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Home»Sections»Energy»Nersa kicks the Karpowership can down the road
Nersa kicks the Karpowership can down the road
Energy By Staff Reporter 13 September 2021
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With the 30 September deadline for financial close looming for controversial electricity generator Karpowership SA's deal with the South African government, energy regulator Nersa kicked a hard discussion about the its generation licence down the road.
Karpowership, a subsidiary of the Turkish Karadeniz Energy Group, was selected as one of the preferred bidders in the department of mineral resources & energy risk mitigation independent power producer programme (RMIPPP) in March.
This programme is aimed as an emergency intervention in the current electricity supply shortage and the projects are supposed to come into operation around August next year to end load shedding.
As the date drew closer, it was clear that the bidders would not be able to overcome several challenges in time
When energy minister Gwede Mantashe announced the first preferred bidders in March, he set the "non-negotiable" deadline for financial close at the end of July.
As the date drew closer, it was clear that the bidders would not be able to overcome several challenges in time and the deadline was shifted to the end of this month – 13 working days away.
Karpowership SA proposes generating a total of 1.2GW of electricity on three floating power stations with a floating storage and regasification unit each, in the harbours of Saldanha, Richards Bay and Ngqura.
This constitutes a major share of the 2GW scope of the RMIPPP.
It requires approval from the Transnet National Ports Authority, which is in the process of being corporatised as a subsidiary of Transnet amid serious concerns regarding its legal status.
The Karpowership proposal has met with fierce resistance – from environmentalists who object to the use of fossil fuels and are concerned about the impact of the operations on marine life, as well as energy analysts who have questioned the wisdom of the 20-year power purchase agreement that would be concluded with Eskom. Eskom's board is reportedly also reluctant to sign such an agreement.
Critics also question the fact that the major infrastructure built – the floating units – will be lost to South Africa at the end of the 20 years as Karpowership will simply be able to take them to another harbour elsewhere in the world.
While Karpowership's proposed unit tariff seems to compare favourably with that of other bidders who rely heavily on renewable energy, it will fluctuate with the international gas price as well as the rand/dollar exchange rate. This poses a huge risk to the consumer, who will ultimately have to pay for the energy through power purchases tariffs.
The company has already faced some headwinds, with the department of environment, forestry & fisheries first reversing its environmental approval and then, after a review, declining it. Karpowership has appealed, but it is not clear when the appeal process will be concluded.
A competitor, DNG Energy, has challenged Karpowership's selection as preferred bidder in court. DNG, which was disqualified, made allegations of corruption in the procurement process and hopes to replace Karpowership as preferred bidder. The high court in Pretoria last week postponed the case until November.
Members of Nersa this past week differed sharply about the approval of Karpowership's licences to generate electricity
Energy expert Chris Yelland this week expressed his doubt whether the Karpowership projects can reach financial close before the court application has been finalised.
Against this background, members of Nersa this past week differed sharply about the approval of Karpowership's licences to generate electricity.
Licence applications from seven of the preferred bidders were served before Nersa's electricity subcommittee on Wednesday, 8 September. This committee normally deals with electricity matters on the basis of reports prepared by Nersa staff. They then make recommendations to the energy regulator meeting for final decision. Some of the members serve in both structures.
While the committee had no objections against the other applications, Nomfundo Maseti, full-time regulator member for piped gas (who also previously acted as member for electricity for an extended time), asked whether Nersa could entertain the Karpowership application while other approvals are still outstanding.
She pointed out that Karpowership has not yet obtained a gas licence and therefore the source and price of the feedstock is still uncertain. She also referred to the outstanding environmental and harbour approvals and uncertainty about the conclusion of a power purchase agreement.
Maseti asked for clarity about the sequence of regulatory approvals and Nersa's role in the matter. "Are we putting the cart before the horses?" she asked.
She emphasised that the Electricity Regulation Act requires the applicant to show its ability to generate power in terms of the licence it applies for and the plan showing how it will do so.
She also asked about an earlier legal opinion Nersa got from senior counsel stating that the regulator must have the information it bases its decision on before it when taking the decision.
Although less vocal, some of the other regulator members had the same concerns.
Investors need the generation licence approval to obtain finance and Nersa should not add to their difficulty
Nhlanhla Gumede, full-time member for electricity, who chaired the meeting, cautioned members to stick to Nersa's mandate. He said while a number of regulators have to give different approvals, Nersa should stick to its mandate and leave the other matters to those regulators.
"That is the guidance I gave to the team (of officials)", he said. He added that the South African environment is extremely difficult for investors. They need the generation licence approval to obtain finance and Nersa should not add to their difficulty.
Gumede said the gas supply will follow once the demand has been created by the Karpowership projects.
Nersa's internal legal advice supported Gumede's position and the committee was advised that Karpowership had shown that it made the necessary applications to other regulators.
Maseti eventually agreed to support a positive recommendation regarding the Karpowership applications to the regulator, provided that the legal opinion she referred to is be made available at the meeting.
It is not clear when the regulator meeting will be scheduled. While it is usually close to the end of the month, an earlier special meeting may be scheduled in light of the looming financial close deadline.
This article was originally published by Moneyweb
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redpajama_set_name: RedPajamaCommonCrawl


The Indian retail sector is on a faster roll than ever before. Rapid urbanization and digitization, rising disposable incomes and lifestyle changes – particularly of the middle-class – are acting as booster rockets for the Indian retail sector, which is projected to grow from US$ 672 billion in 2017 to US$ 1.3 trillion in 2020.
Over the last two decades, the Indian retail market has witnessed phenomenal changes, evolving rapidly from traditional shops to large multi-format stores in malls offering a global experience, and on to the highly tech-driven e-commerce model.
These changes have resulted in unprecedented growth in overall consumption with numbers suggesting that consumer expenditure in India will rise to US$ 3,600 billion by 2020 from US$ 1,824 billion in 2017.


The Fiberbuilt 9 foot octagonal wood market umbrella features a solid Kempas wood two piece pole, ribs, hub and finial. Single sewn-in vent and storage ties come standard. Canopy is attached to wood ribs using sturdy stainless steel rivets. Features a Pulley and Pin lift. Top is made of heavy duty Sunbrella marine grade, solution dyed acrylic fabric.


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require 'vendor/autoload.php';

use Exception;
use Nerrad\BuildMachine\WebHookListener\Http\RequestFactory;

define('CB_WEBHOOK_BASE_PATH', __DIR__ . '/');

//react
try {
    $config = new Config();
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redpajama_set_name: RedPajamaGithub


INDIANAPOLIS - Super Bowl spots are still the hottest ticket in advertising.
NBC has sold all the commercial airtime for the Feb. 5 game in Indianapolis and even has a waiting list of advertisers. The average cost for a 30-second spot this year was $3.5 million, with some time slots costing as much as $4 million.
Seth Winter, senior vice president of NBC Sports group sales & marketing, said in a recent interview that the last time slot was sold just after Thanksgiving. A year ago, Fox Sports said it sold the last of its advertising spots before the end of October.
Slots are still available during NBC's pregame show, and those on the waiting list for the Super Bowl will have an opportunity to advertise if other companies give up their slot.
"There are the usual companies that have supported it in the past," Winter said. "Automotive will be very healthy. Beverages will be very healthy. The movie and snack category continue to be healthy. There will be a few new players and some who have been there, who won't be there."
Winter declined to identify which companies bought ads or dropped out, fearing it could tip off competitors. Anheuser-Busch InBev, Coca-Cola and Godaddy.com are among the recent regulars.
The biggest change this year, Winter said, is advertisers are booking longer spots to showcase their creativity.
"Some of the things I've seen are astonishing," Winter said. "I think you'll see a lot of ads that are humorous and action-filled, with a range of different types of executions. We haven't seen everything yet; we don't see everything until almost the week of (the game)."
The ads must comply with network and NFL standards.
Sports fans also might see the ads more regularly, thanks to NBC's merger with Comcast. NBC officials have used the Super Bowl to sell advertisers on its expanding family of networks, including NBC Sports Network (formerly Versus) and The Golf Channel.


