Biomedical subjects

T T Huynh

Publications and source records attributed to T T Huynh.

35 records · Page 2Linked to original sources

PubMed1999

Functional characterization of alpha1-adrenergic receptors in experimental vein grafts.

BACKGROUND: Studies on the pharmacology of the smooth muscle cells in vein bypass grafts suggest that the function of G-proteins and adrenergic receptors is altered. This study examines the alpha-adrenergic responsiveness of smooth muscle cells in vein bypass grafts as compared with those in the common carotid arteries and external jugular veins. METHODS: New Zealand White rabbits received jugular vein interposition bypass grafts of the common carotid. Vessel segments of the vein bypass grafts harvested after 28 days, common carotid arteries, and external jugular veins were sectioned into 5-mm rings (four per vessel) for studies of isometric tension in response to phenylephrine (10(-10) to 10(-4) M) alone and in the presence of prazosin, an alpha1-adrenergic antagonist; WB4101 and 5-methylurapidil (5-MU), alpha1A antagonists; chloroethylclonidine (CEC); an alpha1B antagonist; or the Gi/o G-protein inhibitor pertussis toxin (PTx). RESULTS: All vessels had prazosin-sensitive responses. The jugular veins appear to have functional alpha1A receptors (WB4101 and 5-MU sensitive, CEC insensitive) which are associated with pertussis toxin-sensitive G-proteins. Carotid arteries appear to have atypical alpha1 receptors (WB4101 and 5-MU insensitive, CEC insensitive) associated with pertussis toxin-insensitive G-proteins. Vein grafts appear to have functional alpha1B receptors (WB4101 and 5-MU insensitive, CEC sensitive) which are associated with pertussis toxin-insensitive G-proteins. CONCLUSIONS: These results show that placement of a vein into the arterial circulation induces a change in alpha1-adrenergic receptor subtypes (alpha1A to alpha1B) and in the G-protein coupling of the receptors (PTx sensitive to PTx insensitive), reflecting a signficant phenotypic change in smooth muscle cell signal transduction.

Adrenergic alpha-Agonists↗

PubMed1999

Early morphology of accelerated vein graft atheroma in experimental vein grafts.

Vein grafts fail because of the development of intimal hyperplasia and atheroma. Recent experimental evidence suggests that the presence of hypercholesterolemia induces a three-fold increase in intimal hyperplasia with early atheroma development within 4 weeks of implantation. We have previously demonstrated endothelial cell preservation and a short-lived (3-day) polymorphonuclear leukocyte infiltrate in vein grafts. The aim of this study is to define the early morphology and ultrastructure of vein grafts implanted into a hyperlipidemic environment to provide a pathological foundation on which to examine the cellular and molecular events that determine this accelerated response. Twenty-one male New Zealand White rabbits underwent a right carotid interposition bypass graft using the ipsilateral external jugular vein; all animals received a 1% cholesterol diet for 4 weeks prior to surgery and continuing postoperatively until harvest. Animals (n = 3 per time point) were sacrificed at 60 min, 1 day, 3 days, 5 days, 7 days, 14 days, and 28 days postoperatively for scanning and transmission electron microscopy of the vein grafts. No concurrent controls were employed. The results of this study suggest that in the presence of hypercholesterolemia, the pathophysiological processes involved in the vein graft are similar to those reported for noncholesterol-fed animals. There is a sustained subendothelial response with the prolonged presence of macrophages and cellular debris and the accumulation of foam cells.

Animals↗

PubMed1999

Combination therapy of cholesterol reduction and L-arginine supplementation controls accelerated vein graft atheroma.

