Displaying publications 101 - 120 of 485 in total

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  1. Al-Herz W, Chou J, Delmonte OM, Massaad MJ, Bainter W, Castagnoli R, et al.
    Front Immunol, 2018;9:3146.
    PMID: 30697212 DOI: 10.3389/fimmu.2018.03146
    Objective: To present the genetic causes of patients with primary immune deficiencies (PIDs) in Kuwait between 2004 and 2017. Methods: The data was obtained from the Kuwait National Primary Immunodeficiency Disorders Registry. Genomic DNA from patients with clinical and immunological features of PID was sequenced using Sanger sequencing (SS), next generation sequencing (NGS) of targeted genes, whole exome sequencing (WES), and/or whole genome sequencing (WGS). Functional assays were utilized to assess the biologic effect of identified variants. Fluorescence in situ hybridization (FISH) for 22q11.2 deletion and genomic hybridizations arrays were performed when thymic defects were suspected. Results: A total of 264 patients were registered during the study period with predominance of patients with immunodeficiencies affecting cellular and humoral immunity (35.2%), followed by combined immunodeficiencies with associated syndromic features (24%). Parental consanguinity and family history suggestive of PID were reported in 213 (81%) and 145 patients (55%), respectively. Genetic testing of 206 patients resulted in a diagnostic yield of 70%. Mutations were identified in 46 different genes and more than 90% of the reported genetic defects were transmitted by in an autosomal recessive pattern. The majority of the mutations were missense mutations (57%) followed by deletions and frame shift mutations. Five novel disease-causing genes were discovered. Conclusions: Genetic testing should be an integral part in the management of primary immunodeficiency patients. This will help the delivery of precision medicine and facilitate proper genetic counseling. Studying inbred populations using sophisticated diagnostic methods can allow better understanding of the genetics of primary immunodeficiency disorders.
    Matched MeSH terms: Immunologic Deficiency Syndromes/diagnosis; Immunologic Deficiency Syndromes/genetics*; Immunologic Deficiency Syndromes/epidemiology*
  2. Tasker PWG, Mollin DL, Berriman H
    Br J Haematol, 1958;4:167-176.
    DOI: 10.1111/j.1365-2141.1958.tb03847.x
    Matched MeSH terms: Vitamin B 12 Deficiency
  3. Ong SG, Ding HJ
    Med J Malaysia, 2019 12;74(6):492-498.
    PMID: 31929474
    INTRODUCTION: Numerous studies have found that a majority of systemic lupus erythematosus (SLE) patients have suboptimal vitamin D levels. The major contributory factor is most likely attributed to sun protection measures in order to avoid SLE flares. The objectives of this research included the assessment of vitamin D status and its association with clinical manifestations of SLE, cardiovascular risk factors, autoantibodies, SLE disease activity and damage accrual.

    METHOD: This retrospective study involved SLE patients who attended the Rheumatology Clinic at the Hospital Kuala Lumpur from January 2014 to December 2016. Vitamin D was categorised as normal, insufficient or deficient, and the clinical variables were compared across vitamin D categories with chi-squared tests and Pearson correlation coefficient.

    RESULTS: We included 216 patients. The mean 25(OH)D concentration was 51.3(Standard Deviation; SD 14.8) nmol/L. Fifty (23.1%) patients had vitamin D deficiency, 120 (55.6%) had vitamin D insufficiency, while 46 (21.3%) had adequate vitamin D levels. There were statistically significant associations between vitamin D status and ethnic group, lupus nephritis and hypertension. No correlations were observed between vitamin D status with SLEDAI score (Pearson correlation coefficient -0.015, p=0.829) as well as SDI score (Pearson correlation coefficient -0.017, p=0.801).

    CONCLUSION: SLE patients should be screened for vitamin D concentrations and their levels optimised.

    Matched MeSH terms: Vitamin D Deficiency/blood*; Vitamin D Deficiency/drug therapy; Vitamin D Deficiency/etiology
  4. Wong CED, Hua K, Monis S, Saxena V, Norazit A, Noor SM, et al.
    J Neurochem, 2021 02;156(4):481-498.
