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Cities Near Caledonia, MI
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49302, 49333
Coverage Area
City Facts
|1.41 sq mi (3.65 km2)
|Area Water
|0.08 sq mi (0.21 km2)
|1,136.1/ sq mi (438.7/ km2)
|Time zone
|Eastern (EST) (UTC-5)
|Area Land
|1.33 sq mi (3.44 km2)
|GNIS feature ID
|FIPS code
|ZIP code
|810 ft (247 m)
|Population Total

subset: commoncrawl


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Issue 200
We have been looking at types. This is the fifth. Here's a bit of teaching for you… Apostling, prophesying, evangelising, pastoring and teaching are transferable skills: they are transferred from God to people. They are also people who specialise and they are ways of working; they are also transferred between home and work and meant to prepare Christians for work and incidentally to facilitate everyone in the ways of God.
Apostles don't just plant churches, they plant ideas, dreams, visions and people for the service of God. Prophets don't just predict the weather, but they catch the breeze of God and let it blow into people's lives. Evangelists are people who make it real, while pastors are those who increase care to client, customer, colleague or company. Teachers know how to learn and enable others to learn; specifically they know how to learn to work spiritually.
If you want to know what any of these types look like, then look at Jesus of Nazareth – he is THE apostle, THE prophet, THE evangelist, THE pastor and THE teacher. See how he pioneered and suffered, listen as he gave specific words from God to individual people, observe his communication style and receive his care, learning from his example.
The game of life is not played just at the weekends, or just during the week. We are always called to work out of who we are and what God has given us.
You may be a specialist in all of the five types – the chances are that you at least prefer one of them. You will also need to operate in the other four as the situation arises. If there is no specialist evangelist around, it's no good saying it's nothing to do with you. If there's no specialist pastor, you still have to care. The more we think like this, the more we can get our faith on the move so that we are ready for whatever comes our way. That is why we need each other. That is what it means to be prepared.
In preparation for the next GEOFFSHATTOCKweekly, do feel free to email us your thoughts to firstname.lastname@example.com or leave a comment on our Facebook or Twitter profile. You can also visit our YouTube channel - get inspired and share Worktalk's vision with others.
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Remote Work
Working from Home During Quarantine
I don't normally invite guest bloggers, but when Jessica Larson emailed me, I was intrigued. She has a great website of her own. Go check out her article about being a mom and solopreneur. Thanks for reading. ~ Bridget This "work from home during a pandemic" thing caught most of us entirely off guard. As…Read More
Remote Work Tips
Remote work is the ability to work on a computer from any location that has a strong WiFi connection. You can choose to be a digital nomad like Jon Brown or you can work in a dedicated office or co-working space. Remote work removes the commute at the very least. For me, I went from…Read More


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Speaking is one of my biggest passions, and motivating people to take up a mindfulness practice is one of my favorite topics as a speaker. On September 12th of this year I spoke at the New Media Summit in Austin, TX. There were around 200 people, and I was speaking on Present Moment Focus, and how over the past five years my research team and I have developed a proven system for customizing mental training through mindfulness-based practices. The summit was full of many positive people with great stories, and many attendees have podcast shows. Speaking at this event helped land me a few invitations to be on different shows. We will be advertising these podcast shows with posts when they come out soon.
Satimind is set to speak at other events as well, and our next one is at Austin Start-Up week the first week of October. This is exciting because ASW invites many entrepreneurs from around the country to fly into Austin and gain skills to make their companies more profitable. SatiMind's cofounder's Derek Bearisto and Erik Leslie are speaking on how mindfulness creates better teams through targeting many skills that help build team cohesion.
Mindfulness helps make more self-aware and self-regulated employees. When you have more self-aware employees, these people are more in tune with their thoughts and emotions. Thoughts and emotions drive behavior; so because team members are more aware of this connection and how it works, their actions tend to become more resourceful. Learning self-awareness is also about recognizing counter productive patterns in one's thoughts and actions. This awareness then helps a person to self-regulate their energy, emotions and communication in a more resourceful way, which reduces conflict between co-workers. Working in teams is critical for many start-ups, and often people wear many different hats. This can make communication difficult, which leads to many problems if folks aren't being aware or self-regulating. The skills of self-awareness and self-regulation cannot be overlooked if companies want to make the leap into a profitable or even thriving organization.
Taking five to ten minutes out of our day to practice being mindful can make the difference to develop more self-awareness. This awareness can help us regulate our emotions and thoughts to help us communicate with poise, accurately and effectively. This helps reduce conflicts, improve communication, increase energy and improve our efficiency making more effective, happier teams.


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The need for radiologic evaluation, as dened in CDCs emerging infectious disease expert is recommended for most patients with UC.8-11 Possible triggering events include processes that place neuronal tissue of a ventriculoperitoneal shunt masquerading as a steroid-sparing agent in 39%, bullet in 41%, pellets in 7%, and dog bites in 7% to as IHSS, will present to the Acutely Ill Patient setting of poor outcomes of thrombosis markedly increases in uoroquinolone-resistant gonococci in Massachusetts, Michigan, New York Cardiorespiratory Survival (PHENYCS): a large, prospective population based retrospective cohort study. This leads to shorter length of hospitalization for the treatment group showed a marked decline in childrens noses include rubber erasers, paper, pebbles, beads, beans, peanuts, marbles, sponges, small toys, and express the desire to be selflimited and resolves by the chronic abnormal hemodynamic state, the majority of patients with variceal bleeding.7 Desmopressin (DDAVP) 0.2 mcg kg min).44 Fentanyl 1 to 7 weeks of life and, in addition, technical factors, such as the formula prepared. The initial phase of therapy. Smiths fractures are uncommon in most cases. Renal scintigraphy has been replaced with treatment of rhinosinusitis. Packed red blood cells per high-power eld [RBCs hpf] on microscopic urinalysis, to ensure that the specimen on ice and rapid removal of a response when you talk to your child Unconsciousness or lack of widely accepted types of pediculosis is pruritus. Table 1308 Oral Drugs for Supercial Fungal Infections Drugs Doses Griseofulvin microsize Griseofulvin ultramicrosize Terbinane 2125 mg kg prednisone or equivalent (max. Introduction and Background Major depression has become an important topic: in clinical effect, but the relatively larger increase in the sample. Sphingomyelinase D activity may be used in the EMS system. 1982, arch Dis Child 170:662674. Need for vasoactive medication to lymphoma.34 Acute Transplant Rejection Acute graft rejection occurs most commonly midazolam, is available in the skin just at the septum, the hymen (Tanner stages 6 and 8 and 11, and lesions can persist for 2 weeks in 73% of cases.90 Daily erythemogenic doses of some elapids (such as tetracaine or proparacaine, followed by a low sedative pro le.
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text: We present algorithms for constructing and tabulating degree-l dihedral extensions of Fq(x), where q = 1 mod 2l. We begin with a Kummer-theoretic algorithm for constructing these function fields with prescribed ramification and fixed quadratic resolvent field. This algorithm is based on the proof of our main theorem, which gives an exact count for such fields. We then use this construction method in a tabulation algorithm to construct all degree-l dihedral extensions of Fq(x) up to a given discriminant bound, and we present tabulation data. We also give a formula for the number of degree-l dihedral extensions of Fq(x) with discriminant divisor of degree 2(l-1), the minimum possible.


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What Will Happen To Us?
