text:
Chinese Delegation Visits ISA Headquarters
JAMAICA, Kingston (21 November 2015) - - On 19 November 2015, a six-member Chinese delegation headed by Mr Lu Hao, Chairman of Environmental Protection and Resources Conservation Committee of National People's Congress of China, visited the headquarters of the International Seabed Authority. During the meeting with the ISA Secretary-General Mr Nii...
Call for Applications: ISA Contractor Training Programmes
JAMAICA, Kingston (14 November 2015) - - ISA continues its call for applications from candidates from developing countries to attend various ISA Contractor training programmes.The training programmes are pursuant to the terms of the contracts for exploration between the contractors and the International Seabed Authority. Member States are encouraged to ensure...
Director for Malaysia's KLRCA Pays Courtesy Call
JAMAICA, Kingston (14 November 2015) - - Datuk Professor Sundra Rajoo, Director of Malaysia's Kuala Lumpur Centre for Arbitration (KLRCA) paid a courtesy call on the Authority on Tuesday 10 November 2015. Professor Rajoo who is in Jamaica on the invitation of the University of the West Indies School of Law shared with the Authority, information about the KLRCA...
ISA and Companhia de Pesquisa de Recursos Minerais of BRAZIL Sign Exploration Contract
KINGSTON, Jamaica (9 November 2015) - - The International Seabed Authority and Companhia De Pesquisa de Recursos Minerais of Brazil (CPRM) have signed a 15-year contract for exploration for cobalt-rich ferromanganese crusts in the Rio Grande Rise in the South Atlantic Ocean. The Contract was signed today, 9 November 2015, in Brasília, by the Secretary-General of the...
Call for Applications : ISA/NORI Training Opportunities
JAMAICA, Kingston (6 November 2015) - - Nauru Ocean Resources Inc. (NORI) is offering two training places for candidates from developing States to attend an Environmental Planning Workshop in Gent, Belgium held by NORI on 11 and 12 December 2015. At the Workshop, NORI will review its plans for conducting environmental baseline studies within its nodule...


text:
Q: Sorting by price/quality ratio I have this trivial problem I can't solve.
I have a list of names with a value (let's say strenght) and a price. I want to understand which is the most convenient depending on the price, a sort of price/quality ratio.
Example
NAME   STRENGTH  PRICE
BOB    48        17
CHRIS  51        17
MARK   49        15

I want to sort this data on the price/quality ratio

A: Let's assume your value (quality) is strength that each player has. It also has its price.
If you want to find out which player is the most valuable, you shall divide strength/price, because in result you'll get how many strength-units you can have for 1 price-unit. The more strength-units for 1 price-unit - the better player is, obviously.
Let's take a look at the data set below (sorted by STR/PRI ratio descending):
NAME   STRENGTH  PRICE  STR/PRI
JOHN   99        15      6,600
MARK   49        15      3,267
CHRIS  51        17      3,000
BOB    48        17      2,823
TOM    5         17      0,294

99 strength and only 15 price? Great, right? His ratio is 6,600.
Wait... 5 strength and 17 price? I wouldn't buy this one, and you? And look - his ratio is only 0,294.
Conclusion? The best player has the highest STR/PRI ratio.
Now if we add PRI/STR column to the table above (sorted from the best to the worst as above):
NAME   STRENGTH  PRICE  STR/PRI     PRI/STR
JOHN   99        15      6,600       0,151
MARK   49        15      3,267       0,306
CHRIS  51        17      3,000       0,333
BOB    48        17      2,823       0,354
TOM    5         17      0,294       3,400

You can easily notice that the best player (John) has the lowest PRI/STR ratio.

A: We've clarified that you mean price/strength ratio.
Here's your original data set:
INDEX      NAME   STRENGTH  PRICE RATIO
1          BOB    48        17    0.354167
2          CHRIS  51        17    0.333333
3          MARK   49        15    0.306122

If I sort these by RATIO in ascending order, the indexes are (3, 2, 1).  I can tell what order NAME, STRENGTH, and PRICE need to be in by using those indexes.
Use any sorting algorithm you wish on the RATIO array and get the indexes back.  Use these to refer to the original data in the order of ascending RATIO.

redpajama_set_name: RedPajamaStackExchange


text:
Jeremy Rosen / August 18, 2016
Black Lives Matter indeed, and so they ought to, all the more for what they have had to endure. But the organization, however noble and justified its beginnings, is in serious danger of marginalizing and undermining itself. For the sake of its cause, I hope it does not fall further into a political trap.
There can be no doubt that black human beings, as well as many others, both of color and of different ethnic and religious backgrounds, have been treated atrociously in the USA (and almost everywhere else in the world, regardless of political or religious creed). For all the moral piety of the Declaration of Independence that declared, "We hold these truths to be self-evident, that all men are created equal, that they are endowed by their Creator with certain unalienable Rights, that among these are Life, Liberty and the pursuit of Happiness," it took a bloody civil war to abolish slavery.
It was not until President Lyndon B. Johnson helped secure the passage of the Civil Rights Act of 1964 (we can argue about Eisenhower), making racial discrimination and segregation illegal, and the Voting Rights Act of 1965, which abolished the poll tax and other means of keeping blacks and poor people from voting, that the USA began to take the noble sentiments seriously.
Despite all this and the fact that a portion of the black population has reached the pinnacles of American society, large numbers of black (and other) citizens remain confined to poor areas with substandard education, housing, and employment. A disproportionate number of blacks sit in American jails, and systemic prejudice remains endemic in pockets throughout the country. Some police forces have a terrible record of discrimination, and poor areas suffering from contamination, like Flint, have been ignored ( and sadly there are plenty of other examples of contaminated water across the US that have not been addressed). Clearly neither money, nor access to local government (Baltimore's administration is almost entirely black), nor affirmative action have resolved what seems to be an intractable problem.
Is there a solution? I cannot think of one. I was brought up in a different culture, one that admittedly believed that self-help was the only way. But then Jews could always hide their identity if they chose to, and most did. Doctrinaire socialism has not found a solution other than blaming others. On the contrary, too often trade unions hold back progress in all these areas, either out of political correctness or vested interest in preserving their power bases and privileges.
That is why the only solution I see is for those who care to speak out, to campaign, to agitate peacefully against prejudice wherever it occurs.
But Black Lives Matter is in danger, unless it wakes up, of becoming another left-wing, political, ideological, lunatic fringe as guilty of prejudice and close-mindedness as any other special interest sector of American society, precisely because it has fallen into bed with crackpot extremists who have pushed it to adopt ideological lies that only prove it is just as politicized as those it claims to speak out against. And politicization only holds back progress. No better example exists than that of civil rights campaigner Al Sharpton, who for all his noise, bluster, and publicity for more than fifty years has achieved bubkas other than self-promotion and wealth.
There is a wider coalition (which Black Lives Matter has allied itself with), called The Movement for Black Lives, which has expanded its remit to deal with universal examples of prejudice and discrimination that it blames on American imperialism. Nothing, you notice, against oppression of human rights by other states, religions, and races. In its manifesto, published on August 1, it pokes its nose into the Israel-Palestine conflict and uses terms that are not only deceitful, but plain and simply wrong. Its motive can only be to ally itself with myopic ideological left-wing ideology with closed minds, and those, both Jewish and non-Jewish, who deny Jews equal rights. You will notice that they say nothing about Indian occupation of Muslim Kashmir.
They claim that the occupation of Palestinian territory is only due to Israeli intransigence and white Imperialism and everything wrong in the Middle Eat is America's fault for supporting Israel. They repeat the tropes of black anti-Semites such as Louis Farrakhan and Malcolm X who thought that Israel was the sole aggressor, rather than an expression of a persecuted people for home rule (support them when they are victims, reject them when they are not). They erroneously think that blacks have more in common with Muslims than with Christians and ignore the fact that Muslim traders were more responsible for slavery, both in time and numbers. And that most slaves were sold to the Americas by black African chieftains for personal gain. Sadly, everyone's hands were sullied by that inhuman trade to some degree, and to pick on only one to blame is simply historical ignorance, if not rabble-rousing prejudice. Unfortunately, this spurious black narrative has infected a whole generation, including novelist Toni Morrison, bestseller Ta-Nehisi Coates, and Bernie Sanders supporters who blame Israel for everything you care to mention.
It is applying terms like apartheid or genocide to Israel's attempts to protect itself (while waiting for a negotiated peace agreement, having relinquished the occupation of Gaza) that betrays prejudice, whether it comes from Jew or non-Jew, black or white. Genocide means destroying a people, but under Israel the Palestinian population has risen not fallen. No mass graves of executed civilians or gassed populations have been found, whereas all this is common place amongst its declared enemies.
If Black Lives Matter is dedicated to removing discrimination in the USA, we should support it wholeheartedly and campaign for it. But if, like the UN, it allies itself uncritically with movements that have political agendas like The Movement of Black Lives, which sticks its nose uncritically into other complicated and complex conflicts, coming down on one side only, I will accuse it of dishonesty, prejudice, and malign intent. It will be in danger of becoming just another corrupt, self-serving political movement. If it continues to support The Movement for Black Lives, it will wither on its own vine.
The Secret War against the Jews
2 thoughts on "Black Lives Matter"
The Levantine Maghrebi says:
Even if everything they claim about Israel is true, it was a really stupid move to take focus off their home priorities to meddle in international affairs. They could make an impact in race relations in the US. Civil disobedience probably alienates some of their potential supporters (I can't say some of their activities in Chi left a good impression on me, but I was pleased that it was mostly nonviolent), but I understand the rationale for such methods. Sticking their noses in a conflict which has been going on for decades, with involvement from the US, EU, UN, Arab League etc, with obscenely staunch, passionate, and even downright bullheaded, supporters on both ends of the conflict, and which really doesn't affect domestic race relations (the Israel-Palestine conflict is younger than the prejudices here, after all), is far beyond the scope of making black lives matter here. I wouldn't be surprised if they get swallowed up by groups like SJP.
Jeremy Rosen says:
Well put. Of course nothing you or I say will make any difference. The blind left wing narrative on Israel and beyond has cast its die and nothing will change an ideologue who has an idee fixe!

