5 hr followed by three rinses in PBS and mounting in Vectashield. Cells were imaged at 20 × on a Zeiss Axio Imager.M1 microscope. All images were imported into Adobe Photoshop and thresholded. ET33-Cre-expressing cells were identified by their tdTomato expression. The somas of Cre-expressing cells were outlined Cisplatin and the average

fluorescence intensity of the VGLUT2 signal within the traced area was measured by using the histogram function. VGLUT2 fluorescence intensity was normalized to soma size for each cell. Data were compared by a Student’s t test. One retina was removed on either P0 or P5 and recordings were performed on P5 or P10, respectively. Brain sections (325 μm) containing the optic tract and dLGN were acutely prepared as previously described (Chen and Regehr, 2000, Koch and Ullian, 2010 and Bickford et al., 2010). Sectioning

was performed in oxygenated cutting solution consisting of 78.3 mM NaCl, 23.0 mM NaHCO3, 23.0 mM dextrose, 33.8 mM choline chloride, 2.3 mM KCl, 1.1 mM NaH2PO4, 6.4 mM MgCl2, and 0.45 mM CaCl2. Brains were incubated for 25 min at 34°C in cutting solution and then transferred to oxygenated ACSF consisting of 125.0 mM NaCl, 25.0 mM NaHCO3, 25.0 mM dextrose, 2.5 mM KCl, 1.25 mM NaH2PO4, 2.0 mM CaCl2, and 1.0 MgCl2 × 6H20. Recordings were made at room temperature. Whole-cell voltage-clamp recordings of dLGN neurons were obtained by using 2.5–3.5 MOhm patch electrodes containing internal solution (35 mM CsF, 100 mM CsCl, 10 mM EGTA, and 10 mM HEPES). Inhibitory inputs were blocked with 20 μM bicuculline

methobromide (Tocris). Recordings were sampled at 10–20 kHz and filtered at Proteases inhibitor 1 kHz. Access resistance was monitored and adjusted to 4–9 MOhms after 70% compensation. A concentric bipolar stimulating electrode was placed just touching the surface of the optic tract next to the ventral LGN and a 1 ms stimulus was delivered every 30 s. A 40 μA stimulus was used because this intensity Non-specific serine/threonine protein kinase evoked action potentials from many RGC axons, typically resulting in maximal postsynaptic responses in control cells. NMDAR-mediated current amplitudes were measured at +40 mV and at a time when the AMPAR-mediated currents no longer contributed to the response, ∼25 ms after the onset of the EPSC. Synaptic currents were analyzed by using Igor Pro, Microsoft Excel, and GraphPad Prism programs. All experiments and analyses were done blind to genotype. Statistical comparisons were made by using a Student’s unpaired t test unless otherwise stated. Mice were anesthetized with isoflurane and their eyelids were gently separated with tweezers. Eyes were numbed with proparacaine and injected with 1.0–2.0 μL of CTb-488 or CTb-594 (0.5% in sterile saline), 1.0 μl for P3 mice, 1.5 μl for P9 mice, and 2.0 μl for P27 mice. Confocal images of dLGN sections were acquired on an Axiovert 200 microscope and Pascal acquisition software.

When analyzing the data from the early MV trial it became clear that there were strong interactions between early MV and NVAS. Early MV had no effect on overall mortality in children who had Selleckchem Alectinib received NVAS, whereas a strong beneficial effect was seen among children who had not received NVAS, either because they had been randomized to placebo or because they had not participated in the NVAS trials [5].

Though neither NVAS nor early MV is currently recommended, the situation may change. Three new NVAS trials are ongoing [7] and NVAS may become policy if these new trials show a beneficial effect. The early MV trial showed a remarkably strong beneficial effect of early MV in children who had not received NVAS. The trial is currently being repeated in several West African countries

which do not use NVAS. If results are replicable early MV may also become policy. It is therefore important to assess whether there is interaction between NVAS and early MV. In the present paper we analyzed the potential interaction between NVAS and early MV in 5141 children who participated in both an NVAS trial and the early MV trial. We compared the mortality of NVAS and placebo recipients: first, in the time window from 4.5 to 8 months for children randomized to early MV or no early MV, and second, from 9 to 17 months in children who had received two MV or one MV, respectively. The study was a reanalysis of previously conducted randomized trials of NVAS and early MV, respectively. The trials were conducted to study the effect of NVAS and MV, respectively, and the idea to study the potential interactions see more between the two interventions only occurred after the completion of the trials. Hence, the size of the present study was not based Levetiracetam on a prespecified hypothesis and corresponding sample size calculations, but defined by the number of children who had participated in both a NVAS trial and the early MV trial. Information on exposure (randomization to NVAS and early MV) and outcome (overall mortality) was available

