Seroprevalence of Toxoplasma gondii and associated risk factors for infection in the Netherlands: third cross-sectional national study.

A third nationally representative serosurvey was performed to study the changes in Toxoplasma gondii (T. gondii) seroprevalence in the Netherlands over a 20-year time span and to identify and confirm risk factors for acquired toxoplasmosis. This cross-sectional study (conducted in 2016/2017) was designed similarly to the previous two studies (1995/1996 and 2006/2007) and included a questionnaire and serum sampling among Dutch residents. Factors associated with seropositivity for T. gondii were determined using multivariable analysis of the questionnaire-derived data. The earlier observed decrease in T. gondii seroprevalence between 1995/1996 and 2006/2007 (from 40.5% to 26.0%) did not continue into 2016/2017 (29.9%). Similarly to the previous studies, the seroprevalence increased with age and varied among regions. In all studies, higher T. gondii seropositivity was associated with increasing age, lower educational level, not living in the Southeast, and eating raw or semi-cooked pork. The incidence of congenital toxoplasmosis was estimated at 1.3/1000 (95% CI 0.9-1.8) live-born children in 2017. As the seroprevalence of T. gondii in the Netherlands did not decrease over the last decade, an increase in public health awareness is needed and prevention measures may need to be taken to achieve a further reduction in T. gondii infections in the Netherlands.

Mpox outbreak in the Netherlands, 2022: public health response, characteristics of the first 1,000 cases and protection of the first-generation smallpox vaccine.

In early May 2022, a global outbreak of mpox started among persons without travel history to regions known to be enzootic for monkeypox virus (MPXV). On 8 August 2022, the Netherlands reported its 1,000th mpox case, representing a cumulative incidence of 55 per million population, one of the highest cumulative incidences worldwide. We describe characteristics of the first 1,000 mpox cases in the Netherlands, reported between 20 May and 8 August 2022, within the context of the public health response. These cases were predominantly men who have sex with men aged 31-45 years. The vast majority of infections were acquired through sexual contact with casual partners in private or recreational settings including LGBTQIA+ venues in the Netherlands. This indicates that, although some larger upsurges occurred from point-source and/or travel-related events, the outbreak was mainly characterised by sustained transmission within the Netherlands. In addition, we estimated the protective effect of first-generation smallpox vaccine against moderate/severe mpox and found a vaccine effectiveness of 58% (95% CI: 17-78%), suggesting moderate protection against moderate/severe mpox symptoms on top of any possible protection by this vaccine against MPXV infection and disease. Communication with and supporting the at-risk population in following mitigation measures remains essential.

Effects of mammal host diversity and density on the infection level of Trypanosoma cruzi in sylvatic kissing bugs.

Several reports have described host species diversity and identity as the most important factors influencing disease risk, producing either dilution or amplification of the pathogen in a host community. Triatomine vectors, mammals and the protozoan Trypanosoma cruzi (Trypanosomatida: Trypanosomatidae) Chagas are involved in the wild cycle of Chagas disease, in which infection of mammals occurs by contamination of mucous membranes or skin abrasions with insect-infected faeces. We examined the extent to which host diversity and identity determine the infection level observed in vector populations (i.e. disease risk in humans). We recorded infection in triatomine colonies and on the coexisting host mammalian species in semi-arid Chile. Host diversity, and total and infected host species densities are used as predictor variables for disease risk. Disease risk did not correlate with host diversity changes. However, the densities of each infected rodent species were positively associated with disease risk. We suggest that the infected host density surrounding the vector colonies is a relevant variable for disease risk and should be considered to understand disease dynamics. It is crucial to pay attention on the spatial scale of analysis, considering the pattern of vector dispersal, when the relationship between host diversity and disease risk is studied.

Seroprevalence and Risk Factors of Lyme Borreliosis in The Netherlands: A Population-Based Cross-Sectional Study.

