Biomedical subjects

Y Wan

Publications and source records attributed to Y Wan.

At least 73 records · Page 4Linked to original sources

PubMed2000

FISH mapping of the sex-reversal region on human chromosome 9p in two XY females and in primates.

Accumulating evidence suggests that haploinsufficiency of a dosage-sensitive gene(s) in human chromosome 9p24.3 is responsible for the failure of testicular development and feminisation in XY patients with monosomy for 9p. We have used molecular cytogenetic methods to characterise the sex-reversing 9p deletions in two XY females. Fluorescence in situ hybridisation (FISH) with YACs from the critical 9p region containing an evolutionarily conserved sex-determining gene, DMRT1, is a very fast and reliable assay for patient screening. Comparative YAC mapping on great ape and Old and New World monkey chromosomes demonstrated that the critical region was moved from an interstitial position on the ancestral primate chromosome to a very subtelomeric position in chimpanzee and humans by a pericentric inversion(s). Pathological 9p rearrangements may be the consequence of an evolutionary chromosome breakpoint in close proximity to the sex-reversal region.

Animals↗

PubMed2000

Contrasting effects of myeloid dendritic cells transduced with an adenoviral vector encoding interleukin-10 on organ allograft and tumour rejection.

Mouse bone marrow-derived myeloid dendritic cells (DC) propagated in granulocyte-macrophage colony-stimulating factor and transforming growth factor-beta1 (TGF-beta1) (so-called 'TGF-beta DC') are phenotypically immature, and prolong allograft survival. Interleukin-10 (IL-10) has been shown to inhibit the maturation of DC by down-regulating surface major histocompatibility complex (MHC) class II, co-stimulatory and adhesion molecule expression. Genetic engineering of TGF-beta DC to overexpress IL-10 might enhance their tolerogenic potential. In this study, adenoviral (Ad) vectors encoding the mouse IL-10 gene were transduced into B10 (H2b) TGF-beta DC. Transduction with Ad-IL-10 at a multiplicity of infection (MOI) of 50-100 resulted in a modest reduction in the incidence of DC expressing surface MHC class II, CD40, CD80 and CD86. Paradoxically, Ad-IL-10 transduction enhanced the allostimulatory activity of DC in mixed leucocyte reactions and cytotoxic T lymphocyte assays, and increased their natural killer cell stimulatory activity. Systemic injection of normal C3H recipients with Ad-IL-10-transduced B10-DC 7 days before organ transplantation, exacerbated heart graft rejection and augmented circulating anti-donor alloantibody titres. Contrasting effects were observed in relation to tumour growth. All mice preimmunized with Ad-IL-10-transduced, tumour antigen (B16F10)-pulsed DC developed palpable tumours, associated with significant inhibition of splenic anti-tumour cytotoxic T lymphocyte generation. Animals pretreated with control Ad-LacZ-transduced, B16F10-pulsed DC however, remained tumour free. These findings are consistent with the multifunctional immunomodulatory properties of mammalian IL-10.

Adenoviruses, Human↗

PubMed2000

Lowering dietary saturated fat and total fat reduces the oxidative susceptibility of LDL in healthy men and women.

The present study examined the effects of reducing dietary total fat and saturated fat (SFA) on LDL oxidative susceptibility in 27 healthy men and women (age 24-65 y). Each subject consumed each of three diets for 8 wk: an average American diet (AAD, 34% energy from fat, 15% from SFA), a Step-1 diet (29% fat, 9% SFA) and a very low SFA diet (Low-Sat, 25% fat, 6% SFA). In vitro LDL oxidation was assessed by copper-mediated oxidation, as measured by the kinetics of conjugated diene formation and lipid peroxide formation. Compared with the AAD, plasma LDL-cholesterol (LDL-C) and HDL cholesterol levels were 8% lower (P: = 0.16 and P: = 0.11, respectively), in subjects when they consumed the Step-1 diet and 11% (P: < 0.03) and 14% (P: < 0.057) lower, respectively, when they consumed the Low-Sat diet. Conjugated diene production and oxidation rate were 7% (P: < 0. 05) and 9% (P: < 0.05) lower, respectively. The reduction of lipid peroxide formation was 9% (P: < 0.05) in subjects when they consumed the Low-Sat diet vs. the AAD. In addition, lipid peroxide and conjugated diene formation were positively correlated with plasma total and LDL-C and apolipoprotein B (apo B) levels (r = 0.5-0.6, P: < 0.001), suggesting that quantity of LDL is an important determinant of oxidative modification. Furthermore, at the same level of apo B or LDL-C, LDL from subjects when they consumed either Step-1 or Low-Sat diets was less susceptible (P: < 0.05) to oxidation than those when they consumed the AAD, suggesting that qualitative changes also affect LDL oxidative susceptibility. Therefore, the benefits of lowering dietary SFA may extend beyond decreasing LDL-C levels and include favorable qualitative changes in LDL that further decrease risk of coronary heart disease.

