Twenty Hebrew-learning infants aged 8 to 11 months were presented with lists of nonsense words featuring the first two patterns (Experiment 1), and 20 were presented with nonsense

words featuring the second two patterns (Experiment 2). The results showed longer listening to CéCeC than to CóCoC lists and to CaCóC than to CaCéC lists, suggesting that infants recognized the common nonadjacent vocalic patterns in both cases. The study thus demonstrates that Hebrew-learning infants are able to disregard check details the intervening consonants within words and generalize their vocalic pattern to previously unheard nonwords, whether this pattern includes identical or different

vowels and regardless of the rhythmic pattern of the word (trochaic or iambic). Analysis of the occurrence of the relevant vowel patterns in input speech in three Hebrew corpora (two addressed to children and one to adults) suggests that exposure to these patterns in words underlies the infants’ preferences. SCH772984 supplier “
“The ability to effectively regulate emotions is a critical component of early socio-emotional development. This longitudinal study examined the developmental trajectories of emotion regulation in a sample of 3-, 5-, and 7-month-olds during an interaction with mothers and fathers. Infants’ negative affect and use of behavioral strategies, including distraction,

self-soothing, and high intensity motor behaviors were rated during the still-face episode of the Still-Face Paradigm. Longitudinal mixed-effects models were tested to determine whether strategies were followed by an increase or decrease in negative affect. Results from mother-infant and father-infant dyads indicated that focusing attention away from the unresponsive parent and engaging in self-soothing behaviors were associated with a subsequent decline in negative affect and the strength of these temporal associations were stable across infancy. In contrast, high-intensity motor behaviors were followed by an increase in negative affect FER and this effect declined over time. No significant effects were found for the behavioral strategy of looking at the parent. Results underscore the importance of considering infant age and the social partner when studying the effectiveness of emotion regulatory strategies in early infancy. “
“We examined how infants’ categorization is jointly influenced by previous experience and how much they shift their gaze back and forth between stimuli. Extending previous findings reported by K. A. Kovack-Lesh, J. S. Horst, and L. M.

1E). Levels of IL-10 were below the detection limit in both groups of mice (data not shown). Finally, analysis of the OVA-stimulated LNC cultures for the proportion of activated T cells showed similar frequency of CD3+CD4+CD44hi T cell in stimulated LNs from WT and PD-1−/− mice (Fig. 1F). Taken together, these results demonstrate that

during breakdown of tolerance and induction of autoimmunity, the absence of PD-1 expression on T cells results in aberrant activation and proliferation of these cells and more severe disease. To identify the potential involvement of microRNAs in PD-1-mediated breakdown of tolerance, we screened the expression of 365 microRNAs by microarray analysis of WT and PD1−/− lymphocytes, isolated from draining LNs of OVA-primed mice, before and after stimulation with OVA (Fig. 2A).

Five microRNAs (miR-21, miR-20a, miR-16, Sorafenib miR-155, and miR-375) differentially expressed after OVA stimulation in WT and PD1−/− cells. MiR-21 was statistically upregulated (2.3-fold) in unstimulated PD1−/− PLX-4720 order compared with WT cells. OVA stimulation induced miR-21 expression to a higher degree in PD-1−/− than WT cells. The effect of PD-1 on miR-21 expression was also validated by real-time PCR analysis (Fig. 2B). To further assess the role of PD-1 as an miR-21 regulator, we inhibited PD-1 by siRNA treatment (Fig. 2C) and tested miR-21 expression. PD-1 inhibition resulted in >11-fold upregulation in miR-21 expression levels, thus confirming the role of PD-1 as negative regulator of miR-21 (Fig. 2D). We next sought to identify whether this regulation occurs at the transcriptional RVX-208 or post-transcriptional level. The observation that PD-1 inhibition by siRNA resulted in upregulation of the primary transcript miR-21 (Fig. 3A) suggests that PD-1 regulates miR-21 transcriptional levels. The previous studies have shown that PD-1 regulates the expression and phosphorylation of STAT5 17. Western blot analysis showed that siRNA inhibition of PD-1 in Jurkat cells resulted in upregulation of STAT5 protein expression and phosphorylation (Fig. 3B). We next analyzed the

known putative promoter area of miR-21 18 for STAT5-binding sites. To this end, we used the TRANSFAC bioinformatic program and identified an evolutionary conserved STAT5 binding site on the miR-21 precursor sequence (Fig. 3C). In support of this, PD-1 inhibition resulted in enrichment of STAT5 binding in miR-21 promoter area (Fig. 3D) and resulted in upregulation of pri-miR-21. Furthermore, concurrent inhibition of PD-1 and STAT5 did not upregulate miR-21 expression (Fig. 3E), suggesting that PD-1 regulates miR-21 expression through STAT5. MicroRNAs exert their function through post-transcriptional inhibition of gene targets 14. Bioinformatic algorithm prediction analysis revealed programmed cell death 4 (PDCD4) as a potential miR-21 gene target.