    PMID: 32583440 DOI: 10.1111/jnc.15108
    Glial cell line-derived neurotrophic factor (GDNF) has been reported to enhance dopaminergic neuron survival and differentiation in vitro and in vivo, although those results are still being debated. Glial cell line-derived neurotrophic factor (gdnf) is highly conserved in zebrafish and plays a role in enteric nervous system function. However, little is known about gdnf function in the teleost brain. Here, we employed clustered regularly interspaced short palindromic repeats/CRISPR-associated protein 9 to impede gdnf function in the maintenance of dopaminergic neuron development. Genotyping of gdnf crispants revealed successful deletions of the coding region with various mutant band sizes and down-regulation of gdnf transcripts at 1, 3 and 7 day(s) post fertilization. Notably, ~20% reduction in ventral diencephalic dopaminergic neuron numbers in clusters 8 and 13 was observed in the gdnf-deficient crispants. In addition, gdnf depletion caused a modest reduction in dopaminergic neurogenesis as determined by 5-ethynyl-2'-deoxyuridine pulse chase assay. These deleterious effects could be partly attributed to deregulation of dopaminergic neuron fate specification-related transcription factors (otp,lmx1b,shha,and ngn1) in both crispants and established homozygous mutants with whole mount in-situ hybridization (WISH) on gdnf mutants showing reduced otpb and lmx1b.1 expression in the ventral diencephalon. Interestingly, locomotor function of crispants was only impacted at 7 dpf, but not earlier. Lastly, as expected, gdnf deficiency heightened crispants vulnerability to 1-methyl-4-phenylpyridinium toxic insult. Our results suggest conservation of teleost gdnf brain function with mammals and revealed the interactions between gdnf and transcription factors in dopaminergic neuron differentiation.
    Matched MeSH terms: Transcription Factors/deficiency*; Zebrafish Proteins/deficiency*; Glial Cell Line-Derived Neurotrophic Factor/deficiency*
  5. Ainoon O, Alawiyah A, Yu YH, Cheong SK, Hamidah NH, Boo NY, et al.
    PMID: 12971572
    Neonatal screening for G6PD deficiency has long been established in many countries. The aim of the study was to determine whether the routine semiquantitative fluorescent spot test could detect all cases of G6PD deficiency, including those cases with partial deficiency (residual red cell G6PD activity between 20-60% of normal). We compared the results of G6PD screening by the semiquantitative fluorescent spot test and quantitative G6PD activity assay on a group of 976 neonates and 67 known female heterozygotes. The values for mean G6PD activity of G6PD-normal neonates and 293 healthy adult females were determined. There was no significant difference in the mean normal G6PD activity between the two racial groups in the neonates (669 Malays, 307 Chinese) and in the 293 healthy adult females (150 Malays, 143 Chinese) group. The values for the upper limits of total deficiency (20% of normal residual activity) for neonates and adult females were 2.92 U/gHb and 1.54 U/gHb, respectively. The upper limits of partial deficiency (60% of normal residual activity) were 8.7 U/gHb and 4.6 U/gHb respectively. The prevalence of G6PD deficiency among the male neonates was 5.1% (26) by both the fluorescent spot test and the enzyme assay method. The G6PD activity levels of all 26 cases of G6PD-deficient male neonates were < 20% normal (severe enzyme deficiency). In the female neonate group, the frequency of G6PD deficiency was 1.3% (6 of 472) by the fluorescent spot test and 9.35% (44 of 472) by enzyme assay. The 6 cases diagnosed as deficient by the fluorescent spot test showed severe enzyme deficiency (< 2.92 U/gHb). The remaining 38 female neonates had partial enzyme deficiency and all were misdiagnosed as normal by the fluorescent spot test. In the female heterozygote group, G6PD deficiency was diagnosed in 53% (35 of 67) by enzyme assay and in 7.5% (4 of 67) of cases by the fluorescent spot test. The 4 cases detected by fluorescent spot test had severe enzyme deficiency (<1.6 U/gHb). The remaining 31 (46.3%) cases, diagnosed as normal by fluorescent spot test, showed partial G6PD deficiency. In conclusion, we found that the semiquantitative fluorescent spot test could only diagnose cases of total G6PD deficiency and misclassified the partially-deficient cases as normal. In this study, the overall prevalence of G6PD deficiency was 3.28% by the semiquantitative fluorescent spot test and 7.17% by enzyme assay. This means that 3.9% of G6PD-deficient neonates were missed by the routine fluorescent spot test and they were found to be exclusively females. This study demonstrates a need to use a method that can correctly classify female heterozygotes with partial G6PD deficiency. The clinical implication is that these individuals may be at risk of the hemolytic complication of G6PD deficiency.