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Frontiers in Neurology
Multiple Sclerosis and Neuroimmunology
New Cerebrospinal Fluid Research to Uncover Mechanisms Driving Neurological and Psychiatric Diseases View all 16 Articles
Thomas Skripuletz
Hannover Medical School, Germany
Anastasia Bougea
Department of Medicine, School of Health Sciences, National and Kapodistrian University of Athens, Greece
Mehmet A. Topçuoğlu
Hacettepe University, Turkey
Current Diagnostic Approaches
Emerging New Diagnostic Biomarkers
Potential New Diagnostic Biomarkers
Front. Neurol., 06 June 2019 | https://doi.org/10.3389/fneur.2019.00568
Primary Angiitis of the Central Nervous System: New Potential Imaging Techniques and Biomarkers in Blood and Cerebrospinal Fluid
Milani Deb-Chatterji*, Simon Schuster, Vivien Haeussler, Christian Gerloff, Götz Thomalla and Tim Magnus
Department of Neurology, University Medical Center Hamburg-Eppendorf (UKE), Hamburg, Germany
Primary angiitis of the central nervous system (PACNS) is an inflammatory brain disease affecting the medium and small vessels of the CNS. Although recent data of patients with PACNS have advanced the understanding of the disease, the diagnosis remains challenging. Clinical presentation of PACNS is broad and unspecific and the majority of the diagnostic approaches are hallmarked by a low specificity. Thus, PACNS is commonly misdiagnosed. In addition, due to its potential aggressive course which may be altered by an adequate immunosuppressive treatment, delineation from other vasculopathies and PACNS mimics is crucial. New diagnostic tools and biomarkers which increase specificity and facilitate the diagnosis for patients with suspected PACNS are highly desirable. This short review summarizes the current procedures within the diagnostic process and aims to illustrate its difficulties and challenges. Furthermore, it highlights emerging biomarkers in the cerebrospinal fluid and peripheral venous blood as well as novel potential imaging tools that may corroborate the diagnosis. With new imaging techniques and a panel of biomarkers the certainty of the diagnosis may be increased and diagnostic processes more accelerated in the future.
Primary angiitis of the central nervous system (PACNS) is a poorly understood disease which is restricted to the small- and medium-sized vessels of the brain and spinal cord. It is a rare disease with an estimated incidence of 2.4 cases per 100,000 person-years and an equal frequency in women and men (1). All age groups may be affected, whereas 50% are 37–59 years of age. Of note, PACNS is also a rare cause of stroke and remains an important differential diagnosis in younger (<45 years) adults (2.2%) (2, 3). Diagnosis is extremely hampered by the paucity of specific clinical symptoms and by the low specificity of the diagnostic approaches. Thus, establishing a reliable diagnosis remains challenging and PACNS is often misdiagnosed. In addition, two different subtypes of the disease have been reported, the small (SVV) and medium vessel variant (MVV), with different diagnostic phenotypes which increases the diagnostic challenge. While the MVV shows remarkable vascular irregularities in angiography procedures, current angiography techniques do not have a sufficient resolution to detect vessel abnormalities if the disease is limited to a small-vessel involvement. Moreover, since aggressive immunosuppressive therapy is mandatory to avert the often fatal course of the disease, exclusion from other etiologies is crucial. The aim of this short review is to give an overview of the current diagnostic procedures in PACNS and emphasize its difficulties. It further highlights new potential biomarkers in the cerebrospinal fluid (CSF) and peripheral venous blood as well as imaging markers that may increase the diagnostic accuracy.
The clinical presentation of PACNS is broad and unspecific. Thus, the average time to diagnosis may be several months (4). The symptoms vary from cognitive dysfunction, subacute, and progressive headache, seizures to focal neurological symptoms (5). Amongst others, the differential diagnosis includes e.g., hemorrhagic or ischemic stroke, neoplasia, encephalitis, dementia, migraine, multiple sclerosis. One of the most important differential diagnosis is the reversible cerebral vasoconstriction syndrome (RCVS) which bears the closest resemblance to PACNS with similar abnormalities in angiography. Recent studies provided new insights in diagnosing and distinguishing RCVS from PACNS by taking into account the patients' variables on admission (clinical symptoms, initial brain imaging etc.) (6, 7). However, diagnosis and distinction from this non-inflammatory vasculopathy is still difficult. In 1988, Calabrese and Mallek (8) proposed diagnostic criteria for PACNS which include a history or presence of a neurological deficit unexplained by any other cause after a thorough examination, evidence of vasculitis either by histopathology or angiography with characteristic changes of vasculitis and exclusion of a systemic vasculitis or any other condition to which the angiographic changes can be secondary. Birnbaum et al. (9) modified these criteria and differentiated between a "probable" and "definite" diagnosis. While definite PACNS is defined by histopathological evidence, all other cases are categorized as suspected PACNS. These revised criteria aimed at preventing inadequate and uncontrolled application of immunosuppressive treatment. To date, the diagnostic workup encompasses extensive laboratory examinations including an immunological screening and CSF analysis, MRI, angiography, and histopathology. Most of the tests are done to rule out differential diagnosis, such as systemic vasculitis (autoimmune or infectious), non-inflammatory vasculopathies (e.g., RCVS), or malignant disorders (e.g., lymphoproliferative diseases). Most of the patients (80–90%) show a pleocytosis (about 10–20 cells/ml) and/or increased protein levels (about 120 mg/ml) (4). However, these abnormalities in CSF are unspecific and, of note, an initial normal CSF does not exclude the diagnosis (10). In addition, there is currently no evidence of differences in CSF findings between the two disease variants. For brain imaging in PACNS, MRI remains the modality of choice. Fluid attenuated inversion recovery (FLAIR)—imaging, T1- and T2-weighted imaging, diffusion-weighted imaging (DWI), susceptibility-weighted imaging (SWI), time–of-flight MR angiography (TOF) and contrast medium-enhanced imaging are required sequences. Most of the patients with PACNS (90–100%) show abnormal MRI findings (9, 11). Typical changes include diffuse white and gray matter changes, contrast medium enhanced parenchymal lesions, leptomeningeal enhancement (12), parenchymal hemorrhages as well as microbleeds (13, 14). Tumor-like mass lesions have also been reported (15). Even a generalized atrophy in the MRI scan can be a sign of PACNS (16). Furthermore, MR angiography (MRA) can be applied. While in patients with SVV brain vessels in MRA are commonly unremarkable, vessel abnormalities are likely to be detected in MVV. Typical irregularities comprise peripheral alternating stenosis/occlusions and dilatation as well as vessel wall thickening in different vascular territories. However, none of these findings are specific, but a normal MRI scan in combination with a normal CSF result rule out the diagnosis of PACNS (17, 18). The current gold standard for vessel imaging in PACNS is digital subtraction angiography (DSA). Its reported overall sensitivity varies between 40 and 90% (4, 19, 20). This high range is most likely explained by the different subtypes of the disease (21, 22). Whereas, DSA may reveal remarkable vascular irregularities in patients with a predominant MVV, it shows unconspicious vessels in SVV. Currently, DSA has only a resolution for vessels >500 μm in diameter (23), thus, the SVV is typically "angiography-negative." In addition, despite having a higher sensitivity in distal vessels and the posterior circulation (24) compared to MRA, the DSA provides information on changes in vessel contours only and not on the underlying pathological process (25). In particular, distinguishing non-inflammatory vasculopathies (e.g., RCVS or artherosclerosis) remains a challenge. Hence, DSA also has a low specificity. To date, brain biopsy is the only eligible technique to establish a definite diagnosis of PACNS. An optimal biopsy should contain samples from the dura, leptomeninges, cortex and white matter (26). However, the sensitivity of brain biopsy is also low (54–83%) (20, 21, 27). This broad range may be explained by the different case series including SVV and MVV. Notably, about one fourth of all autopsy-documented cases of PACNS were false-negative (28). In particular, in patients with MVV histopathology is frequently false-negative, probably due to abnormalities of medium-sized vessels that are rather detectable by angiography but not covered by brain biopsy (22). The rate of positive results can be increased by targeting MRI positive lesions (18). Three histopathological patterns are known in PACNS so far: granulomatous (58%), lymphocytic (28%) and necrotizing (14%), but they often overlap. The amyloid-ß angiitis (ABRA) with ß-amyloid depositions in the brain vessel walls is considered to be a subset of the granulomatous pattern. To date, no clear difference in clinical symptoms, aggressiveness of the disease, or treatment response between these patterns has been reported.
Due to the variable clinical presentation of PACNS, the lack of specific diagnostics and its differences between SVV and MVV (diverse DSA/MRA results, diverse biopsy results if derived from the right frontal lobe) a definite diagnosis is still a challenge. Additional diagnostic approaches are required to increase certainty. Thus, in the following we focus on potential, novel diagnostic imaging techniques and biomarkers in the CSF and blood to diagnose PACNS.
Interleukin-17 in the Cerebrospinal Fluid
A promising marker for PACNS in the CSF is interleukin-17 (IL-17). IL-17 is a pro-inflammatory cytokine and a potent mediator in cellular immunity. It plays a pivotal role in the pathogenesis of systemic vasculitis, in particular, antineutrophil cytoplasmatic antibodies (ANCA)-associated vasculitis (AAV), or giant cell arteritis (29). Previously, we reported that IL-17 produced by CD4+-T-cells in the CSF was elevated in patients with PACNS (sensitivity 73%, specificity 100%) (Figure 1A) (30). Elevated IL-17 levels were persistent in patients with active PACNS and patients in remission, thus indicating IL-17 being a more specific biomarker of cerebral vasculitis than the cell count or protein elevation in the CSF and being crucial also in the pathogenesis of PACNS. These findings merit the attempt of making IL-17 a target for novel therapeutic interventions. Interestingly, humanized anti-IL-17 antibodies as a treatment approach were already shown to induce clinically relevant responses in patients with psoriasis and rheumatoid arthritis (31). However, the promising results of IL-17 analyses in PACNS need to be verified in larger patient cohorts.
Figure 1. (A) Morphology of circulating endothelial cells (CEC, green) with Dynabeads™ (black) attached after immunomagnetic isolation from peripheral blood of a patient with PACNS displayed under a fluorescence microscope. CECs were isolated by CD 146-coated Dynabeads™ and with a fluorescence-coated (FITC) lectin (Ulex europaeus agglutinin 1, UEA-1) in an endothelial cell specific double-staining method. Afterwards CECs were enumerated in a counting chamber using a fluorescence microscope. (B) FACS plot of expanded T helper cells from a patient with biopsy proven PACNS. CSF cells were expanded in the presence of feeder cells, IL-2 und PHA for 2 weeks and an intracellular cytokine staining for IL-17 and IFNγ was performed.
Amyloid-beta A4 Protein (APP) in the Cerebrospinal Fluid
Mass-spectrometry-based techniques allow the assessment of a significant fraction of the proteome in biofluids without a pre-selection of target proteins. Ruland et al. reported a significantly lower abundance of proteins in the CSF of patients with PACNS (32). In particular, reduced APP concentrations were detected, a protein indicative for nervous system damage or pathology. Based on these findings the authors speculate that this protein may serve as a surrogate marker of brain injury in cerebral vasculitis. Further studies will have to validate these findings.
Circulating Endothelial Cells in the Peripheral Venous Blood
