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Intersection syndrome is a condition that should be differentiated from DeQuervain's stenosing tenosynovitis, as there are many subtle differences in treatment and prognosis. We present a case of intersection syndrome, describing its characteristic clinical and anatomic features, and highlighting differences in the areas of diagnosis and treatment relative to the better known DeQuervain's tenosynovitis.

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OBJECTIVE: The audiological examination of this patient was to determine the degree and type of hearing loss that was incurred from apparent dimethylmercury poisoning. DESIGN: This was a single subject case study design. Audiologic tests were selected to help determine sensory from neural and/or central auditory system dysfunction. RESULTS: This patient demonstrated an inability to understand speech, both in formal and informal assessments, yet relatively good hearing sensitivity for pure tones bilaterally. Distortion product otoacoustic emissions showed only minimal deficits in each ear. The auditory brain stem response was abnormal bilaterally, indicating neural and/or central involvement. CONCLUSION: Dimethylmercury poisoning, in this case, resulted in compromise of the auditory neural system with little effect on the sensory (cochlea) mechanism.

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A 34-year-old woman, 12 weeks pregnant, presented with an acute monoarthritis. Gout was proven by joint aspiration. The gout was multifactorial in origin. Only 2 cases of gout during pregnancy have been described previously.

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Elderly individuals not only live longer but are also more active than in the past. Accompanying this increase in activity is the number of older trauma victims. The effect of aging on response to injury is reviewed, and the initial evaluation and treatment of geriatric trauma are delineated in this article. Specific injuries of note include head and chest wall injury; pulmonary and cardiac contusion; abdominal trauma; and aortic, spinal, and musculoskeletal injury.

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A multidisciplinary referral center was established at a university hospital for prospectively assessing patients with possible Lyme disease. Borrelia burgdorferi is not known to be endemic in this region, but considerable anxiety about Lyme disease has developed among the general public. Sixty-five patients were referred for suspected Lyme borreliosis. Detailed histories were obtained and physical examinations were performed; patients were investigated aggressively in accordance with their symptom complexes. Strict diagnostic criteria consistent with published standards were applied. Only two of the 65 patients were judged to have probable Lyme disease. Definite major alternate diagnoses were made for 50 patients (77%); firm medical diagnoses (11 dermatologic, 9 rheumatologic, 9 infectious disease, 6 gastrointestinal, 4 neurological, and 2 miscellaneous) were made for 41 patients (63%); and major psychiatric diagnoses were made for 9 patients (14%). Probable diagnoses of chronic fatigue syndrome and fibromyalgia were made for 11 patients (17%). The conditions of four patients (6%) were undiagnosed. A referral center for patients with suspected Lyme disease can be useful even in an area of nonendemicity, and careful clinical assessment will reveal treatable alternate diagnoses for many patients with suspected Lyme disease.

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Bilateral Achilles tendon rupture is an unusual injury. This rare entity usually occurs in patients on chronic steroid therapy or with underlying disease. Bilateral Achilles tendon rupture is extremely rare in a previously healthy individual. A case involving traumatic Achilles tendon rupture as a result of a sky diving accident is reported. Evaluation of patients with suspected Achilles tendon rupture is briefly reviewed.

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Pregnant hamsters were treated with selenite, selenate, and selenomethionine during the critical stages of embryogenesis. The dosing regimens were oral, intravenous, and osmotic minipump infusion. Malformations, mainly encephaloceles, were noted with oral and intravenous selenite and selenate but were associated with maternal toxicity manifested by inanition and weight loss. Fetal body weights and lengths were reduced in a dose-dependent manner with the inorganic forms. Single oral doses of selenomethionine above 77 mumol/kg induced similar malformations but not when the dose was delivered orally over four days nor by minipump over several days. Fetal body weights and lengths were decreased by selenomethionine in a dose-dependent manner. Maternal toxicity was pronounced with the higher doses of selenomethionine. Assigning a specific teratogenic effect to selenium is confounded by maternal toxicity.

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A normally teratogenic dose of cadmium ions administered to hamsters late in gestation does not cross the placental barrier nor does it result in placental pathology. Our finding, which differs from data for other rodents, may be due to differences in the chemical status of cadmium in the placental cytosols.