redpajama_set_name: RedPajamaCommonCrawl


text:
In Memoriam: Â The S.H.I.E.L.D. Agent that Tony Stark Called Out for Playing 'Galaga' on the Hellicarrier in 'The Avengers'
Tony Matutai 5 years ago
There are some emotional wounds that will just never heal right. You can patch them up as best you can, work them over as therapeutically as you like, but they're there to stay. No matter how you might try to fight against it, no matter how you might try to forget or move on with your life, there will always be a hole in your heart the exact size and shape of what you once had: now lost forever.
The final moments of Avengers: Infinity War were traumatic for many fans. We had been with these characters for more than a decade now. We had grown up and grown old with them. They were our heroes, our roles models. We looked up to the sky and saw hope: champions of truth, justice and the American way who would never — could never — let us down, even on their worst days.
Everybody lost somebody that day. As likely as not, they lose several somebodies: cherished loved ones and treasured friends alike. My wife joked about taking a bereavement day from work in the morning, but I know she really wanted to. Hell, we all could have used one.
Reports are still coming in about how badly Thanos hit us: about all the brave men and women who ultimately lost their lives for one man's damnedable ambitions. It's likely that we won't know the extent of the devastation until well after the fact. Taking account of what was taken from it is pretty hard without any bodies to tally up, after all.
We will not forget the names of the fallen. We cannot bring ourselves to forget T'Challa, Parker, Strange, Barnes, Wilson, Maximoff, Quill, Groot, Drax, Mantis and Hill. And now we have one more name to add to that resplendent list of heroes: Galaga Guy.
Real heroes don't wear capes. They don't insulate themselves in armor. They don't have magic hammers. Real heroes are the regular men and women of the world who put themselves in daily risk despite not having any of the powers or gadgets or gizmos that all the headliners have. Real heroes don't need all the fame and glory that comes with publicizing their name for all to see: the only thing that they need is the assurance that, when the dust settles, they made a difference.
Galaga Guy was one such hero. We may never know his name, but his deeds will surely outlive us all. A brave SHIELD agent fighting on the front lines of freedom, he was always there when the action was fiercest and courage was in shortest supply.
He is, of course, best remembered for the instrumental role that he played during and before the famed Battle of New York, when the rogue Asgardian Loki infiltrated Earth's defenses and lead an invasion of Chitauri raiders into the heart of New York City. The Avengers stole all the credit for the city's defense, of course, but we won't forget the real heroes from that day.
Galaga Guy wasn't just a SHIELD agent, though. He was avid gamer, best remembered for his dedication to the retro classic Galaga, which he was known to occasionally sneak away from his official duties on the Hellicarrier bridge to play while the world below was safeguarded by their constant vigil. His gaming skills even drew the attention of Tony Stark upon entering the beating heart of SHIELD's global mission, who couldn't help but comment "That man is playing Galaga! Thought we wouldn't notice. But we did."
Infinity War co-director Joe Russo broke the news earlier this week. On May 7th, Russo announced that "he got snapped in the middle of a Galaga game. He was seconds away from his all-time high score… He's gone."
Galaga Guy was survived by the remaining half of SHIELD (just not the same half that includes Nick Fury). His contributions to our continued safety (at least the half of us that remain) will not soon be forgotten. You will be missed, dear friend.
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I cover updates on the latest celebrity gossip, TV show ratings, and interviews with actors and actresses from popular shows. I also do recaps of episodes and predictions for future storylines. My articles are an excellent resource for television fans looking to stay up-to-date on the latest happenings in the entertainment industry.
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text:
'It made me shudder' - Chorley residents' horror after severed dog's head found on door handle
Great Meadow, Astley Village
A community has been left shocked and horrified after a severed dog's head was found on the door handle of a house.
READ THE ORIGINAL STORY HERE: Severed dog's head left on door handle
Police are urging the public to help them catch the sadistic thug who carried out the vile act.
A former mayor described the incident as the 'sign of a psychopath'.
The gruesome discovery is said to have left the householder traumatised.
Officers were called to the property in Great Meadow, Astley Village, on Sunday morning.
They found the head of a dog, believed to be a Yorkshire terrier, on the door handle.
"This was extremely distressing for the occupant who found the dog," said a police spokesman.
"At this time, we have no idea why this has happened."
News of the shocking find prompted scores of people to express their shock and disgust on social media.
One said: "How could enyone do such a cruel, sadistic thing?"
Another wrote: "That's horrific. Who the hell does something like that?"
Laura Lennox, chairman of Astley Village Parish Council, said she had just returned from holiday to learn of the incident.
Pizza takeaway plan at iconic landmark branded 'ludicrous'
"Oh my god. that's disgusting. I'm absolutely horrified," she said.
"I'm totally stunned and shocked because Astley Village has been very quiet and peaceful in the past, so to have something like this is horrible.
"It made me shudder.
"I just hope somebody comes forward and tells the police where it might have come from."
Councillor Mark Perks represents Astley Village on Chorley Council and Clayton with Whittle division
on Lancashire County Council.
The former Mayor of Chorley described the incident as "horrendous" and "evil".
"It's the sign of a psychopath," he said.
"If there's someone living in the village like that it can lead to other things."
He said he had contacted Chorley council, the police and Place for People to manage properties in the area, to ask for their response.
He said: "The need to give some reassurance, particulalry in Great Meadow, but generally in the village.
"In all the years as a councillor, I've never come across that."
Chorley Council said their animal welfare officer received a call about the incident at the weekend and that the matter was passed to the police.
The police spokesman said: "If you have any information or are missing a dog, which is described, possibly as a terrier then please get in touch with PC Chris Hilton on 101 quoting log LC-20180520-0514.
"Alternative you can email 6977@lancashire.pnn.police.uk or contact CrimeStoppers anonymously."


Aftermarket Chevrolet GPS Navigation Head Unit is specially designed to replace Chevrolet Captiva factory standard radio(No navigation system). It has the same frame, plug and harness as original radio, totally plug and play.
The cruise constant speed control system (if your vehicle has) will be invalind after install this radio.


text:
<?php

namespace Application\Migrations;

use Doctrine\DBAL\Migrations\AbstractMigration;
use Doctrine\DBAL\Schema\Schema;

/**
 * Auto-generated Migration: Please modify to your needs!
 */
class Version20170430000911 extends AbstractMigration
{
    /**
     * @param Schema $schema
     */
    public function up(Schema $schema)
    {
        // this up() migration is auto-generated, please modify it to your needs
        $this->abortIf($this->connection->getDatabasePlatform()->getName() !== 'mysql', 'Migration can only be executed safely on \'mysql\'.');

        $this->addSql('ALTER TABLE ticket DROP FOREIGN KEY FK_97A0ADA37B00651C');
        $this->addSql('DROP INDEX IDX_97A0ADA37B00651C ON ticket');
        $this->addSql('ALTER TABLE ticket CHANGE status status INT NOT NULL');
    }

    /**
     * @param Schema $schema
     */
    public function down(Schema $schema)
    {
        // this down() migration is auto-generated, please modify it to your needs
        $this->abortIf($this->connection->getDatabasePlatform()->getName() !== 'mysql', 'Migration can only be executed safely on \'mysql\'.');

        $this->addSql('ALTER TABLE ticket CHANGE status status INT DEFAULT NULL');
        $this->addSql('ALTER TABLE ticket ADD CONSTRAINT FK_97A0ADA37B00651C FOREIGN KEY (status) REFERENCES status (id)');
        $this->addSql('CREATE INDEX IDX_97A0ADA37B00651C ON ticket (status)');
    }
}

redpajama_set_name: RedPajamaGithub


Moaraq is an ancient technique that has been perfected in the Middle East and Far East. It involves placing wood, glass, and other materials into pictures and other designs. The designs are then glued to a surface such as wood, then sanded and lacquered. The end result is a magnificent piece of art that will last forever.
Click on a picture for an enlarged view and more details.
Please provide the item number when ordering or making enquiries.