Circulating endothelial cells (CECs) are known as markers of endothelial damage (33, 34). Inflammatory or non-inflammatory endothelial damage or mechanical injury can lead to the detachment of endothelial cells from the vessel wall. Thereafter, CECs can easily be detected in the blood by immunomagnetic isolation (Figure 1B) or flow cytometry (35). Preliminary studies of AAV showed increased CEC levels in patients with an active disease (36) whereas the number of CECs decreased under successful immunosuppressive treatment. Likewise, lower numbers of CECs were detected in patients with non-inflammatory vascular diseases, such as stroke and myocardial infarction (34, 37, 38). Of note, similar results were observed in patients with PACNS. We demonstrated that CECs were significantly elevated in patients with active PACNS while being decreased under successful immunosuppressive medication, in healthy controls and patients with stroke and cerebrovascular risk factors (39). Hence, CECs may potentially contribute to the diagnosis in biopsy negative cases and monitor the success of immunosuppressive treatment. However, although being a promising biomarker, studies with larger patient numbers are required to verify these results.
High-Resolution Magnetic Resonance Vessel Wall Imaging (HR-MRI)
Commonly used imaging modalities fail to distinguish between inflammatory and non-inflammatory vasculopathies. Preliminary studies demonstrated the possibility of outlining the vessel wall by contrast enhancement (40–42). In enhanced MR imaging of the vessel walls ("dark blood imaging") the signal of the blood is suppressed and discrimination of the vessel wall from the lumen is increased (Figure 2). This HR-MRI can be performed as T1-weighted, T2-weighted or proton density-weighted sequences (43). This technique has already been used to distinguish PACNS from other vasculopathies (40, 42). In more detail, in PACNS a predominantly smooth, concentric, and long-segment wall thickening with strong enhancement and a perivascular edema were observed (44). Arteriosclerotic plaques exhibit a more eccentric, irregular, and short-segment wall thickening without perivascular edema and only mild enhancement depending on composition and activity of the plaque (25, 42). However, the distinction might still be difficult and this MRI sequence might rather help to differentiate PACNS from vasculopathies of young adults such as RCVS (41, 44). Notably, HR-MRI is merely capable of detecting the MVV with its current capacity of vessel resolution. However, this imaging technique is quickly developing and might soon lead to an improved discrimination between the MVV of PACNS and other intracranial vasculopathies (45). Of note, with higher resolutions it will be able to detect changes even in small vessels. Given that treatment can also affect the imaging findings, e.g., less enhancement under immunosuppressive or antiviral therapy (43, 46), it might also have the potential to monitor disease activity, which would make it extremely valuable for clinical trials (43, 47).
Figure 2. Cranial MRI, coronal T1-weighted-(dark-blood) sequence demonstrating contrast enhancement of the vessel wall in the first segment of the left middle cerebral artery.
Endothelial Progenitor Cells in the Peripheral Venous Blood
Another potential biomarker in PACNS are the endothelial progenitor cells (EPCs). In contrast to CECs, EPCs are considered to play a pivotal role in vascular regeneration and endothelial renewal (34). They are bone marrow-derived cells and originate from hematopoietic progenitor cells. EPCs are believed to be mobilized by various factors (e.g., vascular endothelial growth factor, VEGF), migrate to the site of endothelial injury, integrate in the endothelial cell layer and differentiate to mature endothelial cells (48). Interestingly, an inverse relationship of CECs and EPCs in patients with systemic vasculitis was previously reported (49). CEC values were highly elevated immediately after endothelial injury and decreased over time. In contrast, the EPC counts were low at time of endothelial injury and increased in the equal time course. Notably, similar results were observed in patients with Kawasaki disease, acute coronary syndrome and ischemic stroke (50–52). Hence, EPCs are presumed to be a marker for vascular or endothelial repair in inflammatory and non-inflammatory vasculopathies. However, EPCs have heretofore not been investigated, but these findings warrant the analysis of EPCs in PACNS.
Von Willebrand Factor Antigen in the Peripheral Venous Blood
The von Willebrand factor antigen (vWF-Ag) is a plasma protein which is mainly synthesized from endothelial cells. Its function includes platelet aggregation and adhesion. If endothelium is damaged, e.g., by inflammation, increased levels of vWF-Ag may then be detected in blood. In fact, vWF-Ag was previously suggested as a potential biomarker in patients with systemic vasculitis. In patients suffering from Behçet disease and AAV, vWF-Ag levels were increased compared to controls (53–55). However, these elevated levels were observed in an active stage of disease and remained increased under remission. In contrast, in patients with Granulomatosis with Polyangiitis and Kawasaki disease vWF-Ag levels correlated well with disease activity (56, 57). Likewise, a recent study demonstrated that vWF-Ag may be a marker for disease activity in childhood PACNS (58). Elevated levels were detected in active disease and normalized under successful treatment. These results justify further analyses in adult PACNS.
High Resolution Digital Subtraction Angiography
High resolution digital subtraction angiography including a 3D rotation technique provides a visualization of smaller vessels than with commonly used angiography techniques. A recent study demonstrated that this tool can display small branches (e.g., perforators) of the basilar artery (59). Fukuda et al. (60) described a fusion technique using two three-dimensional DSA images with precise information of the angio-architecture of arterial-venous malformations. The exact structure and location of the fistula, feeders, and drainers with high spatial resolution were obtained. Another novel technique to visualize small vessels beyond the spatial resolution of commonly used imaging modalities is the time-resolved 3D rotational angiography (4D DSA) (61). In particular, for proximal stenosis of the middle cerebral artery local collateral networks can be displayed and microangio-architecture in dural arteriovenous fistulas (dAVF) or arteriovenous malformations (AVM) can be visualized (62). Notably, 4D DSA might reduce the radiation and contrast agent dose and can be less time consuming compared to commonly used methods. In summary, novel imaging techniques in DSA could potentially provide more detailed information on smaller cerebral vessels due to higher spatial resolution. These imaging sequences were applied to studies of AVMs, dAVFs and aneurysms so far. They might also be applied to the SVV of PACNS to further increase the diagnostic specificity.
Positron Emission Tomography (PET)
Fluor-desoxy-glucose (FDG)-PET is a functional imaging technique in nuclear medicine. It uses FDG as the radiopharmaceutical and depicts metabolic activity in the body by visualization of glucose uptake in tissues. Hence, inflamed vessel walls can be uncovered. In fact, in patients with biopsy proven giant cell arteriitis, FDG-PET was successfully applied and showed a high sensitivity and specificity (63). In addition, Novikov et al. demonstrated that PET can be a valuable diagnostic tool in patients with medium vessel involvement (64) and, thus, may contribute to depict inflammation of the vessel walls in patients with inconclusive diagnostic results (65). Of note, FDG-PET was previously applied to follow up and monitor disease activity in vasculitis (66, 67). However, small-vessel involvement cannot be detected by this imaging modality (68).
This short review summarizes current diagnostic procedures applied to primary CNS vasculitis and aims at illustrating the difficulties and challenges in diagnosing PACNS. It further presents novel emerging and potential biomarkers which might facilitate the diagnostic process in the future. New biofluid and imaging markers may increase the certainty of the diagnosis. Biomarkers in the CSF (IL-17, APP) and peripheral venous blood (CEC, EPC, vWF-Ag) seem to be promising approaches, although potential differences in results between SVV and MVV remain to be determined. The ultimate goal would be to identify a panel of markers that might increase the diagnostic accuracy in PACNS in the future. In addition, novel potential imaging techniques, e.g., PET or different high resolution DSA-based techniques, can visualize smaller vessels or inflammatory vessel walls and, therefore, might support the diagnostic work. Data on these diagnostic tools are currently preliminary and, thus, need to be verified in larger patient cohorts or still need to be investigated in adult patients with PACNS. However, they might advance the diagnostic workflow in the future and aid to an accelerated diagnosis in patients lacking histological evidence, hence, in patients with suspected disease. They are promising diagnostic approaches that justify future attempts of investigation.
MD-C: substantial contribution to the conception and design of the work; acquisition, analysis and interpretation of data for the work; drafting the work and revising it critically for important intellectual content. SS: interpretation of data for the work; revising it critically for important intellectual content. VH: analysis and interpretation of data for the work; revising it critically for important intellectual content. CG: analysis and interpretation of data for the work; drafting of the work and revising it critically for important intellectual content. GT: analysis and interpretation of data for the work; drafting of the work and revising it critically for important intellectual content. TM: conception and design of the work; analysis and interpretation of data for the work; drafting of the work and revising it critically for important intellectual content. All authors provide approval for publication of the content. All authors agree to be accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved.
CG received fees as a consultant or lecture fees from Amgen, Bayer Vital, Bristol-Myers Squibb/Pfizer, Boehringer Ingelheim, Sanofi Aventis. GT received fees as a consultant or lecture fees from Acandis, Bayer Vital, Bristol-Myers Squibb/Pfizer, Boehringer Ingelheim, Daichii Sankyo, GlaxoSmithKline, and Stryker. TM received fees as a consultant or lecture fees from Boehringer Ingelheim, Novartis, Merck-Serono, Grifols, CSL-Behring and he received research fees from BMBF, DFG, EU, Werner-Otto-Stiftung, Schilling-Stiftung, Novartis, Merck-Serono.
The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
1. Salvarani C, Brown RD Jr., Hunder GG. Adult primary central nervous system vasculitis. Lancet. (2012) 380:767–77. doi: 10.1016/S0140-6736(12)60069-5
2. Marini C, Totaro R, De Santis F, Ciancarelli I, Baldassarre M, Carolei A. Stroke in young adults in the community-based L'Aquila registry: incidence and prognosis. Stroke. (2001) 32:52–6. doi: 10.1161/01.STR.32.1.52
3. Yesilot Barlas N, Putaala J, Waje-Andreassen U, Vassilopoulou S, Nardi K, Odier C, et al. Etiology of first-ever ischaemic stroke in European young adults: the 15 cities young stroke study. Eur J Neurol. (2013) 20:1431–9. doi: 10.1111/ene.12228
4. Salvarani C, Brown RDJr, Calamia KT, Christianson TJ, Weigand SD, Miller DV, et al. Primary central nervous system vasculitis: analysis of 101 patients. Ann Neurol. (2007) 62:442–51. doi: 10.1002/ana.21226
5. Lucke M, Hajj-Ali RA. Advances in primary angiitis of the central nervous system. Curr Cardiol Rep. (2014) 16:533. doi: 10.1007/s11886-014-0533-0
6. Singhal AB, Topcuoglu MA, Fok JW, Kursun O, Nogueira RG, Frosch MP, et al. Reversible cerebral vasoconstriction syndromes and primary angiitis of the central nervous system: clinical, imaging, and angiographic comparison. Ann Neurol. (2016) 79:882–94. doi: 10.1002/ana.24652
7. Rocha EA, Topcuoglu MA, Silva GS, Singhal AB. RCVS2 score and diagnostic approach for reversible cerebral vasoconstriction syndrome. Neurology. (2019) 92:e639–47. doi: 10.1212/WNL.0000000000006917
8. Calabrese LH, Mallek JA. Primary angiitis of the central nervous system. Report of 8 new cases, review of the literature, and proposal for diagnostic criteria. Medicine. (1988) 67:20–39. doi: 10.1097/00005792-198801000-00002
9. Birnbaum J, Hellmann DB. Primary angiitis of the central nervous system. Arch Neurol. (2009) 66:704–9. doi: 10.1001/archneurol.2009.76
10. Schmidley JW. 10 questions on central nervous system vasculitis. Neurologist. (2008) 14:138–9. doi: 10.1097/NRL.0b013e31815bdc2b
11. Salvarani C, Brown RD Jr., Christianson T, Miller DV, Giannini C, Huston J III, et al. An update of the Mayo Clinic cohort of patients with adult primary central nervous system vasculitis: description of 163 patients. Medicine. (2015) 94:e738. doi: 10.1097/MD.0000000000000738
12. Zuccoli G, Pipitone N, Haldipur A, Brown RD Jr., Hunder G, Salvarani C. Imaging findings in primary central nervous system vasculitis. Clin Exp Rheumatol. (2011) 29(1 Suppl 64):S104–9. Available online at: https://www.clinexprheumatol.org/abstract.asp?a=4879
13. Ay H, Sahin G, Saatci I, Soylemezoglu F, Saribas O. Primary angiitis of the central nervous system and silent cortical hemorrhages. AJNR Am J Neuroradiol. (2002) 23:1561–3. Available online at: http://www.ajnr.org/content/23/9/1561.long