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Fourteen untrained females (age 19 +/- 1, range 18-21) were studied to examine the heart rate-VO2 relationship during a single aerobic dance training session. These findings were used to help explain the changes in VO2max resulting from an aerobic dance training program. VO2max and body composition were determined before and after an 8 wk training period. In addition, the heart rate-VO2 responses to an aerobic dance training session were monitored and compared to the heart rate responses of treadmill jogging performed at the same VO2. The aerobic dance session elicited a significantly lower oxygen pulse than did treadmill exercise (7.2 +/- 0.3 vs 8.1 +/- 0.8 ml.beat-1; P less than 0.01). There were no significant changes in percent body fat, whereas VO2max increased by 11% (34.4 +/- 0.9 vs 38.1 +/- 0.8 ml.kg-1.min-1; P less than 0.05). No significant changes in any of the parameters tested were observed in 10 untrained controls. These findings indicate that the heart rate elicited from aerobic dance represents a lower relative exercise intensity (VO2) than that of running. Therefore, the assumption that aerobic dance training produces the same cardiovascular adaptations as running training when performed at the same target rate may be unwarranted.

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Pregnant Syrian hamsters were given a dose of 3.9 micromoles cadmium ion/kg (radiolabelled with 109cadmium) on days 7, 8, 9, and 11 of gestation. Animals were sacrificed on day 13 of gestation and maternal blood, liver, kidney, placentas, and fetuses collected. No pathology was observed in placentas or fetuses. Maternal liver accounted for 61% of the total cadmium injected (15.6 micromoles/kg dam), maternal kidney 4%, and placentas 0.24%. Maternal blood and fetuses contributed negligibly to the total body burden of cadmium. Gel filtration experiments indicated two major cadmium fractions in maternal liver, maternal kidney, and placental cytosols, one at the excluded volume and another nearly twice the excluded volume. Further purification and characterization of the cadmium fraction eluting at twice the excluded volume in the gel filtration experiments showed it to be cadmium metallothionein. Ion exchange chromatography on DEAE Sephacel revealed two forms of cadmium metallothionein in the cytosols of maternal liver and placentas. Maternal kidney cytosols contained one cadmium metallothionein. Amino acid analyses suggest that the thionein components of placental cytosols are synthesized in situ.

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We determined the concentration and chemical status of arsenic in the placentas of hamsters following continuous exposure via the osmotic minipump to minimally and frankly teratogenic doses of arsenate. Close to 70% of the placental arsenic is bound to macromolecules, two-thirds of which is dialyzable. The remaining 30% of arsenic consists of low molecular weight species, predominantly inorganic arsenic. This mix is the same for minimally teratogenic and frankly teratogenic doses of arsenate.

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The teratogenic effect of cadmium can be diminished by a number of mechanisms including zinc and pretreatment with cadmium and mercury. In this study, the oral administration of alpha-mercapto-beta-(2-furyl)-acrylic acid (MFA) protects against cadmium-induced malformations and embryonic death. This protection is probably mediated by the chelation of the cadmium ion rather than metallothionein (MT) synthesis.

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Hamster dams dosed continuously with arsenate and exposed to short-term hyperthermia produced a greater percentage of malformed offspring than did hamster dams dosed with arsenate alone. Hamsters receiving both treatments possessed elevated arsenic concentrations in the maternal blood and placentas immediately after cessation of the hyperthermic insult. Blood levels of arsenic were the same as those of animals not receiving the heat treatment within several hours post-hyperthermia; however, arsenic concentrations remained elevated in placentas, the duration being dependent on the dose of arsenate. We suggest that the rise in placental arsenic concentrations is the basis of the increase in the production of fetal malformations for hamsters treated continuously with arsenate and heat stressed during critical organogenesis.

