Intradepartmental System of Allocating Operating Room Block Time and its Financial Impact at The University of New Mexico Department of Orthopaedics & Rehabilitation: A Preliminary Report

Background: Within a hospital, the operating room (OR) is one of the most critical and expensive resources. Labor productivity is maximized by filling allocated surgical block time with as many hours of cases as possible. We have found that the intradepartmental block time release system at our institution has improved access to operating time, resulting in a substantial financial advantage within the department. Methods: The annual charges and collections produced by the pick-up of intradepartmental released block time during the past 4 fiscal years (July 1-June 30) was assessed at both the main hospital and an outpatient surgical center. Results: There is a general, year-over-year trend of increasing charges and collections from the intradepartmental release of OR time. The average gross collection rate for OR pick-up time is 30%, which matches the average collection rate of about 30% for our department. At the main inpatient hospital, the orthopaedic spine service typically comprises the mostreleased OR block time. In the outpatient setting, typically the orthopaedic hand service captures the most released OR block time. Conclusions: The early release of allocated block time on an internal level may help schedule patients in an easier manner, with decreased patient wait times than other methods, and maintain the overall revenue within the department. Further studies that quantify surgeon satisfaction would help strengthen the use and validation of this system

Global urban environmental change drives adaptation in white clover

Urbanization transforms environments in ways that alter biological evolution. We examined whether urban environmental change drives parallel evolution by sampling 110,019 white clover plants from 6169 populations in 160 cities globally. Plants were assayed for a Mendelian antiherbivore defense that also affects tolerance to abiotic stressors. Urban-rural gradients were associated with the evolution of clines in defense in 47% of cities throughout the world. Variation in the strength of clines was explained by environmental changes in drought stress and vegetation cover that varied among cities. Sequencing 2074 genomes from 26 cities revealed that the evolution of urban-rural clines was best explained by adaptive evolution, but the degree of parallel adaptation varied among cities. Our results demonstrate that urbanization leads to adaptation at a global scale

Oscillation Results for a Class of Nonlinear Fractional Order Difference Equations with Damping Term

The paper studies the oscillation of a class of nonlinear fractional order difference equations with damping term of the form Δψλzηλ+pλzηλ+qλF∑s=λ0λ−1+μ λ−s−1−μys=0, where zλ=aλ+bλΔμyλ, Δμ stands for the fractional difference operator in Riemann-Liouville settings and of order μ, 0<μ≤1, and η≥1 is a quotient of odd positive integers and λ∈ℕλ0+1−μ. New oscillation results are established by the help of certain inequalities, features of fractional operators, and the generalized Riccati technique. We verify the theoretical outcomes by presenting two numerical examples

Modeling and stability analysis of the spread of novel coronavirus disease COVID-19

© 2021 World Scientific Publishing Company.Towards the end of 2019, the world witnessed the outbreak of Severe Acute Respiratory Syndrome Coronavirus-2 (COVID-19), a new strain of coronavirus that was unidentified in humans previously. In this paper, a new fractional-order Susceptible-Exposed-Infected-Hospitalized-Recovered (SEIHR) model is formulated for COVID-19, where the population is infected due to human transmission. The fractional-order discrete version of the model is obtained by the process of discretization and the basic reproductive number is calculated with the next-generation matrix approach. All equilibrium points related to the disease transmission model are then computed. Further, sufficient conditions to investigate all possible equilibria of the model are established in terms of the basic reproduction number (local stability) and are supported with time series, phase portraits and bifurcation diagrams. Finally, numerical simulations are provided to demonstrate the theoretical findings

Protein kinase C beta II suppresses colorectal cancer by regulating IGF-1 mediated cell survival.

Despite extensive efforts, cancer therapies directed at the Protein Kinase C (PKC) family of serine/threonine kinases have failed in clinical trials. These therapies have been directed at inhibiting PKC and have, in some cases, worsened disease outcome. Here we examine colon cancer patients and show not only that PKC Beta II is a tumour suppressor, but patients with low levels of this isozyme have significantly decreased disease free survival. Specifically, analysis of gene expression levels of all PKC genes in matched normal and cancer tissue samples from colon cancer patients revealed a striking down-regulation of the gene coding PKC Beta in the cancer tissue (n = 21). Tissue microarray analysis revealed a dramatic down-regulation of PKC Beta II protein levels in both the epithelial and stromal diseased tissue (n = 166). Of clinical significance, low levels of the protein in the normal tissue of patients is associated with a low (10%) 10 year survival compared with a much higher (60%) survival in patients with relatively high levels of the protein. Consistent with PKC Beta II levels protecting against colon cancer, overexpression of PKC Beta II in colon cancer cell lines reveals that PKC Beta II reverses transformation in cell based assays. Further to this, activation of PKC Beta II results in a dramatic downregulation of IGF-I-induced AKT, indicating a role for PKCs in regulating IGF-1 mediated cell survival. Thus, PKC Beta II is a tumour suppressor in colon cancer and low levels serve as a predictor for poor survival outcome

