Contribution of different causes of death to socioeconomic mortality inequality in Korean children aged 1-9: findings from a national mortality follow-up study.

OBJECTIVES: To determine the contribution of different causes of death to absolute socioeconomic inequalities in mortality for the whole population of children of South Korea aged 1-4 years and 5-9 years. METHODS: A cohort study based on the national birth and death registers of Korea was performed for 3,724,347 children born in 1995-2000 and 657,209 children born in 1995 to analyse mortality among children aged 1-4 and 5-9 years old, respectively. Adjusted mortality, risk difference (RD), slope index of inequality (SII), RR and relative index of inequality were calculated. The contributions of different causes of death to absolute mortality inequalities were calculated as percentages based on RD and SII. RESULTS: Injuries other than from transport accidents contributed the most to total SIIs for male deaths at ages 1-4 (30.0% for father's education). The second largest contribution was from transport accident injuries (19.6% for father's education). For male deaths at ages 5-9, transport accident injuries and other injuries also accounted for most of the educational and occupational differentials in absolute mortality (63.5-90.5%). Patterns in cause-specific contribution to total inequalities in mortality among girls were generally similar to those among boys. CONCLUSIONS: The major contributing causes to absolute socioeconomic inequality in all-cause mortality for children aged 1-9 were external. To reduce the absolute magnitude of socioeconomic inequalities in childhood mortality, policy efforts should be directed towards injury prevention and treatment in South Korea.

Socioeconomic differentials in cause-specific mortality among 1.4 million South Korean public servants and their dependents.

BACKGROUND: A growing number of investigations have explored the contribution of cause of death to socioeconomic inequalities in mortality in Europe and North America, but few such studies have been performed on Asian populations. OBJECTIVES: To analyse the socioeconomic inequality of cause-specific death rates from both an absolute and relative perspective, and to evaluate the contribution of cause of death to total mortality inequality in South Korea. METHODS: Data were obtained from public servant health insurance beneficiary records. 1,403,297 subjects aged 35-64 years were followed for 9 years. Health insurance premium levels were used as a socioeconomic position indicator. The outcome variables were all-cause, 11 broad causes and 41 specific causes of death. Mortality differentials were examined using cause-specific age-adjusted mortality, relative indices of inequality, and slope inequality indices. RESULTS: Graded inverse associations between income and mortality were found for most, but not all, specific causes of death. The major contributors to income differentials in total mortality in men were liver disease (15.4%), stroke (12.8%), land transport accidents (10.0%), lung cancer (7.1%) and liver cancer (7.0%). In women, stroke (30.7%), diabetes (9.1%), land transport accidents (6.6%), liver cancer (6.0%) and liver disease (5.1%) were important. Conclusions The contribution of the cause of death to socioeconomic inequality in mortality in South Korea differed from Western countries. To develop a policy to reduce the magnitude of socioeconomic inequality, an understanding of the major causes of death that contribute to mortality inequality is required.

Investigation of multilayer silicon structures with buried iron silicide nanocrystallites: growth, structure, and properties.

The growth of nanosize islands of iron silicides on Si(100) substrates and epitaxial silicon overgrowth atop them have been studied by low energy electron diffraction and reflectance high energy electron diffraction methods. The near optimal formation conditions of iron silicide islands with high density and minimal sizes have been determined by using of atomic force microscopy. Multilayer (8-10) monolithic structures with buried iron silicide nanocrystallites have been grown after the definition of monocrystalline burying conditions of iron silicides nanocrystallites in silicon lattice. The structure of buried nanocrystallites has been studied in multilayer monolithic heterostructures by high resolution transmission electron microscopy. It was established that in multilayer samples the majority of nanocrystallites have beta-FeSi2 structure, but some of them have gamma-FeSi2 structure. It was observed an influence of additional annealing at 850 degrees C on the morphology and structure of nanocrystallites. By means of deep level transient spectroscopy data one and two trap levels have been observed in multilayer structures (without and with additional annealing, respectively). Photoluminescence spectra have been studied at 4.2 K and the causes of its absence from buried beta-FeSi, NC have been analyzed.

Explaining age-specific inequalities in mortality from all causes, cardiovascular disease and ischaemic heart disease among South Korean male public servants: relative and absolute perspectives.