Lyme borreliosis (LB) is not notifiable in many European countries, and accurate data on the incidence are often lacking. This study aimed to determine the seroprevalence of Borrelia burgdorferi sensu lato (s.l.)-specific antibodies in the general population of The Netherlands, and to determine risk factors associated with seropositivity. Sera and questionnaires were obtained from participants (n = 5592, aged 0-88 years) enrolled in a nationwide serosurveillance study. The sera were tested for B. burgdorferi s.l.-specific IgM and IgG antibodies using ELISA and immunoblot. Seroprevalence was estimated controlling for the survey design. Risk factors for seropositivity were analyzed using a generalized linear mixed-effect model. In 2016/2017, the seroprevalence in The Netherlands was 4.4% (95% CI 3.5-5.2). Estimates were higher in men (5.7% [95% CI 4.4-7.2]) than in women (3.1% [95% CI 2.0-4.0]), and increased with age from 2.6% (95% CI 1.4-4.4) in children to 7.7% (95% CI 5.9-7.9) in 60- to 88-year-olds. The seroprevalence for B. burgdorferi s.l. in the general population in The Netherlands was comparable to rates reported in European countries. The main risk factors for seropositivity were increasing age, being male and the tick bite frequency. The dynamics of LB infection are complex and involve variables from various disciplines. This could be further elucidated using infectious disease modelling.

Initial Variability and Time-Dependent Changes of Neuronal Response Features Are Cell-Type-Specific.

Different cell types are commonly defined by their distinct response features. But several studies proved substantial variability between cells of the same type, suggesting rather the appraisal of response feature distributions than a limitation to "typical" responses. Moreover, there is growing evidence that time-dependent changes of response features contribute to robust and functional network output in many neuronal systems. The individually characterized Touch (T), Pressure (P), and Retzius (Rz) cells in the medicinal leech allow for a rigid analysis of response features, elucidating differences between and variability within cell types, as well as their changes over time. The initial responses of T and P cells to somatic current injection cover a wide range of spike counts, and their first spike is generated with a high temporal precision after a short latency. In contrast, all Rz cells elicit very similar low spike counts with variable, long latencies. During prolonged electrical stimulation the resting membrane potential of all three cell types hyperpolarizes. At the same time, Rz cells reduce their spiking activity as expected for a departure from the spike threshold. In contrast, both mechanoreceptor types increase their spike counts during repeated stimulation, consistent with previous findings in T cells. A control experiment reveals that neither a massive current stimulation nor the hyperpolarization of the membrane potential is necessary for the mechanoreceptors' increase in excitability over time. These findings challenge the previously proposed involvement of slow K+-channels in the time-dependent activity changes. We also find no indication for a run-down of HCN channels over time, and a rigid statistical analysis contradicts several potential experimental confounders as the basis of the observed variability. We conclude that the time-dependent change in excitability of T and P cells could indicate a cell-type-specific shift between different spiking regimes, which also could explain the high variability in the initial responses. The underlying mechanism needs to be further investigated in more naturalistic experimental situations to disentangle the effects of varying membrane properties versus network interactions. They will show if variability in individual response features serves as flexible adaptation to behavioral contexts rather than just "randomness".

Corrigendum: The influence of HIV infection and antiretroviral treatment on pulmonary function in individuals in an urban setting in sub-Saharan Africa.

[This corrects the article DOI: 10.4102/sajhivmed.v22i1.1312.].

High-density lipoprotein cholesterol is positively associated with hypertension in apparently healthy Japanese men and women.

Among five components of metabolic syndrome, high-density lipoprotein (HDL) cholesterol is unique because it is not significantly associated with blood pressure. This study looks at cross-sectional relationships between HDL cholesterol and hypertension using medical check-up data from 1803 apparently healthy Japanese men aged 49.9 +/- 9.0 years, and 1150 Japanese women aged 49.5 +/- 9.0 years. Pearson's correlation coefficients between systolic blood pressure (SBP)/diastolic blood pressure (DBP) and HDL cholesterol were -0.01 (ns)/-0.01 (ns) in men and -0.04 (ns)/-0.01 (ns) in women. The standardised partial regression coefficient of HDL cholesterol for SBP/DBP (mmHg) controlling for age, body mass index (BMI), fasting plasma glucose (FPG), triglycerides, high-sensitivity C-reactive protein (hs-CRP) and low-density lipoprotein (LDL) cholesterol were 0.15 (P < 0.0001)/0.15 (P < 0.0001) in men and 0.10 (P < 0.0001)/0.12 (P < 0.0001) in women. The odds ratio (OR; 95% confidence interval [CI]) of a 1 mg/dL increment of HDL cholesterol for hypertension controlling for age, BMI, FPG, triglycerides, hs-CRP, LDL cholesterol, metabolic syndrome, diabetes, exercise status, drinking status, and smoking status was 1.03 (1.02-1.04; P < 0.001) in men and 1.03 (1.01-1.05; P = 0.002) in women. Thus, HDL cholesterol was independently positively associated with hypertension in apparently healthy Japanese men and women.

