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Biomedical subjects

J J Wood

Publications and source records attributed to J J Wood.

12 recordsLinked to original sources
PubMed1991

Brachial plexopathy in breast carcinoma--an unsolved problem.

Brachial plexus involvement from carcinoma of the breast produces a severe disability which presents difficulties in diagnosis and treatment. Five patients who suffered this complication are described and the problems they present are discussed.

Adult↗
PubMed1987

Immature T lymphocytes after injury characterized by morphology and phenotypic markers.

Changes in the peripheral blood mononuclear cell (PBMC) population in patients following both thermal and nonthermal injury were defined by both morphological characteristics and surface phenotype with the monoclonal antibodies T6, OKT9, OKT10, and OKIa1, using a fluorescence activated flow cytometer with gating to separate small cells of the lymphocyte series from larger forms. Lymphocytes with surface antigens that bind T6, OKT9, and OKT10 are rarely found in the peripheral blood of adult patients, except in those with malignancies of the lymphoid system. In both burn and trauma patients the percentage of lymphocytes in the PBMC population after Ficoll-Hypaque separation was significantly reduced as compared with normal controls due to increases in the number of granulocytes, large granular lymphocytes (LGL), and monocytes, often present in immature forms. T6 cells were found in significantly greater numbers in both burn and nonthermal injury patients than in a control group using both small and wide gate settings on the fluorescence-activated flow cytometer. Significant increases in the number of T9+ cells also were observed in both groups for a prolonged period following injury. Significantly increased numbers of the T10+ and Ia1+ cells were detected in burn patients. The response to injury, therefore, involves the appearance in the peripheral blood of immature cells that may express T6, T9, T10, and Ia1 surface antigens. These cells may be present in quantities otherwise seen only in malignant disease.

Adolescent↗
PubMed1986

Abnormalities of antibody production after thermal injury. An association with reduced interleukin 2 production.

Antibody (Ab) production was studied in 25 burned patients who were immunized with 0.5 mg of tetanus toxoid adsorbed. Anti-tetanus toxoid (TT) Ab was measured by hemagglutination, radial immunodiffusion, and an enzyme-linked immunosorbent assay, and the results for the patients were compared with those for five similarly immunized healthy controls. As measured by hemagglutination, 12 (63%) of 19 patients had lower Ab responses than all five controls (P less than .05 by chi 2), and the median Ab response during the period of maximum response was significantly less than that in controls (8 vs 15.5 log2 maximum dilution; P = .014). After the initial response, serum Ab levels were not maintained in patients, in contrast to controls. This pattern was demonstrated by all three assays; enzyme-linked immunosorbent assay demonstrated that IgG anti-TT Ab was the major class of Ab produced. In nine patients interleukin 2 production by T lymphocytes was measured simultaneously; it was significantly depressed throughout the study except during the period from 36 to 45 days. The Ab response was also impaired in this patient group. Since maintained antibody production in response to TT is known to be T-cell dependent, these results suggest that inadequate interleukin 2 production leading to reduced T-cell help may be responsible for the lack of a persistent Ab response in these burned patients.

Adolescent↗
PubMed1979

Effects of hypoxia and hypotension on oxygen delivery in the brain.

Failure of microvascular re-perfusion, no reflow, of the brain after a period of ischemia has been proposed as the etiology of the cerebral dysfunction frequently seen in patients after resuscitation from hemorrhagic shock. For this investigation rats were stressed by subjecting them to a period of combined hypoxia and hypotension followed by resuscitation. Micro-oxygen electrodes measured brain oxygen tension, thus allowing an assessment of the distribution of cerebral blood flow, during stress and after resuscitation. After resuscitation, a hyperemic response was noted, followed by gradual return of some areas of the brain to normal perfusion, while other areas remained hyperemic for at least 2 hours post-resuscitation. On the basis of these results there appears to be no support for the no-reflow hypothesis. These data imply that therapeutic modalities aimed at increasing cerebral blood flow and oxygenation in the post-resuscitation period are insufficient in themselves for improved survival of patients sustaining a hypotensive, hypoxic episode.

Animals↗
PubMed1978

Restitution of ATP and creatine phosphate after experimental depletion in young, adult, and old rats.

The rates of restitution of skeletal muscle, heart, and brain creatine phosphate and brain ATP, following experimental depletion, were compared in young (3-5 month), adult (12 month) and old (24 month) rats. In skeletal muscle, restitution of creatine phosphate after 3 min of recovery was greatest in the young rats, minimal in the adult animals, and absent in the old animals. In heart muscle, on the other hand, restitution was rapid in all three age groups, and was essentially complete after 60 sec recovery. In brain, restitution of creatine phosphate was rapid and was complete after 10 min recovery in the young and adult rats; restitution was slower and less complete in the old rats. In the old rats there was no restitution of brain ATP during the first 2 min of recovery, after which the rate of restitution paralleled that of the young and adult rats.

Adenosine Triphosphate↗
PubMed1977

Recovery of brain energy metabolism following a period of combined hypoxia and hypotension.

Rats were "stressed" by a 30-min period of hypoxia (FIO2 = 7.5%) and hypotension (x arterial pressure = 30 mm Hg), and then "resusciated" by restoring FIO2 = 30% and reinfusing shed blood to restore arterial pressure toward baseline values. Concentrations of brain phosphocreatine, ATP and lactate were measured after "stress" and 20, 60, and 120 min after "resuscitation". A biphasic response was noted in which ATP was initially restored to baseline values by "resuscitation", and then progressively decreased. Physiologic mechanisms to explain the observed data are presented.

Adenosine Diphosphate↗
PubMed1977

Role of glucose-6-phosphate in cerebral dysfunction following hypoxia and hypotension.

Rats were "stressed" by a 30-minute period of breathing 7.5% oxygen combined with hemorrhagic hypotension (x arterial pressure = 25 mm Hg), and then "resuscitated" by restoring the inspired oxygen concentration to 30% and reinfusing the blood previously removed to produce hypotension. We have previously noted in initial return of brain adenosine-triphosphate to normal after this "stress" followed by a progressive decline during the post-resuscitation period. In this study, substrate deficiency was investigated as a possible etiology for the decreased adenosine-triphosphate. Glucose and glucose-6-phosphate concentrations in the brain were measured before "stress" and after resuscitation and were found not to change, indicating no deficiency of substrate.

Animals↗