An1-03
Ontology highlight
ABSTRACT:
SUBMITTER: Yu Zhang
PROVIDER: OEX00012161 | NODE | 2021-01-29
REPOSITORIES: NODE
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Project description:The adult somatosensory cortex undergoes reorganization in response to changes in peripheral input, such as limb usage patterns or denervation/amputation. This reorganization underlies important phenomena, such as phantom pain, recovery after stroke, and certain forms of learning. Although cellular processes, such as LTP, receptor regulation, axonal growth and synaptic formation have been theorized and studied in relation to cortical reorganization, conclusive evidence remains elusive. The identification of genes up- and down-regulated during reorganization will provide clues for which processes underlie reorganization. Reorganization is likely to involve forms of signaling between cortical neurons (e.g. release of growth factors), which could be identified through gene chip studies. Identification of genes modulated during reorganization will provide specific direction for further studies in the elucidation of the mechanism(s) underlying cortical reorganization. To identify those genes with altered regulation during the cortical reorganization process. We hypothesize that genes regulated during cortical reorganization will be components of the mechanism(s) underlying this important process, and that identification of these genes will provide insight for the design of further studies of cortical plasticity. Cortical reorganization in rat somatosensory cortex (S1) will be induced at the forepaw/lower jaw border by partially denervating the paw. The animals will be recovered and the reorganization allowed to proceed for 3, 7, 14 and 28 days. Control animals will receive a sham denervation. Following the allotted time, the border between the lower jaw and the now silent forepaw cortex will be mapped in vivo. A 500 um wide strip of cortex surrounding the border area will be excised and stored in RNAlater (Qiagen) at 20oC until processed for RNA extraction. The tissue will be dispersed using a disposable pestle and microcentrifuge tube and then homogenized in Qiashredder (Qiagen) columns. RNA will be extracted using a RNeasy Micro Kit. However, if the UCLA center has a rotor/stator homogenizer with a microcentrifuge tube sized probe, we would like to discuss the possibility of performing the RNA extraction there (we would expect a better yield, and cannot locate this equipment at UCR). An initial portion of this study will done for 3 day experimental and sham control animals, plus non-operated animals, with four animals per group. This will be to determine the variability among our samples and to familiarize our personnel with the process. The number of samples/group necessary for the remaining time points may be modified based on the results of the 3 day study. Keywords: time-course
2005-07-06 | GSE2874 | GEO
Project description:Interventions: Start protocol treatment within 8 weeks after surgery.
If it was not possible to start within 8 weeks after surgery, state the reason on the treatment progress record sheet.
Test treatment
UFT is administered orally three times a day (about every 8 hours) avoiding one hour before and after meal, dividing equivalent amount of 300 to 600 mg of tegafur (300 mg/m 2/day). LV (Uzel tablet) is 75 mg/day divided three times a day, and it is orally administered simultaneously with UFT. This is administered for 28 consecutive days, followed by 7 days off. As this is one course, we will implement 5 courses (25W).
Primary outcome(s): Feasibility
An aborted case because of the reason of 1) or 2) is regarded as an event. An aborted case because of the reason of 3) to 5) is regarded as a censored case and calculated the cumulative completion rate by the Kaplan-Meier method or the like. For the calculation of the confidence interval of the cumulative completion rate at 25 weeks after UFT / LV administration, Greenwood’s equation is used.
1) Canceling due to side effects.
2) Canceling due to patient refusal.
3) Canceling due to complications after curative treatment.
4) Canceling due to recurrence or death.
5) Canceling cases due to patient transfers.
