— Jeff Bezos challenged other retailers to pay a $15 hourly minimum.
— The EEOC will be in court April 16 to seek delay for a judge's ruling that requires the agency to collect pay data broken down by race, ethnicity, and gender.
— Trump tried to dump immigrant detainees in Nancy Pelosi's district.
GOOD MORNING! It's Friday, April 12, and this is Morning Shift, your daily tipsheet on labor and immigration news. Send tips, exclusives and suggestions to rrainey@politico.com, thesson@politico.com, ikullgren@politico.com, and tnoah@politico.com. Follow us on Twitter at @RebeccaARainey, @tedhesson, @IanKullgren, and @TimothyNoah1.
AMAZON'S FIGHT FOR $15: Amazon CEO Jeff Bezos urged competitors to match the online superstore's $15 hourly minimum wage plus benefits in a letter to shareholders Thursday, even as those same companies struggle to catch up with Amazon's sales.
"I challenge our top retail competitors (you know who you are!) to match our employee benefits and our $15 minimum wage," Bezos said in the letter, according to the Washington Post (which Bezos owns). "Do it! Better yet, go to $16 and throw the gauntlet back at us. It's a kind of competition that will benefit everyone." Amazon boosted its wage minimum in November (although it also slashed warehouse workers' bonuses and stock option benefits).
HEARING DATE ON EEO-1 DEADLINE: Attorneys representing the Office of Management and Budget and the Equal Employment Opportunity Commission will be in court April 16 for a hearing regarding the deadline for when businesses with 100 or more employees will be required to submit pay data broken down by race, ethnicity, and gender. An Obama-era requirement that the EEOC collect this demographic information was stayed by the Trump administration, but then reinstated by a DC federal court in March. The government said earlier this month that it could manage a September 30 deadline, but Judge Tanya Chutkan hasn't decided whether that will do. Chutkan wasn't pleased to learn that the agency didn't move quickly to alert businesses to the reinstated reporting requirements.
The National Women's Law Center, which challenged the Trump administration's stay of the new pay reporting requirements, has urged Chutkan to reject the EEOC's request. Meanwhile, the American Society of Employers and the DirectEmployers Association have urged Chutkan to put off the deadline to next year, and the Chamber of Commerce has asked Chutkan give employers 18 months to comply. Read the order here.
TRUMP TRIED TO DUMP DETAINEES IN SANCTUARY CITIES: At least twice in the past six months, the Trump White House tried to persuade U.S. Immigration and Customs Enforcement to release detainees in sanctuary cities, Rachael Bade and Nick Miroff report for the Washington Post. One proposed target was Nancy Pelosi's district in San Francisco. "Senior Trump adviser Stephen Miller discussed the proposal with ICE, according to two DHS officials. Matthew Albence, who is ICE's acting deputy director, immediately questioned the proposal in November and later circulated the idea within his agency when it resurfaced in February, seeking the legal review that ultimately doomed the proposal."
"The extent of this administration's cynicism and cruelty cannot be overstated," Pelosi spokeswoman Ashley Etienne told the Post. "Using human beings — including little children — as pawns in their warped game to perpetuate fear and demonize immigrants is despicable." More here.
MCCONNELL SAYS LETS TALK IMMIGRATION: Senate Majority Leader Mitch McConnell said Thursday "it's way past time" to have an "adult bipartisan discussion" with Democrats "about our immigration laws," POLITICO's Marianne LeVine reports.
"I'm willing to enter into a negotiation to see what we can do to fix the problems," the Kentucky Republican said. The Senate last year crafted a bipartisan immigration bill that would have given as many as 1.8 million young undocumented immigrants a path to citizenship while spending $25 billion on border security, but Trump wouldn't support it and the bill died. McConnell stipulated that any alterations to existing law would have to address border security and asylum. More here.
UNEMPLOYMENT CLAIMS DROP TO HISTORIC LOWS: Only 196,000 people filed initial unemployment benefit claims during the week ending April 6, the lowest level since 1969, the Labor Department reported Thursday. But the Associated Press' Christopher Rugaber points out that the historic numbers aren't due only to a tight labor market. "Many states have imposed stricter rules on their unemployment insurance programs — from making it harder to qualify to reducing the duration of benefits to cutting payouts," he writes.
The Labor Department published a proposal last year that would allow states to require a broad swath of applicants for unemployment insurance to pass drug tests. Under the 2012 Middle Class Tax Relief and Job Creation Act, Congress gave states the authority to impose drug tests, but that bill passed at a time when unemployment was high. Democrats agreed to the drug-test provision to secure Republican votes to extend emergency spending for unemployment insurance. The Obama administration then implemented a regulation that limited sharply the population that could be subjected to the drug tests. Then the Trump administration broadened that population, even as unemployment dropped below 4 percent. More from POLITICO's Rebecca Rainey here.
TRUMP SAYS HE'S STILL FRIENDS WITH LABOR: At an event Wednesday in Crosby, Texas, Trump promised the International Union of Operating Engineers that labor "will always have a friend at the White House," the Washington Examiner's Sean Higgins reported. "Under this administration we have ended the war on energy .... and we've put thousands and thousands of patriotic union members like you to work building our energy future," the president said.
But in a March event in Lima Ohio, Trump sang a very different tune. "I sort of don't want to meet" with union leaders, Trump told that crowd. "Because the heads of the union are not honest people. They're not honest." Trump blamed the closing of GM's Lordstown plant on high union dues ("You're paying too much dues"), which didn't make a lot of sense because union dues comes out of workers' pockets, not management's. More from Higgins here.
DUKE DOCTORAL STUDENTS WIN $15 AN HOUR: Doctoral candidates at Duke University will be paid the equivalent of $15 an hour starting in 2022, the university said in an email Thursday. "While the majority of our Ph.D. students already receive year-round funding, we believe that providing 12-month stipends, at the full rate, will enhance the experience for all graduate students." Each grad student will receive $31,160 per academic year (the equivalent of $15 per hour for a full-time employee).
Emory University announced a similar pay raise last year. Nationally, stipends for funded graduate students range from about $13,000 a year to $34,000 a year, according to Inside HigherEd.
"He would say, 'I'm not losing the contract over this – get this case closed,'" according to the former employee. Besh told Reveal that Tesla doesn't pressure him to dismiss injuries and that his determinations are "only based on what the patient needs." More here.
STOP AND SHOP STRIKE: "As many as 31,000 workers at Stop & Shop grocery stores in New England went on strike Thursday after contract negotiations stalled between management and the United Food & Commercial Workers," POLITICO's Ian Kullgren reports. "The union says it is fighting proposed benefit cuts at the same time that Ahold Delhaize, the corporation that owns Stop & Shop, voted to give shareholders an 11 percent dividends increase." More here.
California: Some 3,000 members of the Sacramento City Classroom Teachers Association, went on strike Thursday over what they said was the Sacramento City Unified School District's failure to fulfill the terms of a contract it reached with teachers in 2017. "This strike is to ensure that SCUSD management keeps its promises to our students," said association president David Fisher. "The Sacramento City Teachers Association is the third major teachers union in California to strike this year, following those in Los Angeles and Oakland — all of whom have called for more school funding, smaller class sizes, and support services," POLITICO's Mackenzie Mays reports. More here.
Illinois: Loyola University Chicago graduate workers plan a sit-in Monday to protest the institution's failure to reach a "fair contract" with their union.


The Patented* Design of QMax ETS Maximizes the Performance of all types of electric tracing. Without QMax, much of the length of these systems is heating the airspace around the pipe and relying on ineffective convection heat transfer to heat the pipe and process. This causes localized hot and cold spots along the pipe. QMax ETS creates a conductive path between the electric tracing and the pipe and increases the heating surface area to as much as 2 inches per strip. The energy from the electric tracing is efficiently and effectively transferred into the pipe and process. QMax ETS also extends the life of electric tracin by reducing the temperature of the cable during heating cycles.


The 14 winners of the Knight News Challenge on Libraries announced today by the John S. and James L. Knight Foundation aim to help shape the future of libraries, meeting 21st century information needs as centers for digital learning, data sharing, community connection and discovery.
The winning ideas highlight libraries as essential to addressing information challenges and creating new opportunities for communities to engage with ideas and each other. They position libraries as digital age problem-solvers tackling issues from information literacy for children, to using technology tools to make library collections more accessible and open, to giving people the resources they need to tell deeper stories about their lives and communities. Five of the projects will receive investments of between $150,000 and $393,249 each, while nine will receive $35,000 each to test early-stage ideas.
"The winners show the potential of libraries to innovate and reinvent themselves in response to ever-evolving information needs. We hope they will inspire more innovation in the space and help highlight the many ways libraries can connect communities in the digital age," said John Bracken, Knight Foundation vice president of media innovation.
Launched in February, the Knight News Challenge asked for ideas that serve 21st century information needs, recognizing libraries as vital institutions that can play an essential role in building more informed and engaged communities.
Improve Access to Knowledge and Empower Citizens: Amplify Libraries and Communities through Wikipedia | Online Computer Library Center (OCLC) | $250,000 | Project leads: Sharon Streams and Merrilee Proffitt | Twitter: @oclc, @thinktower, @merrileeiam | Seattle Making library resources more accessible to Wikipedia editors and engaging librarians as contributors to Wikipedia through a national training program that will include community outreach to increase local information literacy.
Full project descriptions for these five projects are found at the bottom.
Digging DEEP: A Digital Extension Education Portal for Community Growth | Pennsylvania State University | $35,000 | Project leads: Rebecca Kate Miller, Lauren Reiter, and Maria Kenney Burchill | Twitter: @psulibs, @rebeccakmiller, @mkburchill | State College, Pennsylvania.
The Knight News Challenge on Libraries launched in February 2016. In January Knight announced 17 winners of the Knight News Challenge on Data which sought ideas that make data work for individuals and communities.


