Publications by authors named "Retno Sutomo"

13 Publications

  • Page 1 of 1

Translation, Adaptation and Psychometric Validation of the Indonesian Version of the Readiness for Hospital Discharge Scale for Parents of Low Birth Weight Infants.

J Pediatr Nurs 2020 Sep - Oct;54:e97-e104. Epub 2020 Jun 7.

Department of Epidemiology, Faculty of Public Health, Hasanuddin University, Makassar, Indonesia. Electronic address:

Purpose: Parental readiness is a requirement for discharge of the high-risk infant from the hospital. Currently, in Indonesia, there are no standard tools to measure parental readiness according to parents' perceptions. This study aimed to undertake cross-cultural adaptation and psychometric validation of the original version (English) of the Readiness for Hospital Discharge Scale (RHDS)-Parent into Bahasa Indonesia.

Design And Methods: The cross-cultural adaptation was comprised of seven steps: forward translation, forward translation review, blind-back translation, back translation review, pilot testing of the pre-final version with mothers of low birth weight (LBW) infants, expert panel for conceptual and content equivalence, and initial psychometric testing. In the fifth and sixth steps, content validity index was estimated. In the seventh step, exploratory factor analysis (EFA) and internal consistency reliability were conducted. In total, 146 mothers of LBW infants were included in the psychometric testing using convenience sampling.

Results: The 22 item Bahasa-RHDS-Parent emerged in a four-factor structure evident from EFA. This version has good reliability with Cronbach alpha values for knowledge and coping ability (0.92), physical-emotional readiness (0.89), pain and power (0.83), expected support (0.80) and 0.90 across the total Bahasa-RHDS-Parent.

Conclusion: The Bahasa-RHDS-Parent presents good cross-cultural adaptation and initial psychometric properties for assessing parental readiness in parents with LBW infants before hospital discharge.

Practice Implications: This questionnaire can be used by nurses to measure readiness for discharge of parents of low birthweight babies. Further testing is needed with a larger sample and parents of children of other ages and conditions for instrument improvement.
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http://dx.doi.org/10.1016/j.pedn.2020.05.010DOI Listing
June 2020

Discharge readiness of Indonesian mother with preterm infant in NICU.

Enferm Clin 2020 03;30 Suppl 2:234-237

Community Health Nursing Department, Faculty of Nursing Universitas Hasanuddin, Indonesia.

Objective: This study aimed to describe Indonesian mother readiness for discharge with Low Birth Weight (LBW) infant.

Method: This paper is part of larger study and using quantitative study. Sampling method was used in this study was convenience sampling to 139 mothers with LBW infant in public hospital in Makassar City, Indonesia. Respondents were given self-assessed questionnaire about their readiness for discharge within 24h before they go home.

Results: Majority (94.5%) of mothers reported that they were ready to go home and 90.6% perceived that their LBW infants were ready for hospital discharge as assessed by the dichotomous answer (i.e. Yes vs. No). The mothers mean overall score of the RHDS was 199 (29.752) which maximum total score 290. The scores on an item of the RHDS was 6.86 (3.164) which maximum item score 10.

Conclusion: Indonesian mother's readiness had lower readiness than other countries. The discharge education program was needed to enhance mother's knowledge of readiness for hospital discharge.
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http://dx.doi.org/10.1016/j.enfcli.2019.07.096DOI Listing
March 2020

Switch from oral to inactivated poliovirus vaccine in Yogyakarta Province, Indonesia: summary of coverage, immunity, and environmental surveillance.

J Infect Dis 2014 Nov;210 Suppl 1:S347-52

World Health Organization, Geneva, Switzerland.

Background: Inactivated poliovirus vaccine (IPV) is rarely used in tropical developing countries. To generate additional scientific information, especially on the possible emergence of vaccine-derived polioviruses (VDPVs) in an IPV-only environment, we initiated an IPV introduction project in Yogyakarta, an Indonesian province. In this report, we present the coverage, immunity, and VDPV surveillance results.

