Search PubMed⌕ Search

Biomedical subjects

D Wu

Publications and source records attributed to D Wu.

At least 379 records · Page 21Linked to original sources
PubMed1996

U50,488H-induced pressor effect in the ovine foetus is mediated by sympathetic activation and vasopressin.

The purpose of this study was to investigate the mechanism behind the increase in blood pressure observed after intravenous administration of U50,488H (trans-3,4-dichloro-N-[2-(1-pyrrolidinyl)cyclohexyl]benzeneacetamide), a selective Kappa-opioid receptor agonist, to the ovine foetus. Intravenous administration of U50,488H (1.0 mg/kg) to the foetus resulted in an immediate increase in foetal blood pressure which lasted 15 min. Pretreatment with phentolamine (1.0 mg/kg i.v.) completely blocked the immediate (1-4 min) pressor effect of U50,488H, but not the subsequent increase in blood pressure after 5 min. In contrast, pretreatment with the vasopressin antagonist ([beta-mercapto-beta, beta-cyclopentamethylene-propionyl)-O-Me2-Tyr,Arg8]vasopressin, 0.06 mg/kg) did not affect the immediate pressor effect of U50,488H, but completely blocked the latter increase in blood pressure after 4 min. These data suggest that the immediate increase in blood pressure caused by U50,488H was mediated by sympathetic activation which was then further sustained by a release of vasopressin.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed1996

Influence of the 20-kDa protein from Bacillus thuringiensis ssp. israelensis on the rate of production of truncated Cry1C proteins.

The potential role of a molecular chaperone on the rate of production of extensively altered Bacillus thuringiensis Cry1C proteins was investigated. Analysis of the proteins produced by the recombinant B. thuringiensis strains showed that the truncated proteins were produced at a low rate. Expression of the 20-kDa protein gene from B. thuringiensis ssp. israelensis in tandem with the truncated-cry1C genes led to the production of a greater amount of proteins. The formation of inclusion bodies, however, did not occur even when the 20-kDa protein gene was expressed.

Bacillus thuringiensis↗
PubMed1996

Pertussis toxin-sensitive activation of phospholipase C by the C5a and fMet-Leu-Phe receptors.

Signal transduction pathways that mediate C5a and fMet-Leu-Phe (fMLP)-induced pertussis toxin (PTx)-sensitive activation of phospholipase C (PLC) have been investigated using a cotransfection assay system in COS-7 cells. The abilities of the receptors for C5a and fMLP to activate PLC beta2 and PLC beta3 through the Gbetagamma subunits of endogenous Gi proteins in COS-7 cells were tested because both PLC beta2 and PLC beta3 were shown to be activated by the betagamma subunits of G proteins in in vitro reconstitution assays. Neither of the receptors can activate endogenous PLC beta3 or recombinant PLC beta3 in transfected COS-7 cells. However, both receptors can clearly activate PLC beta2 in a PTx-sensitive manner, suggesting that the receptors may interact with endogenous PTx-sensitive G proteins and activate PLC beta2 probably through the Gbetagamma subunits. These findings were further corroborated by the results that PLC beta3 could only be slightly activated by Gbeta1gamma1 or Gbeta1gamma5 in the cotransfection assay, whereas the Gbetagamma subunits strongly activated PLC beta2 under the same conditions. PLC beta3 can be activated by Galphaq, Galpha11, and Galpha16 in the cotransfection assay. In addition, the Ggamma2 and Ggamma3 mutants with substitution of the C-terminal Cys residue by a Ser residue, which can inhibit wild type Gbetagamma-mediated activation of PLC beta2, were able to inhibit C5a or fMLP-mediated activation of PLC beta2. These Ggamma mutants, however, showed little effect on m1-muscarinic receptor-mediated PLC activation, which is mediated by the Gq class of G proteins. These results all confirm that the Gbetagamma subunits are involved in PLC beta2 activation by the two chemoattractant receptors and suggest that in COS-7 cells activation of PLC beta3 by Gbetagamma may not be the primary pathway for the receptors.

Amino Acid Sequence↗
PubMed1996

Radiofrequency ablation for supraventricular and ventricular tachycardia in young patients.