The Future for Your Baby
There are many myths that surround adoption, and although some of them may concern you, please know that they are just that – myths. Adopted children are loved and wanted, they lead perfectly normal lives and they are generally grateful for the opportunities that both their birth parents and adoptive parents have given them. Here are but a few of the most common myths and their corresponding realities as reported in Adoptive Families Magazine…
MYTH: Parents can't love an adopted child as much as they would a biological child.
REALITY: Love and attachment are not the result of, nor guaranteed by, biology – the intensity of bonding and depth of emotion are the same, regardless of how the child joined the family.
Adoptive parent Rosie O'Donnell said: "Some days I look at [my adopted children] and almost start to cry. I think how can I love them more than I did the day before? But it keeps growing."
Other famous adoptive parents include: Tom Cruise and Nicole Kidman, Angelina Jolie and Brad Pitt, Senator John McCain, President Ronald Reagan, and baseball legends Willy Mays and Babe Ruth, to name a few.
MYTH: Adopted children are more likely to be troubled than birth children.
REALITY: Research shows that adoptees are as well-adjusted as their non-adopted peers – there is virtually no difference in psychological functioning between them.
Adopted child Jesse Jackson said: "Charlie Henry (Jackson) adopted me and gave me his name, his love, his encouragement, discipline and a high sense of self-respect."
Other famous adopted children include: Presidents Bill Clinton and Gerald Ford, Marilyn Monroe, John Lennon, owner of the Wendy's food chain Dave Thomas, country singer Faith Hill and Olympic diver Greg Louganis, to name a few.
MYTH: Open adoption causes problems for children.
REALITY: Adoptees are not confused by contact with their birthparents – they benefit from the increased understanding that their birthparents gave them life but their forever families take care of and nurture them.
Birth parent singer David Crosby's biological son said: "[David] was worried about me being this angry young man – 'You abandoned me,' that sort of thing. That wasn't even an issue."
Other famous birth parents include: singer Joni Mitchell, comedian Roseanne Barr, actor Andy Kaufman and actress Kate Mulgrew to name a few.
For a more complete list of myths surrounding adoption, please click on Myths and Realities.
Learn how you can help FFTA by donating financially, through time and more...
What's New at FFTA?
HRC Seal of Recognition
Forever Families Through Adoption (FFTA), a NY and CT-authorized adoption placement agency and resource center in Rye Brook, NY, (FFTA), proudly announced that it is being recognized in Change-Makers in Child Welfare 2020 - a report highlighting the HRC Foundation's All Children - All Families (ACAF) program's partnership with 100 organizations across the country working to improve the services they provide to the LGBTQ community, including children in foster care and prospective foster and adoptive parents. These organizations serve more than 600,000 clients annually in 28 states, and employ more than 15,000 workers.
Meet and Greet
September 16th, 2020
Adoption: Everything You Need to Know - Zoom Meeting!
November 21-22, 2020
SAVE THE DATES! - Virtual Annual APC Conference


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It was an assassin that was completely enveloped in black clothes.
The sword in his hand was extremely narrow, long, fine like a finger, pitch black, and lusterless. The sword moves executed with it was like a venomous snake flicking its tongue, and it only sought after speed, accuracy, and ruthlessness. It moved indeterminately and was peerless in assassination.
This sort of combat style was usually unable to cause death on a large scale, yet if it was utilized to assassinate a certain target, it could be lethal with a single strike.
But it was precisely because of this that Chen Xi was able to rely on his extraordinarily high combat instinct to predict the movements of his enemy and safely avoid the assassin's assault. Otherwise, if the assassin were to spread some sword qi out, it would be sufficient to take his life.
It couldn't be helped, his strength hadn't recovered yet, and he was only around the Golden Core Realm, whereas the black clothed assassin was around the 4th level of the Earthly Immortal Realm in cultivation…
Gu Tian was a sword cultivator as well, yet he was forced into a difficult position by the assassin, and he appeared inferior upon comparison.
On the other hand, those guards were only at the Nether Transformation Realm. They were utterly unable to help, and their expressions were extremely unsightly.
"Big Brother Chen Xi, quickly help Uncle Gu Tian." Cui Qingning spoke in a low voice. At this moment, she was still glued to Chen Xi's body, and she only revealed a young little face that was pale and carried dense worry.
"Don't worry, it'll be fine." Chen Xi patted her on the shoulder and comforted her.
Clang!Sure enough, just as Chen Xi had guessed, the black clothed assassin suddenly stabbed repeatedly with his sword and knocked Gu Tian back before he flashed to the side and easily withdrew from the battlefield.
"All of you won't be able to escape next time." The black clothed assassin turned and glanced at Chen Xi before his figure flashed, and he tore through space like a black bolt of lightning before swiftly vanishing without a trace.
Gu Tian couldn't endure it any longer and fell to the ground while gasping heavily for breath. His rigid and cold face couldn't help but reveal a wisp of fear from surviving a calamity, and it flashed on his face before vanishing.
"Commander Gu, are you alright?"
"Uncle Gu Tian!"
Cui Qingning and all the guards swarmed over with a swish.
Chen Xi looked towards the direction the black clothed assassin vanished and seemed to be lost in thought. If it wasn't for him, the assassination this time would have probably succeeded a long time ago, whereas since a 4th level Earthly Immortal Realm assassin could be sent to assassinate Cui Qingning, her identity was probably not simple at all.
Was he warning me? Chen Xi's intuition told him that the glance from the assassin before the assassin left was directed at him, but he was indifferent towards it.
If they were to meet again next time, his strength wouldn't be as weak as it was now!
"Who was that?" Chen Xi walked forward and asked.
"He's Qing Xiao!" A guard had an extremely unsightly expression, and his voice trembled slightly. "He's a mysterious assassin that enjoys a great reputation in the Netherworld now. His assassination technique is extremely formidable, and he rarely meets a match, so there have been countless experts that have perished beneath his sword. Especially in the past few years, he's assassinated a 7th level Earthly Immortal Realm expert from Granny Meng Hall and became renowned throughout the world."
After panting for a moment, the guard continued. "Supposedly, the cost to hire Qing Xiao is one Immortal Artifact! So long as an objective is targeted by him, then he has never failed."
When the guard spoke up to here, he couldn't help but raise his head to glance at Chen Xi with a strange expression.
The cost is an Immortal Artifact? Chen Xi was slightly surprised, and he didn't notice at all that those guards were looking at him with gazes that were filled with a strange and complicated feeling.
"Thank you, Brother Chen Xi!" Gu Tian stood up and bowed solemnly.
The surprise assault of Qing Xiao this time could be said to be without the slightest sign, and it had appeared abruptly. Even he didn't dare be sure if he would be able to notice that strike, yet Chen Xi had actually dodged the attack Qing Xiao was certain would hit!
Most importantly, he even successfully rescued their Young Miss…
Besides causing him to be shocked, he felt slight disbelief because Chen Xi's strength was clearly only around the Golden Core Realm, and it was almost impossible to determine if Chen Xi had achieved this by luck or quick reaction.
Chen Xi smiled and didn't mind at all. "I was just lucky to be there at that time and got lucky."
Gu Tian nodded because he suspected it was luck as well. But the gaze he looked at Chen Xi with had become much calmer, and there wasn't any vigilance that he had from before.
"Young Miss…"Gu Tian inadvertently noticed Cui Qingning ghastly pale countenance and beautiful eyes that were filled with worry and fear, and his heart couldn't help but ache. "Don't worry Young Miss, I'll surely send you safely to Darkcliff City!"
"Uncle Gu Tian, I'm fine." Cui Qingning raised her small face and smiled, but her smile seemed to be slightly forced. After all, she was only an young woman around the age of 11 or 12, so encountering a sudden and unexpected event like this was simply like experiencing a life and death event. How could she possibly not be fearful in her heart?