Front chassis section between main chassis rails inline with the outriggers. Includes all correct holes for heater tube and cable tubing. Laser cut and CNC folded in 1.2mm steel. Fits all years of splitscreen busses from 1955 to 1967.
Rear chassis section between main chassis rails inline with the outriggers. Includes all correct holes for heater tube and cable tubing. Laser cut and CNC folded in 1.2mm steel. Fits all year splitscreen busses from 1955 to 1967.
830mm long section of main chassis rail for all splitscreen busses from 1955 to 1967. Laser cut and CNC folded for consistently accurate panels.
The Top hat section sits between the inner sills and in line with jacking points, outriggers and centre chassis sections, and provides support for the cargo floor. Includes all correct holes for cables and gear shift selector rod. 2 required per vehicle. CNC cut and folded from 1.2mm mild steel, fits all splitscreen busses from 1950 to 1967.
The rear top hat section sits between the inner sills and provides support for the cargo floor. Underside is fully enclosed. Includes all correct holes for cables and gear shift selector rod. CNC cut and folded from 1.2mm mild steel, suitable for years 1959 to 1967.
Rear left chassis rail repair section for all post Barndoor splitscreen buses. Laser cut and CNC folded for consistently accurate panels.
Rear right chassis rail repair section for all post Barndoor splitscreen buses. Laser cut and CNC folded for consistently accurate panels.
Front chassis cross member with master cylinder mount for left hand drive split screen vans from 1955 to 1967.
Front chassis cross member with master cylinder mount for right hand drive split screen vans from 1955 to 1967.
Left side front chassis repair section, behind the front beam. Laser cut and CNC folded in 2mm steel.
Right side front chassis repair section, behind the front beam. Laser cut and CNC folded in 2mm steel.
Front left chassis repair section, includes mounting points for the front bumper bracket. Laser cut and CNC folded from 2mm steel.
Front right chassis repair section, includes mounting points for the front bumper bracket. Laser cut and CNC folded from 2mm steel.
Front left chassis leg with steering box support fittings.
Laser cut and CNC folded from 1.5mm mild steel for a perfect fit. Includes captive nuts for the steering box, sleeve for the brake pedal shaft, and tab for the return spring.
Steering support for right hand drive splitscreen busses from 1955 to 1967. Laser cut and CNC folded from 1.5mm steel, includes the sleeve for the brake pedal and tab for the return spring. Also includes all mounting holes for the steering box itself.
Front left jacking point, fits to the end of the chassis outrigger and inside of the inner sill. Laser cut and formed in 2mm steel. Suitable for all years of splitscreen busses from 1950 to 1967.
Front right jacking point. Fits to the end of chassis outrigger and inside of inner sill. Laser cut and formed in 2mm steel. Suitable for all years of splitscreen busses from 1950 to 1967.
Middle left outrigger. Fits between the main chassis rail and the rear jacking point, below the top hat section. Laser cut and CNC folded from 1.2 mild steel. Suitable for all years from 1950 to 1967.
Guide tube for the accelerator cable. 2400mm long, 8mm outer diameter, 1mm wall thickness. 1 required per vehicle.
Guide tube for the clutch cable. 1845 mm long, 12mm outer diameter, 1mm wall thickness. 1 required per vehicle.
Guide tube for the handbrake cable. 1535mm long, 12mm outer diameter, 1mm wall thickness. Sold individually, 2 required per vehicle.
Guide tube for heater control cable. 2775 mm long, 8mm outer diameter, 1mm wall thickness. Sold individually, 2 required per vehicle.
Steel heater tube to pass through centre chassis sections. 1270mm Long, 70mm outer diameter and 1mm sidewall. See below for various fitting uses.
Stainless steel jubilee clip for the heat exchanger to body tube.
Guide tube for main gear linkage rod through chassis. 1475mm long, 30mm outer diameter, 1mm wall thickness.


text:
Q: Android LiveData: Transformation switchMap: Apply filter on the original list and show the filtered data public class FlightViewModel extends BaseViewModel {

    private FlightRepository flightRepository;
    private MediatorLiveData<Resource<FlightSearchMainOuterModel>> mSearchFlights = new MediatorLiveData<>();
    private MediatorLiveData<Resource<FlightSearchMainOuterModel>> mOriginalList = new MediatorLiveData<>();
    private MediatorLiveData<Resource<FlightSearchMainOuterModel>> mSortedSearchFlights = new MediatorLiveData<>();

    public FlightViewModel(@NonNull Application application) {
        super(application);
        flightRepository = FlightRepository.getInstance(application);
    }

    @Override
    public void updateResults() {

    }

    public void postFlightSearch() {

        mSearchFlights.addSource(flightRepository.postFlightSearchData(requestJson), mSearchFlights::setValue);
    }

    public LiveData<Resource<FlightSearchMainOuterModel>> getFlightResult() {
        return Transformations.map(mSearchFlights, input -> {

            if (input == null || input.data == null || input.status != Resource.Status.SUCCESS)
                return null;

            if (input.status == Resource.Status.SUCCESS && input.data != null) {
                if (input.data.getError().getErrorCode().equalsIgnoreCase("1")) {
                    FlightSearchModel flightSearchModel;
                    List<FlightSearchMainOuterResultOnwordReturnModel> onword = input.data.getResults().getOnword();
                    for (FlightSearchMainOuterResultOnwordReturnModel onwordLiveData : onword) {
                        flightSearchModel = onwordLiveData.getSegments().get(0);
                        flightSearchModel.getDurationFormat(onwordLiveData.getSegments());
                    }
                    return Resource.cloneResource(input, input.data);
                }
            } else if(input.status == Resource.Status.LOADING){
                return Resource.loading(null);
            } else {
                return Resource.error("Error! Please try again.", null);
            }

            return null;
        });

    }

    public void copyToOrignal(){
        mOriginalList = new MediatorLiveData<>();
        mOriginalList.setValue(mSearchFlights.getValue());
    }

    public LiveData<Resource<FlightSearchMainOuterModel>> getSortedFlightResult() {
        return mSortedSearchFlights;
    }

    public void nonStop(boolean isOneStop) {
        copyToOrignal();
        LiveData<Resource<FlightSearchMainOuterModel>> onwordLiveData = Transformations.map(mOriginalList, input -> {
            if (input == null || input.data == null || input.status != Resource.Status.SUCCESS)
                return null;

            List<FlightSearchMainOuterResultOnwordReturnModel> onwordNewList = new ArrayList<>();

            List<FlightSearchMainOuterResultOnwordReturnModel> onword = input.data.getResults().getOnword();
            if (onword.size() > 0) {

                if(isOneStop){
                    for(int i =0; i<onword.size(); i++){
                        if(onword.get(i).getSegments().size()>1 || !onword.get(i).getSegments().get(0).getNumberofStops().equalsIgnoreCase("0")){
                            onwordNewList.add(onword.get(i));

                        }
                    }
                }else {
                    for(int i =0; i<onword.size(); i++){
                        if(onword.get(i).getSegments().size()==1){
                            if(onword.get(i).getSegments().get(0).getNumberofStops().equalsIgnoreCase("0")){
                                onwordNewList.add(onword.get(i));
                            }
                        }
                    }
                }
                input.data.getResults().setOnword(onwordNewList);
            }
            return Resource.cloneResource(input, input.data);
        });

        mSortedSearchFlights.addSource(onwordLiveData, mSortedSearchFlights::setValue);

    }

}

In mSearchFlights I'm getting the whole list on which I have to apply filter. After applying one filter the mSearchFlights original list gets filtered even after copying the data in another liveData. So while applying filter second time it works on the filtered list rather than the original one list which is mSearchFlights. So please help me in applying the filter.
In the fragment I'm observing the two livedata which is same :
flightViewModel.getFlightResult().observe(this, flightSearchModelResource -> {
            if (flightSearchModelResource == null)
                return;
            if (flightSearchModelResource.status == Resource.Status.SUCCESS && flightSearchModelResource.data != null) {

                if (flightSearchModelResource.data.getError().getErrorCode().equalsIgnoreCase("1")) {
                    firstOrderAdapter.setData(flightSearchModelResource.data.getResults().getOnword());

                } else {
                    Utils.toastLong(getContext(), flightSearchModelResource.data.getError().getErrorMessage());

                }
            }
        });

flightViewModel.getSortedFlightResult().observe(this, flightSearchModelResource -> {
            if (flightSearchModelResource == null)
                return;
            if (flightSearchModelResource.status == Resource.Status.SUCCESS && flightSearchModelResource.data != null) {

                if (flightSearchModelResource.data.getError().getErrorCode().equalsIgnoreCase("1")) {
                    if(flightSearchModelResource.data.getResults().getOnword().size()>0){
                        firstOrderAdapter.setData(flightSearchModelResource.data.getResults().getOnword());

                    }
                } else {
                    Utils.toastLong(getContext(), flightSearchModelResource.data.getError().getErrorMessage());

                }
            }
        });

A: Please read this document and apply switchMap transformation to your source livedata. It will not alter your original source LiveData values.

redpajama_set_name: RedPajamaStackExchange


Blossom Basket Florist carries a wide selections of green plants and planters. We offer a wide variety sizes and styles to express your heartfelt condolences. Blossom Basket Florist offers sympathy plant delivery to homes in Urbana, Champaign, all of Champaign Country and nationwide.


