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  1. Sharma A, Sharma C, Sharma L, Wal P, Mishra P, Sachdeva N, et al.
    Can J Physiol Pharmacol, 2024 May 01;102(5):305-317.
    PMID: 38334084 DOI: 10.1139/cjpp-2023-0259
    Mostly, cardiovascular diseases are blamed for casualties in rheumatoid arthritis (RA) patients. Customarily, dyslipidemia is probably the most prevalent underlying cause of untimely demise in people suffering from RA as it hastens the expansion of atherosclerosis. The engagement of inflammatory cytokines like tumor necrosis factor-α (TNF-α), interleukin-1 (IL-1), interleukin-6 (IL-6), etc., is crucial in the progression and proliferation of both RA and abnormal lipid parameters. Thus, lipid abnormalities should be monitored frequently in patients with both primary and advanced RA stages. An advanced lipid profile examination, i.e., direct role of apolipoproteins associated with various lipid molecules is a more dependable approach for better understanding of the disease and selecting suitable therapeutic targets. Therefore, studying their apolipoproteins is more relevant than assessing RA patients' altered lipid profile levels. Among the various apolipoprotein classes, Apo A1 and Apo B are primarily being focused. In addition, it also addresses how calculating Apo B:Apo A1 ratio can aid in analyzing the disease's risk. The marketed therapies available to control lipid abnormalities are associated with many other risk factors. Hence, directly targeting Apo A1 and Apo B would provide a better and safer option.
    Matched MeSH terms: Apolipoproteins B/blood; Apolipoproteins B/metabolism
  2. Kamal A, Kanchau JD, Shahuri NS, Mohamed-Yassin MS, Baharudin N, Abdul Razak S, et al.
    Am J Case Rep, 2023 Apr 27;24:e939489.
    PMID: 37185657 DOI: 10.12659/AJCR.939489
    BACKGROUND In Malaysia, the prevalence of genetically confirmed heterozygous familial hypercholesterolemia (FH) was reported as 1 in 427. Despite this, FH remains largely underdiagnosed and undertreated in primary care. CASE REPORT In this case series, we report 3 FH cases detected in primary care due to mutations in the low-density lipoprotein receptor (LDLR), apolipoprotein-B (APOB), and proprotein convertase subtilisin/kexin type 9 (PCSK9) genes. The mutations in case 1 (frameshift c.660del pathogenic variant in LDLR gene) and case 2 (missense c.10579C>T pathogenic variant in APOB gene) were confirmed as pathogenic, while the mutation in case 3 (missense c.277C>T mutation in PCSK9 gene) may have been benign. In case 1, the patient had the highest LDL-c level, 8.6 mmol/L, and prominent tendon xanthomas. In case 2, the patient had an LDL-c level of 5.7 mmol/L and premature corneal arcus. In case 3, the patient had an LDL-c level of 5.4 mmol/L but had neither of the classical physical findings. Genetic counseling and diagnosis were delivered by primary care physicians. These index cases were initially managed in primary care with statins and therapeutic lifestyle modifications. They were referred to the lipid specialists for up-titration of lipid lowering medications. First-degree relatives were identified and referred for cascade testing. CONCLUSIONS This case series highlights different phenotypical expressions in patients with 3 different FH genetic mutations. Primary care physicians should play a pivotal role in the detection of FH index cases, genetic testing, management, and cascade screening of family members, in partnership with lipid specialists.
    Matched MeSH terms: Apolipoproteins B/genetics; Apolipoproteins B/therapeutic use
  3. Ng PY, Nafi SNM, Jalil NAC, Kueh YC, Lee YY, Zin AAM
    Croat Med J, 2023 Feb 28;64(1):29-36.
    PMID: 36864816
    AIM: To assess the association of the expression of apolipoprotein B (apoB) and 4-hydroxynonenal (4HNE) with the clinicopathological data of patients with colorectal cancer (CRC).

    METHODS: We obtained 80 CRC histopathological specimens sent to the Pathology Laboratory of Hospital Universiti Sains Malaysia from 2015 to 2019. Data on demographic factors, body mass index (BMI), and clinicopathological characteristics were also collected. Formalin-fixed paraffin-embedded tissues were stained by using an optimized immunohistochemical protocol.

