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Biomedical subjects

R D Neumann

Publications and source records attributed to R D Neumann.

96 records · Page 6Linked to original sources
PubMedDate not supplied

Antisense radiotherapy: targeting full-size mdrl mRNA with 125I-labelled oligonucleotides.

PURPOSE: Antisense radiotherapy is an approach based on the targeting of mRNA of specific genes by complementary oligonucleotide probes labelled with an Auger-electron-emitting radioisotope. Decay of the Auger emitter should specifically destroy the targeted mRNA while producing minimal damage to the rest of mRNA pool and the nuclear DNA. The feasibility of this approach was investigated by using full-length human multidrug-resistance gene (mdr1) mRNA as a target. MATERIALS AND METHODS: Antisense oligonucleotides were labelled with [125I] I-dCTP by primer extension and annealed to target mRNA. Breaks in the target mRNA were analysed by denaturing polyacrylamide gel electriphoresis. RESULTS: The efficiency of 125I-labelled antisense oligonucleotides in producing RNA strand breaks was tested on short synthetic RNA and DNA targets. The position and specificity of 125I-induced breaks in the full-length mRNA were then tested and compared with the cleavage of the target by RNase H. The distribution of the breaks in the longer mRNA is different from that in the short RNA targets, most likely due to a complex folding of RNA strands in the full-length mRNA. CONCLUSIONS: The authors posit that 125I-labelled antisense probes could be useful not only for targeting mRNA, but also as probes for mRNA folding in vivo.

Deoxycytosine Nucleotides↗
PubMedDate not supplied

1982 George Simon Memorial Fellowship Award. Experimental studies with 111indium-labeled platelets in pulmonary embolism.

The effects of several potential modifiers on the detection of experimental pulmonary emboli by indium-111-labeled autologous platelets were studied. Contrast material did not affect embolus visualization; heparin prevented it, but its effect was not irreversible. The addition of exogenous thrombin to the experimental thrombus was not necessary for successful detection of the resulting emboli. Indium-111-oxine detected a small number of emboli without in vitro platelet labeling. Acutely embolized thrombi up to 72 hours old were readily identified by labeled platelets, but emboli older than 24 hours were almost impossible to detect. There was evidence suggesting propagation of emboli within the pulmonary arteries.

Acute Disease↗
PubMedDate not supplied

Platelet kinetics and biodistribution in canine endotoxemia.

Kinetics and magnitudes of changes in Indium-labeled platelet biodistribution were studied in dogs given E. coli endotoxin. Marked, reversible, dose-dependent shifts of platelets from blood to lung and apparently irreversible shifts to liver were demonstrated. These were contemporaneous with alterations in blood gases and in pulmonary and systemic hemodynamics. Morphologic studies revealed atelectasis, sequestration of leukocytes and platelets in the lungs, and mild interstitial pulmonary edema. This study provides in vivo quantification of labeled platelet response to a specific stimulus, and illustrates a method that could be applied to more extensive study of blood element participation in acute lung injury.

Animals↗
PubMedDate not supplied

The influence of heparin on the in vivo distribution of IN-111 labeled platelets.

We investigated the influence of heparin (H) (bolus i.v.; 100-200 I.U./kg.) on the in vivo distribution and accumulation of autologous indium-111-platelets (In-111-P) on experimental pulmonary emboli (PE) in a canine model. Using a thrombin clot formation technique, we induced pulmonary emboli in ten dogs; three dogs were treated with heparin (H), and seven were not (NH). Of five control animals without PE, two were heparinized (H-control) and three were not (NH-control). Animals were sacrificed after 4 to 5 hours of serial blood sampling and sequential scintigraphy. We observed that heparin increased the recovery of In-111-P in the peripheral blood circulation of both control and PE dogs, and reduced the liver uptake of In-111-P in the PE dogs. No PE could be detected while the dogs were fully heparinized, but as the heparin effect dissipated over time, the deposition of In-111-P permitted the scintigraphic detection of PE.

Animals↗
PubMedDate not supplied

Shoulder strength following acromioclavicular injury.

The acromioclavicular (AC) joint enjoys the dubious distinction of being one of the few joints in the body whose total dislocation is routinely treated by simply leaving the joint dislocated. Adherents of both conservative and operative treatment have presented reasons for their viewpoints. Residual shoulder weakness has been offered as a sequela of untreated acromioclavicular injury and a reason for repairing the joint. An objective evaluation of shoulder strength would be valuable in determining the optimum treatment for this injury. The purpose of our study was to quantitate, using the Cybex II, the residual shoulder weakness following various modes of treatment. Seventeen patients with Grade III AC separations and eight patients with Grade II AC sprains were reviewed. Nine of the Grade III injuries were treated and eight nonoperatively. All Grade II injuries were treated nonsurgically. All patients were tested on the Cybex II isokinetic dynamometer at both slow and fast speeds through various ranges of motion. Grade III injuries treated nonoperatively showed no significant strength deficits. Surgically treated Grade III injuries had a significant strength deficit in vertical abduction at fast speeds (19.8%) when compared to the uninjured shoulder. Interestingly, the Grade II injuries led to a significant weakness in horizontal abduction (24.3%) at fast velocity. Evaluation of subjective results showed that Grade III injuries treated conservatively had the most pain and stiffness, despite their strong shoulders. Patients with Grade III injuries treated operatively rated their overall outcome below that of those treated conservatively.(ABSTRACT TRUNCATED AT 250 WORDS)

Acromioclavicular Joint↗