Hyperlipidemia contributes to the development of intimal hyperplasia and accelerated atheroma in vein bypass grafts. Dietary cholesterol reduction and oral supplementation with L-arginine have been shown to reduce accelerated atheroma in experimental vein grafts. This study extends these observations by examining the effect of the combination therapy of cholesterol reduction and L-arginine supplementation on the development of intimal hyperplasia in vein grafts in hypercholesterolemic animals. Thirty New Zealand White rabbits had a carotid vein bypass graft performed and were sacrificed at 28 days postoperatively either for morphology (light and electron microscopy) and videomorphometry, or for in vitro contractile studies. Twenty animals received a 1% cholesterol diet for 4 weeks prior to surgery. This diet was continued until harvest in ten animals. Ten cholesterol-fed animals received L-arginine supplementation (2 g/kg/day, p.o.) for 7 days preoperatively and thereafter until harvest and in addition were returned to a normal diet on the day of surgery. The last ten animals were controls (normal diet). Combined cholesterol reduction and L-arginine supplementation prevented accelerated atheroma in vein grafts, halted the change in enhanced smooth muscle cell contractility, and improved endothelial cell function. Early postoperative therapy targeting atheroma development in the high-risk patient could offer significant morphological and functional benefits.

Animals↗

PubMed1999

Alterations in wall tension and shear stress modulate tyrosine kinase signaling and wall remodeling in experimental vein grafts.

PURPOSE: Hemodynamic alterations have been implicated as major stimuli for the development of intimal hyperplasia in vein grafts that are implanted in the arterial circulation. Tyrosine kinase is known to mediate cell signaling. However, its role with in vivo mechanotransduction is not yet well defined. We used a novel bioprosthetic collagen tube to provide an external support to vein grafts and examined the subsequent changes in hemodynamics, tyrosine kinase signaling, wall remodeling, and vasomotor function. METHODS: Carotid interposition bypass grafting was performed with the reversed jugular vein in New Zealand white rabbits. In the experimental group (n = 15), after the completion of the proximal anastomosis, the vein was passed through a 4-mm collagen tube and the distal anastomosis was performed. The tube support was fashioned to completely cover the vein grafts. The control animals (n = 14) had no tube support. After surgery, the blood pressure and flow rate were measured and the wall tension and shear stress were calculated in the vein grafts on day 3 or day 28 (n = 5 per group). Tyrosine phosphorylation was assessed with the Western blot test in vein grafts at day 3 (n = 4 per group). The intimal and medial dimensions of the vein grafts were assessed with videomorphometry on day 28 (n = 5 per group). The cumulative dose response curves of the vein grafts to contractile and relaxant agonists were determined in isometric tension studies on day 28 (n = 5 per group). RESULTS: The use of tube support reduced wall tension 1.7-fold (P <.01) and increased shear stress 4.8-fold (P <.001) without altering the flow rate or blood pressure. The tyrosine kinase activity was reduced 15-fold (P <.001) in the tube-supported vein grafts. The intimal thickness was reduced by 45% in the tube-supported vein grafts as compared with the control grafts (46 +/- 2 mm vs 84 +/- 5 mm, respectively; P <.0001), and the media thickness was reduced by 20% (63 +/- 8 mm vs 79 +/- 4 mm, respectively; P <.05). Isometric tension studies showed preservation of contractile function and modulation of endothelial-dependent dysfunctional relaxation in tube-supported vein grafts. CONCLUSION: These results show that reduced wall tension and increased shear stress with an external tube support can effectively modulate the signaling, functional, and hyperplastic responses in vein grafts. We conclude that this simple strategy deserves further study and clinical consideration.

Animals↗

PubMed1999

Differential effects of chemical sympathectomy on expression and activity of tyrosine hydroxylase and levels of catecholamines and DOPA in peripheral tissues of rats.

