The six seed ROIs selected for this analysis were defined in the left hemisphere according to anatomical criteria (see Experimental Procedures; see also Figure S1 and

Table S1 available online) and included the lateral prefrontal cortex (LPFC), posterior part of inferior frontal gyrus (IFG), “hand knob” area of central sulcus (CS), anterior intraparietal sulcus (aIPS), posterior part of superior temporal gyrus (STG), and lateral occipital sulcus (LO). Selecting right hemisphere ROIs would have yielded a complementary analysis with equivalent findings. Strong correlations with the seed time course were found in voxels adjacent to the location of the seed (white ellipses, Navitoclax research buy Figure 1) and in voxels located in the homologous

area of selleckchem the contralateral right hemisphere. Note two important points. First, the voxels that exhibited correlation with each seed showed high spatial selectivity with very little overlap across seeds: this means that the spontaneous activity found for each seed and its corresponding contralateral location was relatively unique and different from that found for each of the other seeds and their contralateral locations. Second, the strength and spread of correlation in the contralateral locations are qualitatively similar across groups in all areas except for STG and IFG, which appear abnormally reduced in the autism group. Voxel-by-voxel comparisons showed that toddlers with autism exhibited significantly weaker interhemispheric correlations than both typically developing and language-delayed toddlers in the STG, a cortical area commonly associated with language processing (Figure 2). The comparisons of the heptaminol autism group to each of the other groups were independent of one another, yet both revealed significant synchronization differences only in voxels located within the STG. This analysis was performed by first computing the correlation between the time course of each left-hemisphere voxel and the time course of its corresponding contralateral right-hemisphere

voxel in each subject. This gave us an interhemispheric correlation value for each pair of corresponding left/right voxels, which signified their synchronization strength. We then performed a t test for each voxel, contrasting the correlation values across individuals of different groups. This analysis yields symmetrical results across the two hemispheres, hence the presentation of the voxel-wise group differences only on the left hemisphere. Presenting the results on the right hemisphere yields a reciprocal “mirror image. The results found in STG raised the possibility that poor interhemispheric synchronization may be a characteristic of the language system in toddlers with autism. To evaluate this further, we performed an ROI analysis in six anatomically defined ROIs that included two putative language areas, STG and IFG, and four control areas, LO, aIPS, CS, and LPFC.

For DRD4, the variable number of tandem repeats (VNTR) has been shown to affect DRD4 functioning (Schoots and van Tol, 2003). Individuals carrying the 7 repeat (7R) VNTR of DRD4 (from now on referred to as L-DRD4) have a reduced sensitivity to dopamine when compared to individuals carrying only shorter variants (S-DRD4) (Asghari et al., 1995 and Oak et al., 2000). Functioning of the dopaminergic system, especially in the striatum, has been associated with individual differences

in reward-related traits, such as impulsivity and novelty seeking (Cloninger, 1987), and to disorders that involve enhanced reward-seeking, including substance use disorders (Hyman et al., 2006). As such, it has been suggested that individuals with hypodopaminergic functioning, including L-DRD4 and those carrying the A1 allele of the TaqIA polymorphism, are more likely to manifest drug-seeking behavior in order to Doxorubicin order compensate for their reduced sense of reward (Blum et al., 2000). Although these polymorphisms have indeed been associated with, among others, alcohol-related phenotypes, smoking and illicit substance abuse, other studies have failed to replicate such associations or have found opposing links (Lusher et al., 2001, Noble, 2003 and McGeary et al.,

2007). Only few studies have examined the genetic effects of DRD2 and DRD4 on substance use and abuse during Screening Library in vitro adolescence, and with mixed results. For instance, whereas sons of alcoholics carrying the A1 allele of the DRD2 TaqIA polymorphism have been found to try and get

