Biomedical subjects

H M Jones

Publications and source records attributed to H M Jones.

At least 37 records · Page 2Linked to original sources

PubMed1995

Accessory cells do not contribute to G-CSF or IL-6 production nor to rapid haematological recovery following peripheral blood stem cell transplantation.

Haemopoietic recovery is more rapid after peripheral blood stem cell (PBSC) transplantation than after autologous bone marrow transplantation, and the aim of this study was to assess the role of the large number of lymphocytes and monocytes (accessory cells) in a PBSC leukapheresis product in this rapid regeneration. Haematological recovery was therefore assessed in 10 PBSC recipients with lymphoma or myeloma in whom monocytes and T cells were depleted by a median of 2.3 and 3.3 logs by CD34+ cell selection using the CEPRATE SC stem cell concentration system and compared with recovery in 59 recipients who received whole PBSC. After allowing for the number of progenitor cells reinfused, there was no significant delay in engraftment induced by accessory cell depletion. Plasma levels of granulocyte-colony stimulating factor (G-CSF), granulocyte/monocyte-colony stimulating factor (GM-CSF), interleukin-6 (IL-6), stem cell factor (SCF) and macrophage-inhibition factor-alpha (MIP-1-alpha) during the transplant procedure were similar whether or not accessory cells were given. The G-CSF and IL-6 levels rose between days 5 and 14 post transplantation to approximately 1 ng/ml and 50 pg/ml respectively. This study indicates that accessory cells reinfused with PBSC collections are not responsible for the subsequent cytokine profile or rapid haematological recovery.

Adolescent↗

PubMed1994

The effects of gestation on circulating progenitor cells.

The frequency of BFU-E in second-trimester fetal blood (484 +/- 104/10(5)) falls progressively during gestation to a value of 69 +/- 41/10(5) in cord bloods of 36 weeks gestation and beyond, but this is still significantly greater than adult blood values of 14 +/- 8 (P < 0.01). BFU-E obtained from unfractionated peripheral blood mononuclear cells from fetuses/neonates less than 36 weeks gestation were more sensitive to erythropoietin than adult BFU-E, but the sensitivity of highly purified BFU-E obtained from second-trimester fetal liver was similar to that in adult cells. Almost maximal growth of BFU-E from purified fetal progenitor cells could be achieved with erythropoietin alone, whereas adult cells required the presence of other factors with 'burst-promoting activity'.

Cell Division↗

PubMed1994

Development of a simplified single-apheresis approach for peripheral-blood progenitor-cell transplantation in previously treated patients with lymphoma.

PURPOSE: The aims of this study were to develop a simplified, safe, and cost-effective peripheral-blood progenitor-cell (PBPC) mobilization protocol. PATIENTS AND METHODS: Twenty-six patients with relapsed or resistant lymphomas were entered onto a sequential cohort study in which schedules of various granulocyte colony-stimulating factor (G-CSF) were administered after cyclophosphamide 1.5 g/m2. Hematologic recovery after high-dose carmustine (BCNU) etoposide, cytarabine, and melphalan (BEAM) chemotherapy was compared with that of 46 patients who received autologous bone marrow transplantation (ABMT) without growth factors and 28 patients who received ABMT followed by G-CSF. RESULTS: When G-CSF (10 micrograms/kg/d) was administered from the day after the cyclophosphamide, neutropenia developed on day 8 followed by an abrupt increase in the WBC count. The optimal time for PBPC harvesting was the day on which the postnadir WBC count was greater than 8.0 x 10(9)/L, as shown by CD34+ cell counts and granulocytic-macrophage colony-forming cell (GM-CFC) assays. The reproducibility of the response was such that routine monitoring of CD34+ cell counts and GM-CFC was not necessary. A single leukapheresis on this day was adequate for prompt hematologic engraftment, and posttransplant G-CSF made little further impact on the rapid recovery. Compared with both control groups, the use of PBPC led to more rapid neutrophil recovery, markedly accelerated platelet recovery, less use of antimicrobial agents and parenteral nutrition, and more than 10 days earlier discharge from hospital. All of these differences were highly significant (P < .01). CONCLUSION: A simplified mobilization protocol is described that requires only one apheresis to achieve rapid hematologic engraftment.

Adult↗

PubMed1994

The effects of recombinant human granulocyte-macrophage colony stimulating factor on the neutrophil respiratory burst in the term and preterm infant when studied in whole blood.