"Up in the Air," "Precious" and "Inglourious Basterds" led the Screen Actors Guild Awards with three nominations each Thursday, among them honors for George Clooney, Diane Kruger and Mo'Nique.
The World War II rewrite "Inglourious Basterds" and the Harlem story "Precious: Based on the Novel `Push' By Sapphire" are competing for the guild's overall cast prize, along with the 1960s British drama "An Education," the Iraq War tale "The Hurt Locker" and the musical "Nine."
Other TV comedies nominated for best cast are "Curb Your Enthusiasm," "Glee," "Modern Family" and "The Office."
Last year's drama cast winner, "Mad Men," is nominated again, along with "The Closer, "Dexter," "The Good Wife" and "True Blood."


text:
Virology Journal
The viral distribution and pathological characteristics of BALB/c mice infected with highly pathogenic Influenza H7N9 virus
Xiao-Xin Wu1 na1,
Song-Jia Tang2 na1,
Shu-Hao Yao3 na1,
Yu-Qin Zhou4 na1,
Lan-Lan Xiao1,
Lin-Fang Cheng1,
Fu-Ming Liu1,
Nan-Ping Wu1,
Hang-Ping Yao ORCID: orcid.org/0000-0001-6742-70741 &
Lan-Juan Li1
Virology Journal volume 18, Article number: 237 (2021) Cite this article
The highly pathogenic Influenza H7N9 virus is believed to cause multiple organ infections. However, there have been few systematic animal experiments demonstrating the virus distribution after H7N9 virus infection. The present study was carried out to investigate the viral distribution and pathological changes in the main organs of mice after experimental infection with highly pathogenic H7N9 virus.
Infection of mice with A/Guangdong/GZ8H002/2017(H7N9) virus was achieved via nasal inoculation. Mice were killed at 2, 3, and 7 days post infection. The other mice were used to observe their illness status and weight changes. Reverse transcription polymerase chain reaction and viral isolation were used to analyse the characteristics of viral invasion. The pathological changes of the main organs were observed using haematoxylin and eosin staining and immunohistochemistry.
The weight of H7N9 virus-infected mice increased slightly in the first two days. However, the weight of the mice decreased sharply in the following days, by up to 20%. All the mice had died by the 8th day post infection and showed multiple organ injury. The emergence of viremia in mice was synchronous with lung infection. On the third day post infection, except in the brain, the virus could be isolated from all organs (lung, heart, kidney, liver, and spleen). On the seventh day post infection, the virus could be detected in all six organs. Brain infection was detected in all mice, and the viral titre in the heart, kidney, and spleen infection was high.
Acute diffuse lung injury was the initial pathogenesis in highly pathogenic H7N9 virus infection. In addition to lung infection and viremia, the highly pathogenic H7N9 virus could cause multiple organ infection and injury.
Virus infection is a serious human health problem, and influenza virus is one of the major pathogenic viruses [1, 2]. Over the past 100 years, there have been many influenza epidemics, with the Spanish flu outbreak in the early twentieth century being the worst. In the past 20 years, there have also been several serious influenza infection outbreaks. In 1997, high pathogenic H5N1 avian influenza virus crossed the species barrier to infect humans [3]. To date, the H5N1 outbreak has caused more than 800 infections, with more than 400 deaths, with a mortality rate of more than 50%. In 2009, the H1N1 pandemic appeared in the American continent. Since 2009, the H1N1 pandemic has spread worldwide, killing more than 200,000 people. In 2013, the novel H7N9 avian virus started to infect humans, causing more than 1500 infections, with a fatality rate as high as 40% [4]. In 2017, the H7N9 virus mutated and changed to a highly pathogenic H7N9 virus [5, 6]. Since then, 32 cases of human infection with highly pathogenic H7N9 virus have occurred in eight provinces in China, with a mortality rate of around 50% [7]. Fortunately, in order to control and eradicate the H7N9 virus, many actions had been taken including closing live poultry markets and culling poultry, standard bioinformatics analysis for monitoring virus evolution, the establishment of the platform for influenza research, early-warning, and introduction of the bivalent H5/H7 vaccine in poultry [8,9,10,11,12,13]. Several studies reported that the use of the poultry vaccine could reduce the H7N9 virus prevalence in poultry and successfully eliminate the human infection with H7N9 virus [11,12,13]. However, the H7N9 virus has not been eradicated in poultry in China, and might escape from the vaccine-induced immunity [14]. At the same time, the influenza virus is still changing, different viruses are emerging, and a novel H7N9 virus might appear again, causing new threats to human health [14].
Many clinical and epidemiological studies have shown that H7N9 displays obvious family aggregation, indicating that close contact between people might lead to H7N9 infection [15,16,17,18,19]. Once H7N9 increases its adaptability to human receptors to acquire human transmission ability, it will lead to an influenza epidemic and mass infection [20]. Fortunately, a recent study reported that the highly pathogenic H7N9 viruses isolated from poultry between 2018 and 2019 have weakened ability to bind to human-type receptors but high affinity to bind to avian-type receptors [14]. Highly pathogenic H7N9 viruses isolated from avian species have low-to-moderate pathogenicity in mice, but after replication in mammalian hosts, the H7N9 influenza viruses could easily acquire the mutations (PB2 627 K or PB2 701 N) and then become more virulent in mice [5, 13, 14]. With the evolution and recombination, the highly pathogenic H7N9 viruses may also has the potential to infect human. Mortality could also increase because of mutations in highly pathogenic H7N9 virus. Therefore, on the one hand, we should study the affinity of the virus to receptor, and on the other hand, we should also study the pathogenic characteristics of the virus, especially its multiple organ distribution and pathological characteristics after virus infection.
Many influenza viruses have been reported have acquired an extra-pulmonary infection ability [21, 22]. Clinically, the most frequently described symptoms are viral encephalitis and viral myocarditis [1, 23, 24]. The H1N1 virus has been confirmed to cause viremia, which led to brain infection. H5N1 has also been confirmed to cause viremia [25]. Viremia could more often be detected in fatal cases rather than in nonfatal cases [26]. H5N1 pathogenesis is characterised by intense inflammatory responses and a high viral load. The morbidity of H5N1 viruses is associated with their extra-pulmonary [27,28,29,30]. The plasma of patients was shown to contain H7N9 virus RNA; however, this did not correlate with the clinical outcome. H7N9 virus RNA could also be detected in urine and faeces [31]. We have confirmed the presence of viremia in highly pathogenic H7N9 infections. The initial infection site of highly pathogenic H7N9 is the lung. Lung infection is the main manifestation, and it will eventually develop to multiple organ failure [32]. Patients infected with H7N9 virus developed cytokine storms and viremia, and died from multiple organ failure. Whether multiple organ failure is an inflammatory response caused by lung infection, or a later viral, multi-organ infection is unclear, and solving this problem would guide treatment. There is currently limited clinical and pathological research on H7N9 virus infection, and there have been few systematic animal experiments to prove the virus distribution after highly pathogenic H7N9 virus infection [33]. To answer the above questions, we designed experiments in mice infected with highly pathogenic H7N9 viruses to clarify the viral distribution and pathological changes to important organs after viral infection.
Animal experiment ethical statement
Specific-pathogen-free (SPF) female BALB/c mice (n = 31, 6–8 weeks old) were obtained from the Experimental Animal Center of Zhejiang Province, China. All animal experiments were carried out following the principles of the Guide for the Care and Use of Laboratory Animals of Zhejiang Province. The Ethics Committee of the First Affiliated Hospital, Zhejiang University School of Medicine, approved the present study. A bio-safety level 3 laboratory at the First Affiliated Hospital, Zhejiang University School of Medicine was used to perform all the H7N9 virus experiments (Registration No. CNAS BL0022).
Viruses and cells
The American type culture collection (Rockville, MD, USA) provided the Madin-Darby canine kidney cell line (MDCK). MDCK cells were cultured using Dulbecco's modified Eagle's medium (DMEM; Cat#11965092, Gibco, Grand Island, NY, USA) containing 10% foetal bovine serum (FBS; Cat#10100147, Thermo Fisher Scientific, Waltham, MA, USA) at 37 °C in a 5% CO2 atmosphere. The present study used a A/Guangdong/GZ8H002/2017(H7N9) virus (GenBank: MF455313-455320) isolated from an infected patient in Guangzhou, China, in 2017. Viruses were grown in the allantoic cavities of 9-day-old SPF embryonated chicken eggs at for 72 h 37 °C. The harvested allantoic fluid was tested using a haemagglutinin (HA) assay. Fifty microliters of allantoic fluid was diluted at 1:2 using phosphate-buffered saline (PBS; Cat#20012500BT, Gibco) in a 96-well blood coagulation plate. Then, an equal volume of 1% chicken red blood cells were added, and observed at room temperature for 30–45 min. The highest dilution at which blood coagulation appeared was the HA titre. Allantoic fluid aliquots containing the virus were placed in a − 80 °C freezer until further use.
Virus median tissue culture infectious dose (TCID50) determination
MDCK cells were inoculated into 96-well cell culture plates at 3 × 104 cells/well (in 100 μl). The virus was diluted in viral growth liquid 10 times continuously, from 10–1 to 10−10, and the last two rows were reserved for the controls. After cells grew into a single layer in the 96-well plate, the medium was removed, the wells were rinsed with sterile PBS once, and the diluted virus (100 μl/well) was added to the wells, with each concentration infecting cells in four wells. A normal cell control well (virus free) was set. The 96-well plate was incubated at 37 °C in a 5% CO2 incubator for 2 h, and then washed two times with PBS. The normal control well and the virus infection wells then received virus growth fluid (DMEM with 1% FBS; 100 μl/well). The microtitre plate was incubated for 72 h in a 5% CO2 incubator at 37 °C. The HA assay was then used to identify positive or negative wells. The TCID50 was calculated according to a previously published method [34].
Inoculation of the virus
Fifty microliters of 106 TCID50 of A/Guangdong/GZ8H002/2017(H7N9) virus was inoculated into the mice intranasally. The control group (n = 5) received the same volume of PBS. The mice (n = 14) were observed for signs of death, weight loss, and illness post-infection. Some mice (n = 12) were sacrificed humanly at 2, 3, and 7 days post infection (dpi). Their serum and organs (spleens, livers, kidneys, hearts, brains, and lungs) were excised or collected. The organs were dived into parts, one of which was fixed in 10% buffered formalin, and the other subjected to viral isolation and quantitative PCR to detect virus levels.
Organ histopathology
Haematoxylin eosin (HE) staining of organ tissues was performed. The organ tissues were also subjected to Immunohistochemistry (IHC) staining. Organ tissues were embedded in paraffin and sectioned. The sections were then de-waxed and heated in citrate buffer. H2O2 (0.3%) in methanol was used to quench endogenous peroxidase activity. Sections were blocked for 2 h with Three percent bovine serum albumin (BSA; Cat#H1130, Solarbio, Tongzhou, Beijing, China) in PBS was used to block the sections for 2 h. The sections were then incubated at 4 °C overnight (12 h) with a 1:200 dilution of rabbit polyclonal antibodies recognizing H7N9 (Cat#GTX125989, GeneTex, Irvine, CA, USA). EnVision System reagents (Cat#K5007, DAKO, Glostrup, Denmark) were used to detect the bound antibodies. HE was used to counterstain all the slides.
Virus isolation from mouse serum and organs
Virus isolation was attempted from serum sampled at 2, 3, and 7 dpi. The allantoic cavities of 9-day-old SPF embryonated chicken eggs were injected with approximately 100 µl of serum and cultured in an incubator for 72 h at 37 °C. Thereafter, the allantoic fluid was sampled and subjected to an HA assay.
The tissue leachate was obtained as follows: 1 ml of sterile PBS was added to the frozen tissues in storage tubes, and then the tissue was cut using sterile scissors in the biosafety cabinet. The tubes were centrifuged at 500 × g for 10 min. Then, 200 μl of the supernatant was used to isolate the virus. The virus separation from the tissue leachate was similar to serum virus separation procedure.
Determination of the virus titre of organs
One millilitre of sterile PBS was added to the frozen tissues in storage tubes, and then the tissue samples were cut using sterile scissors in the biosafety cabinet. The tubes were then centrifuged at 500 × g for 10 min. Then, 200 μl of the supernatant was added with 800 μl Trizol to extract the RNA. Quantitative real-time PCR (qPCR) was then used to calculate the amount of the virus. qPCR was carried out using an H7N9 nucleic acid quantitative detection kit (Cat#Z-RR-0309-02; Zhijiang biological technology Co., Ltd. (Shanghai, China). Nineteen microlitres of H7N9 nucleic acid PCR detection reaction mixture and 1 μl of quantitative PCR enzyme were mixed by vortexing and then centrifuged at 500 × g for several seconds. This mixture was added to the PCR reaction tube, together with 5 μl of the RNA sample, for a total reaction volume of 25 μl. The tube was covered, centrifuged briefly, and subjected to the following PCR conditions: 40 cycles of 45 °C for 10 min, 95 °C for 15 s, and 60 °C for 60 s. The relative quantity of H7N9 virus was determined by the cycle threshold (Ct) value.
GraphPad Prism 5 (GraphPad Software, Inc., La Jolla, CA, USA) was used for the statistical analyses of the survival rate and weight data. Statistical analyses of the data for weight was conducted using Mann–Whitney test. P-values < 0.05 were considered statistically significant.
The change in weight and the survival status of the H7N9-infected mice
After H7N9 challenge, the mice lost weight, displayed signs of illness, and eventually died. Up to 2 dpi, the H7N9-infected mice showed mild illness, with a minor decrease in appetite and activity. The weight of the mice increased slightly over the first two days (Fig. 1A). However, subsequently, the weight of the mice decreased sharply (Fig. 1A, C, D), reaching a weight loss of nearly 20% (Fig. 1A). After 2 dpi, The health of the mice deteriorated gradually. The mice showed signs of a relatively acute clinical disease, manifested by poor appetite, ruffled fur, and inactivity. By 7 dpi, the death rate of the mice was more than 64% (Fig. 1B). The remaining live mice had signs of severe respiratory disease, such as respiratory distress and an increasing lack of appetite. By 8 dpi, all the mice had died (Fig. 1B). Throughout the observation period, the mice in the uninfected control group remained healthy, with no obvious loss of weight or illness.
Changes in the weights of the experimental mice and their survival curve. A The weight change of the experimental mice. B The survival curve of the experimental mice. C The comparison of weights between the normal group and virus infection group 5 days post infection. D The comparison of weights between the normal group and virus infection group 7 days post infection. GZ8H: A/Guangdong/GZ8H002/2017(H7N9); *P-values < 0.05 were considered statistically significant
Histopathology of organs
HE staining was used to evaluate the histopathology of lung tissue. The number and appearance of the lesions varied at different dpi. At 2 dpi, the mice showed a lesion with inflammatory cell infiltration, exudation, and intra-alveolar haemorrhage. At 3 dpi, the mouse lungs showed pathological changes in the exudate and severe multifocal interstitial inflammatory hyperaemia. At 7 dpi, the lung lesions were larger compared with those at 2 and 3 dpi, and many patchy lesions had fused. At this time point, the intra-alveolar haemorrhage area was enlarged (Fig. 2A). As the dpi increased, varying degrees of lung injury were revealed using immunohistochemical staining. Lung tissue, particularly the bronchiolar epithelium, showed the presence of viral antigens. The mice at 3 and 7 dpi suffered severe injury, with many viral antigens being detected (Fig. 2A).
Histopathology of lung, brain, and heart tissue. A Immunological and HE staining of mouse lungs at 2, 3, and 7 days post infection. B Immunological and HE staining of mouse brains at 2, 3, and 7 days post infection. C Immunological and HE staining of mouse hearts at 2, 3, and 7 days post infection. The viral antigen is shown using a red arrow. HE: Haematoxylin and eosin; IHC: Immunohistochemistry; dpi: days post infection
