Showing papers by "University of Tennessee Health Science Center published in 1990"
TL;DR: It is recommended that all pregnant women having any of these symptoms should have a complete blood cell count with platelet and liver enzyme determinations irrespective of maternal blood pressure, because of the high maternal and perinatal mortality and morbidity reported with the presence of this syndrome.
591 citations
TL;DR: This phase separation technique provides a rapid and gentle method for removing endotoxin from protein solutions, and retained normal functions when treating proteins treated by this procedure.
549 citations
TL;DR: The sensitivity of the giant aspiny interneuron to a relatively small number of proximal afferent synaptic contacts, its tonic firing, and its widespread dendritic and axonal fields place it in an excellent position to act as a modulator of the excitability of neostriatal projection neurons in advance of the onset of movement-related neostRIatal activity.
Abstract: Intracellular recordings were made in vivo from 9 giant aspiny neurons in the neostriatum of urethane-anesthetized rats. The cells were identified by intracellular staining with HRP or biocytin. The neurons exhibited morphological features typical of neostriatal cholinergic interneurons. Six of the cells were obtained from intact animals, while 3 were recorded from rats with ipsilateral hemidecortications. Giant aspiny neurons were characterized by their slow irregular but tonic (3–10/sec) spontaneous activity and long-duration action potentials. Examination of the underlying membrane potential trajectories during spontaneous firing revealed that individual action potentials were triggered from spontaneous small (1–5 mV) depolarizing potentials. These spontaneous potentials exhibited the voltage sensitivity of ordinary EPSPs. They were much less frequent during the 80–200 msec pause in tonic afferent input that follows the excitation evoked by cortical or thalamic stimulation, and were decreased in frequency in decorticate animals. Their rise times and half-widths matched those expected for unitary synaptic potentials placed proximally on the surface of the neurons. Low-intensity stimulation of neostriatal afferents produced small short-latency EPSPs that appeared to be composed of responses identical to the spontaneous depolarizing potentials. The latencies of the EPSPs evoked from the cerebral cortex and thalamus were consistent with a monosynaptic input from both structures, but the maximal size of the EPSPs was much smaller than that evoked in spiny neurons, suggesting that a smaller number of afferent inputs make synapses with each of the aspiny cells. Giant aspiny neurons exhibited much larger input resistances and longer time constants than spiny neostriatal neurons. They also exhibited relatively linear steady-state current-voltage relationship compared to spiny projection cells. Input resistances ranged from 71–105 M omega, and time constants ranged from 17.8–28.5 msec. Analysis of the charging transients in response to current pulses yielded estimates of dendritic length of approximately 1 length constant. Repetitive firing of the neurons was limited by a powerful spike afterhyperpolarization and by a strong spike frequency adaptation. The sensitivity of the giant aspiny interneuron to a relatively small number of proximal afferent synaptic contacts, its tonic firing, and its widespread dendritic and axonal fields place it in an excellent position to act as a modulator of the excitability of neostriatal projection neurons in advance of the onset of movement-related neostriatal activity.
509 citations
TL;DR: Assessment instruments are particularly useful in screening for problems that often go undetected in older patients and can provide information about conditions and abilities or limitations that are not regularly assessed in standard clinical practice.
Abstract: Structured assessment instruments are particularly useful in screening for problems that often go undetected in older patients. In addition, such instruments can provide information about conditions and abilities or limitations that are not regularly assessed in standard clinical practice. Often, their administration is delegated to other health professionals, but these tools still provide useful information to the physician. Clinicians should view assessment instruments as they would any other clinical test. They should be familiar with the strengths, weaknesses, and precision of any test used and understand how best to use the test as an adjunct to clinical practice. In addition, clinicians must learn to focus on functional status, in terms of both assessment and outcome, in their care of older patients.
426 citations
TL;DR: The study indicates that, in the striatum, immunocytochemistry for PV selectively stains GABAergic interneurons and that the neurons are incorporated in a feed-forward inhibitory circuit of the Striatum.