text:
500,000 people forced to flee wildfires in Oregon as federal officials investigate potential mass arson
Sunday, September 13, 2020 by: JD Heyes
Tags: arson, arsonist network, California, coordinated attacks, disaster, domestic terror, evacuations, federal law enforcement antifa, fires, law enforcement, Oregon, reparations from whites, rule of law, sabotage, terrorism, Washington
(Natural News) Federal officials are looking into whether a series of wildfires burning out west are at least partially the result of arson as more than a half-million people in Oregon alone were forced to flee their homes.
On the anniversary of the deadliest terrorist attack in U.S. history, fire officials in Oregon were ordering people to evacuate the heavily-populated northwest portion of the state as fires burned out of control.
The Epoch Times reported:
People evacuated statewide because of fires had climbed to an estimated 500,000—more than 10 percent of the 4.2 million people in the state, the Oregon Office of Emergency Management reported late Thursday.
One fire approached Molalla, triggering a mandatory evacuation order for the community of about 9,000 people located 30 miles (48 kilometers) south of Portland. A police car rolled through the streets with a loudspeaker blaring "evacuate now."
The evacuees included inmates housed at a women's prison located less than a mile from Interstate 5 in the suburbs of Portland, where Antifa and Black Lives Matter thugs have been purposely trying to burn down police, government, and federal buildings all summer long.
The women's prison was not yet being directly threatened by flames, however, but officials with the Oregon Department of Corrections said the inmates were evacuated "out of an abundance of caution."
Two large fires were threatening to converge into one massive conflagration by Friday, officials said, nothing that firefighters in Clackamas County were ordered to temporarily disengage because of growing danger.
Meanwhile, officials attempted to calm nerves and reassure the public as well as residents who were ordered to leave their homes. Police said they would be beefing up patrols in the area to prevent looting — and with so much Antifa and BLM around, no doubt that's a necessary course of action to take.
Local fire officials said on Twitter: "To be clear, your firefighters are still working hard on the wildfires in Clackamas County. They are taking a 'tactical pause' to allow firefighters to reposition, get accountability & evaluate extreme fire conditions."
"We haven't abandoned you," the fire officials added.
As to the cause of at least some of the fires, federal law enforcement officials believe they are part of a "coordinated and planned" attack. We reported:
Many of these arson attacks are being strategically coordinated to destroy suburban areas in the Western United States. Law enforcement are putting everyone on high alert to help identify "opportunists" who seek to set communities ablaze. They have apprehended a number of arsonists and warn that there are still some on the run.
Specifically, law enforcement officials have arrested Christine Comello, 36, for allegedly starting several fires including one involving a pallet outside of a commercial business and another that was set to blow up an old oil drum.
Also, Elias Newton Pendergrass, 44, is suspected of igniting a fire that torched some 400 acres, which caused residents west of Eugene to bail out. As of this writing, he is still on the loose.
And Anita Esquivel, 37, is suspected of lighting fires along Highway 101 near Salinas, Ore.
"We are reacting to a coordinated series of attempts to start fires anywhere and everywhere in Oregon. Public and Private lands, incorporated and unincorporated areas," federal officials said, adding that all indications are the fires are part of a larger "coordinated effort" to commit arson in regions of the state that are not very well protected.
In all, wildfires are burning in Oregon, California, and Washington state, according to Law Enforcement Today, which added in a Breaking News alert that federal officials warned there could be more "attacks" soon.
"By all indications so far in the preliminary stages of these investigations there is a coordinated effort on the part of these individuals to start fires in areas that are the least protected and most vulnerable then slowing working their way into more populated areas and neighborhoods," officials said.
LawEnforcementToday.com
TheEpochTimes.com
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Next : Texas lawmaker implores state AG to launch child endangerment probe into Netflix over "Cuties" film sexualizing young girls
More news on arson
Trump-supporting farmer's equipment burned down in possible "politically-motivated arson"
Portland demonstrators set fire to billboard advertisement with pro-police message outside police union building
Obama praises left-wing terrorism, violence and arson as the "new normal in America"
Minneapolis laws barring business owners from protecting property resulted in widespread death and destruction
New report shows platforms run by Big Tech companies enable Antifa violence
So-called "protests" are clearly being orchestrated by well-funded, shadowy villains
Portland Mayor Ted Wheeler wants police officer deputization to end so that violent criminals can be given a pass by the corrupt local DA
Suspected arsonists arrested for setting rural fires in Washington state amid blazing wildfires
Breonna Taylor verdict sparks arson, property destruction and shooting of police officers in Louisville
"Regular attendee" of anti-police demonstrations in Seattle arrested for arson
https://www.naturalnews.com/2020-09-13-500000-people-forced-flee-wildfires-oregon-federal-officials-investigate-mass-arson.html
500,000 people forced to flee wildfires in Oregon as federal officials investigate potential mass arson

redpajama_set_name: RedPajamaCommonCrawl


text:
Home News U.S. Declines to Defend Trump Ally in Lawsuit Over Jan. 6 Riot
U.S. Declines to Defend Trump Ally in Lawsuit Over Jan. 6 Riot
WASHINGTON — The Justice Division declined on Tuesday to defend a congressional ally of former President Donald J. Trump in a lawsuit accusing them each of inciting supporters at a rally within the hours earlier than the Jan. 6 storming of the Capitol.
Regulation enforcement officers decided that Consultant Mo Brooks, Republican of Alabama, was appearing exterior the scope of his duties in an incendiary speech simply earlier than the assault, in response to a court docket submitting. Mr. Brooks had requested the division to certify that he was appearing as a authorities worker in the course of the rally; had it agreed to defend him, he would have been dismissed from the lawsuit and america substituted as a defendant.
"The file signifies that Brooks's look on the Jan. 6 rally was marketing campaign exercise, and it's no a part of the enterprise of america to select sides amongst candidates in federal elections," the Justice Division wrote.
"Members of Congress are topic to a bunch of restrictions that fastidiously distinguish between their official features, on the one hand, and marketing campaign features, on the opposite."
The Justice Division's choice reveals it's prone to additionally decline to offer authorized safety for Mr. Trump within the lawsuit. Authorized consultants have carefully watched the case as a result of the Biden Justice Division has continued to combat for granting immunity to Mr. Trump in a 2019 defamation lawsuit the place he denied allegations that he raped the author E. Jean Carroll and stated she accused him to get consideration.
Such a substitution gives broad protections for presidency officers and is usually reserved for presidency staff sued over actions that stem from their work. Within the Carroll case, the division cited different defamation lawsuits as precedent.
The Brooks choice additionally ran counter to the Justice Division's longstanding broad view of actions taken within the scope of a federal worker's employment, which has served to make it tougher to make use of the courts to carry authorities staff accountable for wrongdoing.
Attorneys for the Home additionally stated on Tuesday that they declined to defend Mr. Brooks within the lawsuit. On condition that it "doesn't problem any institutional motion of the Home," a Home lawyer wrote in a court filing, "it isn't applicable for it to take part within the litigation."
The Justice Division and Home filed their briefs on Tuesday, the deadline set by Decide Amit P. Mehta of the Federal District Courtroom for the District of Columbia. The lawsuit, filed in March by Consultant Eric Swalwell, Democrat of California, accuses Mr. Brooks of inciting a riot and conspiring to forestall an individual from holding workplace or performing official duties.
Mr. Swalwell accused Mr. Brooks, Mr. Trump, his son Donald Trump Jr. and his onetime private lawyer Rudolph W. Giuliani of enjoying a key function in inciting the Jan 6. assault throughout a rally close to the White Home within the hours earlier than the storming of the Capitol.
Citing excerpts from their speeches, Mr. Swalwell accused the boys of violating federal legislation by conspiring to forestall an elected official from holding workplace or from performing official duties, arguing that their speeches led Mr. Trump's supporters to imagine they had been appearing on orders to assault the Capitol.
Mr. Swalwell alleged that their speeches inspired Mr. Trump's supporters to unlawfully pressure members of Congress from their chambers and destroy components of the Capitol to maintain lawmakers from performing their duties.
Through the rally, Mr. Brooks instructed attendees that america was "in danger in contrast to it has been in many years, and maybe centuries." He stated that their ancestors "sacrificed their blood, their sweat, their tears, their fortunes and generally their lives" for the nation.
"Are you keen to do the identical?" he requested the gang. "Are you keen to do what it takes to combat for America?"
Mr. Swalwell stated defendants in his lawsuit had incited the mob and had continued to stoke false beliefs that the election was stolen.
"As a direct and foreseeable consequence of the defendants' false and incendiary allegations of fraud and theft, and in direct response to the defendants' categorical requires violence on the rally, a violent mob attacked the U.S. Capitol," Mr. Swalwell stated in his criticism. "Many members within the assault have since revealed that they had been appearing on what they believed to be former President Trump's orders in service of their nation."
In June, Mr. Brooks requested that the Justice Division defend him within the case. He cited the Westfall Act, which basically substitutes the Justice Division because the defendant when federal staff are sued for actions deemed throughout the scope of their employment, in response to a court document.
He described his speech on Jan. 6 as a part of his job, saying that his duties embody delivering speeches, making pronouncements on coverage and persuading lawmakers.
Mr. Trump has not sought to have the federal government substitute for him as a defendant within the lawsuit beneath the Westfall Act. However he has argued in court docket filings that the statements he made on Jan. 6 are lined by broad immunity, that he couldn't be sued for making them and that the lawsuit violated his free speech rights.
Ought to a decide deny Mr. Trump's claims, he might ask the Justice Division to intervene on his behalf. However its choice in Mr. Brooks's case lowered the probabilities that it'll comply.
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All participants will receive conference proceedings, summarizing the the contributions of participants.
The capacity of the conference is about 70 people, including 40 people from the supported target groups of this project (see below).
Participation in the conference's participants from academic and R&D staff and students in selected fields (nanotechnology, nanomodification) subsidized by the project NANOcontact.
Academic and other university staff, professionals, involved in education, research and development, working at Masaryk University, at University of West Bohemia and at the Technical University of Liberec.
Academic and other university staff, professionals, involved in education, research and development, working in academic and scientific research organizations in the Czech Republic except Prague.
Students of Physics and Managment and discipline involve in nanotechnologies and nanomaterials.
For more information on the number of supported people, and whether you qualify for obtaining support, please contact the contact person (Adam Pazourek).
Templates for creating abstracts to conference proceedings, will see ANNEX at bottom of page.Program - Invited lectures + schedule will be added later and will be avilable for download in the ANNEX.


text:
Q: Replace packages unsupported in Ubuntu with packages from Debian On an installation of Ubuntu 18.04, ubuntu-support-status --show-unsupported shows several unsupported packages. This is a known issue with Ubuntu that the LTS promise is only for packages in main, but many setups require packages from universe and multiverse. Now, the clean solution would be to use Debian instead. However, this is a VM in a computing center, and they do not offer Debian at the moment. So I'm stuck with Ubuntu.
What about replacing the unsupported packages with packages from the Debian main repository? Any experiences with that? What would be the necessary technical steps?
I'm also contemplating using do-release-upgrade in order to go to 19.04, hoping that it will support all the relevant packages.
Any other ideas how to deal with this situation?
Addendum: To some degree, a solution is to use an nspawn container. I give a basic howto on setting up such a container (does not address private user configuration, though) and some comments on how to get XFS filesystem quotas inside of the container.
Side note: The computing center in the meantime offered me to install Debian on the VM, so the problem no longer persists for me. But maybe this will be helpful to others. I also like to add that I find the current state of Ubuntu unacceptable; you cannot have unsupported packages on a production system. Some of the unsupported packages are pretty standard ones (such as nslcd and fail2ban), and are suggested by Ubuntu's official howtos.

A: *

*Have your system use as most official packages as possible, then build from sources everything else.