Methods: In Yogyakarta, we established environmental surveillance starting in 2004; and conducted routine immunization coverage and seroprevalence surveys before and after a September 2007 switch from oral poliovirus vaccine (OPV) to IPV, using standard coverage and serosurvey methods. Rates and types of polioviruses found in sewage samples were analyzed, and all poliovirus isolates after the switch were sequenced.

Results: Vaccination coverage (>95%) and immunity (approximately 100%) did not change substantially before and after the IPV switch. No VDPVs were detected. Before the switch, 58% of environmental samples contained Sabin poliovirus; starting 6 weeks after the switch, Sabin polioviruses were rarely isolated, and if they were, genetic sequencing suggested recent introductions.

Conclusions: This project demonstrated that under almost ideal conditions (good hygiene, maintenance of universally high IPV coverage, and corresponding high immunity against polioviruses), no emergence and circulation of VDPV could be detected in a tropical developing country setting.
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http://dx.doi.org/10.1093/infdis/jiu060DOI Listing
November 2014

A novel mutation at the N-terminal of SMN Tudor domain inhibits its interaction with target proteins.

J Neurol 2007 May 6;254(5):624-30. Epub 2007 Apr 6.

Dept. of Public Health, Kobe University Graduate School of Medicine, 7-5-1 Kusunoki-cho, Chuo-ku, Kobe, 650-0017, Japan.

Although most patients with spinal muscular atrophy (SMA) are homozygous for deletion of the SMN1 gene, some patients bear one SMN1 copy with a subtle mutation. Detection of such an intragenic mutation may be helpful not only in confirming diagnosis but also in elucidating functional domains of the SMN protein. In this study, we identified a novel mutation in SMN1 of two Japanese patients with type I SMA. DHPLC and sequencing analysis revealed that they harbored a point mutation in SMN1 exon 3, 275G > C, leading to tryptophan-to-serine substitution at amino acid 92 (W92S) at the Nterminal of SMN Tudor domain. In-vitro protein binding assays showed that the mutation severely reduced interaction of the domain with SmB protein and fibrillarin, suggesting that it impairs the critical function of SMN. In conclusion, we reported here that a novel mutation, W92S, in the Tudor domain affects the interaction of SMN with the target proteins.
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http://dx.doi.org/10.1007/s00415-006-0410-xDOI Listing
May 2007

Evaluation of mutation effects on UGT1A1 activity toward 17beta-estradiol using liquid chromatography-tandem mass spectrometry.

J Chromatogr B Analyt Technol Biomed Life Sci 2006 Jun 28;838(1):9-14. Epub 2006 Feb 28.

Department of Public Health, Kobe University Graduate School of Medicine, Kobe 650-0017, Japan.

Mutations in the gene encoding UDP-glucuronosyltransferase 1A1 (UGT1A1) may reduce the glucuronidation of estradiol, bilirubin, etc. In the present study, we used a liquid chromatography-tandem mass spectrometry (LC/MS/MS) method to assay the activities of recombinant mutated UGT1A1 toward 17beta-estradiol (E2), by determining its glucuronide (E2G) content. Direct evidence for glucuronide formation was provided by E2G-specific ion peaks. The UGT1A1 activities of G71R (exon 1), F83L (exon 1), I322V (exon 2) and G493R (exon 5) mutants were 24, 30, 18 and 0.6% of the normal UGT1A1 activity, respectively. In conclusion, our study showed that LC/MS/MS enabled accurate evaluation of the effects of mutations on recombinant UGT1A1 activity towards E2.
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http://dx.doi.org/10.1016/j.jchromb.2006.01.030DOI Listing
June 2006

Screening for G71R mutation of the UGT1A1 gene in the Javanese-Indonesian and Malay-Malaysian populations.

Pediatr Int 2004 Oct;46(5):565-9

Department of Pediatrics, Kobe University Graduate School of Medicine, Japan.