In addition, Rorγt+ ILC numbers were also reduced upon specific deletion of AhR in Rorγt-expressing cells (including ILCs) [[56]]. Together these data indicate that the effects of AhR-deficiency on

Rorγt+ ILCs are cell intrinsic. Interestingly, the reduction of Rorγt+ ILC numbers, induced by ablation of AhR, was observed only after birth. GS-1101 purchase During fetal development, and early after birth, the ILC22 numbers in AhR-deficient mice are comparable to those in wild type mice, indicating that AhR is not required for development of these cells [[54]]. However, after weaning, the numbers of Rorγt+ ILCs in AhR-deficient mice steadily decrease [[54]]. Maintenance of ILC numbers is not a consequence of AhR activation by products of colonizing microbiota, because the difference in ILC22 numbers between wt and AhR-deficient animals is not affected by treatment with a mix of antibiotics [[54]]. Also, the observation that germ-free animals do not show reductions in gut residing Rorγt+ ILC numbers [[55, 57]] is consistent with the notion

that products from commensals are not required for the maintenance of these cells. It is controversial whether dietary products are the AhR ligands responsible for the maintenance of gut-residing Rorγt+ ILCs, as observed for IELs [[53]]. In one study, it was found that mice fed with a diet free of AhR-binding phytochemicals showed decreased numbers of Rorγt+ ILCs, causing a lack of CPs and Tyrosine-protein kinase BLK ILFs [[55]]. Addition of indole-3-carbinol, a dietary product, restored the Rorγt+ ILC numbers [[55]]. Another study, however, suggested that endogenous ABT-199 in vitro AhR ligands, including the tryptophane catabolite kynurenine, were potent regulators of Rorγt+ ILC maintenance as removal of dietary AhR ligands in that study did not disturb Rorγt+ ILC homeostasis and function [[56]]. The differences may be due to different types of controlled diets used by the different groups.

Further experiments should aim to resolve these discrepancies. The mechanisms by which AhR controls Rorγt+ cell numbers are not fully understood. Microarray analysis of Rorγt+ cells from wt and AhR-deficient mice suggested that Notch 1 is a downstream target of AhR [[56]]. Consistent with this, administration by gavage of the toxin TCCD (2,3,7,8-tetrachlorodibenzo-p-dioxin) resulted in the upregulation of Notch1 and Notch2 in gut Rorγt+ ILCs. Evidence for a role of Notch in AhR-mediated maintenance of Rorγt+ ILCs was provided by the observation that mice deficient for RBP-Jk, an essential partner of Notch, showed substantially reduced numbers of NKp46-expressing Rorγt+ ILCs and, although less prominently, of CD4+ Rorγt+ ILCs (LTi cells) also [[56]]. However, there were differences between the AhR- and RBP-Jk-deficient mice, in that in the latter, cryptopatches and ILFs were largely intact, whereas they were greatly reduced in AhR-deficient mice [[56]].

The method also combined measurement of changes in Ca2+i using fluo-4 and excitation at 490 nm. Results:  After establishing loading conditions, a linear relationship was demonstrated between Em and fluorescence signal in FRET dye-loaded HEK cells held under voltage clamp. Over the voltage range from −70 to +30 mV, slope (of FRET signal vs. voltage, m) = 0.49 ± 0.07, r2 = 0.96 ± 0.025. Similar data were obtained in cerebral artery SMCs, slope (m) = 0.30 ± 0.02, r2 = 0.98 ± 0.02. Change in FRET emission ratio over the holding potential of −70 to +30 mV was 41.7 ± 4.9% for HEK cells and 30.0 ± 2.3%

