Monday, October 27, 2008

God Said " Go somewhere and sit. Let me do my work"

Ephesians 2


Amplified

1AND YOU [He made alive], when you were dead (slain) by [your] trespasses and sins
2In which at one time you walked [habitually]. You were following the course and fashion of this world [were under the sway of the tendency of this present age], following the prince of the power of the air. [You were obedient to and under the control of] the [demon] spirit that still constantly works in the sons of disobedience [the careless, the rebellious, and the unbelieving, who go against the purposes of God].
3Among these we as well as you once lived and conducted ourselves in the passions of our flesh [our behavior governed by our corrupt and sensual nature], obeying the impulses of the flesh and the thoughts of the mind [our cravings dictated by our senses and our dark imaginings]. We were then by nature children of [God's] wrath and heirs of [His] indignation, like the rest of mankind.

Message
1-6
It wasn't so long ago that you were mired in that old stagnant life of sin. You let the world, which doesn't know the first thing about living, tell you how to live. You filled your lungs with polluted unbelief, and then exhaled disobedience. We all did it, all of us doing what we felt like doing, when we felt like doing it, all of us in the same boat. It's a wonder God didn't lose his temper and do away with the whole lot of us. Instead, immense in mercy and with an incredible love, he embraced us. He took our sin-dead lives and made us alive in Christ. He did all this on his own, with no help from us! Then he picked us up and set us down in highest heaven in company with Jesus, our Messiah.

Relationship With Jesus = Garment = Chosen States Maintenance?

The Story of the Wedding Banquet
Rev. James Peterson

1-3 Jesus responded by telling still more stories. "God's kingdom," he said, "is like a king who threw a wedding banquet for his son. He sent out servants to call in all the invited guests. And they wouldn't come!

4"He sent out another round of servants, instructing them to tell the guests, 'Look, everything is on the table, the prime rib is ready for carving. Come to the feast!'

5-7"They only shrugged their shoulders and went off, one to weed his garden, another to work in his shop. The rest, with nothing better to do, beat up on the messengers and then killed them. The king was outraged and sent his soldiers to destroy those thugs and level their city.

8-10"Then he told his servants, 'We have a wedding banquet all prepared but no guests. The ones I invited weren't up to it. Go out into the busiest intersections in town and invite anyone you find to the banquet.' The servants went out on the streets and rounded up everyone they laid eyes on, good and bad, regardless. And so the banquet was on—every place filled.

11-13"When the king entered and looked over the scene, he spotted a man who wasn't properly dressed. He said to him, 'Friend, how dare you come in here looking like that!' The man was speechless. Then the king told his servants, 'Get him out of here—fast. Tie him up and ship him to hell. And make sure he doesn't get back in.'

14"That's what I mean when I say, 'Many get invited; only a few make it.'"

Tuesday, October 21, 2008

Thank God for Beth Caravalho



Thank God for YOU TUBE

I hope I can get some words from the Word of God to be sung to some of these tunes
I am sure this music is played to praise God in Heaven now as we speak

Ministry

You gotta love it. Love your church. Jesus loved you like this!

Even if you would rather be fishing or in a ministy wtih limelight of the church. YOU could complain all day about being neglected, not having your cash donations counted, egregious ingratitude of the leadership, members borrowing money with no intent on paying back, false teaching, support of the enemy (spouse in divorce), not getting any support during a season of being poor in Spirit, defending past leadership mistakes, more attention to outside ministries than to those that you are in in his church, promising to marry daughter and then backing out, and over all treating you as an enemy of Christ.
There may have been a major scandal involving the leadership and you without fail took up for him whcih cost you. You may have a member of his fraternity and your church literally treat you as a heathen and deny your ministry. Remember what happened to Jesus. If it happened to him, guess what?
It is not about you but about those you serve, the kids in the case of youth ministry.

Beth Caravalho


Beth Carvalho
From Wikipedia, the free encyclopedia


Elizabeth Santos Leal de Carvalho (born May 5, 1946 in Rio de Janeiro) is a Brazilian samba singer, guitarist, cavaquinist and composer.

Biography
Carvalho was raised in a middle class family in Rio de Janeiro's South Zone. Her father, João Francisco Leal de Carvalho, was a lawyer. She grew up in contact with different types of music. Her father used to take her to samba school rehearsals, and her mother was an appreciator of classical music who encouraged her to become a ballerina. She started playing the guitar as a teenager, and got involved with the emerging Bossa Nova movement, winning a nationwide song contest on TV at the age of 19. Her first record was 1968's "Andança", carrying the song of same name which she had defended in a festival, which brought her to prominence. Although she started her career with Bossa Nova, that was an ephemeral phase which lasted less than one year - Beth started dedicating herself entirely to samba just as her fame began, working with legendary composers such as Nelson Sargento.