Study Design: single arm study, open(masking not used), no treatment control/standard of care control, single assignment, treatment purpose
| 2615636 | ecrin-mdr-crc
Project description:Background: The importance of print health literacy is widely recognized, but oral literacy has been largely ignored. Because much health information is conveyed via spoken word, an inaccurate or incomplete comprehension of spoken health messages may have important consequences. This study explored the extent to which listeners understood critical concepts in spoken messages about cancer prevention and screening.Methods: Forty-four adults from three health plans took part in a 1-hour interview. Participants viewed six brief media clips from TV or the Web about cancer prevention and screening. Each clip contained multiple messages. Participants paraphrased the clips? main points and key concepts. We coded the accuracy of participants? responses with respect to the message content.Results: Of 44 participants, aged 41 to 70, 52% were female; 48% were non-white; and 5% had a high school education or less. Messages were generally understood by most participants but some participants misunderstood critical cancer prevention concepts. Nine of 44 could not define the term ?at risk.? Others provided approximately accurate synonyms, such as ?susceptible to,? or ?inclined to,? or gave examples of risk factors (e.g. fair skin for skin cancer) that indicated a partial understanding of the concept. In response to a news report about a comprehensive cancer study synthesizing the results of 7,000 clinical trials, 10% of the participants viewed the study size as small, or mistook the number of trials for number of patients. Some participants had trouble distinguishing ?screening? and ?prevention,? apparently believing that screening is inherently preventive.Conclusions: Most participants in this sample of moderately to well-educated adults understood the main points contained in spoken messages about cancer screening and prevention. However, important concepts such as ?at risk? (applicable to conditions besides cancer), were sometimes misunderstood. Similarly, some participants had difficulty understanding the strength of research evidence and the value of multiple studies. Comprehension depends on foundational knowledge, which even educated lay people may be missing. Speakers, whether news anchors or providers?cannot assume that listeners understand critical health concepts even if the words themselves seem simple.
| S-EPMC2842424 | biostudies-other
Project description:The highest genetic type 1 diabetes risk is conferred by HLA class II haplotypes defined by alleles at the HLA-DR and -DQ loci. The combination of HLA-DQA1*03:01 and DQB1*03:02 alleles (summarized as 'HLA-DQ8') is reported to be among the two most prevalent HLA class II haplotypes in Caucasian type 1 diabetes patients. This classification is based on conventional genotyping of exon 2 of the DQ gene locus and excludes exon 3. In this study, HLA genotyping on the type 1 diabetes susceptibility loci HLA-DRB1, DQA1 and DQB1 was performed using a high-resolution next generation sequencing method. In addition to the routinely examined exon 2, exon 3 was also sequenced. Samples from 229 children with type 1 diabetes were included and compared to a cohort of 9,786 controls. In addition to previously described HLA-DQ haplotypes in type 1 diabetes patients, we found that as well as HLA-DQA1*03:01,HLA-DQA1*03:03 also contributed to HLA-DQ8. HLA-DQA1*03:03 differs from HLA-DQA1*03:01 by one nucleotide substitution in exon 3 at position 160, leading to a single amino acid replacement. DRB1*04:05 was exclusively associated with DQA1*03:03 whereas the DRB1*04:01 haplotype comprised either DQA1*03:01 or DQA1*03:03. Significantly increased type 1 diabetes risk was confirmed for all these haplotypes with only minor differences between DQA1*03:01 and DQA1*03:03 alleles. This study identified the HLA-DQA1*03:03 allele as an addition to the already known type 1 diabetes risk haplotypes, and can contribute to more precise HLA genotyping approaches.
| S-EPMC8701008 | biostudies-literature
Project description:HLA-C*03:03:01:52N differs from HLA-C*03:03:01:01 by one nucleotide substitution at position gDNA 202 (A>G) in Intron1.
| S-EPMC9542030 | biostudies-literature
Project description:Homology models of amidase-03 from Bacillus anthracis were constructed using Modeller (9v2). Modeller constructs protein models using an automated approach for comparative protein structure modeling by the satisfaction of spatial restraints. A template structure of Listeria monocytogenes bacteriophage PSA endolysin PlyPSA (PDB ID: 1XOV) was selected from protein databank (PDB) using BLASTp with BLOSUM62 sequence alignment scoring matrix. We generated five models using the Modeller default routine in which initial coordinates are randomized and evaluated by pseudo-energy parameters. The protein models were validated using PROCHECK and energy minimized using the steepest descent method in GROMACS 3.2 (flexible SPC water model in cubic box of size 1 Å instead of rigid SPC model). We used G43a1 force field in GROMACS for energy calculations and the generated structure was subsequently analyzed using the VMD software for stereo-chemistry, atomic clash and misfolding. A detailed analysis of the amidase-03 model structure from Bacillus anthracis will provide insight to the molecular design of suitable inhibitors as drug candidates.