Background: There are significant differences in the prevalence and severity of neonatal jaundice among various populations. Recently, it has been reported that a mutation of the UGT1A1 gene, glycine to arginine at codon 71 (G71R), is related to the development of neonatal jaundice in East Asian populations. However, whether the G71R mutation contributes to the high incidence of neonatal jaundice in different Asian populations remains unknown. The authors screened for this mutation in the Javanese-Indonesian and Malay-Malaysian populations.

Methods: One hundred and thirty-six subjects were enrolled in this study: 68 Javanese-Indonesian adults and 68 Malay-Malaysian newborns (32 with jaundice and 36 without jaundice). Denaturing high-performance liquid chromatography (DHPLC) was used to screen for the G71R mutation, and the results were confirmed by nucleotide sequencing analysis.

Results: With DHPLC, the authors easily and clearly detected seven subjects carrying the G71R mutation: two Javanese-Indonesian adults and five Malay-Malaysian newborns. In the 68 Javanese-Indonesian adults, the genotype distribution for G71R mutation was 66 G/G, two G/R and no R/R genotypes, and the mutated allele frequency was 0.015. In the 68 Malay-Malaysian newborns, genotype distribution for the mutation was 63 G/G, five G/R and no R/R genotypes, and the mutated allele frequency was 0.037. The genotype distributions did not differ significantly between the newborns with jaundice and those without jaundice.

Conclusion: The G71R mutation is present, but very rare, in Javanese-Indonesians and Malay-Malaysians. Thus, G71R mutation may not contribute to the high incidence of the neonatal jaundice in South-east Asian populations. DHPLC analysis is a very useful method for detecting the G71R mutation.
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http://dx.doi.org/10.1111/j.1442-200x.2004.01959.xDOI Listing
October 2004

C677T mutation in the MTHFR gene was not found in patients with frontoethmoidal encephalocele in East Java, Indonesia.

Pediatr Int 2004 Aug;46(4):409-14

Division of Public Health, Department of Environmental Health and Safety, Brawijaya University, Malang, Indonesia.

Background: Frontoethmoidal encephalocele (FEE) is a neural tube defect (NTD) characterized by a congenital bone defect in the anterior cranium and herniation of the intracranial mass through the defect. The C677T mutation in the 5,10-methylenetetrahydrofolate reductase gene (MTHFR) has been reported as a genetic risk factor for spina bifida. However, the role of the MTHFR in the pathogenesis of FEE remains to be clarified.

Methods: A hospital-based survey of FEE patients who were referred to the Department of Neurosurgery and Plastic Surgery, Malang General Hospital, East Java, Indonesia was conducted. Genetic screening of MTHFR substitutions in 13 patients and eight mothers from 11 affected families were performed using a combination of polymerase chain reaction (PCR), denaturing high-performance liquid chromatography (DHPLC), and direct sequencing.

Results: In total, 130 patients with FEE among 138 NTD patients (94.2%) were identified. The ratios of cranial encephalomeningocele to spinal meningocele (32 : 1) and of FEE to occipital encephalomeningocele (32 : 1) were higher than those in other populations. Five substitutions were detected in the MTHFR: C121T, C677T, C1060T, A1298C, and G1793A. No significant differences were found in the frequency of each nucleotide substitution between patients or mothers and controls. In addition, none of the subjects in this study were homozygous for T at nucleotide position 677.

Conclusion: FEE is the most common form of NTD in East Java, Indonesia. Genetic analysis of 11 affected families suggests that the MTHFR gene is not associated with the development of FEE, although the number of FEE families analyzed in this study was very limited.
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http://dx.doi.org/10.1111/j.1442-200x.2004.01927.xDOI Listing
August 2004

Deletion of the SMN1 and NAIP genes in Vietnamese patients with spinal muscular atrophy.

Kobe J Med Sci 2003 ;49(3-4):55-8

Division of Pediatrics, Department of Development and Aging, Kobe University Graduate School of Medicine, Japan.