intoxicated on alcohol more often, and to experience their first marijuana high on a younger age (Conner et al., 2005), community and clinical studies did not identify any direct genetic effects on quantity (Hopfer et al., 2005) and frequency of alcohol consumption (Guo et al., 2007 and van der Zwaluw et al., 2009), problematic alcohol or other drug use (Esposito-Smythers et al., 2009) and early onset alcohol use disorder (Sakai et al., 2007) in adolescents younger than 19 years old. In the latter study, 93% of the adolescents with early onset alcohol use disorder reported comorbid cannabis abuse or dependence, suggesting absence MTMR9 of effects of DRD2 TaqIA on comorbid alcohol and cannabis use disorder (Sakai et al., 2007). When the focus is on DRD4 and adolescent substance use, findings from a high-risk community sample indicate that male, but not female, 7R carriers drink higher amounts of alcohol per occasion and have greater lifetime rates of heavy drinking than male participants without this allele (Laucht et al., 2007). Contrastingly, McGeary et al. (2007) did not find support for an association between L-DRD4 and adolescent alcohol use, nor marijuana use, in a clinical sample of adolescents. In conclusion, a small number of studies assessing the direct effects of the DRD2 and DRD4 polymorphisms on various alcohol and cannabis-related phenotypes during adolescence has yielded inconsistent results.

Threlfell et al. (2012) also demonstrated that optical stimulation of thalamic projections to ChIs could mimic the effect of direct activation of ChIs, raising the remarkable possibility that the thalamic intralaminar nuclei can control DA release—a situation they are well positioned to do, given their sensitivity to salient stimuli (Matsumoto Ivacaftor solubility dmso et al., 2001). The paper in Cell Reports by Cheer’s group ( Cachope et al., 2012) describes a very similar

scenario in the ventral striatum-nucleus accumbens (NAc). In addition to showing that optogenetic stimulation of a population of ChIs induces DA release in slices of the NAc, Cachope et al. show that the same thing happens in vivo. One apparent point of divergence with the Threlfell et al. work is the

inferred role of glutamate. Threlfell et al. found no effect of glutamate receptor antagonists on the ChI-induced DA release, but Cheer’s group did find a partial reduction in release with the antagonism of AMPA receptors. They linked this to the recently described corelease of glutamate and ACh by ChIs ( Higley et al., 2011). However, because this release is rapidly http://www.selleckchem.com/products/OSI-906.html lost at the normal spiking rates of ChIs, its enhancement of DA release would be limited to rebound spiking after a long pause. How does Threlfell et al.’s discovery change our understanding of the striatum? First, their work has vindicated the findings of the French group led by Glowinski, who emphasized intrastriatal

control of DA release decades ago but who had few adherents. Clearly, DA release is not driven solely by the substantia nigra. Quite remarkably, even the thalamus can drive DA release in the striatum through the mechanism that Cragg and colleagues have outlined. either Moreover, the model that DA and ACh simply oppose one another—as in the feud metaphor—needs to be fundamentally revised. A revision doesn’t mean, however, that these two neurotransmitters are bosom buddies. DA does suppress ACh release, even if the converse is not true. Moreover, there is still compelling evidence that DA and ACh can have opposed effects on striatal physiology. For example, the induction of long-term depression at corticostriatal synapses of principal spiny projection neurons (SPNs) is promoted by an elevation in DA and a fall in ACh (Bagetta et al., 2011 and Wang et al., 2006). In indirect pathway SPNs that express D2 DA receptors, DA clearly depresses intrinsic excitability, and ACh increases it through activation of M1 muscarinic receptors (Gerfen and Surmeier, 2010). In direct pathway SPNs that express D1 DA receptors, the situation appears to be more nuanced by the coexpression of M1 and M4 muscarinic receptors. In vitro studies of ACh regulation of DA have been plagued by the difficulty in selectively stimulating particular microcircuits. When and where you stimulate matters, as shown by both Threlfell et al. and Cachope et al.

Given the large number of comparisons, some statistically significant differences in this study may have occurred by chance. Another limitation of this study is the lack of a control group, which may affect the interpretation of the results. Nevertheless, previous short-term (i.e., PI3K inhibitor 4–15 weeks) Tai Chi intervention studies found positive results in the Tai Chi group in comparison with a sedentary group.26 and 27 Therefore, the outcome pre-test is used as the baseline, and further studies are needed to understand the mechanisms of

the effect of Tai Chi on balance. Our preliminary findings indicate that Tai Chi may be a positive method for improving balance and other physical functions, such as RT and flexibility, among the older males. Longer-term studies involving additional factors related to balance are needed to improve our understanding of the biological mechanisms by which Tai Chi affects balance. This study was supported by the Major Program of Shanghai Science Technical Committee, Shanghai (No. 08490512800) and Shanghai Key Disciplinary Areas III of China

(No. S30803). “
“Central sensitization has become an important topic in the study of whiplash-associated dissorders.1, 2, 3, 4 and 5 It has been postulated that chronic pain in whiplash-associated PI3 kinase pathway disorders is the result of or involves the phenomenon of central sensitisation.1, 2 and 3 That is, following acute whiplash injury, and resolution of the inflammation and process of healing of the peripheral Phosphoprotein phosphatase pathology, it is postulated that some individuals continue to have pain in the absence of a peripheral stimulus. This phenomenon is called central sensitisation.