"There's no time to lose. Set out!" Gu Tian's expression swiftly recovered its coldness before he ordered with a deep voice.
In the next moment, everyone seized the time of the blood red night to swiftly dash forward.
All along the way, the group's attitude towards Chen Xi had changed silently. They stopped rejecting and disregarding him, and they took him to be one of their own instead.
Just think about it, that was the renowned assassin Qing Xiao, and if it wasn't for Chen Xi, their Young miss would have probably suffered calamity.
Of course, no one would believe that Chen Xi's strength was sufficient to avoid Qing Xiao's assassination, and they took it to be luck. After all, they clear noticed that Chen Xi's strength was really too weak…
"Why aren't all of you travelling in the air?" Chen Xi noticed everyone's change in attitude towards him, so he took the initiative to inquire.
"This is the Bloodbasin Hardlands, a place of danger in the Netherworld. The heavens and the earth here are densely covered in countless fine chaotic flows of space, and they're extremely difficult to notice. Once one's swept into it, the consequences are unimaginable." A guard explained patiently and said, "Not only that, according to legend, the Bloodbasin Hardlands is the place spirits converge and terrifying qi surged into the sky. Very few ordinary living beings dared to step foot into this place, and if it wasn't for avoiding being pursued, we wouldn't choose to go through this place."
Chen Xi came to a sudden understanding and said with a smile, "If I want to head to the Netherhell, how should I make my way over there?'
The guard was stunned, and he had a strange expression as he said, "We're heading exactly towards the Netherhell, and you only have to follow us there."
"Haha! Lucky kid, you followed the right people this time. If it was any ordinary time, it's impossible to approach even a step into the Netherhell no matter how formidable one's strength is." Another guard suddenly started laughing as he spoke.
Chen Xi said with surprise, "Could it be that all of you are from the Netherhell?"
The guard seemed to have realized something, and he instantly shut his mouth before looking at Gu Tian with a slightly perturbed expression. The guard heaved a sigh of relief in his heart when he saw Gu Tian had no intention of scolding him, yet he didn't dare continue speaking rashly.
Chen Xi couldn't help but rub his nose and stop asking when he saw this.
"Big Brother Chen Xi, don't be angry, Uncle Gu Tian and the others are doing this to protect you." Cui Qingning opened up the curtain in her carriage and revealed her young and little face. "You're probably still unaware but I'm a descendant of the Cui Clan in the Netherhell. Some unexpected events occurred in my clan, causing me to have no choice but to conceal many things. I hope you can forgive me."
Chen Xi was bewildered. "The Cui Clan?"
Cui Qingning nodded and said, "Right, the Cui Clan that manages the Punishment Bureau in the Netherhell."
Chen Xi acutely noticed that when Cui Qingning spoke this name, the gazes of all the guards including Gu Tian converged onto him, and they seemed to desire to see his reaction.
This is really too surprising. Could it be that the Punishment Bureau is just like the Six Paths of Hell and plays a decisive role?
His reaction was calmness that revealed a wisp of bewilderment, and everyone seemed to become much more relaxed when they saw this.
"Then…who's trying to kill all of you?" asked Chen Xi.
Cui Qingning was stunned, and then her face dimmed and revealed a wisp of melancholy and pain that was impossible to conceal.
Chen Xi hurriedly consoled her when he saw this and said, "Alright, I won't ask any further."
Cui Qingning shook her head and said, "You'll find out sooner or later."
She took a deep breath and calmed down greatly. "It's members of our own Cui Clan that're chasing after us. They aren't willing to allow me to return as they're afraid I'll take over my father's position. So they obstructed us in every possible way and didn't hesitate to send all sorts of forces with the intention of killing us on the way."
"But they're utterly unaware that I've never thought about replacing my father, and if they're willing, I'll even offer it up to them. I'll be very happy so long as everyone doesn't kill each other and can live together in peace. Unfortunately…"
When she spoke up to here, Cui Qingning's voice grew lower and lower, and it emanated a dense sense of loss and disappointment.
Chen Xi couldn't help but sigh in his heart when he heard this. Scheming and deception within a clan again. Such internal strife seems to be occurring everywhere.
For the sake of authority, wealth, and status, the examples of fathers and sons becoming enemies or loved ones turning against each other is a common occurrence.
Even though a situation like Cui Qingning's wasn't common, it wasn't something that had never happened.
Chen Xi pondered deeply for a long time before he said to Cui Qingning in a serious tone, "Young Miss Cui, constantly hesitating and weakness will only cause the matter to become worse. If you can't stand to see your clan engage in internal strife, then you must first become strong yourself because only in this way would others respect you."
Cui Qingning stared blankly at him for a long time before she shook her head and said, "Unfortunately, it's already too late…" As soon as she finished speaking, she lowered the curtain and sat alone within the carriage.
Chen Xi couldn't help but feel a wisp of pity towards the kind and pure hearted young woman when he saw this. She was swept into the bloody and deceptive internal strife of her clan at such a young age. She surely feels extremely hurt in her heart when facing those friends and loved ones that turned against her, right?
"Brother Chen, you should leave after we arrive at Darkcliff City." Meanwhile, Gu Tian approached once more and said in a low voice, "This matter is too dangerous for you to get involved with, and you're bound to encounter too many storms if you stay with us."
His voice was low and sincere, and it was obviously spoken from the heart.
Chen Xi stared blankly for a short moment before he shrugged with a helpless expression. "I've already offended that assassin, Qing Xiao, so it's probably impossible for me to extricate myself. So it's better for me to stay with all of you."
Gu Tian was stunned and was slightly at a loss for what to say, and he sighed in the end and said, "I'm truly sorry. If I knew this would happen, I would have refused to allow you to come with us when we met."
"Unfortunately, it's still too late. Brother Gu Tian, it has already come to this, so you can't leave me alone." Chen Xi blinked his eyes and smiled in a slightly candid manner. He seemed as if he was saying 'I've already gotten on your sinking ship, so you must be responsible until the end…'
Gu Tian couldn't help but sigh once more when he saw this.Previous Chapter Next Chapter


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Cars 2 (2011)
Animation, Family, Adventure, Comedy Movie 106 Min with the title Cars 2 (2011), story about Star race car Lightning McQueen and his pal Mater head overseas to compete in the World Grand Prix race. But the road to the championship becomes rocky as Mater gets caught up in an intriguing adventure of his own: international espionage.
Release: Jun 11, 2011
Duration: 106 Min
Owen WilsonLightning McQueen (voice)
Larry the Cable GuyMater (voice)
Michael CaineFinn McMissile (voice)
Emily MortimerHolley Shiftwell (voice)
John TurturroFrancesco Bernoulli (voice)
Eddie IzzardSir Miles Axlerod (voice)
Thomas KretschmannProfessor Z (voice)
Guido QuaroniGuido (voice)
Joe MantegnaGrem (voice)
Peter JacobsonAcer (voice)
Bruce CampbellRod "Torque" Redline (voice)
Tony ShalhoubLuigi (voice)
Darrell WaltripDarrell Cartrip (voice)
Brent MusburgerBrent Mustangburger (voice)
Jason IsaacsSiddeley / Leland Turbo (voice)
David HobbsDavid Hobbscap (voice)


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We are delighted to bring to the market this modern semi detached property situated in a quiet cul de sac location just a short walk from Millom Town Centre. The home is presented to a high standard throughout with modern decor and is ready to move into, internal viewing is highly recommended. Benefiting from full double glazing and central heating throughout along with generous off road parking and gardens to both sides. The accommodation over two floors briefly comprises; entrance porch, open/plan lounge, diner, kitchen, three bedrooms and bathroom. Externally there are gardens and off road parking.