Or:

*

*Find a simple way to use Debian from Ubuntu, like a chroot jail, or by using Docker.


text:
Amblypsilopus discretifasciatus är en tvåvingeart som först beskrevs av Macquart 1850.  Amblypsilopus discretifasciatus ingår i släktet Amblypsilopus och familjen styltflugor. Inga underarter finns listade i Catalogue of Life.

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redpajama_set_name: RedPajamaWikipedia


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redpajama_set_name: RedPajamaGithub


Acid-base disorders occur commonly in clinical medicine. Although the degree of acidosis or alkalosis that results is rarely life threatening, the careful evaluation of the acid-base status of the patient often provides insight into the underlying medical problem. Moreover, the pathophysiology and differential diagnosis of these disorders can be approached quite logically with a minimum of laboratory and clinical data. An effective approach to clinical acid-base disorders is accomplished most easily with a stepwise pathophysiologic approach.
Human acid-base homeostasis normally involves the tight regulation of CO2 tension by respiratory excretion and plasma bicarbonate [HCO3–] concentration by renal HCO3– reabsorption and elimination of protons (H+) produced by metabolism. The pH of body fluids (which can be sampled easily) is determined by the CO2 tension (in arterial blood, PaCO2) and the [HCO3–]. Primary derangements of CO2 tension are referred to as respiratory disturbances, whereas primary derangements of [HCO3–] are called metabolic disturbances (1).
In this chapter, we first review acid-base chemistry and physiology and then present a pathophysiologic approach to the diagnosis and management of metabolic acidosis and alkalosis.
The chemistry of acids, bases, and buffers and the normal physiology of acid and bicarbonate excretion (2, 3) are described in detail in several excellent reviews and are summarized only briefly in this section.
important point, suppose 1 mL of 0.1 mol/L HCl is added to 9 mL of distilled water, the [H+] would increase from 10-7 to 10-2 mol/L. In other words, the pH would fall from 7.0 to 2.0. However, if we added 1 mL of 0.1 mol/L HCl to 9 mL of a 1 mol/L phosphate buffer (pK = 6.9) at pH 7.0, most of the dissociated H+ from HCl would combine with dibasic phosphate (HPO42-) and only slightly change the ratio of dibasic to monobasic (H2PO4–) phosphate. In fact, the pH would fall by only about 0.1 pH units. The addition of acid has been buffered by the phosphate dissolved in water. Another way to think about this is that the pH was stabilized by substances that bound the free H+ released by the HCl, in this case the phosphate. Such substances are called buffers (4).
which is attributed to Henderson in 1909.
In the above equations, [HCO3–] is expressed in mM (or mEq/L) and PaCO2 is expressed in torr (or mm Hg). Convenient expression allows us to view acid-base disorders as being attributable to the numerator of the ratio (metabolic processes), the denominator (respiratory processes), or both (mixed or complex acid-base disorders) (Fig. 3-1) (1).
in other words, to consider acids as electron acceptors rather than proton donors. In concrete terms, acid is generated when a substrate is metabolized to something more anionic (e.g., glucose is metabolized to lactate through the Embden-Meyerhof glycolytic pathway). Conversely, if a substrate is metabolized to something more cationic (e.g., lactate is metabolized to CO2 and H2O via the tricarboxylic acid [TCA] cycle), then acid is consumed (9). Because of the importance of the bicarbonate buffer system in the overall acid-base homeostasis, we generally consider the addition of a proton as equivalent to the decrease in total body HCO3– and loss of a proton as a gain in HCO3– (9).
Figure 3-1 Modified Henderson-Hasselbalch equation, portraying the interacting effects of the primary acid-base disturbance and the secondary mechanisms on the pH.
This approach to understanding acid-base metabolism has led to its practical application in treating the acidosis of chronic renal failure with peritoneal dialysis. Although the lactate-based dialysate (generally at about 35 mM) has a pH of only 6.0, virtually all of the lactate is ionized; bicarbonate is generated and the acidosis is corrected via metabolism largely through the TCA cycle to CO2 and H2O (10).
acid load must be excreted by the kidney to maintain acid-base homeostasis. The easiest way to understand the molecular processes involved in renal acid excretion is to separate renal acid-base handling itself into two functions: bicarbonate reabsorption and net acid excretion (NAE) (12).
In recent years, our understanding of the renal cellular transport proteins that effect H+ extrusion has expanded significantly. We now know that in addition to the sodium-proton exchanger (Na+/H+ exchanger) that exchanges one H+ for one sodium molecule, the sodium phosphate symporter that transports one sodium with one monobasic phosphate molecule, and the vacuolar H+ ATPase that directly pumps H+ into the tubular lumen (13, 14, 15, 16, 17, 18, 19), other transport proteins may be of considerable importance. These other transport proteins include the family of chloride-bicarbonate symporters and exchangers, the "colonic" H+/K+ ATPase, and the Na+/K+ ATPase (20, 21, 22, 23). These transport proteins are expressed to different degrees in the different nephron segments depending on the function of the cell type within that nephron section.
On a more global basis, there is a tight link between acid secretion and the reclamation of filtered bicarbonate as well as the production of new bicarbonate by the kidney. For example, the reclamation of HCO3– filtered from the blood occurs when HCO3– formed inside the renal tubular cells by either H+ secretion or ammonium (NH4+) synthesis is transported back into the blood via the basolateral Na+(HCO3–)3 symporter (23) or a Cl–/HCO3– antiporter (13, 24). Alternatively, bicarbonate can be secreted by certain cells of the collecting duct in exchange for chloride (25).
When plasma is filtered at the glomerulus, HCO3– enters the tubule lumen. Mechanistically, each HCO3– that is reclaimed requires the epithelial secretion of one H+. This is accomplished largely by an Na+/H+ exchanger on the luminal membrane, although an electrogenic H+ ATPase also may be involved. On an organ physiology level, HCO3– reabsorption can be considered in terms of the plasma threshold (PT) for bicarbonate, that is, the plasma HCO3– concentration at which HCO3– begins to appear in the urine. In terms of the maximal net activity of tubular HCO3– reabsorption (also called Tmax), assuming glomerular filtration rate (GFR) of 100 mL/min and a plasma [HCO3–] of 24 mM, the renal tubules must secrete about 2.4 mmol of H+ per minute to reclaim all of the filtered HCO3–. Therefore, HCO3– reclamation by the tubules involves a tremendous amount of H+ secretion. Bicarbonate reclamation is coupled tightly to sodium reabsorption and also is sensitive to a number of other influences. As the Tmax for HCO3– increases, the PT for HCO3– increases. Conversely, decreases in Tmax result in decreases in the PT. In particular, states of extracellular fluid (ECF) expansion and decreases in PCO2 decrease the apparent Tmax for HCO3–, whereas ECF contraction and increases in PCO2 increase the apparent Tmax for HCO3–. Parathyroid hormone (PTH) inhibits proximal tubule HCO3– reabsorption and lowers the apparent Tmax and PT for HCO3–. Most (but not all) of this HCO3– reabsorption (about 85-90%) occurs in the proximal tubule (3).
Carbonic anhydrase that is present both intracellularly and on the tubular surface of the brush border of the proximal tubule allows the secreted H+ that combines with tubular fluid HCO3– to form H2CO3. This H2CO3 rapidly dissociates to form H2O and CO2 that can readily permeate proximal tubule cell membranes. Intracellularly, carbonic anhydrase catalyzes the formation of H2CO3 again, which subsequently dissociates into HCO3– and H+. Finally, HCO3– leaves the cell via several bicarbonate transport proteins, including the Na+(HCO3–)3 symporter and the Cl–/HCO3– exchanger (26). The secreted H+ also titrates citrate, another form of alkali (27). This process is shown schematically in Figure 3-2.
NAE is the net amount of H+ eliminated from the body. If we postulate that an excreted HCO3– molecule negates the value of an excreted H+, then we can consider NAE by the kidney to be the amount of H+ (both buffered and free) excreted in the urine minus the amount of HCO3– excreted in the urine. As discussed, H+ secretion into the tubule lumen mandates 1:1 stoichiometric HCO3– transport across the basolateral segment into the extracellular space; therefore, NAE represents the amount of new HCO3– generated by the kidneys and added to the body stores.
Figure 3-2 Schematic depicting proximal tubule HCO3– reclamation process. Two vehicles for apical H+ secretion: Na+/H+ exchanger (lightly shaded ellipse) and H+ ATPase (filled ellipse on apical side) are shown. Some basolateral ion pumps and exchangers, including the Na+/K+ ATPase (filled circle), Na+(HCO3–)3 symporter (open circle), and HCO3–/Cl– exchanger (lightly shaded ellipse), are also shown. The role of carbonic anhydrase (CA) both in the tubular cell and on the brush border in HCO3– reabsorption also is depicted.
NAE is accomplished primarily through elimination of titratable acid (which is mostly phosphate) and nontitratable acid (in the form of NH4+) (12). These terms refer to clinical chemistry titration techniques by which known amounts of alkali were added to urine until a color change with a pH indicator (e.g., phenolphthalein) occurred. This color change occurred above the pK for the phosphate buffer system but below the pK for ammonia-ammonium (about 9). It must be stressed that the NAE is relatively insensitive to the urine pH. This concept is illustrated by the observation that addition of 1 mmol of HCl to 1 L of distilled water results in a pH of 3 (corresponding to an H+ concentration of 10-3 mol/L). Therefore, in the extreme case (i.e., no buffers in the urine at all), extremely acidic urine (i.e., a very low pH) could eliminate very few protons from the body. There are several clinical settings discussed later in which acidic urine is elaborated, but NAE is insufficient. NAE requires the adequate function of both the proximal tubule to synthesize NH4+ (which generates an HCO3– molecule) and the distal tubule and collecting tubules where H+ and NH4+ secretion occur (26).
Proton secretion by the distal nephron involves the production of an electrogenic gradient that favors H+ secretion produced by removal of sodium from the luminal fluid and direct pumping of H+ into the tubular lumen. The latter is accomplished by the activities of vacuolar H+ ATPase and the H+/K+ ATPase in type A intercalated cells. Notably, chloride exchange with bicarbonate on the basolateral side of these distal tubular cells allows for proton secretion to be translated into bicarbonate addition to the blood. Finally, the epithelial membrane must not allow back leak of H+ or loss of the electrogenic gradient. Under normal circumstances, humans can elaborate a urine pH as low as 4.4, representing a 1,000:1 gradient of H+ between tubular fluid and cells. However, the excretion of NH4+, which is discussed later, is of much greater importance in terms of NAE than is the level of urine pH achieved (28).
NAE is sensitive to a variety of factors, including the plasma K concentration (increases in plasma K decrease NH4+ excretion, whereas decreases enhance H+ secretion by the distal nephron) and the effects of aldosterone. By stimulating the renin-angiotensin-aldosterone system, ECF contraction enhances distal acid secretion (29).
sodium-hydrogen exchanger isoform 4 (NHE4) to the tubular interstitial space (32). This ultimately results in the increase in the medullary concentration of NH4, which is highest in the inner medulla. This NH4+ is then taken up by distal convoluted tubule and collecting duct cells, substituting for K+ using the basolateral Na+/K+ ATPase of the inner medullary collecting duct or as NH3 (after losing H+) utilizing ammonia-specific transporters Rhesus Glycoproteins (Rhbg and Rhcg) along with a component of diffusive absorption. Collecting duct ammonia secretion involves parallel secretion of NH3 utilizing Rhcg of the apical membrane or by its diffusive capacity along with cytosolic H+ generated by carbonic anhydrase II-mediated mechanism. H+ secretion across the apical membrane is primarily mediated by H+-ATPase and H+-K+ ATPase pumps. In the tubular lumen, H+ titrates luminal NH3 to form NH4+ and maintains low NH3 concentration in the urinary space, which is necessary for continued NH3 secretion (33). The net generation of any HCO3– from αKG metabolism is ultimately dependent on the excretion of NH4+. This is because if this NH4+ molecule is not excreted in the urine but rather is returned via the systemic circulation to the liver, it is used to form urea at the expense of generating an H+. Thus, the HCO3– molecule that was generated by the metabolism of the αKG will be neutralized, and no change in acid-base status will occur (30).
Difficulties in the routine clinical measurement of urinary NH4+ concentrations have delayed our appreciation of its importance in net acid-base balance during pathophysiologic conditions including chronic metabolic acidosis or acid loads (31). However, recent observations by Batlle et al. (34) suggest that the urinary [NH4+] may be inferred fairly accurately by calculations based on urinary electrolyte concentrations as is discussed subsequently.
Although the topic under discussion is "renal" acid-base metabolism, the liver may be significantly involved. Hepatic glutamine synthetase expression appears to be regulated by pH as well as protein ingestion (35, 36, 37). Perhaps more importantly, administration of amino acids via a parenteral rather than the enteral route often is accompanied by acid retention (38).
Metabolic acidosis is a systemic disorder characterized by a primary decrease in [HCO3–]. This may occur in three ways: (a) the addition of strong acid that is buffered by (i.e., consumes) HCO3–; (b) the loss of HCO3– from body fluids, usually through the GI tract or kidneys; and (c) the rapid addition to the ECF of nonbicarbonate solutions (dilutional acidosis). No organic anion is generated when HCO3– is lost or diluted. Reciprocal increases in the serum chloride concentration occur to preserve electroneutrality. Thus, these forms of metabolic acidosis generally are referred to as hyperchloremic or nonanion gap metabolic acidosis. When an organic acid consumes HCO3–, its organic anion is generated and may be retained in the ECF and serum. The serum chloride concentration does not increase with organic acidosis. An increase in the anion gap marks the existence and concentration of the organic anion (39).
The hallmark of metabolic acidosis is a fall in plasma [HCO3–]. We stress that the fall in [HCO3–] always is mitigated by the participation of other buffers in both the ECF and the intracellular fluid (ICF). Roughly one-half of an administered acid load is buffered by nonbicarbonate buffers (40). Bone is an important buffer pool in states of chronic metabolic acidosis. In fact, the leaching of calcium from bone is one of the major deleterious effects of chronic metabolic acidosis (41, 42, 43).
acid-base disturbance. Conversely, an exaggerated fall in PaCO2 producing a normal pH indicates the presence of respiratory alkalosis in the setting of a complex or mixed acid-base disturbance (44). The mechanism by which metabolic acidosis induces hypocapnia appears to be mediated in part by peripheral pH receptors in the carotid body, but mostly by central nervous system (CNS) pH receptors. This point is supported by the time course, specifically the temporal delay observed for respiratory compensation seen in experimental metabolic acidosis (45). The degree of chronic compensation varies from person to person; however, based on a large volume of clinical data, we can state with some confidence that the appropriate fall in PaCO2 (in torr) should be 1 to 1.5 × the fall in [HCO3–] (in mM) (44). Oral acid loading in normal subjects produced a rapid fall in PCO2 that reached a steady state after 30 minutes that was 0.85 times the fall in HCO3–, thus providing direct evidence for the rapid respiratory response to metabolic acidosis in humans (46).
