Biomedical subjects
Publications and source records attributed to M Brooks.
A case of osteomylitis of the foot and ankle bones with subsequent complications is presented. Antibiotic therapy was unsuccessful and a below-knee amputation was performed. A comparison of the various Mycobacteria species and their role as etiologic agents in osteomyelitis follows.
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An infant, whose mother was treated for thyrotoxicosis during pregnancy, appeared normal at birth, but laboratory data were indicative of hypothyroidism. On the sixth day of life the infant had clinical and laboratory evidence of hyperthyroidism. A plan of management is proposed for infants born to thyrotoxic mothers.
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A case of chordoma involving the thoracic spine (T12) is reported. The plain film findings included lytic obstruction and partial collapse of a single vertebral body. Noncontrast CT and CT following Metrizamide myelography revealed vertebral body destruction with paravertebral and intraspinal soft tissue masses. Unusual findings in the case included a photon deficient area on nuclear medicine corresponding to the lesion and normal vascularity on spinal angiography. We know of no previous report describing chordoma as a "cold" defect on bone scanning.
The addition of a spin-lock preparatory sequence to a Carr-Purcell-Meiboom-Gill (CPMG) imaging sequence provides a method which allows an accurate and simple comparison of T1p and T2 contrast. Sagittal and axial brain images, produced with the application of a three pulse preparatory spin-lock sequence prior to a sixteen-echo CPMG imaging sequence, are compared with images acquired without the spin-lock sequence. The CPMG sequence uses non-selective refocusing pulses. Therefore, observed echo signals accurately reflect T2 relaxation. This allows a convenient method for assessing the degree to which T1p and T2 contrast differ. The spin-lock CPMG (SL-CPMG) images were acquired with a spin-locking field amplitude of 0.4 G and resemble heavily T2-weighted images at 0.15 T. Quantitative analyses of signal intensities from edema and normal brain tissue confirm the qualitative observations. This in vivo method should prove useful for determining when the additional RF power deposition associated with spin-locking techniques will provide an alternate form of tissue contrast than that available from additional echo collection.
A frequent legal argument raised in defense of men accused of paternity, but not excluded by genetic tests, is that the probabilities of paternity of falsely accused men are similar to those of biologic fathers. This assertion was tested in a computer simulation experiment that used a database of 15,000 actual paternity cases to provide red cell and HLA phenotypes of mothers, children, and putative fathers. Tests had a combined probability of exclusion of 97.3 percent. Equal numbers of true and false fathers were generated from the data by computer to achieve a prior probability of paternity of 0.5. True fathers' phenotypes were those of unexcluded men from actual cases (Group A) or of mothers from actual cases (Group B) in which paternity was not excluded. The false father group was created by assigning the phenotypes of racially identical men who were selected at random from among cases other than their own. Probabilities of paternity were calculated for the men in each group and were classified into descriptive intervals. The frequency of men in each group was compared in each interval. The frequency distributions of probabilities of paternity for true fathers and unexcluded, falsely accused men (false fathers) were markedly dissimilar.
Many different inherited bleeding disorders have been identified in dogs, defined on the basis of quantitative, functional, or structural defects in specific hemostatic proteins or pathways. Most of these disorders are caused by single-gene defects and biochemical assays provide an accurate measure of disease phenotype. Phenotypic disease classifications, however, are often genetically heterogeneous. Protein-based carrier detection assays are fast, inexpensive, and do not require specific identification of causative mutations. The limitations of these tests arise from variable "overlap" regions between carrier and clear dogs, influencing positive and negative predictive values of carrier detection tests within breed populations. Molecular diagnostic techniques enhance the accuracy of carrier detection, providing their clinical application takes into account the molecular heterogeneity underlying naturally occurring hemostatic defects in dogs.
We studied the development of implicit and of verbally declared knowledge for normal human subjects who learned an unfamiliar motor task in one learning session. The exploratory nature of motor learning and a special period for optimizing skill were followed in real time. Subjects understood the goal for task success, but they had to learn a motor strategy of what pattern of serial movements to make and the tactics of how much to scale their amplitudes and timing. We compared the time course for acquiring tactical skill with that for acquiring knowledge of strategy and of tactics, and their necessary cues. Implicit and declarative knowledge were distinguished from one another by correlating subjects' verbal self-reports with movement kinematics and their results. Implicit generation of the correct strategy and of the tactics developed in an exploratory manner from the beginning of the learning session. Implicit strategy learning soon gave way to conscious efforts, but tactical learning remained implicit until its first unambiguous verbal declaration (with one exception). First strategy declarations were voiced before those for tactics, during trial-and-error learning that did not require task success, and referred to reversing the direction of hand movements (one exception). In contrast, first declarations of tactics almost always required actual or imminent success, referred to when direction was to be reversed, and it was achieved near the top of a sigmoid learning curve that rose to tactical skill (with one exception). During the sigmoid rise, movement amplitudes and timing were optimized in a distinct manner, although tactics usually adapted thereafter to movements of more moderate speed that could still be successful.
