Changes of the intestinal microbiota along the gut of Japanese Eel (Anguilla japonica).

Fish intestine contains different types of microbiomes, and bacteria are the dominant microbiota in fishes. Studies have identified various core gut bacteria in fishes. However, little is known about the composition and their relative functions of gut microbial community along the intestine. To explore this, the current study investigated the microbial community distribution along the gut in Anguilla japonica. By 16S rRNA gene sequencing, we profiled the gut microbiota in eel along the three regions (anterior intestine (AI), the middle intestine (MI) and the posterior intestine (PI)). Results suggested that the three regions did not have significant differences on the observed species and diversities. The cluster tree analysis showed that the bacteria community in MI was closer to PI than the AI. The dominant bacteria in AI were the Proteobacteria, in which the majority was graduated replaced by Bacteroidetes along the gut to PI region. Through PICRUSt analysis, shifts in the bacterial community along the gut were found to affect the genetic information processing pathways. Higher levels of translation and transcriptional pathway activities were found in MI and PI than in AI. The dominant bacterial species were different among the regions and contributed to various biological functions along the gut.

Developmental toxicity of the common UV filter, benophenone-2, in zebrafish embryos.

Benozophenone (BP) type UV filters are extensively used in the personal care products to provide protection against the harmful effects of UV radiation. BPs are one of the primary components in the UV filter family, in which benophenone-2 (BP2) is widely used as a UV filter reagent in the sunscreen. Humans used these personal care products directly on skin and the chemicals will be washed away to the water system. BP2 has been identified as one of the endocrine disruptor chemicals, which can inference the synthesis, metabolism, and action of endogenous hormones. Environmentally, it has been found to contaminate water worldwide. In this study, we aimed to unfold the possible developmental toxicology of this chemical. Zebrafish are used as the screening model to perform in situ hybridization staining to investigate the effects of BP2 on segmentation, brain regionalization, and facial formation at four developmental stages (10-12 somite, prim-5, 2 and 5 days post-fertilization). Results showed 40 µM (9.85 mg L-1) or above BP2 exposure in zebrafish embryos for 5 days resulted in lipid accumulation in the yolk sac and facial malformation via affecting the lipid processing and the expression of cranial neural crest cells respectively. To conclude, the study alarmed its potential developmental toxicities at high dosage exposure.

Osmotic stress transcription factor 1b (Ostf1b) promotes migration properties with the modulation of epithelial mesenchymal transition (EMT) phenotype in human embryonic kidney cell.

Osmoregulation is an essential mechanism for euryhaline fish. Gill cells undergo rapid mechanism to maintain the cellular homeostasis during osmotic stress. Reports have suggested that gill cells may be able to migrate between primary filament and secondary lamella during seawater acclimination. However, the factor that can trigger such process is not well-known. Previously, we identified the osmotic stress transcription factor 1b (Ostf1b) in medaka and found that it is an early hypertonic responsive gene and can activate the c-Jun N-terminal kinase (JNK) pathway. In this report, we aim to know if Ostf1b plays the role in the migration. Ostf1b was ectopic expressed in the human embryonic kidney cell line (HEK293) to understand the Ostf1b function. Results clearly demonstrated that Ostf1b could constitutively activate the Rho kinase 1 (ROCK1) and myosin light chain 2 (MLC2) signalling pathway that promotes cell migration, epithelial mesenchymal transition (EMT) and cytoskeletal dynamics through stress fibre formation. The study supports the notion of cell migration and cytoskeleton rearrangement theories in osmoregulation.

Medaka osmotic stress transcription factor 1b (Ostf1b/TSC22D3-2) triggers hyperosmotic responses of different ion transporters in medaka gill and human embryonic kidney cells via the JNK signalling pathway.