The influence of HIV infection and antiretroviral treatment on pulmonary function in individuals in an urban setting in sub-Saharan Africa.

BACKGROUND: With the roll-out of antiretroviral treatment (ART), the life expectancy of people with HIV and, hence, morbidity from non-communicable diseases, including pulmonary diseases, have increased. OBJECTIVES: This research study aims to investigate whether HIV infection and ART use are associated with pulmonary function, given the high frequency of pulmonary infections, including tuberculosis (TB), associated with HIV. METHOD: Adults living with HIV (ART-naïve, on first- or second-line ART), and age and sex matched HIV-negative controls were included in a cross-sectional study in Johannesburg, South Africa. Spirometry was performed to determine lung function, measuring the forced expiratory volume in one second (FEV1), the forced vital capacity (FVC) and the FEV1/FVC ratio before (pre), and after (post), short-acting bronchodilator. The association of HIV infection and ART use with pulmonary function was analysed using linear regression models, adjusting for age, gender, body surface area (BSA), employment, education, smoking and TB. RESULTS: Overall, 548 participants (62% women) were included with a mean age of 38 (standard deviation [s.d.] 9.5) years. No effect of HIV or ART on post-FEV1 was observed in adjusted analysis. Additional adjustment for TB resulted in a higher post-FEV1 in participants on ART compared with HIV-negative participants, whereas TB was associated with a lower FEV1. No effect of HIV and ART on post-FEV1/FVC was observed. CONCLUSION: HIV infection and ART use were not associated with reduced pulmonary function in this urban African population. Tuberculosis showed a mediating effect on the association between HIV, ART and pulmonary function.

Noxa, a BH3-only member of the Bcl-2 family and candidate mediator of p53-induced apoptosis.

A critical function of tumor suppressor p53 is the induction of apoptosis in cells exposed to noxious stresses. We report a previously unidentified pro-apoptotic gene, Noxa. Expression of Noxa induction in primary mouse cells exposed to x-ray irradiation was dependent on p53. Noxa encodes a Bcl-2 homology 3 (BH3)-only member of the Bcl-2 family of proteins; this member contains the BH3 region but not other BH domains. When ectopically expressed, Noxa underwent BH3 motif-dependent localization to mitochondria and interacted with anti-apoptotic Bcl-2 family members, resulting in the activation of caspase-9. We also demonstrate that blocking the endogenous Noxa induction results in the suppression of apoptosis. Noxa may thus represent a mediator of p53-dependent apoptosis.

Induction of Sp1 in differentiating human embryonal carcinoma cells triggers transcription of the fibronectin gene.

Cells of the human embryonal carcinoma line NEC14 proliferate as densely packed clusters consisting of small, polygonal stem cells and do not express a detectable level of fibronectin (FN). Upon induction of differentiation by treatment with N,N'-hexamethylene bisacetamide (HMBA), the level of FN mRNA increased steeply within 24 h and FN began to be accumulated, along with the organization of actin filaments in the cells. The FN promoter elements required for the activation were analyzed in reference to a cluster of GC boxes by using the chloramphenicol acetyltransferase (CAT) gene fused to 5' sequential-deletion derivatives of the promoter and promoters carrying base substitutions in the GC boxes. Among four GC boxes, GC boxes 2 and 3 had the greatest effect on promoter activation, and base substitutions in these GC boxes resulted in 80% reduction in promoter activity. The pattern of DNA-protein complex formation with these GC boxes changed drastically after induction of differentiation. The extract prepared from undifferentiated NEC14 cells formed fast-migrating complexes (UnD complexes), while the extract prepared from NEC14 cells treated with HMBA for 24 h formed slow-migrating complexes containing Sp1. Both complexes were formed predominantly with GC box 2. Base substitutions within the GC boxes completely abolished the formation of both UnD and Sp1 complexes. Consistent with these changes, the Sp1 level increased steeply within 24 h. Induction of Sp1 expression in NEC14 cells effectively stimulated the promoter activity of the transfected FN promoter-CAT constructs. These results indicate that activation of the FN promoter in differentiating NEC14 cells occurs by the steep induction of Sp1, which prevents an undifferentiated cell factor from binding to the Sp1 sites.

Cloning and characterization of a GC-box binding protein, G10BP-1, responsible for repression of the rat fibronectin gene.