To investigate further the susceptibility to infection of newborn infants, particularly those born prematurely, we have used a "whole blood" flow cytometric assay to compare the respiratory burst activity in recombinant human granulocyte-macrophage colony stimulating factor "primed" neutrophils obtained from healthy adults, term infants, and preterm newborn infants. The use of whole blood avoids prior cell separation procedures that may cause artifactual activation or priming. In healthy adults (n = 21), the bacterial cell wall peptide N-formyl-methionyl-leucyl-phenylalanine induced little neutrophil respiratory burst activity, suggesting that the circulating cell is relatively quiescent. Prior exposure to recombinant human granulocyte-macrophage colony stimulating factor augmented the median N-formyl-methionyl-leucyl-phenylalanine response by 425%. In cord blood from full-term neonates (n = 9), recombinant human granulocyte-macrophage colony stimulating factor produced less enhancement of the N-formyl-methionyl-leucyl-phenylalanine response (345%), but the absolute level of respiratory burst activity was at least as great as in adults, suggesting that the neutrophils are fully functional and partially primed after delivery. In preterm infants receiving intensive care (n = 10), the degree of priming was similar to that in neutrophils from term infants (344%), although the absolute level of respiratory burst activity was reduced (p = 0.0003). In response to stimulation with phorbol ester, 73.5% (18-99%) (median and range) of neutrophils obtained from adults and 77.6% (50-92%) from term babies exhibit respiratory burst activity detectable in the whole blood assay. However, in neutrophils obtained from preterm infants, there was a significant reduction in the phorbol ester-induced respiratory burst, with only 32.9% (21-61%) of cells responding (p = 0.0129).

Adult↗

PubMed1994

The formation of human synovial joint cavities: a possible role for hyaluronan and CD44 in altered interzone cohesion.

During fetal development, cavitation occurs within the primitive skeleton along planes destined to become the articular surfaces of synovial joints. A histochemical study of human fetal limbs was undertaken to identify the cell types involved in this cavitation and the possible role of interactions between cells and extracellular matrix. Cryostat sections were stained with antibodies to CD68, factor VIII related antigen, prolyl hydroxylase, beta 1 integrin, VCAM-1, proliferating cell nuclear antigen, chondroitin-4 sulphate, chondroitin-6-sulphate, hyaluronan synthase and CD44. Similar sections were reacted for uridine diphosphoglucose dehydrogenase (UDPGD) and acid phosphatase activity. Hyaluronan was demonstrated using an aggrecan core protein hyaluronan binding region probe. Macrophages were present prior to cavitation in the periphery of joint interzones but not at the presumptive joint line in the central interzone. Fibroblastic cells were present throughout. Absence of local VCAM-1 expression indicated that cavitation was temporally distinct from full fibroblast-like synoviocyte differentiation. CD44 was expressed by interzone cells at all stages. Staining for hyaluronan and hyaluronan synthase, but not chondroitin sulphates was present in the interzone before and at the time of cavitation. UDPGD activity was increased in a narrow band of cells at the presumptive joint line prior to cavitation. These findings suggest that joint cavitation is dependent on the behaviour of fibroblastic cells and/or adjacent chondrocytes, rather than macrophages. Since UDPGD activity is involved in hyaluronan synthesis, it is proposed that joint cavitation is facilitated by a rise in local hyaluronan concentration in an area of tissue where cohesion is dependent on the interaction between cellular CD44 and extracellular hyaluronan. As proposed by Toole et al. (1984) such a local rise in hyaluronan concentration may lead to a switch from intercellular cohesion to dissociation, leading to tissue cavitation.

Ankle Joint↗

PubMed1994

Isolation and ex vivo expansion of CD34+ cells from cord blood using dextran sedimentation and avidin column selection.

Human umbilical cord bloods were fractionated by unit gravity sedimentation in 1% (v/v) dextran, followed by immunoaffinity selection for CD34+ stem and progenitor cells. Dextran sedimentation alone enabled recovery of more than 80% of the nucleated cells present and 90% of the CD34+ cells, as determined by flow cytometry. The addition of an immunoaffinity selection step for CD34+ cells resulted in a 134-fold enrichment for CD34+ cells, with a mean yield of 64 +/- 15%. The resultant CD34+ population contained almost half the CFU-GM activity initially present in the cord bloods and could be expanded ex vivo in liquid culture.