The SMN1 and NAIP genes are related to the development of spinal muscular atrophy (SMA), which is characterized by degeneration of motor neurons leading to progressive muscular weakness and atrophy. The SMN1 gene is homozygously deleted in most SMA patients, and now recognized as a responsible gene for SMA. The NAIP gene is often deleted in the SMA patients with the severest form of SMA, and now considered to be a modifying factor of the severity of SMA. Our previous study of five Vietnamese SMA patients showed that the SMN1 gene deletion was detected in one patient, although the NAIP gene deletion was not detected in any patients. In this study, we analyzed 12 Vietnamese SMA patients who were not enrolled in the previous study. The SMN1 gene was homozygously deleted in six out of 12 patients, and the NAIP gene deletion was detected in five patients. Taken together with our previous data, the SMN1 gene deletion was detected in seven out of 17 Vietnamese SMA patients and the NAIP gene deletion in five out of 17 Vietnamese SMA patients. These studies suggest that the SMN1 and NAIP gene deletions are not rare in Vietnamese SMA patients. Thus, the confirmation of SMA-related gene deletion will also be a useful tool for the diagnosis of SMA in Vietnam.
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June 2004

The C677T mutation in the methylenetetrahydrofolate reductase gene among the Indonesian Javanese population.

Kobe J Med Sci 2002 Dec;48(5-6):137-44

Division of Public Health, Department of Environmental Health and Safety, Kobe University Graduate School of Medicine 7-5-1 Kusunoki-cho, Chuo-ku, Kobe 650-0017, Japan.

The presence of the C677T mutation in the methylenetetrahydrofolate reductase (MTHFR) gene has been regarded as a genetic risk factor for coronary artery diseases and neural tube defects. Although the prevalence of this mutation has been reported from various ethnic populations, few data concerning Indonesian populations are available. We have investigated the frequency of the mutation in 68 Indonesian Javanese (residents of Java Island) and compared it with the data from 244 Japanese (residents of Honshu Island). The frequencies of the three genotypes in Javanese were C/C 0.84, C/T 0.16 and T/T 0.00, whereas those in Japanese were C/C 0.39, C/T 0.48 and T/T 0.13. The rarity of the T/T genotype in the Indonesian Javanese population may be due to malnutrition in pregnant women, because insufficient intake of folate is considered to be a survival disadvantage for fetuses with the T/T genotype. In conclusion, homozygosity for the C677T mutation in the MTHFR gene does not constitute a genetic risk factor for coronary artery diseases and neural tube defects in the Indonesian Javanese population.
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December 2002

Correlation between SMN2 copy number and clinical phenotype of spinal muscular atrophy: three SMN2 copies fail to rescue some patients from the disease severity.

J Neurol 2002 Sep;249(9):1211-9

Division of Public Health, Department of Environmental Health and Safety, Faculty of Medicine, Kobe University Graduate School of Medicine, 7-5-1 Kusunoki-cho, Chuo-ku, Kobe, 650-0017, Japan.

Spinal muscular atrophy (SMA) is a common autosomal recessive neuromuscular disorder that is characterized by degeneration of the anterior horn cells of the spinal cord, which leads to the axial and limb weakness associated with muscle atrophy. SMA is classified into three groups based on the clinical severity: type I (severe), type II (intermediate) and type III (mild). All three clinical subtypes of SMA are caused by mutations of the SMN1 gene. More than 95 % of SMA patients show homozygous deletion of SMN1. It is thought that SMN2, which is a highly homologous gene of SMN1, compensates for the SMN1 deletion to some degree. To clarify the relationship between SMN2 and the disease severity of SMA, we performed fluorescence-based quantitative polymerase chain reaction assay of the copy number of SMN2 in 27 patients (11 type I and 16 type II-III) homozygous for SMN1 deletion. The SMN2 copy number in type II-III patients was 3.1 +/- 0.3 (mean +/- SD), which is significantly higher than that observed in type I patients, 2.2 +/- 0.6 (P < 0.01). However, three of the 11 type I patients carried 3 SMN2 copies. A type I patient with 3 SMN2 copies was studied further. RT-PCR analysis of the patient showed a trace of full-length SMN2 mRNA species, but a large amount of the truncated SMN2 mRNA species lacking exon 7. In conclusion, SMN2 alleles are not functionally equivalent among SMA patients, although in general the SMN2 copy number is correlated with the severity of SMA. Genetic background influencing splicing mechanisms of the SMN2 gene may be more critical in some SMA patients.
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http://dx.doi.org/10.1007/s00415-002-0811-4DOI Listing
September 2002

No relationship exists between itai-itai disease and TA repeat polymorphisms of the estrogen receptor alpha gene.