The kidney provides the mechanism for the third line of defense to pH changes. However, this mechanism is rather slow compared to buffering (which begins immediately) and respiratory compensation (which begins within 15-30 minutes), since it takes up to 5 days to become maximal. NAE is increased in response to either metabolic acidosis (unless the kidney is the cause) or respiratory acidosis. This increase in NAE is largely NH4+ excretion because titratable acid excretion is limited by the amount of excreted phosphate, which changes very little. Metabolic acidosis increases the processing of glutamine into NH4+, which, in turn, leads to enhanced generation of HCO3–, by both transcriptional and translational regulations of key enzymes in this pathway (47). Chronic metabolic acidosis increases renal endothelin-1 activity that activates the NHE3 sodium-hydrogen ion antiporter on the proximal tubule brush border (48). Thus, both the generation of new HCO3– via the glutamine system and the enhancement of HCO3– reabsorption and titratable acid formation are stimulated. Of interest, the hypocapnia that occurs because of respiratory compensation actually limits renal correction in metabolic acidosis (49). Note that renal correction never corrects the pH to normal until the disorder causing HCO3– loss or acid generation is halted.
Mild degrees of acidemia generally are well tolerated, at least acutely, and even may afford some physiologic advantages, such as favorable oxygen delivery from hemoglobin. However, with marked acidemia, pH < 7.10, myocardial contractility is depressed and peripheral resistance falls (50, 51). These manifestations may be a result of the effect of acidosis to depress both vascular and myocardial responsiveness to catecholamines as well as innate myocardial contractility. Both myocardial β-adrenergic receptor density and physiologic responses to β agonists appear to be decreased by metabolic acidosis (52, 53).
Clearly, metabolic acidosis induces an intracellular acidosis in myocytes (48, 49). This intracellular acidosis in turn impairs contractile responses to normal or even elevated cytosolic calcium concentrations (54, 55). Alterations in troponin I-troponin C interactions mediated by low pH appear to shift the sensitivity of troponin C to calcium (56). Additionally, impairment of actin-myosin cross-bridge cycling caused by increases in the concentration of inorganic phosphate in the monovalent form may be involved in the decreased calcium sensitivity and contractile dysfunction seen with acidosis (57). The increase in monovalent inorganic phosphate results both from the acidic environment, which increases the ratio of monovalent to divalent inorganic phosphate, and from an impairment of myocardial energy production, which increases the total intracellular concentration of inorganic phosphate (58, 59). Metabolic acidosis and hypoxia appear to additively or synergistically impair myocardial function, a phenomenon consistent with the monovalent inorganic phosphate hypothesis (60). The vasodepressor effect of acidosis likely results from similar molecular mechanisms (61).
of increases in prostaglandin E2 (PGE2) production (64). This aspect is extremely important in determining treatment of renal tubular acidosis (RTA) or the acidosis of chronic renal failure.
Simple metabolic acidosis is characterized by a decrease in blood pH, [HCO3–], and PCO2 (through compensation). Note that a failure to lower the PCO2 by 1 to 1.5 × the fall in [HCO3–] indicates the coexistence of respiratory acidosis (44). The clinical implications of this are quite profound because this failure of compensation may signify impending severe respiratory failure. Serum electrolytes reveal a fall in [TCO2]. Acidosis tends to shift potassium out of cells in a rather complex manner (65), and renal potassium excretion tends to increase in many states of metabolic acidosis. Normal or increased serum potassium in the face of decreased total body potassium stores occurs commonly in cases of metabolic acidosis (Chapter 5) (65). Some states of metabolic acidosis are characterized by the retention of an organic anion generated in concert with HCO3– consumption (organic acidosis), whereas others are not (hyperchloremic). The screening of plasma for such organic anions is not practical on a routine, immediate basis; thus, a calculation performed on the serum electrolytes called the serum anion gap (SAG) is employed (66).
Normally, the SAG is about 9 (6-12 mEq/L). Although the SAG is used routinely in the differential diagnosis of metabolic acidosis, we stress that it is a relative rather than absolute indicator of the underlying pathophysiology. Note that the maintenance of stoichiometry (i.e., 1 mEq increase in anion gap for every 1 mmol decrease in HCO3–) depends on the clearance mechanisms for the anion as well as the myriad factors that influence HCO3– concentration. Therefore, some organic acidoses may manifest trivial or even no increase in the anion gap, whereas some hyperchloremic acidoses may have coincidental increases in the anion gap. This must be kept in mind when evaluating the differential diagnosis of metabolic acidosis. However, a major increase in the anion gap (e.g., SAG >26 mEq/L) always implies the existence of an organic acidosis (67).
If we look at the changes in the SAG and compare it to changes in HCO3– concentrations, additional insights can be made. This is often referred to as the "Delta gap" = Delta SAG – Delta Serum [HCO3–] or the "Delta-Delta." It takes advantage of the assumption that with a pure organic metabolic acidosis, the fall in HCO3– and the increase in SAG should be equal (with the disclaimers stated above). Ergo, if the Delta gap is very positive (i.e., >6), it suggests that there must be another process generating alkali. Conversely, if the Delta gap is very negative (i.e., <-6), it suggests that there is another source of acid that does not result in an increase in SAG, ergo a concomitant nonanion gap metabolic alkalosis.
then we see that this is determined largely by the amount of NH4+ in the urine that holds true in clinical studies of metabolic acidosis (34). In contrast to the SAG, which is useful in many settings of clinical acid-base diagnosis and therapy, the UAG has a very narrow clinical application in the differentiation of renal from nonrenal causes of nonanion gap metabolic acidosis (68).
The differential diagnosis of metabolic acidosis generally is approached clinically by using the SAG. Those acidosis states associated with retention of an organic anion are classified as increased anion gap or simply anion gap metabolic acidosis. Those acidosis states not associated with retention of an organic anion are classified as nonanion gap or hyperchloremic metabolic acidosis (66). These disorders are listed in Table 3-1.
Diarrhea is the most common cause of hyperchloremic metabolic acidosis and always should be considered early in the differential diagnosis. The concentration of HCO3– in diarrheal fluid is generally greater than that of plasma. In the extreme case of cholera, patients may lose up to 20 L/day of fluid containing 30 to 50 mEq/L of HCO3– (69). However, hypovolemic shock likely will cause lactic acidosis and increase the anion gap in that situation. Ileostomy fluid is also rich in HCO3–, especially early after construction (70).
The diagnosis of diarrheal loss of HCO3–, however, may be difficult in the very young or very old (71). In the former case, the distinction between diarrhea and an underlying RTA is extremely important. The UAG may be very helpful in this setting. Patients with diarrhea as a cause of metabolic acidosis typically have a very negative UAG (i.e., urinary chloride exceeds the sum of urinary NA+ + K+ by >10 mEq/L) reflecting the presence of ample urinary NH4+ concentrations, whereas patients with all forms of distal RTA have positive UAGs reflecting the inadequate urinary NH4+ concentrations present (34).
The succus entericus and pancreatic and biliary secretions are rich in HCO3– and poor in Cl–. The succus entericus has a daily volume of 600 to 700 mL but may be increased in disease states. Biliary secretions amount to >1 L/day of fluid, with [HCO3–] approaching 60 mmol/L. Pancreatic secretion may exceed 2 L/day, with [HCO3–] approaching 120 mmol/L. Therefore, it is not surprising that GI drainage or fistulas could cause significant metabolic acidosis (72).
The technique of simultaneous kidney/pancreas transplant (SPK) has been used for the treatment of type I diabetic patients with end-stage renal disease (73). When urinary drainage of the HCO3–-rich exocrine secretions of the pancreatic allograft is employed rather than enteric drainage, this addition of pancreatic exocrine fluid causes urinary loss because the bladder cannot absorb the pancreatic secretion. Thus, SPK with urinary drainage is often associated with significant normal anion gap metabolic acidosis (74, 75). Many of these patients require sodium bicarbonate supplementation (as high as 100-150 mEq/day) on a chronic basis. The incidence of metabolic acidosis can be significantly lowered with enteric drainage compared to urinary drainage because the intestine can absorb the HCO3– (76).
Patients may require urinary diversion from normal egress through the bladder for a variety of reasons. Approaches to this include the creation of an ileal loop conduit or, less commonly, drainage of the ureters into the sigmoid colon (ureterosigmoidostomy) (77). Although metabolic acidosis can develop with both procedures, it is more severe with ureterosigmoidostomy. The pathophysiology for both situations is the bowel mucosal secretion of HCO3– in exchange for Cl– during water reabsorption, which may lead to significant HCO3– losses in the GI tract effluent (72). Newer reconstructive procedures including ileal neobladders, which minimize the time of contact between urine and bowel mucosa, have been successful in limiting HCO3– loss (78).
Cholestyramine is a nonabsorbable anion exchange resin used to bind bile acids in the gut for a variety of purposes, including the treatment of obstructive liver disease as well as hypercholesterolemia and the management of acute diarrhea in children (79). However, this resin has some affinity for HCO3– and may exchange Cl– for HCO3– across the bowel mucosa. In conditions of renal insufficiency where new HCO3– generation is impaired, in volume depletion or patients taking spironolactone, hyperchloremic metabolic acidosis has been reported (80).
The divalent cations, calcium or magnesium, are absorbed incompletely in the GI tract. If large amounts of these cations are ingested in soluble form (e.g., as the Cl2 salts), then the unabsorbed Ca2+ or Mg2+ reacts with HCO3–, which has been exchanged across the mucosa for Cl–, to form an insoluble salt. Thus, plasma HCO3– falls to a moderate degree (81).
while referring to this nomenclature. RTAs can be divided into those characterized by disturbed distal nephron function (i.e., impaired NAE) and those caused by impaired proximal HCO3– reabsorption (82). Distal RTAs are divided into those associated with hypokalemia (83) and those associated with hyperkalemia, which may be further subdivided into RTA caused by hypoaldosteronism and RTA characterized by a general distal tubular defect (84).
Proximal RTA, also called type II RTA, is an uncommon but very interesting disorder (85, 86). Basically, the acid-base disturbance is caused by impairment in proximal tubular reabsorption of HCO3–, the nephron site where 85% of HCO3– usually is reabsorbed. The delivery of HCO3–-rich fluid to distal nephron sites leads to substantial bicarbonaturia, when plasma levels of HCO3– are normal, as well as urinary losses of potassium and sodium. Thus, patients present with hypokalemia and hyperchloremic metabolic acidosis. When the plasma concentration of HCO3– is maintained at normal by administration of HCO3–, fractional HCO3– excretion (i.e., the fraction of filtered HCO3– that is excreted in the urine) exceeds 15%.
In physiologic terms, the apparent Tmax and PT for HCO3– are significantly reduced in patients with proximal RTA. However, once a level of plasma HCO3– is achieved that is below the patient's PT for HCO3–, renal acid handling is normal. In other words, NAE equals dietary and endogenous acid production rates and the subject comes into a steady state of acid-base balance, albeit at a moderately reduced plasma HCO3– concentration (and a mild reduction in systemic pH). Because a steady state in acid handling is achieved, patients with proximal RTA have less severe acidosis as well as less nephrocalcinosis (which results from bone calcium mobilization from acidosis) than patients with distal RTAs (see the following).
The problem with proximal HCO3– reabsorption may occur independently but more commonly coexists with other defects in proximal nephron function, such as decreased reabsorption of glucose, amino acids, phosphate, and uric acid. The term Fanconi syndrome is employed when general proximal nephron function is disturbed (87). Patients with full-blown Fanconi syndrome may have severe osteomalacia and malnutrition in addition to the mild metabolic acidosis associated with proximal RTA (88). Proximal RTA may occur as a primary disorder and present in infancy or may be acquired in the course of other diseases or as a result of exposure to substances toxic to this nephron segment. A list of causes of proximal RTA is shown in Table 3-2. Treatment of this condition is approached by addressing the underlying cause, but if this is ineffective, administration of large amounts of HCO3– (10-15 mmol/kg/day) and potassium to compensate for ongoing potassium losses in the urine caused by the bicarbonaturia is necessary. This is necessary to avoid growth retardation in children and osteopenia, which may be produced by even mild degrees of acidemia (89).
The distal RTAs are characterized primarily by impaired NAE, which is due, at least in part, to impaired NH4+ excretion. The central role of impaired NH4+ excretion in this disorder is highlighted by a recent clinical study in which all patients with either hypokalemic distal RTA (also called type I or classic distal RTA) or hyperkalemic distal RTA (previously referred to as type IV RTA), caused by either hypoaldosteronism or a generalized tubular defect, had a positive UAG reflecting decreased NH4+ excretion. How NH4+ excretion is impaired in this diverse set of clinical disorders is still incompletely understood (84, 90).
Hypokalemic distal RTA has long been considered a disorder of the collecting duct in which the quantity of H+ secretion is inadequate to effect the necessary NAE for the subject to maintain acid-base balance. Clinically, patients with hypokalemic distal RTA present with hyperchloremic metabolic acidosis but are unable to acidify their urine (pH < 5.5 is commonly used) in response to an acid challenge. It must be stressed that the failure to acidify the urine does not fully explain the defect in NAE, which is primarily caused by an associated defect in NH4+ excretion (91). However, the failure to acidify the urine under conditions of systemic acidosis historically has been considered the clinical hallmark of hypokalemic distal RTA. The physiologic mechanisms for this impaired acidification have been a topic of interest for some time and are summarized with clinical examples in Table 3-3. Basically, four mechanisms have been suggested for impaired acidification by the distal nephron: (a) back leak through a leaky epithelium; (b) pump failure, where the H+ ATPase cannot pump sufficient amounts of H+; (c) voltage defect, where a favorable transepithelial voltage cannot be generated (e.g., decreased sodium delivery to the distal nephron or decreased sodium reabsorption in the distal nephron); or (d) rate defect/NH4+ defect, where urinary pH is reduced but NH4+ excretion and NAE cannot be increased to normal amounts. Hypokalemic distal RTA appears to be caused by either back leak or pump failure. Patients may have an isolated defect in the H+/K+ ATPase or the vacuolar ATPase (92). Hyperkalemic distal RTAs are probably caused by either voltage defect or rate defect/NH4+ defect (84).
in the urinary collecting system (i.e., renal pelvis, ureters, and urinary bladder), where the surface area for CO2 absorption is small. This CO2 essentially is trapped, and, when normalized for the blood PCO2 (i.e., the difference between urine and blood), is a marker for the rate of distal H+ secretion. Patients with back leak or pump failure generally have a small difference between urine and blood PCO2 (<20 torr).


