The histologic diagnosis was based on the presence of signet ring cells filled with cytoplasmic mucus-containing vacuoles compressing and displacing the nucleus into a peripheral crescent alongside the cell wall. The component signet ring cells are variable; it is >75% in almost half the cases.5 Our first case was an invasive tumor, which extended to the perivesical fat. Indeed, the insidious progression

of this entity explains the local character already advanced at diagnosis. At the time of diagnosis, about 25% of patients have distant metastases and approximately 50% have stage IV disease.6 Primary signet ring cell carcinoma of the urinary bladder has an ominous prognosis as it is diagnosed at an advanced stage. The treatment is surgical and consists of an early radical cystectomy. Resection is often incomplete with

no clear margins on the specimen.7 Considering the rarity of this histologic type of tumor, there is no consensus regarding the management after HKI 272 surgical care. Chemotherapy and radiation therapy are discussed. Adjuvant chemotherapy with 5-fluorouracil associated with adriablastin or bleomycin seems to give favorable responses, by analogy with stomach plastic linitis.8 Our second patient had no palliative chemotherapy because of altered general condition. The primary SRCC of the urinary bladder is a rare and aggressive tumor; the histologic I-BET151 purchase type justifies a surgical strategy associated with a multidisciplinary approach. Prognosis is poor although some patients may benefit from surgical resection. Adjuvant chemotherapy should be discussed even if consensual attitude has not been defined. “
“A rare variant of lipoma, angiomyxolipoma (vascular myxolipoma) was first reported by Mai et al1 in 1996. The tumor was composed of an admixture of myxoid stroma, mature adipose tissue, and vascular crotamiton channels. Since then, an additional 17 cases have been reported across a broad age range and in different locations. We report the first case in English medical literature of renal angiomyxolipoma in an adult male. Among adult soft-tissue tumors, adipose tissue tumors are by far the most common.

Although ordinary subcutaneous lipomas do not represent a major diagnostic problem, the remaining benign tumors and tumor-like lesions of adipose tissue can be more challenging, especially if occurring at unusual locations and/or containing other tissue elements.2 and 3 Our case will be the 18th reported case of angiomyxolipoma and the first of renal origin. A review of the literature along with a discussion of diagnosis and follow-up are illustrated in the report. We report a 43-year-old man who presented to our urology clinic with left flank pain of 1-year duration. On investigation, he was discovered to have bilateral kidney masses and splenomegaly after a computed tomography (CT) scan (Fig. 1). Radiologic findings were highly suspicious for lymphoma in the presence of splenomegaly and distal ileal wall thickening.

Serum-resistant strains down-regulate complement activation on their surface by expressing PorB molecules that bind C4b-binding protein or factor H [21]. Phase

variation of glycosyltransferase genes can cause production of LOS species that are more resistant to bactericidal antibodies [22]. Survival of Gc within PMNs may prolong infection and increase dissemination and transmission and occurs by mechanisms not yet fully elucidated [23]. During acute infections, Gc induces a purulent exudate that consists of PMNs, exfoliated epithelial cells, and intracellular and extracellular Gc. The capacity of Gc to evade the inflammatory response is supported Pomalidomide research buy by the observation that Gc colonization levels are similar in BALB/c and C57/BL6 mice despite marked differences in vaginal PMN influx

[24]. Elevated proinflammatory cytokines and chemokines have Decitabine been detected in experimentally infected men [25], but not in naturally infected women unless coinfected with another STI pathogen [26]. In the mouse model Gc selectively induces Th17 cells, which leads to the recruitment of innate defense effectors including PMNs and results in faster clearance of infection [27]. Signaling through TLR4 is critical for Th17 responses in vitro [27] and in vivo [28], and colonization load is increased in TLR4-deficient mice [28]. Gonococcal LOS-mediated signaling through lectins such as DC SIGN induces cytokine production [29] and both PorB and the H.8 lipoprotein stimulate TLR2 leading to NF-κB activation, inflammatory cytokine production, and dendritic cell (DC) maturation [30] and [31].