Arch Toxicol 2002 Aug 29;76(8):467-9. Epub 2002 May 29.

Department of Environmental Health and Safety, Faculty of Medicine, Kobe University Graduate School of Medicine 7-5-1 Kusunoki-cho, Chuo-ku, Kobe, 650-0017, Japan.

Itai-itai (ouch-ouch) disease is a syndrome accompanied by bone mineral disorders that may be related to oral cadmium exposure. Itai-itai predominantly affects postmenopausal women with a history of multiple childbirth. In a previous study we have examined the genotype distributions of PvuII and XbaI restriction fragment length polymorphisms of the estrogen receptor alpha (ER alpha) gene in patients with itai-itai disease and compared them with those of controls. However, no significant differences were shown between the genotype distributions of the patients and controls. In the present study, we determined the TA repeat polymorphisms of the patients and controls. The distributions of the patients were: HH 25.0%, HL 50.0%, and LL 25.0%; where HH includes two alleles with a high number of TA repeats (TA> or =16), HL includes one high number allele and one low number allele (TA< or =15), and LL includes two alleles with a low number of TA repeats. These patients' distributions were not significantly different from those of the controls. Although our sample number was limited, we concluded that a polymorphism variant of the ER alpha gene is not a predisposing factor for itai-itai disease.
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http://dx.doi.org/10.1007/s00204-002-0361-7DOI Listing
August 2002

Novel missense mutation of the UGT1A1 gene in Thai siblings with Gilbert's syndrome.

Pediatr Int 2002 Aug;44(4):427-32

Department of Development and Aging, Faculty of Medicine, Kobe University Graduate School of Medicine, Japan.

Background: Gilbert's syndrome is a common inherited disorder of bilirubin metabolism contributing to the development of neonatal jaundice and causing recurrent jaundice after the neonatal period. In the patients with Gilbert's syndrome, mutations have been reported in the promoter and exons of the uridine diphosphate-glucuronosyl transferase 1 (UGT1A1) gene on chromsome 2q37, which encodes bilirubin uridine diphosphate-glucuronosyltransferase. However, the genetic basis of Gilbert's syndrome, including its inheritance trait, remains to be clarified.

Methods: Patients 1 and 2 were Thai sisters with Gilbert's syndrome. They had a history of prolonged neonatal jaundice and showed recurrent jaundice after their infancy, while the parents showed no symptoms. To search for the mutation in the patients, all exons of the UGT1A1 gene were amplified by polymerase chain reaction (PCR) and sequenced directly. The frequency of the mutation in controls was studied by PCR-restriction enzyme digestion method.

Results: The patients were homozygous for a novel single transition of T to C at nucleotide position 247 (exon 1), which would predict a substitution of leucine for phenylalanine at codon 83 of the enzyme protein. No other mutation was detected in any regions except exon 1. The parents with no symptoms showed heterozygosity for the mutation. Among the 110 Japanese controls, no homozygous individuals and three heterozygous individuals for the mutation were identified, giving a mutated allele frequency of 0.0136.

Conclusions: A novel missense mutation in the UGT1A1 gene was identified in two Thai siblings with Gilbert's syndrome. The affected family showed that homozygosity for the mutation may lead to apparent symptoms and that the syndrome was inherited as an autosomal recessive trait. The mutation does not explain a high incidence of neonatal jaundice in Japan, because it is very rare in the Japanese population.
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August 2002