The brain tissue samples were also subjected to HE staining. As the dpi increased, the H7N9-infected showed more severe pathological changes. Brain IHC staining revealed abundant H7N9 antigens at 7 dpi (Fig. 2B). These results suggested that the brain was infected by the virus.
HE staining was also used to examine the heart histopathology. The number and appearance of the lesions varied according to the dpi. At 3 and 7 dpi, IHC staining revealed large amounts of H7N9 antigens in the heart (Fig. 2C). These results suggested that from 3 dpi, the heart became infected with the virus.
HE staining of kidney tissue revealed that H7N9 infection caused more severe pathological changes over time. At 3 and 7 dpi, IHC staining showed large quantities of H7N9 antigens in the kidneys (Fig. 3A). These results suggested that from 3 dpi, the kidneys became infected with the virus.
Histopathology of kidney, liver, and spleen tissue. A Immunological and HE staining of mouse kidneys at 2, 3, and 7 days post infection. B Immunological and HE staining of mouse livers at 2, 3, and 7 days post infection. C Immunological and HE staining of mouse spleens at 2, 3, and 7 days post infection. The viral antigen is shown using a red arrow. HE: Haematoxylin and eosin; IHC: Immunohistochemistry; dpi: days post infection
HE staining liver tissue was also revealed that the number and appearance of the lesions varied according to the dpi. At 3 and 7 dpi, IHC staining detected H7N9 viral antigens in the liver (Fig. 3B). These results suggested that from 3 dpi, the liver became infected with the virus.
HE staining of spleen tissue revealed that H7N9 infection caused more severe pathological changes over time. At 3 and 7 dpi, IHC staining detected H7N9 viral antigens in the spleen (Fig. 3C). These results suggested that from 3 dpi, the spleen became infected with the virus.
Isolation of the virus from mouse serum and organs
Live H7N9 virus could be isolated from the serum of infected mice persistently until death (Table 1). At 2 dpi, H7N9 virus was isolated from the lung one of three mice. Virus could also be isolated from mice at 3 and 7 dpi. However, 2 and 3 dpi, no H7N9 virus could be isolated from brain samples. By contrast, at 7 dpi, H7N9 virus was isolated from all mouse brains. At 2 dpi, no H7N9 virus was isolated from heart samples, whereas at 3 dpi, virus could be isolated from the heart of one of three mice. At 7 dpi, the virus was isolated from three of six mouse hearts. At 2 dpi, no H7N9 virus could be isolated from the kidney samples. At 3 and 7 dpi, the virus was isolated from the kidney of one of three mice and two of six mice, respectively. The H7N9 virus was not isolated from the liver at 2 dpi. At 3 dpi and 7 dpi, virus was isolated from the liver of one of three and one of six mice respectively. At 2 dpi, no H7N9 virus could be isolated from the spleen samples. At 3 dpi and 7 dpi, virus was isolated from the spleen of one of three mice and two of six mice, respectively.
Table 1 The H7N9 virus isolated from serum and different tissues of mice
The amount of virus in mouse organs
Quantitative PCR was used to evaluate the amount of virus in mouse organs. The RNA level was represented by the Ct value. A Ct value > 38 was considered negative. The lower the Ct value, the higher the virus content. The RNA level was relatively low in mouse lungs at 2 dpi, but increased sharply at 3 dpi and again at 7 dpi (Fig. 4). The RNA level was relatively low in the brains of the mice at 2 and 3 dpi, but increased to a high level at 7 dpi. The RNA level was relatively low in the hearts of mice at 2 dpi. However, the virus content in the heart was relatively high in one of three mice at 3 dpi and in three of six mice at 7 dpi. The RNA level was relatively low in the kidneys of the mice at 2 dpi. However, the virus content in the kidney was relatively high in one of the mice at 3 dpi and in two of six mice at 7 dpi. The RNA level was relatively low in the livers of the mice at 2 dpi. However, the virus content in the liver was relatively high in one of three mice at 3 dpi and in one 1 of six mice at 7 dpi. The RNA level was relatively low in the spleens of mice at 2 dpi. However, the virus content in the spleen was relatively high in one of three mice at 3 dpi and in two of six mice at 7 dpi.
Reverse transcription-polymerase chain reaction results in different tissues of each group of mice. A Reverse transcription-polymerase chain reaction results in lungs of each group of mice. B Reverse transcription-polymerase chain reaction results in brains of each group of mice. C Reverse transcription-polymerase chain reaction results in hearts of each group of mice. D Reverse transcription-polymerase chain reaction results in kidneys of each group of mice. E Reverse transcription-polymerase chain reaction results in livers of each group of mice. F Reverse transcription-polymerase chain reaction results in spleens of each group of mice. dpi: days post infection; The H7 and N9 gene levels are shown as the cycle threshold (Ct) value; A Ct value > 38 was considered negative
We have confirmed that viremia was associated with the high mortality caused by highly pathogenic H7N9. Lung infection is the main manifestation, and the virus eventually causes multiple organ failure. Multiple organ failure might have many causes, including a systemic inflammatory response resulting from pulmonary infection [35], but might also be caused by late multiple organ infection. In the present study, we found that in mice infected with the A/Guangdong/GZ8H002/2017(H7N9) virus. Their weight decreased sharply from 3 dpi. Our results suggested that in the early phase of infection (up to 2 dpi), lung lesions were few and the virus titre was low. During this early period, the other organs were not infected. The first two days is a very important time window for early diagnosis and treatment. In a previous study of in patients with H7N9 viral infection, the early use (in the first 48 h of illness) of a neuraminidase inhibitor decreased the duration of viral shedding and improved survival [36]. In addition, as the virus has changed, the time of antiviral use has been extended to fully control the infection [36]. Thus, in highly pathogenic H7N9 virus infection, antiviral treatment should be started as early as possible. We observed that on the third day post infection, the disease burden increased sharply, enhancing the risk of multiple organ infection, which would require a longer period of antiviral therapy and might result in multiple organ injury.
In our previous study, the H7N9 virus was not lethal to mice [34]. In other previous studies, the highly pathogenic H7N9 viruses isolated from the avian species could replicate in the airway of mice but were no lethal to mice [5]. However, with the evolution of H7N9 highly pathogenic viruses, some of the viruses became highly virulent in mice. Recent studies have shown that after circulation in poultry for a few weeks, some viruses acquired the ability to kill mice [13]. Once the virus obtained the PB2 701 N or PB2 627 K mutation, its virulence in mice could increase over 10,000-fold [5, 13, 14]. In another study, the authors using the highly pathogenic H7N9 viruses isolated from the avian species between 2018 and 2019 to infect the mice, some mice were detected with brain and spleen infection, but the authors have not explore the infection in other major organs like hearts, kidneys and livers [14]. However, in our present study, all the mice infected with highly pathogenic H7N9 were dead by the 8th day post infection with multiple organ injuries.
K526R in PB2 gene can increase pathogenicity to mice in the absence of E627K and D701N mutations [37]. M535L in PB2 gene has been reported to increase viral polymerase activity [38]. Having both K526R and M535L mutations in PB2 gene might be responsible for the increased viral virulence of A/Guangdong/GZ8H002/2017(H7N9) virus, which required further verification by reverse genetic techniques. The highly pathogenic H7N9 virus induced a more enhanced immune response than the low pathogenic H7N9 virus. Pathogenicity of high pathogenic H7N9 was increased by inducing a stronger cytokine storm [39]. The cause of death in mice is considered to be a result of increased replication capacity of highly pathogenic H7N9 virus, which is observed as rapid viral replication in lungs of mice on 3–4 dpi, the lung blood barrier breaking, viremia and other organs infection, later multi-organ infection and failure [39]. It simultaneously induced a cytokine storm, resulting in multi-organ function impairment [39]. Direct damage caused by high pathogenic H7N9 virus and immune damage together contribute to death in mice.
Heart, kidney, and liver injuries are common in influenza infection [22, 40, 41]. Moreover, influenza A (H1N1) has been detected in patients' pericardial and myocardial tissues [42, 43]. These studies suggest that infection-associated cardiac injury is caused by direct viral invasion. Heart changes have also been reported during H7N9 infection. For example, in 203 out of 321 patients, evidence of cardiac injury was observed [44]. Cardiac injury was associated with severe infections, acute respiratory distress syndrome, and the associated settings of the mechanical ventilator and was linked higher mortality during hospitalization [44]. In our study, heart infection was confirmed in mice. Heart infection might also be the cause of high rates of pathogenic H7N9 mortality. Therefore, we should closely monitor myocardial function in patients infected with highly pathogenic H7N9.
In our study, during the late stage of infection, all the mice showed brain infection. Influenza-associated encephalopathy might be another important cause of death in patients with influenza [45]. Seasonal and pandemic H1N1 infections in 2009 were found to cause encephalopathy in patients [46, 47]. In a previous study, the highly pathogenic H7N9 virus exhibited enhanced virulence and extended viral tropism in mice compared with low pathogenic H7N9 viruses [48]. Meanwhile, the highly pathogenic H7N9 virus has been proven to replicate in brain tissues in animal models [48]. H5N1 virulence in mice correlates with that in humans; therefore, we could speculate that highly pathogenic H7N9 strains that caused fatalities in mice would also show increased lethality in humans [12, 13]. When the patients develops multiple organ injuries and brain infection, they should receive urgent intensive care treatment. In the intensive care unit, we should maintain organ function, strengthen antiviral treatment, and provide life support treatment. Such comprehensive treatment can save patients' lives [4, 49]. At the same time, we should pay attention to a patient's intracranial pressure and note any changes to their mental capacity [50].
In summary, influenza virus mutations increase infection rates in humans and may also lead to pathogenic enhancement. We should closely monitor the H7N9 virus because it might gain greater multi-organ infection capacity through mutations, leading to higher fatality rates. Acute diffuse lung injury is the initial stage of pathogenesis in highly pathogenic H7N9 virus infection. In addition to lung infection and viremia, the highly pathogenic H7N9 virus can cause multiple organ infection and injury, which should receive more research attention. Therefore, early diagnosis, early use of drugs or neutralization antibodies to control the virus, and the prevention and control of multiple organ infection are very important.
PB2:
Polymerase basic protein 2
SPF:
Specific-pathogen-free
MDCK:
Madin-Darby canine kidney
DMEM:
Dulbecco's modified Eagle's medium
FBS:
Foetal bovine serum
Haemagglutinin
PBS:
Phosphate-buffered saline
TCID50 :
Median tissue culture infectious dose
dpi:
Days post infection
HE:
Haematoxylin eosin
IHC:
qPCR:
Ct:
Cycle threshold
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Zhang Y, Liu J, Yu L, Zhou N, Ding W, Zheng S, et al. Prevalence and characteristics of hypoxic hepatitis in the largest single-centre cohort of avian influenza A(H7N9) virus-infected patients with severe liver impairment in the intensive care unit. Emerg Microbes Infect. 2016;5:e1. https://doi.org/10.1038/emi.2016.1.
Davoudi AR, Maleki AR, Beykmohammadi AR, Tayebi A. Fulminant myopericarditis in an immunocompetent adult due to pandemic 2009 (H1N1) influenza A virus infection. Scand J Infect Dis. 2012;44(6):470–2. https://doi.org/10.3109/00365548.2011.631575.
Calabrese F, Carturan E, Chimenti C, Pieroni M, Agostini C, Angelini A, et al. Overexpression of tumor necrosis factor (TNF)alpha and TNFalpha receptor I in human viral myocarditis: clinicopathologic correlations. Mod Pathol. 2004;17(9):1108–18. https://doi.org/10.1038/modpathol.3800158.
Gao C, Wang Y, Gu X, Shen X, Zhou D, Zhou S, et al. Association between cardiac injury and mortality in hospitalized patients infected with avian influenza A (H7N9) virus. Crit Care Med. 2020;48(4):451–8. https://doi.org/10.1097/CCM.0000000000004207.
Britton PN, Blyth CC, Macartney K, Dale RC, Li-Kim-Moy J, Khandaker G, et al. The spectrum and burden of influenza-associated neurological disease in children: combined encephalitis and influenza sentinel site surveillance from Australia, 2013–2015. Clin Infect Dis. 2017;65(4):653–60. https://doi.org/10.1093/cid/cix412.
Kawashima H, Morichi S, Okumara A, Nakagawa S, Morishima T, collaborating study group on influenza-associated encephalopathy in J. National survey of pandemic influenza A (H1N1) 2009-associated encephalopathy in Japanese children. J Med Virol. 2012;84(8):1151–6. https://doi.org/10.1002/jmv.23317.
Mylonaki E, Harrer A, Pilz G, Stalzer P, Otto F, Trinka E, et al. Neurological complications associated with influenza in season 2017/18 in Austria—a retrospective single center study. J Clin Virol. 2020;127:104340. https://doi.org/10.1016/j.jcv.2020.104340.
Sun X, Belser JA, Pappas C, Pulit-Penaloza JA, Brock N, Zeng H, et al. Risk assessment of fifth-wave H7N9 influenza A viruses in mammalian models. J Virol. 2019. https://doi.org/10.1128/JVI.01740-18.
Cantan B, Luyt CE, Martin-Loeches I. Influenza infections and emergent viral infections in intensive care unit. Semin Respir Crit Care Med. 2019;40(4):488–97. https://doi.org/10.1055/s-0039-1693497.
Studahl M. Influenza virus and CNS manifestations. J Clin Virol. 2003;28(3):225–32. https://doi.org/10.1016/s1386-6532(03)00119-7.
We would like to thank Professor Fu-Chun Zhang (Guangzhou Eighth People's Hospital) for kindly providing H7N9 virus used in the present study. We also thank the native English speaking scientists of Elixigen Company for editing our manuscript.
This work was supported by China Postdoctoral Science Foundation (Grant Number 2020T130102ZX), the Postdoctoral Science Foundation of Zhejiang Province (Grant Number ZJ2020031), the Natural Science Foundation of Zhejiang Province (Grant Number LQ21H190004), and the Medical and Health Science and Technology Program of Zhejiang Province (Grant Numbers 2020379356 and 2020377610). The funding sources had no role in the study design; in the writing of the report; or in the decision to submit the paper for publication.
Xiao-Xin Wu, Song-Jia Tang, Shu-Hao Yao and Yu-Qin Zhou have contributed equally to this work
State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, National Clinical Research Centre for Infectious Diseases, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, The First Affiliated Hospital, Zhejiang University School of Medicine, 79 Qing Chun Road, Hangzhou, 310003, Zhejiang, China
Xiao-Xin Wu, Lan-Lan Xiao, Lin-Fang Cheng, Fu-Ming Liu, Nan-Ping Wu, Hang-Ping Yao & Lan-Juan Li
Plastic and Aesthetic Surgery Department, Affiliated Hangzhou First People's Hospital, Zhejiang University School of Medicine, Hangzhou, 310000, Zhejiang, China
Song-Jia Tang
Department of Stomatology, Wenzhou Medical University Renji College, Wenzhou, 325035, Zhejiang, China
Shu-Hao Yao
Department of Respiratory Medicine, The Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou, 310016, Zhejiang, China
Yu-Qin Zhou
Xiao-Xin Wu
Lan-Lan Xiao
Lin-Fang Cheng
Fu-Ming Liu
Nan-Ping Wu
Hang-Ping Yao
Lan-Juan Li
HY, NW, and LL designed the experiments. XW, ST, SY, YZ, LX, LC, and FL performed the experiments. XW and ST drafted the manuscript. All authors participated in revising the manuscript. All authors read and approved the final manuscript.
Correspondence to Hang-Ping Yao or Lan-Juan Li.
All mouse experiments were carried out following the Guide for the Care and Use of Laboratory Animals of Zhejiang Province. The Ethics Committee of the First Affiliated Hospital, Zhejiang University School of Medicine approved the study.
All data generated or analysed during this study are included in this published article.
Wu, XX., Tang, SJ., Yao, SH. et al. The viral distribution and pathological characteristics of BALB/c mice infected with highly pathogenic Influenza H7N9 virus. Virol J 18, 237 (2021). https://doi.org/10.1186/s12985-021-01709-7
Highly pathogenic H7N9
Multiple organ injury
Viral distribution
Pathological changes
Influenza viruses