text:
Q: How to differentiate users in web application How to differentiate users, after they log in into their account, in the way that they cannot see and edit other users' data? Is it a good approach to remember somehow user id during logging procedure and then make queries like WHERE user_id=x? or is there any other smart way?
Basically, I am using spring framework for logging procedure, but I am not really advanced user of this framework. After user log in they have to insert some informations about themselves to the database (i.e. name, surname, e-mail etc) and fill in their timetables. I don't really know how to get id of current user to let them edit and insert only their own data.

A: yes, you should store their user id in a session variable (if you don't know what sessions are look those up too)

A: You can always get the current logged in user using SecurityContextHolder.
SecurityContextHolder has the logged in user for the current thread.
Authentication authentication = SecurityContextHolder.getContext().getAuthentication();
if (authentication != null && !authentication.getPrincipal().toString().equalsIgnoreCase("anonymous")) {
    User loggedInUser = (User) authentication.getPrincipal();
}


If you are visiting XperiSoft Limited by road please use ME5 9SD for Satellite Navigation guidance.
From the Junction 3 of the M2, take directions for Chatham. After joining the A229, you should drive for about 1/4 mile where will find us on the left just next to the Holiday Inn Hotel.
Chatham Station is a mainline station from London. The easiest terminal stations in London are London Victoria, St Pancras or Charing Cross if travelling to Chatham.
A Taxi rank is available outside of Chatham Station, or a 101 bus is available from the Bus Station adjoining Chatham Station. A 101 bus travelling to Maidstone stops opposite the Holiday Inn Hotel and entrance to the the Innovation Centre.
If you would like to know more about our products and services, we're here to help.
You can call us, email us or use the Contact Form.
The organisation you work for.
A contact number or email we can use.
Information you send us for contact requests will be used only for that purpose and is acquired only on the basis of consent.
XperiSoft Limited is based in Medway, Kent with easy access to London and the rest of the United Kingdom.


