Purdue's athletic department had its best finish in the Learfield Directors Cup standings in nearly a decade but more is expected in 2018-19

About 50 people gathered Saturday afternoon at West 62nd Street and Michigan Road to protest the fatal police shooting of Dreasjon "Sean" Reed.

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When a famed Egyptian actor revealed his daughter had transitioned, the reaction was unconventional.

The SLGA retail store and the private off sale in La Loche are closed for two weeks, the province announced.

History of Machu Picchu

Archaeological evidence uncovered around the site suggests that the area was first used for agricultural purposes back in 760 B.C.

The war of Vilcambamba Pachacutec in 1440 established the first settlement at the site. It was called the Tahuantinsuyo Empire which was later followed by the formation of the government of Manco Capac.

It is thought that Machu Picchu was first inhabited by 300-1000 inhabitants, who were of the highest Class or "llactas".

The valleys around these areas were important for their agricultural contribution, however after death of the Emperor Pachacutec, it lost it's importance, with the establishment of new sites like Ollaytantambo and Vilcambamba. The building of these new sites by his successors, in more accessible terrain made Machu Picchu less appealing.

From 1527 to 1532, two brothers Huáscar and Atahualpa fought against each other in a civil war over the Inca Empire. Their father, Inca Huayna Capac had given each brother a section of the empire to manage, one in Huáscar in Cuzco and Atahualpa in Quito. When Huayna Capac and his heir, Ninan Cuyuchi, died somewhere between 1525 and 1527, the two brothers Atahualpa and Huáscar went to war over who should rule.  The population who had come to live in the Machu Picchu area from rural or remote locations left after the war ended to return to where they came from. Later another brother, Manco Inca was sent into exile in Vilcambamba, and Machu Picchu was deserted.

Antonio Raimondi was an Italian geographer and scientist from Milan who visited Machu Picchu in 1851. In 1867 Augusto Berns arrived to mine the site.

Hiram Bingham re-discovered the ruins in 1911. He documented and publicised his "discovery".

Hiram Bingham

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The following article, Rep. Ilhan Omar Asks For Contributions To Her Campaign To Help MN Food Bank…Food Bank Director Says Omar Has Nothing To Do With Project: “I have no idea where this money is going”, was first published on 100PercentFedUp.com.

Ilhan Omar is a lot of things. First, and foremost, she’s deceitful. David Steinberg of PJ Media was one of the first investigative journalists to break the story about the anti-Semitic, freshman lawmaker’s marriage to her immigrant brother while she was still married to her first husband, who she has since divorced after having an […]

Continue reading: Rep. Ilhan Omar Asks For Contributions To Her Campaign To Help MN Food Bank…Food Bank Director Says Omar Has Nothing To Do With Project: “I have no idea where this money is going” ...

The following article, NYC Nurse Steals Credit Card From 70-Yr-Old Dying COVID-19 Patient On Ventilator, was first published on 100PercentFedUp.com.

"She is a despicable human being"

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6 February 2014 , Volume 70, Number 1

Republic of Guinea

Population: 10,000,000 (2009 estimate CIA World Factbook), GDP per Capita: $588.00, Official language: French, Capital and largest city: Conakry, Area: 245,857 km2, Independence: From France, 2 October 1958

Members Event

Event participants

Richard Heald, CEO, UK India Business Council (UKIBC)
Manoj Ladwa, Communications Director, Narendra Modi for Prime Minister Campaign
Dr Gareth Price, Senior Research Fellow, Asia Programme, Chatham House

Chair: Adam Roberts, South Asia Bureau Chief, Delhi, The Economist

Members Event

Event participants

Parag Khanna, Author, Connectography: Mapping the Global Network Revolution

Elizabeth Spiers wrote about an incident where Jared Kushner used the memorial of an employee to congratulate himself for success.

Nepal protested India's inauguration of a new road to China that passes through territory claimed by Kathmandu on Saturday, with police arresting dozens demonstrating close to India's embassy. Indian defence minister Rajnath Singh on Friday inaugurated via video link the 80-kilometre (50 miles) long road from Ghatiabagarh in northern Uttarakhand state to the Lipu Lekh pass high in the Himalaya. The pass is claimed by Nepal based on an 1816 treaty that defines its western border with India.

In a tweet Saturday morning, Tesla's chief executive said it would file a lawsuit against county officials over not being able to run its factory.