INSTALLATION DESIGN 15 8. ENVIRONMENTAL IMPACT 19 9. IMPACT ON HUMAN HEALTH 20 10. FINAL CONSIDERATIONS 22 pag. PRACTICAL GUIDE FORoutdoor lighting PRACTICAL GUIDE FORoutdoor lighting . Light pollution can be defined as the direct or indirect entry of artificial light into the environment. We can, however, prevent pollution from the emission of luminous flux from artificial …... Learn from a practicing design Engineer on the systematic methodology by which a designer should proceed in designing a work holding fixture with hydraulic clamping for a milling operation.
6/05/2012 · If you do a lot of boards, and work out how long you take to manually dimension a board or how long you take to make a fancy (but ultimately, shaky jig) and spend per board getting it accurate this approach makes a lot of sense. Obviously there is knock-on effect with pre radiused frets and fret press cauls seeing the same surface every time and there is less time cleaning up bumpy and lumpy the phantom of the psyche pdf It is important to develop an assistive jig, which is that have fully criterion to work out the problem. Hopefully the concepts that have been generated can diminish an accident to the workers and can reduce the cost of polishing process..
Ejectors must be provided to force the work out of the jig or fixture due to o In case work piece is heavy. Enough clearance must be provided to allow for variations in component size. The design should allow easy and quick loading or unloading of the work piece. o Any use of lubricant oil creates a film between surfaces which causes the work piece to stick to the surface of jig or fixture rational equations word problems worksheet pdf Well, last weeks video went over better than I ever expected! I guess it really fills a need for a lot of woodworkers. Not everyone has a saw with the ability to take a stack set, or maybe simply like me they don't have the money to spend on one.
7/02/2012 · From measurements on the kreg jig, the narrow tip on the drill bit is 15/32" long, and the tip tends to stop about 1/16" from the bottom of the jig. So, that means 15/32" + 1/16" = 17/32" of the screw length is embedded in the pocket hole side of the joint.
Objective : Design Validation of Welding fixture, Holding Systems, Pallet Tooling, Weld gun and EOAT has done and reported in the issue list with suggestion for the Designers. Weld gun Selection for all Welding station Collision free path creation for the whole line Offline programming for all the Robots RDS and Weld Matrix Creation.
This paper is designed for bearing processing technology and fixture. The main task is to work out the half fine milling under 36mm, Φ18 holes, bearing the processing technology of the rules of procedure, and write CARDS.