Tyrosine hydroxylase (TH) mRNA and activity and concentrations of 3,4-dihydroxyphenylalanine (DOPA) and catecholamines were examined as markers of sympathetic innervation and catecholamine synthesis in peripheral tissues of sympathectomized and intact rats. Chemical sympathectomy with 6-hydroxydopamine (6-OHDA) markedly decreased norepinephrine and to a generally lesser extent TH activities and dopamine in most peripheral tissues (stomach, lung, testis, duodenum, pancreas, salivary gland, spleen, heart, kidney, thymus). Superior cervical ganglia, adrenals and descending aorta were unaffected and vas deferens showed a large 92% decrease in norepinephrine, but only a small 38% decrease in TH activity after 6-OHDA. Presence of chromaffin cells or neuronal cell bodies in these latter tissues, indicated by consistent expression of TH mRNA, explained the relative resistance of these tissues to 6-OHDA. Stomach also showed consistent expression of TH mRNA before, but not after 6-OHDA, suggesting that catecholamine synthesizing cells in gastric tissue are sensitive to the toxic effects of 6-OHDA. Tissue concentrations of DOPA were mainly unaffected by 6-OHDA, indicating that much of the DOPA in peripheral tissues is synthesized independently of local TH or sympathetic innervation. The differential effects of chemical sympathectomy on tissue catecholamines, DOPA, TH mRNA and TH activity demonstrate that these variables are not simple markers of sympathetic innervation or catecholamine synthesis. Other factors, including presence of neuronal cell bodies, parenchymal chromaffin cells, non-neuronal sites of catecholamine synthesis and alternative sources of tissue DOPA, must also be considered when tissue catecholamines, DOPA and TH are examined as markers of sympathetic innervation and local catecholamine synthesis.

Animals↗

PubMed1999

Controlling transplant vasculopathy in cryopreserved vein grafts with polyethylene glycol and glutathione during transport.

BACKGROUND: the biological characteristics of cryopreserved allografts are poorly understood, although many factors are known to influence their outcome. This study examines the development of transplant vasculopathy in both fresh and cryopreserved vein allografts and specifically assesses the efficacy of a transport solution containing 10% polyethylene glycol and 10 microM glutathione (PEG/GSH). METHODS: jugular veins were harvested from control donor rabbits and transplanted as interposition carotid bypass grafts in 30 New Zealand White (NZW) rabbits. Ten received the fresh jugular veins (fresh). Ten animals received jugular veins which had been harvested, transported in a physiological solution, cryopreserved and stored in a standard fashion (cryopreserved). Ten animals received jugular veins which had been harvested, transported in the same solution with the addition of PEG/GSH, cryopreserved and stored in a standard fashion (PEG/GSH). Cryopreserved jugular veins were stored for 6 weeks before transplantation. All animals were sacrificed 28 days postoperatively. Vein grafts were perfusion-fixed and wall dimensions were determined by planimetry. RESULTS: all transplanted grafts were patent at harvest. The control cryopreserved vein grafts showed a 54% increase in mean intimal thickness (63+/-10 micron vs. 41+/-3 micron p<0.05) but no change in mean medial thickness (125+/-9 micron vs. 119+/-13 micron; p = N.S. ) compared to the fresh allograft. Transport of the grafts in PEG/GSH solution resulted in the abolition of the increase in intimal thickness (41+/-4 micron; p <0.01) associated with cryopreservation without a change in medial thickness (140+/-15 micron; p = N.S.) compared to the cryopreserved allograft. CONCLUSION: cryopreserved vein grafts develop significant intimal hyperplasia compared to freshly transplanted grafts. The use of PEG/GSH in the transport solution significantly reduces this transplant graft intimal hyperplasia to that which develops in fresh grafts and may lead to improvements in the clinical use of cryopreserved veins.

Animals↗

PubMed1999

Characterization of a palmitoyl-acyl carrier protein thioesterase (FatB1) in cotton.