Antigens, CD↗

PubMed1993

Painful transthoracic needle biopsy: a sign of neurogenic tumor.

Neurogenic tumors most commonly appear initially as posterior mediastinal masses. These tumors, however, may occur in other intrathoracic locations and present a diagnostic challenge. In such cases transthoracic fine-needle aspiration (FNA) often is used to make a definitive diagnosis. This procedure usually does not result in severe pain. We report two patients who experienced severe pain during transthoracic FNA of neurogenic tumors. We believe that severe pain associated with transthoracic needle biopsy of an intrathoracic mass is suggestive of a neurogenic tumor. When pain accompanies this procedure, a cytopathologist should be notified so that specific immunostaining techniques can be performed to confirm the diagnosis.

Adult↗

PubMed1993

Expression and dynamic modulation of the human granulocyte colony-stimulating factor receptor in immature and differentiated myeloid cells.

In this study we have examined the expression and modulation of the human granulocyte colony-stimulating factor (G-CSF) receptor (R) in immature and differentiated myeloid cells using a 125I labelled human G-CSF analogue (TG50). Equilibrium binding data revealed a single affinity class of receptor on all cell types expressing G-CSFR (KD 235-606 pM) with neutrophils expressing 2883 +/- 672 Rs/cell. Rapid internalization of surface receptor-bound ligand at 37 degrees C was detected in both immature cells (U937) and neutrophils with > 70% of specifically bound ligand internalized within 5 min. Concentration-response data showed that the level of occupancy of neutrophil G-CSFRs by ligand at 37 degrees C was approximately 5-fold greater than predicted by equilibrium binding data and correlated closely with concentration-response data for biological activity. Re-expression of G-CSFRs following down-regulation by internalization was not detected. Down-regulation of the neutrophil G-CSFR by several agents including granulocyte-macrophage colony-stimulating factor (GM-CSF), tumour necrosis factor (TNF), lipopolysaccharide (LPS), f-met-leu-phe (fMLP), phorbol ester (TPA) and C5a was observed at 37 degrees C but not at 4 degrees C. In contrast, G-CSFRs on immature myeloid cells were significantly down-regulated by TPA only. Differentiation of myeloid leukaemic cell line HL-60 with DMSO, a frequently used model of granulocytic differentiation, was associated with a significant reduction in G-CSFR expression (11 +/- 5% of control) whereas treatment with retinoic acid led to increased G-CSFR expression (161 +/- 3%).

Binding, Competitive↗

PubMed1993

Dynamic modulation of the cell surface expression of the granulocyte-macrophage colony-stimulating factor receptor.

The GM-CSF receptor (GM-CSFR) is composed of alpha and beta subunits. Surface expression of the alpha chain alone leads to low affinity GM-CSF binding and of both subunits to high affinity binding; the beta chain is required for transducing a proliferative signal. Studies of GM-CSFR expression have concentrated largely on static events occurring under conditions of binding equilibrium. We have examined the dynamic regulation of high and low affinity GM-CSFR expression in neutrophils (1100 +/- 200 R/cell, KD 50 +/- 15 pM) and a GM-CSF dependent human leukaemic cell line, TF-1 (2000 +/- 450 R/cell KD 15 +/- 5 pM) and 8600 +/- 1150 R/cell KD 1.8 +/- 0.3 nM). The addition of GM-CSF to TF-1 cells (350 pM, 4 h at 37 degrees C) caused a reduction in subsequent binding of 125I-GM-CSF at low ligand concentration (100 pM) (following a low pH wash to remove surface bound ligand) to 16 +/- 4% and a reduction in binding at high ligand concentration (2 nM 125I-GM-CSF) to 36 +/- 9% of control. Scatchard analysis showed complete down-regulation of high affinity GM-CSFR and a significant reduction in low affinity GM-CSFR. In neutrophils, concentration-response curves of ligand induced receptor down-regulation at 37 degrees C showed that observed down-modulation was more than 10-fold greater than predicted by static equilibrium binding data and correlated closely with GM-CSF priming of the neutrophil respiratory burst. The addition of IL-3 to TF-1 cells at 37 degrees C reduced 100 pM 125I-GM-CSF binding to 18 +/- 4% and 2 nM 125I-GM-CSF binding to 46 +/- 5% of control. TF-1 cells, but not neutrophils, were able to re-express GM-CSFR following removal of GM-CSF from medium. TF-1 proliferation assays showed that pulsed GM-CSF (0.35-3.5 nM) for up to 4 h did not cause a significant increase in 3H-thymidine incorporation which required the continued presence of GM-CSF (control 2875 +/- 208 cpm, pulsed GM-CSF 5 ng/ml 4972 +/- 1344, continuous GM-CSF 5 ng/ml 17249 +/- 2982). Therefore, proliferation of TF-1 cells required the continued presence of GM-CSF at a time when there was no detectable surface high affinity GM-CSFR.(ABSTRACT TRUNCATED AT 400 WORDS)

Cells, Cultured↗

PubMed1993

In vivo and in vitro effects of 3-hydroxypyridin-4-one chelators on murine hemopoiesis.

