Elimination of microfilaria in dogs infected with zoonotic Dirofilaria repens would be desirable to reduce further spread. Moxidectin has demonstrated efficacy against microfilariae and safety in dogs infected with Dirofilaria immitis and could be an option for controlling D. repens microfilariae. A field study with 64 dogs previously confirmed positive for D. repens microfilaria was conducted in Hungary, in which a spot-on product (Advocate, Bayer) was tested. Treatments were applied to 44 dogs once a month for 3 months (five dogs) or 6 months (22 dogs), alternatively every 2 weeks for 6 months (17 dogs). Twenty dogs remained untreated. Microfilaria counts were performed once a month and for a further 6 months following the last treatment. Two weeks after the first treatment, 38 of 44 dogs were microfilaria negative. Four weeks after the initial treatment, one dog still showed a low microfilaria count. Following the second treatment, all treated dogs were negative. This status was maintained during the 6-month observation period after the last treatment. These data demonstrate the successful long-lasting elimination of microfilariae. Moreover, it may be supposed that adult D. repens were killed based on the observation that no further microfilariae were seen up to 6 months after the end of the treatment period.
Abstract-The authors tested 123 genotypes described in 54 papers published in the journal Neurology between 1999 and 2002 to ascertain whether these genotype distributions deviated from Hardy-Weinberg equilibrium (HWE). Unreported deviations from HWE in 19 genotype distributions described in 11 of the papers were discovered. The authors also report additional information that could have been extracted after calculating HWE and conclude that HWE values should be mandatory in population genetic studies published in Neurology. NEUROLOGY 2004;63:357-358 The gene frequencies at a locus in a randomly interbreeding diploid population and population genotype frequencies remain constant from generation to generation if mating is random and if mutation, selection, and migration do not occur. A mathematical formula created by Hardy and Weinberg 1-4 allows for this equilibrium to be tested in studied populations.The Hardy-Weinberg law is suitable for testing the hypothesis of panmixia (random mating within a breeding population) and evolutionary stasis. It is a null hypothesis in genetic studies for testing the suitability of the enrolled reference population and for detecting even weak associations between genotype and disease. However, Hardy-Weinberg equilibrium (HWE) is not always calculated and published in papers investigating population genetics, as we found after reviewing a sample of papers published in recent volumes of Neurology.Subjects and methods. We reanalyzed genotypes described in papers published in Neurology between 1999 and 2002. Enrollment criteria were investigation of biallelic genetic polymorphisms with Mendelian inheritance and case-control study design. We calculated HWE values for each published genotype in each subject group using the Arlequin program (http://anthropologie. unige.ch/arlequin/). 6,7 The level of significance was set at p Ͻ 0.05.
5-fluorouracil (5-FU) is widely used in the treatment of gastric and colorectal cancer. Recent microrarray studies associated different gene lists with 5-FU resistance. A major challenge in the genomic era is to find the most validated genes, and to decipher the regulatory networks responsible for the expression changes in a set of co-regulated transcripts. Our aim was to find genes repeatedly associated with 5-FU resistance, and to identify transcription factors (TFs) having overrepresented binding sites (TFBSs) in the promoter regions of genes associated with 5-FU resistance. Materials and Methods: The analyzed data originated from 5 different publications describing genome-wide gene expression patterns associated with 5- FU resistance in gastric and colorectal cancer. First, a data warehouse containing all genes associated with resistance was set up. 39 genes were identified which were repeatedly associated with resistance. Of these, using the EZ-Retrieve web service, proximal promoter sequences were available for 33 genes. The MotifScanner software was used to detect TFBSs in this set of sequences. Results: A total of 200 different TFBSs were identified. Using the statistics tool of the Java program TOUCAN, 4 binding sites were found to be significantly overrepresented: NFKappaB50 (p = 0.01), EGR2 (p = 0.027), EGR3 (p = 0.007), and NGFIC (or EGR4) (p = 0.001). These genes intercept apoptotic pathways at multiple locations in the tumor cells. Conclusion: We identified a consensus gene list associated with 5-FU resistance, performed an in silico comparative promoter analysis, and highlighted the potential implication of some TFs in the development of chemoresistance.