Eukaryotic cells undergo rapid regulatory processes to maintain cellular homeostasis upon osmotic stress. In fishes, gill epithelial cells play main roles in these processes. Although osmoregulatory functions of fish gills have been well studied, little is known about the underlying mechanisms, particularly the hypertonic-induced signalling pathways during osmotic stress. This study reports for the first time on the osmo-sensing signal cascade that related to the medaka osmotic stress transcription factor 1 (Ostf1), a hypertonic induced immediate early gene, under hypertonic stress. Quantitative real-time PCR showed the rapid increase of Ostf1 in gill after transfer of medaka from fresh water to 50% seawater; particularly Ostf1b whose mRNA expression increased to 4 folds at 0.5h and reached to 10 folds at 6h after the transfer. The in vivo knockdown of Ostf1b profoundly inhibited SEK and JNK phosphorylation, but not p38 and ERK phosphorylation in the medaka gill tissue. To further investigate the possible role of Ostf1b in the JNK pathway, Ostf1b was ectopically expressed in HEK293 cells. Results indicated that Ostf1b is a downstream target of SEK and JNK and exerts a positive feedback loop on the JNK signalling pathway via activation of GCK and/or MLK3 proteins. Additionally, MAPK inhibitors experiments suggested that activation of the JNK pathway by hypertonicity is involved in the maintenance of Ostf1b stability, which in turn provides continuous stimulation of GCK for JNK phosphorylation. Lastly, changes in transcription levels of different water/ion transporters were found in knockdown or ecoptic over-expression of Ostf1b in medaka gills and human embryonic kidney cells, suggesting the role of Ostf1b in modulation of critical water channel/ion transporters during osmotic stress.

Modulation of ion transporter expression in gill mitochondrion-rich cells of eels acclimated to low-Na(+) or-Cl(-) freshwater.

In this study, we aimed to establish an experimental model to study the role of the gill mitochondrion-rich cells (MRCs) of freshwater fish in Na(+) uptake and to examine the effect of adjusting external Na(+) and Cl(-) ions on selected ion transporters in gill MRCs. Japanese eels (Anguilla japonica) acclimated to deionized (DI) water for 2 weeks were transferred directly to (a) ion-supplemented artificial freshwater (AF), (b) Na(+) -deficient AF, or (c) Cl(-) -deficient AF for 2 days. The effects of the transfer on the expression levels of ion transporters in isolated gill cells were investigated. Our data demonstrated that the 2-day acclimation in ion-supplemented AF, Na(+) -deficient AF, or Cl(-) -deficient AF led to a significant increase in serum osmolarity attributed mainly to an increase in serum Na(+) and/or Cl(-) levels when compared with DI-acclimated eel. Significant inductions of V-type H(+) -ATPase (V-H(+) -ATPase) and cotransporter (NBC1) mRNA expression in gill MRCs were detected in AF-acclimated fish. In fish acclimated to Na(+) -deficient AF, mRNA expression levels of V-H(+) -ATPase, NBC1, and Na(+) /H(+) -exchanger-3 (NHE3) were significantly increased in MRCs. Fish acclimated to Cl(-) -deficient AF showed no observable change in expression levels of ion transporters in gill MRCs. In addition, expression levels of ion transporters in pavement cells were stable throughout the 2-day experiments. These data indicate that the level of Na(+) in freshwater is important for altering the mRNA expression of ion transporters in gill MRCs, which supports the notion that gill MRCs play important roles in freshwater Na(+) uptake.

A positive role for c-Abl in Atm and Atr activation in DNA damage response.

DNA damage triggers Atm- and/or Atr-dependent signaling pathways to control cell cycle progression, apoptosis, and DNA repair. However, how Atm and Atr are activated is not fully understood. One of the downstream targets of Atm is non-receptor tyrosine kinase c-Abl, which is phosphorylated and activated by Atm. The current view is that c-Abl relays pro-apoptotic signals from Atm to p73 and p53. Here we show that c-Abl deficiency resulted in a broad spectrum of defects in cell response to genotoxic stress, including activation of Chk1 and Chk2, activation of p53, nuclear foci formation, apoptosis, and DNA repair, suggesting that c-Abl might also act upstream of the DNA damage-activated signaling cascades in addition to its role in p73 and p53 regulation. Indeed, we found that c-Abl is required for proper activation of both Atm and Atr. c-Abl is bound to the chromatin and shows enhanced interaction with Atm and Atr in response to DNA damage. c-Abl can phosphorylate Atr on Y291 and Y310 and this phosphorylation appears to have a positive role in Atr activation under genotoxic stress. These findings suggest that Atm-mediated c-Abl activation in cell response to double-stranded DNA breaks might facilitate the activation of both Atm and Atr to regulate their downstream cellular events.