The effects of 3-hydroxypyridin-4-one (HPO) iron chelators and desferrioxamine (DFO) on murine hemopoiesis in vivo and in vitro have been compared in order to investigate the mechanism by which leucopenia in mice and granulocytopenia in man occurs with 1,2-,dimethyl-HPO (CP20). Administration of 60 doses of 200 mg/kg CP20 to Balb/c mice resulted in significant anemia, lymphopenia and granulocytopenia accompanied by bone marrow hypocellularity. DFO and CP94 (1,2,diethyl-HPO) at the same dose also caused lymphopenia but marrow cellularity was unaffected. When marrow from untreated mice was incubated with HPOs and DFO, erythroid burst-forming cells (BFU-E) and granulocyte/macrophage colony forming units (CFU-G+Mac), colony growth was inhibited in a dose-dependent manner at micromolar concentrations. The addition of iron to saturate the chelators abrogated the effects of DFO, but not those of the HPOs. With the HPO-iron complexes, addition of sufficient iron to saturate the transferrin in the medium reversed the inhibitory effects of the relatively hydrophilic CP20-iron complex but not those of the more lipophilic CP94-iron complex. Addition of further iron-saturated transferrin also corrected inhibition by the CP94-iron complex. These results show that HPO-iron complexes potentially have antiproliferative effects unlike DFO-iron complex (FO). The difference in the relative effects of CP20 to CP94 on hemopoiesis in vivo and in vitro suggests that additional factors to those inhibiting hemopoiesis in marrow cultures may operate with the long-term administration of iron chelators in vivo.

Animals↗

PubMed1992

Down-regulation of human protein kinase C alpha is associated with terminal neutrophil differentiation.

We have established an RNase protection method to quantify the expression of mRNA for the human protein kinase C (PK-C) isoforms alpha, beta 1, beta 2, and gamma. This was used to investigate whether each isoform is differentially expressed during the differentiation of hematopoietic cells. Myeloid and lymphoid cells express PK-C alpha, beta 1, and beta 2 mRNAs in various proportions. PK-C gamma mRNA was detected in human brain, but not in hematopoietic cells. PK-C alpha mRNA decreases as HL-60 cells mature to a neutrophil phenotype in response to retinoic acid, but its abundance does not change during monocytic differentiation in response to vitamin D3. PK-C alpha mRNA and protein were undetectable in peripheral blood neutrophils, but are present in monocytes. The mRNAs for PK-C beta 1 and beta 2 isoforms increase during HL-60 differentiation and are expressed in both neutrophils and monocytes. Therefore, the PK-C alpha isoform is specifically down-regulated during human neutrophil terminal differentiation. These data suggest that mature neutrophil functions do not require the PK-C alpha isoform.

Calcitriol↗

PubMed1992

Evaluation of the humoral immune response in trachoma to Chlamydia trachomatis major outer membrane proteins by sequence-defined immunoassay.

The Chlamydia trachomatis immunodominant major outer membrane protein (MOMP) is both a target of neutralizing antibodies and the serotyping antigen and thus has been a focus of diagnostic, seroepidemiologic, and experimental investigations. The microimmunofluorescence (MIF) test has been the principal tool in serologic investigations of chlamydial infections but is difficult and expensive for routine use; moreover, since it uses whole organisms as antigen, it is incapable of revealing the molecular specificity of the humoral response to infection. These limitations were resolved by using synthetic peptides corresponding to serovar-specific antigenic regions of MOMP in an ELISA-based format to analyze the serospecificity of sera from trachoma cases. The ELISA reaction to the surface-exposed MOMP sequence variable segment 1 was immunodominant and serovar-specific and was in concordance with serovar specificity according to paired MIF test determinations. Understanding the patterns of humoral responses to MOMP determinants in patient populations will advance our knowledge of their role in the immunobiology of naturally acquired infection.