Prolonged or strong activity of dorsal horn neurons caused by repeated or sustained noxious stimulation may subsequently lead to increased neuronal responsiveness or central sensitisation.6 and 7 Neuroplasticity and subsequent central nervous system sensitization include altered function of chemical, electrophysiological, and pharmacological systems.8, 9 and 10 These changes cause exaggerated perception of painful stimuli (hyperalgesia), a perception of innocuous stimuli as painful (allodynia) and may be involved in the generation of referred pain and hyperalgesia across multiple spinal segments.11, 12, 13 and 14 Nevertheless, the extent to which it is a result or a cause of chronic pain (or both) has not been fully elucidated.1 The presence of ongoing signs of central sensitization may reflect a lack of recovery, but measurement of central sensitization in the primary care setting is challenging, requiring either specific physical examination measures or instruments.2 Recovery from whiplash injury can be assessed by a number of measures.

Therefore, PlexB-mediated Sema-2b signaling solidifies specific projection positioning originally established by the Robo code. Together, these two distinct Robo and plexin guidance cue signaling modules function in a sequential and complementary fashion to specify both long range medial-to-lateral positioning (Robo) and short-range local fasciculation (PlexB). PlexA, the other Drosophila plexin receptor, and its ligand Sema-1a are specifically required for the proper formation of the 1D4-l pathway ( Winberg et al., 1998b and Yu et al., 1998). However, Sema-1a Sirolimus mw does not show

restricted expression within the medio-lateral axis of the nerve cord analogous to that observed for Sema-2b ( Yu et al., 1998), suggesting a different mechanism may underlie Sema-1a–PlexA regulation

of fasciculation in the most lateral CNS longitudinal region. Following medio-lateral specification by Slit-Robo VRT752271 clinical trial signaling and general organization of longitudinal regions by Sema-plexin signaling, additional cues are likely to mediate local interactions among neural processes already restricted to defined regions in the neuropile. Several cell surface proteins may serve such functions; for example, the cell adhesion molecule (CAM) connectin, like Sema-2b, shows exquisitely restricted expression along a subset of longitudinal projections (Nose et al., 1992). More widely expressed CAMs also play important roles in maintaining the fasciculated state of longitudinally projecting processes that are part of the same connective; indeed, in the absence of the Drosophila Ig super family member FasII, axons that contribute to the MP1 pathway show reduced association when examined at high resolution ( Lin et al., 1994). Therefore, an ensemble of short-range cues expressed in distinct subsets of longitudinally projecting neurons allows for individual pathways to be established following more global restriction to appropriate locations, and as we demonstrate here, this process is critical for the neural circuit function. It seems likely that similar mechanisms underlie the segregation of complex trajectories, the establishment

of laminar organization, and the formation of discrete neural maps in other regions of invertebrate Thymidine kinase and vertebrate nervous systems ( Matsuoka et al., 2011 and Sanes and Yamagata, 2009). Our analyses allow for a comparison between the effects of the secreted semaphorins Sema-2a and Sema-2b on both CNS interneuron trajectories and sensory afferent targeting within the CNS. We observed in both LOF and GOF genetic paradigms that Sema-2a acts as a repellent, consistent with previous observations (Ayoob et al., 2006, Bates and Whitington, 2007, Carrillo et al., 2010, Matthes et al., 1995, Winberg et al., 1998a and Zlatic et al., 2009). Sema-2b, in contrast, serves an opposite guidance function and promotes neurite fasciculation.