    Matched MeSH terms: Glucosephosphate Dehydrogenase Deficiency/blood*; Glucosephosphate Dehydrogenase Deficiency/genetics; Glucosephosphate Dehydrogenase Deficiency/epidemiology
  6. Ainoon O, Yu YH, Amir Muhriz AL, Boo NY, Cheong SK, Hamidah NH
    Hum Mutat, 2003 Jan;21(1):101.
    PMID: 12497642 DOI: 10.1002/humu.9103
    We performed DNA analysis using cord blood samples on 86 male Malay neonates diagnosed as G6PD deficiency in the National University of Malaysia Hospital by a combination of rapid PCR-based techniques, single-stranded conformation polymorphism analysis (SSCP) and DNA sequencing. We found 37.2% were 871G>A (G6PD Viangchan), 26.7% were nt 563 C>T (G6PD Mediterranean) and 15.1% were 487G>A (G6PD Mahidol) followed by 4.7% 1376G>T (G6PD Canton), 3.5% 383T>C (G6PD Vanua Lava), 3.5% 592C>T (G6PD Coimbra), 2.3% 1388G>A (G6PD Kaiping), 2.3% 1360C>T (G6PD Union), 2.3% 1003G>A (G6PD Chatham), 1.2% 131C>G (G6PD Orissa) and 1.2% 1361G>A (G6PD Andalus). Seventy-one (82.6%) of the 86 G6PD-deficient neonates had neonatal jaundice. Fifty seven (80%) of the 71 neonates with jaundice required phototherapy with only one neonate progressing to severe hyperbilirubinemia (serum bilirubin >340 micromol/l) requiring exchange transfusion. There was no significant difference in the incidence of neonatal jaundice, mean serum bilirubin level, mean age for peak serum bilirubin, percentage of babies requiring phototherapy and mean number of days of phototherapy between the three common variants. In conclusion, the molecular defects of Malay G6PD deficiency is heterogeneous and G6PD Viangchan, Mahidol and Mediterranean account for at least 80% of the cases. Our findings support the observation that G6PD Viangchan and Mahidol are common Southeast Asian variants. Their presence in the Malays suggests a common ancestral origin with the Cambodians, Laotians and Thais. Our findings together with other preliminary data on the presence of the Mediterranean variant in this region provide evidence of strong Arab influence in the Malay Archipelago.
    Matched MeSH terms: Glucosephosphate Dehydrogenase Deficiency/diagnosis; Glucosephosphate Dehydrogenase Deficiency/ethnology; Glucosephosphate Dehydrogenase Deficiency/genetics*
  7. Iwai K, Hirono A, Matsuoka H, Kawamoto F, Horie T, Lin K, et al.
    Hum Genet, 2001 Jun;108(6):445-9.
