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Biomedical subjects

P L Goldberg

Publications and source records attributed to P L Goldberg.

7 recordsLinked to original sources

Rearrangement of adherens junctions by transforming growth factor-beta1: role of contraction.

The signal transduction pathways that lead to disruption of pulmonary endothelial monolayer integrity by transforming growth factor-beta1 (TGF-beta1) have not been elucidated. The purpose of this investigation was to determine whether disassembly of the adherens junction is temporally associated with the TGF-beta1-induced decrease in pulmonary endothelial monolayer integrity. Measurement of albumin clearance and electrical resistance showed that monolayer integrity started to decrease between 1 and 2 h post-TGF-beta1 treatment and continued to slowly decrease over the next 6 h. Immunofluorescence microscopy of monolayers between 2 and 3 h post-TGF-beta1 showed that beta-catenin, plakoglobin, alpha-catenin, and cadherin-5 were colocalized both at the cell periphery and in newly formed bands that are perpendicular to the cell-cell border. At 4 h post-TGF-beta1, cells began separating; however, beta- and alpha-catenin, plakoglobin, and cadherin-5 could still be found at the cell periphery at areas of cell separation and in strands between separated cells. By 8 h, these junctional proteins were no longer present at the cell periphery at areas of cell separation. The myosin light chain kinase inhibitor KT-5926 prevented the TGF-beta1-induced change in integrity but did not inhibit the formation of actin stress fibers or the formation of bands containing adherens junction proteins that were perpendicular to the cell-cell junction. Overall, these results suggest that adherens junction disassembly occurs after cell separation during TGF-beta1-induced decreases in pulmonary endothelial monolayer integrity and that the loss of integrity may be due to the activation of a myosin light chain kinase-dependent signaling cascade.

Animals↗

Should x-rays be ordered to find a bee's stinger?

On several occasions, we have been asked to locate bee stingers so that they could be removed. The studies were negative, and we did not know if identification was even possible. An experiment was done using both film screen studies and xerograms at various techniques to attempt to locate a honey bee stinger. The stinger could not be identified.

Animals↗

Pulmonary candidiasis in infants: clinical, radiologic, and pathologic features.

Although systemic candidiasis is common in hospitalized patients, invasive pulmonary candidiasis is rare and generally considered of secondary importance when found at autopsy. Autopsy records for a 12 year period were reviewed and 15 infants were found in whom systemic candidiasis was considered the primary or a major contributory cause of death. Significant pulmonary involvement was found in 14. There were three characteristic histologic patterns of pulmonary candidiasis: (1) embolic (arterial-invasive) (seven cases); (2) disseminated (capillary-invasive) (four cases); and (3) bronchopulmonary (air space-invasive) (three cases, including one congenital infection). An indwelling vascular catheter or infected cutdown wound was the portal of entry in every case of the embolic form of pulmonary candidiasis. Systemic and pulmonary Candida infections were rarely diagnosed during life. The typical radiographic appearance was progressive air space consolidation, although two infants with the embolic form of pulmonary candidiasis had focal cavitation. In general, there was poor correlation between the radiologic and pathologic findings, and pathologic findings other than pulmonary candidiasis undoubtedly accounted for many of the radiologic abnormalities observed. There were no radiologic findings that could be used to differentiate the three histologic forms of lung involvement in these patients. Small lung nodules, the earliest histologic lesion of pulmonary candidiasis, were not seen in any patient owing to the presence of other lung disease and suboptimal radiographic technique.

Autopsy↗

Circulating somatostatin after food and glucose in man.

Using a recently validated radioimmunoassay, changes in circulating somatostatin have been measured in normal subjects after food (a standard breakfast), and oral and intravenous glucose. After the standard breakfast, a clear and sustained rise in plasma somatostatin was seen in all subjects from a mean value (+/-1 SE) of 28 +/- 7 pg/ml to a mean peak value, at 60 min of 57 +/- 11 pg/ml. When glucose was taken by mouth a significant but smaller rise was seen, but intravenous glucose caused no significant change in plasma somatostatin. A rise in circulating somatostatin after feeding has not previously been demonstrated in normal man and it is suggested that somatostatin may have an important endocrine role in the gut.

Adult↗