The relatively high level of palmitic acid (22 mol%) in cotton seeds may be due in part to a palmitoyl-acyl carrier protein (ACP) thioesterase (PATE), which prefers C16:0-ACP as its substrate. In embryo extracts, PATE activity was highest at the maximum rate of reserve accumulation (oil and protein), occurring about 30-35 d post anthesis. Thioesterase activity toward oleoyl-ACP was relatively similar at all developmental stages examined, but was considerably lower than the PATE activity. In developing seeds and in cotyledons and hypocotyls of seedlings, the PATE activity predominated. A cotton PATE cDNA clone isolated by screening a cDNA library with a heterologous Arabidopsis FatB1 probe has a 1.7-kb insert sequence with an open reading frame of 410 amino acids, lacking codons for the three N-terminal amino acids. The predicted amino acid sequence of the cotton PATE preprotein has a characteristic stromal-targeting domain and a 63% identity to the Arabidopsis long-chain acyl ACP-thioesterase FatB1 sequence. Alkaline blot hybridization of cotton genomic DNA with the Arabidopsis FatB1 probe suggested the presence of at least two FatB1 thioesterase genes in cotton. Relative cotton FatB1 transcript abundance was compared by RT-PCR and slot blot analysis in total RNA extracts from embryos, seedlings and leaves of mature plants. The cotton FatB1 mRNA apparently was expressed in all tissues but paralleled the profiles of PATE enzyme activity and seed oil accumulation in embryos.

Acyl Carrier Protein↗

PubMed1999

External support modulates G protein expression and receptor coupling in experimental vein grafts.

BACKGROUND: Intimal hyperplasia remains the leading cause of vein graft failure. Various external stenting devices have been shown to reduce the development of intimal hyperplasia in vein grafts. Mitogenic and mechanotransduction signals are known to be mediated by G protein-coupled receptors. Therefore in this study we examined the alterations in G protein expression and receptor coupling in vein grafts stented with external tube support. METHODS: Thirty New Zealand White male rabbits had a right carotid interposition bypass graft with use of the ipsilateral jugular vein. Fifteen animals received external support and 15 were controls. In a subset the animals either had removal of the external support or a sham-control neck exploration at 14 days after the initial implantation (n = 5 per group). RESULTS: External support reduced G alpha i3 proteins by 30% in vein grafts without changes in G alpha s by Western blot. Vein grafts with external support were significantly less sensitive to pertussis toxin inactivation than controls were in response to both norepinephrine and serotonin. A 24% decrease in intimal thickness was maintained after withdrawal of the initial external support. CONCLUSIONS: The placement of an external support is associated with alternations in G protein expression and receptor coupling function in vein grafts. The results of this study suggest that the development of vein graft intimal hyperplasia may involve G protein-mediated events.

Animals↗

PubMed1998

Local inhibition of tyrosine kinase activity markedly attenuates the development of intimal hyperplasia in experimental vein grafts.

BACKGROUND: Intimal hyperplasia is due to the migration and proliferation of vascular smooth muscle cells after bypass surgery. Tyrosine kinases are involved in many signal transduction pathways including cell proliferation. This study examines the effects of local treatment with the tyrosine kinase inhibitor, tyrphostin AG-51, on the formation of intimal hyperplasia in vein grafts. MATERIALS AND METHODS: Thirty-nine New Zealand White rabbits underwent interposition bypass grafting of the carotid artery using the jugular vein. In the first group (TKI), tyrphostin AG-51 (5 mg), dissolved in 600 microliter of dimethyl sulfoxide and Ringer's lactate (2:1, v:v), was used to incubate the veins ex vivo prior to grafting and delivered locally in 2.5 ml of 30% pluronic gel after grafting. The second group (DMSO) received the same treatment but without tyrphostin. In the third group (control), tyrphostin and DMSO were omitted from the incubation and gel delivery solutions. Postoperatively, vein grafts were harvested on Day 3 for Western analysis using an antiphosphotyrosine antibody (PY-20) to assess for tyrosine kinase activity, and on Day 28 for either morphologic or contractile function studies. RESULTS: Local application of the TKI to vein grafts resulted in a 49% reduction in intimal hyperplasia compared to DMSO-treated vein grafts (31 +/- 4 micrometer vs. 61 +/- 5 micrometer, P < 0.01). Treatment with DMSO alone reduced intimal hyperplasia by 28% compared to control (85 +/- 4 micrometer, P < 0.05). The contractile responses in the DMSO and TKI-treated vein grafts were equivalent. Western analysis showed a 39-fold decrease in tyrosine phosphorylation with TKI treatment compared to control. CONCLUSION: This study demonstrates that local short-term treatment with TKI produces a 49% reduction in intimal hyperplasia and suggests that phosphorylation of tyrosine residues is involved in the signaling pathways leading to the development of intimal hyperplasia in vein grafts.