Radiofrequency ablation therapy was conducted in 86 consecutive children and young patients with a mean age of 14 +/- 3 years (range = 3-18). Fifty-two patients had Wolff-Parkinson-White syndrome, one had re-entry tachycardia incorporating a nodoventricular fiber, 22 had atrioventricular node re-entry tachycardia, two had atrial tachycardia and nine had idiopathic ventricular tachycardia. Radiofrequency ablation was successful in 50 of the 52 patients (96%) with Wolff-Parkinson-White syndrome and the one with nodoventricular fiber. Radiofrequency modification of the atrioventricular node using the inferior approach was successful in eliminating atrioventricular node re-entry tachycardia in 20 of the 22 patients (91%). Radiofrequency ablation in the two patients with atrial tachycardia was unsuccessful. Of the nine patients with idiopathic ventricular tachycardia, eight from the left ventricle and one from the right ventricular outflow tract, eight were successfully ablated (88%). Follow-up over a period ranging from 1 to 46 months (21 +/- 13) revealed a recurrence of tachycardia in seven patients; a late electrophysiological study in 38 patients revealed the induction of tachycardia in 11 patients (seven with accessory pathway-mediated tachycardia, three with atrioventricular node re-entry tachycardia and one with idiopathic ventricular tachycardia). All 11 patients were successfully ablated by a second trial. In conclusion, radiofrequency ablation therapy is effective and safe in pediatric patients with supraventricular and ventricular tachycardia and should be considered as the therapy of choice in this group of patients.

Adolescent↗
PubMed1996

Identification of a phospholipase C beta2 region that interacts with Gbeta-gamma.

To delineate the phospholipase C (PLC; EC 3.1.4.3) beta2 sequences involved in interactions with the beta-gamma subunits of G proteins, we prepared a number of mammalian expression plasmids encoding a series of PLC beta2 segments that span the region from the beginning of the X box to the end of the Y box. We found the sequence extending from residue Glu-435 to residue Val-641 inhibited Gbeta-gamma-mediated activation of PLC beta2 in transfected COS-7 cells. This PLC beta2 sequence also inhibited ligand-induced activation of PLC in COS-7 cells cotransfected with cDNAs encoding the complement component C5a receptor and PLC beta2 but not in cells transfected with the alpha1B-adrenergic receptor, suggesting that the PLC beta2 residues (Glu-435 to Val-641) inhibit the Gbeta-gamma-mediated but not the Galpha-mediated effect. The inhibitory effect on Gbeta-gamma-mediated activation of PLC beta2 may be the result of the interaction between Gbeta-gamma and the PLC beta2 fragment. This idea was confirmed by the observation that a fusion protein comprising these residues (Glu-435 to Val-641) of PLC beta2 and glutathione S-transferase (GST) bound to Gbeta-gamma in an in vitro binding assay. The Gbeta-gamma-binding region was further narrowed down to 62 amino acids (residues Leu-580 to Val-641) by testing fusion proteins comprising various PLC beta2 sequences and GST in the in vitro binding assay.

Amino Acid Sequence↗
PubMed1996

Selective G protein coupling by C-C chemokine receptors.

The C-C chemokines are major mediators of chemotaxis of monocytes and some T cells in inflammatory reactions. The pathways by which the C-C chemokine receptors activate phospholipase C (PLC) were investigated in cotransfected COS-7 cells. The C-C chemokine receptor-1 (CKR-1), the MCP-1 receptor-A (MCP-1Ra), and MCP-1Rb can reconstitute ligand-induced accumulation of inositol phosphates with PLC beta2 in a pertussis toxin-sensitive manner, presumably through G beta gamma released from the Gi proteins. However, these three receptors demonstrated different specificity in coupling to the alpha subunits of the Gq class. While none of the receptors can couple to Galphaq/11, MCP-1Rb can couple to both Galpha14 and Galpha16, but its splicing variant, MCP-1Rb, cannot. Since MCP-1Ra and -b differ only in their C-terminal intracellular domains, the C-terminal ends of MCP-1Rs determine G protein coupling specificity. CKR-1 can couple to Galpha14 but not to Galpha16, suggesting some of the C-C chemokine receptors, unlike the C-X-C chemokine receptors, discriminate against Galpha16, a hematopoietic-specific Galpha subunit. The intriguing specificity in coupling of the Gq class of G proteins implies that the chemokines may be involved in some distinct functions in vivo. The commonality of the chemokine receptors in coupling to the Gi-Gbetagamma-PLC beta2 pathway provides a potential target for developing broad spectrum anti-inflammatory drugs.