Functional hyperemia is attenuated after experimental and clinical focal ischemia, (Girouard and Iadecola, 2006). It is currently unclear whether this reduction represents a decoupling of functional hyperemia by impaired cerebrovascular reactivity (Kim et al., 2005 and Rossini et al., 2004), or whether neurovascular coupling is preserved, but has a reduced amplitude because the underlying

neuronal activity is attenuated (Bundo et al., 2002, Weber et al., 2008 and Zhang and Murphy, 2007). Moreover, ischemia also reduces the ability of endothelial Autophagy Compound Library solubility dmso cells to initiate vasodilation (Kunz et al., 2007). Functional hyperemia is also reduced following global cerebral hypoxia (Schmitz et al., 1998), and in arterial hypertension (Girouard and Iadecola, 2006). In addition, pericyte-mediated contraction of capillaries may also contribute to the perturbation of blood flow after cerebral high throughput screening assay ischemia (Yemisci et al., 2009). During migraine aura, as well as after stroke,

traumatic brain injury, and subarachnoid hemorrhage, spreading waves of neuronal depolarization occur (Lauritzen et al., 2011). In the healthy brain and during migraine aura, these events are associated with a transient increase in local CBF (Hadjikhani et al., 2001 and Lauritzen, 1987), and do not induce overt neuronal injury (Nedergaard and Hansen, 1988). However, during ischemia, as well as after brain injury or hemorrhage, the coupling between these neuronal depolarization waves and CBF is inverted, such that the increased neuronal activity is accompanied by a drop of CBF to ischemic levels, indicating that this inverted neurovascular coupling may contribute to tissue damage (Dohmen et al., 2008, Dreier et al., 2009, Petzold et al., 2003 and Shin et al., 2006). Functional hyperemia is also perturbed in Alzheimer’s disease (Iadecola, 2004). In patients, resting CBF is reduced early in the disease (Johnson and Albert, 2000), and functional hyperemia is significantly impaired in animal models and patients (Hock et al., 1996, Nicolakakis et al., only 2008, Niwa et al., 2000b, Park et al., 2004, Park et al., 2008, Shin et al., 2007, Smith

et al., 1999 and Tong et al., 2005). Amyloid-β, the main constituent of amyloid plaques in the brains of patients with Alzheimer’s disease, is vasoactive in vitro (Crawford et al., 1998) and in vivo (Niwa et al., 2000b), and soluble amyloid-β contributes to the reduction of functional hyperemia in animal models in vivo (Niwa et al., 2001b and Park et al., 2004), although it has also been suggested that insoluble amyloid plaques and amyloid angiopathy are necessary for this effect (Christie et al., 2001, Hu et al., 2008 and Shin et al., 2007). This perturbation of neurovascular coupling, together with nonvascular mechanisms triggering neurodegeneration, may have synergistic detrimental effects on cognition and memory in this disease (Iadecola, 2004).

One or two micromolars dynamin 1 were incubated with equimolar CSPα or Hsc70 in the presence of 1 mM ATP at 37°C. The incubation mixtures were first separated on a Superose 6 column or directly analyzed on SDS-PAGE and immunoblotted

for dynamin 1. Synaptosomes were preincubated for 15 min at 37°C and then incubated for 1 min at room temperature after adding 1 mM DSS. The reaction was stopped by adding 100 mM Tris-HCl (pH 8.0) for 15 min at room temperature. All values are presented as the mean ± SEM, and p < 0.05 was considered statistically significant. Calculations were performed using the GraphPad Prism 4 software (San Diego, CA, USA). We would like to thank Thomas Südhof, Pietro De Camilli, Art Horwich, Thomas Biederer, and members of our laboratory Ibrutinib research buy for critical discussions related to this paper. We would like to thank Karina Vargas for technical help with electron microscopy

and Ivacaftor nmr Becket Greten-Harrison for quantitative immunoblotting of human brain samples. This work was supported by the YCCI Scholar Award (CTSA Grant UL1 RR024139; to S.S.C.), R01NS064963 (to S.S.C.), an Anonymous Foundation (to S.S.C.), W.M. Keck Foundation grant (to S.S.C.), NIDA Neuroproteomic Pilot Grant (5 P30 DA018343-07; to S.S.C.), Anderson Fellowship (to Y-Q.Z.), NSF Graduate Research Fellowship (to M.X.H.), and AG14449 (to S.D.G.). “
“Motorneuron nerve terminals host thousands of synaptic vesicles (Rizzoli and Betz, 2005) that release neurotransmitters upon the arrival of action potentials (Katz, 1969). Many motorneurons trigger hundreds of thousands of action potentials a day (Hennig and Lømo, 1985) driving synaptic vesicles into multiple cycles of rapid exo- and endocytosis (Maeno-Hikichi et al., 2011). The synaptic vesicle cycle is governed by precisely regulated, extremely fast, and spatially restricted