Identification and characterization of the hypoxia-responsive element in human stanniocalcin-1 gene.

In this study, we aimed to identify the hypoxia-inducible factor-1 (HIF-1) binding motif in human STC1 gene promoter and to characterize the associated gene transactivation mechanism. Using normoxic human nasopharyngeal cancer cells (CNE2), we manipulated the stability of HIF-1 alpha protein by overexpressing HIF-1 alpha or the silencing of prolyl hydroxylase-2 (PHD2), to illustrate HIF-1 activation of STC1 promoter-driven luciferase activity. Subsequently luciferase activities of the deletion and mutated STC1 promoter constructs were investigated in HIF-1 overexpressed cells. The data revealed the presence of an authentic HRE motif in STC1 gene. This result was further supported by the chromatin immunoprecipitation (ChIP) assay. Using a similar experimental treatment, however, had no significant effect on the expression level of STC1 mRNA and protein. Moreover the activation of STC1 expression can be restored by the silencing of "factor inhibiting HIF-1" (FIH-1) in either HIF-1 overexpressed or PHD2 silenced cells. The data implied that the HIF-1-mediated STC1 gene expression required the recruitment of p300. This presumption was confirmed by the use of p300 inhibitor, chetomin and HIF-1 alpha/p300 re-ChIP assay. Collectively our data provide the first evidence to show that STC1 is a FIH-inhibited gene with a functional HRE motif located at the upstream region between -2322/-2335. The data support the need for further investigation to reveal if STC1 can be used as a novel tumor marker for HIF-1 induction and for the monitoring of anti-angiogenic therapy.

Inverse method to estimate kinetic degradation parameters of grape anthocyanins in wheat flour under simultaneously changing temperature and moisture.

Thermal and moisture effects on grape anthocyanin degradation were investigated using solid media to simulate processing at temperatures above 100 degrees C. Grape pomace (anthocyanin source) mixed with wheat pastry flour (1: 3, w/w dry basis) was used in both isothermal and nonisothermal experiments by heating the same mixture at 43% (db) initial moisture in steel cells in an oil bath at 80, 105, and 145 degrees C. To determine the effect of moisture on anthocyanin degradation, the grape pomace-wheat flour mixture was heated isothermally at 80 degrees C at constant moisture contents of 10%, 20%, and 43% (db). Anthocyanin degradation followed a pseudo first-order reaction with moisture. Anthocyanins degraded more rapidly with increasing temperature and moisture. The effects of temperature and moisture on the rate constant were modeled according to the Arrhenius and an exponential relationship, respectively. The nonisothermal reaction rate constant and activation energy (mean +/- standard error) were k(80 degrees C, 43% (db) moisture) = 2.81 x 10(-4)+/- 1.1 x 10(-6) s(-1) and DeltaE = 75273 +/- 197 J/g mol, respectively. The moisture parameter for the exponential model was 4.28 (dry basis moisture content)(-1). One possible application of this study is as a tool to predict the loss of anthocyanins in nutraceutical products containing grape pomace. For example, if the process temperature history and moisture history in an extruded snack fortified with grape pomace is known, the percentage anthocyanin loss can be predicted.

Histone deacetylase inhibitor-induced cellular apoptosis involves stanniocalcin-1 activation.