Adult↗

PubMed2000

Temporally distinct and ligand-specific recruitment of nuclear receptor-interacting peptides and cofactors to subnuclear domains containing the estrogen receptor.

Ligand binding to estrogen receptor (ER) is presumed to regulate the type and timing of ER interactions with different cofactors. Using fluorescence microscopy in living cells, we characterized the recruitment of five different green fluorescent protein (GFP)-labeled ER-interacting peptides to the distinct subnuclear compartment occupied by blue fluorescent protein (BFP)-labeled ER alpha. Different ligands promoted the recruitment of different peptides. One peptide was recruited in response to estradiol (E2), tamoxifen, raloxifene, or ICI 182,780 incubation whereas other peptides were recruited specifically by E2 or tamoxifen. Peptides containing different sequences surrounding the ER-interacting motif LXXLL were recruited with different time courses after E2 addition. Complex temporal kinetics also were observed for recruitment of the full-length, ER cofactor glucocorticoid receptor-interacting protein 1 (GRIP1); rapid, E2-dependent recruitment of GRIP1 was blocked by mutation of the GRIP1 LXXLL motifs to LXXAA whereas slower E2 recruitment persisted for the GRIP1 LXXAA mutant. This suggested the presence of multiple, temporally distinct GRIP 1 recruitment mechanisms. E2 recruitment of GRIP1 and LXXLL peptides was blocked by coincubation with excess ICI 182,780. In contrast, preformed E2/ER/GRIP1 and E2/ER/LXXLL complexes were resistant to subsequent ICI 182,780 addition whereas ICI 182,780 dispersed preformed complexes containing the GRIP1 LXXAA mutant. This suggested that E2-induced LXXLL binding altered subsequent ligand/ER interactions. Thus, alternative, ligand-selective recruitment and dissociation mechanisms with distinct temporal sequences are available for ER alpha action in vivo.

Active Transport, Cell Nucleus↗

PubMed2000

UV-induced expression of GADD45 is mediated by an oxidant sensitive pathway in cultured human keratinocytes and in human skin in vivo.

The expression of GADD45 was examined in cultured skin keratinocytes and in human skin in vivo following UV irradiation. Northern blot analysis revealed that UV-induced the expression of GADD45 (alpha, beta, gamma) in a time- and dose-dependent manner. Messenger RNA of GADD45 (alpha, beta, gamma) increased within 30 min, peaked at 4 h and remained elevated for at least 8 h following UV irradiation in vitro and in vivo. Maximal induction of GADD45alpha was approximately 5-fold compared to the level in sham-irradiated controls. Similarly H2O2 and IL-1 also induced GADD45alpha expression in cultured human keratinocytes. The kinetics of induction of GADD45alpha by H2O2, IL-1beta and UV were very similar. Interestingly, UV-induced GADD45alpha expression was inhibited by diphenylene iodonium (DPI), an inhibitor of NADPH oxidase, and antioxidant, N-acetyl-L-cysteine (NAC), indicating the involvement of reactive oxygen species in UV signaling. Previously we have shown that EGF receptor activation by UV is prerequisite for subsequent activation of NADPH oxidase and generation of reactive oxygen species. We therefore examined the effect of EGF receptor inhibitor on UV-induced GADD45alpha expression. Our results showed that PD168393, a potent EGF receptor inhibitor, blocked UV-induced GADD45alpha expression. Collectively, our data suggest that UV-induced GADD45alpha expression occur via an EGF receptor-mediated oxidative pathway sensitive to antioxidant regulation.

Acetylcysteine↗

PubMed2000

Cytotoxic effects of 5-fluorocytosine on melanoma cells transduced with cytosine deaminase gene.