14. de Boysson H, Zuber M, Naggara O, Neau JP, Gray F, Bousser MG, et al. Primary angiitis of the central nervous system: description of the first fifty-two adults enrolled in the French cohort of patients with primary vasculitis of the central nervous system. Arthrit Rheumatol. (2014) 66:1315–26. doi: 10.1002/art.38340
15. Kumar RS, Singh A, Rathore C, Kesavadas C. Primary angiitis of central nervous system: tumor-like lesion. Neurol India. (2010) 58:147–9. doi: 10.4103/0028-3886.60417
16. Bonstrup M, Ott K, Glatzel M, Magnus T. Frontal lobe dementia syndrome as a first manifestation of primary angiitis of the central nervous system (PACNS). Clin Neurol Neurosurg. (2016) 141:92–4. doi: 10.1016/j.clineuro.2015.12.016
17. Stone JH, Pomper MG, Roubenoff R, Miller TJ, Hellmann DB. Sensitivities of noninvasive tests for central nervous system vasculitis: a comparison of lumbar puncture, computed tomography, and magnetic resonance imaging. J Rheumatol. (1994) 21:1277–82.
18. Schuster S, Magnus T. [Primary central nervous system vasculitis]. Z Rheumatol. (2015) 74:862. doi: 10.1007/s00393-015-0007-9
19. Harris KG, Tran DD, Sickels WJ, Cornell SH, Yuh WT. Diagnosing intracranial vasculitis: the roles of MR and angiography. AJNR Am J Neuroradiol. (1994) 15:317–30.
20. Marsh EB, Zeiler SR, Levy M, Llinas RH, Urrutia VC. Diagnosing CNS vasculitis: the case against empiric treatment. Neurologist. (2012) 18:233–8. doi: 10.1097/NRL.0b013e31825c6d23
21. Calabrese LH, Furlan AJ, Gragg LA, Ropos TJ. Primary angiitis of the central nervous system: diagnostic criteria and clinical approach. Cleve Clin J Med. (1992) 59:293–306. doi: 10.3949/ccjm.59.3.293
22. Schuster S, Bachmann H, Thom V, Kaufmann-Buehler AK, Matschke J, Siemonsen S, et al. Subtypes of primary angiitis of the CNS identified by MRI patterns reflect the size of affected vessels. J Neurol Neurosurg Psychiatr. (2017) 88:749–55. doi: 10.1136/jnnp-2017-315691
23. Bhattacharyya S, Berkowitz AL. Primary angiitis of the central nervous system: avoiding misdiagnosis and missed diagnosis of a rare disease. Pract Neurol. (2016) 16:195–200. doi: 10.1136/practneurol-2015-001332
24. Eleftheriou D, Cox T, Saunders D, Klein NJ, Brogan PA, Ganesan V. Investigation of childhood central nervous system vasculitis: magnetic resonance angiography versus catheter cerebral angiography. Dev Med Child Neurol. (2010) 52:863–7. doi: 10.1111/j.1469-8749.2009.03591.x
25. Dutra LA, de Souza AW, Grinberg-Dias G, Barsottini OG, Appenzeller S. Central nervous system vasculitis in adults: An update. Autoimmun Rev. (2017) 16:123–31. doi: 10.1016/j.autrev.2016.12.001
26. Parisi JE, Moore PM. The role of biopsy in vasculitis of the central nervous system. Semin Neurol. (1994) 14:341–8. doi: 10.1055/s-2008-1041093
27. Miller DV, Salvarani C, Hunder GG, Brown RD, Parisi JE, Christianson TJ, et al. Biopsy findings in primary angiitis of the central nervous system. Am J Surg Pathol. (2009) 33:35–43. doi: 10.1097/PAS.0b013e318181e097
28. Cupps TR, Moore PM, Fauci AS. Isolated angiitis of the central nervous system. Prospective diagnostic and therapeutic experience. Am J Med. (1983) 74:97–105. doi: 10.1016/0002-9343(83)91125-7
29. Kallenberg CG. Pathophysiology of ANCA-associated small vessel vasculitis. Curr Rheumatol Rep. (2010) 12:399–405. doi: 10.1007/s11926-010-0138-6
30. Thom V, Schmid S, Gelderblom M, Hackbusch R, Kolster M, Schuster S, et al. IL-17 production by CSF lymphocytes as a biomarker for cerebral vasculitis. Neurol Neuroimmunol Neuroinflamm. (2016) 3:e214. doi: 10.1212/NXI.0000000000000214
31. Hueber W, Patel DD, Dryja T, Wright AM, Koroleva I, Bruin G, et al. Effects of AIN457, a fully human antibody to interleukin-17A, on psoriasis, rheumatoid arthritis, and uveitis. Sci Transl Med. (2010) 2:52ra72. doi: 10.1126/scitranslmed.3001107
32. Ruland T, Wolbert J, Gottschalk MG, Konig S, Schulte-Mecklenbeck A, Minnerup J, et al. Cerebrospinal fluid concentrations of neuronal proteins are reduced in primary angiitis of the central nervous system. Front Neurol. (2018) 9:407. doi: 10.3389/fneur.2018.00407
33. Erdbruegger U, Haubitz M, Woywodt A. Circulating endothelial cells: a novel marker of endothelial damage. Clin Chim Acta. (2006) 373:17–26. doi: 10.1016/j.cca.2006.05.016
34. Schmidt DE, Manca M, Hoefer IE. Circulating endothelial cells in coronary artery disease and acute coronary syndrome. Trends Cardiovasc Med. (2015) 25:578–87. doi: 10.1016/j.tcm.2015.01.013
35. Erdbruegger U, Woywodt A, Kirsch T, Haller H, Haubitz M. Circulating endothelial cells as a prognostic marker in thrombotic microangiopathy. Am J Kidney Dis. (2006) 48:564–70. doi: 10.1053/j.ajkd.2006.06.013
36. Woywodt A, Streiber F, de Groot K, Regelsberger H, Haller H, Haubitz M. Circulating endothelial cells as markers for ANCA-associated small-vessel vasculitis. Lancet. (2003) 361:206–10. doi: 10.1016/S0140-6736(03)12269-6
37. Haubitz M, Woywodt A. Circulating endothelial cells and vasculitis. Intern Med. (2004) 43:660–7. doi: 10.2169/internalmedicine.43.660
38. Woywodt A, Gerdes S, Ahl B, Erdbruegger U, Haubitz M, Weissenborn K. Circulating endothelial cells and stroke: influence of stroke subtypes and changes during the course of disease. J Stroke Cerebrovasc Dis. (2012) 21:452–8. doi: 10.1016/j.jstrokecerebrovasdis.2010.11.003
39. Deb M, Gerdes S, Heeren M, Lambrecht J, Worthmann H, Goldbecker A, et al. Circulating endothelial cells as potential diagnostic biomarkers in primary central nervous system vasculitis. J Neurol Neurosurg Psychiatr. (2013) 84:732–4. doi: 10.1136/jnnp-2012-303335
40. Kuker W, Gaertner S, Nagele T, Dopfer C, Schoning M, Fiehler J, et al. Vessel wall contrast enhancement: a diagnostic sign of cerebral vasculitis. Cerebrovasc Dis. (2008) 26:23–9. doi: 10.1159/000135649
41. Swartz RH, Bhuta SS, Farb RI, Agid R, Willinsky RA, Terbrugge KG, et al. Intracranial arterial wall imaging using high-resolution 3-tesla contrast-enhanced MRI. Neurology. (2009) 72:627–34. doi: 10.1212/01.wnl.0000342470.69739.b3
42. Saam T, Habs M, Cyran CC, Grimm J, Pfefferkorn T, Schuller U, et al. [New aspects of MRI for diagnostics of large vessel vasculitis and primary angiitis of the central nervous system]. Radiologe. (2010) 50:861–71. doi: 10.1007/s00117-010-2004-y
43. Lehman VT, Brinjikji W, Kallmes DF, Huston JR, Lanzino G, Rabinstein AA, et al. Clinical interpretation of high-resolution vessel wall MRI of intracranial arterial diseases. Br J Radiol. (2016) 89:20160496. doi: 10.1259/bjr.20160496
44. Obusez EC, Hui F, Hajj-Ali RA, Cerejo R, Calabrese LH, Hammad T, et al. High-resolution MRI vessel wall imaging: spatial and temporal patterns of reversible cerebral vasoconstriction syndrome and central nervous system vasculitis. AJNR Am J Neuroradiol. (2014) 35:1527–32. doi: 10.3174/ajnr.A3909
45. Mossa-Basha M, Hwang WD, De Havenon A, Hippe D, Balu N, Becker KJ, et al. Multicontrast high-resolution vessel wall magnetic resonance imaging and its value in differentiating intracranial vasculopathic processes. Stroke. (2015) 46:1567–73. doi: 10.1161/STROKEAHA.115.009037
46. Noh HJ, Choi JW, Kim JP, Moon GJ, Bang OY. Role of high-resolution magnetic resonance imaging in the diagnosis of primary angiitis of the central nervous system. J Clin Neurol. (2014) 10:267–71. doi: 10.3988/jcn.2014.10.3.267
47. Kissin EY, Merkel PA. Diagnostic imaging in Takayasu arteritis. Curr Opin Rheumatol. (2004) 16:31–7. doi: 10.1097/00002281-200401000-00007
48. Liao S, Luo C, Cao B, Hu H, Wang S, Yue H, et al. Endothelial progenitor cells for ischemic stroke: update on basic research and application. Stem Cells Int. (2017) 2017:2193432. doi: 10.1155/2017/2193432
49. de Groot K, Goldberg C, Bahlmann FH, Woywodt A, Haller H, Fliser D, et al. Vascular endothelial damage and repair in antineutrophil cytoplasmic antibody-associated vasculitis. Arthr Rheum. (2007) 56:3847–53. doi: 10.1002/art.23070
50. Nakatani K, Takeshita S, Tsujimoto H, Kawamura Y, Tokutomi T, Sekine I. Circulating endothelial cells in Kawasaki disease. Clin Exp Immunol. (2003) 131:536–40. doi: 10.1046/j.1365-2249.2003.02091.x
51. Massa M, Rosti V, Ferrario M, Campanelli R, Ramajoli I, Rosso R, et al. Increased circulating hematopoietic and endothelial progenitor cells in the early phase of acute myocardial infarction. Blood. (2005) 105:199–206. doi: 10.1182/blood-2004-05-1831
52. Bogoslovsky T, Chaudhry A, Latour L, Maric D, Luby M, Spatz M, et al. Endothelial progenitor cells correlate with lesion volume and growth in acute stroke. Neurology. (2010) 75:2059–62. doi: 10.1212/WNL.0b013e318200d741
53. Direskeneli H, Keser G, D'Cruz D, Khamashta MA, Akoglu T, Yazici H, et al. Anti-endothelial cell antibodies, endothelial proliferation and von Willebrand factor antigen in Behcet's disease. Clin Rheumatol. (1995) 14:55–61. doi: 10.1007/BF02208085
54. Beyan E, Sadikoglu B, Ertugrul E, Beyan C. Von Willebrand factor antigen levels in Behcet disease. Am J Hematol. (2005) 79:70–2. doi: 10.1002/ajh.20317
55. Salmela A, Ekstrand A, Joutsi-Korhonen L, Raisanen-Sokolowski A, Lassila R. Activation of endothelium, coagulation and fibrinolysis is enhanced and associates with renal anti-neutrophil cytoplasmic antibody-associated vasculitis. Nephrol Dial Transplant. (2015) 30(Suppl 1):i53–9. doi: 10.1093/ndt/gfu379
56. D'Cruz D, Direskeneli H, Khamashta M, Hughes GR. Lymphocyte activation markers and von Willebrand factor antigen in Wegener's granulomatosis: potential markers for disease activity. J Rheumatol. (1999) 26:103–9.
57. Falcini F, Generini S, Pignone A, Leoncini G, Cimaz R, Partsch G, et al. Are angiotensin converting enzyme and von Willebrand factor circulating levels useful surrogate parameters to monitor disease activity in Kawasaki disease? Endothelium. (1999) 6:209–15. doi: 10.3109/10623329909053411
58. Cellucci T, Tyrrell PN, Pullenayegum E, Benseler SM. von Willebrand factor antigen–a possible biomarker of disease activity in childhood central nervous system vasculitis? Rheumatology. (2012) 51:1838–45. doi: 10.1093/rheumatology/kes156
59. Lescher S, Samaan T, Berkefeld J. Evaluation of the pontine perforators of the basilar artery using digital subtraction angiography in high resolution and 3D rotation technique. AJNR Am J Neuroradiol. (2014) 35:1942–7. doi: 10.3174/ajnr.A3981
60. Fukuda K, Higashi T, Okawa M, Iwaasa M, Abe H, Inoue T. Fusion technique using three-dimensional digital subtraction angiography in the evaluation of complex cerebral and spinal vascular malformations. World Neurosurg. (2016) 85:353–8. doi: 10.1016/j.wneu.2015.08.075
61. Kammerer S, Mueller-Eschner M, Berkefeld J, Tritt S. Time-resolved 3D rotational angiography (4D DSA) of the lenticulostriate arteries: display of normal anatomic variants and collaterals in cases with chronic obstruction of the MCA. Clin Neuroradiol. (2017) 27:451–7. doi: 10.1007/s00062-017-0578-8
62. Lescher S, Gehrisch S, Klein S, Berkefeld J. Time-resolved 3D rotational angiography: display of detailed neurovascular anatomy in patients with intracranial vascular malformations. J Neurointerv Surg. (2017) 9:887–94. doi: 10.1136/neurintsurg-2016-012462
63. Prieto-Gonzalez S, Depetris M, Garcia-Martinez A, Espigol-Frigole G, Tavera-Bahillo I, Corbera-Bellata M, et al. Positron emission tomography assessment of large vessel inflammation in patients with newly diagnosed, biopsy-proven giant cell arteritis: a prospective, case-control study. Ann Rheum Dis. (2014) 73:1388–92. doi: 10.1136/annrheumdis-2013-204572
64. Novikov PI, Meshkov AD, Moiseev SV. Positron emission tomography in giant cell arteritis: a new diagnostic tool? Ann Rheum Dis. (2014) 73:e70. doi: 10.1136/annrheumdis-2014-206227
65. Abdel Razek AA, Alvarez H, Bagg S, Refaat S, Castillo M. Imaging spectrum of CNS vasculitis. Radiographics. (2014) 34:873–94. doi: 10.1148/rg.344135028
66. Berlit P. Diagnosis and treatment of cerebral vasculitis. Ther Adv Neurol Disord. (2010) 3:29–42. doi: 10.1177/1756285609347123
67. Pacheco Castellanos Mdel C, Minguez Vega M, Martinez Caballero A, Bernabeu Gonzalvez MP. Early diagnosis of large vessel vasculitis: usefulness of positron emission tomography with computed tomography. Reumatol Clin. (2013) 9:65–8. doi: 10.1016/j.reumae.2013.01.005
68. Wengenroth M, Saam T, Hahnel S. [Neuroimaging of cerebral vasculitis]. Radiologe. (2016) 56:52–69. doi: 10.1007/s00117-015-0053-y
Keywords: PACNS, biomarker, vasculitis, cerebrospinal fluid, peripheral venous blood, imaging, circulating endothelial cells
Citation: Deb-Chatterji M, Schuster S, Haeussler V, Gerloff C, Thomalla G and Magnus T (2019) Primary Angiitis of the Central Nervous System: New Potential Imaging Techniques and Biomarkers in Blood and Cerebrospinal Fluid. Front. Neurol. 10:568. doi: 10.3389/fneur.2019.00568
Thomas Skripuletz, Hanover Medical School, Germany
Anastasia Bougea, National and Kapodistrian University of Athens, Greece
Mehmet Akif Topçuoǧlu, Hacettepe University, Turkey
Copyright © 2019 Deb-Chatterji, Schuster, Haeussler, Gerloff, Thomalla and Magnus. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
*Correspondence: Milani Deb-Chatterji, m.deb-chatterji@uke.de


