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Biomedical subjects

D L Greenberg

Publications and source records attributed to D L Greenberg.

8 recordsLinked to original sources

Genetic variation across the historical range of the wild turkey (Meleagris gallopavo).

Genetic differences within and among naturally occurring populations of wild turkeys (Meleagris gallopavo) were characterized across five subspecies' historical ranges using amplified fragment length polymorphism (AFLP) analysis, microsatellite loci and mitochondrial control region sequencing. Current subspecific designations based on morphological traits were generally supported by these analyses, with the exception of the eastern (M. g. silvestris) and Florida (M. g. osceola) subspecies, which consistently formed a single unit. The Gould's subspecies was both the most genetically divergent and the least genetically diverse of the subspecies. These genetic patterns were consistent with current and historical patterns of habitat continuity. Merriam's populations showed a positive association between genetic and geographical distance, Rio Grande populations showed a weaker association and the eastern populations showed none, suggesting differing demographic forces at work in these subspecies. We recommend managing turkeys to maintain subspecies integrity, while recognizing the importance of maintaining regional population structure that may reflect important adaptive variation.

Animals↗

Hippocampal volume in geriatric depression.

BACKGROUND: There is a growing literature on the importance of hippocampal volume in geriatric depression. METHODS: We examined hippocampal volume in a group of elderly depressed patients and a group of elderly control subjects (N = 66 geriatric depressed patients and 18 elderly nondepressed control subjects) recruited through Duke's Mental Health Clinical Research Center for the Study of Depression in the Elderly. The subjects received a standardized evaluation, including a magnetic resonance imaging scan of the brain. Patients had unipolar major depression and were free of comorbid major psychiatric illness and neurologic illness. Differences were assessed using t tests and linear regression modeling. RESULTS: Accounting for the effects of age, gender, and total brain volume, depressed patients tended to have smaller right hippocampal volume (p =.014) and left hippocampal volume (p =.073). Among depressed patients, age of onset was negatively but not significantly related to right hippocampal volume (p =.052) and to left hippocampal volume (p =.062). We noted that among subjects with either right or left hippocampal volume of 3 mL or less, the vast majority were patients rather than control subjects. CONCLUSIONS: These results support a role for hippocampal dysfunction in depression, particularly in late-age onset depression. Longitudinal studies examining both depressive and cognitive outcomes are needed to clarify the relationships between the hippocampus, depression, and dementia.

Aged↗

Self-reported exercise tolerance and the risk of serious perioperative complications.

BACKGROUND: Impaired exercise tolerance during formal testing is predictive of perioperative complications. However, for most patients, formal exercise testing is not indicated, and exercise tolerance is assessed by history. OBJECTIVE: To determine the relationship between self-reported exercise tolerance and serious perioperative complications. METHODS: Our study group consisted of 600 consecutive outpatients referred to a medical consultation clinic at a tertiary care medical center for preoperative evaluation before undergoing 612 major noncardiac procedures. Patients were asked to estimate the number of blocks they could walk and flights of stairs they could climb without experiencing symptomatic limitation. Patients who could not walk 4 blocks and climb 2 flights of stairs were considered to have poor exercise tolerance. All patients were evaluated for the development of 26 serious complications that occurred during hospitalization. RESULTS: Patients reporting poor exercise tolerance had more perioperative complications (20.4% vs 10.4%; P<.001). Specifically, they had more myocardial ischemia (P = .02) and more cardiovascular (P = .04) and neurologic (P = .03) events. Poor exercise tolerance predicted risk for serious complications independent of all other patient characteristics, including age (adjusted odds ratio, 1.94; 95% confidence interval, 1.19-3.17). The likelihood of a serious complication occurring was inversely related to the number blocks that could be walked (P = .006) or flights of stairs that could be climbed (P = .01). Other patient characteristics predicting serious complications in multivariable regression analysis included history of congestive heart failure, dementia, Parkinson disease, and smoking greater than or equal to 20 pack-years. CONCLUSION: Self-reported exercise tolerance can be used to predict in-hospital perioperative risk, even when using relatively simple and familiar measures.

Aged↗

Protease-activated receptor 1 is the primary mediator of thrombin-stimulated platelet procoagulant activity.