Carvalho is a very important artist in the history of samba, for she has celebrated and brought stronger light, with great reverence, to the work of legendary composers such as Cartola, Nelson Cavaquinho & Guilherme de Brito in times where they weren't receiving the attention they deserved. Almost all of her records have songs by these composers, among other legendary sambistas such as Nelson Sargento and the Old Guard of Portela. Her samba school is Mangueira, but that didn't stop her from revering and recording dozens of songs from composers of Portela, the other most traditional samba school in Rio de Janeiro.



Beth Carvalho performing in Paris during the year of Brazil in France. 2005
Later, in the late 1970s and early 80's, Beth helped bring to light the work of the incipient pagode artists from Cacique de Ramos, such as Almir Guineto, Jorge Aragão and the Fundo de Quintal group. Then, in 1983, she introduced him who would become the major samba name in the 90's and contemporary Brazil, Zeca Pagodinho. Beth has always cultured her habit of giving underrated composers the recognition they deserve, and for that she is regarded as the madrinha do samba (samba godmother), for always trying to get the songwriters known, even when they're not the ones singing the songs (something for which Cristina Buarque also deserves credit). She was a driving force in the modernization of samba in the 80s, and at the same time rejected commercial pop trends in samba arrangements, culturing the samba tradition.
In the 1990s, Beth's popularity wasn't the strongest, but she was always popular. She recorded an album dedicated to the samba from São Paulo, retorting the famous axiom which states that São Paulo is the grave of samba. In 1998 she recorded an album dedicated entirely to the pagode classics, Pérolas do Pagode (Pagode Pearls).
In the new millennium, Beth is working more than ever, releasing CDs and DVDs. With a career that spans 40 years, she is already a historical figure in Brazilian culture, and recognizedly the samba dame with the most substantial opus in Brazil, without diminishing others such as Clara Nunes and Cristina Buarque.

Not For Married Folks Only - for singles if you do not know where your spouse is (literally/figuratively)



To Breathe Correctly is to make love to yourself. Love yourself and your temple. It is where He resides. Think on these things as you watch this!
The law woke up and quickened sin, yet we need to strengthen our relationship with Him. (Read your Word, Pray, and Confess your sin. Do all this in the bathroom or closet with the lights out. Watch what happens. Put on your whole armor before you leave Ephesians 6:12- )

Monday, October 20, 2008

I told you

Nature Biotechnology 26, 1053 - 1054 (2008) doi:10.1038/nbt1008-1053
CD20 blockers eye crowded rheumatology market
George S Mack