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Resident Evil 7: Biohazard from Capcom is a true return to form for the series, mixing horror, a first-person perspective, and an intriguing story in one amazing package.
It also features numerous types of collectibles to discover. This guide features screenshots and descriptions of every Antique Coin collectible, which help you unlock new weapons, items, and achievements!
Antique Coins are a collectible with a purpose. At two points in the game (the Trailer safe room in the Yard and the Swamp safe room), they can be exchanged for three items: Steroids (3 coins), a Stabilizer (6 coins), and the 44 Magnum pistol (9 coins).
There are 18 Antique Coins on Easy or Normal difficulty. Madhouse difficulty has 33 coins of its own to collect, but this guide focuses on the Easy/Normal coins. If you collect a coin but die before saving the game or reaching a checkpoint, you'll need to get it again for it to count towards the 'Pelicans in your Pocket' Achievement. It requires all 18 coins to be collected in one playthrough.
We've divided the collectibles by the location in which they're found, so you'll always be able to tell if you've gone too far or need to backtrack.
Naturally, some of these Antique Coin locations might involve mild spoilers.
The first area of the game, and one that we'll revisit at the end as well. As you play through, be sure to check out our comprehensive Achievement Guide, Files Guide, and Mr. Everywhere Statues Guide so you don't miss any Achievements or collectibles along the way.
The first coin requires special action be taken during the Derelict House Footage videotape sequence before picking the coin up in the present. As soon as the videotape starts, take a few steps back and get the Lockpick from the ground. Enter the Guest House and use the Lockpick on the drawer in the kitchen.
After completing the videotape and before entering the secret passage, head back to the Kitchen as Ethan. You can now open the drawer to find the coin.
Survive the boss battle in the Guest House Attic and Ethan will end up in the Main House, a major area that he'll be revisiting throughout the game.
After Jack starts chasing you for the first time, quickly find the Hatch Key at the east side of the hallway. Take the hatch in the Pantry to the underground passage. The Antique Coin sits on top of a riding lawnmower.
After the Garage boss battle, take the Ox Statuette and use it to enter the Main Hall. Inside, walk along the wall and you'll discover the coin inside of a drawer in the northeastern corner.
On the second floor, enter the Recreation Room from the southern entrance. Straight ahead, you'll find the coin on a small shell beside a basket (right beside Mr. Everywhere #4).
On the second floor, head west from the Recreation Room to the Bathroom. Check the toilet bowl for a shiny, totally germ-free coin.
From the Drawing Room (where you found Mr. Everywhere # 5), take the western door to the unnamed room just before the Monitoring Room. You'll find the coin in an ashtray on the table.
In the Basement Processing Area, head west past the Incinerator Room door. Pry open the corrugated room divider. Immediately left from that divider, you'll find a wooden pallet leaning against the wall and the coin in a nearby hole in the wall. Get the Processing Area Map from the nearby shelf while you're there.
After defeating the Morgue boss, you can use the three Dog's Heads to open the back door of the Main House and enter the Yard.
Right when you enter the Yard from the back door of the Main House, step off the porch and turn right. You'll find the coin in a planter besides the steps. Be sure to grab the first Repair Kit while you're out here, too.
Inside the Trailer safe room, it's sitting right next to the birdcage on the table that costs nine coins to open. How convenient!
After accepting the phone call in the Trailer, head northeast through the Yard to the Old House. You can build the Burner Flamethrower in this area, as well as take the first step towards acquiring the Grenade Launcher.
Take the passage from the Dining Room to the Cellar (where we found Mr. Everywhere #9). You'll find the coin sitting on a cart just before the door to the Cellar.
Once you have the Crank, head to the boardwalk area where you got the Burner Nozzle. Roast the insect nest, and then use the Crank to raise the northern bridge. You'll find the coin inside the outhouse on top of the toilet – just right of the chest that contains the Crow Key.
On the second floor, in the room with the scale attached to a door, check the chest of drawers in the corner for the coin.
Once you get the Blue and Yellow Key Cards from the Main House, go back to the Yard and use the keys on the western door to enter the Testing Area. Note that you can't return to the Main House or Old House once you're inside.
In the first floor western corner room that contains four tripwire bombs, first disarm the bombs. Then check the drawer in the table for a coin. You'll also find the third Steroids and an exploding crate in the nearby locker.
After defeating the Fat Molded boss, take the elevator to the second floor. Immediately outside of the room with the burnt corpse (the Rest Area, where we found File #22), the coin awaits on a wall shelf.
After leaving the Testing Area and defeating the Boat House boss, you'll make a decision that affects which ending you'll receive. Next comes the Wrecked Ship area. The first portion of the ship has two highly missable Antique Coins – you won't be able to return after progressing further into the area.
The Wrecked Ship portion of the game starts on floor S3. As soon as you reach S1, prepare to look for this coin. From the Office, drop down into the hatch after the flashback occurs. In the crawlspace, turn right at the first fork. The coin lies at the end of the path.
After the crawlspace, you'll emerge on floor S2. Climb the ladder there that leads to the first floor. Immediately following the ladder climb, you'll jump into a pool of water. The coin is hidden beside a plant in the northwestern corner of the water.
This coin is found inside the locked toolbox on the third floor, just past the elevator shaft. To get it, you'll first have to retrieve the Lockpick on the second floor.
After you've solved the painting puzzle in the Lounge on the second floor, head out of the Dining Room and straight into the northeastern room with the ladder. Climb the ladder, and take the Lockpick from the orange box. Shoot the Mr. Everywhere statue (#17), and then make your way back to the locked box in the Control Room of the third floor.
Near the end of the Wrecked Ship, you'll battle a Fat Molded in the No. 1 Engine Room on floor S2. The hallway immediately after that room has a box on the wall that must be opened with Corrosives. You'll find the coin inside.
That's the last Antique Coin on Easy and Normal playthroughs! If you're hunting down all the collectibles, you still have five Files and three Mr. Everywhere statues left to go before the end of the game.
For more help, check out our Achievement Guide, Files Guide, and Mr. Everywhere Statues Guide. You also don't want to miss our full review!