The Flying Cross Men's Dress Pants are the top choice of the U.S. Navy for service dress uniforms. Finely crafted of the highest-quality wool, blended with polyester for durability, these pants are perfect for your next official occasion. Reap the benefits of our rigorous attention to detail, including exacting quality standards and all U.S. made components.


text:
Q: How do I list installed software with the installed size? I would like to have a list of the installed software on my machine, with the disk space consumed by them alongside. I would prefer to be able to order by largest/smallest, but that is not a necessity.
I am the sort of person who will install software to try it, and never clean up after myself.
As a result, my 7GB (Windows and my Data are on separate partitions, as well as a swap area) Ubuntu 11.04 partition is suffering, and has started regularly showing warning messages.

A: Another option is to use the dpigs application from the debian-goodies package:
NAME
   dpigs - Show which installed packages occupy the most space

SYNOPSIS
   dpigs [options]

DESCRIPTION
   dpigs sorts the installed packages by size and outputs the largest ones. Per
   default dpigs displays the largest 10 packages. You can change this value by
   using the -n option (see "OPTIONS"). The information is taken from the dpkg
   status file with grep-status(1).

OPTIONS
   -h, --help
       Display some usage information and exit.

   -n, --lines=N
       Display the N largest packages on the system (default 10).

   -s, --status=FILE
       Use FILE instead of the default dpkg status file (which is /var/lib/dpkg/status
       currently).

   -S, --source
       Display the largest source packages of binary packages installed on the system.

A: dpkg-query -W -f='${Installed-Size;8}  ${Package}\n' | sort -n

shows you a package list sorted by size

A: You can view such a list in the terminal-based package manager Aptitude:

*

*Open Aptitude with sudo aptitude.

*Hit S (capital S) and type ~installsize at the prompt.  (The ~ is for descending sort; you can omit it if you want the smallest packages on top.)

*By now, packages are sorted by size inside each hierarchical level. To get an overview, you'll want as few levels as possible.  Hit G and enter status at the prompt.  Now all installed packages are in a single section, sorted by size.

A: You can do this graphically in Synaptic .
First ensure that you enabled the Installed Size and Download size columns (or only one if you want that one).

*

*To do this, go to Settings > Preferences and choose Columns and Fonts, then tick the columns you want to see.

*Then click OK.

*

*Once they are enabled, you can list the packages you have installed by download/installed size by click on the column.

*

*Please note: I do not have my packages listed in that way this screen shot, but it works.

A: Preferred solution
I have found a shorter answer, not requiring aptitude:
dpkg-query -Wf '${Installed-size}\t${Package}\n' | column -t

Old proposed solution
The show command of aptitude is able to show the installed size of a package.
I have this little script, that make use of aptitude (to install separately) to have a list of all installed packages with sizes:
#!/bin/bash

export LC_ALL=C

aptitude show $(dpkg-query -Wf '${Package}\n') |
  awk '$1 == "Package:"     { name = $2 }
       $1 == "Uncompressed" { printf("%10s %s\n", $3, name) }' |
  awk '$1 ~ /k/ { $1 *= 1 }; $1 ~ /M/ { $1 *= 1024 }
       { printf("%9d %s\n", $1, $2)}'

Size are expressed in kilobytes, and are approximate, as returned by aptitude show pkg.
The script can be improved using a single awk invocation (but I'm lazy :-)

A: The other answers here list both installed and deinstalled packages.
The following lists only those which are currently installed:
dpkg-query -W -f='${Installed-Size;8}\t${Status;1}\t${Package}\n' | grep -v "\sd\s" | sort -n | cut -f1,3-

What it does:

*

*Query the installed size, status and name of all packages

*Filter out deinstalled packages

*Cut the status column from the output

Output resembles:
...
22376   vim-runtime
26818   linux-image-3.8.0-32-generic
28673   libc6-dbg
35303   libpython3.3-dev
40303   valgrind
40731   linux-firmware
41516   smbclient
58704   linux-headers-3.8.0-26
58733   linux-headers-3.8.0-32
93566   linux-image-extra-3.8.0-32-generic

A: Here's a variation of Drew Noakes's answer but with awk doing the heavy lifting:
#!/bin/sh

dpkg-query --show --showformat='${Package}\t${Installed-size}\t${Status}\n' |
    awk '
{
    # evaluate installed packages only
    if($3 == "install"){
        packages[$1] = $2
    }
}

END {
    # sort packages by size (change 'asc' to 'desc' to reverse the order)
    PROCINFO["sorted_in"] = "@val_num_asc"
    for (i in packages){
        printf "%05.2fM | %s\n",
        packages[i] / 1024, # convert from kilobytes to megabytes
        i
    }
}
'

The output


text:
NEW YORK, COLORADO BOWLERS SELECTED AS YOUTH AMBASSADORS OF THE YEAR
ARLINGTON, Texas – Courtney Morelli of Selden, New York, and Tanner Ausec of Colorado Springs, Colorado, have been selected as the United States Bowling Congress Youth Ambassadors of the Year.
The annual award recognizes a male and a female USBC Youth bowler for exemplary contributions in the sport outside of league or tournament play, academic accomplishments, and community involvement.
Selected by the International Bowling Campus Youth Committee, based on submitted applications, Morelli and Ausec each will receive a $1,500 scholarship.
Morelli has been a member of the Long Island USBC Youth Leaders program since 2013, and currently serves as treasurer. She chairs the Fundraising and Recruitment committees, and mentors new members.
She also is the vice president of the New York State Youth Leaders board, which she has served on for the last two years.
"Receiving this award is an incredible honor," Morelli said. "I absolutely love participating in Youth Leaders events and helping out in any way possible. This is such a validation to all the years I've spent participating as a Youth Leader and furthering the bowling program."
While her work with the Youth Leaders program has helped the local and state association, it also has taught Morelli valuable skills.
"I have always been a shy kid, and joining this program has really built up my confidence," Morelli said. "I have developed my social skills and how to interact with adults. My organization and planning skills have really improved, as well as my problem-solving skills."
A senior at Newfield High School, she has been a member of the school's bowling team since the seventh grade. She also competes in a travel league.
She plans to study business administration in the fall.
Ausec currently is serving his third one-year term as a youth director on the Pikes Peak USBC board, ensuring local youth are represented and served through tournaments and awards programs.
"I have been fortunate to receive so much from the local bowling community," Ausec said. "Whether through coaching, equipment, or knowledge, there have always been people to support me. As I grew up, I learned to understand the importance of giving back wherever possible, which is why I began coaching. This award is an acknowledgment of not only my efforts to give back to the game, but recognition of all that I have received from my local bowling community, as well."
A senior at Rampart High School, Ausec has a 4.19 grade-point average and ranks sixth in his class. On the lanes, he helped Rampart win back-to-back state team titles the past two seasons.
He started coaching youth bowlers at King Pin Lanes in Colorado Springs four years ago, as part of a National Junior Honor Society community service requirement. He said he quickly realized how much he enjoyed teaching the basic skills of the sport, and it gave him a greater appreciation of those who coached him.
"Coaching has taught me a number of things, but first and foremost it is a constant reminder that bowling should always be fun," Ausec said. "It has also taught me to be a better student of the game, and my skill level has benefited because of it."
Ausec will attend the University of Wisconsin-Whitewater in the fall and plans to bowl for the Warhawks.
Morelli and Ausec may have the opportunity to serve on the IBC Youth Committee and be eligible for additional scholarship funds. Youth Ambassadors selected to serve on the IBC Youth Committee must be at least 18 years old as of Aug. 1 in year of selection.


text:
Hiram Gray (July 10, 1801 in Salem, Washington County, New York – May 6, 1890 in Elmira, Chemung County, New York) was an American lawyer, jurist, and politician from New York who served one term in the U.S. House of Representatives from 1837 to 1839. He was also a judge at both the federal and state levels.

Education
He graduated from Union College in 1821. Then he studied law, was admitted to the bar in 1823, and commenced practice in Elmira, New York.

US Congress
Gray was elected as a Democrat to the 25th United States Congress, and served from March 4, 1837, to March 3, 1839.

New York state judiciary
He was Judge of the Sixth Judicial District from 1846 to 1847. He was a justice of the New York Supreme Court from 1847 to 1859, and was ex officio a judge of the New York Court of Appeals in 1851 and 1859. He was a Commissioner of Appeals from 1870 to 1875.

Gray wrote the majority opinion in the case of Lawrence v. Fox, 1859, giving contractual rights to the third-party Lawrence in a debt collection case.

Death
Gray was buried at the Woodlawn Cemetery in Elmira.

References

External sources

The New York Civil List compiled by Franklin Benjamin Hough (pages 351 and 356; Weed, Parsons and Co., 1858)
 Court of Appeals judges

1801 births
1890 deaths
New York Supreme Court Justices
Judges of the New York Court of Appeals
People from Salem, New York
Politicians from Elmira, New York
Union College (New York) alumni
Democratic Party members of the United States House of Representatives from New York (state)
19th-century American politicians
19th-century American judges


text:
using System;
using System.Collections.Generic;
using System.Linq;
using System.Text;
using System.Windows.Forms;
using Cesto.Config;

namespace Cesto.WinForms
{
	public interface IConfigParameterEditor
	{
		string TextValue { get; }
		Control Control { get; }
		IConfigParameter Parameter { get; }

		void Initialize(IConfigParameter parameter);
	}
}


Glasser SA, Charney S, Dervisis NG, et al.
J Am Anim Hosp Assoc 2014;50:96-104.
An image-guided robotic stereotactic radiosurgery (SRS) system can be used to deliver curative-intent radiation in either single fraction or hypofractionated doses. Medical records for 19 dogs with nonlymphomatous nasal tumors treated with hypofractionated image-guided robotic stereotactic body radiotherapy (SBRT), either with or without adjunctive treatment, were retrospectively analyzed for survival and prognostic factors. Median survival time (MST) was evaluated using Kaplan-Meier survival curves. Age, breed, tumor type, stage, tumor size, prescribed radiation dose, and heterogeneity index were analyzed for prognostic significance. Dogs were treated with three consecutive-day, 8-12 gray (Gy) fractions of image-guided robotic SBRT. Overall MST was 399 days. No significant prognostic factors were identified. Acute side effects were rare and mild. Late side effects included one dog with an oronasal fistula and six dogs with seizures. In three of six dogs, seizures were a presenting complaint prior to SBRT. The cause of seizures in the remaining three dogs could not be definitively determined due to lack of follow-up computed tomography (CT) imaging. The seizures could have been related to either progression of disease or late radiation effect. Results indicate that image-guided robotic SBRT, either with or without adjunctive therapy, for canine nonlymphomatous nasal tumors provides comparable survival times (STs) to daily fractionated megavoltage radiation with fewer required fractions and fewer acute side effects.