    PMID: 11499668
    Glucose-6-phosphate dehydrogenase (G6PD) deficiency is a heterogeneous enzyme abnormality with high frequency in tropical areas. We performed population screening and molecular studies of G6PD variants to clarify their distribution and features in Southeast Asia. A total of 4317 participants (2019 males, 2298 females) from 16 ethnic groups in Myanmar, Lao in Laos, and Amboinese in Indonesia were screened with a single-step screening method. The prevalence of G6PD-deficient males ranged from 0% (the Akha) to 10.8% (the Shan). These G6PD-deficient individuals and 12 G6PD-deficient patients who had been diagnosed at hospitals in Indonesia and Malaysia were subjected to molecular analysis by a combination of polymerase-chain-reaction-based single-strand conformation polymorphism analysis and direct sequencing. Ten different missense mutations were identified in 63 G6PD-deficient individuals (50 hemizygotes, 11 heterozygotes, and 2 homozygotes) from 14 ethnic groups. One missense mutation (1291 G-->A) found in an Indonesian Chinese, viz., G6PD Surabaya, was previously unknown. The 487 G-->A (G6PD Mahidol) mutation was widely seen in Myanmar, 383 T-->C (G6PD Vanua Lava) was specifically found among Amboinese, 871 G-->A (G6PD Viangchan) was observed mainly in Lao, and 592 C-->T (G6PD Coimbra) was found in Malaysian aborigines (Orang Asli). The other five mutations, 95 A-->G (G6PD Gaohe), 1003 G-->A (G6PD Chatham), 1360 C-->T (G6PD Union), 1376 G-->T (G6PD Canton), and 1388 G-->A (G6PD Kaiping) were identified mostly in accordance with distributions reported previously.
    Matched MeSH terms: Glucosephosphate Dehydrogenase Deficiency/enzymology; Glucosephosphate Dehydrogenase Deficiency/genetics*; Glucosephosphate Dehydrogenase Deficiency/epidemiology
  8. Azira N MS, Zeehaida M
    Trop Biomed, 2012 Dec;29(4):626-31.
    PMID: 23202608
    Trichuris dysentery syndrome is caused by Trichuris trichiura which contributes to one of the most common helminthic infections in the world. It is associated with heavy colonic infection that manifests as mucoid diarrhoea, rectal bleeding, rectal prolapse, iron deficiency anaemia, and finger clubbing. Here, we report a case of trichuris dysentery syndrome complicated with severe chronic iron deficiency anaemia in a 4-year-old girl who required blood transfusion. The nematode was visualized on stool microscopic and colonoscopic examination. A longer duration of anti-helminthic treatment is required to achieve effective and better outcome.
    Matched MeSH terms: Anemia, Iron-Deficiency/diagnosis*; Anemia, Iron-Deficiency/parasitology; Anemia, Iron-Deficiency/pathology*
  9. Noh LM, Nasuruddin BA, Abdul Latiff AH, Noah RM, Kamarul Azahar MR, Norzila MZ, et al.
    Med J Malaysia, 2013;68(1):13-7.
    PMID: 23466760
    To determine the clinical and epidemiological characteristics of patients seen with primary immunodeficiencies referred at four Malaysian Hospitals between 1987 to 2007.
    Matched MeSH terms: Immunologic Deficiency Syndromes
  10. Ainoon O, Boo NY, Yu YH, Cheong SK, Hamidah HN
    Hematology, 2006 Apr;11(2):113-8.
    PMID: 16753852 DOI: 10.1080/10245330500155184
    A 2-year-old Chinese boy was referred to Hospital UKM for investigation of recurrent episodes of dark-coloured urine and pallor since birth. He was born prematurely at 34 weeks gestation and developed severe early-onset neonatal jaundice requiring exchange blood transfusion. Screening at birth showed Glucose-6-phosphate dehydrogenase (G6PD) deficiency. On admission, physical examination revealed pallor, jaundice and mild hepatomegaly. Results of laboratory investigations showed a hemoglobin level of 11.0 g/dl with a hemolytic blood picture, reticulocytosis of 20% and red cell G6PD activity reported as undetectable. The patient's DNA was analysed for G6PD mutations by PCR-based techniques and DNA sequencing and results showed a 24 bp deletion of nucleotide 953-976 in the exon 9 of the G6PD gene. DNA analysis was also performed on blood samples of the patient's mother and female sibling confirming their heterozygous status, although both showed normal red cell G6PD activity levels. The patient was discharged well and his parents were appropriately advised on the condition and the importance of taking folic acid regularly. This is a first case report in Malaysia of G6PD deficiency causing chronic-hemolytic anemia. The rare 24 bp deletion causes the G6PD Nara variant, previously reported only in two other unrelated males, a Japanese and a Portuguese both with chronic hemolytic anemia.