protein-protein interactions. Exemplary reactions are the priming of SNARE complex to trigger fast Ca2+ dependent exocytosis and the dynamin1-dependent retrieval of plasma membrane (Slepnev and De Camilli, 2000 and Sudhof, 2004). Although not well known yet, the effect of the maintained synaptic activity is probably a source of protein-stress causing subtle, but nevertheless cumulative, damage see more in protein folding. Under those conditions, molecular chaperones act to save proteins from irreversible unfolding. Indeed, vertebrate synapses are probably endowed by chaperones that protect proteins from stress-dependent degradation and prevent long term failures of nerve terminal function (Muchowski and Wacker, 2005). However, the most vulnerable synaptic proteins and the mechanisms protecting them are poorly understood. The existence of those mechanisms is supported by studies in which cysteine string protein-α (CSP-α) expression has been inactivated in knock-out mice (Chandra et al., 2005 and Fernández-Chacón et al., 2004; Schmitz et al., 2006).

Gerstner, Jr. Young Investigators Award (J.A.K.). The content of this study is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health. “
“Network oscillations in the theta and gamma frequency range are thought to represent key reference signals for temporal encoding of information

in neuronal ensembles (Buzsáki and Draguhn, 2004 and Lisman and Jensen, 2013). The power of theta-gamma oscillations is particularly high in the dentate gyrus of the hippocampal formation (Bragin et al., BTK inhibitor 1995 and Csicsvari et al., 2003). However, the underlying synaptic mechanisms are unclear (Buzsáki, 2002). The classical view suggests that theta activity is driven by cholinergic or GABAergic LY2157299 input from the medial septum (Stewart and Fox, 1990 and Freund and Antal, 1988), while gamma activity is generated by GABAergic interneurons via recurrent or mutual inhibition mechanisms (Bartos et al., 2007; Figure 1A). In apparent contrast, previous studies demonstrated that theta-gamma oscillations in the dentate gyrus are markedly reduced by lesions of the entorhinal cortex (Bragin et al., 1995), suggesting a potential role of excitatory inputs for both theta and gamma rhythms in behaving animals (Figure 1B). However, the temporal structure of the excitatory input and its correlation with the local field potential (LFP) are unknown. Dissecting

the synaptic mechanisms underlying rhythmic patterns in the LFP has remained difficult, since perisomatic inhibition and dendritic excitation produce indistinguishable current sink-source patterns (Mann et al., 2005). Theta-gamma oscillations are thought to have important computational functions in the network. First, they may represent a reference signal for

temporal encoding of information (Lisman and Jensen, 2013). Second, they facilitate communication between principal neurons by synchronization (Fries, 2009 and Akam and Kullmann, 2010). Recent modeling suggested that gamma oscillations could also contribute to the selection of cells that receive the highest excitation level by a “winner takes all” mechanism (de Almeida et al., 2009a and de Almeida et al., 2009b). Such a mechanism during may be particularly useful in the dentate gyrus, where it could potentially participate in both pattern separation and the conversion of grid into place codes (Hafting et al., 2005 and Leutgeb et al., 2007). However, it is not known whether the properties of excitatory postsynaptic currents (EPSCs) and inhibitory postsynaptic currents (IPSCs) in hippocampal granule cells (GCs) are consistent with the predictions of such a model regarding temporal and spatial characteristics (e.g., gamma modulation and network coherence; de Almeida et al., 2009a and de Almeida et al., 2009b). In the present paper, we intended to address three major questions.

Subjects were shown the first four parts in one session. After a short break, the second four parts were VEGFR inhibitor shown. Movie scenes at the end of fourth part and eighth part were matched to the movie scenes at the end of the first session and the second session of the Princeton movie study. Subjects were instructed simply to watch and listen to the movie and pay attention. The movie was projected with an LCD projector onto a rear projection screen that the subject could view through a mirror. The soundtrack for the movie was

played through headphones. In the face and object study, subjects viewed static, grayscale pictures of four categories of faces (human female, human male, monkeys, and dogs) and three categories of objects (houses, chairs, and shoes). Images were presented for 500 ms with 2 s interstimulus intervals. Sixteen images from one category were shown in each block, and subjects performed a one-back repetition detection task. Repetitions were different pictures of the same face or object. Blocks were separated by 12 s blank intervals. One block of each stimulus category was presented in each of eight runs. In the animal