Activation of NLRP3 inflammasomes in human enough monocytic cells or DCs by Gc results in the production of the inflammatory cytokines IL-1β and IL-18 and pyronecrosis of the cells [32] and [33] (Fig. 1). The adaptive response to Gc is ineffective as evidenced by the fact that repeat infections are common. The humoral response to uncomplicated Gc infections is poor. Quantitative evaluation of serum and local antibody responses in both female and male subjects presenting with uncomplicated cervicitis or urethritis showed at best only modest responses to antigens expressed by the homologous clinical isolates. Antibody responses were not sustained over the few weeks of follow-up, and there was no discernable memory arising from known prior episodes of infection [26] and [34]. These results are consistent with earlier reports by others (reviewed in [35]). Insights into the mechanisms by which Gc interferes with immune responses are being elucidated (Fig. 1). In mice, Gc suppresses the development of Th1- and Th2-driven adaptive immune responses by mechanisms dependent on TGF-β and IL-10 as well as type 1 regulatory T cells [36] and [37] (Liu et al., Mucosal Immunol, in press).

IgA levels in serum induced by i.n. immunization were around one to two orders of magnitude higher than those induced by i.d. immunization, suggesting that the NP themselves do not inherently drive IgA switching. We believe it is more likely that the route of immunization has an important role at inducing serum IgA as has been previously suggested [39] and [40]. TSA HDAC supplier We speculate that gp140-specific IgA plasma cells induced in the nasal cavity may home to spleen or bone marrow. It is worth noting

that levels of gp140-specific IgG and IgA were also enhanced in the nasal cavity. This suggests that wax NP may also have utility for delivering of immunogens against respiratory pathogens. M-cells of NALT are thought to play an important role in the uptake of NP in rodents and humans and are absent in vaginal and rectal mucosa [41], [42] and [43]. The nasal route has been extensively studied not only for vaccination purposes [44], [45], [46] and [47] but also for the delivery of drugs [48], and NP have been used nasally to induce immune responses to TT Selleck Thiazovivin [49] and HIV [50]. Induction of systemic and mucosal immune responses to HIV after nasal immunization of mice [51] and [52], guinea pigs [51] and macaques [5] with HIV-gp120 Ag has been described previously.

In the latter, serum and vaginal Ab responses were induced after nasal immunization only when followed by one or two intramuscular boosts. These levels were highly enhanced in vagina after challenge with SHIV, suggesting that the nasal priming induced effective memory responses at mucosal level [5]. In our mouse model, three nasal immunizations were enough to induce high levels of IgG and IgA in serum and vagina. It remains to be confirmed whether this immunization protocol with NP will work similarly in macaques or humans, or whether these Abs would be neutralizing.

secondly Therefore, further studies are warranted that assess homologous and heterologous immunization protocols to determine the feasibility of using these NP, as effective delivery systems of HIV Ags, in the development of mucosal vaccination in humans. Particle Science Inc has IP rights and economical interests in carnauba wax based nanoparticles mentioned in this article. This work was funded by a grant to SGUL by the Bill & Melinda Gates Foundation and the Wellcome Trust, under the Grand Challenges in Global Health Initiative. We are indebted to the Fondation Dormeur for funding of equipment used in the course of this study. We thank Professors Ralf Wagner and Hans Wolf, University of Regensburg and GENEART AG for the CN54-expressing plasmid. We thank Simon Jeffs, Sueli Vieira and Saba Hussein for work on gp140 cloning and expression. CN54-gp140 used in this study was produced under contract by Polymun Scientific GmbH. Griet Van Roey is supported by a EUROPRISE studentship funded by the European Union.

21 For studies that did not present mean differences and confidence intervals, these estimates were calculated using the confidence selleck compound interval calculator downloaded from the PEDro website. Due to the clinical heterogeneity of the studies included in this

systematic review and the variability between health conditions assessed, a meta-analysis was not possible. Therefore, the data analysis was descriptive. For the primary outcomes of pain intensity and disability, descriptive forest plots without pooling were performed for better visualisation. In all cases of multiple follow up points, only the longest-term measurement point available was plotted. Disability scales were converted to a common 0–100 scale. Forest plots were performed only for comparisons with two or more studies. RevMan 5.1 was used for the analysis. The overall

quality of the evidence and the strength of recommendations were evaluated using the GRADE approach.22 The GRADE approach specifies four levels of quality (high, moderate, low and very low). The overall evidence was downgraded depending on the presence of five factors: Panobinostat cell line limitations (due to risk of bias); consistency of results; directness (eg, whether participants are similar to those about whom conclusions are drawn); precision (ie, sufficient data to produce narrow confidence intervals); and other (eg, publication bias). The quality of evidence was then classified for each outcome according to the following criteria: There are consistent findings among many at least 75% of the participants from low risk of bias studies; consistent, direct and precise data; and no known or suspected publication biases. Further research is unlikely to change either the estimate or confidence in the results. One of the domains is not met. Further research is likely to have an important impact on confidence in the estimate of effect