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Serious suggestions have been made that dietary supplementation with folic acid (FA) and perhaps other vitamins during pregnancy may reduce the incidence of neural tube defect (NTD) in human newborns. The purpose of these experiments was to evaluate the effect of continuous infusion of FA on the incidence of NTDs induced by arsenate. This teratogen induces NTDs in up to 90% of golden hamster fetuses when administered acutely during critical stages of embryogenesis. FA was administered by subcutaneously implanted osmotic minipumps beginning on the 6th day of gestation, 48 h before an acutely administered dose of sodium arsenate. The protective effect of FA was examined at three teratogenic dose levels of arsenate: optimal, with 905 NTDs, intermediate, with 38% NTDs, and low, with 20% NTDs. Fetuses were recovered at day 13 of gestation and examined for NTDs and other malformations. Maternal red cell folate levels were determined on day 8, 48 h after implantation of the pumps. The results show that the maternal red blood cell level of FA can be significantly increased within 48 h by chronic infusion to levels which are almost two times (550 ng/ml) control levels. There was no significant protection against arsenate-induced NTDs following FA supplementation at any of three levels of this teratogen.

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We have determined the concentration, availability, and chemical status of radiolabeled arsenic in the blood of pregnant hamsters at the beginning (morning of Day 8) and the end (morning of Day 9) of the critical period of embryogenesis. Hamster dams were exposed to teratogenic doses of arsenate by means of osmotic minipumps implanted on the morning of Day 6 of the gestation period. Whole blood arsenic concentrations were the same for 48 and 72 hr postimplant. The arsenic concentration of plasma equaled that of red cells. Plasma arsenic was not bound to macromolecules and had the same chemical status 48 and 72 hr postimplant. Arsenate was the dominant form (67% of the total). However, the presence of dimethylarsinic acid and arsenite indicates that the pentavalent species was metabolized. Red cell arsenic was bound to macromolecules in the cell sap. Seventy percent of red cell sap arsenic was dialyzable 48 hr postimplant, but only 56% 72 hr postimplant. Arsenate was the dominant dialyzable red cell species on Day 8 and arsenite was the major dialyzable form on Day 9. Our findings demonstrate a relationship between the maternal blood concentration and chemical status of arsenic and the presence of malformations resulting from a constant rate exposure of pregnant hamsters to arsenate via the osmotic minipump.

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We have determined the concentration and chemical composition of arsenic in the blood of pregnant hamsters between 0.2 and 6 hr after an intraperitoneal injection of a teratogenic dose of radiolabeled sodium arsenate on the morning of the eighth day of gestation. Arsenic was present in plasma and red cells 0.20 hr postinjection. The plasma arsenic concentration reached a maximum of 220 mumole/kg blood near 0.5 hr postinjection. Plasma arsenic existed entirely as low-molecular-weight species. Both arsenite and dimethylarsinate (DMA) were present in plasma 0.20 hr postinjection, indicating that arsenate reduction and methylation of arsenic are rapidly initiated. However, the arsenite contribution remained small while the DMA contribution increased with time. Red cell arsenic included macromolecular arsenic (AsP) as well as three low-molecular-weight forms. The contribution of DMA remained small, but arsenite and AsP contributions increased with time. These findings identify the maternal blood concentration and chemical status of arsenic following the administration of a teratogenic dose of arsenate during the period of organogenesis. They could prove useful for predicting the likelihood of a teratogenic outcome in other mammalian species.

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We have examined the teratogenic and embryotoxic effects of constant-rate exposure of pregnant hamsters to arsenate by means of subcutaneous implants of osmotic minipumps. Different total exposure regimens were established by varying the duration of minipump implants and by varying the concentration of arsenate in the minipumps. Dams were killed on Day 13 of pregnancy, 5 days after the critical stage of organogenesis. Numbers of resorptions, dead fetuses, and living fetuses were obtained. Fetal weights, crown-rump lengths, and the incidence of malformations were recorded. Control animals were treated identically with minipumps containing demineralized water. The percentage of malformations per litter, a direct measure of teratogenesis, was dependent only upon the concentration of arsenate in the minipumps. The minimum teratogenic response was achieved with a dose of 70 mumol/kg dam/24 hr during the critical stages of organogenesis. The embryotoxic (fetotoxic) indicators, fetal weight and crown-rump length, decreased with increases in exposure time and with increased concentrations of arsenate. The resorption rate also depended directly upon duration of exposure and concentration of arsenate in the minipump.

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