    Matched MeSH terms: Glucosephosphate Dehydrogenase Deficiency/diagnosis; Glucosephosphate Dehydrogenase Deficiency/genetics*; Glucosephosphate Dehydrogenase Deficiency/epidemiology
  11. Hassan R, Abdullah WZ, Nik Hussain NH
    PMID: 16438162
    The purpose of this study was to detect the frequency of iron deficiency anemia in women attending their first antenatal clinic at a Maternal and Child Health Clinic in Kubang Kerian, a district of Kelantan that is located on the East coast of Malaysia. A cross-sectional study was done over a two-month period and fifty-two Malay women were enrolled in this study. Red blood cell indices and serum ferritin were used as a screening tool for anemia and iron status. Eighteen patients (34.6%) were anemic. The majority were classified as having mild anemia (90%). Four of them had hypochromic microcytic anemia. Of 52 women, 7 had iron deficient erythropoiesis and 11 (61.1%) had iron deficient anemia. The prevalence of iron deficiency anemia in pregnant women was 21.2%, which is similar to other developing countries. The serum ferritin level was significantly associated with the hemoglobin level (p=0.003). Other red blood cell indices were not useful in predicting iron deficient erythropoiesis. It is important to detect iron deficient erythropoiesis during the first antenatal check-up, as it is an early manifestation of iron deficiency anemia. In conclusion, screening for iron deficient is recommended during first antenatal visit because iron deficiency anemia is still the leading cause of nutritional deficiency in pregnant women. This will initiate an early therapeutic intervention so as to reduce public health problem.
    Study site: Hopital Universiti Sains Malaysia (HUSM) and the Maternal and Child Health Clinic, Kubang Kerian, Kelantan, Malaysia
    Matched MeSH terms: Anemia, Iron-Deficiency/blood; Anemia, Iron-Deficiency/diagnosis; Anemia, Iron-Deficiency/epidemiology*
  12. Khor GL, Chee WS, Shariff ZM, Poh BK, Arumugam M, Rahman JA, et al.
    BMC Public Health, 2011;11:95.
    PMID: 21310082 DOI: 10.1186/1471-2458-11-95
    Deficiencies of micronutrients can affect the growth and development of children. There is increasing evidence of vitamin D deficiency world-wide resulting in nutritional rickets in children and osteoporosis in adulthood. Data on the micronutrient status of children in Malaysia is limited. The aim of this study was to determine the anthropometric and micronutrient status of primary school children in the capital city of Kuala Lumpur.
    Matched MeSH terms: Vitamin D Deficiency/blood; Vitamin D Deficiency/complications; Vitamin D Deficiency/epidemiology*
  13. Amini F, Ismail E, Zilfalil BA
    Intern Med J, 2011 Apr;41(4):351-3.
    PMID: 21507164 DOI: 10.1111/j.1445-5994.2011.02456.x
    This study aims to define the prevalence and the molecular basis of G6PD deficiency in the Negrito tribe of the Malaysian Orang Asli. Four hundred and eighty seven consenting Negrito volunteers were screened for G6PD deficiency through the use of a fluorescent spot test. DNA from deficient individuals underwent PCR-RFLP analysis using thirteen recognized G6PD mutations. In the instances when the mutation could not be identified by PCR-RFLP, the entire coding region of the G6PD gene was subjected to DNA sequencing. In total, 9% (44/486) of the sample were found to be G6PD-deficient. However, only 25 samples were subjected to PCR-RFLP and DNA sequencing. Of these, three were found to carry Viangchan, one Coimbra and 16, a combination of C1311T in exon 11 and IVS11 T93C. Mutation(s) for the five remaining samples are unknown. The mean G6PD enzyme activity ranged 5.7 IU/gHb in deficient individuals. Our results demonstrate that the frequency of G6PD deficiency is higher among the Negrito Orang Asli than other Malaysian races. The dual presence of C1311T and IVS11 T93C in 64% of the deficient individuals (16/44) could well be a result of genetic drift within this isolated group.
    Matched MeSH terms: Glucosephosphate Dehydrogenase Deficiency/ethnology*; Glucosephosphate Dehydrogenase Deficiency/genetics*; Glucosephosphate Dehydrogenase Deficiency/epidemiology
  14. Yusoff H, Wan Daud WN, Ahmad Z
    Iran J Public Health, 2013;42(5):467-71.