A Mass Communication student of Delta State University (DELSU), Elozino Ogege, who was declared missing last week has been found dead with her tongue and breasts severed from her body.
Her body was found at about 2:00a.m. by residents along Ekrejeta road in Abraka community, Ethiope-East Local Government Area of the state. Students living in the community said suspected ritualists, popularly called 'Yahoo Boys', might have killed Elozino.
The Delta State chairman of the Committee for the Defence of Human Rights (CDHR), Comrade Prince Kehinde-Taiga speaking with newsmen yesterday said CDHR would champion calls for the redeployment of the Commissioner of Police, CP Muhammad Mustafa, from the state if he fails to bring the perpetrators of the dastardly act to justice.
This is coming on the heels of the discovery of the lifeless body of a two-year-old boy, which has left residents of Abraka community, Delta State, looking for answers. The body was discovered on Saturday by an electricity transformer along Umono Road, Abraka, Ethiope East Local Government Area of the state, after his parents were reported to have raised the alarm that their son was missing.
Father of the deceased, Johnson Oghenevo, who spoke to journalists in the area, alleged that his son was taken away by unknown persons while the infant was playing outside their apartment on Friday. He added that efforts towards locating his whereabouts proved abortive.


A dining table can be expanded with one or two leaves to seat more diners.
Most dining tables have leaves that allow the table to expand from being able to seat four to six people to seating as many as 12. When not in use on the table, these leaves are subject to damage in storage or being misplaced. If you need to replace a table leaf, instead of undertaking the difficult task of custom building a leaf and trying to match the wood, fit and finish, build a quick fill-leaf that will fit within the table and be functional. As long as you cover the table with a tablecloth, no one will be the wiser.
Separate the two halves of the table until the ends won't separate farther. Measure the gap between the two halves of the table to determine how many 18-inch-wide leafs your table will accommodate. Measure the width of the table to determine the length of the leaf.
Scribe the 18-inch width and length of the leaf onto a sheet of 3/4-inch MDF using a pencil and a straightedge. Don safety glasses. Cut out the section of MDF on the pencil lines using a table saw.
Measure the thickness of the dining table's top, from the top of the expandable rails to the top of the tabl,e and subtract the thickness of the MDF from this shim thickness. Cut a piece of two-by-four to 18 inches. Rip two strips from this piece to the shim thickness.
Position the MDF between the table halves, aligned with the side of the table fitted with dowel holes. Place the two shims on top of the MDF, each aligned with one of the table rails beneath the MDF. Drill a shallow 3/32-inch pilot hole through the middle of the shim into the MDF using a power drill. Insert a countersink into the drill chuck and add a countersink to the pilot hole. Insert a 3/4-inch wood screw through the countersunk pilot hole to join the shim to the MDF. Repeat with an additional screw about 1 inch in from each end of the shim, before attaching the other shim with three screws in the same manner.
Flip over the MDF and center the board against the dowel-hole side of the table, with the shims riding on top of the table rails. Check to see that the MDF leaf is the same height as the table top. If the leaf is too high or too low, remove the shims and cut and install two shims of the proper thickness to allow the leaf to match the height of the rest of the table.
Measure the thickness of the dowel pins on the pin side of the table (typically 1/4 inch), and cut the same number of 1-inch-long dowel pins as are found on the table. Insert each of these pins into the holes on the appropriate half of the table.
Slide the leaf so it is against the newly inserted dowels, and mark hole locations for drilling holes on the leaf. Slide the leaf to the opposite side of the table and mark hole locations for the existing pins on the table. Drill the holes at the desired locations before putting a few drops of glue into each of the holes on the pin side of the leaf and inserting the dowel pins.
Place the leaf on the table and close the two halves of the table around the leaf, checking to see that the pins align, and the tabletop is smooth and continuous across the entirety of the table.
Install a router bit matching the chamfer or other bead on the edge of the two halves of the table into a woodworking router. Adjust the height of the bit to match the height of the edge bead, then remove the leaf from the table and apply a matching bead to only the two short sides of the leaf. Give the beads a light sanding with sandpaper and reinsert the leaf for a final test before placing a tablecloth over the entire table.
Most table leaves are 18 inches in width, but your table might be able to accommodate two leaves. Measuring the distance between the two halves of the table determines how many leaves your table can handle.
If your table has an apron, you may with to fabricate a matching apron so anyone reaching underneath the leaf will not notice the leaf is missing the table apron.
Baylor, Chris. "How to Replace Dining Table Leaves." Home Guides | SF Gate, http://homeguides.sfgate.com/replace-dining-table-leaves-51598.html. Accessed 18 April 2019.
How Wide Is an 8-Person Round Table?


text:
package com.enjoy.love.common.util;

import java.io.ByteArrayInputStream;
import java.io.ByteArrayOutputStream;
import java.io.IOException;
import java.io.ObjectInputStream;
import java.io.ObjectOutputStream;

import com.enjoy.love.common.log.CommonLogger;
import com.enjoy.love.common.log.CommonLoggerFactory;
import com.enjoy.love.common.log.LogUtil;

public class CommonSerializerUtil {
	private final static CommonLogger serializerLogger = CommonLoggerFactory
			.getLogger(CommonSerializerUtil.class);

	public static byte[] serialize(Object obj) throws IOException {
		ByteArrayOutputStream bis = null;
		ObjectOutputStream os = null;
		byte[] byteArray = (byte[]) null;
		try {
			bis = new ByteArrayOutputStream();
			os = new ObjectOutputStream(bis);
			os.writeObject(obj);
			os.flush();
			byteArray = bis.toByteArray();
		} catch (IOException e) {
			LogUtil.error(e, serializerLogger,
					"Object convert to bytes array fail:object={0}", obj);
			throw e;
		} finally {
			closeOutputStream(os, bis);
		}
		return byteArray;
	}

	public static Object deSerialize(byte[] byteArray) throws IOException,
			ClassNotFoundException {
		ByteArrayInputStream bos = null;
		ObjectInputStream ois = null;
		Object obj = null;
		try {
			bos = new ByteArrayInputStream(byteArray);
			ois = new ObjectInputStream(bos);
			obj = ois.readObject();
		} catch (IOException e) {
			LogUtil.error(e, serializerLogger,
					"bytes array convert to object fail:byteArray={0}",
					byteArray);
			throw e;
		} catch (ClassNotFoundException e) {
			LogUtil.error(e, serializerLogger,
					"bytes array convert to object fail:byteArray={0}",
					byteArray);
			throw e;
		} finally {
			closeInputStream(bos, ois);
		}
		return obj;
	}

	private static void closeOutputStream(ObjectOutputStream os,
			ByteArrayOutputStream bis) throws IOException {
		if (os != null) {
			try {
				os.close();
			} catch (IOException e) {
				LogUtil.error(e, serializerLogger,
						"close objectOutputStream fail:object={0}", os);
				throw e;
			}
		}
		if (bis != null) {
			try {
				bis.close();
			} catch (IOException e) {
				LogUtil.error(e, serializerLogger,
						"close byteArrayOutputStream fail:object={0}", os);
				throw e;
			}
		}
	}

	private static void closeInputStream(ByteArrayInputStream bos,
			ObjectInputStream ois) throws IOException {
		if (bos != null) {
			try {
				bos.close();
			} catch (IOException e) {
				LogUtil.error(e, serializerLogger,
						"close objectInputStream fail:object={0}", bos);
				throw e;
			}
		}
		if (ois != null) {
			try {
				ois.close();
			} catch (IOException e) {
				LogUtil.error(e, serializerLogger,
						"close byteArrayInputStream fail:object={0}", ois);
				throw e;
			}
		}
	}
}


text:
The Weird and Wonderful Marmozets is the debut studio album by the English alternative rock band Marmozets. It was released by Roadrunner Records on 29 September 2014. The album was very well received by music critics, receiving a 9/10 score from Metal Hammer upon release, and winning the Kerrang! Award for Best Album in 2015. In July 2016, Metal Hammer placed the album 70th in their list of the 100 Greatest Albums of the 21st Century so far.

Track listing

Credits
Writing, performance and production credits are adapted from the album liner notes.

Personnel
Marmozets
 Becca Macintyre – vocals
 Sam Macintyre – guitar, vocals
 Jack Bottomley – guitar
 Will Bottomley – bass, vocals
 Josh Macintyre – drums

Additional musicians
 Larry Hibbitt – percussion, keyboard
 Sem Schaap - Piano

Production
 Larry Hibbitt – production
 James Mottershead – engineering
 Tom Woodstock – editing
 Corey Moore – assistant tracking engineer
 Michael H. Brauer – mixing
 Mark Bengston – mix assistant, Pro Tools engineering
 D. Sardy – mixing of "Why Do You Hate Me?"
 Ryan Castle – mix engineering
 Cameron Barton – engineering
 Joe LaPorta – mastering

Artwork and design
 Hayes Hopkinson – artwork
 Tom Barnes – photography
 Briggs Design – layout

Studios
 Chairworks, West Yorkshire, UK – tracking
 Artspace Studio, London, UK – tracking of "Move, Shake, Hide"
 Xylo Sound, London, UK – recording of vocals, overdubs
 Electric Lady Studios, New York City, NY, USA – mixing
 Hillside Manor – mixing of "Why Do You Hate Me?"
 Sterling Sound, NY, USA – mastering

Charts

References

External links

  The Weird and Wonderful Marmozets at Roadrunner Records

2014 debut albums
Marmozets albums
Roadrunner Records albums