for arterial SMCs. The FRET signal was also shown to be modulated by KCl-induced depolarization high throughput screening compounds in a concentration-dependent manner. Further, in isolated arterial SMCs, KCl-induced depolarization (60 mM) www.selleckchem.com/products/Rapamycin.html measurements occurred with increased fluo-4 fluorescence emission (62 ± 9%) and contraction (−27 ± 4.2%). Conclusions:  The data support the FRET-based approach for measuring changes in Em in arterial SMCs. Further, image-based measurements of Em can be combined with analysis of temporal changes in Ca2+i and contraction. “
“Please cite this paper as: Zhang (2011). Effect

of Suspending Viscosity on Red Blood Cell Dynamics and Blood Flows in Microvessels. Microcirculation 18(7), 562–573. To obtain a better understanding of the beneficial effect of high plasma viscosity observed in hemodilution and resuscitation experiments, we conducted a computational study to investigate

the suspending viscosity effect on red blood cell (RBC) dynamics and blood flow behaviors in microvessels. For single RBCs in simple shear or channel flows, RBCs appear more flexible as indicated by the tank-treading motion in shear flows and the strong transverse migration in channel flows. For the multiple RBC flows in straight channels, our results indicate no significant change with the suspending viscosity in stable flow structure and hemorheologic behaviors, under both constant Cepharanthine flow and forcing conditions. However, due to the increase in apparent cell deformability in a more viscous medium, the cell-free layer (CFL) can be established in a shorter distance along the channel. Considering the multilevel bifurcated structure of the microvascular network, this change in CFL development distance may affect the phase skimming and RBC separation processes at the downstream bifurcation, and therefore the microcirculation performance in the tissue. This may suggest a possible mechanism for the high functional capillary density associated with a high suspending viscosity observed in experiments. “
“Please cite this paper as: Folkesson KT, Samuelsson A, Tesselaar E, Dahlström B, Sjöberg F.

The etiology of AOSD remains unknown but viral infection has been suspected in its pathogenesis. Death in association with systemic features such as hepatic failure, amyloidosis, infection and disseminated intravascular coagulation has been reported and progression

into macrophage activation syndrome (MAS) is known. Several clinical and biochemical markers of inflammation observed in AOSD are similar to those of the systemic inflammatory response syndrome as fever, neutrophilia and hepatic acute phase protein synthesis are prominent in AOSD. Reducing TNF-α is often without effect whereas anakinra results in a rapid resolution of systemic and local manifestations of the disease within hours and days of the initial subcutaneous injection selleck kinase inhibitor 60. Reducing IL-1β activity in AOSD is now the standard therapy. Systemic onset juvenile idiopathic arthritis (SOJIA) is thought to be an auto-immune disease and treatable with tocilizumab (anti-IL-6 receptor); however, the disease has the characteristics of an auto-inflammatory disease

with increased secretion of IL-1β from blood monocytes and dramatic https://www.selleckchem.com/products/DAPT-GSI-IX.html responses to anakinra or canakinumab in patients resistant to glucocorticoids 22. SOJIA patients usually do not respond to anti-TNF-treatment 22, 61. Gattorno et al. 20 reported heterogeneous responses to IL-1 blockade by anakinra, with approximately one-half of the patients treated with anakinra experiencing rapid improvement whereas the other half exhibited either an incomplete or no response.

The responders in that study were characterized by higher absolute neutrophil counts but a lower number of disease-active joints before entering the trial. Thus, it is likely that a more systemic disease predicts a positive response to IL-1 blockade. Indeed, clinical experience reveals that in approximately 50% of SOJIA patients, arthritis tends to remit when the systemic features are controlled. In the other half, unremitting chronic arthritis Reverse transcriptase and joint damage occurs. Thus, durable treatment of SOJIA patients depends on the phase of the disease, that is, whether it is systemic or arthritic. Whereas anakinra treatment of SOJIA does not distinguish between a causative role for IL-1α or IL-1β, sustained responses to canakinumab have been consistently observed implying a role for IL-1β. MAS is also known as hemophagocytic syndrome and there is an inherited variant of MAS due to a mutation in perforin. Another related disease is termed cytophagic histiocytic panniculitis, which is characterized by daily high spiking fevers and severe panniculitis 62, 63. There is abnormal activation and proliferation of well-differentiated macrophages/histiocytes, together with increased phagocytic activity.