Fibronectin (FN) is an extracellular matrix protein that connects the extracellular matrix to intracellular cortical actin filaments through binding to its cell surface receptor, alpha5beta1, a member of the integrin superfamily. The expression level of FN is reduced in most tumor cells, facilitating their anchorage-independent growth by still unclarified mechanisms. The cDNA clone encoding G-rich sequence binding protein G10BP-1, which is responsible for repression of the rat FN gene, was isolated by using a yeast one-hybrid screen with the G10 stretch inserted upstream of the HIS3 and lacZ gene minimal promoters. G10BP-1 comprises 385 amino acids and contains two basic regions and a putative zipper structure. It has the same specificity of binding to three G-rich sequences in the FN promoter and the same size as the G10BP previously identified in adenovirus E1A- and E1B-transformed rat cells. Expression of G10BP-1 is cell cycle regulated; the level was almost undetectable in quiescent rat 3Y1 cells but increased steeply after growth stimulation by serum, reaching a maximum in late G1. Expression of FN mRNA is inversely correlated with G10BP-1 expression, and the level decreased steeply during G1-to-S progression. This down regulation was strictly dependent on the downstream GC box (GCd), and base substitutions within GCd abolished the sensitivity of the promoter to G10BP-1. In contrast, the level of Sp1, which competes with G10BP for binding to the G-rich sequences, was constant throughout the cell cycle, suggesting that the concentration of G10BP-1 relative to that of Sp1 determines the expression level of the FN gene. Preparation of glutathione S-transferase pulldowns of native proteins from the cell extracts containing exogenously or endogenously expressed G10BP-1, followed by Western blot analysis, showed that G10BP-1 forms homodimers through its basic-zipper structure.

G10BP, an E1A-inducible negative regulator of Sp1, represses transcription of the rat fibronectin gene.

Downregulation of the fibronectin (FN) gene in a rat 3Y1 derivative cell line, XhoC, transformed by the adenovirus E1A and E1B genes seems to be caused by the induction of a negative regulator, G10BP, which binds to three G-rich sequences in the promoter (T. Nakamura, T. Nakajima, S. Tsunoda, S. Nakada, K. Oda, H. Tsurui, and A. Wada, J. Virol. 66:6436-6450, 1992). These are the G10 stretch and two GC boxes consisting of the G10 stretch with one internal C residue insertion. The recognition sequences of G10BP and Sp1 (GGGCGG) overlap in these GC boxes. To analyze the mechanism of the downregulation, G10BP was purified by DNA affinity chromatography, and its molecular mass was estimated to be about 30 kDa. The promoter was modified by substituting the sequence GGGG with ATCC or CTTA in these G-rich sequences, leaving the Sp1 motif intact, and by replacing the Sp1 motif by the T stretch. Transcription of FN promoter-chloramphenicol acetyltransferase fusion genes carrying the base substitution in one or more of these G-rich sequences both in vivo and in vitro revealed that the base substitution in any G-rich sequence results in reduction of promoter activity, although the downstream GC box (GCd) plays a primary role. The addition of G10BP severely inhibited the activities of the FN promoters carrying the wild-type GCd in vitro, while the promoters carrying the mutant GCd were unaffected. The binding affinity of G10BP and Sp1 to each of the G-rich sequences, analyzed by gel shift assays, indicated that G10BP binds strongly to the GCd, moderately to the G10 stretch, and weakly to GCu, while Sp1 binds strongly to GCu, moderately to GCd, and weakly to the G10 stretch. Sp1 binding to GCd and the G10 stretch was inhibited by G10BP, while binding to GCu was unaffected. These results indicate that FN gene transcription is inhibited in XhoC cells primarily by exclusion of Sp1 binding to GCd by G10BP and that G10BP is a new class of Sp1 negative regulator.

Varying the ratio of dietary n-6/n-3 polyunsaturated fatty acid alters the tendency to thrombosis and progress of atherosclerosis in apoE-/- LDLR-/- double knockout mouse.