from the trial databases. The Bandim Health Project (BHP) maintains a demographic surveillance system in six suburban districts of the capital of Guinea-Bissau and covers approximately 102,000 inhabitants. There are three health centers in the study area, one has a maternity ward. The national hospital where many women from the study area give birth is a few kilometers away. BHP assistants are placed at the health centers and the hospital to register all study area children. All houses in the study area are visited monthly to register new pregnancies and births. All children below 3 years of age are followed through home visits every third month. UNICEF classifies Guinea-Bissau as having vitamin A deficiency as a public health problem [8]. The country has implemented VAS campaigns for children between 6 months and 5 years of age.

In the 1960s, it was demonstrated that X-irradiated sporozoites confer protective immunity in mice [3]; and the cloning of the gene encoding CSP from the monkey malaria parasite P. knowlesi [4] led to hopes that the homologous protein might form the basis of a vaccine against human malaria parasites. The pace of clinical trials of vaccines based on CSP and other malaria surface proteins from the two most MLN8237 in vitro widespread human malaria parasites, P. falciparum and P. vivax, has increased dramatically in the past decade, but so far the results have been mixed [2]. One of the major challenges

facing vaccine developers is the high level of naturally occurring polymorphism at several of the loci encoding surface proteins of P.

falciparum and P. vivax [5]. In the case of the CSP of P. falciparum, polymorphic variants in epitopes for host CD4+ T cell recognition have been shown not to be cross-reactive [6], implying that vaccines which rely on the use of these epitopes Src inhibitor to stimulate an immune response will fail to provide protection against all naturally occurring parasite variants [5]. At the CSP locus of P. falciparum, there is evidence that the polymorphism in T-cell epitopes is maintained by balancing selection driven by host T cell recognition [7], [8], [9] and [10]. not Likewise, several other loci encoding malaria cell surface proteins show evidence of selectively maintained polymorphism [8], [11], [12] and [13]. Even under balancing selection, because of the role of genetic drift, the level of polymorphism that can be maintained is expected to be a function of the effective population size [14] and [15]. Consistent with theoretical expectations, there is evidence that population bottlenecks can effect the level of polymorphism at antigen-encoding loci of malaria parasites. For example, the

locus encoding apical membrane antigen-1 (AMA-1) of P. vivax shows considerably reduced polymorphism in Brazil in comparison to the Old World, reflecting a bottleneck in colonization of the New World [10] and [16]. Likewise, studies of P. falciparum populations on Pacific islands have revealed relatively low levels of polymorphism at several antigen loci, as expected in the case of founder effects in the colonization of islands by the parasite [17] and [18]. On the other hand, local populations in Old World mainland areas where malaria has long been present, such as Southeast Asia, have revealed substantial levels of polymorphism at antigen-encoding loci [9], [10], [12] and [19]. Given these high levels of polymorphism, the design of a locality-specific vaccine that provides immunity against all locally occurring variants seems problematic.

Mice were maintained at Montana State University Animal Resources Center under pathogen-free conditions in individual ventilated cages under HEPA-filtered barrier conditions and

were fed sterilized food and water ad libitum. For intranasal (i.n.) immunization study, mice at 8–10 wks of age were immunized with each DNA vaccine (80 μg/dose) on wks 0, 1, and 2 with each dose administered over a two-day period. On wks 8 and 9, mice were nasally boosted with 25 μg of recombinant F1-Ag protein [27] plus 2.5 μg of cholera toxin (CT; List Biological Laboratories, Campbell, CA) adjuvant. Before challenge, a final Veliparib in vitro boost of DNA vaccine (100 μg) and F1-Ag protein (25 μg) plus CT adjuvant was given i.n. on wk 12. AZD6738 solubility dmso One group of mice was immunized only with Fl-Ag, as described. For intramuscular (i.m.) immunization study, mice were immunized i.m. with each DNA vaccine on wks 0, 1, and 2. For i.m. immunizations,

