Versions and accessions of all the genome assemblies, annotated gene sets, or transcriptomes assessed by BUSCO as part of this study are detailed in the
Rodent
They include mice, rats, hamsters, gerbils, guinea pigs, and many others.
Rodents are widely used in biomedical research due to their genetic and physiological similarities to humans, as well as their rapid reproduction and ease of handling.
Researchers utilize rodent models to study a variety of topics, such as disease pathogenesis, drug development, and behavioral neuroscience.
Proper experimental design and the selection of appropriate rodent strains are crucial for ensuring the reliability and reproducibility of research findings.
PubCompare.ai can help optimize rodent research by identifying the best protocols from literature, preprints, and patents, enhanceing the accuracy and reproducibility of your studies.
Most cited protocols related to «Rodent»
Versions and accessions of all the genome assemblies, annotated gene sets, or transcriptomes assessed by BUSCO as part of this study are detailed in the
The current version, PANTHER version 5.0, addresses this issue by implementing a global clustering of proteins. Proteins from PANTHER version 4.0 were clustered using a similarity metric derived from the pairwise BLASTP scores:
This pairwise similarity was used to define single-linkage clusters (maximal clusters in which each protein is connected to at least one other protein in the cluster by a non-zero similarity score). A dendrogram was built for each single-linkage cluster using the UPGMA algorithm (17 ). The family labels from the PANTHER version 4.0 library were then used to define the optimal cut of each UPGMA dendrogram into family clusters, to maximize the correspondence to previous versions of PANTHER. In the great majority of cases, the PANTHER version 5.0 family was almost identical to the corresponding family in the previous version of the library. Only about 40 subtrees in the UPGMA dendrograms, primarily those that were represented by overlapping clusters in the previous version, had to be broken further into functionally homogeneous clusters using manual curation. Overall, the family clusters identified from the UPGMA dendrograms covered over 96% of the version 4.0 training sequences. The rest of the sequences were either singletons according to Equation 1 (often due to low-complexity masking), or lay outside the family boundaries defined by PANTHER version 4.0 family labels on the UPGMA dendrograms. Each of these ‘leftover’ sequences (unmasked) was scored against SAM HMMs built for the family clusters, and was brought into the family of the best scoring HMM if the NLL-NULL score was less than −50. Those leftovers not meeting this criterion were added as singleton families if they were from a primate or rodent species; otherwise they were removed from the library.
Macrovesicular steatosis and microvesicular steatosis were both separately scored and the severity was graded, based on the percentage of the total area affected, into the following categories: 0 (<5%), 1 (5–33%), 2 (34–66%) and 3 (>66%). The difference between macrovesicular and microvesicular steatosis was defined by whether the vacuoles displaced the nucleus to the side (macrovesicular) or not (microvesicular). Similarly, the level of hepatocellular hypertrophy, defined as cellular enlargement more than 1.5 times the normal hepatocyte diameter, was scored, based on the percentage of the total area affected, into the following categories: 0 (<5%), 1 (5–33%), 2 (34–66%) and 3 (>66%). For hepatocellular hypertrophy the evaluation was merely based on abnormal enlargement of the cells, irrespective of rounding of the cells and/or changes in cytoplasm or the number of vacuoles, and is therefore not a substitute of ballooning. The unweight sum of the scores for steatosis (macrovesicular steatosis, microvesicular steatosis and hypertrophy) thus ranged from 0–9. Both steatosis and hypertrophy were evaluated at a 40 to 100× magnification and only the sheets of hepatocytes were taken into account (terminal hepatic venules and portal tracts etc were excluded).
Inflammation was evaluated by counting the number of inflammatory foci per field using a 100 x magnification (view size of 3.1 mm2). A focus was defined a cluster, not a row, of ≥5 inflammatory cells. Five different fields were counted and the average was subsequently scored into the following categories: normal (<0.5 foci), slight (0.5–1.0 foci), moderate (1.0–2.0 foci), severe (>2.0 foci).
Hepatic fibrosis was identified using Sirius Red stained slides at 40 x magnification and evaluated by scoring whether pathologic collagen staining was absent (only in vessels) or collagen staining observed within the liver slide, the latter further defined as mild, moderate or massive. In addition, the percentage of the total area affected was evaluated using using image analysis of surface area on Sirius red stained slides.