and may change the estimate. Two of the domains are not met. Further research is very likely to have an important impact on confidence in the estimate of effect and is likely to change the estimate. Three of the domains are not met and the results are very uncertain. No randomised trials were identified that addressed this outcome. Single studies with a sample size smaller than the optimal information size (n = 300) were considered to yield very low-quality evidence if there was also a high risk of bias (PEDro score < 6) or low-quality evidence if there was a low risk of bias (PEDro score ≥ 6). From the search strategy, 275 potentially relevant studies were retrieved. Of these, 12 studies were considered eligible for data analysis.3, 4, 5, 11, 12, 13, 14, 23, 24, 25, 26 and 27 The flow of studies through the selection process is presented in Figure 1. The 12 eligible trials were published between 2008 and 2013. The sample sizes ranged from 10 to 76 participants12 and 13.

Found: C 63.56, H 5.03, N 6.98. 5-(4-Hydroxybenzylidene)-N-[2-(4-methoxyphenyl)-2-oxoethyl]-1,3-thiazolidine-2,4-dione (3f): Pale yellow solid, IR (KBr, cm−1): 3031, 1734, 1632, 1463, 1408, 1183, 633. 1H NMR (300 MHz,

DMSO-d6, δ ppm): 9.3 (s, 1H, OH), 7.7–8.2 (m, 8H, Ar), 8.1 (s, 1H, CH), 5.05 (s, 2H, CH2), 3.78 (s, 3H, OCH3). Anal. calcd. for C19H15NO5S: C 61.78, H 4.09, N 3.79. Found: C 61.88, H 3.97, N 3.66. 5-(4-Hydroxy-3-methoxybenzylidene)-N-[2-(4-methoxyphenyl) -2-oxoethyl]-1,3-thiazolidine-2,4-dione (3g): Pale yellow solid, IR (KBr, cm−1): 3012, 1732, 1638, 1465, 1408, 1194, 1189, 634. 1H NMR (300 MHz, DMSO-d6, δ ppm): 9.4 (s, 1H, OH), 7.5–8.1 find more (m, 8H, Ar), 7.9 (s, 1H, CH), 4.9 (s, 2H, CH2), 3.54 (s, 6H, OCH3). Anal. calcd. for C20H17NO6S: C 60.14, H 4.29, N 3.51.

Found: C 60.02, H 4.17, N 3.44. 5-(3,4-Dimethoxybenzylidene)-N-[2-(4-methoxyphenyl)-2-oxoethyl]-1,3-thiazolidine-2,4-dione (3h): Pale yellow crystals, IR (KBr, cm−1): 3031, 1775, 1656, 1451, 1202, 1156, 645. 1H NMR (300 MHz, DMSO-d6, δ ppm): 7.65–8.2 learn more (m, 8H, Ar), 7.8 (s, 1H, CH), 5.3 (s, 2H, CH2), 3.72 (s, 9H, OCH3). Anal. calcd. for C21H19NO6S: C 61.01, H 4.63, N 3.39. Found: C 60.87, H 4.44, N 3.19. 5-(Benzylidene)-N-(4-nitrobenzyl)-1,3-thiazolidine-2,4-dione (4a): Beige colour solid, IR (KBr, cm−1):