OBJECTIVE: To examine age-specific patterns in the ability of major cardiovascular risk factors to explain relative and absolute socioeconomic inequalities in mortality from all causes, cardiovascular disease (CVD), and ischaemic heart disease (IHD). DESIGN: Prospective cohort study. SETTING: South Korea. SUBJECTS: 575 377 male public servants aged 30-64 with 16 998 deaths between 1995 and 2003. MAIN OUTCOMES: All-cause, CVD, and IHD mortality. RESULTS: Four cardiovascular risk factors (cigarette smoking, blood pressure, fasting serum glucose, and serum total cholesterol) were significantly associated with mortality risk. Changing relationships in socioeconomic distribution of risk factors with age were observed. The magnitude of reduction in percent change in absolute risk was greater than that in relative risk. While the risk factors explained only 15.2% of excess RR for all-cause mortality in low-income men aged 30-44, the absolute excess risk of all-cause mortality was reduced by 48.3% when the risk factors were removed from the whole population. This pattern was generally true for all causes, CVD, and IHD, and true for all age groups and risk factors examined. Cigarette smoking and hypertension were the leading contributors in explaining relative and absolute inequality in mortality. CONCLUSION: Policy efforts to eliminate major cardiovascular risk factors in the general population may have a significant effect on reducing the absolute burden of socioeconomic inequality in mortality. Policy efforts to attenuate socioeconomic inequality in cardiovascular risk factors need to be directed to younger age groups in South Korea.

Trends in socioeconomic health inequalities in Korea: use of mortality and morbidity measures.

STUDY OBJECTIVE: To examine trends in educational mortality and morbidity inequalities in Korea. DESIGN: Census data (1990, 1995, 2000) and death certificate data (1990-91, 1995-96, 2000-01) were used for mortality. For morbidity, four waves (1989, 1992, 1995, and 1999) of Social Statistics Survey from Korea's National Statistical Office were used. Morbidity indicators were self rated health and self reported illness in the past two weeks. Trends were studied using indices for both the relative and absolute size of socioeconomic inequalities in health. SETTING: South Korea. Patients (or Participants): Representative annual samples of the adult population aged 30-59 in Korea. MAIN RESULTS: Based on trends in relative index of inequalities, the relative level of socioeconomic mortality inequality remained virtually unchanged in men and women in the past 10 years. Meanwhile, inequalities in self rated health have increased over time in both sexes. Most of the total increase in health inequalities happened between 1995 and 1999. Inequalities in self reported acute illness increased in the past 10 years. CONCLUSIONS: The rise in inequalities in morbidity requires increased social discourse and policy discussions about health inequalities in Korean society.

The 2.0 A crystal structure of cephalosporin acylase.

BACKGROUND: Semisynthetic cephalosporins are primarily synthesized from 7-aminocephalosporanic acid (7-ACA), which is usually obtained by chemical deacylation of cephalosporin C (CPC). The chemical production of 7-ACA includes, however, several expensive steps and requires thorough treatment of chemical wastes. Therefore, an enzymatic conversion of CPC to 7-ACA by cephalosporin acylase is of great interest. The biggest obstacle preventing this in industrial production is that cephalosporin acylase uses glutaryl-7ACA as a primary substrate and has low substrate specificity for CPC. RESULTS: We have solved the first crystal structure of a cephalosporin acylase from Pseudomonas diminuta at 2.0 A resolution. The overall structure looks like a bowl with two "knobs" consisting of helix- and strand-rich regions, respectively. The active site is mostly formed by the distinctive structural motif of the N-terminal (Ntn) hydrolase superfamily. Superposition of the 61 residue active-site pocket onto that of penicillin G acylase shows an rmsd in Calpha positions of 1.38 A. This indicates structural similarity in the active site between these two enzymes, but their overall structures are elsewhere quite different. CONCLUSION: The substrate binding pocket of the P. diminuta cephalosporin acylase provides detailed insight into the ten key residues responsible for the specificity of the cephalosporin C side chain in four classes of cephalosporin acylases, and it thereby forms a basis for the design of an enzyme with an improved conversion rate of CPC to 7-ACA. The structure also provides structural evidence that four of the five different classes of cephalosporin acylases can be grouped into one family of the Ntn hydrolase superfamily.