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My Greatest Olympic Prize by Jesse Owens Analysis
August 21, 2020 December 12, 2019 by Website Contributors
This inspirational story about enduring friendship and relentless effort was written in an autobiographical account by the world-famous athlete Jesse Owens. The title of the story itself holds a more meaningful connection in the life of the author. It is generally understood that Jesse Owens is talking about the Olympic Prize he won in one of the greatest sporting events of all time in the year 1960. However, on deeper reflection, the readers get to know that Jesse is not talking about material possessions like the gold medals at all. In fact, the title of the story refers to his friendship with Luz Long who was a formidable player in the German team. Despite being rivals the two sports people come together as men leaving their differences aside to share a bond worth more than any prize.
The style and technique of writing is simple and unbiased which has helped the author paint a perfect picture of human flaws and redeeming qualities. As it is an autobiographical account the whole story is from the viewpoint of one character that is also the central character of the story. The events unfold at a natural straightforward pace without any usage of major symbolism or other literary devices. The narrative is impressive in its simplicity and effectively registers the deeper meaning of self-less acts even in the face of adversity. Although the author has no experience as a writer he has managed to bring out the emotions of the two main characters quiet well.
Themes: My Greatest Olympic Prize
Thebasic theme of the story centres on the positivity of true sportsmanship and how we can come together as human beings to participate in fair play. Often we see players getting emotionally tormented after a failure in the sporting event. The author wishes to address this problem by giving instances from his own life and explains that sports can at best be a good game or a dream but true friendships are over and above such momentary passions. Compromising the bond of humanity based on social divisions and prejudices is not worth any conflict.
Character Sketch: My Greatest Olympic Prize
The character we first get introduced in the story is that of Jesse Owens and it's his tale so we get a first-hand perspective of the actual events as they happened. He is a hot-blooded athlete with an eye for victory as he wishes to answer back to the people who wronged him with his medals. He gains a better conscience and feels inspired upon his fateful meeting with a German rival.
The figures of Luz Long and Hitler both hail from the same nation of Germany but their beliefs and characters are poles apart. As the story is based on a real event the characters are also real and we find many conflicting traits in the personality of these two people who apparently belong to the same nation. In fact, Luz Long is a man Hitler counts upon during the finals of the Olympics. Nevertheless, Luz Long proves to be a far better and braver man than Hitler ever could be. While Hitler was promoting the idea of a superior race, Luz gave a very important lesson on the true nature and bond of humanity.
The Olympics game of 1960 and the present audience together as a body has also been presented as a character in the story. The excitement for the game is palpitating and can be felt if we read in between the lines. People from everywhere came together to cheer and applaud Jesse Owens as he was performing not only to win but to also defeat a dangerous social prejudice.
Conclusion: My Greatest Olympic Prize
The spectators often only see the performances of the athletes during a game or a match. They fail to see or acknowledge the hardships and struggles that every sportsperson endures before a game. This autobiographical account by Jesse Owens gives the readers a report on how the impossible can be made possible and what goes on in the backend of every outstanding performance in the world of sports.
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My Greatest Olympic Prize Summary by Jesse Owens
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This article is from the Encyclopedia of North Carolina edited by William S. Powell. Copyright © 2006 by the University of North Carolina Press. Used by permission of the publisher. For personal use and not for further distribution. Please submit permission requests for other use directly to the publisher.
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Scottish Settlers
by Robert J. Cain, 2006
Additional research provided by Lloyd Johnson, David A. Norris, and George W. Troxler.
See also: Argyll Colony; Crofter Immigration; Gaelic Language; Highland Games; Highland Scots; Cape Fear Valley Scottish Festival
Scots—as individuals and in families—have been in North Carolina since the beginning of permanent settlement. The first Proprietary governor of Albemarle, William Drummond, was born in Scotland, and later Scots-such as the Glaswegian Thomas Pollock, who came to North Carolina in 1683-achieved prominence in the mercantile and political life of the colony. The earliest surviving court and land grant records reveal modest numbers of distinctively Scottish names.
The first sizable group of Scots to arrive in North Carolina in a body was the so-called Argyll Colony of 1739, which came from the Highland county of Argyll and settled on the Cape Fear River between Cross Creek and the Lower Little River. Numbering some 350 men, women, and children, the group was led by Highland gentry who provided much of the financing for the venture and received the largest grants of land. Gabriel Johnston, a Lowland Scot and North Carolina governor from 1734 to 1752, was accused of showing favoritism to his compatriots, and the General Assembly exempted the newcomers from taxation for ten years after their arrival.
The second large wave of Highland immigrants began in the late 1760s and reached its peak in 1774. It is not known exactly how many Highlanders came to North Carolina, but in 1784 James Knox estimated that 20,000 Highlanders migrated to America during this second wave. Most of the Highlanders who came as part of the second wave settled in the Upper Cape Fear region that includes modern-day Cumberland, Harnett, Hoke, and Moore Counties. Many Highlanders lived in the rural areas on the roads leading to the town of Cross Creek (later Fayetteville), which was chartered by the General Assembly in 1760. The abundance of pine trees in the Sandhills enabled these settlers to make their living in naval stores, extracting the sap and processing it into tar, pitch, and turpentine, which they sent down the Cape Fear River to Wilmington on flatboats made of logs. Many Highlanders were also small farmers growing crops and raising horses, cattle, and hogs.
Other individuals and families found their way directly from the Scottish Highlands to North Carolina during the remainder of the colonial era, mainly through the ports of Brunswick and Wilmington. The colony, in fact, came to be extolled as "the best poor man's country" as promotional tracts and letters home praised its climate and soil and the ease with which land could be acquired. Lowland Scots also immigrated individually or in small groups to North Carolina and other colonies throughout the seventeenth and eighteenth centuries. Because Lowland Scots were widely dispersed and more readily assimilated in the colonies, their story is less easily told than that of their Highland compatriots. While there were far fewer Lowland Scots than Highland Scots in North Carolina, some Lowlanders filled important roles as merchants, high-ranking officials, or military officers. Others ranged from poor immigrants and indentured servants to well-educated teachers, physicians, and clergymen.
The migration of Scotch-Irish settlers to America began in the 1680s but did not occur in large numbers until the 1720s. Pennsylvania was the most popular destination, but Scotch-Irish immigrants also settled in South Carolina, New Jersey, and Maryland. The Scotch-Irish, or Ulster Scots, were descendants of the Lowland Scots, whom James I of England had settled in Ulster, the northern and most isolated and conservative part of Ireland. During the reign of Elizabeth I, the native aristocracy of Ulster had rebelled against the English government and its newly established Anglican Church. The earliest concentrated settlement of Scotch-Irish immigrants in North Carolina was in Duplin and New Hanover Counties around 1740. The Scotch-Irish were also the largest ethnic group among the settlers in the Carolina backcountry in the eighteenth century, and they were the largest group among the pioneers who crossed the Blue Ridge and Allegheny Mountains and settled in southwestern North Carolina in the late eighteenth and early nineteenth centuries.
Although the Scottish emigrants, in coming to America, were assured freedom to exercise their Presbyterian religion at a time when the Stuart monarchy favored spreading the Anglican Church throughout the British Isles, the most important motivation for Scottish emigration was economic. Profound changes in agricultural organization following the Jacobite insurrection of 1745 raised rents to unprecedented heights and resulted in large numbers of evictions. Entire communities often emigrated, with the enterprise many times being organized by "tacksmen"-leaseholders who traditionally held long leases from the landowner and in turn rented to tenants.
Several North Carolina Scots gained prominence in the colony, with Governor Johnston, Royal Council member John Rutherfurd, and official and planter James Murray being examples. Scots were also important in the religious life of the colony, being well represented among both Presbyterian and Anglican clergy. A Scottish immigrant, James Innes, was a notable military leader in the French and Indian War (1754-63). The military prowess of North Carolina Loyalist Scots was put to the test at the Battle of Moore's Creek Bridge in February 1776. Although they suffered a bloody defeat in that contest, Scots constituted the backbone of North Carolina Loyalism throughout the war, and with the establishment of independence many of them sought refuge in the British colonies of Nova Scotia and New Brunswick.
After the Revolutionary War, Scottish immigration to North Carolina gradually resumed and continued until the War of 1812. The number of immigrants who came to the state during this period is unknown, but Scottish port records of the 1790s and the opening years of the nineteenth century list several dozen emigrant vessels clearing for North Carolina, mainly Wilmington. After the War of 1812, at least a trickle of immigration resumed: in 1820, for example, a ship carrying migrants was cleared from Campbelltown to Wilmington. The U.S. Census of 1850 listed some 1,200 Scottish-born citizens in North Carolina, most of them residing in the counties of Cumberland, Moore, Robeson, and Richmond. In the census of 1880 the number was down to some 400. A Scottish corporation in the 1880s purchased land in Madison and Haywood Counties with a view to bringing in Scottish settlers. The venture was unsuccessful, as was the effort to bring Highland crofters (tenant farmers) to the Sandhills at about the same time. A similar attempt of the early 1890s to attract Scots to the lands of J. Bryan Grimes in Pitt County fared little better.
Immigrants from the Scottish Highlands often retained distinctive elements of their culture. The Gaelic language was spoken by some to at least a limited extent until the mid-nineteenth century. Presbyterianism continues to flourish in the areas of Scottish settlement, and Scottish music influenced the development of local musical forms. Clan societies and the Highland Games at Grandfather Mountain and elsewhere in North Carolina continue to help keep alive a sense of the importance of the state's Scottish heritage.
Tyler Blethen and Curtis Wood Jr., From Ulster to Carolina: The Migration of the Scotch-Irish to Southwestern North Carolina (1986).
David Dobson, Scottish Emigration to America, 1607-1785 (1994).
Ian C. C. Graham, Colonists from Scotland: Emigration to Scotland in the Eighteenth Century (1956).
Duane Meyer, The Highland Scots of North Carolina, 1732-1776 (1961).
Saint Andrews Scottish Heritage Center: #
Explanation of the terms in the Scottish Dialect. Some eighteenth century tracts concerning North Carolina, 1927; by Boyd, William Kenneth, 1879-1938. North Carolina Department of Cultural Resources Digital Collections.
Colonial Record Project, NC Office of Archives & History, James Murray and John Rutherford: http://www.ncpublications.com/colonial/Bookshelf/Schaw/murray.htm
James Innes, NC Historical Marker D-90, NC Office of Archives and History.
Flora MacDonald, NC Historical Marker K-38, NC Office of Archives and History.
List of Land Grants to Scottish Settlers: Colonial and State Records of North Carolina, Documenting the American South, UNC Libraries.
Highland Heritage Scottish Americans in the American South, by Celeste Ray, UNC Press.
MacQueens of Queensdale: a biography of Col. James MacQueen and his descendants with an introduction containing a history of the origin of the clan MacQueen by Hon. A.W. Maclean, and the proceedings of the first Clan MacQueen meeting, at Maxton, N.C., June 3 to 5, 1913, by MacElyea, Annabella Bunting, 1916. North Carolina Department of Cultural Resources Digital Collections.
Expanding to the west: Settlement of the Piedmont region, 1730 to 1775 By J. Edwin Hendricks and Christopher E. Hendricks, LearnNC.
Scottish heritage at Linville By Celeste Ray, LearnNC.
MacPherson Church, NC Historical Marker I-13, NC Office of Archives & History.
Flora McDonald College, May Day Scotch Dancers doing the Scottish Fling, dated between 1910-1916. From the Barden Collection, North Carolina State Archives, call #: N.53.16.3780. Available from https://www.flickr.com/photos/north-carolina-state-archives/2348111892/ (accessed August 14, 2012).
Colonial period (1600-1763)
American Revolution (1763-1789)
UNC Press
Cain, Robert J.
Johnson, Lloyd
Norris, David A.
Troxler, George W.
Origin - location:
Hoke County
New Hanover County
Robeson County
Encyclopedia of North Carolina, University of North Carolina Press.
1 January 2006 | Cain, Robert J.; Johnson, Lloyd; Norris, David A.; Troxler, George W.
Doing some research on my
Permalink Submitted by Jason George (not verified) on Thu, 12/31/2020 - 11:28
Doing some research on my maternal grandparents and wondering how the Crawford family and the Bowlin (lots of spelling variations in this surname) fit into the Scots-Irish history of North Carolina? Lots of family in Rutherfordton and Gaston area.
Hi Jason!
Permalink Submitted by tthompson on Mon, 01/04/2021 - 14:33
Thank you for your comment and for visiting NCpedia! I am forwarding your inquiry over to our Reference Team at slnc.reference@ncdcr.gov so that they can provide you with further assistance. A staff member from our library will be reaching out to you via e-mail soon!
Taylor Thompson, Government & Heritage Library
I've been tracing the
Permalink Submitted by Melissa Campbell (not verified) on Fri, 11/13/2020 - 16:22
I've been tracing the Campbell line through my family and have hit a dead end at Edward Campbell Sr. who lived from 1746-1825 and may or may not have been born in Cumberland NC. The closest I've found to a link to his parentage is a will from an Archibald Campbell in 1763 to 3 people whose names match Edward and his siblings. Any help would be greatly appreciated.
Thank you for your comment! I am forwarding your inquiry to our library's Reference Team so that they can provide you with further assistance. A staff member of our library should be reaching out to you via e-mail soon!
My research includes any
Permalink Submitted by Jean (not verified) on Mon, 10/05/2020 - 14:14
My research includes any plantation acres willed to a former slave.
I'm researching Scottish
Permalink Submitted by John McInnis (not verified) on Sat, 07/25/2020 - 11:03
I'm researching Scottish immigrants from the McInnis Family name. Any information would be greatly appreciated
I am stuck at my 3rd gr
Permalink Submitted by Dorothy McDonald (not verified) on Sat, 06/06/2020 - 14:46
I am stuck at my 3rd gr-grandparents, Elizabeth Searcy (1785? Rutherford County, NC; father Richard Searcy, 1766 Albemarle, VA-abt. 1831 Rutherford County, NC) and a "McDaniel". Any assistance would be most appreciated.
My ancestor, Neill McNeill
Permalink Submitted by Donald Aubrey M... (not verified) on Wed, 06/03/2020 - 11:12
My ancestor, Neill McNeill came to Bladen (later Cumberland) in the 1740s. He located on Cape Fear River area. His son Roger had Rogers Meeting House before the Bluff Church was organized. Neill left a will dated May, 1764 and mentioned children Catherine, Margaret, Flora, Mary, Ann, Roger, and Henry. I have tried for quite some time to obtain information on his family. i am a descendant of Roger's son Hector born 12/12/1785. i welcome with much interest any and all information on my family from the Cape Fear region. Many thanks in advance, I am grateful for your assistance.
I am researching my genealogy
Permalink Submitted by Judy Carpenter Hamby (not verified) on Thu, 04/09/2020 - 18:36
I am researching my genealogy from the Western NC Counties. I was born in Avery County, which was composed of parts of surrounding counties in 1911. I have many questions, but I will ask for input on just my paternal side at this time. My DNA and some things that I gathered when I was young indicate that my father's family was German, centered somewhat near Bavaria, but that could not necessarily be directly from the ancestors' origins that I am looking for. Someone had told my father that an ancestral name could have originally have been Zimmerman, but that doesn't necessarily make it correct. Another account from 'Avery County Heritage, Volume 2'related by Elias' youngest son, Clare, that an unusual accent and manner of speech in the family was thought by linguists to be directly related to early Elizabethan English. My paternal grandmother was born a Stamey. She married my biological grandfather William Carpenter, who died and then she married Schyler Anderson Carpenter. I know the Stamey family history in what is now Avery County back to Ephraim Alexander Stamey, who was born near Morganton (Burke Co.) about 1805. He married Nancy Howard. One of his sons, Rev. Elias Stamey settled in what was then Mitchell County. That exact area in what is now called Stamey Branch or Pyatte in Avery County. Elias married several times, but his marriage to his second wife, Mahalia Dellinger Stamey produced Charles (Charlie) 1871-1938, who married Suzy McKinney. They are the parents of my grandmother, Bertie Stamey who married my biological grandfather, William (Will) Carpenter. Will and Bertie are the parents of my late father, William Arnold Carpenter who was born on August 18, 1925. My father married Anna Belle Riddle from the Beech Mountain area of Avery County that was once in Watauga County. I have hit a wall, so to speak, and would be grateful for any information about the origins of the branch of my father's Carpenter family and/or my grandmother's Stamey family. I have been able to obtain volumes II and III of Avery County Heritage, and The Heritage of Watauga County, NC Volume II, but I have been looking for the first volume of either for a long time without success. I got the other Avery County books by going to the history museum in Newland, but they didn't have the first volume. Please let me know if anyone knows how I might find the first volume of either County. I would be very grateful for that and for any information via this forum. Thank you.
I am an Irish descendant of
Permalink Submitted by Paul Wayne Moore (not verified) on Sun, 03/15/2020 - 02:03
I am an Irish descendant of Robert Moore, Robert Mayfield Moores that settled somewhere in Caswell County, North Carolina. Late 1700's they packed up and moved to what was then Robertson County, Tennessee. They were early tobacco farmers as well as educators in the "New Land" of that day. Do you know of or have records of what I understand is an extinct county from that area of the state? Family records document at least three 50 acre properties being sold after deaths of family members. This info is in a family Bible of kinfolks in Texas. By my records, all members of the immediate family had passed or moved to the Nashville area by the end or early beginning of the 1800's because of the failures of the soils to grow the dark fire tobacco. Your help would very much be appreciated. Sincerely, Paul Wayne Moore.
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One of the great advantages of being in Hungary long-term, be it to live or because you are filming in Hungary, is that you get to become acquainted with local traditions and culture. And around the winter holidays this is particularly gratifying, because that means holiday food. Lots and lots of holiday food. This is especially fortuitous in Hungary, which in addition to having the most dynamic cuisine in Central Europe, is also known for its scrumptious holiday treats. In Hungary, holiday food is social currency. You give it to friends, colleagues, and of course family.
But -- you may ask -- what makes Hungarian holiday food so special? Well we are here with a rundown on Christmas food from Hungary, and you can decide for yourself if it isn't something really worth celebrating. So let's have a look at a few of the delicious foods people who live in Hungary will be gorging on over this holiday season.
First up is beigli (sometimes spelled bejgli). There can never be enough beigli around the holidays. This loglike confection is actually a pastry that is rolled around a sweet filling, which in hungary is traditionally poppy seed or apple walnut, or just walnut, though in a quest to keep it current, various jams, nutella, and other off-the-cuff fillings can be found. Its distinctive egg glazing makes it attractive under the holiday lights. Though small in size, beigli is in fact quite heavy. The pastry is wonderful when eaten with both dry and sweet white wines, of which there are no shortage in Hungary.
Mézeskalács, or in loose translation, Hungarian gingerbread, is also omnipresent, particularly in households and schools. Basically it's a softer, airier, less aggressively spiced gingerbread that is shaped into cookie form and decorated with frosting. Of all the Hungarian holiday foods, this one benefits most from being home-made, as the store bought variety tends to dry out and not be as lovingly decorated.
Finally, no Christmas is complete without szaloncukor - or 'parlor candies' - which are colorfully wrapped candies that double as Christmas tree ornaments. Fondant is the primary component of the sweet, which is then dipped in chocolate before being wrapped, usually in bright foil, to reflect the light of fire or Christmas lights. According to Wikipedia, almost a kilo and a half of szaloncukor are eaten per family each year around the holidays.
Luckily, a plucky American vlogger went and put together a video of her favorite Hungarian Christmas foods, which you can watch below. Like with most such videos, her enthusiasm makes up for her ppronunciation. It's good to be generous around the holidays when it comes to this and so much more.
Eat Your Lentils, and Have a Happy, Lucky New Year!