    PMID: 23802103
    This study was carried out to compare the effect between nutrition education intervention and non-nutrition education intervention on awareness regarding iron deficiency among schooling adolescents in Tanah Merah, one of rural district in Kelantan, Malaysia.
    Matched MeSH terms: Anemia, Iron-Deficiency
  15. Moy FM, Hoe VC, Hairi NN, Vethakkan SR, Bulgiba A
    Public Health Nutr, 2017 Jul;20(10):1844-1850.
    PMID: 27086558 DOI: 10.1017/S1368980016000811
    OBJECTIVE: To determine the association of vitamin D status with depression and health-related quality of life among women.

    DESIGN: This was a cross-sectional study conducted among women in Kuala Lumpur, Malaysia. Sociodemographic characteristics, physical activity status, perceived depression and health-related quality of life were assessed via a self-administered questionnaire. Fasting blood samples were taken for the analysis of 25-hydroxyvitamin D, parathyroid hormone, fasting blood glucose and full lipid profile. Complex samples multiple logistic regression analysis was performed.

    SETTING: Public secondary schools in Kuala Lumpur, Malaysia.

    SUBJECTS: Seven hundred and seventy female teachers were included.

    RESULTS: The mean age of participants was 41·15 (95 % CI 40·51, 41·78) years and the majority were ethnic Malays. Over 70 % of them had vitamin D deficiency (<20 ng/ml or <50 nmol/l) and two-thirds were at risk for depression. In the multivariate analysis, ethnic Malays (adjusted OR (aOR)=14·72; 95 % CI 2·12, 102·21) and Indians (aOR=14·02; 95 % CI 2·27, 86·59), those at risk for depression (aOR=1·88, 95 % CI 1·27, 2·79) and those with higher parathyroid hormone level (aOR=1·13; 95 % CI 1·01, 1·26) were associated with vitamin D deficiency, while vitamin D deficiency was negatively associated with mental health-related quality of life (Mental Component Summary) scores (aOR=0·98; 95 % CI 0·97, 0·99).

    CONCLUSIONS: Vitamin D deficiency is significantly associated with depression and mental health-related quality of life among women in Kuala Lumpur, Malaysia.

    Matched MeSH terms: Vitamin D Deficiency/blood*; Vitamin D Deficiency/epidemiology*; Vitamin D Deficiency/psychology
  16. Riahi S, Mei IL, Idris FB, George E, Noor SM
    PMID: 26863862
    Pre-donation screening declarations and hemoglobin (Hb) testing are measures used to determine the quality of donated blood. The copper sulphate (CuSo4) method used to screen for blood abnormalities can give inaccurate results if strict quality control is not applied. Blood donors who are carriers of thalassemia and those with mild iron deficiency anemia (IDA) are usually asymptomatic and frequently missed at blood donation. The aim of this study was to evaluate the red blood cell (RBC) indices related disorders among blood donors who were deemed qualified to donate blood after screening with CuSo4 method. One hundred fifty-eight volunteer blood donors at the Universiti Putra Malaysia (UPM), who had passed the CuSo4 screening method, were recruited for this study. Their bloods specimens were examined with a complete blood count. Subjects with a low mean corpuscular hemoglobin (MCH) level were examined further by checking a serum ferritin level, Hb quantification, and molecular analysis to examine for common RBC disorders. Fourteen point six percent of subjects had a low Hb level, two (1.3%) had IDA and four (2.5%) had thalassemia or some other hemoglobinopathy. Using a MCH level < 27 pg as a cut-off point, 58 subjects (36.7%) had suspected IDA, thalassemia or some other hemoglobinopathy. Eight point nine percent of subjects with a normal Hb level had thalassemia, and 3.8% had IDA. Malaysia has a high prevalence of thalassemia and other hemoglobinopathies. Pre-donation accurate screening is crucial to protect the quality of blood transfusion products. Public education regarding RBC disorders especially among blood donors is important.