"Do opposites attract? Or do similarities attract?"
Well, do opposites or similarities attract? Although I did not see the show, what the program is asking is question that has multiple and widely varying answers. I don't think there is one definitive answer, but a wide range based on individual circumstances and feelings. As we are all individuals, for some may find comfort in a mate that is similar in culture and ideals, as for others it may be the differences which promote the excitement and interest between them that provides the attraction.
A very good question that will be debated until the end of time, since we are all different in our own way which makes each of us interesting in our own right.
Thanks for your comment. I agree with your point. There's not one and only way to define what constitutes good relationship, and what leads to happy marrriage, since we are all different. Thank you very much for sharing your opinion with me.


text:
No Other Movie Has 100% Rating With So Many Reviews
'Lady Bird' manages the feat with 170 critics on Rotten Tomatoes
By Newser Editors, Newser Staff
Posted Nov 28, 2017 5:00 PM CST
This image released by A24 Films shows Saoirse Ronan and Lucas Hedges in a scene from "Lady Bird." (Merie Wallace/A24 via AP)
The early reviews of the movie Lady Bird were fantastic, and that track record is holding up in unprecedented fashion. Slate points out that the movie written and directed by Greta Gerwig has just notched a record on Rotten Tomatoes. It had 170 reviews as of Tuesday afternoon and yet still maintained a 100% positive rating from critics. (Audiences were a little less kind, at 87%.) Other movies have a 100% rating, but none has achieved that rank with so many reviews. Now in second place is Toy Story 2, which has 163 reviews.
"This is completely amazing and so incredibly appreciated by the entire team that made Lady Bird," Gerwig tells Rotten Tomatoes. "We are all on cloud nine and using our tomato emoji more than we ever thought possible." Here's the trailer for the movie, a coming-of-age story about a teenage girl (Saoirse Ronan) in Sacramento. Laurie Metcalf plays her mother. (Read more Rotten Tomatoes stories.)


text:
Music Video: Ziggy Marley & The Melody Makers Perform Their Hit 'Look Who's Dancing' Live
by Stan on Tuesday, July 3, 2012 at 9:02 pm EDT in Arts & Entertainment, Music
I'd long forgotten about this amazing upbeat reggae tune from Bob Marley's eldest son's 1989 album, One Bright Day.
A wake amidst a torrential downpour couldn't bring you down with this song playing in the background.
What a melody! What a performance!
Recorded live on "Sessions At West 54th" in 1999, here is Ziggy Marley & the Melody Makers:
[youtube]http://www.youtube.com/watch?v=IYSeuddZjBE[/youtube]
LISTEN: Reggae Great Delroy Wilson Sings 'This Life Makes Me Wonder'
by Stan on Monday, March 7, 2011 at 1:01 pm EDT in Arts & Entertainment, Music
In 1961, a thirteen year old Delroy Wilson began his music career in Kingston, Jamaica, recording ska hits penned by Lee "scratch" Perry, Coxsone Dodd, amongst others. His music evolved with the sounds of 60's Jamaica from ska to rocksteady and eventually to reggae. By the late-60s/early-70s he was one of the most influential reggae recording stars on the island.
He first toured the U.K. in 1970, where British reggae label Trojan Records had him record a number of songs — a move that would help him to expand his European footprint.
By the mid-70s many British punks, including The Clash's Joe Strummer, counted themselves as Delroy Wilson fans. Strummer, at the time, attended a reggae concert at the Hammersmith Palais to see Wilson and fellow Kingston musicians Dillinger and Leroy Smart perform. Expecting a rebellious 'roots reggae' performance, Strummer felt disappointed by their sets, claiming them to be "all very Vegas."
British film director and musician Don Letts, who attended the show with Strummer, reflected on the evening: "I think that show was an eye opener for [Strummer], realizing that all these people were trying to get out of the ghetto roots life."
The event inspired Strummer to pen the lyrics for one of The Clash's biggest hits: "White Man In Hammersmith Palais." In it you can hear Strummer shout out "Delroy Wilson, your cool operator."
Wilson died at the age of 46 on March 6, 1995 of cirrhosis of the liver. He is often noted for his soulful vocals and melancholy lyrics. Of his many great songs, one of my personal favorites is his 1968 recording, "This Life Makes Me Wonder." The lyrics are simple, yet strangely haunting, and the music is just so damned melodic:
This life makes me wonder
how to live another day to come
I feel the strong of the hand of one that I was depending on
It takes a friend… to be a friend
It takes a friend… to stop a friend
ENJOY:
[youtube]http://www.youtube.com/watch?v=WoqwAJoWBbM[/youtube]
Delroy Wilson's greatest hits album, Once Upon A Time, which features this song, can be downloaded here:
By Aravind Adiga
By Richard Price
By David Nicholls
The Snapper
By Roddy Doyle
Citizen Vince
By Jess Walter
City of Thieves
By David Benioff
By Joseph O'Neill
By Jonathan Tropper
The Curious Incident of the Dog in the Night-Time
By Mark Haddon