    RESULTS: Patients were mostly older than 50 years, male, Malay, and overweight or obese. A high apoB expression was observed in 87.5% CRC samples (70/80), while a high 4HNE expression was observed in only 17.5% (14/80) of CRCs. The expression of apoB was significantly associated with the sigmoid and rectosigmoid tumor sites (p =0.001) and tumor size 3-5 cm (p =0.005). 4HNE expression was significantly associated with tumor size 3-5 cm (p =0.045). Other variables were not significantly associated with the expression of either marker.

    CONCLUSION: ApoB and 4HNE proteins may play a role in promoting CRC carcinogenesis.

    Matched MeSH terms: Apolipoproteins B*
  4. Perak AM, Ning H, Kit BK, de Ferranti SD, Van Horn LV, Wilkins JT, et al.
    JAMA, 2019 May 21;321(19):1895-1905.
    PMID: 31112258 DOI: 10.1001/jama.2019.4984
    IMPORTANCE: Favorable trends occurred in the lipid levels of US youths through 2010, but these trends may be altered by ongoing changes in the food supply, obesity prevalence, and other factors.

    OBJECTIVE: To analyze trends in levels of lipids and apolipoprotein B in US youths during 18 years from 1999 through 2016.

    DESIGN, SETTING, AND PARTICIPANTS: Serial cross-sectional analysis of US population-weighted data for youths aged 6 to 19 years from the National Health and Nutrition Examination Surveys for 1999 through 2016. Linear temporal trends were analyzed using multivariable regression models with regression coefficients (β) reported as change per 1 year.

    EXPOSURES: Survey year; examined periods spanned 10 to 18 years based on data availability.

    MAIN OUTCOMES AND MEASURES: Age- and race/ethnicity-adjusted mean levels of high-density lipoprotein (HDL), non-HDL, and total cholesterol. Among fasting adolescents (aged 12-19 years), mean levels of low-density lipoprotein cholesterol, geometric mean levels of triglycerides, and mean levels of apolipoprotein B. Prevalence of ideal and adverse (vs borderline) levels of lipids and apolipoprotein B per pediatric lipid guidelines.

    RESULTS: In total, 26 047 youths were included (weighted mean age, 12.4 years; female, 51%). Among all youths, the adjusted mean total cholesterol level declined from 164 mg/dL (95% CI, 161 to 167 mg/dL) in 1999-2000 to 155 mg/dL (95% CI, 154 to 157 mg/dL) in 2015-2016 (β for linear trend, -0.6 mg/dL [95% CI, -0.7 to -0.4 mg/dL] per year). Adjusted mean HDL cholesterol level increased from 52.5 mg/dL (95% CI, 51.7 to 53.3 mg/dL) in 2007-2008 to 55.0 mg/dL (95% CI, 53.8 to 56.3 mg/dL) in 2015-2016 (β, 0.2 mg/dL [95% CI, 0.1 to 0.4 mg/dL] per year) and non-HDL cholesterol decreased from 108 mg/dL (95% CI, 106 to 110 mg/dL) to 100 mg/dL (95% CI, 99 to 102 mg/dL) during the same years (β, -0.9 mg/dL [95% CI, -1.2 to -0.6 mg/dL] per year). Among fasting adolescents, geometric mean levels of triglycerides declined from 78 mg/dL (95% CI, 74 to 82 mg/dL) in 1999-2000 to 63 mg/dL (95% CI, 58 to 68 mg/dL) in 2013-2014 (log-transformed β, -0.015 [95% CI, -0.020 to -0.010] per year), mean levels of low-density lipoprotein cholesterol declined from 92 mg/dL (95% CI, 89 to 95 mg/dL) to 86 mg/dL (95% CI, 83 to 90 mg/dL) during the same years (β, -0.4 mg/dL [95% CI, -0.7 to -0.2 mg/dL] per year), and mean levels of apolipoprotein B declined from 70 mg/dL (95% CI, 68 to 72 mg/dL) in 2005-2006 to 67 mg/dL (95% CI, 65 to 70 mg/dL) in 2013-2014 (β, -0.4 mg/dL [95% CI, -0.7 to -0.04 mg/dL] per year). Favorable trends were generally also observed in the prevalence of ideal and adverse levels. By the end of the study period, 51.4% (95% CI, 48.5% to 54.2%) of all youths had ideal levels for HDL, non-HDL, and total cholesterol; among adolescents, 46.8% (95% CI, 40.9% to 52.6%) had ideal levels for all lipids and apolipoprotein B, whereas 15.2% (95% CI, 13.1% to 17.3%) of children aged 6 to 11 years and 25.2% (95% CI, 22.2% to 28.2%) of adolescents aged 12 to 19 years had at least 1 adverse level.