3113, 1737, 1660, 1524, 1417, 692. 1H NMR (300 MHz, DMSO-d6, δ ppm): 7.2–8.1 (m, 9H, Ar), 8.04 (s, 1H, CH), 5.1 (s, 2H, CH2). Anal. calcd. for C17H12N2O4S: C 59.99, H 3.55, N 8.23. Found: C 59.78, H 3.46, N 8.11. 5-(4-Chlorobenzylidene)-N-(4-nitrobenzyl)-1,3-thiazolidine-2,4-dione (4b): Pale yellow crystals, IR (KBr, cm−1): 3034, 1735, 1680, 1545, 1282, 1401, 756, 697. 1H NMR (300 MHz, DMSO-d6, δ ppm): 7.5–8.3 (m, 8H, Ar), 7.98 (s, 1H, CH), 4.95 (s, 2H, CH2). MS (ESI, Ketanserin m/z):374 (M+). Anal. calcd. for C17H11ClN2O4S: C 54.48, H 2.96, N 7.47, O 17.08. Found: C 54.23, H 2.65, N 7.22, O 17.01. N-(4-Nitrobenzyl)-5-(4-nitrobenzylidene)-1,3-thiazolidine-2,4-dione (4c): Half-white crystals, IR (KBr, cm−1): 3028, 1698, 1632, 1538, 1505, 1431, 638. 1H NMR (300 MHz, DMSO-d6, δ ppm): 7.1–8.1 (m, 8H, Ar), 7.8 (s, 1H, CH), 4.85 (s, 2H, CH2). Anal. calcd. for C17H11N3O6S: C 52.99, H 2.88, N 10.9. Found: C 52.79, H 2.75, N 10.76. 5-(4-Methoxybenzylidene)-N-(4-nitrobenzyl)-1,3-thiazolidine-2,4-dione (4d): Half-white solid, IR (KBr, cm−1): 2841, 1737, 1683, 1506, 1407, 1184, 702.

The ability to walk 800 m and climb a flight of stairs http://www.selleckchem.com/products/ink128.html has been used in previous studies to measure mobility-related disability (Guralnik et al 2000, Guralnik et al 1995). Inpatients in aged care rehabilitation are likely to have intermediate levels of disability. That is, they are likely to have greater mobility limitations than those who return home directly but to be more physically and mentally able than those who are admitted directly to residential care. Identification of rehabilitation patients at risk of ongoing mobility-related

disability may help clinicians target provision of interventions for mobility-related disability (such as exercise programs and occupational therapy) to Angiogenesis inhibitor those who need it most. To our knowledge no models have been developed for identifying those aged care rehabilitation inpatients who will experience ongoing mobility-related disability. Therefore the research questions for this study were: 1. What is the prevalence of mobility-related disability 3 months after discharge from inpatient aged care rehabilitation? The 3-month follow-up period was chosen because we sought to investigate relatively short-term outcomes in order to guide discharge planning. The study was a prospective, inception cohort study in which predictors were collected from

consecutive new admissions to aged care rehabilitation units at two metropolitan public hospitals in Sydney, Australia. Data were collected from medical records, from interviews with participants during hospital admission, and from physical tests in the 48 hours prior to discharge by a research physiotherapist (EB or MT). The order of test administration was altered to suit individual participants. The outcome of interest – mobility-related disability – was collected at three months after participants left hospital first via phone calls from EB and MT and postal questionnaires. All patients admitted to the aged care rehabilitation units between August 2005 and April 2007 were considered for inclusion in the study. They were excluded if they were deemed by the investigators

or by hospital staff to be too medically unstable to complete the measurements safely or did not speak conversational English and an interpreter was not available. The predictors were: current co-morbidity, pre-admission mobility, and discharge cognition, pain, vision, muscle strength, and mobility. We chose measures that were relatively easy to use in a clinical situation, had previously been found to be predictive of falls or disability, and/or were commonly used clinically. Co-morbidity was measured as the number of medical conditions and symptoms reported in the medical records. Pre-admission mobility was measured as the participant’s perception of whether they could walk 800 m and climb a flight of stairs in the three months prior to the hospital admission.

We also must not ignore the complexity of integrated record development and annual maintenance of these documents,

including the annual procurement and periodic revision processes as well as more complex discussions of sustainable financing across contributing programmes, all of which inherently creates scenarios of increased risk of stock-outs or shortages of cards for the annual birth cohort. Good clinical and public health practice benefits from good documentation standards that reflect the importance of complete, timely, and accurate recording of information. Immunization programme documentation standards, Abiraterone molecular weight as reflected by our review of home-based vaccination records, differ substantially from country to country

and at times within countries. Implementation of documentation standards and operational 3-MA mouse practice in the field likely varies even more so. Our review assessed the content of cards based on instructions and content as printed and cannot detect variations in field use which likely exist (e.g., stamps that might be used in some fields or practices of recording additional information in a field such as recording lot number in a column labelled “comments”). The World Health Organization is currently refining guidelines for the content and basic structure of home-based child vaccination records. Although that work is on-going, we would like to highlight the following items which are almost certainly to be reflected in the guidelines

in as much as these are derived from general principles of high quality medical records, whether paper- or computer-based. • Perhaps unique to home-based paper records, the physical medium (e.g., water- and tear-resistant paper, heavier card stock paper) used for the document is important to consider given the often harsh conditions to which the document is exposed. Alternatively or in addition, a protective sheath or sleeve can be considered to protect the record. In summary, the role of the home-based vaccination record as basic medical record is clear. The different forms of home-based child vaccination records those [7] reflects integration with other child survival programme areas; however, it remains an open question as to whether there are related adverse impacts on the quality of documentation following receipt of immunization services. We expect home-based vaccination records to continue to evolve particularly with respect to adoption of new and more effective designs and incorporation of technology such as use of bar codes or embedded microchips to facilitate transitions to electronic based systems.