A circulating anticoagulant was detected in a 2-year-old Chesapeake Bay Retriever with hemolytic anemia, nephrotic syndrome, thrombocytopenia, polyarthropathy, and pulmonary thromboembolism. A persistent prolongation of the activated partial thromboplastin time (aPTT) was detected, and it did not correct with repeated administration of fresh frozen plasma. The aPTT was still prolonged, with a 1:1 mixture of patient's plasma and normal dog plasma in vitro, suggesting the presence of a circulating inhibitor. Results of assays to characterize the inhibitor were compatible with those described for the lupus anticoagulant in human patients with systemic lupus erythematosus. Paradoxically, patients having the lupus anticoagulant are at increased risk for thrombosis. Pulmonary thromboembolism has been described as a frequent complication of immune-mediated hemolytic anemia in the dog, and the presence of a circulating anticoagulant should be considered as a potential mechanism.
Twenty-two cats with liver disease were evaluated for coagulation abnormalities including alterations in prothrombin time, activated partial thromboplastin time, thrombin time, factor VII activity, and platelet count. The purpose of the study was to determine the prevalence of coagulation abnormalities in this population of cats, classify abnormalities according to underlying pathogenesis, and determine if serum biochemical parameters typically used as indicators of liver disease showed any correlation with the coagulation abnormalities present. Study results indicated that at least 1 coagulation abnormality was present in 82% of the cats. Prolongation of prothrombin time was most common (16/22 cats) and factor VII activity was below reference range (< 60%) in 15 cats. When classified according to underlying pathogenesis, vitamin K deficiency was the most common abnormality found (11/22). Other abnormalities were less common and included hepatic synthetic failure (3/22), indeterminate (3/22), and disseminated intravascular coagulation (1/22). Increase in alkaline phosphatase (ALP) activity was the only biochemical abnormality that showed statistically significant correlation with coagulation abnormalities (P = .023). Cats with marked increases in ALP activity were more likely to have coagulation abnormalities than those with only mild increases in ALP activity.
The sensitivities and specificities of 3 commercial serum fibrin(ogen) degradation product (FDP) kits and 1 plasma FDP kit for the detection of FDPs in dogs were determined. Blood was collected for measurement of serum and plasma FDP concentrations from 30 healthy dogs and from 20 dogs that fulfilled clinical and laboratory criteria for disseminated intravascular coagulation. To determine the effect of hemolysis on FDP results, blood was collected simultaneously into Bothrops atrox venom-based and thrombin-based serum collection tubes for measurement of FDPs using a single serum FDP kit. The sensitivity (80-95%) and specificity (90-100%) for a positive or negative FDP result, regardless of concentration, was similar for all kits. Kits yielded discordant results in individual dogs and FDP concentrations obtained from 1 serum FDP kit were consistently higher than those from the other kits. Serum prepared from venom-based collection tubes was significantly more hemolyzed than serum prepared from thrombin-based collection tubes or citrated plasma. Hemolysis did not affect the FDP results. On the basis of these results, we conclude that commercial latex agglutination kits for detection of FDPs in serum and plasma samples from human patients are valid for use in dogs. The plasma FDP assay is a viable alternative to currently used serum FDP assays and has the advantage of using a single (citrated plasma) sample for measuring coagulation parameters and FDP concentration.
The effect of daily doses of 5-15 mg of methimazole on the platelet count, prothrombin time (PT), activated partial thromboplastin time (APTT), and proteins induced by vitamin K absence or antagonists (PIVKA) clotting time in 20 hyperthyroid cats was determined. No significant (P > .05) difference was found in median platelet count. PT, APTT, or PIVKA clotting time before treatment compared to median values at 2-6 weeks or > or =7-12 weeks of methimazole treatment. No cat had a prolonged APTT at any time. At 2-6 weeks of methimazole treatment, 1 cat each developed thrombocytopenia or prolonged PIVKA clotting time despite initially normal values. Three cats had abnormal coagulation tests (prolonged PT [n = 1] and PIVKA clotting time [n = 3]) before treatment that fluctuated during treatment. Excluding the 3 cats that had abnormal PIVKA clotting time before treatment, prolonged PIVKA clotting time developed in 6% (1/17; 95% confidence interval, 0-28%) cats treated with methimazole for 2-6 weeks. Seemingly. doses of methimazole commonly used to treat hyperthyroidism in cats do not cause alteration in PT and APTT, and only rarely prolong PIVKA clotting time. Nevertheless, abnormal PIVKA clotting time may explain bleeding tendencies unassociated with thrombocytopenia in methimazole-treated hyperthyroid cats.
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