    CONCLUSIONS AND RELEVANCE: Between 1999 and 2016, favorable trends were observed in levels of lipids and apolipoprotein B in US youths aged 6 to 19 years.

    Matched MeSH terms: Apolipoproteins B/blood*
  5. Gajra B, Candlish JK, Heng CK, Mak JW, Saha N
    Hum Biol, 1997 Oct;69(5):629-40.
    PMID: 9299883
    Associations among seven apolipoprotein B (APOB) gene polymorphisms [C-T promoter site; Leu-Ala-Leu signal peptide (SP) insertion/deletion; AG C,G site at codon 71; AG A1,D site at codon 591; XbaI site at codon 2488; AG H,I site at codon 3611; and AG T,Z site at codon 4154] were investigated in 195 members of an Orang Asli (aborigine) population from western Malaysia. Frequencies of the rare alleles for all these polymorphisms turned out to be low when compared with European but not Asian populations. The AG H,I site was not polymorphic. The highly polymorphic sites are in linkage disequilibrium among themselves, as shown by their delta values: SP 24,27 and AG C,G, 0.68; SP 24,27 and AG A1,D, 0.71; XbaI and AG C,G, 0.64; XbaI and AG A1,D, 0.57; SP 24,27 and XbaI, 0.48; and AG C,G and AG A1,D, 0.68. Ten unequivocal haplotypes on the basis of six sites (excluding the promoter polymorphism) were observed, and they represent 80% of the sample. The frequency of haplotype SP27,G,A1,X-,I,T, defined by the common homozygotes at all the sites for the APOB gene was 0.7, compared with 0.22 in Europeans. The ancestral haplotype SP27,G,D,X-,I,T was present at low frequency (0.01) in both the Orang Asli and Europeans. A cladogram constructed on the basis of haplotypes in the Orang Asli shows two different lines of evolution and that other haplotypes evolved by subsequent mutations on the ancestral haplotype.
    Matched MeSH terms: Apolipoproteins B/genetics*
  6. Yang CL, Chao YJ, Wang HC, Hou YC, Chen CG, Chang CC, et al.
    Nanomedicine, 2021 10;37:102450.
    PMID: 34332115 DOI: 10.1016/j.nano.2021.102450
    Epigenetic inhibitors have shown anticancer effects. Combination chemotherapy with epigenetic inhibitors has shown high effectiveness in gastric cancer clinical trials, but severe side effect and local progression are the causes of treatment failure. Therefore, we sought to develop an acidity-sensitive drug delivery system to release drugs locally to diminish unfavorable outcome of gastric cancer. In this study, we showed that, as compared with single agents, combination treatment with the demethylating agent 5'-aza-2'-deoxycytidine and HDAC inhibitors Trichostatin A or LBH589 decreased cell survival, blocked cell cycle by reducing number of S-phase cells and expression of cyclins, increased cell apoptosis by inducing expression of Bim and cleaved Caspase 3, and reexpressed tumor suppressor genes more effectively in MGCC3I cells. As a carrier, reconstituted apolipoprotein B lipoparticles (rABLs) could release drugs in acidic environments. Orally administrated embedded drugs not only showed inhibitory effects on gastric tumor growth in a syngeneic orthotopic mouse model, but also reduced the hepatic and renal toxicity. In conclusion, we have established rABL-based nanoparticles embedded epigenetic inhibitors for local treatment of gastric cancer, which have good therapeutic effects but do not cause severe side effects.
    Matched MeSH terms: Apolipoproteins B/genetics; Apolipoproteins B/pharmacology*; Apolipoproteins B/chemistry
  7. Razman AZ, Chua YA, Mohd Kasim NA, Al-Khateeb A, Sheikh Abdul Kadir SH, Jusoh SA, et al.
    Int J Mol Sci, 2022 Nov 29;23(23).