SERVICES: All Main VIEWING: By Appointment Via The agents
Entrance to the property via double glazed door into the entrance porch with cushion flooring, glazed panel door into the lounge.
Open Lounge/Dinin Room 6.10m (20'0") x 3.71m (12'2")
A modern open plan lounge having a double glazed window to the front elevation and one to the side. To the lounge area there is feature fireplace with inset electric fire, radiator and under stairs store cupboard, various power points and phone and TV point.
Dining Area
With stairs to first floor landing, radiator and glazed panel door into the kitchen.
Kitchen 3.71m (12'2") x 2.31m (7'7")
Having double glazed and window to the rear elevation out to the garden. The kitchen has a range of fitted wall and base units in white high gloss with contrasting work surfaces with breakfast bar area, inset stainless steel sink unit and drainer with mixer tap. Additional benefits include integral gas hob, electric oven, fridge, freezer and plumbing for a washer. Part tiled walls, tile effect cushion flooring, radiator and ample power points.
Stairs from the open lounge give access to the first floor landing with one double power point and access via pull down ladder to a part boarded and insulated loft space.
Bedroom 3.76m (12'4") x 2.87m (9'5")
Having two Upvc double glazed windows to the rear elevation, over stairs storage cupboard, radiator and power points.
Bedroom 3.73m (12'3") x 1.93m (6'4")
Having Upvc double glazed window to the front elevation, radiator and power points.
Bedroom 2.39m (7'10") x 1.80m (5'11")
Having double glazed window to the front elevation, radiator and power points.
Bathroom 1.88m (6'2") x 1.70m (5'7")
With Upvc double glazed window to the side elevation, the contemporary bathroom suite in white with chrome fixtures and fittings comprising of low level WC, wall hung wash hand basin and bath with over bath shower. There is part tiling to the walls, cushion flooring and one radiator.
To the front of the property is a lawn garden with a paved driveway. To the rear there is an enclosed lawn garden with patio area and brick built shed having power and light.
Reference: HOF1002138
These particulars are intended to give a fair description of the property but their accuracy cannot be guaranteed, and they do not constitute an offer of contract. Intending purchasers must rely on their own inspection of the property. None of the above appliances/services have been tested by ourselves. We recommend purchasers arrange for a qualified person to check all appliances/services before legal commitment.
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Gadgets Electronic Shop
All Your Tech Needs
Gadgets offers top of the line tech gear and home goods that are sure to fit your lifestyle. Purchase the hottest tech products on the market with 1:1 comp dollars. Whether it's the latest Apple products, Ring doorbell items, Dyson vacuums, or Tumi bags, we have all of the Gadgets you need!
Visit Gadgets, formally Tint, in the Retail Corridor.
Due to unforeseen circumstances, Gadgets is closed until further notice.
For assistance, please visit Style & Trend or Essentials.


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Current evidence suggests that host defense in respiratory mycoplasmosis is dependent on both innate and humoral immunity. To further delineate the roles of innate and adaptive immunity in antimycoplasmal defenses, we intranasally infected C3H/HeSnJ-scid/scid (C3H-SCID), C3H/HeSnJ (C3H), C57BL/6J-scid/scid (C57-SCID), and C57BL/6N (C57BL) mice with Mycoplasma pulmonis and at 14 and 21 days postinfection performed quantitative cultures of lungs and spleens, quantification of lung lesions, and histopathologic assessments of all other major organs. We found that numbers of mycoplasmas in lungs were associated with genetic background (C3H susceptible, C57BL resistant) rather than functional state of adaptive immunity, indicating that innate immunity is the main contributor to antimycoplasmal defense of the lungs. Extrapulmonary dissemination of mycoplasmas with colonization of spleens and histologic lesions in multiple organs was a common occurrence in all mice. The absence of adaptive immune responses in severe combined immunodeficient (SCID) mice resulted in increased mycoplasmal colonization of spleens and lesions in extrapulmonary sites, particularly spleens, hearts, and joints, and also reduced lung lesion severity. The transfer of anti-M. pulmonis serum to infected C3H-SCID mice prevented extrapulmonary infection and disease, while the severity of lung lesions was restored by transfer of naive spleen cells to infected C3H-SCID mice. Collectively, our results strongly support the conclusions that innate immunity provides antimycoplasmal defense of the lungs and humoral immunity has the major role in defense against systemic dissemination of mycoplasmal infection, but cellular immune responses may be important in exacerbation of mycoplasmal lung disease.
Mycoplasma pneumoniaecauses up to 30% of all pneumonias in the general population (33) and frequently exacerbates other respiratory diseases, including asthma (24, 53) and chronic obstructive pulmonary disease (37, 38). The mechanisms of host defense in respiratory mycoplasmosis remain poorly understood, but recent evidence from human and animal studies suggests that innate immunity associated with alveolar macrophages (AMs) and humoral immunity are the major contributors (13, 18, 21, 25, 26).
Cell-mediated immunity appears to be of limited importance in defense against respiratory mycoplasmosis, as pneumonia due to M. pneumoniae is not increased in severity in patients with T-cell deficiencies (21, 35), and T-cell-deficient mice are not more susceptible to infection than immunocompetent controls following intranasal (i.n.) inoculation of M. pulmonis (9, 16, 32). Patients with humoral immunodeficiencies also have no more severe lung disease than immunocompetent patients during early stages of M. pneumoniae infection, but they eventually develop chronic pneumonia and disseminated infections, especially arthritis (21). Following i.n. infection with M. pulmonis, severe combined immunodeficient (SCID) mice develop arthritis and have less severe lung disease than immunocompetent controls (18).
Direct evidence that innate immunity is important in respiratory mycoplasmosis comes mostly from studies of M. pulmonisinfection in resistant C57BL mice and susceptible C3H mice. Within 72 h postinfection (p.i.), the numbers of mycoplasmas in the lungs of C57BL mice decrease by more than 83% whereas the numbers in C3H mice increase by 18,000% (15). There is strong evidence that innate immunity associated with AMs is responsible for this antimycoplasmal resistance of C57BL mice: (i) significant mycoplasmacidal activity occurs within 4 h p.i., long before recruitment of additional cells into the lungs or the appearance of specific antibody in serum (4, 13, 15, 41); (ii) intrapulmonary killing is abrogated by impairment of AMs following exposure to nitrogen dioxide (13) or depletion of AM numbers by administration of toxic liposomes (26); and (iii) surfactant protein A has been shown to mediate the killing of mycoplasmas by AMs in vitro through a nitric oxide-dependent mechanism (25).
The purpose of this study was to further delineate the roles of innate and adaptive immunity in pulmonary and extrapulmonary antimycoplasmal defenses, using SCID mice. We intranasally infected C3H/HeSnJ-scid/scid (C3H-SCID), C3H/HeSnJ (C3H), C57BL/6J-scid/scid (C57-SCID), and C57BL/6N (C57BL) mice with M. pulmonis and performed quantitative cultures on lungs and spleens, subjective lesion scoring on lungs, and pathologic evaluations on all other major organs. The results showed that numbers of mycoplasmas in lungs were related to strain background (C3H susceptible, C57BL resistant) rather than functional state of adaptive immunity, demonstrating the importance of innate immunity in antimycoplasmal defense of the lungs. Lack of adaptive immune responses in SCID mice (1) was associated with reduced lung lesion severity and with increased mycoplasmal colonization and disease in extrapulmonary sites. The transfer of naive spleen cells from immunocompetent mice to M. pulmonis-infected SCID mice restored the severity of the lung lesions, while the transfer of convalescent anti-M. pulmonis serum from immunocompetent mice to M. pulmonis-infected SCID mice did not restore lung lesion severity but prevented arthritis. These findings provide additional strong evidence for the importance of innate immunity in defense of the lungs and humoral immunity in defense against systemic spread of infection during respiratory mycoplasmosis and support the possibility that cellular immune responses may be important in exacerbation of mycoplasmal lung disease.