424 citations
TL;DR: In this article, a cDNA encoding human neutrophil collagenase from a lambda gt11 cDNA library constructed from mRNA extracted from the peripheral leukocytes of a patient with chronic granulocytic leukemia was identified and sequenced.
417 citations
TL;DR: The data suggest that keratan sulfate, alone or in combination with other molecules expressed by the roof plate, may be responsible, in part, for the inhibition of axon elongation through the roof Plate in the embryonic spinal cord.
391 citations
TL;DR: It is concluded that the treatment of selected elderly patients in a specialized geriatric rehabilitation unit improves function, decreases the risk of nursing home placement, and may reduce mortality.
Abstract: We conducted a randomized trial in a community rehabilitation hospital to determine the effect of treatment in a geriatric assessment unit on the physical function, institutionalization rate, and mortality of elderly patients. Functionally impaired elderly patients (mean age, 78.8 years) who were recovering from acute medical or surgical illnesses and were considered at risk for nursing home placement were randomly assigned either to the geriatric assessment unit (n = 78) or to a control group that received usual care (n = 77). The two groups were similar at entry and were stratified according to the perceived risk of an immediate nursing home placement. After six months, the patients treated in the geriatric assessment unit had significantly more functional improvement in three of eight basic self-care activities (P less than 0.05). Those in the lower-risk stratum had significantly more improvement in seven of eight self-care activities. Both six weeks and six months after randomization, significantly more patients treated in the geriatric assessment unit than controls (79 vs. 61 percent after six months) were residing in the community. During the year of follow-up, the control patients had more nursing home stays of six months or longer (10 vs. 3; P less than 0.05). However, there was no difference between the groups in the mean number of days spent in health care facilities (acute care hospital, nursing home, or rehabilitation hospital). Survival analysis showed a trend toward fewer deaths among the patients treated in the geriatric assessment unit, and mortality was significantly reduced in the patients considered to be at lower risk of immediate nursing home placement (P less than 0.05). We conclude that the treatment of selected elderly patients in a specialized geriatric rehabilitation unit improves function, decreases the risk of nursing home placement, and may reduce mortality. The beneficial effects on mortality and function appear greatest for patients at a moderate rather than high risk of nursing home placement.
370 citations
TL;DR: It is concluded that estrogen replacement after menopause prolongs survival when coronary artery disease is present, but it has less effect in the absence of coronary arteries disease.
Abstract: The relationship among postmenopausal estrogen use, coronary stenosis, and survival was examined retrospectively in 2268 women undergoing coronary angiography. The patients were selected for study if their age was 55 years or older at the time of angiography or if they had previously undergone bilateral oophorectomy. Postmenopausal estrogen use in 1178 patients with coronary artery disease (greater than 70% stenosis) and 644 patients with mild to moderate coronary artery disease (5% to 69% stenosis) was compared with 446 control subjects (0% stenosis) using life-table analysis. Over 10 years of follow-up, there was no significant difference in survival among patients initially free of coronary lesions on arteriography who had either never used (377) or ever used (69) estrogens. Among patients with mild to moderate coronary stenosis, 10-year survival of those who had never used estrogens was 85.0% and it was 95.6% among 99 "ever users." Survival was 60.0% among those with more than 70% coronary stenosis who had never used estrogen and it was 97.0% among 70 ever users. The "never users" group were older (65 vs 59 years), had a lower proportion of cigarette smokers (40% vs 57.1%), a higher proportion of subjects with diabetes (21.7% vs 12.9%) and hyperlipidemia (58% vs 44%), and approximately equal numbers of hypertensives (56.0% vs 54.3%). Cox's proportional hazards model was used to estimate survival as a function of multiple covariables. Estrogen use was found to have a significant, independent effect on survival in women. We conclude that estrogen replacement after menopause prolongs survival when coronary artery disease is present, but it has less effect in the absence of coronary artery disease.
352 citations
TL;DR: Projections from the basolateral nucleus of the amygdala to the frontal cortex and the striatum were studied by using Phaseolus vulgaris‐leucoagglutinin (PHA‐L) anterograde tracing technique in the rat.