Our previous studies have demonstrated the involvement of HIF-1 and p53 in the regulation of stanniocalcin-1 (STC1) gene transcription in human cancer cells. In this study, we reported that the treatment of human colon adenoma HT29 cells with a histone deacetylase (HDAC) inhibitor (i.e. trichostatin A, TSA) induced both cellular apoptosis and STC1 expression. The activation of STC1 expression was also observed in other TSA-treated human cancer cells (i.e. SKOV3, CaCo-2, Jurkat and CNE-2 cells). STC1 mRNA was rapidly induced within 4 h in TSA-treated HT29 cells, and was found to be transcriptionally regulated and was independent of new protein synthesis as revealed by ActD and CHX treatment respectively. The induction was correlated with increased cellular levels of acetyl histone H3 and H4 and acetyl NFkappaB. Chromatin immunoprecipitation (ChIP) assay showed the increased binding of acetyl histone H3 and H4 to STC1 promoter in the TSA-treated cells. A cotreatment of HT29 cells with a NFkappaB inhibitor (parthenolide) significantly inhibited the TSA-induced cellular levels of acetyl NFkappaB p65 and abolished the stimulation of STC1 gene expression. ChIP assay also demonstrated that TSA treatment increased while TSA/parthenolide cotreatment decreased NFkappaB p65 binding to STC1 gene promoter. In the STC1-luciferase promoter construct (1 kb) study, the data implied that the promoter can be activated by TSA treatment. Interestingly, the promoter region contains 2 putative NFkappaB binding sites. Consistent with the STC1mRNA expression data, TSA/parthenolide cotreatment also significantly inhibited the TSA-induced STC1 promoter-driven luciferase activity. Importantly, TSA-induced apoptotic process was found to be significantly reduced by the silencing of STC1 expression. This is the first study to show that histone hyper-acetylation and the recruitment of activated NFkappaB stimulated STC1 gene expression. In addition, our results support the notion that STC1 is a pro-apoptotic factor.

Bifunctional modulating effects of an indigo dimer (bisindigotin) to CYP1A1 induction in H4IIE cells.

In this study, we measured and characterized the bifunctional effects of a newly identified natural compound-bisindigotin (SLY-1), isolated from leaf extracts of Isatis indigotica, to CYP1A1/EROD activities in H4IIE cells. The compound, SLY-1 (1muM) elicited a transitory and significant induction of CYP1A1 RNA/protein levels and EROD activities in the cells. Maximum levels of CYP1A1 expression and EROD induction were attained at 8 and 12h of post-treatment, respectively. Thereafter the induction decreased significantly. Similar profile of CYP1A2 and CYP1B1 mRNA induction was observed. In contrast TCDD elicited CYP1A1/EROD induction was persistent. The transitory effect by SLY-1 is most likely due to the clearance of SLY-1 by cellular metabolism. Taken together the observation indicated that SLY-1 is an Ah receptor agonist for CYP1A1/CYP1A2/CYP1B1/EROD induction. Interestingly in the TCDD/SLY-1 cotreatment study, although synergistic effects on CYP1A1 expression and EROD induction were observed at 4-8h, significant inhibitory effects to TCDD induced CYP1A1 protein and EROD activity were detected at 12-24h of post-treatment. Because there was no significant reduction of CYP1A1, CYP1A2 or CYP1B1 transcript levels between TCDD- and TCDD/SLY-1 treated cells, the data pointed to the translational and/or post-translational inhibitory effect. The cellular signal transduction system may be modulated following exposure to SLY-1. To investigate the possible mechanisms involved, various specific kinase inhibitors or activators (chelerythrin, PD98059, U0126, ZM336372, SB202190, PKA inhibitor PKI (6-22) amide, and dbcAMP) were used for the assessment. Chelerythrine, PD98059 or dbcAMP treatment in TCDD induced cells showed significant inhibitory effects on CYP1A1 mRNA/protein expressions and EROD activities. U0126 had no observable EROD inhibitory effect. ZM336372 or SB202190 showed inhibition only at EROD activities. The results indicated that the SLY-1 inhibitory effect was possibly not mediated by the cAMP/PKA, PKC or MEK pathways. Nevertheless our results indicate that SLY-1 is not only an inducer of the CYP1A1 system, but also a potent inhibitor of CYP1A1 enzyme.

