Biomedical subjects
Publications and source records attributed to J H Jacoby.
This paper reviews the pathophysiological mechanism of quadriceps tendon rupture and its diagnosis by means of medical imaging including radiography, sonography, and magnetic resonance imaging (MRI). MRI findings are emphasized.
The authors discuss the advantages and limitations of radiographic modalities in assessing traumatic rupture of the thoracic aorta (TRTA). TRTA is one of the most frequent causes of death from high-speed deceleration accidents and other blunt trauma sustained during motor vehicle accidents.
The authors discuss computed tomography (CT) and magnetic resonance imaging (MRI) findings of herpes encephalitis as important adjuncts to the early diagnosis of this entity. The patient was a 42-year-old HIV-negative male who presented with a history of dizziness, headaches, and fever.
Magnetic resonance imaging (MRI) has proved to be an excellent diagnostic tool in evaluating the musculoskeletal system. This article illustrates one particular facet of musculoskeletal MRI: investigation of the rotator cuff tendon complex.
In Radiology Rounds, the authors presents a case history, mammogram, and discussion of causes of diseases simulating carcinoma of the breast. The patient is a 59-year-old female. The diagnosis is edema of the breast secondary to congestive heart failure, mimicking carcinoma.
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UNLABELLED: Our patient exhibited typical characteristics of giant cavernous hemangioma by CT and MR, and was asymptomatic. We have concluded, therefore, that this did not represent a malignant lesion. In general, however, one must exhibit a reasonable degree of caution in applying this diagnosis, adhere strictly to the criteria described, and recognize the clinical setting of the patient. DIAGNOSIS: Giant cavernous hemangioma of the liver.
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The effects of chemically, i.e., streptozotocin-induced diabetes or induced hyperglycemia on dopamine and serotonin release in striatum were examined in vivo in rats by employing voltammetry. In the acutely diabetic state, an increased (67%) striatal dopamine release was seen, whereas in the chronically diabetic state, striatal dopamine release was increased, but not to the same extent (19%). The acutely diabetic rat, in which electrochemical signals for serotonin were studied 3 days after the single intraperitoneal injection of STZ, responded with a significant increased release of serotonin (62%). Chronically diabetic rats showed a reversal of serotonin release to basal values. When L-tryptophan was injected in nondiabetic rats, the results showed a decrease (45%) in striatal dopamine release. Injection of L-tryptophan into nondiabetic rats produced a significant increase (25%) over control values in the striatal release of serotonin. The maximum increase was most evident 90 min after injection and the increase remained elevated an additional 90 min. Long term diabetic animals showed a significant decrease (73%) in striatal dopamine release after L-tryptophan. Long term diabetes produced a significant inhibition of serotonin release over control values to 70% below baseline levels. The effects of hyperglycemia on non-diabetic rats were a decreased (52%) striatal dopamine release and an increased (304%) striatal serotonin release. These changes imply that the untreated diabetic state is associated with progressive impairment of neurotransmitter release. These data can be interpreted as implying that mood changes may be related to impaired neurotransmitter availability in the diabetic state.
Extracellular serotonin in striatum was studied in untreated streptozotocin-induced diabetic rats and in untreated nondiabetic rats that served as age-, food-, and sex-matched controls. Extracellular serotonin was studied under anesthesia in vivo and dynamically with voltammetry. The results showed that an early and significant increase in extracellular serotonin occurred in striatum in the untreated acutely (3 days) diabetic rat. In untreated long-term (3-7 weeks) diabetic rats, however, the increase in serotonin in extracellular fluid in striatum decreased and returned to normal. The findings show a change in serotonergic function in acutely diabetic rats. The serotonergic alteration may have psychotherapeutic implications.
In vivo voltammetry was used to measure the synaptic release of rat striatal dopamine and serotonin after the administration of the amino acid L-tryptophan to streptozocin-induced diabetic rats. Dopamine and serotonin release from rat striatum was studied at a short-term or acute (3-day) interval and a long-term or chronic (3- to 7-wk) interval after the induction of diabetes. The study was also done in age-, sex-, and food-matched controls. The findings show that L-tryptophan decreased dopamine release from rat striatum in nondiabetic rats. The decreased striatal dopamine release, after L-tryptophan administration, was exacerbated in acutely diabetic rats and further exacerbated in chronically diabetic rats. By contrast, rat striatal serotonin release predictably increased after L-tryptophan injection in nondiabetic rats. A further increased striatal serotonin release was seen in acutely diabetic rats. Chronically diabetic rats, however, responded to L-tryptophan with a dramatic and significant decrease in striatal serotonin release. The results show that in acutely diabetic and normal rats, L-tryptophan administration reduced striatal dopamine and increased striatal serotonin release, whereas in chronically diabetic rats, the release of both biogenic amines was decreased. The findings indicate that the progression of diabetes is associated with an impaired ability to release primary neurotransmitter biogenic amines.
Adult rats received intraventricular injections of 5,7-dihydroxytryptamine (5,7-DHT) to destroy serotonin (5-HT)-containing nerve terminals throughout the brain. When the animals were killed 3 or 21 days later, we observed a marked decrease in 5-HT content in septum and hippocampus and a parallel decline in in vitro high affinity 5-HT uptake. 5-Hydroxyindoleacetic acid (5-HIAA) concentrations also were reduced but by a much smaller extent, resulting in significant increases in the ratio of 5-HIAA to 5-HT. These changes were accompanied by similar increases in the ratio of tryptophan hydroxylase (TPH) activity to 5-HT content. The relative increases in TPH activity resulted from two temporally distinct processes, the first of which appeared to be an activation that could be mimicked in vitro by Ca2+-dependent phosphorylation. We conclude that, after partial damage to 5-HT neurons, there is a compensatory increase in the synthesis and release of 5-HT from those terminals that remain.
The rate of brain 5-hydroxytryptamine (serotonin) synthesis and turnover in streptozotocin-diabetic rats was assessed using three separate methods: the rate of 5-hydroxytryptophan accumulation following decarboxylase inhibition with Ro 4-4602; the decline in 5-hydroxyindoleacetic acid levels following monoamine oxidase inhibition with pargyline; and the rate of 5-hydroxyindoleacetic acid accumulation following blockade of acid transport with probenecid. Each of the three methods revealed that 5-hydroxytryptamine synthesis and turnover is decreased by 44-71% in diabetic rats with plasma glucose levels of between 500 and 600 mg%. In addition, the levels of free and bound plasma tryptophan were measured and the levels of the free amino acid were found to be the same in control and diabetic rats. Since diabetic rats exhibit a 40% decrease in brain tryptophan, the free tryptophan level in plasma does not predict brain tryptophan levels in diabetic rats. These data are discussed within the context of psychiatric disturbances experienced by diabetic patients.
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