When trial results for a novel cancer drug were trumpeted in July, the rheumatology field felt the ripples. The drug is ofatumumab, a monoclonal antibody (mAb) targeting the CD20 molecule on B lymphocytes. Its makers, London-based GlaxoSmithKline (GSK) and Genmab of Copenhagen, announced that the mAb had met its primary and secondary endpoints in chronic lymphocytic leukemia (CLL). But with two double-blind phase 3 studies of ofatumumab for rheumatoid arthritis already underway in Italy and Eastern Europe, these companies are clearly looking beyond cancer indications to lucrative autoimmune disease markets for their second-generation molecule.
The idea is to follow the trail blazed by Genentech of South San Francisco, Roche of Basel and Biogen-Idec of Cambridge, Massachusetts, with Rituxan (rituximab), their anti-CD20 chimeric mAb. Rituxan was approved by the US Food and Drug Administration to treat B-cell lymphomas and leukemias in 1997 and then as a third-line therapy against rheumatoid arthritis in 2006. Currently marketed by Roche in Europe as MabThera, it surpassed $5 billion in worldwide sales in 2007 alone.
GSK has invested heavily in ofatumumab. The company made headlines at the end of 2006 when the licensing agreement to co-develop this fully human IgG1- mAb for cancer and rheumatoid arthritis was announced. The deal, potentially worth $2.1 billion, saw Genmab receive an upfront $102 million as a sweetener for their anti-CD20 mAb. GSK also took a 10% stake in the biotech firm by purchasing $357 million in shares. The transaction was deemed to be the largest ever in Europe for a single product; if all milestones are met it will exceed the $2.0 billion deal between New York–based Bristol-Myers Squibb and New York–based ImClone Systems for blockbuster cancer chimeric mAb Erbitux (cetuximab).
The meteoric rise of tumor necrosis factor (TNF)- blockers over the past decade ushered in the age of biologic therapies for rheumatoid arthritis. Anti-TNF agents—Enbrel (etanercept), Humira (adalimumab) and Remicade (infliximab)—are now labeled for second-line use after failure of methotrexate and nonsteroidal anti-inflammatory drugs (NSAIDs). But there is no product that works for everyone—about a third of those with rheumatoid arthritis do not respond to first- or second-line therapy.
Rituxan is currently a third-line therapy for rheumatoid arthritis after failure of methotrexate and anti-TNF- products. "We'd like to try it in patients much earlier on, and we're working towards that at the moment," says immunologist Geraldine Cambridge, who has collaborated for many years with rheumatologist Jonathan Edwards, both of the Center for Rheumatology Research at University College London. The two have done much of the basic science groundwork as well as overseen clinical trials over the past decade to establish the effectiveness of B-cell depletion with CD20 blockade. "You need to get these patients in remission as early as possible," she says. "If you lose one year while patients are slowly failing on methotrexate and TNF-inhibitors, that means they've lost their job by then and will probably never get back to work again."
The clinical approach by which B cells are ablated to treat rheumatoid arthritis has only recently gained acceptance. Treatment with Rituxan has brought relief to many patients whose synovitis symptoms, including pain and stiffness, subside, as do the swollen hand joints that accompany the more advanced stages of the disease. Today treating rheumatoid arthritis with anti-CD20 blockers is well accepted, but this was not the case a few short years ago.
The transformation in thinking began in 1997 when Rituxan was approved for blood cancers. As the drug became accessible to investigators like Cambridge and Edwards, they were able to test the idea that B cells were driving autoimmune disease. This was anathema at the time because most research in autoimmunity focused on T cells. The confusion is understandable because B cells and T cells signal back and forth continuously in a highly integrated and dynamic network. B cells present antigens to T cells, which in turn activate and excite B cells to produce autoantibodies such as rheumatoid factor. These RF antibodies latch on to the Fc portions of IgGs to form immune complexes, which in turn trigger a cascade of events that finally attract macrophages and neutrophils. As these phagocytic cells engulf immunocomplexes, they release lysosomal enzymes that ratchet up inflammation and further damage the synovial apparatus, leading to chronic disease.
Anti-CD20 agent Rituxan interrupts this self-perpetuating cycle by wiping out B-cell populations. This may seem an extreme measure, but it has allowed a sizable proportion of rheumatoid arthritis patients to manage their disease. Not all CD20 blockers are equivalent, however. CD20 is a tetra-membrane-spanning protein with a rather serpentine configuration weaving in and out of the B-cell membrane. Different anti-CD20 antibodies might bind epitopes far apart on the molecule, and these differences could account for variations in intracellular signaling cascades affecting potency, efficacy or even immunotoxicity. Different antibody formats may also have different advantages in terms of functionality, pharmacodynamics and pharmacokinetics.
One novel antibody format targeting CD20 currently under development is Seattle-based Trubion Pharmaceuticals' TRU-015. This molecule—one third of the size of a true antibody—consists of single-chain variable regions (VL and VH) that bind CD20, which are fused by means of a modified human IgG1 hinge domain to engineered constant regions that encode human IgG1 constant heavy domains (CH2 and CH3). Because the fusion protein includes the Fc portion it allows antibody-dependent cellular cytotoxicity (ADCC) to take place whereas its smaller size is thought to improve tissue biodistribution.
In collaboration with Madison, New Jersey-based Wyeth, Trubion is studying this anti-CD20 scFv-Fc fusion protein (TRU-015) in phase 2 trials for rheumatoid arthritis and in preclinical development for systemic lupus erythematosus (SLE). CEO and founder Peter Thompson says the product is "significantly attenuated" with respect to complement-dependent cellular cytotoxicity (CDCC) of B cells, but "very potent" with respect to ADCC and direct apoptotic activity (these are two of the mechanisms by which existing anti-CD20 antibodies are thought to deplete B cells). Such toned-down CDCC activity, relative to Rituxan, is presumably advantageous because complement cascades have been shown to herald signs and symptoms of some infusion reactions, which can range from very mild to severe. "We have not really seen grade three or grade four infusion reactions with TRU-015 in contrast to the experience previously published with Rituxan," says Thompson. Trubion also has another scFv-Fc fusion (SBI-087) targeting CD20 in phase 1 trials for SLE and rheumatoid arthritis.
In the early days of Rituxan as a rheumatoid arthritis treatment, rheumatologists were concerned over what might happen if the patient's B-cell population were to be wiped out, and if their immunoglobulin levels were to drop to unacceptably low levels. Some of these worries have now been dispelled. B cells give rise to long-lived immunoglobulin-producing plasma cells that persist for many months, and because they do not have the CD20 antigen on their cell surfaces, these plasma cells remain untouched by anti-CD20 agents. Also, plasma cells retain some memory of previous exposures to infectious agents, so they continue to offer protection to the patient. "Patients treated with rituximab [Rituxan] still mount an immunoglobulin response to vaccines after rituximab therapy," says rheumatologist Peter Taylor, who is head of clinical trials at the Kennedy Institute of Rheumatology in London. "But humoral responses can be reduced," he says.
The critical question for clinicians is what happens to the patients' bone marrow stem cells and their ability to generate plasma cells after repeated cycles of anti-CD20 therapy. As bone marrow precursors are not CD20 positive, presumably they are not affected by anti-CD20 agents. "In my own practice, we've gotten up to four or five cycles," says Taylor. Cambridge and Edwards have doubled the cycles without observing substantial drops in immunoglobulin levels. They believe that after B cells in the periphery are depleted, the bone marrow somehow reboots to produce new lymphocytes that no longer churn out rheumatoid arthritis–causing autoantibodies. Indeed, Cambridge has been tracking a group of rheumatoid arthritis patients whose symptoms have not returned for 18 months after the last Rituxan treatment. Cambridge won't go out on a limb and say there's been a complete response, but she says, "One patient has been in remission for three years or longer."
Still, Taylor expresses some mild concerns. "When you get past about five or six cycles of therapy, there is a proportion of patients with robust and well-maintained, really good responses, that at some point don't recover B-cell levels, and their immunoglobulin levels drop down below the normal range," he says. "If B-cell depletion were thought to be the optimal therapy for individuals with rheumatoid arthritis, it may have a finite shelf life as to how long you could use that approach. It may be perhaps that you could use rituximab [Rituxan] in a responsive patient for 5 years, 10 years or 12 years. But it's not yet clear that you could go on [long term], as we do, with methotrexate for a lifetime."
Time will tell if newer anti-CD20 therapies in pipelines work any better. Because ofatumumab is fully human and Rituxan is chimeric, the supposition is that ofatumumab would present fewer infusion reactions or other adverse events, particularly the human anti-chimeric antibody response. But not much information is publicly available, and, in fact, there have been no head-to-head trials of ofatumumab versus Rituxan in rheumatoid arthritis. Taylor is principal investigator in one ongoing phase 3 trial of ofatumumab for rheumatoid arthritis, which is scheduled to wrap up in 2011, but a confidentiality agreement prevents him from discussing it.
One thing Taylor will say, however, is that there's been a revolution in the mind-set of rheumatologists around the globe, who are losing their trepidation about using cancer drugs in rheumatoid arthritis patients. "I think there's a massive change," he says. "People often use the phrase 'aggressive early therapy'. To me, it really means optimally suppressing synovitis."