Low MiR-187 Expression Promotes Resistance to Chemoradiation Therapy In Vitro and Correlates with Treatment Failure in Patients with Esophageal Adenocarcinoma

Abstract Esophageal adenocarcinoma (EAC) has a poor prognosis and is increasing in incidence in many Western populations. Neoadjuvant chemoradiation therapy (CRT) followed by surgery is increasingly the standard of care for locally advanced EAC; however, resistance to treatment is a significant clinical problem. The identification of both novel biomarkers predicting response to treatment and novel therapeutic targets to enhance the efficacy of CRT is key to improving survival rates in EAC. In this study, we performed global microRNA (miRNA) profiling of pretreatment EAC biopsies and identified 67 miRNAs significantly altered in patients who are resistant to CRT. One of these miRNAs, miR-187, was significantly decreased in pretreatment EAC tumors from patients having a poor response to neoadjuvant CRT, highlighting downregulation of miR-187 as a potential mediator of treatment resistance in EAC. In vitro, miR-187 was demonstrated to play a functional role in modulating sensitivity to X-ray radiation and cisplatin in EAC and its dysregulation was demonstrated to be due to chromosomal alterations. In vitro, miR-187 altered expression of a diverse array of pathways, including the immune regulator complement component 3 (C3), serum levels of which we have previously demonstrated to predict patient response to CRT. In vivo, expression of C3 was significantly increased in tumors from patients having a poor response to CRT. This study highlights for the first time a role for miR-187 as a novel biomarker of response to CRT and a potential therapeutic target for enhancing the efficacy of CRT in EAC

Combining 1,4-dihydroxy quininib with Bevacizumab/FOLFOX alters angiogenic and inflammatory secretions in ex vivo colorectal tumors

Background: Colorectal cancer (CRC) is the second most common cause of cancer-related mortality worldwide with one in every five patients diagnosed with metastatic CRC (mCRC). In mCRC cases, the 5-year survival rate remains at approximately 14%, reflecting the lack of effectiveness of currently available treatments such as the anti-VEGF targeting antibody Bevacizumab combined with the chemotherapy folinic acid, fluorouracil and oxaliplatin (FOLFOX). Approximately 60% of patients do not respond to this combined treatment. Furthermore, Bevacizumab inhibits dendritic cell (DC) maturation in poor responders, a key process for tumor eradication. Method: Following drug treatment, secreted expression levels of angiogenic and inflammatory markers in tumor conditioned media generated from human ex vivo colorectal tumors were measured by ELISA. Dendritic cell phenotypic and maturation markers were assessed by flow cytometry. Results: Our novel compound, 1,4-dihydroxy quininib, acts in an alternative pathway compared to the approved therapy Bevacizumab. 1,4-dihydroxy quininib alone, and in combination with Bevacizumab or FOLFOX significantly reduced TIE-2 expression which is involved in the promotion of tumor vascularization. Combination treatment with 1,4-dihydroxy quininib significantly increased the expression level of DC phenotypic and maturation markers. Conclusion: Our results indicate the anti-angiogenic small molecule 1,4-dihydroxy quininib could be an alternative novel treatment in combination therapy for CRC patients

Expression of protein kinase C gamma promotes cell migration in colon cancer

Despite extensive efforts, Protein Kinase Cs (PKCs) have proven to be an intractable target in cancer therapies. Traditionally it was accepted that PKCs act as tumour promoters, however new research suggests that PKCs may play an important role in the suppression of cancer. A challenge in targeting PKCs is the limited data available in patient samples. One of the PKC isozymes, PKC gamma, is thought to be present only in the brain and has been largely neglected in the context of cancer. Analysis of gene expression levels of PKC gamma in patient matched normal and colon cancer tissue samples revealed an up-regulation of the gene in the cancer tissue of 54% of the patients examined. Mechanistically we demonstrate that a reduction in the levels of PKC gamma in the colon cancer cells inhibits cell migration and foci formation. Further to this, we observe an increase in cell adhesion and proliferation following the reduction of PKC gamma levels in the cell. Thus, PKC gamma plays a key role in colon cancer; making it an important isozyme that needs to be reconsidered in the context of cancer therapies