Spatial autocorrelation analysis of health care hotspots in Taiwan in 2006

<p>Abstract</p> <p>Background</p> <p>Spatial analytical techniques and models are often used in epidemiology to identify spatial anomalies (hotspots) in disease regions. These analytical approaches can be used to not only identify the location of such hotspots, but also their spatial patterns.</p> <p>Methods</p> <p>In this study, we utilize spatial autocorrelation methodologies, including Global Moran's I and Local Getis-Ord statistics, to describe and map spatial clusters, and areas in which these are situated, for the 20 leading causes of death in Taiwan. In addition, we use the fit to a logistic regression model to test the characteristics of similarity and dissimilarity by gender.</p> <p>Results</p> <p>Gender is compared in efforts to formulate the common spatial risk. The mean found by local spatial autocorrelation analysis is utilized to identify spatial cluster patterns. There is naturally great interest in discovering the relationship between the leading causes of death and well-documented spatial risk factors. For example, in Taiwan, we found the geographical distribution of clusters where there is a prevalence of tuberculosis to closely correspond to the location of aboriginal townships.</p> <p>Conclusions</p> <p>Cluster mapping helps to clarify issues such as the spatial aspects of both internal and external correlations for leading health care events. This is of great aid in assessing spatial risk factors, which in turn facilitates the planning of the most advantageous types of health care policies and implementation of effective health care services.</p

Novel Quinazolinone MJ-29 Triggers Endoplasmic Reticulum Stress and Intrinsic Apoptosis in Murine Leukemia WEHI-3 Cells and Inhibits Leukemic Mice

The present study was to explore the biological responses of the newly compound, MJ-29 in murine myelomonocytic leukemia WEHI-3 cells in vitro and in vivo fates. We focused on the in vitro effects of MJ-29 on ER stress and mitochondria-dependent apoptotic death in WEHI-3 cells, and to hypothesize that MJ-29 might fully impair the orthotopic leukemic mice. Our results indicated that a concentration-dependent decrease of cell viability was shown in MJ-29-treated cells. DNA content was examined utilizing flow cytometry, whereas apoptotic populations were determined using annexin V/PI, DAPI staining and TUNEL assay. Increasing vital factors of mitochondrial dysfunction by MJ-29 were further investigated. Thus, MJ-29-provaked apoptosis of WEHI-3 cells is mediated through the intrinsic pathway. Importantly, intracellular Ca2+ release and ER stress-associated signaling also contributed to MJ-29-triggered cell apoptosis. We found that MJ-29 stimulated the protein levels of calpain 1, CHOP and p-eIF2α pathways in WEHI-3 cells. In in vivo experiments, intraperitoneal administration of MJ-29 significantly improved the total survival rate, enhanced body weight and attenuated enlarged spleen and liver tissues in leukemic mice. The infiltration of immature myeloblastic cells into splenic red pulp was reduced in MJ-29-treated leukemic mice. Moreover, MJ-29 increased the differentiations of T and B cells but decreased that of macrophages and monocytes. Additionally, MJ-29-stimulated immune responses might be involved in anti-leukemic activity in vivo. Based on these observations, MJ-29 suppresses WEHI-3 cells in vitro and in vivo, and it is proposed that this potent and selective agent could be a new chemotherapeutic candidate for anti-leukemia in the future

The ERK and JNK pathways in the regulation of metabolic reprogramming.

Most tumor cells reprogram their glucose metabolism as a result of mutations in oncogenes and tumor suppressors, leading to the constitutive activation of signaling pathways involved in cell growth. This metabolic reprogramming, known as aerobic glycolysis or the Warburg effect, allows tumor cells to sustain their fast proliferation and evade apoptosis. Interfering with oncogenic signaling pathways that regulate the Warburg effect in cancer cells has therefore become an attractive anticancer strategy. However, evidence for the occurrence of the Warburg effect in physiological processes has also been documented. As such, close consideration of which signaling pathways are beneficial targets and the effect of their inhibition on physiological processes are essential. The MAPK/ERK and MAPK/JNK pathways, crucial for normal cellular responses to extracellular stimuli, have recently emerged as key regulators of the Warburg effect during tumorigenesis and normal cellular functions. In this review, we summarize our current understanding of the roles of the ERK and JNK pathways in controlling the Warburg effect in cancer and discuss their implication in controlling this metabolic reprogramming in physiological processes and opportunities for targeting their downstream effectors for therapeutic purposes.Brunel Research Initiative & Enterprise Fund, Brunel University of London (to CB), Kay Kendall Leukemia Fund (KKL443) (to CB), 250 Great Minds Fellowship, University of Leeds (to SP), AMMF Cholangiocarcinoma Charity (to SP and PMC), and Bloodwise (17014) (to SP and CB)

Cell-Based Functional IgE Assays Are Superior to Conventional Allergy Tests for Shrimp Allergy Diagnosis.

BackgroundThe diagnosis of shellfish allergy currently relies on patient history, skin prick test (SPT), and serum specific IgE (sIgE) quantification. These methods lack sufficient diagnostic accuracy, whereas the gold standard of oral food challenges is risky and burdensome. Markers of reactivity and severity of allergic reactions to shellfish will improve clinical care of these patients.ObjectivesThis study compared the diagnostic performance of SPT, sIgE, basophil activation test (BAT), and IgE crosslinking-induced luciferase expression (EXiLE) test for shrimp allergy.MethodsThirty-five subjects with documented history of shrimp allergic reactions were recruited and grouped according to results of double-blind, placebo-controlled food challenge (DBPCFC). In addition to routine diagnostics, BAT (Flow CAST) and EXiLE test with shrimp extract and tropomyosin were performed.ResultsOf 35 subjects, 15 were shrimp allergic with pruritus, urticaria, and itchy mouth on DBPCFC, whereas 20 were tolerant to shrimp. Tropomyosin only accounted for 53.3% of sensitization among subjects with challenge-proven shrimp allergy. BAT using shrimp extract as stimulant showed the highest area under curve value (0.88), Youden Index (0.81), likelihood ratio (14.73), odds ratio (104), and variable importance (4.27) when compared with other assays and tropomyosin diagnosis. Results of BAT significantly correlated with those of EXiLE (r&nbsp;= 0.664, P &lt; .0001).ConclusionsBAT is a more accurate diagnostic marker for shrimp allergy than SPT and shrimp sIgE, whereas the EXiLE test based on an IgE crosslinking assay is a good alternative to BAT. Tropomyosin may not be the most important shrimp allergen in Chinese, which warrants further investigation to search for other major allergens and diagnostic markers