species study, subjects viewed static, color pictures of six animal species (ladybug beetles, luna moths, mallard ducks, yellow-throated warblers, ring-tailed lemurs, and squirrel monkeys). Stimulus images showed full bodies of animals cropped out from the original background and Bortezomib overlaid on a uniform gray background. Images subtended approximately 10° of visual angle. These images were presented to subjects using a slow event-related design with a recognition

memory task. In each event, three images of the same species were presented for 500 ms each in succession followed by 4.5 s of fixation cross. Each trial consisted of six stimulus events for each species plus one 6 s blank event (fixation cross only) interspersed with the stimulus events. Each trial was followed by a probe event, and the subject indicated whether the probe event was identical to any of the events seen during the trial. Order of events was assigned pseudorandomly. Six trials were presented in each Rolziracetam of ten runs, giving 60 encoding events per species for each subject. Data were preprocessed using AFNI (Cox, 1996; http://afni.nimh.nih.gov). All further analyses were performed using MATLAB (version 7.8, MathWorks) and PyMVPA (Hanke et al., 2009; http://www.pymvpa.org). Software for hyperalignment is available as part of PyMVPA (Hanke et al., 2009; http://www.pymvpa.org), and data from these studies also can be downloaded from the PyMVPA website. Activation in a set of voxels at each time point can be considered as a vector in a high-dimensional Euclidean space with each voxel as one dimension. We call this a time-point vector and the space of voxels a voxel space.

, 2006). One could explain this as an effect of parasite strain sub-structuring

leading to differential transmission among definitive host species. In contrast, Rudge et al. (2009) HKI272 reported a clustering of isolates from dogs and bovines in marshland areas and humans, rodents and dogs in highland areas of China, but often found little differentiation among parasite sub-populations of different host types in sympatry. These authors suggested that patterns may differ even among local villages or between years ( Rudge et al., 2009). In contrast to S. japonicum, S. mekongi is regarded as a parasite maintained mostly through transmission via human populations. S. mekongi uses the snail Neotricula aperta as its intermediate host and published records identify the following foci of S. mekongi transmission: Ban Hat-Xai-Khoun, Khong Island, southern Laos ( Harinasuta and Kruatrachue, 1962); Kratie in Kratie

Province, northeastern Cambodia, approximately 180 km downstream of Khong Island ( Audebaud et al., 1968); and San Dan, Sambour District, also in Kratie Province ( Biays et al., 1999). All the aforementioned sites lie along the lower Mekong River. More recently, transmission of the parasite has been discovered in tributaries of the Mekong river, but also within the Mekong Basin, namely at Sa Dao in the Xe Kong river of Cambodia ( Attwood et al., 2004). The potential human population at risk from Gemcitabine Mekong schistosomiasis is currently over 1.5 million ( Attwood et al., 2008), with around 800 people infected in Laos and around 2000 in Cambodia (crude estimates

based on prevalence data in Urbani et al., 2002 and Muth et al., 2010). At Sa Dao, no human infections were detected in 2004, but the disease re-emerged in 2005 ( Sinuon et al., 2007). In addition, in 2004 the prevalence of infection among N. aperta collected at Sa Dao was 0.14% ( Attwood et al., 2004). Similarly, despite an almost eight-fold reduction in the prevalence in the human population at Khong Island in Laos (1969–2003), the estimated prevalence in the local N. aperta populations had changed little ( Attwood et al., 2001). These observations Terminal deoxynucleotidyl transferase suggest that there may be a significant zoonotic component to the transmission of S. mekongi. Prevalences of 12.2% and 3.6% for pigs (in Laos) and dogs (in Cambodia), respectively, provide direct evidence for the importance of reservoir hosts ( Strandgaard et al., 2001 and Matsumoto et al., 2002). Surveys of cows, water buffalo, pigs, horses and field rats in 5 villages of Kratié Province (Cambodia) failed to detect any infection with S. mekongi (see ( Matsumoto et al., 2002). Historical surveys have detected no natural infections in water buffalo ( Schneider, 1976) and reported a similar prevalence in dogs at Kratié ( Iijima et al., 1971), suggesting that the recent findings represent a long term equilibrium state. Human schistosomiasis in Malaysia is caused by S. malayensis.