The C-type lectin receptors (CLRs) form a family of pattern recognition receptors that recognize numerous pathogens, such as bacteria and fungi, and trigger innate immune responses. The extracellular carbohydrate-recognition domain (CRD) of CLRs forms a globular structure that can coordinate a Ca2+ ion, allowing receptor interactions with sugar-containing ligands. Although well-conserved, the CRD fold can also display differences that directly affect the specificity of the receptors for their ligands. Here, we report crystal structures at 1.8–2.3 Å resolutions of the CRD of murine dendritic cell-immunoactivating receptor (DCAR, or Clec4b1), the CLR that binds phosphoglycolipids such as acylated phosphatidyl-myo-inositol mannosides (AcPIMs) of mycobacteria. Using mutagenesis analysis, we identified critical residues, Ala136 and Gln198, on the surface surrounding the ligand-binding site of DCAR, as well as an atypical Ca2+-binding motif (Glu-Pro-Ser/EPS168–170). By chemically synthesizing a water-soluble ligand analog, inositol-monophosphate dimannose (IPM2), we confirmed the direct interaction of DCAR with the polar moiety of AcPIMs by biolayer interferometry and co-crystallization approaches. We also observed a hydrophobic groove extending from the ligand-binding site that is in a suitable position to interact with the lipid portion of whole AcPIMs. These results suggest that the hydroxyl group-binding ability and hydrophobic groove of DCAR mediate its specific binding to pathogen-derived phosphoglycolipids such as mycobacterial AcPIMs.

Bacterial products such as lipopolysaccharides (or endotoxin) cause systemic inflammation, resulting in a substantial global health burden. The onset, progression, and resolution of the inflammatory response to endotoxin are usually tightly controlled to avoid chronic inflammation. Members of the NF-κB family of transcription factors are key drivers of inflammation that activate sets of genes in response to inflammatory signals. Such responses are typically short-lived and can be suppressed by proteins that act post-translationally, such as the SOCS (suppressor of cytokine signaling) family. Less is known about direct transcriptional regulation of these responses, however. Here, using a combination of in vitro approaches and in vivo animal models, we show that endotoxin treatment induced expression of the well-characterized transcriptional repressor Krüppel-like factor 3 (KLF3), which, in turn, directly repressed the expression of the NF-κB family member RELA/p65. We also observed that KLF3-deficient mice were hypersensitive to endotoxin and exhibited elevated levels of circulating Ly6C+ monocytes and macrophage-derived inflammatory cytokines. These findings reveal that KLF3 is a fundamental suppressor that operates as a feedback inhibitor of RELA/p65 and may be important in facilitating the resolution of inflammation.

Protease-activated receptor 2 (PAR-2) is activated by secreted proteases from immune cells or fungi. PAR-2 is normally expressed basolaterally in differentiated nasal ciliated cells. We hypothesized that epithelial remodeling during diseases characterized by cilial loss and squamous metaplasia may alter PAR-2 polarization. Here, using a fluorescent arrestin assay, we confirmed that the common fungal airway pathogen Aspergillus fumigatus activates heterologously-expressed PAR-2. Endogenous PAR-2 activation in submerged airway RPMI 2650 or NCI–H520 squamous cells increased intracellular calcium levels and granulocyte macrophage–colony-stimulating factor, tumor necrosis factor α, and interleukin (IL)-6 secretion. RPMI 2650 cells cultured at an air–liquid interface (ALI) responded to apically or basolaterally applied PAR-2 agonists. However, well-differentiated primary nasal epithelial ALIs responded only to basolateral PAR-2 stimulation, indicated by calcium elevation, increased cilia beat frequency, and increased fluid and cytokine secretion. We exposed primary cells to disease-related modifiers that alter epithelial morphology, including IL-13, cigarette smoke condensate, and retinoic acid deficiency, at concentrations and times that altered epithelial morphology without causing breakdown of the epithelial barrier to model early disease states. These altered primary cultures responded to both apical and basolateral PAR-2 stimulation. Imaging nasal polyps and control middle turbinate explants, we found that nasal polyps, but not turbinates, exhibit apical calcium responses to PAR-2 stimulation. However, isolated ciliated cells from both polyps and turbinates maintained basolateral PAR-2 polarization, suggesting that the calcium responses originated from nonciliated cells. Altered PAR-2 polarization in disease-remodeled epithelia may enhance apical responses and increase sensitivity to inhaled proteases.

Prevention of aberrant cutaneous wound repair and appropriate regeneration of an intact and functional integument require the coordinated timing of fibroblast and keratinocyte migration. Here, we identified a mechanism whereby opposing cell-specific motogenic functions of a multifunctional intracellular and extracellular protein, the receptor for hyaluronan-mediated motility (RHAMM), coordinates fibroblast and keratinocyte migration speed and ensures appropriate timing of excisional wound closure. We found that, unlike in WT mice, in Rhamm-null mice, keratinocyte migration initiates prematurely in the excisional wounds, resulting in wounds that have re-surfaced before the formation of normal granulation tissue, leading to a defective epidermal architecture. We also noted aberrant keratinocyte and fibroblast migration in the Rhamm-null mice, indicating that RHAMM suppresses keratinocyte motility but increases fibroblast motility. This cell context–dependent effect resulted from cell-specific regulation of extracellular signal-regulated kinase 1/2 (ERK1/2) activation and expression of a RHAMM target gene encoding matrix metalloprotease 9 (MMP-9). In fibroblasts, RHAMM promoted ERK1/2 activation and MMP-9 expression, whereas in keratinocytes, RHAMM suppressed these activities. In keratinocytes, loss of RHAMM function or expression promoted epidermal growth factor receptor–regulated MMP-9 expression via ERK1/2, which resulted in cleavage of the ectodomain of the RHAMM partner protein CD44 and thereby increased keratinocyte motility. These results identify RHAMM as a key factor that integrates the timing of wound repair by controlling cell migration.