100 μg DNA were administered with a needle into the tibialis anterior muscles of the two hind legs, as previously described [28]. On wks 8 and 9, mice were nasally boosted with 25 μg of F1-Ag protein plus 2.5 μg of CT (List Biological Laboratories) adjuvant. Before challenge, a final boost of DNA vaccine (100 μg) i.m. and F1-Ag protein (25 μg) plus CT adjuvant was given i.n. on wk 12. To test the efficacy of the LTN DNA vaccines against pneumonic challenge, immunized mice were transported to Colorado State University, acclimated for at least 7 days, and subjected to nasal challenge with 100 LD50 of Y. pestis Madagascar strain (MG05) >2 wks after the last immunization, as previously described [25] and [27]. All mice care and procedures were in accordance with institutional policies for animal health and well-being. Blood was collected from the saphenous vein. Fresh fecal pellets from individual mice were solubilized in sterile PBS containing 50 μg/ml of soybean trypsin inhibitor (Sigma–Aldrich) by vortexing for 10 min at 4 °C. much After microcentrifugation, supernatants were collected and frozen at −30 °C until assay. Serum and fecal Ab titers were determined

by ELISA. Briefly, recombinant F1- or V-Ag [27] in sterile PBS was coated onto Maxisorp Immunoplate II microtiter plates (Nunc) at 50 μl/well. After overnight incubation at room temperature, wells were blocked with PBS containing 1% BSA for 1 h at 37 °C; individual wells were loaded with serially diluted mouse serum or fecal samples in ELISA buffer (PBS containing 0.5% BSA and 0.5% Tween 20) overnight at 4 °C. Ag-specific Abs were reacted with HRP-conjugated goat anti-mouse IgG, IgA, IgG1, IgG2a, or IgG2b Abs (Southern Biotechnology Associates) for 90 min at 37 °C. The specific reactions were detected with soluble enzyme substrate, 50 μl of ABTS (Moss), and absorbance was measured at 415 nm after 1 h incubation at room temperature using Bio-Tek Instruments ELx808 microtiter plate reader. Endpoint titers were determined to be an absorbance of 0.

8%) in 100 mL of diluents acetonotrile:water:methanol (3:3:4) in a 100 mL volumetric flask (stock solution A). The stock solution of Fexofenadine hydrochloride (1200 μg/mL) was prepared by dissolving 120 mg of Fexofenadine hydrochloride (99.6%) in 100 mL of same diluent (stock solution B). For analysis of the tablet dosage form, twenty tablets were weighed individually and their average weight was determined. The tablets were crushed to fine homogenous powder and quantity equivalent to one tablet (about 75 mg of homogeneous www.selleckchem.com/products/z-vad-fmk.html powder) were transferred in a 50 mL volumetric flask. Added about 50 mL of diluent

to the volumetric flask, shaken for 10 min and then sonicated for 15 min. The solution was allowed to stand at room temperature for 20–30 min and filtered through Whatman no. 41 filter paper. 2.0 mL of filtrate was quantitatively transferred to a 10 mL volumetric flask and solution was diluted up to the mark with diluent. The identities of both the compounds were established by comparing retention time of the sample solution with those of standard solution and result were determine as shown in Table 2 and Fig. 1. The linearity of analytical method is its ability to elicit test results that are directly proportional A-1210477 concentration to the concentration of analyte in sample within a given range. The linearity was performed by five different concentration were injected and calibration curve were plotted as shown in Figs. 3 and 4. The linearity for

Montelukast Sodium and Fexofenadine hydrochloride was found to be 12.5–37.5 μg/ml and 150–450 μg/ml respectively and 3-Dimensional plot of calibration curve as shown in Fig. 2. The precision of an analytical method is the degree of agreement among individual test results when the method is applied repeatedly to multiple samplings of homogenous samples. It provides an indication science of random error results and was expressed

as coefficient of variation (CV). Intraday and interday precision was determined in terms of % RSD. Intraday precision was determined by analyzing in combined solution their respective calibration range for five times in the same day. Interday precision was determined by analyzing MONT and FEXO in for five days. ⇒ Procedure for intraday precision: combined solution containing of mixture of MONT and FEXO as 12.5 + 150 μg/mL, 25 + 300 μg/mL, 37.5 + 450 μg/mL were injected into the system with stated chromatographic conditions and analyzed for five times on the same day and %RSD was calculated. Accuracy may often be expressed as percentage recovery. It was determined by calculating the recovery of MONT and FEXO by application of the analytical method to mixtures of the drug product contents to which known amount of analyte have been added within the range of the method. The L.O.D. was estimated from the set of five calibration curves. LOD=3.3×(S.D./Slope)LOD=3.3×(S.D./Slope)Where, S.D. = Standard deviation of the Y-intercepts of the 5 calibration curves. The L.O.Q.