Central administration of Y2R agonists have failed to alter anxiety-like behavior in a number of studies (Broqua and et al, 1995, Heilig and et al, 1989, Britton and et al, 1997 and Sorensen and et al, 2004). However, agonism of Y2R in the locus coeruleus and lateral septum produces anxiolytic effects, whereas Y2R are required for NPY-mediated anxiolysis in the hippocampus (Kask et al., 1998a, Kask et al., 1998b, Kask et al., 1998c, Trent and Menard, 2013 and Smialowska and et al, 2007). Y2R agonism in the basolateral amygdala has bidirectional effects on anxiety in the social interaction test, with low agonist doses generating anxiety and high doses decreasing anxiety (Sajdyk et al., 2002). A recent study

indicates that knockout of the Y2R in GABAergic neurons located Trametinib research buy in the central nucleus of the amygdala was anxiogenic specifically in female mice (McCall et al., 2013). Contrasting reports indicate that Y2R antagonism in the central nucleus of the amygdala is anxiolytic (Kallupi et al., 2013), and that ablation of Y2R in either the basolateral or central nucleus of

the amygdala Selleckchem Crizotinib produces an anxiolytic phenotype (Tasan et al., 2010). Global deletion of Y2R reduces anxiety in the elevated plus maze, light–dark, open-field, and marble burying tests (Tasan and et al, 2009, Painsipp et al., 2008, Painsipp and et al, 2008 and Tschenett and et al, 2003), and Y2R deficient mice exhibit reduced neuronal activation upon exposure to an anxiogenic environment (Nguyen et al., 2009). Taken together, this evidence isothipendyl suggests that Y2R may function in a regionally specific and neurochemically selective fashion. The Y4R and Y5R also have putative roles in rodent anxiety-like behavior. Similar to Y2R mutant mice, deletion of the Y4R also reduces anxiety-like behavior in a number of rodent paradigms

(Tasan and et al, 2009 and Painsipp and et al, 2008). Knockout of the Y4R with the Y2R enhances the anxiolytic phenotype observed following deletion of either receptor alone (Tasan et al., 2009). Finally, pharmacological studies indicate that Y5R ligands may have promising anxiolytic properties. A Y5R antagonist blocked the anxiolytic effects of a Y2R agonist in the basolateral amygdala (Sajdyk et al., 2002), while i.c.v. delivery of a Y5R agonist produced anxiolytic effects (Sorensen et al., 2004). Y5R can form heterodimers with Y1R (Gehlert et al., 2007), and these receptor subtypes are colocalized in the basolateral amygdala, hippocampus, and hypothalamus (Wolak and et al, 2003, Longo and et al, 2014, Oberto and et al, 2007 and Fetissov et al., 2004). Y1 and Y5 receptors act synergistically in the regulation of energy homeostasis (Mashiko et al., 2009). Although the combined effects of Y1 and Y5 receptor agonists have not been tested in the context of anxiety thus far, the notion of co-activating these receptors could be valuable in the development of pharmacotherapeutics for enhanced anxiolytic effects.

This hypothesis was based on two main observations: first, the routine childhood vaccinations have non-specific effects, the live BCG and MV reduce mortality more than can be explained by prevention of the target diseases [11] and [12], whereas the inactivated DTP vaccine is associated with increased

mortality in areas with herd immunity to pertussis [13] and [14]; second, the mortality benefit pattern after VAS resembles that of vaccines, with a beneficial effect in the time windows dominated by BCG (at birth) and MV (after 6 months of age) but no beneficial effect between 1 and 5 months of age, in the time window of DTP [10]. The hypothesis implied that VAS would probably be beneficial when provided with the live BCG and MV, but harmful when provided with DTP vaccine. We have subsequently tested the hypothesis in observational studies [15] and [16], randomized trials BKM120 supplier [1], [2], [3] and [17] and by reanalyzing old trials [18] and we have been able to show repeatedly that VAS and vaccines interact.