Animals↗
PubMed1996

Cardiovascular and respiratory actions of U50,488H in the unanaesthetized ovine foetus.

In an effort to evaluate the feasibility of kappa-opioid receptor agonists for use in pregnancy, we have investigated the actions of U50,488H (trans-3,4-dichloro-N-methyl-N-[2-(1- pyrrolidinyl)cyclohexyl]benzeneacetamide) on cardiovascular and respiratory control in the unanaesthetized ovine foetus. Intravenous administration of U50,488H (1.0 mg/kg) to the foetus resulted in an immediate increase in foetal blood pressure (P < 0.0001) and heart rate (P < 0.0001) which lasted 15 min, followed by a prolonged loss of heart rate variability for up to 3 h. There was also a significant suppression of foetal breathing movements for 2-3 h (P < 0.008). Pretreatment with naloxone (12 mg/h) completely blocked the hypertensive and tachycardiac response to U50,488H, but was unable to prevent the loss of variation in heart rate or respiratory depression. These data suggest that U50,488H can exert direct cardiovascular and respiratory actions in the ovine foetus via both opioid and non-opioid mechanisms. The naloxone-insensitive suppression of foetal breathing would severely limit the use of U50,488H as an obstetrical analgesic.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed1996

Left ventricular fibromuscular band is not a specific substrate for idiopathic left ventricular tachycardia.

BACKGROUND: A fibromuscular band has been detected in patients with idiopathic left ventricular tachycardia, and this band has been suggested to be the anatomic substrate for the arrhythmia. Whether the fibromuscular band is a specific substrate for the tachycardia was systematically evaluated in a large group of consecutive patients with and without idiopathic left ventricular tachycardia. METHODS AND RESULTS: Conventional transthoracic two-dimensional echocardiography and multiplane transesophageal echocardiography were performed in 18 patients with idiopathic left ventricular tachycardia that was responsive to calcium blockers (group 1, tachycardia patients) and 40 patients with paroxysmal supraventricular tachycardia (group 2, control patients). There were 17 men and 1 woman, with a mean age of 29 +/- 11 years, in group 1 patients, and 21 men and 19 women, with a mean age of 42 +/- 12 years, in group 2 patients. The QRS morphology during tachycardia in group 1 patients displayed a pattern of right bundle-branch block with superior axis in 15 patients, indeterminate axis in 2 patients, and inferior axis in 1 patient. Radiofrequency ablation successfully eliminated the tachycardia in all 18 patients; the successful ablation site was located at the inferior apical septum in 11 patients, at the midseptum in 6 patients, and at the anterior lateral wall in 1 patient. Transthoracic echocardiography detected the fibromuscular band in 11 of the 18 patients, whereas multiplane transesophageal echocardiography detected the band in 17 of 18 patients. The fibromuscular band extended from the interventricular septum to the apex of the left ventricle. In group 2 patients, transthoracic echocardiography detected the fibromuscular band in 22 and multiplane transesophageal echocardiography detected the band in 35 of the 40 patients. The presence of a fibromuscular band in these two groups of patients was not statistically different. CONCLUSIONS: The presence of a left ventricular fibromuscular band is not a specific anatomic substrate for idiopathic left ventricular tachycardia.

Adult↗
PubMed1996

Recombinant PSP94 (prostate secretory protein of 94 amino acids) demonstrates similar linear epitope structure as natural PSP94 protein.

PSP94 has the potential to be a useful diagnostic marker and therapeutic agent in prostate cancer. Recently, different immunoassay systems for quantitative analysis of PSP94 in clinical samples have been developed, but the epitope structure of PSP94 protein has not been elucidated. In this study, we report an Escherichia coli expression system for recombinant GST-PSP94 fusion protein. GST-PSP94 contains antigenic determinants similar to natural PSP94 protein (determined both by Western blotting experiments and by ELISA) and can be used to study the structure of natural PSP94 antigen. Since GST-PSP94 was expressed in E. coli and purification involved a denaturing process, we propose that the epitope structure of PSP94 is linear and largely dependent on the primary amino acid sequence, rather than conformational structure. This hypothesis was supported by reciprocal competition in ELISA among natural, GST-PSP94 fusion protein, and purified recombinant PSP94 protein. The results demonstrate that the various forms of PSP94 can compete with each other in binding to rabbit PSP94 polyclonal antibody, although the natural PSP94 has a slightly higher affinity. When natural and recombinant PSP94 protein were denatured in vitro with urea and alkali, no effect on the binding to antibody was found. The epitope activity of natural PSP94 was also shown to be resistant to the treatment of detergent and reducing agent. The location of one of the linear epitopes recognized by the PSP94 antibody was determined to be in the N-terminus by using two synthetic peptides representing N- and C-terminal sequences. Competitive ELISA between the N-terminal peptide and PSP94 protein indicate that both natural and GST-PSP94 have similar immunoactive N-termini.