Abstract: Projections from the basolateral nucleus of the amygdala (BLA) to the frontal cortex and the striatum were studied by using Phaseolus vulgaris-leucoagglutinin (PHA-L) anterograde tracing technique in the rat. PHA-L injections into the rostral part of the BLA resulted in a dense labeling of fibers with boutons in the dorsal bank of the rhinal fissure and in the lateral and the medial agranular cortex. PHA-L injections into the caudal part of the BLA produced a dense labeling of fibers in the medial surface of the frontal cortex. In most of the cortical regions, labeled fibers were predominantly distributed in two bands: one in the deep part of layers I and II and the other, heavier band, in layers V and VI. PHA-L injections into the rostral BLA resulted in a dense labeling of fibers with boutons in the olfactory tubercle, the rostral and caudolateral portion of the nucleus accumbens, and a large region of the caudate-putamen. The labeled area of the caudate-putamen included the rostroventral area, the central area, and the area caudal to the anterior commissure and dorsal and lateral to the globus pallidus. PHA-L injections into the caudal BLA produced fiber labeling in the most rostromedial area of the caudate-putamen facing the lateral ventricle, the medial portion of the nucleus accumbens, and the lateral septum. In the rostroventral striatum, PHA-L-labeled fibers selectively innervated the matrix compartment that contains abundant somatostatin-immunoreactive fibers. Compartmental segregation was less clear in the caudodorsolateral caudate-putamen and in the nucleus accumbens. Electron microscopy revealed that PHA-L-labeled boutons in the striatum contained abundant, small, round vesicles. These boutons formed asymmetrical synapses with dendritic spines of striatal neurons.
348 citations
TL;DR: T(1;14)(p32;q11) translocations and tald rearrangements disrupt the coding potential of tal‐1 in an equivalent manner, and thereby generate a common genetic lesion shared by a significant proportion of T‐ALL patients.
Abstract: The tal-1 gene is altered as a consequence of the t(1;14) (p32;q11) chromosome translocation observed in 3% of patients with T cell acute lymphoblastic leukemia (T-ALL). tal-1 encodes a helix-loop-helix (HLH) domain, a DNA binding and dimerization motif found in a number of proteins involved in cell growth and differentiation. We now report that an additional 25% of T-ALL patients bear tal-1 gene rearrangements that are not detected by karyotype analysis. These rearrangements result from a precise 90 kb deletion (designated tald) that arises independently in different patients by site-specific DNA recombination. Since the deletion junctions resemble the coding joints of assembled immunoglobulin genes, tald rearrangements are likely to be mediated by aberrant activity of the immunoglobulin recombinase. Moreover, t(1;14)(p32;q11) translocations and tald rearrangements disrupt the coding potential of tal-1 in an equivalent manner, and thereby generate a common genetic lesion shared by a significant proportion of T-ALL patients.
TL;DR: The main lines of evidence are assembled that suggest the presence of several novel subtypes for both D1 and D2 dopamine receptors and it is predicted that molecular cloning will, in the near future, confirm their existence.
TL;DR: The findings emphasize the need for intensive monitoring of women with preeclampsia throughout hospitalization and underscore the importance of maternal stabilization before and during transfer.
TL;DR: Results are consistent with the hypothesis that chorea results from preferential loss of striatal neurons projecting to the lateral globus pallidus and that rigid‐akinetic HD is a consequence of the additional loss of Striatal neurons projection to the medial segment of the pallidum.