Amino Acid Sequence↗

PubMed1992

The effect of macrophage colony-stimulating factor on haemopoietic recovery after autologous bone marrow transplantation.

Macrophage colony-stimulating factor (M-CSF) is active in the late stages of monocyte maturation, activates mature monocyte-macrophages and enhances their production of various other cytokines. We have examined the effects of a 21 d course of escalating doses of M-CSF purified from human urine (hM-CSF) on recovery following autologous bone marrow transplantation (ABMT) in 20 patients with malignant lymphomas. Four patients were treated at each dose level of 4, 8, 16, 32 and 64 x 10(6) U/m2/d and results compared to 46 concurrent controls. There was no significant difference in recovery to an absolute neutrophil count (ANC) of 0.5 x 10(9)/l (median 20 d in hM-CSF group versus 22 in controls) or in recovery of platelets to 50 x 10(9)/l (32 d versus 39 d, 0.05 less than P less than 0.1); hM-CSF patients received a median of 81 platelet units following ABMT (controls 112 units, P = NS). hM-CSF patients had a median of 5.5 d with fever greater than 37.5 degrees C (control 8, P = NS), received parenteral antibiotics for 14.5 d (control 17, P = NS) and had a 50% incidence of bacteraemia (control 48%). hM-CSF treated patients were discharged by a median of day 29 following transplantation (control 33, P less than 0.05). Platelet and neutrophil recovery correlated significantly with the number of marrow mononuclear cells (MNC) reinfused in the hM-CSF group (P = 0.05 and P = 0.014 respectively) but not in controls. Subgroup analysis showed that hM-CSF patients receiving greater than 2 x 10(8) MNC/kg body weight reached an ANC of 0.5 x 10(9)/l by a median of day 16.5 (control 18.5, NS), became platelet transfusion independent by day 17 (control 29, P less than 0.05) and reached a platelet count of 50 x 10(9)/l by day 21 (control 40, P less than 0.05). No significant toxicity attributable to hM-CSF treatment was seen. These results suggest that hM-CSF accelerates platelet recovery following ABMT and that relatively large marrow innocula are required to see this effect.

Adult↗

PubMed1992

Fc gamma RII, but not erythropoietin or GM-CSF, mediates calcium mobilization in fetal hemopoietic blast cells.

A proportion of fetal liver hemopoietic blast cells express Fc gamma RII, and addition of the anti-Fc gamma RII monoclonal antibody CIKM5 induces a rise in calcium in these cells in suspension. Although these cells are thus capable of mobilizing intracellular calcium in response to surface receptor mediated events, neither granulocyte-macrophage colony-stimulating factor (GM-CSF) nor erythropoietin produced detectable changes in intracellular calcium ion concentration in these cells.

Antibodies, Monoclonal↗

PubMed1991

Lack of effect of granulocyte-macrophage and granulocyte colony-stimulating factors on cultured human endothelial cells.

The hematopoietic growth factors, granulocyte-macrophage colony-stimulating factor (GM-CSF) and granulocyte colony-stimulating factor (G-CSF), enhance the effector functions of mature myeloid cells, including the interaction with vascular endothelium. We examined the direct effect of recombinant human GM-CSF (rhGM-CSF) and recombinant human G-CSF (rhG-CSF) on the growth and function of cultured human umbilical vein endothelial cells (HUVEC). Endothelial cell growth supplement (ECGS) increased the proliferation of passaged and primary cells by 305% +/- 45% (mean +/- SEM, n = 5, P less than .01) over control cells at 4 days; GM-CSF and G-CSF had no effect. Endothelial cell procoagulant activity was increased after 4-hour incubation with recombinant interleukin-1 beta (IL-1 beta) 10 U/mL and recombinant tumor necrosis factor (TNF) 10 U/mL to 1,721% +/- 376% (n = 7, P less than .005) and 247% +/- 71% (n = 4) of control levels, respectively. gamma-Interferon (gamma-IFN) 50 U/mL had no direct effect of its own but was able to prime the response to IL-1 beta. There was no direct or priming effect of GM-CSF (1 ng to 1 microgram/mL) on the expression of procoagulant activity in endothelial cells. GM-CSF and G-CSF (1 ng/mL to 1 microgram/mL) had no effect on the expression of either tissue plasminogen activator (tPA) or plasminogen activator inhibitor-1 (PAI-1) by endothelial cells. The secretion of tPA by endothelial cells was increased, however, after 24-hour incubation with thrombin 4 U/mL (314% +/- 72% of control levels, n = 5, P less than .025). The production of PAI-1 was increased by TNF 200 U/mL (241% +/- 44% of control, n = 3, P less than .005), thrombin 4 U/mL (180% +/- 12% of control, n = 5, P less than .0005) and IL-1 beta 10 U/mL (275% +/- 44% of controls, n = 5, P less than .0005). In four experiments, endothelial cells showed no specific binding of 125I-GM-CSF, whereas peripheral blood (PB) neutrophils demonstrated the presence of 802 +/- 78 high-affinity receptors for GM-CSF. Thus, we found no effect of rhGM-CSF or rhG-CSF on the proliferation activities by these cells. These findings are in accordance with the lack of demonstrable receptors for GM-CSF on cultured HUVEC.