Animals↗
PubMed1996

Characterization of a collagenous cementum-derived attachment protein.

We report further characterization of a cementum-derived protein that promotes the adhesion and spreading of periodontal cells. The cementum attachment protein (CAP) was extracted from bovine cementum, separated by diethylamino ethyl (DEAE)-cellulose chromatography, and purified by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and C18 reverse phase high performance liquid chromatography. The purified preparation contained a single protein band migrating with M(r) 56,000. It did not cross-react with polyclonal antibodies to osteopontin, vitronectin, or other attachment proteins. The attachment activity was resistant to chondroitinase ABC digestion. An internal amino acid sequence of six peptides was determined by microsequencing, and the peptide sequences were not present in other attachment proteins described in cementum. Four sequences contained Gly-X-Y repeats typical of collagen helix. One 17 amino acid peptide had 82% homology with a type XII collagen domain. However, bovine type XII collagen did not promote fibroblast attachment. Although another 19-amino-acid-long peptide had 95% homology to bovine alpha 1 [I], two other peptides were only 74% and 68% homologous, and the CAP was not recognized by anti-type I collagen antibody. The attachment activity of CAP was susceptible to bacterial collagenase. The CAP did not cross-react with antibodies to type V, XII, and XIV collagens. These data and our previous immunostaining data indicate that the CAP is not related to other collagens or attachment proteins and that it is a collagenous attachment protein localized in cementum.

Animals↗
PubMed1996

Glutamic acid decarboxylase 65 and 67 isoforms in fetal, neonatal and adult porcine islets: predominant beta cell co-localization by light and confocal microscopy.

Glutamic acid decarboxylase (GAD) has been shown to exist as two isoforms with molecular weights of 65 kD (GAD65) and 67 kD (GAD67) in the central nervous system as well as in several non-neuronal tissues, including the pancreatic islets. Recently, this enzyme has been proposed as a key beta-cell autoantigen in insulin-dependent diabetes mellitus (IDDM). In the present study, we used double label light and confocal microscopy to examine the expression of the two GAD isoforms in islet cells of fetal, neonatal and adult porcine pancreas. We also aimed to identify the islet cell-type(s) which co-express GAD. In the adult pig, GAD65 was localized exclusively in most of the beta cells, whereas GAD67, in addition to being present in a majority of the beta cells, was also seen in a proportion of glucagon and somatostatin labelled cells. In the 90-day fetus and the 7-day neonate, while GAD65 was also observed in a majority of beta cells, a proportion of glucagon cells also co-expressed this isoform. The cellular expression of GAD67 in the fetal and neonatal stages was similar to that in the adult. Detailed confocal analysis of GAD65 immunoreactive cells showed a granular cytoplasmic staining, with labelled granules often concentrated in specific perinuclear regions, possibly the Golgi apparatus. In contrast, GAD67 positive cells showed more diffuse cytoplasmic staining. The predominant expression of both the isoforms in porcine beta cells suggests that islet cells from this species may act as a suitable cellular model for study of GAD autoreactivity during the early stages of IDDM.

Animals↗
PubMed1996

Effect of vitamin E on human aortic endothelial cell responses to oxidative injury.