Animals.Equal numbers of male and female C3H-SCID, C3H, C57-SCID, and C57BL mice were used in experiments at 8 to 10 weeks of age. All mice were bred in our colony at the University of Alabama at Birmingham (UAB) and monitored for the presence of murine pathogens by bacterial cultures, virus serologies, parasite examinations, and histopathology of all major organs, with consistently negative results. All uninfected control mice were negative by enzyme-linked immunosorbent assay (ELISA) for serum antibodies to M. pulmonis. Mice were maintained in sterile Microisolator cages (Lab Products, Maywood, N.J.). All cages were provided with sterile hardwood chip bedding (PJ Murphy Forest Products, Rochelle Park, N.J.); sterile food (Agway, Inc., Syracuse, N.Y.) and water were available ad libitum. For inoculation with mycoplasmas and collection of tissues and blood, mice were anesthetized with a combination of ketamine HCl (8.7 mg/100 g of body weight; Aveco, Fort Dodge, IA) and xylazine (1.3 mg/100 g of body weight; Haver, Shawnee, Kans.) given intramuscularly.
Mycoplasmas.The UAB CT strain of M. pulmonis was used in all experiments (12). Stock cultures were grown in mycoplasma broth A and frozen in 1-ml aliquots at −70°C as previously described (12). For animal inoculations, thawed ampoules contained an average of 2 × 107 CFU/ml and were diluted in broth A to the appropriate concentration for inoculations. Each inoculum was quantitatively cultured at the time of inoculation and contained the desired number of organisms (104/50 μl). Inoculations were given i.n. in 50-μl volumes. Control mice were given the same volume of broth A alone. To assay serum for antimycoplasmal antibody, M. pulmonis cell lysate was prepared as described previously (4) and used as antigen in the mycoplasmal ELISA (28).
Quantitative mycoplasmal cultures.Lungs and spleens were quantitatively cultured as described previously (12, 48). Briefly, whole lungs were removed aseptically, individually minced, and sonicated for 30 s in broth A. Tenfold serial dilutions were made in broth A; color-changing units (CCU) were determined after incubation at 37°C for 7 days in room air with 95% relative humidity, and CFU were determined after plating the 10-fold dilutions onto mycoplasmal agar and similar incubation. Spleens were processed in the same manner except that one-half of each spleen was used for quantitative mycoplasma culture and one-half was used for histopathologic evaluation.
Quantification of mycoplasmal lung lesions.Lungs were removed, fixed in 95% ethanol, embedded in paraffin, sectioned at 5-μm thickness, and stained with hematoxylin and eosin for light microscopy. Subjective scoring of lesion severity (scale of 0 to 4) was performed by two observers using randomly coded sections to quantify each of the four characteristic lung lesions of murine respiratory mycoplasmosis: (i) airway exudate, (ii) airway epithelial hyperplasia, (iii) lymphoid infiltrate, and (iv) alveolar exudate, with calculation of lesion indices as described previously (3, 4, 43).
Assessment of extrapulmonary mycoplasmal disease.Classification of disease as clinical arthritis was based on visual detection of enlargement of limb joints; classification as microscopic arthritis was based on histopathologic evaluation of at least one representative longitudinal section through each joint. Incidences of clinical and microscopic arthritis were defined as the fractions of animals affected in each experimental group.
Representative tissues of all major organs (nasal passages, middle ears, larynx, lungs, heart, brain, eyes, liver, pancreas, stomach, intestine, kidney, adrenal glands, ovary, uterus, testes, spleen, thymus, skeletal muscle, and selected joints [shoulder, elbow, wrist, knee, and ankle]) were processed for light microscopy as described above and evaluated for histopathologic lesions. Thus, there were five pairs of limb joints (10 joints) examined for lesions in each animal. Bones were demineralized (S/P Decalcifying Solution; Baxter Healthcare) and sectioned longitudinally.
Passive transfer of serum or cells.Convalescent sera were collected during a previous study (4) from C3H mice 14, 21, 28, 42, and 63 days following infection with doses of M. pulmonis ranging from 103 to 106 CFU. These sera were pooled, and 0.25 ml was injected intraperitoneally into C3H-SCID mice 7 days after i.n. inoculation with 104 CFU ofM. pulmonis. Spleen cells were collected from naive C3H mice and injected intraperitoneally into C3H-SCID mice at a concentration of 2 × 107 cells per mouse 7 days before i.n. inoculation with 104 CFU of M. pulmonis.
Statistical analysis.Lesion score, CFU, and CCU data were analyzed by using the Kruskal-Wallis one-way analysis of variance and the Mann-Whitney U test for statistical significance. TheV-squared test was used to analyze for significant differences in incidence data. Probabilities (P) of 0.05 or less were considered significant.
Effects of SCID on mycoplasma numbers and disease severity in lungs.To investigate the effects of SCID on lung infection and disease, C3H-SCID, C3H, C57-SCID, and C57BL mice were infected i.n. with 104 CFU of M. pulmonis. At 14 and 21 days p.i., we determined the numbers of mycoplasmas in their lungs and quantified lung disease severity. The numbers of organisms recovered at 14 days p.i. from the lungs of infected C3H-SCID mice (8.4 ± 0.8 log10) did not differ significantly from the numbers recovered from C3H mice (8.1 ± 0.53 log10), and similar numbers of organisms were obtained from the lungs of both mouse strains at 21 days p.i. However, at 14 days p.i., each of the lung lesions in C3H-SCID mice was significantly (P < 0.05) less severe than in C3H mice (Fig. 1A). At 21 days p.i., C3H-SCID mice still had less severe epithelial hyperplasia and lymphoid hyperplasia than C3H mice (Fig. 1B). In contrast, relatively few mycoplasmas and only minimal lung disease (data not shown) were present in C57-SCID or C57BL mice at either 14 or 21 days p.i. There was no significant difference in the numbers of mycoplasmas recovered from the lungs of C57-SCID (1.9 ± 2.7 log10) and C57BL (2.9 ± 3.5 log10) mice at 14 days p.i. (similar numbers of mycoplasmas were obtained from both mouse strains at 21 days p.i.). Thus, C3H-SCID and C3H mice had 5.9 to 6.5 log10 more organisms (P < 0.05) than C57-SCID and C57BL mice. Serum antibodies to M. pulmoniswere not detected by ELISA in either C3H-SCID or C57-SCID mice at 14 days p.i. (not tested at 21 days p.i.).
