“Un-balanced” Economic Growth

Since the elasticity of substitution between capital and labor is not always one, and since technical progress is not always Harrod-neutral, it is desirable to have an endogenous growth model that admits all sizes of the elasticity and all known technology modes. We derive an equation to do just that, fully describing the per capita income growth rate at all times. It shows a typical economy needing hundreds if not thousands of years to reach its long term growth rate, leading to the conclusion that even the short run may be very long indeed.The elasticity of substitution, Non-Harrod-neutral technology, short-run growth

Continuous Monitoring of Distributed Data Streams over a Time-based Sliding Window

The past decade has witnessed many interesting algorithms for maintaining statistics over a data stream. This paper initiates a theoretical study of algorithms for monitoring distributed data streams over a time-based sliding window (which contains a variable number of items and possibly out-of-order items). The concern is how to minimize the communication between individual streams and the root, while allowing the root, at any time, to be able to report the global statistics of all streams within a given error bound. This paper presents communication-efficient algorithms for three classical statistics, namely, basic counting, frequent items and quantiles. The worst-case communication cost over a window is $O(\frac{k} {\epsilon} \log \frac{\epsilon N}{k})$ bits for basic counting and $O(\frac{k}{\epsilon} \log \frac{N}{k})$ words for the remainings, where $k$ is the number of distributed data streams, $N$ is the total number of items in the streams that arrive or expire in the window, and $\epsilon < 1$ is the desired error bound. Matching and nearly matching lower bounds are also obtained.Comment: 12 pages, to appear in the 27th International Symposium on Theoretical Aspects of Computer Science (STACS), 201

Peri-prostatic fat volume measurement as a predictive tool for castration resistance in advanced prostate cancer

Background: Obesity and aggressive prostate cancer (PC) may be linked, but how local peri-prostatic fat relates to tumour response following androgen deprivation therapy (ADT) is unknown. Objective: To test if peri-prostatic fat volume (PPFV) predicts tumour response to ADT. Design, setting, and participants: We performed a retrospective study on consecutive patients receiving primary ADT. From staging pelvic magnetic resonance imaging scans, the PPFV was quantified with OsirixX 6.5 imaging software. Statistical (univariate and multivariate) analysis were performed using R Version 3.2.1. Results and limitations: Of 224 consecutive patients, 61 with advanced (≥T3 or N1 or M1) disease had (3-mm high resolution axial sections) pelvic magnetic resonance imaging scan before ADT. Median age = 75 yr; median PPFV = 24.8 cm3 (range, 7.4–139.4 cm3). PPFV was significantly higher in patients who developed castration resistant prostate cancer (CRPC; n = 31), with a median of 37.9 cm3 compared with 16.1 cm3 (p &lt; 0.0001, Wilcoxon rank sum test) in patients who showed sustained response to ADT (n = 30). Multivariate analysis using Cox proportional hazards models were performed controlling for known predictors of CRPC. PPFV was shown to be independent of all included factors, and the most significant predictor of time to CRPC. Using our multivariate model consisting of all known factors prior to ADT, PPFV significantly improved the area under the curve of the multivariate models receiver operating characteristic analysis. The main study limitation is a relatively small cohort to account for multiple variables, necessitating a future large-scale prospective analysis of PPFV in advanced PC. Conclusions: PPFV quantification in patients with advanced PC predicts tumour response to ADT

The RNA-binding protein hnRNPA2 regulates β-catenin protein expression and is overexpressed in prostate cancer

The RNA-binding protein hnRNPA2 (HNRNPA2B1) is upregulated in cancer, where it controls alternative pre-mRNA splicing of cancer-relevant genes. Cytoplasmic hnRNPA2 is reported in aggressive cancers, but is functionally uncharacterized. We explored the role of hnRNPA2 in prostate cancer (PCa). Methods: hnRNPA2 function/localization/expression in PCa was determined using biochemical approaches (colony forming/proliferation/luciferase reporter assays/flow cytometry/immunohistocytochemistry). Binding of hnRNPA2 within cancer-relevant 3′-UTR mRNAs was identified by bioinformatics. Results: RNAi-mediated knockdown of hnRNPA2 reduced colony forming and proliferation, while hnRNPA2 overexpression increased proliferation of PCa cells. Nuclear hnRNPA2 is overexpressed in high-grade clinical PCa, and is also observed in the cytoplasm in some cases. Ectopic expression of a predominantly cytoplasmic variant hnRNPA2-ΔRGG also increased PCa cell proliferation, suggesting that cytoplasmic hnRNPA2 may also be functionally relevant in PCa. Consistent with its known cytoplasmic roles, hnRNPA2 was associated with 3′-UTR mRNAs of several cancer-relevant mRNAs including β-catenin (CTNNB1). Both wild-type hnRNPA2 and hnRNPA2-ΔRGG act on CTNNB1 3′-UTR mRNA, increasing endogenous CTNNB1 mRNA expression and β-catenin protein expression and nuclear localization. Conclusion: Nuclear and cytoplasmic hnRNPA2 are present in PCa and appear to be functionally important. Cytoplasmic hnRNPA2 may affect the cancer cell phenotype through 3′-UTR mRNA-mediated regulation of β-catenin expression and other cancer-relevant genes

AMP-activated protein kinase (AMPK) as a potential therapeutic target independent of PI3K/Akt signaling in prostate cancer

Depletion of cellular energy activates the AMP-activated protein kinase (AMPK) to favor energy-producing catabolic processes during tumorigenesis. Using a panel of in vitro cell lines and resected tumors, we investigated the therapeutic value of manipulating AMPK in prostate cancer (PC). Phospho-AMPK expression was significantly elevated in human PC cells and clinical PC samples. In clinical PC, we observed a trend for increasing phospho-AMPK with increasing Gleason sum score; Phospho-AMPK expression was associated with phospho-ACC (p=0.0023). Using the paired PC3 and PC3M cells to model progressive androgen-independent PC, treatment with either 5-aminoimidazole-4-carboxamide riboside (AICAR) or A-769662 suppressed proliferation, migration and invasion in both cell lines, and down-regulated mTOR and P70S6Ki levels regardless of the Akt status. Involvement of AMPK was confirmed by Compound C (AMPK inhibitor) and siRNA-mediated AMPK silencing. Despite similar functional responses in PC3 and PC3M cells, AMPK activation resulted in sustained phospho-Akt activation in PC3M cells, but not in PC3 cells. This prompted the addition of the PI3K inhibitor LY-294002 to AICAR treatment of PC3M cells in a proliferation assay. Interestingly, we found no synergistic effects upon combined treatment. Collectively, these findings support AMPK as a potential therapeutic target independent of PI3K/Akt signalling