45%) in non-site-specific assay. In plasmid nicking assay, the extracts (except hexane and chloroform extracts) were found to be effective in preventing the degradation of supercoiled plasmid DNA from hydroxyl radical into linear and open circular forms. The results showed that the extracts

(methanol, ethyl acetate and water extract) have potent hydroxyl radical scavenging activity. These activities could be due to the presence of terpenoids and phenolic compounds in extracts as determined using IR and 1H NMR during the phytochemical studies of the extracts of roots of the plant. 27 Antioxidants are molecules which can safely interact with free radicals and terminate the chain reaction before vital molecules get damaged. The free radical damage can be prevented by several enzymes and the principal antioxidants Torin 1 concentration such as vitamin E, beta-carotene, and vitamin C, present in the defense system of our body. Several studies have shown that plant phenolics also have antioxidant properties.28, 29 and 30 Natural polyphenols can have simple structures for example phenolic acid, phenylpropanoids, flavonoids or they can have structure like polymers e.g., lignins, melanins, tannins.31 Free radical scavenging property, metal chelating property, effects on cell signaling pathways and on gene expression contributes to the potential of phenolics as antioxidant therapeutic agents.32 S. oleosa has been

found as potent antioxidant due to those the presence of phenolic compounds. 33 Thind et al evaluated the antiradical properties and determined the total phenolic Luminespib manufacturer content in methanolic extract/fractions from bark of S. oleosa by several in vitro systems – 2,2′-diphenyl-1-picrylhydazyl (DPPH), deoxyribose degradation (non-site-specific and site- specific), reducing power, chelating power, plasmid nicking assays and by Folin-Ciocalteu’s

method, 34 respectively. Results revealed that residue fraction which was obtained by drying the supernatent of the precipitate had greater free radical scavenging activity than the precipitate and aqueous extract as the content of phenolic compounds present in the extracts follows the order; residue fraction (942 mg/g gallic acid equivalents) > aqueous extract (896 mg/g gallic acid equivalents) > precipitate (604 mg/g gallic acid equivalent) and the potential of antioxidant activity of the extract also follows the same order as determined by the assays thus reconfirming the fact that antioxidant activity depends on the phenolic contents in the extract. 33 Studies have been carried out on the antimicrobial activity of S. oleosa showing great potential of the plant as an upcoming antimicrobial agent. Archana Moon 35 deliberated the same, in which clinical isolates from methanolic extracts of the plant were examined against defiant drug strains of Escherichia coli, Staphylococus aureus, Klebsiella.

On the other hand, members are intentionally selected to avoid representation of special interests of the organizations that they belong to. Members are appointed for one legislative mandate (four years) and can sit for a maximum of 12 years. There are also ex officio members, which include FOPH representatives

(the commission’s Secretariat) and a Swissmedic representative. They can participate in the commission’s meetings but they Dinaciclib manufacturer have no voting rights. Representatives of pharmaceutical companies can be invited to present data, but this occurs outside of official meetings, and they do not participate in the meetings. The CFV members work for the CFV without pay during their four-year legislative mandate, which is in accordance with

the Swiss “militia system” (a voluntary public work system). This is a demonstration of their commitment and belief that vaccination issues must be addressed at the highest levels in Switzerland. The members are reimbursed for travel expenses and they receive a nominal compensation for attending this website meetings. As vaccination recommendations have a significant impact on public health, the CFV aims to ensure that analyses of issues and data, which lead to vaccination recommendations, are carried out independently and free of any direct or indirect pressure. Thus, the CFV deems it necessary to avoid situations where personal or institutional interests, whatever their nature may be (financial or other), may affect the integrity or impartiality of its work. Experts approached for participation in the CFV must describe in detail their relations with the pharmaceutical industry and identify all