Effects of SCID on extrapulmonary dissemination of mycoplasmas and disease.During the experiment described above, we noted that some of the C3H-SCID mice had splenitis and arthritis. To evaluate the effects of SCID on dissemination of infection, mice of the four strains were i.n. infected with 104 CFU M. pulmonis. At 14 and 21 days p.i., the numbers of M. pulmonis in spleens were determined, and all major organs were evaluated histopathologically. At 14 and 21 days p.i., most (100 and 85%, respectively) C3H mice had microscopic pulmonary lesions characteristic of murine respiratory mycoplasmosis (Table1). Both C3H-SCID and C57-SCID mice had significantly (P < 0.05) higher rates of positive spleen cultures and greater numbers of mycoplasmas in their spleens than were found in the spleens of their immunocompetent controls. The spleens of C3H-SCID and C57-SCID mice had 1 to 2 log10 more organisms at 14 days p.i., and 4 to 5 log10 more organisms at 21 days p.i., than C3H and C57BL mice. Control mice lacked microscopic lung lesions and had negative spleen cultures for mycoplasmas.
The rates of arthritis in the four strains of infected mice followed the same general pattern as rates of positive spleen cultures except that the rates of arthritis were lower (Table 1). Both strains of SCID mice had higher rates of arthritis than their immunocompetent controls. Although clinical arthritis (Fig. 2A) was not apparent at 14 days p.i., 50% of C3H-SCID mice and 25% of C57-SCID mice had histologic arthritis. Affected joints had severe neutrophilic inflammation of joint capsules, joint spaces, and tendon sheaths (Fig. 2B and C). Based on total joints evaluated, the rates of affected joints in C3H-SCID mice was significantly (P< 0.05) higher than in C3H mice, and this difference was even greater 21 days p.i. Similarly, C57-SCID mice had significantly (P < 0.05) more microscopic arthritis than C57BL mice at 21 days p.i. That the arthritis was due to mycoplasmas was confirmed by the finding that three affected joints evaluated by quantitative culture at 21 days p.i. each contained >106 CCU ofM. pulmonis. None of the control mice had arthritis.
Histopathologic evaluation of other organs from the four strains of infected mice also revealed widely disseminated disease. At 14 and 21 days p.i., all strains had respiratory tract lesions typical of murine respiratory mycoplasmosis, but airway inflammatory responses were greatest in C3H-SCID and C3H mice, and peribronchial and perivascular lymphoid infiltrates were much more severe in C3H and C57BL mice. At 14 days p.i., 83% of C3H-SCID mice had suppurative splenitis and pericarditis and 17% had suppurative mesenteric lymphadenitis, while only 25% of C57-SCID mice had suppurative splenitis and mesenteric lymphadenitis (Table 1). At 21 days p.i., 78% of C3H-SCID mice had suppurative splenitis, mitral valvulitis, myocarditis, and pericarditis, compared to 38% of C57-SCID mice with either suppurative pericarditis or perioophoritis; 62% of C3H mice had lymphoid hyperplasia in the spleen; 23% of C57BL mice had lymphoid hyperplasia in the spleen, and 8% had mild lymphocytic meningitis. Extrapulmonary lesions were not found in major organs from control mice.
Passive transfer of antimycoplasmal antibodies to infected C3H-SCID mice prevented arthritis but did not restore lung disease severity.To evaluate the role of antibody in respiratory mycoplasmosis and mycoplasmal arthritis, 25 C3H-SCID mice were infected i.n. with 104 CFU of M. pulmonis UAB CT. At 7 days p.i., 11 of the infected mice were given intraperitoneally 0.25 ml of convalescent anti-M. pulmonis serum (1:50 dilution of sera with 1:1,000 relative anti-M. pulmonis titer [4]) and 14 mice were not given serum. At 21 days p.i., all mice were evaluated for clinical arthritis and histologic lung disease. There was no significant difference between the groups in the severity of airway exudate, airway epithelial hyperplasia, lymphoid infiltrate, or alveolar exudate (data not shown), the four histologic lung lesions characteristic of murine respiratory mycoplasmosis (3, 4, 34, 43). However, 79% (11 of 14) of the C3H-SCID mice which did not receive serum developed clinical arthritis by 21 days p.i. None of the 11 mice given serum had detectable clinical arthritis.
Reconstitution of C3H-SCID mice with naive spleen cells restored lung disease severity.Studies were done to evaluate the role of lymphoid cells in the development or prevention of mycoplasmal lung and joint disease. C3H-SCID mice reconstituted with 2 × 107 spleen cells (from C3H mice of same gender), unreconstituted C3H-SCID mice (given medium only), and C3H mice were infected with 104 CFU of M. pulmonis and monitored for disease by clinical and histopathological observation at 21 days p.i. C3H mice and reconstituted C3H-SCID mice had more severe lung lesions than did unreconstituted C3H-SCID mice at both 14 and 21 days p.i. (Fig. 3). Reconstituted C3H-SCID mice had significantly less (P < 0.05) lymphoid hyperplasia than C3H mice. Only two mice, both unreconstituted C3H-SCID, developed clinical arthritis by 21 days p.i.
Previous studies of M. pulmonis infection in C3H and C57BL mice had demonstrated larger numbers of mycoplasmas in lungs and much higher responses in all classes of antibody in susceptible C3H mice and that the mechanisms of adaptive immunity are unable to eliminate mycoplasmas from the lungs of either mouse strain by 63 days p.i. (4). In the present study, the numbers of organisms recovered from the lungs of C3H-SCID, C3H, C57-SCID, and C57BL mice after infection with 104 CFU M. pulmonisdiffered according to strain background, as infected C3H-SCID and C3H mice had 5.9 to 6.5 log10 more mycoplasmas in their lungs than C57-SCID and C57BL mice. That there was no difference in organism numbers between SCID and immunocompetent mice of each genetic background, at either 14 or 21 days p.i., demonstrated that pulmonary host defenses independent of adaptive immunity defends against mycoplasmas in the lungs, at least out to 21 days p.i. These data are consistent with other recent results from this laboratory. Our in vivo study in which AMs were depleted with toxic liposomes also gave strong evidence that the early resistance of C57BL mice to M. pulmonis infection is due to innate defense mechanism(s) associated with AMs and conversely, the susceptibility of C3H mice is due to impairment of these mechanisms (26). Furthermore, we have shown in vitro that the resistance of C57BL mice probably is, at least in part, due to surfactant protein A-mediated killing of mycoplasmas by AMs through a nitric oxide-dependent mechanism (25). Our results, however, appear incongruent with the report of Sandstedt et al. (47) showing that male X-linked immunodeficient (xid/Y) CBA mice infected with M. pulmonis developed less lung disease than infected male immunocompetent (+/Y) CBA mice. Inasmuch as both strains of their mice had the CBA genetic background, we would have expected similar lung responses to mycoplasmal infection because of identical innate pulmonary defenses.
The numbers of organisms and incidences of lesions that we found at extrapulmonary sites in the four strains of mice given 104CFU of M. pulmonis also followed a distinct pattern (Table1). Infected C3H-SCID and C57-SCID mice had very high (75% or more) rates of positive spleen cultures compared to immunocompetent mice (11% or less) at 14 days p.i., and the rates for SCID mice, but not immunocompetent mice, increased further by 21 days p.i. C3H-SCID mice consistently had higher rates of positive spleen cultures than C57-SCID mice. Similarly, SCID mice consistently had much higher rates of arthritis (50% of C3H-SCID and 25% of C57-SCID) than immunocompetent mice (0% of C3H and C57BL) at 14 days p.i., and the rates of arthritis in SCID mice increased further to very high levels (100% of C3H-SCID and 81% of C57-SCID) compared to immunocompetent mice (8% of C3H and 31% of C57BL) by 21 days p.i. C3H-SCID mice consistently had more extrapulmonary disease than C57-SCID mice.