To investigate the cytotoxic effects of 5-fluorocytosine on melanoma cells genetically modified with cytosine deaminase gene, the gene was transduced into the tumor cells with the retroviral method. The cytotoxicity effects of 5-fluorocytosine on the tumor cells were measured with the MTT assay and clonogenic assay. It was found that the prodrug 5-fluorocytosine had significant cytotoxic effects on melanoma cells transduced with cytosine deaminase in vitro. The IC50 value of 5-fluorocytosine on transgenic and nontransgenic melanoma cells was 572 microg/mL(-1) and 3870 microg/mL(-1), respectively. Our experiment demonstrated the potential value of the cytosine deaminase gene/5-fluorocytosine system in the treatment of melanoma.

3T3 Cells↗

PubMed2000

Potentiation of BCNU anticancer activity by O6-benzylguanine: a study in vitro and in vivo.

O6-Alkylguanine-DNA alkyltransferase (O6-AGT), a constitutively expressed DNA repair protein, removes alkyl groups from the O6-position of guanine in DNA. Tumor cells with high O6-AGT activity are resistant to nitrosoureas and other agents that form toxic O6-alkyl adducts. We evaluated O6-benzylguanine (O6-BG) for its activity to inhibit O6-AGT and potentiate 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) in O6-AGT-positive human gastric adenocarcinoma cell line, BGC-823 and its tumor xenograft. The sensitivity of BGC-823 cells to BCNU was increased by pretreatment for 2 hours with 1.5 to 6.0 microg/mL O6-benzylguanine. O6-benzylguanine (0.75-6.0 microg/mL) completely and rapidly suppressed the O6-AGT activity of cells for up to 12 hours. When given i.p. 2 hours before BCNU (25 mg/kg) to animals bearing s.c. tumors, O6-BG (90 mg/kg) produced a growth delay of 38.6 days in human gastric adenocarcinoma xenograft. Furthermore, O6-BG significantly inhibited the O6-AGT activity of tumor tissue and induced evident apoptosis. These results suggest that combination of O6-BG with BCNU may have a significant therapeutic effect in the treatment of mer + tumor.

Alkyl and Aryl Transferases↗

PubMed2000

[Research on the regular pattern of Ag-NOR changes in patients with cancer].

OBJECTIVE: To correlate the relationship between rDNA transcriptional activity of CD4+ helper T cells and immunity in patients with cancer through silver stainability of nucleolus organizing regions (Ag-NORs). METHODS: The Th(CD4+) rDNA transcriptional activity was compared among patients with cancer, infectious diseases, non-cancerous non-infectious diseases through image analysis. RESULTS: Th(CD4+) rDNA transcriptional activity was decreased extremely in patients with cancer, but increased in patients with inflammation compared with normal controls. CONCLUSION: The analysis of Th(CD4+) rDNA transcriptional activity may serve as a new tumor marker for tumor diagnosis and differential diagnosis. Therefore, it may provide an innovative and reliable method for clinical cancer diagnosis.

CD4-Positive T-Lymphocytes↗

PubMed2000

[Mutation of human O6-alkylguanine-DNA alkyltransferase confers resistance to O6-benzylguanine].

OBJECTIVE: O6-alkylguanine-DNA alkyltransferase (O6-AGT), capable of repairing DNA damage, is responsible for tumor cell resistance to nitrosourea. While O6-benzylguanine as a selective inhibitor of AGT helps reverse drug resistance, it would aggravate myelo-suppression. This investigation is to generate AGT mutant and see if it would confer resistance to O6-benzylguanine-induced inhibition but leave its alkyltransferase activity intact. METHODS: Human O6-methylguanine-DNA methyltransferase (MGMT) cDNA was mutated by site-directed mutagenesis. The mutant cDNA was transferred into E. coli and the protein expressed was purified. The activity of the mutant MGMT was determined in vitro with O6-(3H)-methylguanine-DNA as substrate. RESULTS: Two mutant MGMT proteins were obtained: G156A and P140A, with glycine-to-alanine mutation at position 156 and proline-to-alanine mutation at position 140, respectively. The AGT activity of both mutants was similar to that of the wild type MGMT. However, their resistance to O6-benzylguanine was significantly increased up to 105.8 and 13.5 fold, respectively as compared to that of the wild type MGMT. CONCLUSION: The results suggested that transduction of the mutant MGMT herein reported into hematopoietic progenitor cells may lead to their selective resistance to the combined use of O6-benzylguanine and alkylating agents designed to overcome tumor resistance to nitrosourea treatment.