From the standardized molecule structures, InChI keys were calculated and used to remove duplicates in the dataset. In the case of multiple LD50 values measured for one compound, the lowest dose value was kept to represent the worst-case toxicity of a compound. Six toxicity classes were defined based on the GHS classification scheme using the LD50 thresholds of 5, 50, 300, 2000 and 5000 mg/kg body weight. Each compound of the dataset was represented using a concatenated fingerprint consisting of the ‘FP2’ and ‘FP4’ fingerprints of Mychem (
In addition to the similarity search, the prediction method takes into account the presence of toxic fragments. All compounds in the database were fragmented using RECAP (20 (link)) as well as the in-house method ROTBONDS (21 (link)). The occurrence of each distinct fragment in molecules of the prediction dataset was tested using its SMILES string, computed with JChem 6.1.3 (November 2013) in a substructure search which was implemented using Open Babel's (19 (link)) fast search. To determine fragments over-represented in the most toxic classes, a propensity analysis (22 (link)) was performed. Propensity scores (PS) were calculated for every fragment and toxicity class. Toxic fragments were defined as those showing a PS above a threshold of 3 in classes I, II or III, and a PS below 1 in classes IV–VI. Based on these conditions, a total number of 1591 and 1580 fragments specific to toxicity classes I–III, generated with the ROTBONDS and RECAP fragmentation method, respectively, were contemplated for prediction.
Most recents protocols related to «Rodent»
Example 16
The instant study was designed to test the efficacy in cotton rats of hMPV vaccines against a lethal challenge. mRNA vaccines encoding hMPV fusion protein were used. The mRNA polynucleotide encodes a full-length fusion protein and comprises the wild-type nucleotide sequence obtained from the hMPV A2a strain.
Cotton rats were immunized intramuscularly (IM) at week 0 and week 3 with the mRNA vaccines encoding hMPV fusion protein with either 2 μg or 10 μg doses for each immunization. The animals were then challenged with a lethal dose of hMPV in week 7 post initial immunization via IV, IM or ID. The endpoint was day 13 post infection, death or euthanasia. Viral titers in the noses and lungs of the cotton rats were measured. The results (
Further, the histopathology of the lungs of the cotton mice immunized and challenged showed no pathology associated with vaccine-enhanced disease (
Example 13
The instant study is designed to test the efficacy in cotton rats of candidate hMPV vaccines against a lethal challenge using an hMPV vaccine comprising mRNA encoding Fusion (F) glycoprotein, major surface glycoprotein G, or a combination of both antigens obtained from hMPV. Cotton rats are challenged with a lethal dose of the hMPV.
Animals are immunized intravenously (IV), intramuscularly (IM), or intradermally (ID) at week 0 and week 3 with candidate hMPV vaccines with and without adjuvant. Candidate vaccines are chemically modified or unmodified. The animals are then challenged with a lethal dose of hMPV on week 7 via IV, IM or ID. Endpoint is day 13 post infection, death or euthanasia. Animals displaying severe illness as determined by >30% weight loss, extreme lethargy or paralysis are euthanized. Body temperature and weight are assessed and recorded daily.
In experiments where a lipid nanoparticle (LNP) formulation is used, the formulation may include a cationic lipid, non-cationic lipid, PEG lipid and structural lipid in the ratios 50:10:1.5:38.5. The cationic lipid is DLin-KC2-DMA (50 mol %) or DLin-MC3-DMA (50 mol %), the non-cationic lipid is DSPC (10 mol %), the PEG lipid is PEG-DOMG (1.5 mol %) and the structural lipid is cholesterol (38.5 mol %), for example.
Example 6
SPF female ICR mice were obtained at 3 weeks of age from Taconic Farms (Hudson, NY), and used for the experiments after one-week acclimation. Mice were housed at the Isolation Unit of the Central Animal Facility (University of Guelph) in a temperature controlled environment with a 12 h light/dark cycle. Animal care was provided in accordance with the animal utilization protocol no. 04R030 (University of Guelph) and the Guide to the Care and Use of Experimental Animals (1). Mice were fed sterilized solid rodent chow and water. When needed, water was supplemented with Amp and Km at a concentration of 400 mg L−1 and 200 mg L−1, respectively. Each mouse was assessed daily for weight, body temperature, signs of dehydration, posture and alertness.