    PMID: 36499307 DOI: 10.3390/ijms232314971
    Familial hypercholesterolaemia (FH) is caused by mutations in lipid metabolism genes, predominantly in low-density lipoprotein receptor (LDLR), apolipoprotein B (APOB), proprotein convertase subtilisin/kexin-type 9 (PCSK9) and LDL receptor adaptor protein 1 (LDLRAP1). The prevalence of genetically confirmed FH and the detection rate of pathogenic variants (PV) amongst clinically diagnosed patients is not well established. Targeted next-generation sequencing of LDLR, APOB, PCSK9 and LDLRAP1 was performed on 372 clinically diagnosed Malaysian FH subjects. Out of 361 variants identified, 40 of them were PV (18 = LDLR, 15 = APOB, 5 = PCSK9 and 2 = LDLRAP1). The majority of the PV were LDLR and APOB, where the frequency of both PV were almost similar. About 39% of clinically diagnosed FH have PV in PCSK9 alone and two novel variants of PCSK9 were identified in this study, which have not been described in Malaysia and globally. The prevalence of genetically confirmed potential FH in the community was 1:427, with a detection rate of PV at 0.2% (12/5130). About one-fourth of clinically diagnosed FH in the Malaysian community can be genetically confirmed. The detection rate of genetic confirmation is similar between potential and possible FH groups, suggesting a need for genetic confirmation in index cases from both groups. Clinical and genetic confirmation of FH index cases in the community may enhance the early detection of affected family members through family cascade screening.
    Matched MeSH terms: Apolipoproteins B
  8. Kyi WM, Isa MN, Rashid FA, Osman JM, Mansur MA
    Malays J Med Sci, 2000 Jan;7(1):16-21.
    PMID: 22844210
    Familial defective apolipoprotein B-100 (FDB) is an autosomal dominant genetic disorder associated with hypercholesterolaemia and premature coronary heart disease. FDB is caused by mutations in and around the codon 3500 of the apolipoprotein B (apo B) gene. Apo B R3500Q mutation is the first apo B mutation known to be associated with FDB and it is the most frequently reported apo B mutation in several different populations. The objective of the present study was to determine the association of apo B R3500Q mutation with elevated plasma cholesterol concentration in Kelantanese population in which both hypercholesterolaemia and coronary heart disease are common. Sixty-two Malay subjects with hyperlipidaemia, attending the lipid clinic at Hospital Universiti Sains Malaysia, Kelantan, were selected for this study. The DNA samples were analysed for the presence of apo B R3500Q mutation by polymerase chain reaction-based restriction fragment analysis method using mutagenic primers. This mutation was not detected in the subjects selected for this study. Apo B R3500Q mutation does not appear to be a common cause of hypercholesterolaemia in Kelantanese Malays.
    Matched MeSH terms: Apolipoproteins B
  9. Lye SH, Chahil JK, Bagali P, Alex L, Vadivelu J, Ahmad WA, et al.
    PLoS One, 2013;8(4):e60729.
    PMID: 23593297 DOI: 10.1371/journal.pone.0060729
    Familial hypercholesterolemia (FH) is an autosomal dominant disorder characterized by elevations in total cholesterol (TC) and low density lipoprotein cholesterol (LDLc). Development of FH can result in the increase of risk for premature cardiovascular diseases (CVD). FH is primarily caused by genetic variations in Low Density Lipoprotein Receptor (LDLR), Apolipoprotein B (APOB) or Proprotein Convertase Subtilisin/Kexin type 9 (PCSK9) genes. Although FH has been extensively studied in the Caucasian population, there are limited reports of FH mutations in the Asian population. We investigated the association of previously reported genetic variants that are involved in lipid regulation in our study cohort. A total of 1536 polymorphisms previously implicated in FH were evaluated in 141 consecutive patients with clinical FH (defined by the Dutch Lipid Clinic Network criteria) and 111 unrelated control subjects without FH using high throughput microarray genotyping platform. Fourteen Single Nucleotide Polymorphisms (SNPs) were found to be significantly associated with FH, eleven with increased FH risk and three with decreased FH risk. Of the eleven SNPs associated with an increased risk of FH, only one SNP was found in the LDLR gene, seven in the APOB gene and three in the PCSK9 gene. SNP rs12720762 in APOB gene is associated with the highest risk of FH (odds ratio 14.78, p<0.001). Amongst the FH cases, 108 out of 141 (76.60%) have had at least one significant risk-associated SNP. Our study adds new information and knowledge on the genetic polymorphisms amongst Asians with FH, which may serve as potential markers in risk prediction and disease management.