    Matched MeSH terms: Anemia, Iron-Deficiency/blood; Anemia, Iron-Deficiency/etiology; Anemia, Iron-Deficiency/epidemiology*
  17. Zheltova AA, Kharitonova MV, Iezhitsa IN, Serebryansky EP, Evsyukov OY, Spasov AA, et al.
    J Trace Elem Med Biol, 2017 Jan;39:36-42.
    PMID: 27908421 DOI: 10.1016/j.jtemb.2016.07.002
    The aim of the present study was to assess whether dietary magnesium deficiency can alter distribution of macroelements and trace elements in different organs and tissues. Experiments were carried out on 12 adult female Wistar rats, which were fed either a diet with low Mg content (≤20mgkg(-1) of diet) (LMgD) or a diet with daily recommended Mg content (≈500mgkg(-1)) as control group (CG) for 70 days. On the 70th day of the experiment heart, aorta, femoral skeletal muscle, forebrain, cerebellum, pituitary gland, thyroid gland, ovaries, uterus, liver, kidneys, and spleen were taken for analysis of mineral content. Concentrations of Fe and Ca were measured by inductively coupled plasma-atomic emission spectrometry, and levels of Na, K, Mg, Co, Cu, Zn, Ni, Se, I were determined by inductively coupled plasma mass spectrometry. On the 70th day, LMgD led to significant reduction of Mg level in red blood cells, plasma, aorta, uterus and thyroid gland compared to CG as well as resulted in significant decrease of Mg/Ca ratio in kidneys, spleen and ovaries. Contrary to this, an increase of Mg/Ca ratio was found in cerebellum of LMgD group. Significant decrease of K concentration was shown in aorta of LMgD animals compared to CG whereas myocardial K concentration was increased in LMgD group. Na level was two-fold higher in skeletal muscles of rats that received LMgD in comparison to CG (p=0.006). Increased concentrations of Fe in ovaries and uterus were found in LMgD. Mg restriction did not affect Zn concentration in any of tasted tissues. Se level was higher in spleen and lower in uterus of LMgD animals compared to CG. MgD was accompanied by increased level of Co in skeletal muscles and decreased its level in kidneys and uterus. LMgD feeding was associated with decreased concentrations of Ni in heart, thyroid gland, spleen, uterus and Co in heart, aorta, liver, kidneys, spleen and ovaries. The changes of Mg, K, Co content were accompanied by dramatic (10-fold) decrease of I concentration in aorta of LMgD animals. LMgD causes decrease of I content in ovaries and increase of I level in uterus vs CG. Thus, distribution of macroelements (Ca, Na, K) was weakly affected by Mg restriction that led to the most evident alterations of Co and Ni tissue levels. Moreover, mineral balance of uterus seems to be the most susceptible to low Mg intake. Hypomagnesaemia resulted in significant changes of 5 studied trace elements (Fe, Se, Cu, Ni and Co).
    Matched MeSH terms: Magnesium Deficiency/blood; Magnesium Deficiency/metabolism*
  18. Quah SW, Abdul Majid H, Al-Sadat N, Yahya A, Su TT, Jalaludin MY
    PLoS One, 2018;13(7):e0200736.
    PMID: 30024934 DOI: 10.1371/journal.pone.0200736
    BACKGROUND: This study is to determine the prevalence and risk factors of vitamin D deficiency (vitamin D ≤ 50 nmol/L) among 15-year-old Malaysian adolescents. By identifying potential risk factors, prevention strategies and interventions can be carried out to improve the vitamin D status in adolescents.