Kevin Bob Roberts

I just love those water scenes

Saturday, October 18, 2008

Moving Toward The Sun

Courtesy of SOHO/EIT consortium

Moving toward the sun, if you could get that close

Artistic work based on work by SOHO/EIT consortium SOHO/EIT

Artistic work based on work by SOHO/EIT consortium

Sun moving

high-res photographs of the sun

Click on this and scroll to see what the sun looks like in stil and animated motion photography

Go to item 9

Friday, October 17, 2008

Colored Black Hole

I have always been blessed. but on 10-16-08, at 2 pm, I was tremendously blessed with the filming of a strange phenomenon which I will just name a Black Hole. It tended to suck light in a counteclockwiwe fashion, just the opposite to what the sun does, from pictures that I have seen.

It was as if living and breathing as an organism. I have 1 hour of this taped and I will give you a clip if God says the same. Please write for the whole hour.

I get the impression of some type of slit-lamp phenomenon, or crystal-prism activity. I will need wome of you physic gurus to figure this out for a Nobel Prize

Wednesday, October 15, 2008

Nice tune


He did not even know the song's name . Pay Jamie Abe. for this one

Pawn Shop Info? From MSN

At People’s Pawn in Springfield, Mass., the collection of DVD players, televisions and other electronics just keeps getting bigger.

As many as 200 a people a day come in to “sell all their stuff so they can get gas money,” said Efren Rivera, who works at the shop. “Some people have to pay their mortgages.”
The story is similar at EZ Cash Pawn in West Palm Beach, Fla., where the shelves are so stacked with electronics, musical instruments, guns, fishing poles, scuba gear — you name it — that people are being turned away.