Reactive oxygen species produced by the cells present in the arterial wall may cause oxidative damage to cellular components altering endothelial cell (EC) function. Changes in the EC function appear to play a key role in the pathogenesis of atherosclerosis. Human aortic endothelial cells (HAEC) were employed to investigate the protective role of vitamin E upon exposure of endothelial cells to oxidative stress in vitro. HAEC assimilate d-alpha-tocopherol from the media in a dose-dependent manner. Exposure of HAEC to 16.5 mM of the free radical generator 2,2'-azobis (2-amidinopropane) hydrochloride (AAPH) for 16 h decreased cell viability (assessed by trypan blue exclusion) from 90 to 28%. HAEC preincubated with vitamin E at 15, 30, and 60 microM prior to the AAPH exposure resulted in a dose-dependent increase in resistance to oxidative stress and increased cell viability by 37, 66, and 85%, respectively. An increase in prostacyclin (PGI2) production by HAEC in response to AAPH exposure was correlated positively with cell damage and negatively with vitamin E concentration. Interleukin (IL)-1 production also increased in parallel with cell damage induced by AAPH. Vitamin E treatment significantly reduced IL-1 production after AAPH exposure. This modulatory role of vitamin E on HAEC function following exposure to an oxidative stress may reflect its antioxidant protection against lipid peroxidation.

Amidines↗
PubMed1996

Catheter-induced atrioventricular nodal block during radiofrequency ablation.

This study examined the incidence and significance of catheter-induced atrioventricular nodal block (AVNB) during a radiofrequency ablation procedure that uses stiff large-tip steerable ablation catheters. AVNB was noted in 10 (1.6%) of 613 consecutive patients undergoing radiofrequency ablation therapy for atrioventricular nodal (AVN) reentrant tachycardia (592 patients) or atrioventricular reentry tachycardia incorporating a midseptal accessory pathway (21 patients). Of these 10 patients, 9 underwent AVN modification for AVN reentrant tachycardia and 1 for ablation of a midseptal accessory pathway. One patient had two episodes of AVNB during two sessions undertaken because of recurrence of tachycardia. No patient had a preexisting conduction defect before the study. In all 10 patients, AVNB was transient, and it lasted for a mean of 9.1 +/- 19 minutes. It occurred during positioning of the ablation catheter in the junctional area before (8 patients) or after (2 patients) the start of radiofrequency current applications. Complete AVNB was noted on six occasions, second-degree AVNB on four occasions, and first-degree AVNB on one occasion. All blocks were associated with narrow QRS ventricular beats and with a site of block proximal to the His bundle. The mean ventricular heart rate during AVNB was 60 +/- 23 beats/min. Two patients had transient asystole, with one having loss of consciousness. No patient required special treatment for heart block. One-to-one conduction resumed after repositioning of the catheters, and the subsequent ablation procedure was successfully completed in 8 of the 10 patients. During a follow-up of 20 +/- 12 months, none of the patients had severe dizziness or syncope, and none required implantation of a permanent pacemaker. In conclusion, transient AVNB due to mechanical injury occurs during positioning of a stiff large-tip steerable ablation catheter in the junctional area. Delivery of radiofrequency current to the site that provokes catheter-induced AVNB should be avoided.

Adolescent↗
PubMed1996

Radiofrequency ablation therapy of the posteroseptal accessory pathway.

Among 652 patients with Wolff-Parkinson-White syndrome who underwent radiofrequency ablation in this laboratory, 139 (21%) were found to have a total of 146 posteroseptal accessory pathways. Ablation was conducted by the regular transvenous or transaortic approach; ablation from cardiac venous structures was used only if regular approaches were unsuccessful. Of the 146 posteroseptal accessory pathways, 94 were successfully ablated from the left posteroseptal region and 45 from the right posteroseptal region. In 3, successful ablation of the accessory pathway required delivery of the current to the proximal coronary sinus, and in 1 it required delivery of the current to both the atrial and ventricular aspects of the tricuspid valve at the right posteroseptum. Thus, the accessory pathway was successfully ablated in 143 (98%) of 146 instances or in 136 (98%) patients. In 3 patients, ablation was unsuccessful despite delivery of current to the left posteroseptum, the right posteroseptum, the proximal coronary sinus, and the middle cardiac vein. Seventy-seven (57%) patients with an initial success, including 9 patients with resumed preexcitation or recurrence of paipitations, underwent a follow-up electro-physiologic study 90 +/- 72 days after ablation. Of these 9 patients, the initial successful ablation site was the right posteroseptum in 7 and the left posteroseptum in 2. The accessory pathways were ablated successfully by subsequent trials in 8 patients, whereas in 1 the accessory pathway was severely damaged. Thus radiofrequency ablation of posteroseptal accessory pathways can be achieved by the regular transvenous or transaortic approach; delivery of current to the coronary sinus or middle cardiac vein is unnecessary in most patients.