Abstract: Neuropeptide immunohistochemistry was used to test several hypotheses of the anatomical bases of chorea and rigidity-akinesia. To test the hypothesis that elevated concentration of striatal somatostatin causes chorea, we visually compared the density of striatal neurons containing somatostatin and neuropeptide Y in brains affected by choreic or rigid-akinetic Huntington's disease (HD). The density of these neurons was elevated in both rigid-akinetic and choreic HD specimens with an apparently normal total number of these neurons, indicating that elevated somatostatin concentration, by itself, does not lead to chorea. We tested the hypothesis that rigid-akinetic HD results from deficient dopaminergic nigrostriatal neurotransmission by examining tyrosine hydroxylase-immunoreactive (TH-IR) neurons in the substantia nigra. In rigid-akinetic HD brains, there was no obvious reduction of nigral TH-IR neurons, indicating that rigid-akinetic HD is probably not due to loss of nigral dopaminergic neurons. Finally, we also examined the status of striatal projection neurons and found near total loss of all striatal neurons projecting to the lateral globus pallidus, medial globus pallidus, and substantia nigra in brains affected by rigid-akinetic HD in contrast to the preservation of neurons projecting to the medial globus pallidus in choreic HD. These results are consistent with the hypothesis that chorea results from preferential loss of striatal neurons projecting to the lateral globus pallidus and that rigid-akinetic HD is a consequence of the additional loss of striatal neurons projecting to the medial segment of the pallidum.
TL;DR: The neurotransmitter organization of striatal projection neurons appears to be less complex than once thought and each neuron utilizes multiple neuroactive substances to influence target neurons, simplifying understanding of neurotransmission between these neurons and their target areas.
TL;DR: Analysis with restriction-fragmentlength polymorphisms (RFLPs) has localized the Huntington's disease gene close to the telomere of the short arm of chromosome 4.
Abstract: HUNTINGTON'S disease is an autosomal dominant disease characterized by slowly progressive personality changes, dementia, and movement disorders.1 , 2 The average age at onset is 30 to 40 years, and the disease lasts for an average of 15 to 20 years. Analysis with restriction-fragmentlength polymorphisms (RFLPs) has localized the Huntington's disease gene close to the telomere of the short arm of chromosome 4.1 2 3 Prominent striatal atrophy with loss of striatal neurons and relative sparing of fibers of passage and afferent axons is the pathological hallmark of Huntington's disease.4 Recent studies have demonstrated a distinct pattern of vulnerability of striatal neurons in Huntington's . . .
TL;DR: Heterogeneous groups of neurons exist in the PPN in terms of morphology, transmitter phenotypes and electrical membrane properties, as indicated by in vitro parasagittal slice preparation data.
TL;DR: Treatment of maternal blood pressure in mild chronic hypertension during pregnancy did not improve perinatal outcome and there were no differences among the groups regarding gestational age at delivery, birth weight, incidence of fetal growth retardation, or neonatal head circumference.
TL;DR: Investigation of cartilage from arthritic joints of rats immunized with type II collagen suggests that chondrocytes may play a direct role in the earliest stages of the degradation of their own matrices, and that stromelysin is responsible for proteoglycan degradation in early inflammatory arthritis.
Abstract: Articular cartilage from arthritic joints of rats immunized with type II collagen is severely depleted of proteoglycans. Depletion begins within 48 hours after the onset of inflammation, prior to extensive pannus formation, and may represent a critical first step in cartilage destruction. We have immunolocalized stromelysin, an enzyme that is believed to play a major role in the pathologic degradation of proteoglycans, in the joints of rats with collagen-induced arthritis. Immunoperoxidase staining of frozen tissue sections demonstrated the presence of stromelysin in both the synovium and chondrocytes. In contrast, collagenase was localized primarily to the pannus-cartilage junction. Neither enzyme was detectable in joints from normal animals. To test the hypothesis that chondrocytes respond directly to inflammatory mediators by increasing the production of stromelysin, isolated chondrocytes were incubated with various concentrations of interleukin-1. The culture media were also assayed for the presence of stromelysin by immunoreactivity on Western blots and by analysis of enzymatic activity on casein substrate gels. A 3-fold increase in a doublet of proteins synthesized in response to 10 units/ml of interleukin-1 was observed. These proteins also immunoreacted with the stromelysin antibody and degraded casein. Northern blotting results established that the increased levels of stromelysin were accompanied by increases in stromelysin-specific messenger RNA levels. These results suggest that stromelysin is responsible for proteoglycan degradation in early inflammatory arthritis, and that chondrocytes may play a direct role in the earliest stages of the degradation of their own matrices.
