Gun Violence in Chicago, 2016

A total of 764 people were murdered in Chicago in 2016. They were sons, brothers, and fathers; sisters, daughters, and mothers; they were, as the title of The New York Times reporter Fox Butterfield's book on urban violence noted, All God's Children. This report represents a first step towards understanding what happened with the goal of helping the city of Chicago prevent another year like the one that just passed.We draw on data obtained from the Chicago Police Department (CPD) and other sources to provide a more complete picture of the change in our city's crime problem in 2016. Our analysis highlights a number of key facts that are important for understanding what happened, but also raises some new puzzles as well. While this report focuses on establishing basic facts and avoids delving too deeply into solutions, we will continue to partner with policymakers, the civic community, and local nonprofits to identify promising approaches for moving forward. We plan to share our thinking about how to reduce violence in Chicago, informed by the best available data and research, in other venues in the future.Between 2015 and 2016, Chicago experienced 58 percent more homicides and 43 percent more non-fatal shootings. Annual increases of this size are not unprecedented among American cities, particularly in recent years, but are rare for a city of Chicago's size. One striking feature of Chicago's increase in gun violence is how sudden it was: as of December 2015, there was no indication that gun violence was on the verge of rising sharply. But in January 2016, homicides and shootings surged relative to their 2015 levels and remained higher in almost every month that followed, threatening 20 years of progress on violent crime in Chicago. This increase was mostly in gun crimes; other crimes did not change by nearly as much.The characteristics of homicide were generally similar in 2016 and 2015; what changed in Chicago was not so much the nature of our violence problem, but rather its prevalence. Most murders involved guns, occurred in public places, and stemmed from what police believe was some sort of altercation. This violence continues to be very regressive in its impact, disproportionately affecting the city's most disadvantaged residents. Most gun violence victims and suspects were African American men, more often than not having had some prior encounter with the criminal justice system.Compared to other cities, a larger share of homicide suspects in Chicago consists of adolescents, although the majority of all homicide suspects are in their 20s or older. The increase in gun violence occurred disproportionately in several disadvantaged neighborhoods on the city's South and West sides, which now account for an even larger share of the city's homicides. Another change is that from 2015 to 2016, the share of homicides that CPD believes stemmed from an altercation, as well as the share of homicide offenders who were recorded by CPD as having a gang affiliation, seemed to decline.What caused Chicago's sudden surge in gun violence in 2016 remains a puzzle. Weather cannot explain the surge in homicides and shootings, since monthly temperatures in 2016 were close to their historical averages. City spending on social services and public education did not change much in 2016 compared to previous years, and while the state budget impasse disrupted funding for many community organizations, this did not seem to change sharply in December 2015.Most relevant measures of police activity did not change abruptly enough to explain the surge in gun violence. Overall arrests declined in 2016, driven by narcotics arrests, but arrests for violent crimes, including homicides and shootings, barely changed. One policing measure that declined was the chance of arrest for homicides and shootings (the "clearance rate"), which was a result of arrests for these crimes not keeping pace with the increase in gun violence. Another policing measure that declined was the number of investigatory street stops. However, for this to explain why shootings increased in Chicago would also require an explanation for why the previous dramatic decline in street stops in New York City did not lead to more gun violence there.We also cannot know the effect of factors not measurable in the available data, such as any change in street gangs or the use of social media. However, given the timing of the recent increase in gun violence, for any alternative explanation to make sense it would need to involve something that changed abruptly near the end of 2015 and disproportionately affected gun crimes.Not knowing the definitive cause of Chicago's sudden and substantial increase in gun violence does not mean the city should be paralyzed in crafting a response. The solution to a problem need not be the opposite of its cause. One key implication of these data is the importance of a policy response that is focused on the core problem: violence concentrated largely in a moderate number of our most disadvantaged neighborhoods, carried out by teens and young adults in public places with illegally owned, and perhaps increasingly lethal, firearm

Human Dermal Microvascular Endothelial Cells Produce Matrix Metalloproteinases in Response to Angiogenic Factors and Migration