Amino Acid Sequence↗

PubMed2000

[Expression of matrix metalloproteinases and tissue inhibitor of metalloproteinases in colorectal neoplasm].

OBJECTIVES: To explore the relationship of matrix metalloproteinases (MMPs) and tissue inhibitor of metalloproteinases (TIMPs) to the oncogenesis and development of colorectal neoplasm. METHODS: RT-PCR was used to assay the level of MMP-2, MT1-MMP, MMP-7, TIMP-2, TIMP-3 mRNA in 28 cases of colorectal cancer, including tumor tissue and surrounding normal tissue. RESULTS: MMP-2, MT1-MMP, TIMP-2 and TIMP-3 were over-expressed in tumor and normal tissues, and MMP-7 was strong-expressed in tumor tissue but was weak-expressed only in one case of normal tissue. The expression of MMP-7 in tumor tissue was correlated to Dukes stage (P < 0.01). The expression of TIMP-2 in tumor tissue with positive-node was much higher than that with negative-node (P < 0.01). The expression of TIMP-3 was decreased with the Dukes stage and the depth of invasion (P < 0.01). There were no correlations between MMPs and TIMPs (P > 0.1). CONCLUSIONS: The expression of MMP-7 mRNA has a high specificity in colorectal cancer. MMP-7 may become a sensitive tumor marker. Inducing TIMP-2, TIMP-3 or suppressing MMP-2, MT1-MMP, MMP-7 mRNA's expressions may inhibit the invasion and metastasis of cancer.

Adult↗

PubMed2000

[Lymph node metastasis and the extent of lymph node dissection for gastric cancer: report of 326 cases].

OBJECTIVE: To investigate the pattern of lymph node metastasis and the extent of lymph node dissection for gastric cancer. METHODS: 326 patients with gastric cancer admitted from 1990 to 1999 were analyzed retrospectively after D(2), D(3) or D(3) plus para-aortic lymphadenectomy (D(3) + PAL). RESULTS: The total incidence of lymph node metastasis was 69.9%; node involvement was 15.4% and 77.4% respectively for early gastric cancer and advanced gastric cancer. Depth of invasion, tumor size and histology affected lymph node metastasis significantly (P < 0.05). For T(1) patients, node involvement was mainly confined to N(1) and one patient had N(2) metastasis; 8.1% of T(2) patients and 28.7% of T(3), T(4) patients had N(3), M(1) lymph node metastasis. Among 107 patients who received D(3) + PAL, 16a2b1 lymph node metastasis was found in 15.0%. The patients who had 16a2b1 node involvement were all suffered from advanced gastric cancer and N(1)-N(2) node metastasis. In the patients with serosal invasion-positive tumors or tumors size over 5 cm, the incidence of 16a2b1 metastasis was high, and that of entire stomach cancer was up to 38.5%. The 3-year and 5-year survival rates for D(3) + PAL group were 60.7% and 50.0% respectively. After D(3) + PAL, the 1-and 2-year survival rate, of patients with 16a2b1 metastasis were 60.0%, 50.0% respectively. CONCLUSIONS: D(2) lymphadenectomy should be taken for patients with early gastric cancer and D(3) lymphadenectomy for those with relatively early' advanced gastric cancer. For advanced gastric cancer with suspect or confirmed N(1)-N(2) node metastasis, tumor size over 5 cm and/or serosa invasion, D(3) plus para-aortic lymphadenectomy appears to be a necessary surgical procedure.

Adult↗

PubMed2000

[mRNA expression of hyaluronan synthase in the endolymphatic sac cells of guinea pigs].

OBJECTIVE: To detect the mRNA expression of hyaluronan synthase in the endolymphatic sac cells of guinea pigs. METHODS: After consulting gene bank, we analyzed conservative sequence of hyaluronan synthases in different species, detected the mRNA expression of hyaluronan synthase in the endolymphatic sac cells of guinea pigs with oligonucleotide probe by hybridization in situ. RESULTS: mRNA of hyaluronan synthase was strongly expressed in some epithelial cells of endolymphatic sac, coupled with negative expression in negative control groups. CONCLUSION: It confirms that endolymphatic sac cells can synthesize hyaluronan.

Animals↗

PubMed1999

Enhanced immune response to the melanoma antigen gp100 using recombinant adenovirus-transduced dendritic cells.