    METHODS AND FINDINGS: Stratified random sampling design was used to select adolescents from 15 urban and rural secondary schools in Selangor, Perak and Kuala Lumpur, Malaysia. Data collection was carried out from 1st April 2014 to 30th June 2014. Information regarding socio-demographic characteristics, sun exposure and sun protective behaviours, clinical data and environmental factors were collected. Blood for total vitamin D was sampled. Descriptive and multivariate logistic regressions were performed. Total 1061 participants were analyzed (62% were female; mean age 15.1 ± 0.4 years). The prevalence of vitamin D deficiency was 33%. Mean vitamin D was lower in female (53 ± 15 nmol), obese (body fat percentage (≥25%m; ≥33.8%f) (56 ± 16 nmol/L), Malays (58 ± 18 nmol/L) and Indians (58 ± 15 nmol/L). In multivariate analysis, female (OR = 5.5; 95% CI: 3.4-7.5), Malay (OR = 3.2; 95% CI: 1.3-8.0), Indian (OR = 4.3; 95% CI: 1.6-12.0) and those always wearing long sleeve (OR = 2.4; 95% CI: 1.1-5.4) were more likely to have vitamin D deficiency. For female participants, ethnicity {Malays (OR = 6.7; 95% CI: 2.0-18.5), Indian (OR = 4.5; 95% CI: 1.8-19.3)} was an important risk factors. Cloud cover, school residence, skin pigmentation, sun-exposure and sun-protective behaviours were not significant risk factors. The limitation of this study was recall bias as it relied on self-reported on the sun exposure and protective behaviours. The diet factors were not included in this analysis.

    CONCLUSIONS: The prevalence of Vitamin D deficiency among Malaysian adolescents was considerable. Gender, ethnicity and clothing style were important risk factors.

    Matched MeSH terms: Vitamin D Deficiency/ethnology; Vitamin D Deficiency/epidemiology*
  19. Nik Shanita S, Siti Hanisa A, Noor Afifah AR, Lee ST, Chong KH, George P, et al.
    PMID: 30360488 DOI: 10.3390/ijerph15112332
    The present study aimed to report the prevalence of anaemia and iron deficiency (ID) and to explore the associations among socio-demographic characteristics, nutritional status and inflammation status in the occurrence of anaemia and ID in a nationally representative sample of Malaysian primary schoolchildren. Using data from the South East Asian Nutrition Surveys (SEANUTS), 544 Malaysian children aged 7 to 12 years were included in this secondary analysis. Blood samples were drawn for haemoglobin and serum ferritin analysis while C-reactive protein (CRP) and α-1-acid glycoprotein (AGP) were measured to detect inflammation. Prevalence of anaemia and ID were 4.0% and 5.2%, respectively. There were significantly more anaemic indigenous bumiputra children (9.9%) than Chinese children (0.6%). Correction for inflammation did not change the prevalence of ID. More overweight/obese children than thin/normal weight children were found to have elevated acute phase protein (APP). Children with elevated inflammatory markers had significantly higher ferritin level than children without inflammation. Periodic health assessments of anaemia and ID at the population level to monitor and clarify the epidemiology of health problems are required to inform public health policies and strategies.
    Matched MeSH terms: Anemia, Iron-Deficiency/blood; Anemia, Iron-Deficiency/epidemiology*
  20. Almoudi MM, Hussein AS, Abu Hassan MI, Schroth RJ
    Pediatr Int, 2019 Apr;61(4):327-338.
    PMID: 30740822 DOI: 10.1111/ped.13801
    Dental caries and vitamin D inadequacy are known to affect children worldwide. Vitamin D has a vital role in tooth formation. There is growing evidence linking suboptimal serum vitamin D level with dental caries in children. This paper reviews the literature on both the prevalence of dental caries and of vitamin D deficiency in children in four Asian regions, discusses their associated risk factors, and reviews the global evidence on the association between dental caries and vitamin D in children. Caries prevalence in children ranged from 40% to 97% in Eastern Asia, 38-73.7% in Southern Asia, and 26.5-74.7% in Western Asian countries. Moreover, a higher prevalence of vitamin D deficiency in Asian children was identified, even in countries in equatorial regions, ranging from 2.8% to 65.3% in Eastern Asia, 5-66.7% in Southern Asia, 4-45.5% in Western Asia and 38.1-78.7% in Central Asian countries. Obesity, age, female gender, higher latitude, season, darker skin pigmentation, sunlight protection behaviors, less sunlight exposure and low intake of food containing vitamin D were important factors associated with lower serum vitamin D in Asia. Suboptimal vitamin D level in children may be a significant risk factor for dental caries, and requires further research to ascertain such an association in children in Asia, as well as to understand its exact influence on caries risk and development.
    Matched MeSH terms: Vitamin D Deficiency/complications; Vitamin D Deficiency/epidemiology*
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