    Matched MeSH terms: Apolipoproteins B/genetics*
  10. Khoo KL, Van Acker P, Tan H, Deslypere JP
    Med J Malaysia, 2000 Dec;55(4):409-18.
    PMID: 11221151
    A total of 86 unrelated Malaysian patients with familial hypercholesterolaemia (FH) were studied for mutations in their low-density lipoprotein receptor (LDL-R) gene. Amongst them, 23 had a LDL-R gene mutation, while none having an Apolipoprotein B-3500 (Apo B-3500) mutation. Patients with the LDL-R gene defect appeared to have a higher level of low-density lipoprotein cholesterol (LDL-C), an increased incidence of xanthomas and coronary heart disease (CHD), but no relationships were found between the type of LDL-R gene mutations and their lipid levels or clinical signs of CHD. In contrast to Western data, our findings seemed to indicate a predominance of mutations in the ligand binding domain and an absence of Apo B-3500 gene mutation. The latter finding may offer a genetic basis as to why Asian patients with familial hypercholesterolaemia have lower LDL-C levels and less premature CHD than their Western counterparts.
    Matched MeSH terms: Apolipoproteins B/genetics
  11. Saha N, Wong HB
    Biol. Neonate, 1987;52(2):93-6.
    PMID: 3115319
    The mortality from coronary artery disease (CAD) in Indians is more than three times that in the Chinese and Malays of Singapore. Serum total and HDL cholesterol as well as apolipoprotein (Apo) AI, AII and B levels were determined in a group of 349 newborns (cord blood) from both sexes in these three ethnic groups in order to examine if a trend is reflected at birth. Both serum LDL cholesterol and Apo B levels were low in the newborn, while HDL cholesterol and Apo AII levels were almost the same as in adults. Serum Apo AI levels were also low in newborns. No consistent difference as to ethnic group or sex was observed in any of the parameters investigated, except that the females had significantly higher levels of serum Apo AI in all the ethnic groups. Serum total and HDL cholesterol levels in Singapore newborns were comparable to those reported in Caucasians and Asians. The trends of incidence of CAD were not reflected in the lipid profiles studied at birth.
    Matched MeSH terms: Apolipoproteins B/blood*
  12. Khoo KL, van Acker P, Defesche JC, Tan H, van de Kerkhof L, Heijnen-van Eijk SJ, et al.
    Clin Genet, 2000 Aug;58(2):98-105.
    PMID: 11005141 DOI: 10.1034/j.1399-0004.2000.580202.x
    The aim of this study was to detect mutations in the genes coding for the low-density lipoprotein receptor and apolipoprotein B in patients of Southeast Asian origin with clinically diagnosed familial hypercholesterolemia (FH) and to relate these findings with the observed lower incidence of coronary heart disease in this part of the world. A total of 86 unrelated patients with FH were selected on clinical grounds, and complete DNA analysis of the low-density lipoprotein (LDL)-receptor and apolipoprotein B (apoB) genes by DGGE and DNA-sequencing was performed. In the majority (73%) of the cohort studied, no mutations could be detected, even after extensive analysis of the LDL-receptor and apoB genes. However, the 22 patients with a mutation had significantly more xanthomas and a higher incidence of coronary heart disease and levels of low-density lipoproteins were also significantly different. There was no correlation between the type of the mutation and lipoprotein levels or clinical signs of atherosclerosis. The fact that the majority of the FH patients studied had no detectable mutation and that this group had a significant milder phenotype, suggests the presence of a third gene in the Southeast Asian population, predominantly leading to a disorder resembling a milder form of FH. A similar, but less frequent, trait has recently been described in a number of European families.
    Matched MeSH terms: Apolipoproteins B/genetics
  13. Marzuki A, Arshad F, Razak TA, Jaarin K
    Am J Clin Nutr, 1991 04;53(4 Suppl):1010S-1014S.