Glycoprotein 100 (gp100) is one of a series of well-characterized human melanoma-associated antigens expressed by most melanoma cells. Immunization of C57BL/6 mice with an adenovirus (Ad) vector encoding human gp100 (Adhgp100) has been shown to induce limited protective immunity against challenge with murine melanoma B16 cells. In the current study we determined whether gp100-specific immunity can be enhanced using bone-marrow-derived dendritic cells (DCs) transduced with Adhgp100 ex vivo. Subcutaneous injection of Adhgp100-infected DCs resulted in potent T-cell-mediated protective immunity and a greater than 80% reduction of established tumors when administered to B16 tumor-bearing hosts. Compared to direct injection of Adhgp100 vector alone, immunization with Adhgp100-infected DCs induced markedly greater antitumor activity. In vitro CTL analysis demonstrated that DC-Adhgp100 immunization activated both CD4(+) and CD8(+) CTLs, while no lytic activity was generated by vaccination with Adhgp100 alone. In vivo depletion of CD4(+) T cells, but not CD8(+) T cells, completely abrogated CTL activity, suggesting that Adhgp100-transduced DCs result in activation of both CD4(+) and CD8(+) CTLs via a CD4(+)-dependent mechanism. We speculate that this improved efficacy of Adhgp100-transduced DCs compared to direct immunization with Adhgp100 may be the result of direct DC-mediated CD4(+) T cell activation. These results emphasize the importance of CD4(+) T cells in the development of therapeutic antigen-specific cancer vaccines.

Adenoviridae↗

PubMed1999

Endomorphin-1 mediates 2 Hz but not 100 Hz electroacupuncture analgesia in the rat.

This work was designed to elucidate the possible involvement of endogenous endomorphin-I (EM1) in analgesia induced by electroacupuncture of low or high frequencies. Taking radiant heat tail flick latency (TFL) as an indication of nociception, rats were subjected to intrathecal (i.t.) injection of 10 microl antiserum against EM1 (EM1-AS) or normal rabbit serum (NRS, as control) and then followed by 2 or 100 Hz electroacupuncture stimulation for 30 min. The analgesia induced by 2 Hz electroacupuncture was attenuated by i.t. injection of EM1-AS at 1:10 and 1:100 but not at 1:1000 dilution. No such suppressive effect was observed for 100 Hz EA analgesia when EM1-AS was injected i.t. at any dilutions. These results indicate that EM1 is involved in 2 Hz but not 100 Hz electroacupuncture analgesia at spinal level.

Acupuncture Analgesia↗

PubMed1999

Germline mutations in the extracellular domains of the 55 kDa TNF receptor, TNFR1, define a family of dominantly inherited autoinflammatory syndromes.

Autosomal dominant periodic fever syndromes are characterized by unexplained episodes of fever and severe localized inflammation. In seven affected families, we found six different missense mutations of the 55 kDa tumor necrosis factor receptor (TNFR1), five of which disrupt conserved extracellular disulfide bonds. Soluble plasma TNFR1 levels in patients were approximately half normal. Leukocytes bearing a C52F mutation showed increased membrane TNFR1 and reduced receptor cleavage following stimulation. We propose that the autoinflammatory phenotype results from impaired downregulation of membrane TNFR1 and diminished shedding of potentially antagonistic soluble receptor. TNFR1-associated periodic syndromes (TRAPS) establish an important class of mutations in TNF receptors. Detailed analysis of one such mutation suggests impaired cytokine receptor clearance as a novel mechanism of disease.

Amino Acid Sequence↗

PubMed1999

Adenoviral vectors expressing lymphotactin and interleukin 2 or lymphotactin and interleukin 12 synergize to facilitate tumor regression in murine breast cancer models.

We have previously demonstrated that intratumoral injection with Ad vectors expressing IL-2 or IL-12 can induce regression in a murine breast cancer model. These IL-2- or IL-12-induced antitumor responses were mainly mediated by Ag-specific T cells. Lymphotactin is a novel lymphocyte chemokine that can cause local accumulation of CD4+, CD8+, and NK cells. We hypothesized that addition of lymphotactin may enhance the antitumor immune responses induced by locally produced IL-2 and IL-12 as we have previously shown. To this end we constructed two double-recombinant adenoviral vectors expressing lymphotactin along with either IL-2 (Ad5 Lym/IL-2) or IL-12 (Ad5 Lym/IL-12). Subcutaneous injection of polyoma middle T (PyMT) or Neu (8142) transgenically derived breast adenocarcinoma cells, in the hind flank of FVB/n mice, results in the formation of tumor nodules in 14-21 days. We show that these constructs elicit potent antitumor responses when administered intratumorally. The antitumor responses are long lasting as determined by rechallenge experiments and hence demonstrate a protective immunity. These observations indicate that by augmenting the antitumor response with adenoviral vectors expressing lymphotactin in combination with IL-2 or IL-12 is a novel way to enhance immunotherapeutic approaches.