text:
Q: Url to open Android application I'm currently developing an application with Xamarin Forms which I want to be able to open from a simple url.
On iOS part this works fine, but on Android nothing happens when I try to reach my url from chrome.
Here is my MainActivity:
[Activity(Label = "Lockers", Icon = "@drawable/logo", Theme = "@style/MyTheme", MainLauncher = true, ConfigurationChanges = ConfigChanges.ScreenSize | ConfigChanges.Orientation)]
[IntentFilter(new[] { Android.Content.Intent.ActionView },
              DataScheme = "http",
              DataHost = "random.com",
              DataPathPrefix = "/test",
              Categories = new[] { Android.Content.Intent.CategoryDefault, Android.Content.Intent.CategoryBrowsable })]
public class MainActivity : global::Xamarin.Forms.Platform.Android.FormsAppCompatActivity
{
    protected override void OnCreate(Bundle bundle)
    {
        TabLayoutResource = Resource.Layout.Tabbar;
        ToolbarResource = Resource.Layout.Toolbar;

        base.OnCreate(bundle);

        UserDialogs.Init(this);

        global::Xamarin.Forms.Forms.Init(this, bundle);

        App _app = new App();
        LoadApplication(_app);

        if (Intent.HasExtra("al_applink_data"))
        {

            var appLinkData = Intent.GetStringExtra("al_applink_data");

            var alUrl = new Rivets.AppLinkUrl(Intent.Data.ToString(), appLinkData);

            // InputQueryParameters will contain our product id
            if (alUrl != null && alUrl.InputQueryParameters.ContainsKey("id"))
            {
                var id = alUrl.InputQueryParameters["id"];
                NavigationPage nav = _app.MainPage as NavigationPage;
                InputPage page = nav.Navigation.NavigationStack[0] as InputPage;
                page.GenerateContentFromUri(id);
            }
        }
    }
}

When I try to reach http://random.com/test url from chrome app this should normally propose to open the link either from the app or continue with chrome, but nothing is happening, it just goes to the website as if the intent-filter was ignored.
Do you guys know what I might be missing ?