Inhibition of CYP450scc expression in dioxin-exposed rat Leydig cells.

Polychlorinated dibenzo-p-dioxins, such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) have been recognized as highly potent developmental and reproductive toxins. We have previously demonstrated effects of TCDD in modulating the expression of rat Sertoli cell secretory products and markers for cell-cell interaction. In this study, we examined the direct biological effects of TCDD in rat Leydig cell primary cultures. Mature rat Leydig cells were purified by Percoll gradient centrifugation and the cell purity was determined by 3beta-hydroxysteroid dehydrogenase (3beta-HSD) staining and a testosterone induction assay. To examine TCDD-induced biological consequences, we measured the changes in the secretion of progesterone and testosterone, as well as transcript levels of some selected steroidogenic enzymes (i.e. StAR, P450scc, 3beta-HSD and CYP17alpha), in TCDD/human chorionic gonadotropin (hCG) co-treated cells. Our results indicated that TCDD (0.2 or 2 ng/ml) treatment significantly suppressed hCG (5 or 10 ng/ml)-induced testosterone secretion. The suppressive effect aligned with a reduction of progesterone secretion (P<0.05), as well as a decrease of P450scc mRNA and protein expression (P<0.05). The mechanistic action of TCDD was found to be via the reduction of cellular cAMP levels in the hCG-treated cells. This observation was further confirmed, as the TCDD-mediated suppressive effect could be reversed by dibutyryl cAMP co-treatment. The data indicate that TCDD can modulate cAMP signaling in rat Leydig cells to affect the process of steroidogenesis.

Effects of TCDD in modulating the expression of Sertoli cell secretory products and markers for cell-cell interaction.

Among different mammalian tissues, testis is found to be one of the most sensitive organs to TCDD exposure. In this study, primary Sertoli cell culture was established. The purity of the cultured cells was verified using 3beta-hydroxysteroid dehydrogenase, alkaline phosphatase as well as testosterone induction assays. Effects of TCDD in modulating the expression of CYP1A1, aromatase, secretory products (i.e. Mullerian inhibiting substance (MIS), 17beta-estradiol (E(2)) and lactate) and markers for cell-cell interaction (i.e. sertolin and testin) were then examined. Our data demonstrated that Sertoli cells exposed to 0.2-2000 pg/ml of TCDD showed a dose dependent induction of CYP1A1 mRNA. The minimal dose of activation was 2 pg/ml, which indicated that the cell was very sensitive to TCDD exposure. However, there was little or no detectable level CYP1A1 protein and EROD activities found. Dose-dependent inductions of aromatase transcript (200%) and E(2) (20%) secretion were measured. In addition there was a significant reduction (40%) of MIS mRNA. No detectable change in the level of secreted lactate was observed. Sertolin and testin, the gene makers for cell-cell interactions were differentially modulated upon TCDD treatment. Taken together, the results implicated that TCDD exposure might interfere with the normal Sertoli cell functions.

Dioxin-like components in human breast milk collected from Hong Kong and Guangzhou.