Cell Division↗

PubMed1991

Sphingosine inhibits angiotensin-stimulated aldosterone synthesis.

Sphingosine and other protein kinase C inhibitors were tested for their ability to inhibit aldosterone synthesis by bovine adrenal glomerulosa cells. Sphingosine inhibited angiotensin (AII)-stimulated aldosterone synthesis (IC50 of 5 microM). At doses that totally blocked steroidogenesis, sphingosine did not affect protein synthesis or [125I]AII binding to cells. Sphingosine also inhibited dibutyryl cyclic AMP (dbcAMP)-stimulated aldosterone synthesis. Sphingosine inhibited pregnenolone synthesis from cholesterol, but not the conversion of progesterone or 20 alpha-hydroxycholesterol to aldosterone. These results suggest that sphingosine inhibits steroidogenesis at a locus close to that where stimulation occurs by AII and dbcAMP. Other protein kinase C inhibitors were tested. Retinal, 1-(5-isoquinolinesulfonyl)-2-methylpiperazine dihydrochloride (H-7), and staurosporine inhibited aldosterone synthesis stimulated by AII and dbcAMP. Retinal and H-7 also inhibited progesterone conversion to aldosterone, and retinal blocked [125I]AII binding. Staurosporine was more specific, inhibiting AII-stimulated aldosteronogenesis at concentrations which had little effect on conversion of progesterone to aldosterone. Because they inhibited dbcAMP stimulation, none of the inhibitors was sufficiently specific to use as a probe of the role of protein kinase C. The IC50 of sphingosine suggests that this or related products of lipid hydrolysis could act as endogenous regulators of adrenal cell function.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗

PubMed1991

The molecular origin of birefringence in skeletal muscle. Contribution of myosin subfragment S-1.

The state of optical polarization of He-Ne laser light diffracted by single skinned frog skeletal muscle fibers has been determined after decoration of the thin filaments of rigor fibers with exogenous S-1. Light on the first diffraction order was analyzed using optical ellipsometry for changes occurring in total birefringence (delta nT) and total differential field ratio (rT) and the experimental results compared with theoretical predictions. Fibers were examined with SDS-gel electrophoresis and electron microscopy as independent assays of S-1 binding. The binding of S-1 to the thin filaments caused a significant increase in rT and a small but significant decrease in delta nT. Release of bound exogenous S-1 with magnesium pyrophosphate demonstrated that the effect of S-1 on the optical parameters was reversible and both electrophoresis and electron microscopy demonstrated the presence of S-1 specifically bound to the thin filaments. Model simulations based on the theory of Yeh, Y., and R. Baskin (1988. Biophys. J. 54:205-218) showed that the values of delta nT and rT were sensitive to the axial bonding angle of exogenous S-1 as well as to the volume fraction of added S-1. Analysis of the data in light of the model showed that an average axial S-1 binding angle of 68 degrees +/- 7 degrees best fit the data.

Animals↗

PubMed1991

Comparison of plain and alkalinized local anaesthetic mixtures of lignocaine and bupivacaine for elective extradural caesarean section.

We have examined a local anaesthetic mixture of 0.5% bupivacaine 10 ml and 2% lignocaine 10 ml with adrenaline 1 in 200,000, to which 8.4% sodium bicarbonate 2 ml was added, for extradural Caesarean section. The alkalinized mixture of local anaesthetics produced a block of more rapid onset and density than a mixture of bupivacaine and lignocaine alone (P less than 0.001).

Adult↗