other potential conflicts of interest. To ensure maximum transparency, the FDHA only appoints experts who are deemed to be free of such conflicts of interest. Each member of the CFV must declare any interests that very could constitute real, potential or apparent conflicts of interest with industry, either at the individual level or at the institutional level (i.e., the institute that the member is employed by). Members make a formal declaration of interest when they are appointed to the commission, as well as at each CFV meeting. A procedure exists for taking action if a member or chairperson has any apparent interests regarding a vaccine or intervention being discussed. Depending on the situation, a member could be asked to refrain from participating in certain discussions or working groups, or to leave the meeting during certain evaluations, or to be allowed to participate but asked to disclose publicly any interests that might be perceived as a conflict. Description of the directives employed to ensure the integrity and impartiality of CFV’s work can be found in the Déclaration d’intérêts pour les membres de la commission fédérale pour les vaccinations [2] (declaration of interests for members of the Federal Vaccination Commission).

Their baseline characteristics are presented in Table 1. The thirteen participants had moderate to moderately severe airflow obstruction (Knudson et al 1983) and only two patients were slightly breathless at rest (ie, breathlessness = 1 and 0.5 out of 10). One physiotherapist delivered the interventions Trichostatin A price at the Pulmonary Research Room of the Physical Therapy Department

at Khon Kaen University in Thailand. The therapist had a degree in physiotherapy and three years experience working in the Easy Asthma and COPD Clinic of Srinakharind Hospital. The participants found breathing through conical-PEP during exercise to be acceptable and there were no complications or adverse events. The exercise resulted in heart rates that were approximately this website 70% of the age-predicted maximum. The following criteria would have been considered unsafe: SpO2 < 88%, PETCO2 > 50 mmHg, or changes > 20% from control values while using conical-PEP. Oxygen saturation (SpO2) was ≥ 92% during exercise, and there was no evidence of hypercapnia or abnormal electrocardiogram. Group data for lung capacity are presented in Table 2 and for cardiorespiratory function in Table 3. Individual data is presented in Table 4 (see eAddenda for Table 4). Inspiratory capacity increased 200 ml (95% CI 0 to 400) more

after the experimental intervention and slow vital capacity increased 200 ml (95% CI 0 to 400) more after the experimental intervention than the control intervention. Participants exercised for 687 s (SD 287) during the experimental intervention compared with 580 s (SD 248) during the control intervention (mean difference 107 s, 95% CI −23 to 238). Participants stopped exercising either because of breathlessness (n Tryptophan synthase = 6) or

because of leg discomfort (n = 7). The median breathlessness score for all patients was 4 out of 10 (IQR 2.0–5.0) immediately after the experimental intervention, and 4 (IQR 3.0–5.0) after the control intervention. The median leg discomfort was 10 out of 10 (IQR 0–10) immediately after the experimental intervention, and 10 (IQR 0–10) after the control intervention. Change in cardiorespiratory function (heart rate, tidal volume, minute ventilation, PETCO2 or SpO2) from rest to the last 30 s of exercise was not different between the interventions. A longer inspiratory time during the experimental intervention compared with the control intervention (mean difference 0.3 s, 95% CI 0.0 to 0.7) and longer expiratory time (mean difference 0.9 s, 95% CI 0.3 to 1.5) resulted in a slower respiratory rate (mean difference −6.1 breaths/min, 95% CI −10.8 to −1.4). However, this slower respiratory rate did not have any adverse effects on CO2 retention or oxygen saturation. In addition, mouth pressure was 8.5 cmH2O (95% CI 5.9 to 11.2) higher and respiratory flow rate 0.21 L/s (95% CI 0.12 to 0.31) slower during the experimental intervention compared to the control intervention. The I:E ratio went from 1:1.5 to 1:1.

The results have been correlated with the amount of gallic acid, ellagic acid and quercetin, quantified in different plant parts with the help of HPTLC that will validate the medicinal potential of this plant. The authors expect that their HPTLC quantification analyses will be helpful for authentication and quality testing purpose of the marketed plant samples. The different plant parts of S. asoca were collected in March 2010, from the campus

of Bethune College, Kolkata, India. The species was authenticated by Dr. Gour Gopal Maity, Professor of University of Kalyani, who is a renowned scientist in the field of plant taxonomy. Plant samples (bark, leaves and flowers) were washed with Milli-Q water and air-dried at selleck room temperature for 7 days, then oven-dried at 40 °C to remove the residual moisture. The dried plant parts were pulverized and stored in air-tight containers at 4 °C for future use. 50 g of powdered samples of bark, leaves and flowers were extracted with methanol by soxhlation method at 60–80 °C. The three filtrates were separately concentrated in water bath at 40 °C and evaporated under reduced pressure. DPPH was purchased from Sigma–Aldrich Co. (USA). UV–visible spectrophotometer (Shimadzu 1800) was used for recording selleck chemicals the spectra. Gallic acid was obtained from