Administration, Topical↗

PubMed1998

Local delivery of a tissue factor antibody reduces early leukocyte infiltration but fails to limit intimal hyperplasia in experimental vein grafts.

BACKGROUND: Tissue Factor-mediated thrombin generation involves the generation of VIIa and Xa and has been implicated in the pathogenesis of intimal hyperplasia. In experimental vein grafts, Tissue Factor protein is increased over the first 3 days and colocalized with CD18-positive leukocytes; this increase in Tissue Factor precedes the development of intimal hyperplasia. This study further evaluates the potential role of Tissue Factor in vein graft intimal hyperplasia by directly inhibiting Tissue Factor protein. METHODS: New Zealand white rabbits underwent interpositional bypass grafting of the common carotid artery using the external jugular vein. Perioperatively, murine anti-rabbit Tissue Factor antibody (109 microg/ml gel, 12,500x IC50 of Tissue Factor activity) was applied to the adventitial surface of the graft, using a pluronic gel (30% soln.). Tissue Factor antibody treated vein grafts were compared to control and empty gel-treated vein grafts. Vein grafts were examined at 3 days to assess CD18-positive leukocyte infiltration and the presence of residual antibody by Western blotting. At 28 days, intimal and medial dimensions were quantified using videomorphometry. RESULTS: At day 3, there was marked reduction in CD18-positive leukocytes in the Tissue Factor antibody versus control vein grafts (6.3 +/- 4.7 vs 20.8 +/- 7.4 per 200x field, P < 0.05). At 28 days, intimal hyperplasia was similar for the control (70 +/- 4 microm, mean +/- SEM), gel (73 +/- 4 microm), and Tissue Factor antibody (75 +/- 4 microm) vein grafts. However, medial thickness (76 +/- 4 microm;, P < 0.05) was significantly increased compared to the gel treated vein graft (61 +/- 5 microm). CONCLUSION: Local delivery of pharmacologic doses of an anti-rabbit Tissue Factor antibody decreased CD18-positive leukocyte infiltration but failed to limit intimal hyperplasia in experimental vein grafts. The results suggest that inhibition of Tissue Factor protein modulates polymorphonuclear leukocyte-endothelial interactions but not in the subsequent development of intimal hyperplasia. It implies that the relationship between the extrinsic coagulation cascade and intimal hyperplasia in vein grafts is complex.

Animals↗

PubMed1998

Assessment of right ventricular function postretrograde cardioplegia by transesophageal echocardiography.