Matrix metalloproteinases (MMPs) are a family of inducible enzymes that degrade extracellular matrix components, allowing cells to traverse connective tissue structures efficiently. Specific tissue inhibitors (TIMPs) function as physiologic inhibitors of MMP activity. Because neovascularization may require various proteinases, we characterized the profile of metalloenzyme production by microvascular endothelial cells (MEC) and the modulation of expression by phorbol esters (PMA) and by the physiologically relevant cytokines tumor necrosis factor-α (TNF-α), basic fibroblast growth factor, and interferon-γ. MMP expression by MEC and large-vessel human umbilical vein endothelial cells (HUVEC) was determined by enzyme-linked immunosorbent assay, immunoprecipitation, Northern hybridization, and transfection assays. Constitutive expression of MMPs by endothelial cells was low. PMA stimulated the production of collagenase, stromelysin, 92-kDa gelatinase, and TIMP-1 in both endothelial cell types. TIMP-2 was constitutively expressed by MEC and HUVEC, but was down-regulated by PMA. TNF-α induced an endothelial-cell-specific up-regulation of collagenase with a concomitant inhibition of PMA-induced TIMP-1 up-regulation, a response that is distinct from that of fibroblasts. Interferon-γ up-regulated TIMP-1 production by MEC and blocked PMA and TNT-induced up-regulation of collagenase. Northern hybridization assays showed pretranslational control of PMA-, basic fibroblast growth factor-, and TNF-α–induced MM.P expression. Collagenase-promoter CAT constructs containing 2.28 kb of the 5' region of the collagenase gene demonstrated transcriptional regulation. The potential physiologic relevance of such regulation was shown in an in vitro migration assay. MEC were stimulated to migrate by wounding and exposure to TNF-α. Collagenase mRNA was prominently expressed by the migrating cells, as shown by in situ hybridization. In sum, MEC have a unique profile of MMP expression and regulation compared with other cell types, which may be important for wound healing and angiogenesis, particularly during the early phase of migration

Gelatinase B–deficient Mice Are Resistant to Experimental Bullous Pemphigoid

Bullous pemphigoid (BP) is an autoimmune subepidermal blistering disease characterized by deposition of autoantibodies at the basement membrane zone. In an experimental BP model in mice, the subepidermal blistering is mediated by antibodies directed against the hemidesmosomal protein BP180 (collagen XVII, BPAG2), and depends on complement activation and neutrophil infiltration. Gelatinase B is present in BP blister fluid and can cleave BP180. In this study we investigated the role of gelatinase B in the immunopathogenesis of experimental BP using mice containing targeted disruption of the gelatinase B (MMP-9, 92 kD gelatinase) gene. Gelatinase B–deficient mice were resistant to the blistering effect of intracutaneous anti-mBP180 antibodies, although these mice showed deposition of autoantibodies at the basement membrane zone and neutrophil recruitment to the skin comparable to that observed in the control mice. Interleukin 8 given intradermally concomitantly with pathogenic anti-mBP180 elicited a significant neutrophil recruitment into the skin in gelatinase B–deficient mice, but blistering did not occur. However, gelatinase B–deficient mice reconstituted with neutrophils from normal mice developed blistering in response to anti-mBP180 antibodies. These results implicate neutrophil-derived gelatinase B in the pathogenesis of experimental BP and might lead to novel therapeutic strategies for BP

Insights on the Evolution of Prolyl 3-Hydroxylation Sites from Comparative Analysis of Chicken and Xenopus Fibrillar Collagens

Recessive mutations that prevent 3-hydroxyproline formation in type I collagen have been shown to cause forms of osteogenesis imperfecta. In mammals, all A-clade collagen chains with a GPP sequence at the A1 site (P986), except α1(III), have 3Hyp at residue P986. Available avian, amphibian and reptilian type III collagen sequences from the genomic database (Ensembl) all differ in sequence motif from mammals at the A1 site. This suggests a potential evolutionary distinction in prolyl 3-hydroxylation between mammals and earlier vertebrates. Using peptide mass spectrometry, we confirmed that this 3Hyp site is fully occupied in α1(III) from an amphibian, Xenopus laevis, as it is in chicken. A thorough characterization of all predicted 3Hyp sites in collagen types I, II, III and V from chicken and xenopus revealed further differences in the pattern of occupancy of the A3 site (P707). In mammals only α2(I) and α2(V) chains had any 3Hyp at the A3 site, whereas in chicken all α-chains except α1(III) had A3 at least partially 3-hydroxylated. The A3 site was also partially 3-hydroxylated in xenopus α1(I). Minor differences in covalent cross-linking between chicken, xenopus and mammal type I and III collagens were also found as a potential index of evolving functional differences. The function of 3Hyp is still unknown but observed differences in site occupancy during vertebrate evolution are likely to give important clues

Structural Barriers to HIV Prevention and Services: Perspectives of African American Women in Low-Income Communities