Monday, October 13, 2008

Jai Fatigue!

I letter sent to a journalist.

Tumor Necrosis Factor (TNF) is the cytokine (inflammatory culprit) that causes a vasodilation in the face of similar cardiac output. In other words there is less blood going to the brain ( a brain is sensitive to less than 20% of the cardiac output per minute).
This is ultimately where fatigue is felt This fatigue can also be caused by pump failure. Fatigue is a subtle sign of heart dysfunction. This is what is experienced in coronary insufficiency experienced by most senior adults who do not do moderate exercise.
The key is to do work in the garden, walk in the mall, ride a bike in the sun, swim ,
play tennis in moderation in order to encourage the growth of collateral coronary vessels (other than the left anterior main descending , right and circumflex coronary vessels ).
The mitochondria function optimally under conditions of immediate reduction (Vitamin C = stongest reducting agent = electron giving vasodilation ) where the process of oxidation (electron transfer by taking) takes place. Glutathione reserves also function to buffer this process. They do function to perform energy manufacturing
It just so happens that TNF is also responsible for that collateral growth of coronary vessels

I have a proprietary database that I would be more than willing to give information of in order to give you the slant on ANY medical condition . My condition is that all dysfunctional medical conditions are related to cytokines and inflammation and or lack of control of said inflammation. It is the inflammation within the coronary vessels that leads to plaque formation within the coronary vessels , and strokes in the basilar, and carotid arteries. It is the lack of normal inflammation that disallows tumor surveillance and growth formation.

First check out all details sent as to verify their authenticity in this and other articles. You can use Google and my software( I will give you a password) whenever you wish, because you appear to be a servant of the people. Thank you again.

Sincerely,

Alonzo Peters MD
pete4doc@hotmail.com

31 years of service. I picked the right day!

Missed Opportunities. I do not think so!

After going to the 9th-10th grade teaching of SundaySchool at my church, and thanks to the closing of the Medical Library and numerous other blunders on my part, the Lord led me to Holman Street Baptist. There there was a refreshing spirit in the pulpit in a pastor Rains who blessed us all in the Matthew parable of the pearl. Yet the man of the hour was none other than the great teacher-pastor himself Manson B Johnson. This was quite an experience!

tired?

From the Boston Globe

........a new understanding of everyday fatigue - the kind associated with a fundamental lack of energy, not the fatique caused by conditions such as anemia, or a lack of sleep - is emerging from labs around the country. Last month, leading physiologists gathered at the National Institute on Aging, part of the National Institutes of Health, and came up with a new paradigm of what happens in the brain and the rest of the body when a person has subjective feelings of fatigue.
The new understanding "is a fundamental jump forward in the study of fatigue," said Dr. Luigi Ferrucci, one of the conference organizers, and brings with it some good news for the tired among us.Scientists are now convinced that fatigue has a real, molecular basis, and that at least two major biological processes are involved: An excess of natural chemicals called pro-inflammatory cytokines, which the body pumps out in response to infection. And sluggish mitochondria, the tiny organelles

Tricky Dick. Giving honor to those due....indirectly at least. There is dishonor in not honoring the honorable

This is all from MSN!

The first recorded celebration honoring the discovery of America by Europeans took place on October 12, 1792 in New York City. The event, which celebrated the 300th anniversary of Columbus' landing in the New World, was organized by The Society of St. Tammany (also known as the Columbian Order). This is depicted in The Streets of New York, I believe.
San Francisco's Italian community held their first Columbus Day celebration in 1869. In 1892, President Benjamin Harrison urged citizens to participate in the the 400th anniversary celebration of Columbus' first voyage. It was during this event that the Pledge of Allegiance, written by Francis Bellamy, was recited publically for the first time.
Colorado was the first state to observe the holiday in 1905.
In 1937, President Roosevelt proclaimed October 12 as "Columbus Day" and in 1971, President Nixon declared the second Monday of October a national holiday.

Why did Ticky Dick honor those who wanted to forget their African ancestry history?

Tuesday, October 7, 2008

EVENTS-JAZZ HOUSTON

KPFT JAZZ AND STUFF IN THE MILLER THEATRE PARK
Sunday Nov. 9, 2008 3-11 pm
We will be there
as the crowd will

Saturday, October 4, 2008

Friday, October 3, 2008

Entymology and Evans

Now is the time


This is how you participate

Love ya Sis


Sam Buccas-Thursdays


Awesome to HEAR AND SEE

I remember April NY Style

I need more light. Take my word for the artistry

We are have been and will be Family



When I do record a

gain it will be with my family

The Greatest


Artist of musicians and Pan player