Valuing Place in a Chicago Market

This essay approaches the ideas of value and valuing though an exploration of the Maxwell Street market in Chicago, USA. The market was the largest open-air market in North America for much of the twentieth century. From the 1960s onwards it has been subjected to various forms of valuing and devaluing leading to its eventual demise in its historic location in 1994. The essay explores how the market and things in the market entered and left various regimes of value over time. The focus is on the role of hub-caps, home-made instruments called Stradizookys, and the process of tax-increment financing. The essay ends with some thought around order and regulation in the urban landscape.

Protection from muscle damage in the absence of changes in muscle mechanical behavior

Introduction: The repeated bout effect characterizes the protective adaptation after a single bout of unaccustomed eccentric exercise that induces muscle damage. Sarcomerogenesis and increased tendon compliance have been suggested as potential mechanisms for the repeated bout effect by preventing muscle fascicles from being stretched onto the descending limb of the length–tension curve (the region where sarcomere damage is thought to occur). In this study, evidence was sought for three possible mechanical changes that would support either the sarcomerogenesis or the increased tendon compliance hypotheses: a sustained rightward shift in the fascicle length–tension relationship, reduced fascicle strain amplitude, and reduced starting fascicle length. Methods: Subjects (n = 10) walked backward downhill (5 km/h, 20% incline) on a treadmill for 30 min on two occasions separated by 7 d. Kinematic data and medial gastrocnemius fascicle lengths (ultrasonography) were recorded at 10-min intervals to compare fascicle strains between bouts. Fascicle length–torque curves from supramaximal tibial nerve stimulation were constructed before, 2 h after, and 2 d after each exercise bout. Results: Maximum torque decrement and elevated muscle soreness were present after the first, but not the second, backward downhill walking bout signifying a protective repeated bout effect. There was no sustained rightward shift in the length–torque relationship between exercise bouts, nor decreases in fascicle strain amplitude or shortening of the starting fascicle length. Conclusions: Protection from a repeated bout of eccentric exercise was conferred without changes in muscle fascicle strain behavior, indicating that sarcomerogenesis and increased tendon compliance were unlikely to be responsible. As fascicle strains are relatively small in humans, we suggest that changes to connective tissue structures, such as extracellular matrix remodeling, are better able to explain the repeated bout effect observed here

Identification of LIMK2 as a therapeutic target in castration resistant prostate cancer

This study identified LIMK2 kinase as a disease-specific target in castration resistant prostate cancer (CRPC) pathogenesis, which is upregulated in response to androgen deprivation therapy, the current standard of treatment for prostate cancer. Surgical castration increases LIMK2 expression in mouse prostates due to increased hypoxia. Similarly, human clinical specimens showed highest LIMK2 levels in CRPC tissues compared to other stages, while minimal LIMK2 was observed in normal prostates. Most notably, inducible knockdown of LIMK2 fully reverses CRPC tumorigenesis in castrated mice, underscoring its potential as a clinical target for CRPC. We also identified TWIST1 as a direct substrate of LIMK2, which uncovered the molecular mechanism of LIMK2-induced malignancy. TWIST1 is strongly associated with CRPC initiation, progression and poor prognosis. LIMK2 increases TWIST1 mRNA levels upon hypoxia; and stabilizes TWIST1 by direct phosphorylation. TWIST1 also stabilizes LIMK2 by inhibiting its ubiquitylation. Phosphorylation-dead TWIST1 acts as dominant negative and fully prevents EMT and tumor formation in vivo, thereby highlighting the significance of LIMK2-TWIST1 signaling axis in CRPC. As LIMK2 null mice are viable, targeting LIMK2 should have minimal collateral toxicity, thereby improving the overall survival of CRPC patients

Editorial

East Asian Languages and Civilization

Productivity, family planning and reproductive health in Burkina Faso: the PopDev study

Quantitative data from a prospective cohort study of 839 pregnant and/or postpartum women who were between seven months gestation and three months postpartum at recruitment. Participants were interviewed three times over a nine month period. The cohort is a population-representative sample of parturient women in the commune of Bobo-Dioulasso, Burkina Faso. Data were collected relating to socio-demographic characteristics; household assets; reproductive history; women’s work and occupation including both income-generating and non-income generating activities; birth and postpartum preparedness; characteristics of the index delivery; contraceptive history and current use; fertility preferences; health-related functioning (ability to carry out usual daily activities); haemoglobin level; mental health measured through the K10 scale; time use diary; household food security scale

Non-Poisson variations in photomultipliers and implications for luminescence dating

Previous studies have suggested that excess variations from single-photon counting systems used in luminescence dating may result in underestimation of errors and profoundly influence age models. In this study ten different photon counting systems have been investigated to explore this effect with a greater number of photomultiplier types and instrumental architectures. It is shown that radiation induced phosphorescence from F1 feldspar produces a controllable low-level light source whose local variance approximates Poisson expectations. However excess variation in dark counts was observed to varying extents from all systems. The excess variance is slightly anti-correlated with the age of the system, with older devices conforming more closely to Poisson behaviour. This observation does not seem to fit the hypothesis that enhanced levels of helium diffused into older tubes increase non-Poisson components. It was noted that a significant part of the non-Poisson behaviour was associated with multi-event pulse streams within time series. Work was also undertaken to develop mitigation methods for data analysis and to examine the implications for dating uncertainties in a test case. A Poisson-filtering algorithm was developed to identify and remove improbable multi-event streams. Application to data from signal-limited single grains of sediments from a Neolithic chambered tomb in Corsica has shown that, for this case, removing non-Poisson components improves the robustness of retained data, but has less influence on overall dating precision or accuracy. In signal limited applications use of this algorithm to remove one source of excess variation is beneficial. The algorithm and test data are appended to facilitate this.PostprintPeer reviewe

Cholesterol Sulfotransferase SULT2B1b Modulates Sensitivity to Death Receptor Ligand TNFα in Castration-Resistant Prostate Cancer

Cholesterol sulfotransferase, SULT2B1b, has been demonstrated to modulate both androgen receptor activity and cell growth properties. However, the mechanism(s) by which SULT2B1b alters these properties within prostate cancer cells has not been described. Furthermore, specific advantages of SULT2B1b expression in prostate cancer cells is not understood. In these studies, single-cell mRNA sequencing (scRNA-seq) was conducted to compare the transcriptomes of SULT2B1b knockdown (KD) versus Control KD LNCaP cells. Over 2,000 differentially expressed (DE) genes were identified along with alterations in numerous canonical pathways, including the death receptor signaling pathway. The studies herein demonstrate that SULT2B1b KD increases tumor necrosis factor alpha (TNF) expression in prostate cancer cells and results in NF-κB activation in a TNF-dependent manner. More importantly, SULT2B1b KD significantly enhances TNF-mediated apoptosis in both TNF-sensitive LNCaP cells and TNF-resistant C4–2 cells. Overexpression of SULT2B1b in LNCaP cells also decreases sensitivity to TNF-mediated cell death, suggesting that SULT2B1b modulates pathways dictating the TNF sensitivity capacity of prostate cancer cells. Probing human prostate cancer patient datasets further support this work by providing evidence that SULT2B1b expression is inversely correlated with TNF-related genes, including TNF, CD40LG, FADD, and NFKB1. Together, these data provide evidence that SULT2B1b expression in prostate cancer cells enhances resistance to TNF and may provide a growth advantage. In addition, targeting SULT2B1b may induce an enhanced therapeutic response to TNF treatment in advanced prostate cancer