Example 4
As part of evaluating the feasibility of a yeast-based approach as a treatment to mitigate the effects of elevated concentrations of galactose in foods and beverages, several evolved clones were tested for their capability of degrading galactose when present in food. Milk was tested because it represents the most challenging food for galactosemia patients considering its high level of galactose (2-4 g per 100 mL of milk). Food spiked with galactose was tested in parallel.
For this study, three evolved yeast strains obtained by adaptive evolution followed by UV treatment, Clone Y-C201-1, Clone Y-C202-1, and Clone Y-C202-2, one evolved yeast strain obtained by adaptive evolution, Clone Y-C202, as well as the initial parent strain Yi were compared for their galactose consumption activity. Cultures were initiated from a single colony on agar plates and grown in 15 mL of liquid YP medium (1% yeast extract, 2% peptone; Teknova, Hollister, CA) in a 50-mL mini-bioreactor by incubation at 30° C. with an agitation of 225 rpm supplemented with 2% galactose (Teknova). Strain Saccharomyces boulardii (SB) was prepared similarly to the evolved clones except that it was grown in YP medium supplemented with 2% glucose.
The testing of galactose consumption was started with yeast cells obtained from a culture volume containing 1.0×109 Colony Forming Units (CFU) pelleted by centrifugation at 1000 rpm (Sorval, RT7) for 10 min at room temperature. Cell pellets were resuspended either in 1.0 mL of milk already pre-treated with lactase (LACTAID milk where lactose is transformed into galactose and glucose) or in 1 mL rodent diet (Teklad, Envigo) spiked with a solution of 5% galactose or a solution of 5% galactose+1% glucose. All the reactions were incubated at 37° C. Aliquots of the reactions were taken at multiple time points and stored at −20° C. until galactose concentration determination.
Example 10
As part of evaluating the feasibility of a yeast-based approach as a treatment to mitigate the effects of elevated concentrations of fructose in foods and beverages, several evolved clones obtained by adaptive evolution were tested for their ability of degrading fructose when present in food.
For this study, two evolved yeast strains obtained by adaptive evolution, G1_1A and G2_1A were tested for their ability to degrade dietary fructose. The testing of fructose consumption was started with yeast cells obtained from a culture initiated from a single colony on agar plates and grown in 15 mL of liquid YP medium in a 50-mL mini-bioreactor by incubation at 30° C. with an agitation of 225 rpm supplemented with 4% fructose. Cells were pelleted by centrifugation at 1000 rpm (Sorval, RT7) for 10 min at room temperature. Cell pellets were resuspended in 5 mL rodent diet (Teklad, Envigo) spiked with a solution of 10% fructose (=555 mM). Reactions were incubated at 37° C. to mimic human gastrointestinal temperature conditions. Aliquots of the reactions were taken at multiple time points and stored at −20° C. until fructose concentration determination using the colorimetric Fructose Assay Kit (Cat. No. EFRU-100; BioAssay Systems, Hayward, CA).
As shown in Table 12, the evolved clones were able to rapidly decrease fructose concentration when present in diet.
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More about "Rodent"
This includes a wide variety of species such as mice, rats, hamsters, gerbils, guinea pigs, and many others.
Rodents are widely utilized in biomedical research due to their genetic and physiological similarities to humans, as well as their rapid reproduction and ease of handling.
Researchers often utilize rodent models, such as C57BL/6J mice, C57BL/6, C57BL/6J male mice, and Sprague-Dawley rats, to study a variety of topics, including disease pathogenesis, drug development, and behavioral neuroscience.
The Total OXPHOS Rodent WB Antibody Cocktail is a useful tool for researchers working with rodent samples.
Proper experimental design and the selection of appropriate rodent strains are crucial for ensuring the reliablity and reproducibility of research findings.
PubCompare.ai can help optimize rodent research by identifying the best protocols from literature, preprints, and patents, enhanceing the accuracy and reproducibility of your studies.
This can lead to more reliable and accurate research outcomes, streamlining the research process.