The H4IIE rat hepatoma cell line was employed as a cell model to screen 7-ethoxyresorufin O-deethylase (EROD)-TCDD equivalents (EROD-TEQ) of human breast milk samples collected from Hong Kong and Guangzhou, China. The screening methods employed a 96-well plate spectrofluorometer-EROD assay. For cell-line validation, our results demonstrated a dose-dependent increase in the Ah receptor-mediated response (i.e., CYP1A1 mRNA and EROD) of the cells upon exposure to a number of known Ah receptor agonists, including 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), 2,3,7,8-tetrachlorodibenzothiophene, benzo[a]pyrene, and beta-naphthaflavone. TCDD induced CYP1A1 mRNA and EROD was in a close positive correlation (r=0.98). For the screening of dioxin-like compounds, breast milk samples collected during lactation weeks 3-5 were used. One hundred (from Hong Kong) and 48 (from Guangzhou) breast milk samples were assayed, of which 65% and 68% of the samples, respectively, showed detectable dioxin-like activities using the H4IIE cell EROD screening method. For sixty-five samples from Hong Kong the mean EROD-TEQ values ranged from 58.1 to 96.5 pg/g of milk fat for those aged 21-36 years while 32 samples from Guangzhou had mean values of 98.8-202.1 pg/g of milk fat. In comparisons of the EROD-TEQ values for different age groups from both cities, there were no significant differences (P<0.05). However, the mean and median EROD-TEQ values of the Guangzhou population were in general higher than those of the Hong Kong population. The results of the present study indicate that it is feasible to use the H4IIE cell-line as a model for screening dioxin-like compounds in human breast milk. In addition, the method is rapid and cost-effective, particularly for a routine and high-throughput sample screening analysis, compared to the costly and time-intensive chemical analytical techniques.

Modulation of AhR-mediated CYP1A1 mRNA and EROD activities by 17beta-estradiol and dexamethasone in TCDD-induced H411E cells.

TCDD elicits a variety of species- and organ-specific pathological consequences. The differential toxicities are thought to relate to the de novo modulation of TCDD action by endogenous hormones. Previous studies from this laboratory demonstrated a dose- and time-dependent induction of CYP1A1 expression and 7-ethoxyresorufin-O-deethylase (EROD) activities in H4IIE cells by picomolar levels of TCDD treatment. In this study, we examined the hormonal modulation of TCDD-elicited AhR-mediated biochemical responses. Lipid-soluble hormones, 17beta-estradiol (E(2)), diethylstilbestrol (DES), testosterone (T), 5alpha-dihydrotestosterone (DHT), dexamethasone (DEX), and T(3), were studied for their possible interactions with the TCDD-mediated effects. Our results showed that CYP1A1 expression and EROD activities induced by TCDD were potentiated or suppressed, respectively, by DEX or E(2)/DES treatment. Other tested hormones, however, had no significant effect. Using a receptor antagonist (RU486), DEX-mediated potentiation of TCDD-elicited EROD activity was completely abolished. E(2)-mediated suppression, however, was not affected by cotreatment with the estrogen receptor antagonists, 4-hydroxytamoxifen or ICI 182780. Taking a step further to dissect the possible mechanisms involved, with the aid of cycloheximide (CHX), DEX-mediated potentiation was found to depend on the posttranscriptional process. The DEX pretreatment study indicated that the potentiation was a time-dependent process. In contrast, E(2)-mediated suppression did not rely on the synthesis of protein factors. Presumably it might hinder the formation of the activated TCDD/AhR complex and so the subsequent binding on DRE.

Changes in endogenous Zn and Cu distribution in different cytosolic protein fractions in mouse liver after administration of a single sublethal dose of CdCl(2).

The time course of change in tissue Cd, Cu and Zn contents, their distribution in cellular protein fractions as well as the profile of MT gene expression in mouse liver was described over a 7 days period following a single intraperitoneal injection of 2 mg/kg of CdCl(2). The result showed that Cd accumulated rapidly in mouse liver. Between 1 h and 7 days after administration, over 18% of the total Cd administered were found in the liver. Cd administration was also associated with the overexpression of the MT-mRNA. However, the time course of induction was not parallel to the change in tissue Cd content. When separated on a Sephadex G-75 column, majority of Cd was found to bind to the fractions known to contain the metal-binding protein, metallothionein (MT). From day 2 after Cd administration, a small amount of the metal was also found associated with the high molecular weight (HMW) proteins. In addition to Cd, tissue Zn content was affected most during the entire study. There was a significant decrease in tissue Zn content during the initial 8 h but tissue Zn content increased significantly throughout the following 6 days. At 1-7 days, majority of Zn was associated with the HMW protein fraction. Although there was no significant change in total tissue Cu content, distribution of Cu in different protein fractions was detected. While in control animals, Cu was mainly associated with the HMW proteins, some was found in the MT fraction on the second day. On the 7th day, Cu distribution had deteriorated. Together with changes seen in Cd, the results might suggest that injury had occurred in the tissue at this time. The results of the present study showed that Cd caused a change in subcellular distribution of tissue endogenous metals, which might reflect alteration of cellular functional activities.