Adult↗
PubMed1996

B-1a, B-1b and conventional B cell lymphoma from enzootic bovine leukosis.

In order to characterize the phenotypes of tumor cells and to clarify from which B cell lineage the lymphomas were derived, ten cows with enzootic bovine leukosis were examined by means of immunohistologic staining and flow cytometry. The tumor cells expressed mainly major histocompatibility complex (MHC) class II+ (10/10), BoCD11b+ (9/10), IgG1+ (8/10), B-B2+ (8/10) BoCD5+ (7/10), and lambda light chain+ (7/10). Tumor cells from only one animal expressed sIgM+ (1/10). Tumor cells from all ten animals were negative for IgG2, BoCD3, BoCD4, BoCD8, WC1-N2, and IL-2R alpha. The phenotypes of these tumor cells were all slightly different, suggesting that bovine leukemia virus (BLV)-induced lymphoma expresses phenotypic diversity. Moreover, tumor cells from seven cattle coexpressed BoCD5 and BoCD11b (B-1a cells). On the other hand, tumor cells from two of them only expressed BoCD11b (B-1b cells), and those from one were negative for both BoCD5 and BoCD11b (conventional B cells). Therefore, we concluded that BLV-induced lymphoma cells can be derived from B-1a, B-1b and conventional B cells.

Animals↗
PubMed1996

Immunologic effects of marine- and plant-derived n-3 polyunsaturated fatty acids in nonhuman primates.

The effect of marine- and plant-derived n-3 polyunsaturated fatty acids (PUFAs) on T cell-mediated immune response was studied in cynomolgus monkeys. Animals were first fed a 14-wk baseline diet; 10 animals were then fed diets containing 1.3% or 3.3% of energy as eicosapentaenoic acid (EPA) plus docosahexaenoic acid (DHA) which the other 10 were fed diets containing 3.5% or 5.3% of energy as alpha-linolenic acid (ALA) for two consecutive 14-wk periods. Both diets significantly decreased the percentage of T cells (except 1.3% EPA + DHA), T helper cells (except 1.3% EPA + DHA and 3.5% ALA), and T suppressor cells. Proliferative response of lymphocytes to T cell mitogens significantly increased after the diet containing 3.3% EPA + DHA. Interleukin 2 production significantly increased after the diets containing 1.3% and 3.3% EPA + DHA. No significant changes in mitogenic response or interleukin 2 production were found after ALA diets. Feeding 1.3% or 3.3% EPA + DHA or 5.3% ALA significantly suppressed prostaglandin E2 production in response to T cell mitogens. Plasma tocopherol concentrations were decreased significantly only in monkeys fed ALA diets. We conclude that after adjustment for the tocopherol concentration, marine-derived n-3 PUFAs but not plant-derived n-3 PUFAs increased T cell-mediated mitogenic response and interleukin 2 production. This is most likely due to diet-induced quantitative differences in cellular fatty acid composition and, thus, in prostaglandin E2 production and tocopherol status.

Animals↗
PubMed1996

Natural killer cell activity in elderly men is enhanced by beta-carotene supplementation.

Natural killer (NK) cell activity has been postulated to be an immunologic link between beta-carotene and cancer prevention. In a cross-sectional, placebo-controlled, double-blind study we examined the effect of 10-12 y of beta-carotene supplementation (50 mg on alternate days) on NK cell activity in 59 (38 middle-aged men, 51-64 y; 21 elderly men, 65-86 y) Boston area participants in the Physicians' Health Study. No significant difference was seen in NK cell activity due to beta-carotene supplementation in the middle-aged group. The elderly men had significantly lower NK cell activity than the middle-aged men; however, there was no age-associated difference in NK cell activity in men supplemented with beta-carotene. beta-carotene-supplemented elderly men had significantly greater NK cell activity than elderly men receiving placebo. The reason for this is unknown; however, it was not due to an increase in the percentage of NK cells, nor to an increase in interleukin 2 (IL-2) receptor expression, nor to IL-2 production. beta-carotene may be acting directly on one or more of the lytic stages of NK cell cytotoxicity, or on NK cell activity-enhancing cytokines other than IL-2, such as IL-12. Our results show that long-term beta-carotene supplementation enhances NK cell activity in elderly men, which may be beneficial for viral and tumoral surveillance.

Aged↗