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Biomedical subjects

F Welsh

Publications and source records attributed to F Welsh.

29 records · Page 2Linked to original sources
PubMed1976

Macrocheilia due to lymphangiectasia.

A case of symmetrical, diffuse macrocheilia due to lymphangiectasia is presented. No primary cause for this case or for many other pathologic forms of macrocheilia has been established. Tranverse mucosal wedge resection of the lip with mucosal advancement, however, is a satisfactory method of treatment.

Adolescent↗
PubMed1975

Experimental cerebral oligemia and ischemia produced by intracranial hypertension. Part 1: Pathophysiology, electroencephalography, cerebral blood flow, blood-brain barrier, and neurological function.

Cerebral blood flow, electrical activity, and neurological function were studied in rabbits subjected to either 15 minutes of oligemia (20 torr cerebral perfusion pressure) or complete cerebral ischemia produced by cisterna magna infusion. During oligemia, flow was reduced from 68.4 +/- 4.2 ml/100 gm/min to 26.3 +/- 4.4 (p less than .01), and during ischemia animals had no proven flow. By 5 minutes after oligemia or ischemia significant symmetrical hyperemia occurred and there was no evidence of the no-reflow phenomenon. The electroencephalogram became isoelectric significantly later and returned significantly sooner in oligemia than in ischemia. Oligemic animals had earlier and better return of neurological function than their ischemic counterparts, although postinsult hypocapnia improved functional recovery in both groups. These experiments do not support the concept that oligemia is a more severe insult than complete ischemia. In intracranial hypertension produced by this model, the no-reflow phenomenon does not occur.

Animals↗
PubMed1975

Experimental cerebral oligemia and ischemia produced by intracranial hypertension. Part 2: Brain morphology.

The authors studied the morphological sequelae of 15 minutes of cerebral oligemia (20 torr cerebral perfusion pressure) and complete cerebral ischemia produced by raised intracranial pressure in rabbits. Ischemic cell change was present in five of seven ischemic animals; it was most extensive in the striatum and hippocampus, with only a few ischemic nerve cells in the thalamus and neocortex. The brains of control and oligemic animals were normal. These results indicate the following: 1) ischemia is a more severe insult than oligemia; 2) compression ischemia results in a pattern of damage that differs from that produced by other types of ischemia; and 3) the method used to reduce cerebral perfusion pressure is an important factor in determining the pattern and extent of brain damage produced.

Animals↗
PubMed1975

Experimental cerebral oligemia and ischemia produced by intracranial hypertension. Part 3: Brain energy metabolism.

The authors studied the effect on cortical metabolites of intracranial hypertension produced by the infusion of mock cerebrospinal fluid into the cisterna magna in rabbits subjected to 15 minutes of cerebral oligemia (20 torr) or 15 minutes of complete ischemia. In both groups high-energy metabolites were exhausted within the first 5 minutes of the 15-minute insult. Significant recovery of the high-energy intermediates occurred within 15 minutes of reperfusion, well before return of electroencephalogram (EEG) activity. Continued reperfusion, during which electrical activity and function were returning, brought only moderate improvement in energy metabolites. In contrast, severe lactic acidosis persisted at least 15 minutes after insult, but was reduced by the time EEG activity returned. At no time were there striking differences in metabolites between the oligemic and ischemic groups. These results indicate that recovery in general, and the significantly earlier recovery of oligemic as compared to ischemic animals, cannot be explained on the basis of energy supply. Whether the persistence of lactic acidosis is an important factor limiting return of function requires further study.

Adenosine Triphosphate↗
PubMedDate not supplied

A microtiter plate technique for the detection of platelet antibodies and platelet antigen typing.

A microtiter plate assay is described for platelet serologic studies. The assay is based on an indirect radiolabeled antiglobulin test. The test was performed in microtiter wells of 400 microliter capacity manufactured to form strips that fit into a standard 96-well carrier. The strips were broken apart and placed into tubes for counting in a gamma counter. The technique does not require fixation of the platelets to the wells. Freshly collected platelets or platelets that have been stored frozen in 5 percent dimethylsulfoxide can be used. Results are presented using the technique for platelet alloantibody identification, platelet antigen typing, and platelet crossmatching.

Antibodies↗