Instead, we have to manually mark matrix components on each successive image. Thus, we are able to reconstruct the interconnecting fibers also seen in conventional SEM, but as it relies on manual labor, it is not very precise GW-572016 solubility dmso (Fig. 5d). We find this tool very useful for ex vivo imaging of infected tissue. Further improvements in heavy metal contrasting of the specimens could potentially yield better BSED imaging of the matrix. We have tested four different techniques of SEM on P. aeruginosa biofilms (Fig. 6). Each method has obvious drawbacks but also distinct strengths, making it difficult to determine

which method is the most suitable for biofilm visualization. The conventional SEM together with FIB–SEM provides this website good information on spatial structure; however, Fig. 5 shows that the dehydration

preparative step leaves the bacteria exposed. Therefore, the technique is not suitable visualizing substances in the biofilm matrix. Here, the Cryo-SEM and environmental-SEM techniques are more suited, because they appear to leave the matrix unaffected (Fig. 5). However, the problem with these techniques is the poor resolution and hence limited magnification when compared to conventional SEM. Obviously, no single method for visualization exists at present time for visualizing the true architecture of the biofilm matrix. Therefore, it is important to first ask the scientific questions and subsequently chose the most appropriate method. In this study, no single method revealed the true nature of the biofilm, but if combined, the image data from the different methods are better able to predict the true architecture of the matrix. Probably, not many research centers will have all the above methods in hand, but caution should be taken when drawing conclusions based on only one method. Figure 7 outlines the advantageous contribution from each method to a more realistic biofilm structure. The authors would like to thank Grazyna Hahn Poulsen, for the artistic

presentation of the biofilm model, and the Villum Foundation and Novo Nordic Foundation for support to MG. “
“Simultaneous stimulation with antigen and Megestrol Acetate adenosine in mast cells induces a synergistic degranulation response at a low antigen dose that is insufficient to cause secretion by itself. This kind of stimulation is thought to be relevant to the immediate asthmatic response upon bronchial challenge with low-dose allergen. In this context, FcεRI- and adenosine receptor-mediated signalings cooperate to increase degranulation in mast cells. In the present study, we prepared mast cells that have mutations (Y219F/Y225F/Y229F) in three tyrosine residues of the FcεRI β-chain (FcRβ)-ITAM in order to elucidate the molecular mechanisms of degranulation response synergistically elicited by costimulation with low-dose antigen and adenosine. Introduction of mutations in the FcRβ-ITAM abolished the synergistic degranulation response.

5 versus Fostamatinib datasheet 38.5% in lane 5 versus lane 11 to 78.7 versus 21.3% in lane 6 versus lane 12). The densitometry data obtained from multiple blots confirmed the concomitant cytosolic accumulation of p48 and pY-STAT6 accompanied with a nuclear decrease in p48 prominent by 4 h post-IFN-α stimulation (Fig. 4B). Furthermore, co-immunoprecipitation experiments demonstrated that pY-STAT6 strongly interacts with IFN-α-induced pY-STAT2 as well as with p48 in the cytoplasm (Fig. 5A), which is also evident by 4 h after IFN-α treatment. On the other hand, neither STAT1 nor importin-α which is known to mediate

the nuclear translocation of STATs 35, interacted with pY-STAT6 (Fig. S3). By confocal analysis, the concomitant cytoplasmic accumulation of pY-STAT6 (green) and p48 (red), or that of STAT2 (green) and p48 (red) was also confirmed upon 4 h pretreatment of IFN-α followed by IL-4 stimulation (Fig. 5B). Together these data suggest that pY-STAT6 is likely to complex with IFN-α-induced pY-STAT2

and p48, and is retained in the cytosol. The concomitant cytosolic retention of pY-STAT6 by pY-STAT2:p48, and the subsequent decrease in pY-STAT6 nuclear translocation may be responsible for the inhibitory effect of IFN-α on the IL-4-activated CD23 gene expression in B cells (Fig. 1C). The above data indicate that IFN-α and IL-4 treatment induced a concurrent cytoplasmic accumulation and complex Selleckchem Buparlisib formation of the IFN-α-induced pY-STAT2:p48 and the IL-4-induced pY-STAT6 in Ramos B cells. As much as the resulting retention of pY-STAT6 by pY-STAT2:p48 in the cytoplasm may lead to the suppression