We have also learned in the process. Initially, we did not emphasize sex as an important covariate. However, in most [1], [2], [4], [17] and [18], though not all studies [3], [15] and [16], we have found that VAS provided close to DTP had a negative effect for females, but not for males. Furthermore, we had not envisaged that VAS could interact with vaccines given months after. We first became aware AUY 922 of this possibility when analyzing the first NVAS trial, observing an increase in mortality in female NVAS recipients, which occurred when the children

started receiving DTP several months after NVAS [4]. The present analysis suggests that NVAS may interact with vaccines given as much as 4–5 months later. If true, this is surprising, not only because it occurred so many months after NVAS, but also because the interaction between found NVAS and early MV was negative. If anything we would have expected the opposite. The explanation may be the three intermediate DTP vaccinations. In the early MV trial, all children were visited at the ages of DTP1, DTP2, and DTP3 and their mothers were encouraged to bring them for vaccination. Hence, all participants had received three DTP vaccines with short intervals, and they were enrolled in the early MV trial 4 weeks later. The cocktail of first NVAS, then three DTP and then early MV may have been too much. In a trial of BCG revaccination we found a negative effect of receiving BCG at 19 months of age followed by DTP and then VAS in a campaign [19]. We have discovered interactions between NVAS and the following vaccines: DTP (negative for females) [2] and [4], and early MV (negative for males). Furthermore, we have found that NVAS primes a beneficial response to a subsequent dose of VAS provided after 12 months of age, particularly in females [9] and [16].

The lesions observed were smaller in size in comparison to those seen in the non-vaccinated infected animals. No tongue lesions were observed in these two unprotected vaccinated animals. Foot lesions in two of the non-vaccinated

buffalo were observed at 7 dpc, whereas foot lesions in the other four non-vaccinated buffalo were observed at 11 dpc. Only one non-vaccinated buffalo developed a tongue Dolutegravir mw lesion, which was observed at 7 dpc. Five non-vaccinated cattle showed foot lesions at 10 dpc and one showed a foot lesion at 11 dpc. Four of these six unprotected cattle showed tongue or dental pad lesions at 10 dpc, one showed at 7 dpc and the 6th one did not show any tongue or dental pad lesion. Pyrexia (≥39.0 °C to 40.2 °C) was recorded at the same time as the appearance of vesicles, but was less evident in the vaccinated S3I-201 solubility dmso unprotected animals in comparison to the unprotected non-vaccinated animals. A neutralizing antibody titre to FMDV O/IND/R2/75 was detected as early

as 14 dpv and peak antibody titres were obtained at 28 dpv in vaccinated buffalo and cattle. The mean antibody titre in vaccinated buffalo and cattle were 101.2 (95% confidence interval (CI): 100.8–101.7) and 101.5 (95% CI: 101.2–101.8), respectively, at the time of exposure. Two vaccinated buffalo that showed clinical signs had low serum neutralizing antibody titres (100.9; 101.1) whereas a third vaccinated buffalo with low neutralizing antibodies (101.1) at the time of exposure was protected. Following the challenge exposure, the serum neutralising antibody titres were observed in the range of 101.2 to 101.8 up to 32–39 days post challenge in vaccinated buffalo and cattle (Fig. 2). In non-vaccinated control buffalo and cattle a rapid the seroconversion was evident following exposure

to challenge and the antibody titres (101.0 to 101.4) were detected up to 32–39 dpc (Fig. 2). Both vaccinated buffalo and cattle had significantly higher neutralising antibody titres than non-vaccinated control buffalo and cattle at all time points post exposure, but there was no significant difference in serum neutralising antibody titres between vaccinated buffalo and cattle at any time point post exposure. NSP antibodies appeared at 9 dpc in three non-vaccinated buffalo and four non-vaccinated cattle, at 14 dpc in two non-vaccinated buffalo and two non-vaccinated cattle and at 19 dpc in one non-vaccinated buffalo. NSP antibodies were detected at 14 dpc in three vaccinated buffalo and two vaccinated cattle while two vaccinated buffalo and one vaccinated cattle showed NSP antibodies at 32 dpc. One vaccinated buffalo and two vaccinated cattle were not positive for NSP antibodies. Virus replication occurred earlier in non-vaccinated control animals than in the vaccinated animals as was evident from antibody responses against NSP (Fig. 3).