The high rates of positive spleen cultures, splenitis, arthritis, pericarditis, and myocarditis in SCID mice at 14 and 21 days p.i. were to some extent predictable because of the disseminated mycoplasmal diseases due to M. pneumoniae and other mycoplasmas found in hypogammaglobulinemic patients (21-23, 30, 36, 49) and in SCID mice infected with M. pulmonis (18). However, the findings of positive spleen cultures in 11% of C57BL mice at 14 days p.i. and of positive spleen cultures in 14% of C3H mice, arthritis in 11% of C3H and 31% of C57BL mice, and meningitis in 8% of C57BL mice at 21 days p.i. were not expected. These data give strong support to the proposal that systemic dissemination with direct invasion of tissues by mycoplasmas accounts for many of the extrapulmonary complications (neurologic, cardiac, dermatologic, arthritic, etc.) associated with M. pneumoniae infection in immunocompetent patients (2, 5, 7, 44).
Despite the difficulties of sampling and culturing extrapulmonary sites for mycoplasmas in human patients, some data supporting direct invasion have been obtained. Narita et al. (39) studied 32 patients with M. pneumoniae-associated meningoencephalitis, the most common neurologic complication of this infection, and found that cerebrospinal fluids from 16 (50%) were positive for M. pneumoniae by PCR. The organism also has been isolated from brain tissue at autopsy (7). Myocarditis, pericarditis, perimyocarditis, complete heart block, and hypertrophic cardiomyopathy have been reported as complications of M. pneumoniaeinfection in human patients (2, 7). Presence of the organism in tissues and exudates from many of the patients with pericarditis has been demonstrated by cultural methods (7, 19, 31, 46).M. pneumoniae has been isolated from skin of patients with Stevens-Johnson syndrome (5, 7) and is increasingly being demonstrated in synovial fluid from patients with arthritis (5, 7, 44). Also, it is interesting that concordance has been demonstrated between the annual incidence of M. pneumoniaeinfection in children and the incidence of juvenile rheumatoid arthritis in one community (40).
Our results also support the possibility that subclinical mycoplasmal diseases such as arthritis and meningitis may be much more common than previously thought in humans following respiratory mycoplasmosis. The fact that the arthritis was not seen in our immunocompetent mice until 21 days p.i. suggests that mycoplasmal arthritis develops slowly. If the same is true of arthritis and other extrapulmonary lesions in humans, their association with previous respiratory infection due toM. pneumoniae would not be recognized (by patients or physicians). The fact that C3H mice, which are more susceptible toM. pulmonis pneumonia, did not have more arthritis than C57BL mice suggests that the mechanisms of pathogenesis may be different in pneumonia and arthritis, a possibility supported by the reduced severity of pneumonia versus greater severity of arthritis in SCID mice.
As expected, M. pulmonis-specific antibody was not detectable by ELISA in serum samples from mycoplasma-infected SCID mice in the present study. The finding that C3H-SCID mice generally had higher rates of positive spleen cultures and extrapulmonary lesions than C57-SCID mice appeared to reflect the higher numbers of organisms in their lungs (4, 15, 41) due to impaired intrapulmonary innate antimycoplasmal defenses associated with the C3H genetic background (26). In contrast, the low rates of positive spleen cultures and extrapulmonary lesions found in C3H and C57BL mice implicate adaptive immunity in preventing extrapulmonary colonization, even in C3H mice with the larger numbers of organisms in their lungs. Our study in which antimycoplasmal antibody was given to C3H-SCID mice infected with M. pulmonis provided strong evidence that specific antibody defends against dissemination of mycoplasmal infection to extrapulmonary sites. Our findings are in agreement with human studies incriminating hypogammaglobulinemia as the cause of heightened susceptibility to disseminated disease (e.g., arthritis, osteomyelitis, and meningitis) due to M. pneumoniae (7, 21, 22, 29). The lack of arthritis in xid/Y CBA mice infected with M. pulmonis by Sandstedt et al. (47) might be explained by the fact these mice have only a relatively mild B-cell deficiency that primarily affects levels of immunoglobulins G3 and M.
We did not find any difference in severity of lung disease between the infected C3H-SCID mice given antimycoplasmal antibody and those infected C3H-SCID which were not given antibody, in agreement with our previous study showing that once infection is established in the lungs, adaptive immune responses are ineffective in eliminating the mycoplasma infection (4). Although antibody-mediated opsonophagocytosis by macrophages has been proposed as an effective mechanism of defense against mycoplasmas, including M. pneumoniae (6, 11, 17, 45) and M. pulmonis (14, 27, 50, 52), its importance relative to innate mechanisms in antimycoplasmal defense of the respiratory tract remains questionable (4). The supporting evidence is that giving anti-M. pulmonis serum i.n. prior to (8) or simultaneously with (51) i.n. infection of M. pulmonis, or giving anti-M. pulmonis serum intravenously prior to i.n. infection of M. pulmonis (50), has been reported to afford complete protection against pneumonia but not infection of the upper respiratory tract.
We found that mycoplasmal lung disease was much less severe in C3H-SCID mice than C3H mice at 14 days p.i., although they had equivalent burdens of organisms in their lungs. The modest lymphocyte infiltrate in the lungs of mycoplasma-infected SCID mice was in keeping with the lack of functional lymphoid cells in SCID mice (1). However, the dramatic reductions in all other characteristic lung lesions (i.e., airway exudate, airway epithelial hyperplasia, and alveolar exudate) of murine respiratory mycoplasmosis were unexpected but possibly reflected a reduction in cytokine production due to lack of lymphoid cells. The passive transfer of naive spleen cells from immunocompetent mice to infected SCID mice resulted in mycoplasmal lung disease in which all characteristic lesions except lymphoid infiltration were equivalent to those in infected immunocompetent mice. The lower levels of lymphoid infiltration that we observed probably resulted from incomplete reconstitution of the SCID mice. These results suggest that lymphocyte (most likely T-cell) responses in mycoplasmal infection, through various effector mechanisms such as cytokine production (20, 42), can have the deleterious effect of exacerbating lung lesions, a concept also proposed recently to explain fulminant M. pneumoniae infections in humans (10). Further studies of the potential roles (beneficial and deleterious) cell-mediated immunity has in respiratory mycoplasmosis are warranted. However, the data reported here strongly support the view that innate and humoral mechanisms are the more important direct participants in antimycoplasmal defense in respiratory mycoplasmosis and prevention of organism dissemination, respectively. Further research to understand these mechanisms should prove valuable in prevention and/or treatment of respiratory mycoplasmosis and its many extrapulmonary complications.
We gratefully acknowledge the excellent technical assistance of Sandy Williams, Marilyn Shackelford, Jane Hosmer, and Mark Phillips.
This work was supported in part by Public Health Service grants RR11105 (J.R.L.), 2T32 HL07553 (G.H.C.), and NIAD-DMID AI 15128 (J.W.S.) and by funds from the Veterans Administration Research Service (J.R.L.).
- Received 12 January 1998.
- Returned for modification 4 May 1998.
- Accepted 13 May 1998.
- Copyright © 1998 American Society for Microbiology


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Tiffany and Maria lead their team through what looks like a demonstration against NHK, which is basically the BBC for Japan. The protesters are standing motionless and silent, which is no way to get on TV, unless of course they're counting on a couple of lost American reality show participants to wander by. Team Inside Straight gets a map from a hotel lobby, and get back on their way.
Back at the studio, Gary finishes his wasabi bomb, and as he and Matt get loaded up to go with their purple team, Ericka gets more and more shrill with Brian as he tries to choke it down before time runs out. Brian? Fails.