A: Nevermind, everything is fine, I was just trying to type my url directly in the navigation bar of chrome.
To open the application from an url, it should be done by clicking on a link  to make it work

redpajama_set_name: RedPajamaStackExchange


A bison calf was born April 25 on the grounds of the Fermi National Accelerator Laboratory near Batavia.
BATAVIA – Fermi National Accelerator Laboratory's newest addition to its bison herd was staying close to its mother Wednesday afternoon.
The bison calf was born Saturday morning, but Cleo Garcia, senior groundskeeper at Fermilab, hopes it won't be the last one born this spring.
"I'm hoping in the next two weeks for four or five more," said Garcia, who helps take care of the bison. The size of the herd currently is 25, he said.
Although Fermilab is known best for its high energy physics research, the laboratory also maintains a herd of bison. The bison are a popular attraction this time of year because of new calves being born.
Garcia has been working with the bison for five years.
"I like being around animals," he said.
Robert Wilson, Fermilab's first director, brought the first bison – a bull and four cows – to Fermilab in 1969. According to Fermilab officials, Wilson wanted to recognize and strengthen Fermilab's connection to the area's prairie heritage. Today's bison are descendants of those animals.
Bison are the heaviest land mammals in North America. Adult males stand as tall as 6 feet at the shoulders and weigh between 1,000 and 2,000 pounds, according to The Nature Conservancy's website, www.nature.org.
The animals have become a hit with Fermilab campus visitors, who can watch them roam on 80 acres of land. Buffalo is the popular name often used to describe North American bison, but buffalo are distinctly different animals from bison. Although both bison and buffalo belong to the same family, Bovidae, true "buffalo," are native only to Africa and Asia, according to the website www.allaboutwildlife.com.
Visitors are encouraged to see the bison. They can enter the Fermilab site through its Pine Street entrance in Batavia or the Batavia Road entrance in Warrenville. Admission is free, but attendees will need a valid photo ID to enter the site. Summer hours are from 8 a.m. to 8 p.m. seven days a week.


text:
Q: ¿Cómo corrigo "Unable to load the sleep module (no animations available)" de mi trabajo en JavaScript? ¡Hola! Antes que nada, ¡buenas días/tardes/noche! estoy haciendo un bot para Whatsapp. Estoy utilizando la node.js y la librería Venom-bot.
Todo iba bien pero tengo la necesidad de utilizar enlaces y todo eso. Y para eso necesito utilizar lo que es await y async. Les muestro el código.

    const venom = require('venom-bot');

async function wapbot()
{
  venom.create({
    session: 'Digitall', //name of session
    multidevice: false
   }).then((client) =>start(client))
   .catch((erro) => {
      console.log(erro);
    });

async function start(client)
{
   client.onMessage(async(message) =>
  {
      if (message.body==='¡Hola!'){
      client.sendText(message.from, 'Bienvenido al chat de Digitall ¿en qué puedo ayudarte?');
    } else if(message.body==='Big Data'){
      await client.sendLinkPreview(message.from,'https://www.youtube.com/watch?v=V1bFr2SWP1I','Kamakawiwo ole');

    }
  })
}
}

Sin esta parte:
 await client.sendLinkPreview(message.from,'https://www.youtube.com/watch?v=1oMThuGDZwg','Big data');

Funciona muy bien pero al correrlo me sale este error:
"Unable to load the sleep module (no animations available)"
Por lo que veo que tiene que ver con «sleep» pero yo no voy a utilizar ese paquete. Es más, ni siquiera me lo instala. Me sale error. ¿Cómo puedo corregir esto? Soy todavía algo nueva con JavaScript y node.js. Apenas llevo dos semanas estudiando esto.


Nothing to joke about in this subject matter. John Battaglia will die tonight from a lethal injection cocktail administered by the state of Texas. There has been a long history of domestic violence between John Battaglia and his wife Mary Jean Pearle. It was May 2, 2001. The girls no doubt were excited about … More Death Penalty or Not??
2 Comments Death Penalty or Not??


text:
import OpenGL
from OpenGL.GL import *
from OpenGL.GLU import *

import sfml as sf

# create the main window
window = sf.RenderWindow(sf.VideoMode(800, 600), "pySFML - OpenGL"
        , sf.Style.DEFAULT, sf.ContextSettings(32))
window.vertical_synchronization = True

# load a font for drawing some text
font = sf.Font.from_file("resources/sansation.ttf")

# create a sprite for the background
background_texture = sf.Texture.from_file("resources/background.jpg")
background = sf.Sprite(background_texture)

# load an OpenGL texture.
# we could directly use a sf.Texture as an OpenGL texture (with its bind() member function),
# but here we want more control on it (generate mipmaps, ...) so we create a new one from an image
texture = 0
image = sf.Image.from_file("resources/texture.jpg")
glGenTextures(1, texture)
glBindTexture(GL_TEXTURE_2D, texture)
gluBuild2DMipmaps(GL_TEXTURE_2D, GL_RGBA, image.size.x, image.size.y, GL_RGBA, GL_UNSIGNED_BYTE, image.pixels.data)
glTexParameteri(GL_TEXTURE_2D, GL_TEXTURE_MAG_FILTER, GL_LINEAR)
glTexParameteri(GL_TEXTURE_2D, GL_TEXTURE_MIN_FILTER, GL_LINEAR_MIPMAP_LINEAR)

# enable Z-buffer read and write
glEnable(GL_DEPTH_TEST)
glDepthMask(GL_TRUE)
glClearDepth(1)

# setup a perspective projection
glMatrixMode(GL_PROJECTION)
glLoadIdentity()
gluPerspective(90, 1, 1, 500)

# bind our texture
glEnable(GL_TEXTURE_2D)
glBindTexture(GL_TEXTURE_2D, texture)
glColor4f(1, 1, 1, 1)

# create a clock for measuring the time elapsed
clock = sf.Clock()

class Box:
    def __init__(self, value, x, y:
        self.value = value

        # Drawing related metrics
        self.x = x
        self.y = y
        self.sizex = 10
        self.sizey = 10
        self.sizez = 0

    # def translate(self, dx, dy):
    #     self.x += dx
    #     self.y += dy

    # Draw this box at a given location
    def draw(self, x, y):
        # apply some transformations
        glMatrixMode(GL_MODELVIEW)
        glLoadIdentity()
        glTranslatef(i*window.size.x/boardsize, j*window.size.y/boardsize, -100)

        glBegin(GL_QUADS)

        glTexCoord2f(0, 0)
        glVertex3f(-self.sizex, -self.sizey, -self.sizez)
        glTexCoord2f(0, 1)
        glVertex3f(-self.sizex,  self.sizey, -self.sizez)
        glTexCoord2f(1, 1)
        glVertex3f( self.sizex,  self.sizey, -self.sizez)
        glTexCoord2f(1, 0)
        glVertex3f( self.sizex, -self.sizey, -self.sizez)

        glTexCoord2f(0, 0)
        glVertex3f(-self.sizex, -self.sizey, self.sizez)
        glTexCoord2f(0, 1)
        glVertex3f(-self.sizex,  self.sizey, self.sizez)
        glTexCoord2f(1, 1)
        glVertex3f( self.sizex,  self.sizey, self.sizez)
        glTexCoord2f(1, 0)
        glVertex3f( self.sizex, -self.sizey, self.sizez)

        glTexCoord2f(0, 0)
        glVertex3f(-self.sizex, -self.sizey, -self.sizez)
        glTexCoord2f(0, 1)
        glVertex3f(-self.sizex,  self.sizey, -self.sizez)
        glTexCoord2f(1, 1)
        glVertex3f(-self.sizex,  self.sizey,  self.sizez)
        glTexCoord2f(1, 0)
        glVertex3f(-self.sizex, -self.sizey,  self.sizez)

        glTexCoord2f(0, 0)
        glVertex3f(self.sizex, -self.sizey, -self.sizez)
        glTexCoord2f(0, 1)
        glVertex3f(self.sizex,  self.sizey, -self.sizez)
        glTexCoord2f(1, 1)
        glVertex3f(self.sizex,  self.sizey,  self.sizez)
        glTexCoord2f(1, 0)
        glVertex3f(self.sizex, -self.sizey,  self.sizez)

        glTexCoord2f(0, 1)
        glVertex3f(-self.sizex, -self.sizey,  self.sizez)
        glTexCoord2f(0, 0)
        glVertex3f(-self.sizex, -self.sizey, -self.sizez)
        glTexCoord2f(1, 0)
        glVertex3f( self.sizex, -self.sizey, -self.sizez)
        glTexCoord2f(1, 1)
        glVertex3f( self.sizex, -self.sizey,  self.sizez)

        glTexCoord2f(0, 1)
        glVertex3f(-self.sizex, self.sizey,  self.sizez)
        glTexCoord2f(0, 0)
        glVertex3f(-self.sizex, self.sizey, -self.sizez)
        glTexCoord2f(1, 0)
        glVertex3f( self.sizex, self.sizey, -self.sizez)
        glTexCoord2f(1, 1)
        glVertex3f( self.sizex, self.sizey,  self.sizez)

        glEnd()

def boxSpawn():
    # Randomly choose a location for a box to spawn

# start game loop
while window.is_open:

        # process events
        for event in window.events:

                # close window : exit
                if event == sf.CloseEvent:
                        window.close()

                # escape key : exit
                if event == sf.KeyEvent and event.code == sf.Keyboard.ESCAPE:
                        window.close()

                # adjust the viewport when the window is resized
                if event == sf.ResizeEvent:
                        glViewport(0, 0, event.width, event.height)

        # draw the background
        window.push_GL_states()
        window.draw(background)
        window.pop_GL_states()

        # activate the window before using OpenGL commands.
        # this is useless here because we have only one window which is
        # always the active one, but don't forget it if you use multiple windows
        window.active = True

        # clear the depth buffer
        glClear(GL_DEPTH_BUFFER_BIT);

        # we get the position of the mouse cursor, so that we can move the box accordingly
        # x = sf.Mouse.get_position(window).x * 200. / window.size.x - 100.
        # y = -sf.Mouse.get_position(window).y * 200. / window.size.y + 100.

        # for box in boxes:
        #    box.draw()
        for box, i, j in boxIterate():
            # Draw the box that's in grid space i,j

        # draw some text on top of our OpenGL object
        window.push_GL_states()
        text = sf.Text("pySFML / OpenGL demo", font)
        text.color = sf.Color(255, 255, 255, 170)
        text.position = (230, 450)
        window.draw(text)
        window.pop_GL_states()

        # finally, display the rendered frame on screen
        window.display()

# don't forget to destroy our texture
glDeleteTextures(1, texture)