of IL-4 signaling into Baricitinib the nucleus, the retention of pY-STAT2:p48 by pY-STAT6 would have a similar role in the inhibition of nuclear localization of ISGF3 induced by IFN-α. In fact, IL-4 is shown to exert an antagonistic action on IFN-α signaling in certain cell systems 17. As an IFN-α target gene counter-regulated by IL-4 in B lymphoma cells, IRF7 was examined. As a member of IRFs involved in IFN-α response, IRF7 has been reported to be induced via IFN-α-activated ISGF3 in lymphomas and DC, and to play a role in the induction of EBV-transformed lymphoma and the activation of type I IFN genes 17, 36, 37. The quantitative RT-PCR analysis of IRF7 mRNA in Ramos B cells has revealed that IFN-α treatment induced IRF7 at a significant level by 4 to 8 h, and IL-4 reduced IFN-α-induced IRF7 mRNA levels in a time-dependent manner (Fig. 6). The result together with the data from Figs 3–5 raises a possibility that the inhibition of IL-4 on the IFN-α-induced IRF7 gene expression (Fig. 6) is probably interceded by the complex formation and cytoplasmic retention of the pY-STAT6:pY-STAT2:p48.

During these analyses, find protocol it was noticed that there were two forms of cellular mass displaying different histological characteristics (Fig. 2). In one type, cells were confined to a single layer of the skin, surrounded by normal tissue (Fig. 2a,b); however, in the other type,

inflammatory cells were found spread throughout the layers of the skin (Fig. 2c,d). Upon assessment of sections for these characteristics, none of the sections from PC61-treated mice, and around half of the GL113-treated mice, displayed the ‘confined’ phenotype (Fig. 2e). This is noteworthy when compared with the percentage of mice that reject these tumours; approximately 50% in GL113-treated mice and 100% in PC61-treated mice.9 To perform a more quantitative assessment of the differences between cellular masses termed ‘confined’ versus those termed ‘non-confined’, the total volume of each cellular mass within the GL113-treated and PC61-treated groups (> 4 per group),

4 and 24 hr Aloxistatin after tumour cell inoculation, was calculated. These data, shown in Fig. 3(a), corroborated our previous observation in that at 24 hr larger masses were observed in the PC61 group compared with those treated with GL113. At later time-points (96 hr), larger cellular masses were measured in the latter, control group of mice, coinciding with detection of live tumour cells in this group. Live tumour cells were identified by histological examination of H&E-stained Astemizole sections in GL113-treated mice but not in PC61-treated mice. In the former group, within the tumour cell mass, amid cell debris, there are areas of homogeneous healthy cells, forming foci of organized tissue, similar to that seen in large, established tumours (Fig. 3b,c). These data are consistent with the observation that around 50% of mice inoculated with B16FasL develop palpable tumours whereas tumours

are rarely seen in B16FasL-inoculated mice pre-treated with PC61.9 Overall, these data indicate that an inflammatory infiltrate into the tumour creates a disorganized, non-confined mass that is associated with tumour cell death and tumour rejection, favoured by depletion of Treg cells by PC61 mAbs. We were struck by how rapidly Treg-cell depletion affected the accumulation of inflammatory cells at the site of the tumour cell inoculum. The ability of Treg cells to suppress an inflammatory response within hours of an antigenic challenge and at a peripheral site implies that skin-resident Treg cells are rapidly mobilized. To visualize Treg cells at the site of tumour cell challenge, skin sections were stained with Foxp3-specific mAbs. Foxp3+ cells were found in the skin and particularly at the site of tumour cell inoculation (Fig. 4). This is in agreement with other studies reporting Treg-cell identification in the skin of mice16 and humans.17 Stained cells were not observed in sections prepared from PC61-treated mice (data not shown).

Analysis was performed on a BD fluorescence activated cell sorter (FACS) FACSCantos using FACS Diva software. All reagents for immunostaining were from BD Biosciences (San Diego, CA, USA). Plasma levels of GM-CSF (BD Biosciences) and PGE2 (R&D Systems, Minneapolis, MN, USA) were measured by ELISA and performed according to the manufacturers’ instructions. Degree of bone erosion

was analysed by two graders using a previously published staging system [32]. A computed tomography (CT) bone remodelling score was assigned by both graders and then averaged to yield a mean CT bone erosion selleck score for each patient. Graders were blinded to age, race, gender and VD3 status of the patients. Statistical analysis was conducted using GraphPad Prism version 5.02 software (La Jolla, CA, USA). Values were first determined to follow a normal distribution using a D’Agostino and Pearson omnibus normality test. A one-way analysis of variance (anova) with post-hoc unpaired Student’s t-test was then used to determine statistically significant differences between patient