UNLABELLED: The impact of continuous retrograde cardioplegia (RCP) on right ventricular (RV) function was evaluated prospectively with intraoperative transesophageal echocardiography (TEE) in 36 patients (23 males, 13 females) with a mean age of 60.4 years (ages 24-82). Operative procedures included 12 aortic valve replacements, 16 mitral valve repair/replacements, both with or without an associated cardiac operation, and 8 Ross procedures. Mean cardiopulmonary bypass (CPB) time was 123.3 minutes (66-280 minutes) with an average cross-clamp time of 88.9 minutes (43-199 minutes). The amount of cold blood RCP ranged from 3160-18,500 mL (mean = 7382.5), and the average pulmonary artery pressure was 35/18 mmHg. The coronary sinus was distally snared in 11 patients. TEE documented biventricular global dysfunction in two patients and post-CPB with preservation of the left ventricular function in all other patients. Localized akinesis of the RV apex and outflow tract were noted in three patients, and isolated worsening tricuspid insufficiency of moderate to severe intensity in six patients. Two of the six patients with worsening tricuspid insufficiency belonged to the snared coronary sinus group (11 patients). All of the documented RV dysfunctions were new and showed no correlation with the perfusion data. IN CONCLUSION: (1) RV apex, RV outflow tract and tricuspid valve were particularly subject to important dysfunction post-RCP; (2) RCP did not protect RV adequately in 11 patients (31%); and (3) TEE is a convenient intraoperative technique in evaluating RV dysfunction.

Cardiac Surgical Procedures↗

PubMed1998

G protein signaling and vein graft intimal hyperplasia: reduction of intimal hyperplasia in vein grafts by a Gbetagamma inhibitor suggests a major role of G protein signaling in lesion development.

Vein grafting results in the development of intimal hyperplasia with accompanying changes in guanine nucleotide-binding (G) protein expression and function. Several serum mitogens that act through G protein-coupled receptors, such as lysophosphatidic acid, stimulate proliferative pathways that are dependent on the G protein betagamma subunit (Gbetagamma)-mediated activation of p21ras. This study examines the role of Gbetagamma signaling in intimal hyperplasia by targeting a gene encoding a specific Gbetagamma inhibitor in an experimental rabbit vein graft model. This inhibitor, the carboxyl terminus of the beta-adrenergic receptor kinase (betaARK(CT)), contains a Gbetagamma-binding domain. Vein graft intimal hyperplasia was significantly reduced by 37% (P<0.01), and physiological studies demonstrated that the normal alterations in G protein coupling phenotypically seen in this model were blocked by betaARK(CT) treatment. Thus, it appears that Gbetagamma-mediated pathways play a major role in intimal hyperplasia and that targeting inhibitors of Gbetagamma signaling offers novel intraoperative therapeutic modalities to inhibit the development of vein graft intimal hyperplasia and subsequent vein graft failure.

Analysis of Variance↗

PubMed1998

Plasma metanephrines are markers of pheochromocytoma produced by catechol-O-methyltransferase within tumors.

This study examined whether the high sensitivity of plasma free metanephrines for diagnosis of pheochromocytoma may result from production of free metanephrines within tumors. Presence in pheochromocytomas of catechol-O-methyltransferase (COMT), the enzyme responsible for conversion of catecholamines to metanephrines, was confirmed by Western blot analysis, enzyme assay, and immunohistochemistry. Western blot analysis and enzyme assay indicated that membrane-bound and not soluble COMT was the predominant form of the enzyme in pheochromocytoma. Immunohistochemistry revealed colocalization of COMT in the same chromaffin cells where catecholamines are translocated into storage vesicles by the vesicular monoamine transporter. Levels of free metanephrines in pheochromocytoma over 10,000 times higher than plasma concentrations in the same patients before removal of tumors indicated production of metanephrines within tumors. Comparisons of the production of metanephrines in patients with pheochromocytoma with production from catecholamines released or infused into the circulation indicated that more than 93% of the consistently elevated levels of circulating free metanephrines in patients with pheochromocytoma are derived from metabolism before and not after release of catecholamines into the circulation. The data indicate that the elevated plasma levels of free metanephrines in patients with pheochromocytoma are derived from catecholamines produced and metabolized within tumors. Some tumors do not secrete catecholamines, but all appear to metabolize catecholamines to free metanephrines, thus explaining the better sensitivity of plasma free metanephrines over other tests for diagnosis of pheochromocytoma.

Adult↗

PubMed1998

Adenoviral-mediated inhibition of G beta gamma signaling limits the hyperplastic response in experimental vein grafts.