TL;DR: In highly trained athletes, prolonged exercise causes differing responses of the right and left ventricles, which may be due to changes in right ventricular function, shape or compliance.
TL;DR: Evidence in the literature indicates that magnesium sulfate is the ideal anticonvulsant in preeclampsia-eclampsian convulsions, and phenytoin has been recommended as an alternative, however, comprehensive data regarding its safety and efficacy are lacking.
TL;DR: Methods reported here may prove useful for measuring leukocyte influx into inflamed tissues, detecting MPO or EPO deficiencies, and measuring enzyme synthesis and secretion.
TL;DR: It is found that under the influence of muscarinic agonists, the voltage dependence of A-current activation and inactivation is shifted towards more negative membrane potentials and the peak conductance is increased.
Abstract: NEURONS of the neostriatum are richly innervated by cholinergic neurons of intrinsic origin1–3. Both pre- and post-synaptic muscarinic receptors mediate the effects of acetylcholine (ACh) 4–6. Activation of these receptors is functionally significant, particularly in Parkinson's disease7. Current-clamp studies indicate that muscarinic receptors serve to decrease the responsiveness of neostriatal neurons to excitatory inputs8–10. Here we present evidence that this effect is caused, in part, by the muscarinic modulation of the A-current, a transient outward potassium current. The voltage dependence of this current suggets that normally it enhances spike repolarization and slows discharge rate, but does not affect 'synaptic integration'. We find that under the influence of muscarinic agonists, the voltage dependence of A-current activation and inactivation is shifted towards more negative membrane potentials and the peak conductance is increased. Therefore, at relatively hyperpolarized resting potentials, ACh transiently alters the functional role of the A-current, allowing it to suppress excitatory inputs and further slow the discharge rate. But at relatively depolarized resting potentials, ACh increases excitability by removing the A-current through inactivation.
TL;DR: The data suggest that GP IIb-IIIa can exist in multiple conformations in the platelet membrane, D3GP3 binding to GP IIIa can expose the fibrinogen receptor, and the binding of either RGDS peptides or fibr inogen causes exposure of the D3 GP3 epitope.
TL;DR: The minimum incidence of FES in LBPF is 11%, and four patient groups were established: No Qsp, Qsp with pulmonary injury (Qsp + PI), Qsp without pulmonary injury or petechaie (FES - P), and QspWithout pulmonary injury and with petechiae (Fes + P).
Abstract: Hypoxemia following long bone or pelvic fracture (LBPF) is often attributed to fat embolism syndrome (FES), but the true incidence and etiology of postfracture pulmonary shunt (Qsp) are not well defined. Over 12 months, 92 patients with LBPF admitted to a Level I trauma center were prospectively evaluated. Arterial blood gases, Hct, platelet count, serum fibrinogen, serum lipase, and urinary fat bodies (UFB) were determined serially from admission through the fifth hospital day. Patients were evaluated daily by chest x-ray, vital signs, mental status, and presence of petechiae. Four patient groups were established: No Qsp, Qsp with pulmonary injury (Qsp + PI), Qsp without pulmonary injury or petechaie (FES - P), and Qsp without pulmonary injury and with petechiae (FES + P). Qsp indicated by an alveolar/arterial PO2 gradient greater than 100 torr developed in 49 (53%) of the patients. Pulmonary injury was present in 39 (81%) of those 49 and was at least partially responsible for the shunt. The remaining ten patients were diagnosed as having FES; four had petechiae (FES + P) and six were without petechiae (FES - P). The minimum incidence of FES in LBPF is therefore 11%.
TL;DR: Regular case review of short-term returns to the ED should be included in a comprehensive ED-based program of quality assurance.
TL;DR: The presence of abnormal glial arrangements and glycoconjugate boundaries in the cortices of the genetic mutant mouse reeler, and findings on plasticity of boundaries following various perturbations, suggest that boundary expression is controlled by both genetic and epigenetic factors.
TL;DR: It is concluded not only that critically ill pregnant women can be managed successfully in an obstetric intensive care unit but also that critical care is a bona fide part of obstetric practice and has been incorporated into the training program.