Virulence in lymphomagenesis is modulated by alterations in proteins binding to CORE and GRE-LVa elements of the MoMuLV enhancer.

Changing nucleotide 3 of the CORE consensus from T to C has no effect on the binding of a 42 kDa protein, which has little affinity for the CCAAT binding site. Changing nucleotide 6 of the CORE consensus from T to C significantly reduces binding of the 42 kDa protein. Studies on the pathology induced by various MoMuLV mutants with CORE mutations showed that the CORE elements are important in modulating virulence in T-cell lymphomagenesis in BALB/c mice. However, disease specificity appears to be influenced as much by the host as it is by the virus. LVa is preferentially bound to the GRE-LVa sites. Deletion of nucleotide 9 and changing nucleotides 10 and 11 from GG to AA in the GRE-LVa element does not disrupt binding of LVa. Changing nucleotide 10 from G to A and nucleotide 13 from A to T in the GRE-LVa element does not disrupt binding of GR but allows binding of a novel protein which displaces or abolishes binding of LVa. These five nucleotide changes alone do not alter disease specificity and had a minimal effect on virulence in T-cell lymphomagenesis in BALB/c mice. Additionally, changing nucleotide 3 in CORE(a) and nucleotide 6 in CORE(b) does not alter disease specificity but has a small additional effect on virulence in T-cell lymphomagenesis.

The Moloney murine leukemia virus enhancer and its flanking sequences collaborate to determine virulence in T-cell lymphomagenesis.

A panel of recombinant virus genomes was constructed by exchanging homologous genome fragments between the potent T-cell lymphoma inducer Moloney murine leukemia virus (MoMuLV) and its closely related but significantly less virulent relative MoMuLV-TB. Testing of these recombinant viruses in BALB/c mice established that only nucleotide changes within the Clal(-590)-Kpnl(36) fragment altered virulence. Fine analysis of this fragment showed that while mutations within the enhancer of MoMuLV-TB attenuated the latency period most, mutations within the MoMuLV-TB fragments flanking the enhancer also helped reduce the virulence of MoMuLV. The present study also suggests that the small difference in the relative number of lymphomas that developed primarily in the spleens of MoMuLV- or MoMuLV-TB-infected mice may correlate with nucleotide differences between the Clal-Kpnl fragments of the two viruses. However, the significantly greater proportion of premature death observed in MoMuLV-TB-relative to MoMuLV-infected mice could not be correlated with nucleotide differences in a specific genome fragment.

A single mutation in one of the CORE elements of Moloney murine leukemia virus reduced binding of a 42-kDa T lymphoma cell nuclear factor but did not affect lymphomagenesis.

The genetic determinant responsible for virulence in Moloney murine leukemia virus (MoMuLV) induced T-cell lymphomagenesis has recently been mapped [J Virol 63:471-480, 1989] by homologous genomic fragment exchange between MoMuLV and MoMuLV-TB to the Clal/Xbal at the 3' end of the genome. This region of MoMuLV and MoMuLV-TB differs in 11 nucleotides. Of these 11 nucleotide differences, 9 are distributed within the two CORE, the two distal NF1, and the two GRE/LVa elements of the enhancer. Since both the CORE binding sites of MoMuLV-TB are mutated with respect to those of MoMuLV, we compared nuclear proteins of a thymus-bone marrow cell line and a T-lymphoma cell line (EMT), which bind to the wild-type and mutant CORE binding sites. Using both the bandshift assay and southwestern analysis with labeled synthetic deoxyoligonucleotides, we showed that a 42-kDa protein from TB and EMT cells bound specifically to the MoMuLV CORE element. The T----C transversion of nucleotide 6 of the CORE consensus, TGTGGT/CTAA, significantly reduced binding of the 42-kDa TB and EMT cell factors. However, the transversion of nucleotide 3 from T----C had little effect on the binding of the 42-kDa protein to the CORE element. In addition, the 42-kDa protein bound weakly to the CCAAT element of MoMuLV. A recombinant virus, NwtTB-6, was generated by introducing the two CORE mutations of MoMuLV-TB into the MoMuLV genome. Although the latency period of NwtTB-6 in the induction of lymphoma was not significantly different from that of MoMuLV, preliminary findings suggest that the lymphoma induced by NwtTB-6 may be more widely distributed.