We have investigated the influence of dietary n-6/n-3 (ù-6/ù-3) polyunsaturated fatty acid-balance on the tendency to arterial thrombosis and the progress of atherosclerosis in apoE-/- LDLR-/- double knockout mouse. Homozygous apoE-/- LDLR-/- double knockout mouse (DKO mice, 129XC57BL/6J background) and male C57BL/6 mice aged 6 weeks were divided into four groups. Each group was fed a diet containing a different n-6/n-3 ratio (Group l: 0.29; Group 2: 1.43; Group 3: 5.00; Group 4: 8), prepared with high linolenic (LNA) flaxseed oil (n-3 rich) and high linoleic (LA) safflower oil (n-6 rich). There were no statistical differences in the gain in body weight between the four groups. After 16 weeks, plasma triglyceride and LDL levels in Group 1 were significantly lower than in the other groups. Conversely, HDL was the highest. After 8 and 16 weeks, the tendency to arterial thrombosis was assessed using a He-Ne laser-induced thrombosis model. The degree of atherosclerosis was measured using the entire aorta method employing image analysis software. The n-6/n-3 ratio had a dose-dependent antithrombotic effect (thrombus volume decreased 23%, Group 1 vs. Group 4), In addition, the extent of atherosclerosis was less in the animals fed a low n-6/n-3 ratio compared with the high n-6/n-3 ratio group (atherosclerotic area decreased 40%, Group 1 vs. Group 4). The lowest n-6/n-3 ratio tested (0.29) was the most effective in suppressing the thrombotic and atherosclerotic parameters in these DKO mice.

Determination of the active site of CD59 with synthetic peptides.

CD59 inhibits the formation of membrane attack complex (MAC) of human complement by binding to C8 and C9 in the nascent membrane attack complex and inhibiting C9 binding to C8 in C5b-8 and C9 polymerization. Considering five disulfide bridges of CD59, we divided the molecule into two portions and synthesized the two peptides. One represented an amino-terminal half, P1-41, consisting of residues 1-41, while another represented a carboxyl-terminal half, P42-77, consisting of residues 42-77. P1-41 inhibited the MAC formation much more strongly than P42-77, indicating that the amino-terminal half contained the active site. We further synthesized P4-18 that consisted of residues 4-18 and P19-41 that consisted of residues 19-41. The activity of P4-18 was less than that of P19-41. Surprisingly, P19-41 showed higher activity than P1-41 and was comparable to urine CD59. Residues 19-41 were further divided into two portions: P20-25 which consisted of residues 20-25 and P27-38 which consisted of residues 27-38. Although their activities were significantly less than the activity of P19-41, P27-38 showed higher activity than P20-25. Residues 27-38 were further divided into three portions: P27-32 which consisted of residues 27-32, P30-34 which consisted of residues 30-34 and P33-38 which consisted of residues 33-38. When these peptides were assayed for the activities, all of them showed significant activities, even though they needed 10-fold more concentrations than P19-41. These data suggest that the portion made up of residues 27-38 is the active site constituting the binding site to C8 and C9.

Involvement of the IRF family transcription factor IRF-3 in virus-induced activation of the IFN-beta gene.

The virus-induced activation of interferon alpha/beta (IFN-alpha/beta) gene transcription is essential for host defense. The IFN-beta promoter is controlled primarily by the virus-inducible enhancer elements, the IRF-Es. Here we show that IRF-3, an IRF family transcription factor, translocates to the nucleus from the cytoplasm upon virus infection in NIH/3T3 cells. The nuclear IRF-3 is phosphorylated, interacts with the co-activators CBP/p300, and binds specifically to the IFN-beta IRF-E. Furthermore, overexpression of IRF-3 causes a marked increase in virus-induced IFN-beta mRNA expression. Thus, IRF-3 is a candidate transcription factor mediating the activation of the IFN-beta gene.

Determination of carboxyl-terminal residue and disulfide bonds of MACIF (CD59), a glycosyl-phosphatidylinositol-anchored membrane protein.

MACIF (CD59) is a glycosyl-phosphatidylinositol (GPI)-anchored membrane glycoprotein which inhibits the formation of membrane attack complex of human complement. MACIF prepared from human erythrocyte membranes was digested with pronase. When the digest was subjected to two-phase partition with butanol and 0.1 N HCl, the carboxyl-terminal peptide was recovered in the butanol phase because of the attachment of the highly hydrophobic GPI. The amino acid sequence of the peptide was determined to be Asn72 at its amino-terminus and up to Glu76, while the presence of Asn77 was ambiguous. To allow unequivocal determination of the carboxyl-terminus, a soluble form of MACIF was prepared from human urine on a large scale. The carboxyl-terminal peptide from the soluble form was prepared by tryptic digestion followed by reversed-phase HPLC. The sequence and composition of the peptide unequivocally revealed Asn77 as the carboxyl-terminus. The pattern of disulfide bonds of MACIF was also determined with the membrane form as well as the soluble form. Cystine-containing peptides were prepared by chymotryptic and tryptic digestion, purified by HPLC, and their amino acid sequences were determined. The results indicated that disulfide bonds were formed at Cys3-Cys26, Cys6-Cys13, Cys19-Cys39, Cys45-Cys63 (or 64), and Cys63 (or 64)-Cys69.