BACKGROUND: Vein graft intimal hyperplasia is associated with changes in G protein expression. The carboxyl terminus of the beta-adrenergic receptor kinase-1 (beta ARKCT) is known to inhibit G beta gamma-mediated mitogen-activated signaling pathways. This study examines the effects of adenoviral-mediated beta ARKCT infection on the development of intimal hyperplasia in vein grafts. METHODS: New Zealand White rabbits underwent bypass grafting of the carotid artery with the jugular vein. Vein grafts were infected with adenoviral vectors encoding for beta ARKCT (n = 19), beta-galactosidase (n = 3), or empty viral constructs (n = 12). In control animals, vein grafting was performed without infection (n = 10). RESULTS: The efficacy of beta ARKCT infection in vein grafts was verified by reverse transcriptase-polymerase chain reaction. X-gal staining of beta-galactosidase-infected vein grafts demonstrated the transgene in cells throughout the vessel wall. Adenoviral infection of vein grafts without gene transfer did not alter wall thicknesses or sensitivities to contractile agonists, compared with control grafts. beta ARKCT infection, however, reduced intimal thickness by 36% (P < .001) and medial thickness by 24% (P < .001), compared with empty viral infection. beta ARKCT-infected vein grafts also demonstrated increased sensitivity in response to contractile agonists. CONCLUSIONS: These results show that inhibition of G beta gamma signaling with adenoviral-mediated beta ARKCT in vivo infection effectively modifies the structural and functional hyperplastic abnormalities in vein grafts.

Adenoviridae↗

PubMed1995

Propionibacterium acnes endocarditis.

Propionibacterium acnes endocarditis is a rare disease. A case of prosthetic valve endocarditis involving P acnes complicated by multiple mycotic aneurysms is reported. A brief review of the literature is presented.

Aortic Valve↗

PubMed1994

[Ultrasonographic diagnosis of appendicitis. Value and limitations].

Appendicitis is a frequently encountered surgical emergency which can be diagnosed by clinical and laboratory criteria. But there are some atypical cases that ultrasound can help to diagnose. From April the 9th 1992 to April the 11th 1993, we have examined by ultrasound 465 patients entered in our hospital for right lower quadrant pain. 190 patients have been diagnosed as appendicitis and operated (true positive = 124 cases, false negative = 54 cases and false positive = 12 cases). 275 patients have been diagnosed as negative and they are not operated (true = 273 cases, false positive = 2 cases). So in our study, the sensitivity is 70%, the specificity is 95% and the accuracy is 85%. Our scientific report has the objective to show the usefulness and the limits of ultrasound in the diagnosis of appendicitis.

Acute Disease↗

PubMedDate not supplied

Effects of interleukin-1 and gamma interferon on total intracellular magnesium concentration in a murine lymphoid cell line.

Treatment of the pre-B lymphoid cell line 70Z/3 by interleukin-1 alpha (IL-1 alpha) and gamma-interferon (IFN-gamma) induces kappa-immunoglobulin light chain gene expression resulting in surface IgM expression. In this study we examined changes in total intracellular magnesium concentration [Mg]i, in 70Z/3 cells following lymphokine stimulation. After 30 min of treatment, [Mg]i increased by delta [Mg]i = 2.8 +/- 1.1 mM (n = 10, p < 0.025) with IL-1 alpha, and by delta [Mg]i = 3.0 +/- 1.6 mM (n = 8, p < 0.05) with IFN-gamma. After 4 h of treatment, the effect of IL-1 alpha was sustained, delta [Mg]i = 4.0 +/- 0.8 mM (n = 4, p < 0.01), whereas that of IFN-gamma diminished, delta [Mg]i = 0.2 +/- 0.6 mM (n = 7). These cytokines did not induce measurable changes in cell water volume indicating that the lymphokine-induced increase in [Mg]i represented Mg2+ influx.

Animals↗