cohorts and indicated parameters. A Pearson’s correlation analysis was used to determine if there was a correlation between VD3 levels and the aforementioned immune parameters. Two-way anova was conducted to determine if differences observed in VD3 levels were influenced by age, gender, body mass index (BMI) or race. Within the subset of patients whose mean CT bone remodelling score was greater than 0, an unpaired selleck chemicals t-test was used to determine statistical significance those with adequate VD3 (greater than or equal to 32 ng/ml) or insufficient VD3 levels (<32 ng/ml) on the CT bone remodelling score. An unpaired Student's t-test was

used to determine differences in bone erosion scores between VD3-deficient and -insufficient patients. A Pearson’s correlation analysis was used to determine if there was a correlation between VD3 levels and bone erosion severity. In these retrospective studies, we examined PBMCs from patients with CRSsNP, CRSwNP or AFRS to determine if there were differences Celecoxib in circulating numbers of APCs and monocytes compared to controls. First, expression of CD86 was assessed due to its role in Th2 initiation [5,6]. Compared to controls, we found elevated numbers of CD86+ PBMCs in CRSsNP (P = 0·007), CRSwNP (P < 0·0001) and AFRS (P < 0·0001) (Fig. 1a). There was no statistically significant difference between CRSsNP and CRSwNP (P = 0·368) or AFRS (P = 0·190). Next, staining for CD209 and CD68 was conducted to identify circulating DCs and macrophages, respectively, more definitively. Only CRSwNP and AFRS displayed elevated levels of CD209+ DCs (Fig. 1b) compared to control (P < 0·0001 for each group). CRSwNP and AFRS circulating DC numbers were also elevated compared to CRSsNP (P = 0·0001 and P = 0·0014, respectively). Similar to the CD209 results, circulating numbers of CD1c+ DCs (Fig.

, 2000). Chemotherapy with praziquantel is the cornerstone of schistosomiasis control. Assessment of the impact of mass treatment with praziquantel is usually by determining the prevalence of the infection and presence of PPF (Mohamed-Ali et al., 1991). In Sudan, Mohamed-Ali et al. (1991) and Doehring-Schwerdtfeger et al. (1990) reported a reduction of egg excretion and reversibility of PPF 7 and 23 months, respectively, after praziquantel PF-562271 ic50 treatment, while the same finding was reported by Homeida

et al. (1996) after both annual and biennial treatment. Reports by the Homeida group, in their studies in Sudan, have shown that the factors that control fibrosis regression are age, gender and the grade of fibrosis. Young patients with lower PPF grades tend to respond more to antischistosomal chemotherapy (Homeida et al., 1991, 1996; Kheir et al., 2000).

Based on the above findings, and because the SM2 locus was reported to control the progression of the disease (Henri et al., 2002), it was suggested that the regression of PPF (reversibility) could also be under genetic control. Thus, the aim of this study is to evaluate the factors controlling the regression of liver fibrosis in S. mansoni-infected subjects after praziquantel therapy. This study was carried out between 1999 and 2002 in Um-Zukra village, Gezira state, Managil province, Central Sudan. The village is about 350 km south of Khartoum (the capital)

and 110 km west of Wad Medani town, in the Managil extension DNA Damage inhibitor agricultural scheme. The Gezira and Managil irrigated scheme involves about two million acres, cultivated by cotton and other crops, and populated by about 1.5 Acesulfame Potassium million individuals. The study area was selected according to the prevalence of S. mansoni infection. Random stool samples were obtained from different villages in the Gezira state, and examined for S. mansoni eggs. The highest prevalence (50%) was found in Um-Zukra village. The population of Um-Zukra is about 4000individuals (according to a census performed in 1999), belonging to three tribes, mainly the Kawahla (80%), in addition to Rawashda and Galeen (20%). The village is surrounded by cultivated area and the canal is only 450 m from the center of the village. There are two water pumps (wells) that are used for drinking water. The other water source for domestic use (washing and bathing) is the canal. Each house was given a number from 1 to 629. The numbers were written on metallic plates and fixed on all houses, and pedigrees for the study subjects were drawn. Plastic containers for stool samples were distributed to the villagers according to the house and individual numbers. The Schistosoma mansoni egg count g−1 stool was conducted in November 1999 using Kato’s method (Katz et al., 1972) on three stool samples collected on different days before treatment.