Titan Biotech Ltd. (India). Ellagic acid and quercetin were purchased from Sigma–Aldrich Co. (USA). Methanol, toluene, ethyl acetate and formic acid were all of analytical grades and procured from E-Merck (India). Silica gel 60 F254 precoated TLC aluminum plate (Merck, Germany) was used for HPTLC analysis. The evaluation of free radical scavenging activity of each plant extract was carried out using

DPPH assay by adopting spectrophotometric method.16 and 17 Different concentrations of plant extracts were prepared with different plant parts. 1 ml of 300 μM DPPH dissolved in methanol was added to each of the samples (plant extracts) and allowed to stand at room temperature in the dark for 20 min. Same condition was applied for a blank solution which consisted of only 1 ml 300 μM DPPH dissolved in methanol (i.e. without any plant extract). Gallic acid (1 mg/ml) was used as standard control. Each experiment was repeated at least three times. The change in color from deep violet to light yellow was measured at 517 nm using UV–visible spectrophotometer. Cell press The decrease in absorbance was then converted to percentage antioxidant activity using the following formula: Inhibition(%)=Control−Test/Control×100 5 mg each of gallic acid or ellagic acid or quercetin were accurately weighed into a 25 ml of volumetric flask and dissolved in 3 ml of methanol. Each of them was then sonicated for 5 min and the final volume was made upto 5 ml with the same solvent to obtain stock solutions of 1 mg/ml. All the methanolic plant extracts (0.5 g) were dissolved in 10 ml of methanol to get stock solution of 50 mg/ml.

8: other specified congenital malformations of the intestine; ICD-10-CM K38.8: intussusception of the appendix) as well as for possible complications of intussusception, such as bowel obstruction. This data was compared to previously published data from the same hospital (January 1, 1995 to June 30, 2001) that was collected using the similar methodology [11] Patients with primary idiopathic intussusception confirmed by surgery, air or liquid-contrast enema as level 1 according to the Brighton Collaboration Clinical Case Definition, were included in the analysis [15]. To examine the check details possibility of a temporal association

between receipt of a rotavirus vaccine and intussusception, we obtained vaccination records from the Australian Childhood Immunisation

Register [16]. We compared the date of rotavirus immunisation to the recorded date of intussusception diagnosis, the age of each patient at the time of vaccination and the number and date of doses received. Data were entered and stored in a secure Microsoft Access 2003 database. Incidence rates were calculated using age specific population estimates for Victorian children obtained from the Australian Bureau of Statistics for each year of the study [17]. Ninety-five per cent confidence intervals for incidence rates and DNA Damage inhibitor their ratios were calculated using standard methods based on Poisson distribution. Poisson regression analysis was used to estimate incidence rate ratios that describe the difference in incidence rate for each age group from the beginning to the end of the study period. Statistical analysis was performed using Stata 10.0 (StataCorp, College Station, TX, USA). This study was approved by the Ethics in Human Research Committee at the Royal Children’s Hospital, Melbourne. A total of 258 episodes of IS were identified in 230 children aged 24 months or less over the 8-year study period. Thirty-three patients were excluded from the final analysis. This

included 11 patients whose diagnosis was secondary to underlying pathologies such as; Meckel’s Diverticulum (n = 6), duplication cyst (n = 1), prolapsed Methisazone stoma (n = 1) and post operative IS (n = 3). In addition, 21 cases of IS were found to be unproven on surgical or radiological investigations, and 1 case lacked sufficient data to make a complete assessment (n = 1). Approximately 9% (n = 28) of episodes were misclassified or coded incorrectly. Sixty-four cases were identified under codes that could be associated with intussusception and miscoded, although a subset analysis of these cases found no miscoded cases of intussusception. Four cases were not born in Victoria but presented to RCH for diagnosis and treatment of intussusception during the study.