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Biomedical subjects

S Gregory

Publications and source records attributed to S Gregory.

At least 91 records · Page 5Linked to original sources
PubMed1984

Delayed traumatic intracerebral hematoma: report of 15 cases operatively treated.

Fifteen cases of delayed traumatic intracerebral hematoma (DTICH) operatively treated are reported. Patients who are awake or only drowsy on admission (Coma Grades 1 and 2, Grady scale) often undergo dramatic sudden neurological deterioration 48 to 72 hours after admission. Emergency computed tomographic scanning and prompt craniotomy for hematoma evacuation yield excellent clinical results in the majority of cases. Patients presenting in deeper grades of coma (Grades 3 to 5, Grady scale) who develop DTICH do quite poorly, often because the diagnosis is difficult to make and consequently is delayed. The development of DTICH is in our experience highly unpredictable, and often no clear secondary cause (hypercapnia, hypoxia, bleeding diathesis) can be demonstrated.

Adolescent↗
PubMed1981

Lymphoid source and target of murine leukocyte adherence inhibition factor (LAIF).

The cellular source of murine LAIF detected by an indirect leukocyte adherence inhibition (LAI) assay using capillary tubes was investigated using non-inducing peritoneal cells (PC) from normal and spindle-cell sarcoma-bearing A/J mice. Cell populations containing greater than 95% T-cells, B-cells or macrophages were prepared from PC using a series of elimination and enrichment procedures. The in vitro incubation of enriched T-cell populations (less than 0.05% macrophages) from tumor-bearing mice with the specific soluble tumor antigen did not result in the release of detectable levels of LAIF; however, the addition of 10% normal isologous macrophages to the T-cells resulted in a significant release of LAIF. Enriched B-cell populations did not release LAIF either by themselves of when 10% normal isologous macrophages were added. Cell populations containing both T-cells and B-cells produced significant levels of LAIF, but only when suitable numbers of macrophages were present. Treatment with anti-Thy-1.2 alloantiserum and complement resulted in the abrogation of LAIF production by mixed cell populations. Using Lyt-1.2 and Lyt-2.2 alloantisera and complement to prepare either Lyt-1.2 or Lyt-2.2 depleted T-cell populations, it was found that the Lyt-1.2 subpopulation was responsible for the release of LAIF in this test system. LAIF was found to be effective in reducing the glass adherence of macrophages but not of T-cells or B-cells.

Animals↗
PubMed1981

A quantitative determination for the detection of immunoglobulin (IgG) on the surface of platelets.

A sensitive method for the quantitation of IgG on platelets had not been demonstrated until 1975, when Dixon, Rosse, and Ebbert described a quantitative antiglobulin consumption test useful in detecting platelet associated IgG (N Engl J Med 292:230, 1975). A modification of that technique has rendered the assay reproducible and removed the need for daily repetition of a standard IgG titration curve for quantitation. This modification utilizes 1-ethyl-3-3(dimethylaminopropyl)carbodiimide HCl (ECDI) (Sigma, E-7750), in place of chromic chloride, as a coupling agent for attaching IgG (Miles 64-145) to sheep cells (SRC), used as indicator cells. The ECDI consistently couples IgG to SRC and does not subject the SRC to sporadic spontaneous lysis, as does chromic chloride. This modification permits the detection of IgG on platelets (Direct Test), or in sera (Indirect Test) by incubation of a washed platelet pool with sera in vitro, and testing as in the Direct Test. Normal values of 0.01-1.56 and 0.14-1.6 femtograms (F) per platelet have been obtained for the Direct and Indirect Tests, respectively. In six cases of suspected ITP, values ranged 12.0-221.0 F and 2.9-37.6 F for the Direct and Indirect Tests, respectively. In conclusion, in disease states or other abnormal situations, quantities of IgG can be detected that are not usually present on the platelets of normal subjects.

Blood Platelets↗
PubMed1979

Hearing loss in very low birthweight infants treated with neonatal intensive care.

The hearing of 111 perinatal intensive care survivors of birthweights 1500 g or less was assessed at a mean age of 6 1/2 years (range 4--12). These 111 infants included 86% of the long-term survivors of this birthweight cared for in the newborn unit of University College Hospital, London, during the years 1966--72. All these infants were nursed in commercially available incubators for periods ranging from 2 to 80 days (mean 37) in which the mean noise threshold was 65 dB. Ten (9%) had sensory neural nearing losses, one (1%) infant had a congenital conductive hearing loss, and 21 (19%) infants had exudative otitis media with a mean loss of 25 dB. Apnoeic attacks in the neotal period were the most significant predictors of hearing loss in these infants (P less than 0.05) and an indirect serum filirubin level of at least 170 micromol/l (10 mg/100 ml) in the neonatal period had an additive effect (P less than 0.05). There was no evidence that ambient noise had affected the hearing of these very low birthweight infants.

Apnea↗
PubMed1978

Outcome for infants at high risk of major handicap.