Molecular cloning and characterization of MACIF, an inhibitor of membrane channel formation of complement.

Human erythrocytes contain a membrane protein, MACIF, which inhibits the formation of a membrane attack complex (MAC) of complement. We have cloned and sequenced the complementary DNA of MACIF messenger RNA. The amino acid sequence predicted from its nucleotide sequence consists of 128 amino acids. The amino-terminal 25 residues may correspond to a signal peptide. The carboxy-terminal sequence confirmed that MACIF is a glycosylphosphatidylinositol (GPI)-anchored protein. The amino acid sequence of MACIF was partially determined by established techniques for protein chemistry and the resultant sequence was consistent with that predicted from the nucleotide sequence. The results of sequence analyses also suggested that asparagine at the 18th position was N-glycosylated. When mRNA obtained from the MACIF cDNA clone with SP6 RNA polymerase was microinjected into Xenopus oocytes, the oocytes synthesized a product which exhibited MACIF activity and reacted with anti-MACIF antibody. Comparison of the predicted sequence revealed significant homology with mouse Ly-6 antigens.

Purification and characterization of a novel glycoprotein which has significant homology to heavy chains of inter-alpha-trypsin inhibitor family from human plasma.

Plasmapheresis with a dextran sulfate column is a treatment for patients with hypercholesteremia. When proteins bound to the column during the treatment were fractionated to prepare some known proteins, we found a 57 kDa glycoprotein designated GP57 which showed a new N-terminal amino acid sequence. Western-blot analysis of human plasma revealed that only a 120 kDa protein, GP120, reacted with anti-GP57 antibody. Since GP120 and GP57 had an identical N-terminal amino acid sequence, GP120 is probably the intact form of GP57. The isoelectric point of GP120 was 6.8. N-Glycanase treatment decreased the molecular weight of GP120 by 15 kDa. Neuraminidase and O-glycanase, however, did not affect the molecular weight. Amino acid sequence analyses of the lysylendopeptidase digest of GP120 revealed significant homology to the heavy chains of inter-alpha-trypsin inhibitor (ITI) family. Since GP120 showed no bikunin sequence, and chondroitinase treatment and alkaline treatment of GP120 did not affect its molecular weight, we concluded that GP120 was not a complex with bikunin. We designated GP120 as IHRP (ITI heavy chain-related protein).

Isolation and characterization of the human inter-alpha-trypsin inhibitor family heavy chain-related protein (IHRP) gene (ITIHL1).

Inter-alpha-trypsin inhibitor (ITI) family heavy chain-related protein (IHRP) is a novel human glycoprotein that shows significant homology in amino acid sequence to proteins of the ITI family heavy chains from human plasma. Three overlapping clones that encode the human inter-alpha-trypsin inhibitor family heavy chain-related protein (IHRP) gene (ITIHL1) were isolated and characterized. The IHRP gene spans 15 kb and is composed of 24 exons from 27 to 207 bp in size with consensus splice sites. The gene codes for the precursor of IHRP, which is similar to inter-alpha-trypsin inhibitor (ITI) family heavy chains. Two major transcription initiation sites were identified in the 5'-flanking region. They contain putative promoter elements, but no typical TATA box. Some exons of this gene showed significant similarities to those of the ITI-H1 gene in nucleotide length and in intron phasing. The tissue-specific transcription of this gene may be due to the presence of binding sites for the hepatocyte nuclear factors LF-A1, HNF-5, NF-IL6, and C/EBP. This gene was found to be localized very close to another unknown gene related to EST (GenBank accession #: R54643, R50663, R50563, H27139, and R54913).

Tetrasomy 8 in acute myelomonocytic leukemia developing after a gastric cancer operation.

A 70 year-old-Japanese man underwent gastrectomy for early gastric cancer with preoperative hypocellular marrow. Three weeks later, acute myelomonocytic leukemia developed with tetrasomy for chromosome 8 (48,XY,+8,+8). The patient died of leukemia on the 33rd postoperative day. Whether or not the operation triggered the leukemia remains unknown.