Background African American women are at a disproportionate HIV risk compared with other U.S. women. Studies show that complex structural and social determinants, rather than individual behaviors, place African American women at greater risk of HIV infection; however, little is known about women's views of what puts them at risk.AimsThis study sought to comprehend the perceptions of African American women living in low-income housing regarding the factors that influence both their personal sexual health behaviors and use of HIV prevention services. Methods We conducted seven focus groups with 48 African American women from 10 public housing communities in a small city in the southeastern United States. We analyzed the focus group transcripts using thematic data analysis to identify salient themes and points of interest related to the study aim. Results Women identified factors related to the health care system (trustworthiness of the health care system), the external environment (racism, classism, patriarchal structures, and violence/crime), as well as predisposing (health beliefs, stigma, and gender norms), enabling (agency to negotiate gendered power), and need (perceived HIV risk and perceptions of partner characteristics) features of individuals in the population. Conclusion African American women living in public housing are especially vulnerable to HIV infection due to intersectional discrimination based on racism, classism, gender power dynamics, and community conditions. Our findings confirm the need to develop HIV intervention programming addressing intersectional identities of those making up the communities they plan to address, and being informed by those living in the communities they plan to act on

A role for the collagen I/III and MMP-1/-13 genes in primary inguinal hernia?

BACKGROUND: Abnormal collagen metabolism is thought to play an important role in the development of primary inguinal hernia. This is underlined by detection of altered collagen metabolism and structural changes of the tissue in patients with primary inguinal hernia. However, it is still unknown whether these alterations reflect a basic dysfunction of the collagen synthesis, or of collagen degradation. METHODS: In the present study, we analysed type I and type III procollagen messenger ribonucleic acid (mRNA) and MMP-1 and MMP-13 mRNA in cultured fibroblasts from the skin of patients with primary inguinal hernia, and from patients without hernia (controls) by reverse transcription polymerase chain reaction (RT-PCR) and Northern Blot. RESULTS: The results indicated that the ratio of type I to type III procollagen mRNA was decreased in patients with primary hernia, showing significant differences as compared to controls (p = 0.01). This decrease was mainly due to the increase of type III procollagen mRNA. Furthermore, RT-PCR analysis revealed that the expression of MMP-1 mRNA in patients with primary hernia is equivalent to that of controls (p > 0.05). In addition, MMP-13 mRNA is expressed neither in patients with primary hernia nor in controls. CONCLUSION: We concluded that abnormal change of type I and type III collagen mRNAs contribute to the development of primary inguinal hernia, whereas the expressions of MMP-1 and MMP-13 mRNA appears not to be involved in the development of primary inguinal hernia. Thus, the knowledge on the transcriptional regulation of collagen in patients with primary inguinal hernia may help to understand the pathogenesis of primary inguinal hernia, and implies new therapeutic strategies for this disease

Histone deacetylase inhibitors suppress mechanical stress-induced expression of RUNX-2 and ADAMTS-5 through the inhibition of the MAPK signaling pathway in cultured human chondrocytes

Objective: To investigate the inhibitory effects and the regulatory mechanisms of histone deacetylase (HDAC) inhibitors on mechanical stress-induced gene expression of runt-related transcription factor (RUNX)-2 and a disintegrin and metalloproteinase with thrombospondin motif (ADAMTS)-5 in human chondrocytes. Methods: Human chondrocytes were seeded in stretch chambers at a concentration of 5 x 10(4) cells/chamber. Cells were pre-incubated with or without HDAC inhibitors (MS-275 or trichostatin A; TSA) for 12 h, followed by uniaxial cyclic tensile strain (CTS) (0.5 Hz, 10% elongation), which was applied for 30 min using the ST-140-10 system (STREX, Osaka, Japan). Total RNA was extracted and the expression of RUNX-2, ADAMTS-5, matrix metalloproteinase (MMP)-3, and MMP-13 at the mRNA and protein levels were examined by real-time polymerase chain reaction (PCR) and immunocytochemistry, respectively. The activation of diverse mitogen-activated protein kinase (MAPK) pathways with or without HDAC inhibitors during CTS was examined by western blotting. Results: HDAC inhibitors (TSA: 10 nM, MS-275: 100 nM) suppressed CTS-induced expression of RUNX-2, ADAMTS-5, and MMP-3 at both the mRNA and protein levels within 1 h. CTS-induced activation of p38 MAPK (p38), extracellular signal-regulated kinase (ERK), and c-Jun N-terminal kinase (INK) MAPKs was downregulated by both HDAC inhibitors. Conclusion: The CTS-induced expression of RUNX-2 and ADAMTS-5 was suppressed by HDAC inhibitors via the inhibition of the MAPK pathway activation in human chondrocytes. The results of the current study suggested a novel therapeutic role for HDAC inhibitors against degenerative joint disease such as osteoarthritis