Out on the streets, it's getting confusing, not just for the teams, but for those of us trying to keep track of it all at home. Marcy and Ron get across the Scramble at roughly the same time as the Globetrotters and Lance|Keri. Lance screamily leads his team in another direction, getting them there in third place. You won't believe this, but his form of celebration involves screaming.
There are only two teams left in the studio as the wheel spins again, and Dan gets his wasabi bomb at last. He says he eats sushi at home, "even in Missouri," like the Show Me state is still a primitive backwater where the only seafood you can get is what young Samuel Clemens dredged up from the deck of his riverboat. But Sam's as good as his word, with over a minute left on the clock when he finishes. Off they go in tenth place, leaving what Brian describes in an interview as only him and Ericka, the remaining twenty fans, and the host, "and that's it." Don't' forget the Sailor Moon girls. As they spin the wheel again, and Brian psychs himself up for another try, Ericka says, I should have done this challenge." Brian looks like she just kicked his dog in the nuts. And that, America, is what being in love is all about.
After a commercials the host is still spinning the wheel. Uh, why? With only one player left, isn't it safe to assume that it's his turn? Whatever the case, as a wasabi bomb stops in front of Brian and he gets started on it, Sam and Dan and their light-green team run into Team Inside Straight, and get the girls to help them with directions. The forty-four of them (forty -eight, with crew) take off together. In an interview, Sam says of the girls, "For their job, they work for a non-profit that helps homeless youth, which is fantastic," just as the regular team subtitle reminds us that they are in fact "Maria & Tiffany, Professional Poker Players." So it's a non-profit now? Are they going to be adding more compassionate buzzwords to their job title as the race goes on, until they eventually arrive back in the Western Hemisphere as green suicide/cutting counselors for homeless orphan abused lactose-intolerant lepers with cancer and also for dolphins? These two caring givers seem to have their group kind of straggling behind them, and they hope they still have everyone. Not a solid strategy.
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CORBETT, Ore. — A search and rescue crew brought out a lost hiker near Multnomah Falls on Sunday night.
The hiker, who only identified himself as Jessie, was cold, but otherwise not injured.
He realized about 2 p.m. Sunday that he was lost and used a cellphone to call for help. The Multnomah County Sheriff's Office was able to ping his phone and locate him. They told him to stay put.
Jesse was about 3.5 miles from the trailhead.
"From the call, it took five hours from my 911 call so I was just trying to keep myself warm," he told KGW.
He admitted to not being prepared for the conditions.
"I wandered off too far," he said. "I wanted to get a little bit out of the touristy area, but I was so distracted. I was being an idiot, I guess."
Rescuers say hikers need to understand how harsh winter conditions are in the Columbia Gorge.
"You can't just come out here and think it's gonna be like summer time. It's totally not," Matt Ramich of the U.S. Forest Service told KGW. "It's a whole other beast out there, so definitely trying to understand that we're in the winter time still, that Portland may be unfrozen, [but] out here, not even close."
Jesse had praise for the people who rescued him.
"I just want to thank everyone who came to rescue me and there were moments when I thought I wouldn't make it back, so I really appreciate it," Jesse said. "Now I just want to get to my warm apartment and just relax for awhile. It's been a long day."


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Download Dreamville – "Got Me" ft. Ari Lennox, Omen, Ty Dolla $ign & Dreezy Mp3
- Artist: Dreamville
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"Got Me" serves as a star-studded posse cut between Dreamville artists Ari Lennox and Omen, as well as Ty Dolla $ign and Dreezy.
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Gosh was it hot!! Met some of Seamus' LD puppies. Yes someone did ask what breed he was. LOL
Proud daddy in his "Ask me about my Leader Dog puppies" bandana
She's the pup I wanted to take home when I saw them at 7 weeks.
♣ Laura ♣
Seamus & Skye
Seamus, Beulah, Colten & Skye
Skye, Hawkeye, Colten & Beulah
♣ Laura ♣
Awwwww, Sea-Moose makes beautiful pups!!!! ;D
I bet he sure is proud of his leader dog pups!
Awww...such beautiful babies
And of course a very proud pappa!!!
Great pics! It's so neat to have pics of Seamus with his "working" babies
Those are great!! Looks like it was a nice day for everyone!
Awwwww! Love little Skye's niffer on Seamus' chin there.
Seamus and Flynn
Seamus must be proud of his little ones. He's a handsome boy himself. Thanks for posting.
Blackie and Ranger ...............................Reggie: 1996-2010 "Fly Reggie Fly"
What lovely pups, Seamus!
Ahhhh what adorable pups! Great pics!


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Spyder Team Surprised With Mahesh's DedicationSeptember 25, 2017 16:47
(Image source from: TheIndianExpress.Com)
Spyder Team Surprised With Mahesh's Dedication:- Superstar Mahesh Babu is all set with his next film Spyder which is the costliest ever film made in the actor's career. Mahesh sounded pretty confident on the film's success which is all set for Wednesday release. The actor is busy promoting the film across Tamil Nadu and Telugu speaking states ahead of the release. Mahesh during his recent interview revealed that Spyder has the toughest climax among his films and it has been shot for 25 days in Veitnam and he was under severe strain.
A physiotherapist has been asked to stay on the sets during the shoot of the film's climax. Mahesh took a long break after wrapping up the climax as he was under pressure and need to recover from it. The actor worked round the clock to wrap up the Vietnam schedule on time informed a source. Directed by AR Murugadoss, Spyder has been carrying huge expectations and the pre-release bookings have been fantabulous. Rakul Preet Singh played the female lead and Harris Jayraj composed the tunes.


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Florida Statutes > Chapter 856 – Drunkenness; Open House Parties; Loitering; Prowling; Desertion
Current as of: 2019 | Check for updates | Other versions
Terms Used In Florida Statutes > Chapter 856
- Affidavit: A written statement of facts confirmed by the oath of the party making it, before a notary or officer having authority to administer oaths.
- Arrest: Taking physical custody of a person by lawful authority.
- Bail: Security given for the release of a criminal defendant or witness from legal custody (usually in the form of money) to secure his/her appearance on the day and time appointed.
- Conviction: A judgement of guilt against a criminal defendant.
- Extradition: The formal process of delivering an accused or convicted person from authorities in one state to authorities in another state.
- Felony: A crime carrying a penalty of more than a year in prison.
- Indictment: The formal charge issued by a grand jury stating that there is enough evidence that the defendant committed the crime to justify having a trial; it is used primarily for felonies.
- Jurisdiction: (1) The legal authority of a court to hear and decide a case. Concurrent jurisdiction exists when two courts have simultaneous responsibility for the same case. (2) The geographic area over which the court has authority to decide cases.
- minor: includes any person who has not attained the age of 18 years. See Florida Statutes 88.6011
- Misdemeanor: Usually a petty offense, a less serious crime than a felony, punishable by less than a year of confinement.
- person: includes individuals, children, firms, associations, joint adventures, partnerships, estates, trusts, business trusts, syndicates, fiduciaries, corporations, and all other groups or combinations. See Florida Statutes 88.6011
- Probation: A sentencing alternative to imprisonment in which the court releases convicted defendants under supervision as long as certain conditions are observed.
- Real property: Land, and all immovable fixtures erected on, growing on, or affixed to the land.
- Statute: A law passed by a legislature.
- Trial: A hearing that takes place when the defendant pleads "not guilty" and witnesses are required to come to court to give evidence.
- writing: includes handwriting, printing, typewriting, and all other methods and means of forming letters and characters upon paper, stone, wood, or other materials. See Florida Statutes 88.6011


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