Background: Some patients with inflammatory bowel disease (IBD) do not respond to infliximab (IFX) therapy. Gene expression studies revealed genes that may help to predict non-responding IBD patients. Our purpose was to validate the discriminating power of published genes. Methods:Microarray datasets of IBD patients responding or non-responding to IFX were downloaded from GEO database ('transcriptomic arm'). Published genes discriminating responding and non-responding patients were identified in PubMed ('biomarker arm'). Using ROC-analysis, the discriminating performance of genes in 'biomarker arm' were re-tested in each datasets of 'transcriptomic arm'. We also performed an independent analysis of colon biopsy datasets to identify novel discriminating genes. Results:The transcriptomic arm of four GEO datasets (3 and 1 from colon biopsies and blood cells, respectively) included 99 patients (of those, 59 and 40 were IFX responder and non-responder, respectively). Of the 65 candidate genes reported in biopsy specimens 25 genes discriminated significantly (p<0.05) infliximab responders and nonresponders in the three biopsy datasets consistently. Of the 39 candidate genes reported in peripheral blood 9 genes provided significant discrimination after re-testing. Independent analysis of three biopsy datasets identified the top five genes. Three genes (IL13RA2, PTGS2 and WNT5A) were highly effective discriminator in each analysis. Conclusion:This analysis identified IL13RA2, PTGS2 and WNT5A, three genes in colonic tissues of IBD patients as suitable to discrimination between patients responding and non-responding to IFX therapy. These genes encode proteins implicated in intestinal pathology; the high expression in non-responding patients may indicate important targets in IBD therapy.
Tourniquet application proved to be capable of inducing absolute lower limb ischemia, in contrast to infrarenal aortic ligation, where a rich collateral system is considered to help mitigate the injury.
Aural haematoma is treated either by surgical or by conservative treatment. Both techniques usually require several interventions and re-checks. A new operation technique has been evaluated that requires only a single procedure but is as effective as the techniques used previously. The haematoma is opened, cleaned surgically and the two layers of the auricular cartilage are appositioned inside with several suture lines placed on both sides of the incision, alternating the sides approaching to the sagittal cavity. None of the suture lines is stitched through the auricle completely as they all run intradermally on the side of the haematoma and to the cartilage on the other side. Twenty-three dogs with aural haematoma were treated between 2006 and 2012. In 21 (91%) of them, the haematoma healed without any auricle deformity. No secondary intervention was necessary in any of the cases. None of the 23 animals experienced a relapse during follow-up. The new method offers a minor risk of postoperative complications while accomplishing high healing rates.
There is a growing evidence, that antisense transcription might have a key role in a range of human diseases. Although predefined sense-antisense pairs were extensively studied, the antisense expression of the known sense genes is rarely investigated. We retrieved and correlated the expression of sense and antisense sequences of 1182 mouse transcripts to assess the prevalence and to find the characteristic pattern of antisense transcription. We contrasted three Affymetrix MGU74A version 1 mouse genome chips to six MGU74A version 2 chips. For these 1182 transcripts, the version 1 chips contain the antisense sequences of the transcripts presented on the version 2 chips. The original data was taken from the GEO database (GDS431 and GDS432). As the Affymetrix data are semiquantitative, the relative expression levels of antisense partners were analysed. We detected antisense transcription, although the average antisense expression is shifted towards smaller expression values (MGU74A version 1, 516; version 2, 1688). An inverse direct correlation between sense and antisense expression values could be observed at high expression values. At a very high relative expression--above 40,000--the Pearson correlation coefficient is getting closer to -1. Transcripts with high inverse expression ratio may be correlated to the investigated gene (major histocompatibility complex class II trans activator). The ratio of sense to antisense transcripts varied among different chromosomes; on chromosomes 14 and 1 the level of antisense expression was higher than that of sense. We conclude that antisense transcription is a common phenomenon in the mouse genome. The hypothesis of regulatory role of antisense transcripts is supported by the inverse antisense gene expression of highly expressed genes.
This review summarizes the hemorheological changes during gestation and their clinical relevance in pre-eclampsia. The gestational disease named pre-eclampsia, characterized by proteinuria (more than 0.3 g/day) and hypertension (blood pressure above 140/90 mmHg), exists from the 20th gestational week until the sixth postpartum week. Its etiology is complex; the pathomechanism mainly involves disturbances in cross talks among the vegetative system, the placenta and the circulatory system. Soluble factors of placenta mediate circulatory changes, which result in adaptive responses in both vegetative and circulatory systems. Derailment of this adaption, however, leads to increased turbulence and local damages in cellular elements of the circulatory system. The initial local lesion progresses to a generalized form. Later, these events will continue to strengthen their own cycle. As a result, an unstable circulatory state will be established, which causes organ damages.
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