    PMID: 1901440 DOI: 10.1093/ajcn/53.4.1010S
    We studied the effects of saturated (palm olein) and polyunsaturated (soybean oil) cooking oils on the lipid profiles of Malaysian male adolescents eating normal Malaysian diets for 5 wk. Diets cooked with palm olein did not significantly alter plasma total-cholesterol, LDL cholesterol, and HDL cholesterol concentrations or the ratio of total cholesterol to HDL cholesterol compared with diets cooked with soybean oil. However, the diet cooked with palm olein significantly increased apolipoprotein A-I (11%) and apolipoprotein B (9%) concentrations. Unexpectedly, soybean-oil-cooked diets caused a significant increase (47%) in plasma triglycerides compared with palm-olein-cooked diets. We conclude that palm olein, when used as cooking oil, has no detrimental effects on plasma lipid profiles in Malaysian adolescents.
    Matched MeSH terms: Apolipoproteins B/blood
  14. Choong ML, Koay ES, Khaw MC, Aw TC
    Hum Hered, 1999 Jan;49(1):31-40.
    PMID: 9858855
    The allele frequencies for the apolipoprotein B (apo B) 5'-Ins/Del and 3'-VNTR polymorphisms varied significantly (p < 0.01) among Singaporeans of Chinese, Malay and Indian descent. We calculated the unbiased expected heterozygosities for the 5'-Ins/Del polymorphism as 0.3357, 0.1984 and 0.2418, and for the 3'-VNTR as 0.5980, 0.5260 and 0.6749, respectively, in the Chinese, Malays and Indians. Compared to heterozygosities reported for other populations, the Singaporeans differed from most Caucasians in having significantly lower values but were closely related to other non-Caucasians. Thirteen alleles, with a bimodal distribution, were observed at the 3'-VNTR polymorphic locus; the alleles occurring most frequently among the Chinese and Malays were of 35 or 53 repeats, and among the Indians, of 37 or 47 repeats. The Del allele was associated with elevated serum cholesterol (p = 0.023), LDL-cholesterol (LDL-C) (p = 0.001) in the Chinese, and apo B (p = 0.007) in the Indians. Likewise, the larger 3'-VNTR alleles (> 41 repeats) were associated with raised cholesterol (p = 0.018), LDL-C (p = 0.025), and triglyceride (p = 0.001) in the Chinese. The two polymorphisms were not in significant linkage disequilibrium (D = -0.0029, p = 0.494) in the three ethnic groups.
    Matched MeSH terms: Apolipoproteins B/genetics*
  15. Gajra B, Candlish JK, Saha N, Mak JW, Tay JS
    Hum Hered, 1994;44(4):209-13.
    PMID: 8056432
    Members of the Semai group of Orang Asli ('aborigines') in peninsular Malaysia were examined for apolipoprotein E (apo E) variants in relation to plasma total cholesterol (TC), high density lipoprotein cholesterol, low density lipoprotein cholesterol (LDLC), triglycerides (TG), apolipoprotein AI and apolipoprotein B (apo B). The e2 and e4 alleles were found to be higher than in most other groups as reported. The sample as a whole was normotriglyceridaemic (mean plasma TG, 1.5 mmol/l) and very markedly hypocholesterolaemic (mean plasma TC 1.7 mmol/l). The distribution of apo E variants was not related to any of the plasma lipids or apolipoprotein fractions using results from all subjects, but if a distinctly hypertriglyceridaemic sub-section was omitted (TG > 1.7 mmol/l) then apo E variants were determinants of plasma TC, LDLC, and apo B concentrations, the lower values of these being associated with the 2-2 and 2-3 genotypes, and the higher with 3-4, and 4-4.
    Matched MeSH terms: Apolipoproteins B/analysis*
  16. Choong ML, Koay ES, Khoo KL, Khaw MC, Sethi SK
    Clin Chem, 1997 Jun;43(6 Pt 1):916-23.
    PMID: 9191540
    The Arg-to-Trp substitution at codon 3500 in the apolipoprotein (apo) B-100 gene is established as a cause of familial defective apo B-100 (FDB), a functional mutation, resulting in reduced LDL receptor binding and manifest hypercholesterolemia. In a search for similar mutations in 163 Malaysians, we screened the putative receptor-binding region (codons 3456-3553) of the apo B-100 gene by PCR amplification and denaturing gradient-gel electrophoresis. Four single-base mutations were detected and confirmed by DNA sequencing. Two females, a Chinese and a Malay, had the same CGG3500-->TGG mutation, resulting in an Arg3500-to-Trp substitution. This is the second published report of such an independent mutation involving the same codon as the established Arg3500-to-Gln mutation. The two other mutations detected, CTT3517-->CTG and GCC3527-->GCT, resulted in degenerate codons with no amino acid substitutions. All four mutations were associated with a unique apo B haplotype, different from those found in Caucasian FDB patients but concurring with that previously reported for two other Asians with FDB.