Perinatal intensive care had been introduced in University College Hospital, London, by 1966. In the succeeding 10 years, 28-day mortality rates fell among infants of birth weight 1500 g or less. Among the survivors, the incidence of major handicap was 10% or less and the mean IQ increased to within the range expected for a normal population. Of the children aged 8 years or more 76% had no handicaps and were attending normal schools; 18% had minor handicaps or problems for which they were receiving extra help in normal schools; and only 6% were attending special schools. Throughout the 10 years of the study, the overall prognosis for these infants of very low birth weight improved significantly. Results among other high-risk groups were equally encouraging. Analysis of variance of the data from the infants who weighed 1500 g or less at birth indicated that perinatal complications, particularly illnesses associated with abnormal neurological signs or acidaemia in the infants around the time of birth, were the principal factors determining the condition of the survivors at follow-up. Thus, it is likely that additional refinements in the management of the perinatal period may result in further improvements in the prognosis of these and other high-risk newborns.

Achievement↗
PubMed1977

Differentiation of lymphoid cells: the preferential binding of the lipid A moiety of lipopolysaccharide to B lymphocyte populations.

Lipid A, prepared from lipopolysaccharide, was labeled with 125 I. Such iodinated lipid A possesses the full mitogenic activity of untreated lipid A. Comparison of the 125 I-lipid A-binding activity of splenocytes and thymocytes from the same rabbit revealed that the extent of labeling of splenocytes was 10 to 20 times greater than that observed with an equivalent number of thymocytes. A similar preferential binding was detected in comparing cells in mouse and rat. Spleen populations depleted of adherent cells were essentially unaltered with regard to binding when compared to the original population. In addition, spleen cell populations enriched for thymus-derived cells (T cells) exhibited a marked loss of specific binding activity. On the other hand, spleen cell populations enriched for bone marrow-derived cells (B cells) exhibited the expected binding. The difference in binding behavior of B and T cell-enriched populations was confirmed by using three independent techniques to separate B and T cells. These findings are consistent with the mitogenic specificity of lipid A toward B cells rather than T cells and suggest that the observed cellular specificity resides in an early event in mitogenesis, i.e., binding of the mitogen.

Animals↗
PubMedDate not supplied

Measurement of apoptosis, proliferation and three cytokines in 46 patients with myelodysplastic syndromes.

Extensive apoptosis or programmed cell death (PCD) of both hematopoietic (erythroid, myeloid, megakaryocytic) and stromal cells in myelodysplastic syndromes (MDS) cancels the high birth-rate resulting in ineffective hematopoiesis and has been demonstrated as the probable basis for peripheral cytopenias in MDS by our group. It is proposed that factors present in the microenvironment are inducing apoptosis in all the cells whether stromal or parenchymal. To investigate this hypothesis further, bone marrow biopsies from 46 MDS patients and eight normal individuals were examined for the presence of three cytokines, tumor necrosis factor-alpha (TNF-alpha), transforming growth factor-beta (TGF-beta) and granulocyte macrophage-colony stimulating factor (GM-CSF) and one cellular component, macrophages, by the use of monoclonal antibodies immunohistochemically. Results showed the presence of TNF-alpha and TGF-beta in 41/46 and 40/46 cases of MDS respectively, while only 15 cases showed the presence of GM-CSF. Further a significant direct relationship was found between the degree of TNF-alpha and the incidence of PCD (p= 0.0015). Patients who showed high PCD also had an elevated TNF-alpha level. Thus, the expression of high amounts of TNF-alpha and TGF-beta and low amounts of the viability factor GM-CSF may be responsible for the high incidence of PCD leading to ineffective hematopoiesis in MDS. Future studies will be directed at attempting to reverse the lesion in MDS by using anti-TNF-alpha drugs such as pentoxifylline.

Apoptosis↗
PubMedDate not supplied

Degenerate perturbations of protein structure as the mechanism of anaesthetic action.

The interaction of the n-alkanols with lipid bilayers and excitable membranes shows that there is no simple correlation between conduction block and any of the perturbations of bilayer structure currently proposed as unitary mechanisms of local anaesthetic action. We propose instead that the n-alkanols act by direct interaction with target proteins to cause perturbations which depend directly on the precise structure of the alcohol.

Alcohols↗
PubMedDate not supplied

Identification of the breast cancer susceptibility gene BRCA2.

In Western Europe and the United States approximately 1 in 12 women develop breast cancer. A small proportion of breast cancer cases, in particular those arising at a young age, are attributable to a highly penetrant, autosomal dominant predisposition to the disease. The breast cancer susceptibility gene, BRCA2, was recently localized to chromosome 13q12-q13. Here we report the identification of a gene in which we have detected six different germline mutations in breast cancer families that are likely to be due to BRCA2. Each mutation causes serious disruption to the open reading frame of the transcriptional unit. The results indicate that this is the BRCA2 gene.

Amino Acid Sequence↗