Inter-α-inhibitor is a proteoglycan essential for mammalian reproduction and also plays a less well-characterized role in inflammation. It comprises two homologous “heavy chains” (HC1 and HC2) covalently attached to chondroitin sulfate on the bikunin core protein. Before ovulation, HCs are transferred onto the polysaccharide hyaluronan (HA) to form covalent HC·HA complexes, thereby stabilizing an extracellular matrix around the oocyte required for fertilization. Additionally, such complexes form during inflammatory processes and mediate leukocyte adhesion in the synovial fluids of arthritis patients and protect against sepsis. Here using X-ray crystallography, we show that human HC1 has a structure similar to integrin β-chains, with a von Willebrand factor A domain containing a functional metal ion-dependent adhesion site (MIDAS) and an associated hybrid domain. A comparison of the WT protein and a variant with an impaired MIDAS (but otherwise structurally identical) by small-angle X-ray scattering and analytical ultracentrifugation revealed that HC1 self-associates in a cation-dependent manner, providing a mechanism for HC·HA cross-linking and matrix stabilization. Surprisingly, unlike integrins, HC1 interacted with RGD-containing ligands, such as fibronectin, vitronectin, and the latency-associated peptides of transforming growth factor β, in a MIDAS/cation-independent manner. However, HC1 utilizes its MIDAS motif to bind to and inhibit the cleavage of complement C3, and small-angle X-ray scattering–based modeling indicates that this occurs through the inhibition of the alternative pathway C3 convertase. These findings provide detailed structural and functional insights into HC1 as a regulator of innate immunity and further elucidate the role of HC·HA complexes in inflammation and ovulation.

Contact between inflammatory cells and endothelial cells (ECs) is a crucial step in vascular inflammation. Recently, we demonstrated that the cell-surface level of endomucin (EMCN), a heavily O-glycosylated single-transmembrane sialomucin, interferes with the interactions between inflammatory cells and ECs. We have also shown that, in response to an inflammatory stimulus, EMCN is cleared from the cell surface by an unknown mechanism. In this study, using adenovirus-mediated overexpression of a tagged EMCN in human umbilical vein ECs, we found that treatment with tumor necrosis factor α (TNF-α) or the strong oxidant pervanadate leads to loss of cell-surface EMCN and increases the levels of the C-terminal fragment of EMCN 3- to 4-fold. Furthermore, treatment with the broad-spectrum matrix metalloproteinase inhibitor batimastat (BB94) or inhibition of ADAM metallopeptidase domain 10 (ADAM10) and ADAM17 with two small-molecule inhibitors, GW280264X and GI254023X, or with siRNA significantly reduced basal and TNFα-induced cell-surface EMCN cleavage. Release of the C-terminal fragment of EMCN by TNF-α treatment was blocked by chemical inhibition of ADAM10 alone or in combination with ADAM17. These results indicate that cell-surface EMCN undergoes constitutive cleavage and that TNF-α treatment dramatically increases this cleavage, which is mediated predominantly by ADAM10 and ADAM17. As endothelial cell-surface EMCN attenuates leukocyte–EC interactions during inflammation, we propose that EMCN is a potential therapeutic target to manage vascular inflammation.

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Briefing and discussion of the release of the latest paper by MPI's Labor Markets Initiative: The Impact of Immigrants in Recession and Economic Expansion.

Briefing and discussion of the release of the latest paper by MPI's Labor Markets Initiative. Speakers are report author Giovanni Peri, UC Davis Professor of Economics; Ross Eisenbrey, Vice President, Economic Policy Institute; and Demetrios G. Papademetriou, MPI President.

A discussion with the Director of The White House Domestic Policy Council on the content of the new National Integration Plan delivered to the President by the recently created White House Task Force on New Americans, along with the plan for implementation.

A discussion with the Director of The White House Domestic Policy Council on the content of the new National Integration Plan delivered to the President by the recently created White House Task Force on New Americans, along with the plan for implementation.

Testimony of Marc Rosenblum before the Senate Judiciary Committee for the December 2, 2015 hearing on priorities for immigration enforcement and the use of prosecutorial discretion. 

On May 9, 1992, Andy Moog powered the Boston Bruins past the Montreal Canadiens with a 2-0 shutout in Game 4 for a sweep of the Adams Division Finals.

(May 4, 2020) On April 29, 2020, the Swedish National Prosecutor announced that it is investigating a workplace environment crime (arbetsmiljöbrott) after a nurse working at Karolinska University Hospital in Stockholm died of COVID-19. The investigation comes following a report by the local safety representative (skyddsombud), who reportedly claimed that the hospital lacked the appropriate […]