The activation of human platelets by thrombin is mediated primarily by protease-activated receptors (PARs). PAR1 and PAR4 are present on human platelets and are activated by the hexapeptides SFLLRN and GYPGQV, respectively. To further characterize the involvement of PAR1 and PAR4 in platelet activation, the ability of SFLLRN or GYPGQV to generate annexin V binding to newly exposed phospholipids on the platelet surface and generate procoagulant activity has been examined. Exposure of phosphatidylserine and phosphatidylethanolamine on platelets, as determined by an increase in annexin V binding, was strongly stimulated by SFLLRN, thrombin, and collagen, but only to a minor extent by GYPGQV. In a clotting assay initiated with factor VIIa, soluble tissue factor, and calcium, the clotting time in the absence of platelets was >5 min. In the presence of unstimulated platelets, the clotting time was 200 +/- 20 sec. In the presence of platelets activated with SFLLRN or collagen, the clotting time decreased to 100 +/- 10 sec. This shortening of the clotting time is equivalent to about a 5-fold increase in coagulant activity when stimulated platelets are compared with unstimulated platelets and activated platelets are used as a reference. These results indicate that thrombin initiates a very strong response in platelets through PAR1, leading to exposure of anionic phospholipids that support blood clotting. The response mediated by PAR4, however, was limited to platelet aggregation and similar to that triggered in platelets by weaker agonists such as ADP or epinephrine.

Annexin A5↗

Visual memory-deficit amnesia: a distinct amnesic presentation and etiology.

We describe a form of amnesia, which we have called visual memory-deficit amnesia, that is caused by damage to areas of the visual system that store visual information. Because it is caused by a deficit in access to stored visual material and not by an impaired ability to encode or retrieve new material, it has the otherwise infrequent properties of a more severe retrograde than anterograde amnesia with no temporal gradient in the retrograde amnesia. Of the 11 cases of long-term visual memory loss found in the literature, all had amnesia extending beyond a loss of visual memory, often including a near total loss of pretraumatic episodic memory. Of the 6 cases in which both the severity of retrograde and anterograde amnesia and the temporal gradient of the retrograde amnesia were noted, 4 had a more severe retrograde amnesia with no temporal gradient and 2 had a less severe retrograde amnesia with a temporal gradient.

Amnesia↗

Transcriptional regulation of the gene coding for human protein C.

The promoter for the gene coding for human protein C has been characterized as to nucleotide sequences that regulate the synthesis of mRNA. The major transcription start site was found 65 nucleotides upstream from the first intron/exon boundary along with two minor sites. Functional characterization of 1528 base pairs at the 5'-end of the gene was then carried out by chloramphenicol acetyltransferase reporter assays, protection from DNase I digestion, and electrophoretic mobility shift assays employing HepG2 and HeLa cells. One of the upstream regions (nucleotides -25 to +9) contained binding sites for at least two different transcription factors, including a hepatic nuclear factor 1-binding site (-10 to +9) and two overlapping and oppositely oriented hepatic nuclear factor 3-binding sites (-25 to -11). A second major region (PCE1) (+12 to +30) appeared to be a unique, liver-specific regulatory sequence. An Sp1-binding site in exon I (+58 to +65) was also recognized by cotransfection experiments with an Sp1 expression plasmid. Specific mutations in these promoter elements reduced transcriptional activity and abolished the binding of hepatic nuclear proteins. Finally, a strong silencer element (PCS1) (between -162 and -82) and two possible liver-specific enhancer regions (PCE2 and PCE3), which interact coordinately with the promoter elements, were also found (between -1462 and -162).

Base Sequence↗

Changing use of intensive care for HIV-infected patients with Pneumocystis carinii pneumonia.

Clinicians' approach to acute respiratory failure from Pneumocystis carinii pneumonia (PCP) is hypothesized to have gone through three phases: aggressive management due to an absence of data on prognosis (1981-84), withholding of intensive care based on a few small studies showing high case fatality (1985-87), and an increase in intensive care to an intermediate level (1988 forward). Unfortunately, studies of survival from acute respiratory failure among such patients have been small and have been limited to patients in the intensive care unit. To determine whether this three-phase scenario has empirical support, we performed a retrospective chart review of all patients with human immunodeficiency virus (HIV) infection and PCP at a university-affiliated municipal hospital from 1983 to 1990. We identified 180 patients, representing 218 episodes of PCP. The previously hypothesized relationship between intensive care and year of diagnosis was confirmed: intubation rates were 30% before 1985, 0% in 1987, and 12% after 1988 (p = 0.03). Among all patients, the percentage dying in the hospital without intensive care had the opposite relationship with year of diagnosis, increasing from 0% in 1984 to 21% in 1987 and then declining to 0% in 1990 (p = 0.001). Overall mortality from an episode of PCP was 25% and did not change significantly over time. Disease severity also did not change significantly over time. In summary, the significant swings in the use of intensive care for HIV-infected patients with PCP suggest that judgments about the futility of intensive care were strongly influenced by incorrect perceptions of survival.

AIDS-Related Opportunistic Infections↗