text:
Q: Maven assembly plugin: filter not escaping backslash when colons exist I'm filtering some configuration files with the Maven assembly plugin 2.4 and have got the problem that in .bat files, literal backslashes are not escaped when the value contains a colon.
pom.xml:
<plugin>
  <artifactId>maven-assembly-plugin</artifactId>
  <version>2.4</version>
  <configuration>
    <filters>
      <filter>src/assembly/filter.properties</filter>
    </filters>
    <descriptors>
      <descriptor>src/assembly/assembly.xml</descriptor>
    </descriptors>
  </configuration>
</plugin>

filter.properties:
#Double (escaped) backslashes
testPath1 = a\\b\\c
testPath2 = c:\\test
#testPath3 contains no colon
testPath3 = c\\test

test.bat:
REM ${testPath1}
REM ${testPath2}
REM ${testPath3}

test.properties:
path1=${testPath1}
path2=${testPath2}
path3=${testPath3}

assembly.xml:
<assembly xmlns="http://maven.apache.org/plugins/maven-assembly-plugin/assembly/1.1.2" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance"
xsi:schemaLocation="http://maven.apache.org/plugins/maven-assembly-plugin/assembly/1.1.2 http://maven.apache.org/xsd/assembly-1.1.2.xsd">
  <id>distribution</id>
  <formats><format>zip</format></formats>
  <files>
    <file>
      <source>${basedir}/src/assembly/testBat.bat</source>
      <outputDirectory>/</outputDirectory>
      <filtered>true</filtered>
    </file>
    <file>
      <source>${basedir}/src/assembly/testProp.properties</source>
      <outputDirectory>/</outputDirectory>
      <filtered>true</filtered>
    </file>
  </files>
</assembly>

And this produces...
testBat.bat (all backslashes were escaped):
REM a\b\c
REM c:\test\path
REM c\test\path

testProp.properties (backslashes in path2 are not escaped as expected!!!):
path1=a\b\c
path2=c:\\test\\path
path3=c\test\path

Anyone know if this is some kind of special feature, or actually a bug? :)

A: Just as an update, I'm now using Ant's filterset functionality instead of the Maven assembly plugin's filtering. Originally I wanted to create the environment-specific artifacts with Maven, but then, due to having numerous slightly different environments, decided to build just one delivery package with Maven, and then have Ant scripts fill the configuration templates at deploy-time.


text:
Biografia
Fu avviato al sacerdozio ed entrò nel seminario di Alba grazie alla spinta di don Giacomo Alberione, fondatore della Congregazione della Società San Paolo (detta anche Congregazione Paolina). Nel 1917 entrò a farne parte anche il Giaccardo (assumendo il nome di Timoteo), che due anni dopo veniva ordinato sacerdote. Fu uno dei più attivi promotori della terza congregazione paolina, quella delle Pie Discepole del Divin Maestro, che, dopo un difficile cammino, ebbe il riconoscimento ufficiale da parte di Pio XII il 12 gennaio 1948, pochi giorni prima del decesso del Giaccardo.

Culto
Fu beatificato il 22 ottobre 1989 e viene ricordato nel calendario liturgico il 24 gennaio.

Bibliografia
 Mario Sgarbossa, I santi e i beati, Figlie di San Paolo, Milano 1998, ISBN 88-315-1585-3

Voci correlate
 Famiglia Paolina

Altri progetti

Collegamenti esterni

Beati italiani del XX secolo
Beati paolini
Beati proclamati da Giovanni Paolo II

redpajama_set_name: RedPajamaWikipedia


text:
Driver allegedly lied about role in fatal crash
Three men involved in a fatal July 2 car crash were charged in local court Saturday.
Driver allegedly lied about role in fatal crash Three men involved in a fatal July 2 car crash were charged in local court Saturday. Check out this story on guampdn.com: http://www.guampdn.com/story/news/2017/07/18/driver-ysengsong-fatal-crash-allegedly-asked-occupant-take-blame/486756001/
Jerick Sablan, jpsablan@guampdn.com Published 12:47 p.m. ChT July 18, 2017 | Updated 5:12 p.m. ChT July 18, 2017
A combined photo of Reality Joe and Travor Todd Ruben(Photo: Department of Corrections)
The driver who was allegedly driving drunk when he was involved in a fatal crash was asked by his occupant to lie and say he didn't drive, racking up a falsification charge on top of vehicular homicide and other charges, according to a court complaint filed last Saturday.
The July 2 crash on Ysengsong Road, near Kaela's Mart, killed Anna Marie Flores, 58.
Three of the four men in the vehicle were charged in the Superior Court of Guam Saturday.
Reality Joe, aka Rialty Joe (Photo: Department of Corrections)
Reality Joe, aka Rialty Joe, 25, was charged with vehicular homicide while intoxicated, vehicular homicide, driving while under the influence of alcohol with injuries, driving while under the influence of alcohol, reckless driving with injuries and making a false report.
Travor Todd Ruben, 26, and Junior Miurha, 21, were charged with hindering apprehension, falsifying evidence and unsworn falsification. Rueben was also charged with witness tampering.
Allegedly headed to get more beer
Flores was driving a 1997 Mitsubishi Mirage southbound on Ysengsong Road when a 2013 Mazda 3 came out of Clara Street into her lane as it attempted to turn into the parking lot of Kaela's Mart, police said. Flores died the next morning from her injuries.
According to a magistrate's complaint, authorities found several alcohol containers in the center console of the men's vehicle as well as another alcohol container in the right rear door of the vehicle. Both vehicles were noted to have sustained extensive damage as a result of the crash.
Travor Todd Ruben (Photo: Department of Corrections)
When interviews by police on July 6, Ruben allegedly said he was the driver in the crash. Ruben told police he'd been drinking at Miurha's place and his group left to buy more beer when the crash happened, documents state.
Miuraha was interviewed and made statements consistent with those provided by Ruben, documents state.
However, the fourth occupant told police on July 13 that Joe was the one driving the car, documents state.
Police spoke with Joe, and he allegedly told them that he drank five cans of beer before the crash. He admitted to driving the car at the time of the crash, court documents state.
Joe said Ruben asked him to tell police that Ruben was the one driving, not him, documents state. Ruben went to Joe's work days after the crash to again ask him to tell police that he was driving the car, documents state.
Video shows fatal car crash on Ysengsong; 3 men arrested
Anna Marie Blas Flores identified as driver who died in Dededo accident
GPD: Man arrested in Maite hit-and-run that sent CalPac employee to hospital
Read or Share this story: http://www.guampdn.com/story/news/2017/07/18/driver-ysengsong-fatal-crash-allegedly-asked-occupant-take-blame/486756001/


text:
Q: RadioButton Asp.net Hi everyone i made an application in Asp.net that contains a fonctionaliyu that allows a candidate to register to a certain thing via a form the entity contains a property called "Gender" of type "string" in the generated view i change it like this ;
@Html.Label("Male")@Html.RadioButtonFor(model => model.Gender, "Male")

@Html.Label("Female")@Html.RadioButtonFor(model => model.Gender, "Female")
@Html.ValidationMessageFor(model => model.Gender, "", new { @class = "text-danger" })

Is this the right way to do it??Plz  need help


text:
Q: usepgfplotslibrary - undefined control sequence I have problem with following example code:
%& --shell-escape --enable-write-18
\documentclass[a4paper,10pt]{article}
\usepackage[T1]{fontenc}
\usepackage[utf8]{inputenc}
\usepackage{polski}
\usepackage{tikz}
\usepackage{pgfplots}
\usepgfplotslibrary{units}

\begin{document}
    \begin{tikzpicture}
        \begin{axis}[
            use units,
            x unit=m,x unit prefix=k,
            y unit=N,y unit prefix=m,
            xlabel=Distance,ylabel=Force]

            \addplot coordinates {
                (1,2.3)
                (2,2.7)
                (3,2.1)
                (4,1.8)
                (5,1.5)
                (6,1.1)
            };
        \end{axis}
    \end{tikzpicture}
\end{document}

A cannot use units in axis labels.
A similar code was included in this documentation: http://www.iro.umontreal.ca/~simardr/pgfplots.pdf on page 227.
Errors:
Missing \begin{document}. \usepgfplotslibrary{u (followed by: nits})
Package pgfkeys Error: I do not know the key '/pgfplots/use units' and I am going to ignore it. Perhaps you misspelled it.
Package pgfkeys Error: I do not know the key '/pgfplots/x unit' and I am going to ignore it. Perhaps you misspelled it.
Package pgfkeys Error: I do not know the key '/pgfplots/x unit prefix' and I am going to ignore it. Perhaps you misspelled it.
Package pgfkeys Error: I do not know the key '/pgfplots/y unit' and I am going to ignore it. Perhaps you misspelled it.
Package pgfkeys Error: I do not know the key '/pgfplots/y unit prefix' and I am going to ignore it. Perhaps you misspelled it.
Undefined control sequence:  \usepgfplotslibrary (followed by: {units})

What's more, the command \usepgfplotslibrary completely does not work with any other pgfplots library.
I don't know what is wrong, but i have to get this working :/
Thank you in advance for your help.
I'm running Debian Sid. Texlive (2009-11), pgf (2.10-1)

A: When I try your code with the Debian/Ubuntu packages, I get
! Undefined control sequence.
<recently read> \usepgfplotslibrary

l.7 \usepgfplotslibrary
                       {units}

(and if I ignore that error, then your errors follow).
I'd guess that the version of pgfplots in the Debian packages (i.e. in TL 2009) doesn't have any additional libraries and you are looking at the wrong manual. Ubuntu 11.04 (which uses the Debian packages, so I guess Debian Sid is the same) comes with pgfplots 1.2.2, while the current version is 1.4.1.
As always I recommend to install TeX Live directly from TUG instead of using the Debian packages. That way you can always get current package versions by running sudo tlmgr update --all. Alternatively, you can try installing pgfplots directly from CTAN.


