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Participants without amputation exhibited increased rate of change of foot temperature during walking. No differences in peak temperature or rate of temperature change were observed during the baseline or cooldown periods.

The current findings of altered foot temperature for individuals with transtibial amputation and type 2 diabetes suggest a possible reason for the high rates of contralateral limb ulceration and amputation among this population.

The current findings of altered foot temperature for individuals with transtibial amputation and type 2 diabetes suggest a possible reason for the high rates of contralateral limb ulceration and amputation among this population.Regulation of gene expression starts from the transcription initiation. Regulated transcription initiation is critical for generating correct transcripts with proper abundance. The impact of epigenetic control, such as histone modifications and chromatin remodelling, on gene regulation has been extensively investigated, but their specific role in regulating transcription initiation is far from well understood. Here we aimed to better understand the roles of genes involved in histone H3 methylations and chromatin remodelling on the regulation of transcription initiation at a genome-scale using the budding yeast as a study system. We obtained and compared maps of transcription start site (TSS) at single-nucleotide resolution by nAnT-iCAGE for a strain with depletion of MINC (Mot1-Ino80C-Nc2) by Mot1p and Ino80p anchor-away (Mot1&Ino80AA) and a strain with loss of histone methylation (set1Δset2Δdot1Δ) to their wild-type controls. Our study showed that the depletion of MINC stimulated transcription initiation from many new sites flanking the dominant TSS of genes, while the loss of histone methylation generates more TSSs in the coding region. Moreover, the depletion of MINC led to less confined boundaries of TSS clusters (TCs) and resulted in broader core promoters, and such patterns are not present in the ssdΔ mutant. Our data also exhibits that the MINC has distinctive impacts on TATA-containing and TATA-less promoters. In conclusion, our study shows that MINC is required for accurate identification of bona fide TSSs, particularly in TATA-containing promoters, and histone methylation contributes to the repression of transcription initiation in coding regions.

Pharmacists' compliance with a medication partial fill policy at a Veterans Affairs healthcare system has been underwhelming. Academic detailing, an educational outreach approach conducted by trained health care professionals to improve patient care, is an attractive method for improving pharmacists' compliance with the policy.

To evaluate the impact of academic detailing on pharmacists' compliance with the partial fill policy.

A pre-post analysis was performed to evaluate the impact of academic detailing outreach visits on pharmacists' compliance with the partial fill policy. Data collection included all partial fill medication orders verified during the study duration. Student's t-test was used to analyze the change in the day supply of partial fills following the academic detailing intervention. Total partial fill drug expense during the pre- and post-intervention phases was calculated as drug cost plus material cost for each partial fill.

A total of 36 (97.3%) pharmacists received an academic detailing outreach visit. Total percentage of partial fills limited to a 7-day supply was significantly increased following academic detailing outreach visits (49.2% pre-intervention vs. 84.2% post-intervention, p-value <0.001). Total partial fill drug expense decreased from $12,144.42 to $9,713.50. Percentage of partial fills limited to a 7-day supply remained significant during the 6-month follow-up period (p-value = 0.03).

Academic detailing is an effective method for improving pharmacists' compliance with an outpatient pharmacy partial fill policy and decreasing total partial fill drug expense for the pharmacy department.

Academic detailing is an effective method for improving pharmacists' compliance with an outpatient pharmacy partial fill policy and decreasing total partial fill drug expense for the pharmacy department.Y-box binding proteins are members of the family of proteins containing the evolutionarily conserved cold shock domain. Their cellular functions are quite diverse, including transcription and translation regulation, participation in pre-mRNA splicing, mRNA stabilization and packaging into mRNPs, involvement in DNA repair, and some others. To date, we know little about the plausible functional interchangeability of Y-box binding proteins. learn more Our previous finding was that in YB-1-null HEK293T cells the synthesis of YB-3 is enhanced, thus enabling YB-3 to interact with a larger set of mRNAs and compensate for the YB-1 absence. We suggested the existence of a mechanism of YB-3 synthesis regulation by its paralog, YB-1. Here we demonstrate that YB-1 participates in the translational control and stabilization of YB-3 mRNA through untranslated regions of YB-3 mRNA.

B7-H3 is an important immunomodulatory molecule, and clinical studies have confirmed that its expression level is closely correlated with prostate cancer prognosis. However, the mechanism of its biological action is unclear.

An engineered cell line overexpressing B7-H3 was constructed. Cell apoptosis, growth and proliferation assays

and an animal model

were performed to analyze the role and possible mechanism of B7-H3 in promoting prostate cancer progression.

Compared with the control cell line (Mock-RM-1), the B7-H3-overexpressing prostate cancer cell line (B7-H3-RM-1) showed no significant growth differences

, whereas the

tumorigenesis rate of B7-H3-RM-1 was significantly higher than that of Mock-RM-1. These results suggest that B7-H3indirectly, rather than directly, promotes prostate cancer progression. Further analysis revealed that significantly higher levels of myeloid-derived suppressor cells (MDSCs) accumulated

in B7-H3-RM-1 tumor-bearing mice than in Mock-RM-1 mice.

and

experiments showed that B7-H3-RM-1 cells significantly antagonized MDSC apoptosis. To further confirm the role of MDSCs in B7-H3-mediated prostate cancer progression, model mice were pretreated with cyclophosphamide before inoculation to clear immune cells and achieve myelo suppression. The results showed no significant differences in tumor growth between the B7-H3-RM-1 group and the Mock-RM-1 group.

We found, for the first time, that B7-H3 can antagonize MDSC apoptosis, leading to MDSC accumulation in the tumor microenvironment and thereby promoting prostate cancer progression.

We found, for the first time, that B7-H3 can antagonize MDSC apoptosis, leading to MDSC accumulation in the tumor microenvironment and thereby promoting prostate cancer progression.

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