Acute respiratory tract infection: a community-based intervention study in Malaysia.

A community-based intervention trial was conducted in Kelantan, Malaysia with the aim of reducing severe acute respiratory tract (ARI) infection in children. Interventions included health education of mothers on childhood pneumonia and training of health staff on case management. In a house-to-house survey 1382 and 1107 children less than 5 years of age in the intervention and control areas, respectively, were followed up every 2 weeks over a 62-week period. The reduction in the incidence of severe ARI cases in the intervention area was significantly greater than in the control area (P < 0.05). The ARI mortality rates were low in both the intervention and control areas ( < 0.1%). Our results indicate that with relatively inexpensive methods and simple interventions, reduction of severe ARI may be effectively achieved. This has important implications for an ARI control programme in Malaysia and other developing countries.

Ascaris and Trichuris do not contribute to growth retardation in primary school children.

To access the effectiveness of the treatment of soil-transmitted helminthiasis (STH) on the growth of primary school children, 353 children were block stratified to receive either mebendazole plus pyrantel oxantel pamoate every three months or a placebo. The children were followed for two years with 89% completing the trial. Follow-up stools indicated that the treatment was efficacious for ascariasis and trichuriasis. There was virtually no hookworm infection. The children were malnourished as measured by the number below -2 SD of height and weight standards. There was no difference in height or weight between the treatment and control groups by sex initially or at the end of two years of follow-up. The treatment of Ascaris and Trichuris had no effect on growth parameters. The effect of STH on growth may be mediated through hookworm infections.

Acute respiratory infection in Malaysian children.

A cross-sectional community-based survey was conducted to determine the prevalence of acute respiratory infection (ARI) in children below 7 years of age and to obtain baseline information for an intervention programme. A total of 6190 households comprising 38,632 persons with 12,273 children (32 per cent) below 7 years of age were surveyed. Information on socio-demographic variables, environmental sanitation, occurrence of ARI and diarrhoea, treatment seeking behaviour during episodes of those illnesses and immunizations among children were obtained. Thirty per cent of children had experienced ARI in the 2-week period prior to the interview, and 94 per cent had mild ARI, 1 per cent had moderate and 5 per cent had severe ARI. There was lack of concurrence between mother's perception of severity and that of the investigators' (Kappa coefficient = 0.083 (95 per cent CI = 0.017-0.149). Twenty-four and 39 per cent of severe and moderate ARI, respectively, were reported by mothers to be mild. There is cause for concern as these children may not receive timely and appropriate treatment. The findings from this study contribute to identification of target populations and priority areas for health education of the population. The survey has provided useful baseline data for the implementation of an intervention programme for the control of ARI in children.

Cryptosporidiosis among HIV positive intravenous drug users in Malaysia.

A study conducted at the Tampin Drug Rehabilitation Center in Malaysia established a high prevalence (23%) of asymptomatic carriers of Cryptosporidium among exposed HIV positive intravenous drug users (IVDUs). A majority of them were young adults and among the ethnic groups, the Malay HIV positive inmates had the highest prevalence of Cryptosporidium infection.

Intestinal protozoan infections in Malaysia.

Intestinal protozoa are found in all communities in Malaysia and among all ethnic groups. Prevalence of intestinal protozoa is not affected by ethnicity but by living conditions. Communities with both basic amenities of safe water supply and proper toilets have lower prevalence than those with one or none of the amenity. Cryptosporidium is an important intestinal protozoon in Malaysia and should be included in future field and laboratory studies and also in laboratory diagnosis for pathogens. Much interest will be centered on Blastocystis hominis in future studies in view that it may be a cause of diarrhea.