Adenoviridae↗

PubMed1999

Adenovector-mediated gene delivery of interleukin-2 in metastatic breast cancer and melanoma: results of a phase 1 clinical trial.

We conducted a phase 1 trial of direct injection of an E1, E3-deleted adenovirus encoding interleukin-2 (AdCAIL-2) into subcutaneous deposits of melanoma or breast cancer. Twenty-three patients were injected at seven dose levels (10(7)-10(10) p.f.u). Local inflammation was observed at the site of injection in 60% of patients, but side-effects were otherwise minor. Incomplete local tumor regression occurred at the site of injection in 24% of patients, but no conventional clinical responses were seen. Circulating CD4 and CD8 counts fell significantly 24 h after injection. Post-injection biopsies demonstrated tumor necrosis and lymphocytic infiltration with the predominant tumor-infiltrating cells both CD3- and CD8-positive. Vector-derived sequences were detected in 14 of 18 biopsies examined 7 days after injection and vector-derived hIL-2 mRNA was detected in 80% of 7-day biopsies processed after injection of 10(8) p.f.u. of AdCAIL-2 or higher. While IL-2 was detectable by ELISA in tumor biopsies at 48 h, no protein was detectable in injected tumors after 7 days and no circulating IL-2 was detectable at any time-point. No Ad5E1 sequences were detected either before or after injection indicating absence of replication-competent virus or endogenous E1-like sequence; furthermore, only rare vector shedding was detected. Anti-adenovirus and neutralizing antibody titers were elevated 1 month after injection in all patients. This trial therefore confirms the safety of use of adenoviral vectors for gene delivery in humans and demonstrates successful transgene expression even in the face of pre-existing immunity to adenovirus.

Adenoviridae↗

PubMed1999

High-monounsaturated fatty acid diets lower both plasma cholesterol and triacylglycerol concentrations.

BACKGROUND: Low-fat diets increase plasma triacylglycerol and decrease HDL-cholesterol concentrations, thereby potentially adversely affecting cardiovascular disease (CVD) risk. High-monounsaturated fatty acid (MUFA), cholesterol-lowering diets do not raise triacylglycerol or lower HDL cholesterol, but little is known about how peanut products, a rich source of MUFAs, affect CVD risk. OBJECTIVE: The present study compared the CVD risk profile of an Average American diet (AAD) with those of 4 cholesterol-lowering diets: an American Heart Association/National Cholesterol Education Program Step II diet and 3 high-MUFA diets [olive oil (OO), peanut oil (PO), and peanuts and peanut butter (PPB)]. DESIGN: A randomized, double-blind, 5-period crossover study design (n = 22) was used to examine the effects of the diets on serum lipids and lipoproteins: AAD [34% fat; 16% saturated fatty acids (SFAs), 11% MUFAs], Step II (25% fat; 7% SFAs, 12% MUFAs), OO (34% fat; 7% SFAs, 21% MUFAs), PO (34% fat; 7% SFAs, 17% MUFAs), and PPB (36% fat; 8% SFAs, 18% MUFAs). RESULTS: The high-MUFA diets lowered total cholesterol by 10% and LDL cholesterol by 14%. This response was comparable with that observed for the Step II diet. Triacylglycerol concentrations were 13% lower in subjects consuming the high-MUFA diets and were 11% higher with the Step II diet than with the AAD. The high-MUFA diets did not lower HDL cholesterol whereas the Step II diet lowered it by 4% compared with the AAD. The OO, PO, and PPB diets decreased CVD risk by an estimated 25%, 16%, and 21%, respectively, whereas the Step II diet lowered CVD risk by 12%. CONCLUSION: A high-MUFA, cholesterol-lowering diet may be preferable to a low-fat diet because of more favorable effects on the CVD risk profile.

Adult↗