    Matched MeSH terms: Apolipoproteins B/analysis*; Apolipoproteins B/genetics*
  17. Choong ML, Sethi SK, Koay ES
    Hum Biol, 1999 Jun;71(3):381-97.
    PMID: 10380374
    We determined the allelic (X+/X-, M+/M-, and E+/E-) distribution frequencies of the XbaI, MspI, and EcoRI restriction fragment length polymorphisms (RFLPs) in the apolipoprotein B gene in a control group of 374 healthy Chinese, Malays, and Indians and in a hyperlipidemic cohort of 131 Chinese patients. Covariability between the RFLPs and serum lipid, lipoprotein, and apolipoprotein concentrations was also studied. We found a lower frequency (average 0.0829) of the X+ allele and higher frequencies of the E+ (average 0.9452) and M+ (average 0.9772) alleles in our study population compared with frequencies reported in other populations. The 3 polymorphic sites did not contribute to significant variations in lipid levels (p > 0.1 in all cases). Also, there was no significant variation in genotype frequencies between the control subjects and the hyperlipidemic subjects. Despite their relative close proximity within the APOB gene sequence, the 3 polymorphic sites did not show any significant linkage disequilibrium. However, the presence of the X+ cutting site was in linkage disequilibrium with the Del allele of the 5' insertion-deletion polymorphism and the E-allele was in linkage disequilibrium with the 3' VNTR located near the 3' end of the coding region of the APOB gene.
    Matched MeSH terms: Apolipoproteins B/blood; Apolipoproteins B/genetics*
  18. Low PS, Saha N, Tay JS, Hong S
    Acta Paediatr, 1996 Dec;85(12):1476-82.
    PMID: 9001661
    In multiracial Singapore, the prevalence of coronary artery disease is highest in ethnic Indian and lowest in ethnic Chinese populations. Since susceptibility to coronary artery disease is closely associated with plasma lipid traits, we studied the cord blood lipid and apolipoprotein profiles of the three ethnic groups in Singapore to determine if ethnic differences in lipid profile are present at birth. The high-risk lipid traits of high LDL-cholesterol, triglycerides and apo B, low HDL-cholesterol and apo A-I were found to be highest in ethnic Indian and lowest in ethnic Chinese populations. This difference was concordant with the relative coronary mortality rates for their respective adult populations in Singapore.
    Matched MeSH terms: Apolipoproteins B/blood
  19. Chow YL, Teh LK, Chyi LH, Lim LF, Yee CC, Wei LK
    Curr Pharm Des, 2020;26(34):4261-4271.
    PMID: 32534558 DOI: 10.2174/1381612826666200614180958
    Stroke is the second leading cause of death and a major cause of disability worldwide. Both modifiable and non-modifiable risk factors can affect the occurrence of ischemic stroke at varying degrees. Among them, atherosclerosis has been well-recognized as one of the main culprits for the rising incidence of stroke-related mortality. Hence, the current review aimed to summarize the prominent role of lipid metabolism genes such as PCSK9, ApoB, ApoA5, ApoC3, ApoE, and ABCA1 in mediating ischemic stroke occurrence.
    Matched MeSH terms: Apolipoproteins B
  20. Khaleghi S, Aziz AA, Razali N, Junit SM
    Genes Nutr, 2011 Nov;6(4):413-27.
    PMID: 21484159 DOI: 10.1007/s12263-011-0216-z
    In this study, the effects of low and high concentrations of the Anacardium occidentale shoot extracts on gene expression in liver HepG2 cells were investigated. From MTT assays, the concentration of the shoot extracts that maintained 50% cell viability (IC(50)) was 1.7 mg/ml. Cell viability was kept above 90% at both 0.4 mg/ml and 0.6 mg/ml of the extracts. The three concentrations were subsequently used for the gene expression analysis using Affymetrix Human Genome 1.0 S.T arrays. The microarray data were validated using real-time qRT-PCR. A total of 246, 696 and 4503 genes were significantly regulated (P 
    Matched MeSH terms: Apolipoproteins B
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