| S-EPMC2951712 | biostudies-literature
Project description:Transcription activation of latent human immunodeficiency virus-1 (HIV-1) occurs due to HIV-1 rebound, the interruption of combination antiretroviral therapy, or development of drug resistance. Thus, novel HIV-1 inhibitors, targeting HIV-1 transcription are needed. We previously developed an HIV-1 transcription inhibitor, 1E7-03, that binds to the noncatalytic RVxF-accommodating site of protein phosphatase 1 and inhibits HIV-1 replication in cultured cells and HIV-1-infected humanized mice by impeding protein phosphatase 1 interaction with HIV-1 Tat protein. However, host proteins and regulatory pathways targeted by 1E7-03 that contribute to its overall HIV-1 inhibitory activity remain to be identified. To address this issue, we performed label-free quantitative proteome and phosphoproteome analyses of noninfected and HIV-1-infected CEM T cells that were untreated or treated with 1E7-03. 1E7-03 significantly reprogramed the phosphorylation profile of proteins including PPARα/RXRα, TGF-β, and PKR pathways. Phosphorylation of nucleophosmin (NPM1) at Ser-125 residue in PPARα/RXRα pathway was significantly reduced (>20-fold, p = 1.37 × 10-9), followed by the reduced phosphorylation of transforming growth factor-beta 2 at Ser-46 (TGF-β2, >12-fold, p = 1.37 × 10-3). Downregulation of NPM1's Ser-125 phosphorylation was further confirmed using Western blot. Phosphorylation mimicking NPM1 S125D mutant activated Tat-induced HIV-1 transcription and exhibited enhanced NPM1-Tat interaction compared to NPM1 S125A mutant. Inhibition of Aurora A or Aurora B kinases that phosphorylate NPM1 on Ser-125 residue inhibited HIV-1, further supporting the role of NPM1 in HIV-1 infection. Taken together, 1E7-03 reprogrammed PPARα/RXRα and TGF-β pathways that contribute to the inhibition of HIV-1 transcription. Our findings suggest that NPM1 phosphorylation is a plausible target for HIV-1 transcription inhibition.
| S-EPMC9975258 | biostudies-literature
Project description:RNAseq responses in Anopheles coluzzii's 2 days post dsENH_2L-03 injection (treatment) vs dsGFP injection (control).
2024-10-13 | E-MTAB-14478 | biostudies-arrayexpress
Project description:Romidepsin, a potent histone deacetylase inhibitor, has shown activity in preclinical glioma models. The primary objectives of this trial were to determine the pharmacokinetics of romidepsin in patients with recurrent glioma on enzyme-inducing antiepileptic drugs (EIAEDs) and to evaluate the antitumor efficacy of romidepsin in patients with recurrent glioblastoma who were not receiving EIAEDs. Two dose cohorts were studied in the phase I component of the trial (13.3 and 17.7 mg/m(2)/d). Patients in the phase II component were treated with intravenous romidepsin at a dosage of 13.3 mg/m(2)/day on days 1, 8, and 15 of each 28-day cycle. Eight patients were treated on the phase I component. A similar romidepsin pharmacokinetic profile was demonstrated between patients receiving EIAEDs to those not receving EIAEDs. Thirty-five patients with glioblastoma were accrued to the phase II component. There was no objective radiographic response. The median progression-free survival (PFS) was 8 weeks and only 1 patient had a PFS time ≥6 months (PFS6 = 3%). To date, 34 patients (97%) have died, with a median survival duration of 34 weeks. Despite in vitro studies showing that romidepsin is primarily metabolized by CYP3A4, no decrease in exposure to romidepsin was seen in patients receiving potent CYP3A4 inducers. Romidepsin, at its standard dose and schedule, was ineffective for patients with recurrent glioblastomas. ClinicalTrials.gov identifier: NCT00085540.
| S-EPMC3093337 | biostudies-literature
Project description:The novel NKG2C*03 allele encodes a hybrid of the NKG2C*01 and NKG2C*02 primary structures.
| S-EPMC8451841 | biostudies-literature