This entry was posted in Uncategorized and tagged 814 bass crew, dubstep, NatasK by 8BC Art and Music Culture Collective. Bookmark the permalink.
Looking forward to being able to proudly hang a Natask original on my wall!! Boom!!!


The New Face of Chanel Is... Kristen Stewart?
She appeared last night in Dallas at a fashion show/camped-up hoedown to launch the collection, wearing orange leather pants by Chanel. Fashion!
As for why Dallas, the Metiers d'Art is a luxe annual showcase for the brand, which honors different locales each time. Vogue says Dallas and the American West won out this year because of the outsized role Texas played in the company's post-war relaunch. No one seemed particularly excited about Chanel's 1954 comeback collection—except America. Dallas-based Neiman Marcus in particular helped keep the company afloat, and in 1957 Coco Chanel was warmly welcomed on a visit to the city.
Unfortunately, it seems when styling the fashion show Lagerfeld and Co. were unable to restrain themselves from, yup, face paint and faux Native American headdresses.
This really ought to class up the (supposed) feud between KStew and Dior emissary Jennifer Lawrence.


short tower type for LHD models. Identify by imperial threads - reconditioned.
short tower type for RHD models. Identify by imperial threads - reconditioned.
short tower type for LHD models. Identify by metric threads - reconditioned.
short tower type for RHD models. Identify by metric threads - reconditioned.
for RHD models - reconditioned.
for LHD models - reconditioned.


Corporate administrators can add E-Verify users at multiple verification locations. To add an additional user the corporate administrator must provide the user's name, phone number, fax number (optional) and email address. A program administrator at the verification location may also add new users.
If a user leaves the employer or no longer needs access to E-Verify, a corporate administrator or program administrator must delete the user's account. To delete a user account, see Delete User Account – Process Overview in Section 2.5.2.
To add a new E-Verify user, follow the Add New User - Process Overview.
From Company Locations, select Add New User.
NOTE: This is the only opportunity to change the user ID.
The new user will receive their user ID and temporary password by email.


I'm also alive...noone seems to bother though...since I've been forced to change my nick from time to time.
i care, mate. i care.
Giving life to old thread is great.
i just wanna make him feel welcome, you know?
Even though the post is about 14 years old and he more likely hasn't been here in years?
kristen you're still alive!!!!!! omg i thought youd left for good. i havnt talked to you for about 5 minutes! shames on you!


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Probabilistic Latent Semantic Analysis is a novel statistical technique for the analysis of two--mode and co-occurrence data, which has applications in information retrieval and filtering, natural language processing, machine learning from text, and in related areas. Compared to standard Latent Semantic Analysis which stems from linear algebra and performs a Singular Value Decomposition of co-occurrence tables, the proposed method is based on a mixture decomposition derived from a latent class model. This results in a more principled approach which has a solid foundation in statistics. In order to avoid overfitting, we propose a widely applicable generalization of maximum likelihood model fitting by tempered EM. Our approach yields substantial and consistent improvements over Latent Semantic Analysis in a number of experiments.


Today, a serving of Q's relating to student-athletes.
But first, a reminder to those applying for our 10th annual Anne Arundel County Sun Academic-Athletic Team: Get your applications in as soon as possible.
Deadline for entries is March 20; we run the ballot frequently onthese pages.
* I'm sure you know Annapolis is 17-1 overall in hoops and has a school-record 23 consecutive wins over county foes. But did you know the average grade point average of the team members is 2.66, with the lowest GPA being a 2.16?
Did you know that Annapolis sophomore Larry Brown had a 4.0 GPA on his last report card?
Do you realize that a 2.66 GPA is well above the county required 1.66 for high school athletes, and also above the NCAA's new 2.50?
Obviously, Annapolis head coach John Brady and assistant Roy Brown are stressing more than X's and O's, aren't they?
* Have you ever seen a player take over a high school basketball game down the stretch as Rob Wooster did at Severna Park last Tuesday night, hitting a career-high 38 points and pacing the Panthers to a come-from-behind 76-69 victory over the Falcons?
* Is the 6-foot-5 Wooster the best all-around player Brady has had in his 15 years at Annapolis?
"Without question, Rob is the best of all time," said Brady. "The guy is so confident under pressure and can score from anywhere, any way."
Brady says that the late James Butler was the "best one-on-one player we've ever had," but Wooster is the best player, period.
* By the way, these eyes have been watching Wooster since his varsity career began three years ago, but did you know his fourth-period slam dunk against Severna Park was the first I can ever remember from him?
* Didn't Glen Burnie's Vernon Osborne have a great game Friday night in the Gophers' 73-66 mild-upset victory at Old Mill, with 28 points, including 14 of 18 from the floor and two slam dunks?
* Has a girls player ever had back-to-back games like Debbi Daddsof Northeast did last week with 70 points and 57 boards?
* Remember former Meade star and 1989 grad Jay Mouzon, who attended Anne Arundel Community College briefly before having a fall-out with ex-coach Mark Amatucci? Did you know that Mouzon is enrolled at Howard Community College and says he will play there next season?
* Whatever happened to Amatucci anyway?
* Wouldn't Archbishop Spalding make an excellent choice for its new head football coach by hiring long-time Annapolis and North County assistant Del Hughes?
* Is the boys enrollment at Spalding big enough to field a competitive football team?
* With the way her team's play has fluctuated this season and an admitted lack of intensity all too often, is veteran North County coachSally Entsminger pondering retirement?
* Could the county do any better than taking Chesapeake administrator Roy Skiles out of the school system and naming him to replace outgoing Recreation and Parks Director Joe McCann?
* Can you believe Paul's "B" team defeated Paul's so-called "A" team in the Anne Arundel County Billiards League last week?
* With Navy winning the Eastern Collegiate Division championship, 8-4, Sunday over West Chester at Dahlgren Hall, didn't the Mids show the University of Maryland club team, a 5-3 loser to West Chester in the semis, who should be going to the National Club Tournament at Penn State?
Maryland took two of three from Navy, including the Mids' coveted Crab Pot final, and thought it should be going to the nationals. But the bottom line is that Navy finished ahead of the Terps in the regular-season standings and won the league tourney.
Isn't the right team going? Wasn't it a fine gesture on the part of Navy hockey coach Jim Barry to present the league championship trophy to Mids' Sports Information Director Tom Bates?
* With Navy's hoop team at 6-17, what is Coach Pete Herrmann going to talk about on his new Thursday night radio show at Middleton's Tavern in Annapolis? Jerry Hardesty's oyster shooters?
* Can you believe the Baltimore Orioles are sending a hitting instructor to Northeast High on March 23 to work with the Spindler's 50-and-over men's softball team of George "Wacko" Kelch?
"We believe you're never too old to learn," said Kelch.
* Aren't the 50-and-over guys hoping the instructor will not be Brady Anderson?
* Have you pro boxing fans marked Thursday, March 26, as the next date for buffet and bouts at Michael's Eighth Avenue?
* Isn't it great that ex-Andover catcher Earl Williams, who was a surprise release of the Orioles a couple years ago despite a goodseason at Bluefield, is getting another shot at pro baseball in the Chicago White Sox organization?
Williams tried out for a couple ofclubs last spring, to no avail, and spent the summer playing for DanFielder's Arundel Stars unlimited team, hoping someone would notice.The guy has light-tower power, and Jim Gilbert, the Orioles scout who originally signed Williams, recommended him to the pale hose.
* Isn't it great to hear that Brooklyn Park Broncos 12-year-old cheerleader Lauren Pokrywka knocked 'em dead singing the national anthem at the Orioles/Baltimore County Baseball Clinic at Parkville High a few weeks ago?
"Lauren should get a chance to sing 'The Star-Spangled Banner' at the new stadium (Oriole Park at Camden Yards) this year," said Gilbert.
* Did you know that three countians are playing baseball for the Florida International University Sun Blazers this spring: infielder Nathan Harvey of Annapolis, who attended Riverdale Baptist, and Arundel grads Will Trinidad (infielder) and Pat Kahl (catcher)?
* How about Archbishop Spalding junior Zachary Wood, who played for a soccer team from Baltimore that toured Mexico City in late December, being named to the All-Tournament team after leading his team into the finals of the youth tournament?
* Despite recovering from surgery for a couple of slipped disks in his neck, did you know that feisty Dennis Thiele intends to be back out there this spring coaching the girls softball team at Chesapeake?
"You can't keep me away from it," said the veteran coach. "I will be protected and give signals from the dugout. I've got two great assistants in Lin Sullivan and Chip Lewis to help me."
Sullivan will coach third base; Lewis, a former assistant to Don Leonard at Broadneck, will be the JV girls coach at Chesapeake.
* Did you know that Thiele has lost a very good assistant in Jerry McBee, who is going to try his hand at baseball asan assistant to the Cougars' new coach, Jim Simms?
* Isn't Thiele's idea to train a student to coach first base for the Cougars' softball team a good one?
* Aren't the field hockey players at Severna Park fortunate to have veteran coach Lil Shelton not only coaching them in the fall, but watching over them in a winter indoor league at the school this time of the year?
Does this extra work and dedication explain why Severna Park is so dominant in field hockey?
Who said only basketball, soccer and football players specialize?


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