EARLY INFANCY.
Cited by 73

ABSTRACT The urinary metabolites of intramuscularly administered 17β-oestradiol-4- 14 C were studied in three infants born with multiple malformations. Of the radioactive material recovered from the urine less than 5 per cent was in an ether-soluble (»free«) form. Following enzyme hydrolysis, an average of 46 per cent became ether-extractable. Of the remaining material all but some 2 per cent was butanol-soluble. The pattern of urinary metabolites was similar in all subjects. Oestrone, 17β-oestradiol and possibly 2-methoxyoestrone accounted for less than 5 per cent of the total urinary radioactive material. Oestriol, 16α-hydroxyoestrone and 16-oxo-17β-oestradiol comprised an important group of metabolites, representing together some 20 per cent of the total. However, the quantitatively most important metabolite was a hydroxylation product somewhat more polar than 2-hydroxyoestriol. This compound accounted for 16 per cent of the total. It is concluded that the metabolism of 17β-oestradiol in early infancy is characterized by extensive hydroxylation reactions. This pattern of metabolism may indicate one of the mechanisms by which the foetus is protected against steroids with high biological activity.