by Joseph Alton, M.D. and Amy Alton, A.R.N.P. (aka Dr. Bones and Nurse Amy)
Dr. Bones and Nurse Amy, of the Doom and Bloom Hour, are my definitive ?collapse medicine? experts. So I was thrilled when I heard they had published a ?medical survival book and I immediately ordered a copy. When it arrived, I spent several days pouring through it.
I could not be happier, it is outstanding! Dr. Bones and Nurse Amy have written a first of it?s kind, an incredible medical reference in the?previously non-existent?category of collapse medicine.
They tell you what to do when, ?Help is NOT on the way? ever.
Collapse: The situation after a TEOTWAWKI event; modern society, infrastructure, and systems as we know it will no longer exist.
Collapse Medicine: Medical care that will be provided when ?there is no access to modern medical care, and there is NO potential for accessing such care in the foreseeable future.?
First aid books tell us, when treating a critical patient, to first stabilize then transport to a hospital emergency room. This one doesn?t. This one can?t ? in a collapse there won?t be any. This book is written in plain easy to understand English, and it is written for you. You, the non-medical provider who takes it upon his or her self to assume the medical responsibilities for the group; doing your best to keep your people as healthy as you can.
The book begins by teaching you how to become a medical resource. It provides detailed lists of Likely Medical Issues You Will Face, Medical Skills You Will Want To Learn, and Medical Supplies you?ll want/need (including a thorough list of what to stock in your medical kit).
There is not only a valuable section explaining Natural Remedies (including a chapter on Essential Oils) but, whenever possible, it shows you how to effectively use them in conjunction with traditional (allopathic) pharmacology. Someday the only medicines available may be the ones you can grow and gather.
This book is as all-encompassing as I believe it can be. From respiratory infections to fractures to hypothermia to pregnancy and delivery, the chapters and the knowledge continue. There is even a detailed chapter on suturing; including when?and when not?to close a wound. If you can think of a medical problem that you may have to deal with in a collapse, there?s information about it in this book and more. Then, to further your medical education, they include a list of medical reference books you can add to your library and YouTube videos that demonstrate the procedures discussed.
The book concludes with information I don?t believe you?ll find written anywhere else; on the medically controversial topics of stockpiling medications (prescription and over-the-counter), how to use antibiotics (without a doctor?s guidance), and what drug expiration dates really mean.
Finally, I especially appreciate that they dedicated the book to me ? okay, all of us. We, who will take on the medical responsibilities when there are no others; the ones who your group will affectionately call ?Doc?. To us, Doctor Bones and Nurse Amy write, ??we both dedicate this book to those who are willing to take responsibility for the health of their loved ones in times of trouble. We salute your courage in accepting this assignment; have no doubt, it will save lives.?
New York ? Israeli scientists learn to breed black tomatoes, while a top liberal arts college admits to cheating ? and more winners and losers of today's news cycle
GOOD DAY FOR:
The dark side Israeli scientists discover a method for breeding tomatoes that are red on the inside, but black on the outside. [Daily Mail]
Good Samaritans A man returns a lost briefcase containing $8,000 to its rightful owner after the owner drove away with the briefcase on the roof of his car. [The Consumerist]
SEE ALSO: Mr. Big & Tall & Litigious
?
Staying on target Researchers create a self-guided bullet prototype that can strike a target from a mile away. [Business Insider]
BAD DAY FOR:
Safe travels The TSA endures criticism for waiting six hours before alerting police to possible pipe bombs found in a traveler's bag. [Huffington Post]
SEE ALSO: The frequent flier's furniture
?
Cheaters Claremont McKenna College admits to inflating SAT scores for its last seven freshman classes in an attempt to boost its national ranking. [Newser]
Attention spans A new report reveals that a majority of smartphone owners ignore most of the apps they download, opening only five or fewer apps at least once a week. [USA Today]
SEE ALSO: Heavy surveillance
?
For more winners and losers see: Good day, bad day: January 30, 2012
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JCI online early table of contents: Feb. 1, 2012Public release date: 1-Feb-2012 [ | E-mail | Share ]
Contact: Karen Honey press_releases@the-jci.org 734-546-5242 Journal of Clinical Investigation
EDITOR'S PICK: A thought-provoking new therapeutic target for brain cancer?
Glioblastoma multiforme (GBM) is the most common of all malignant brain tumors that originate in the brain. Patients with GBM have a poor prognosis because it is a highly aggressive form of cancer that is commonly resistant to current therapies. New therapeutic approaches are therefore much needed. Joanna Phillips, Zena Werb, and colleagues, at the University of California, San Francisco, have now identified a potential new therapeutic target for the treatment of GBM.
A substantial proportion of GBMs show evidence of abnormal activation of signaling pathways triggered by a cell surface protein known as PDGFR-alpha, and this is thought to drive the tumor. PDGFR-alpha triggers activation of signaling pathways when it binds the growth factor PDGF. Phillips, Werb, and colleagues found that the protein SULF2, which is known to regulate the availability of growth factors such as PDGF, was expressed in primary human GBM tumors and cell lines. Moreover, GBMs characterized by abnormal activation of signaling pathways downstream of PDGFR-alpha showed the strongest SULF2 expression. Importantly, knocking down expression of SULF2 in human GBM cell lines decreased the growth of these cells upon transplantation into mice. Phillips, Werb, and colleagues therefore suggest that SULF2 is a candidate therapeutic target for the treatment of GBM and that assessing its levels could identify tumors dependent on growth factors such as PDGF. The latter is important as PDGFR-alpha and other molecules to which growth factors bind are themselves good therapeutic targets.
TITLE: Heparan sulfate sulfatase SULF2 regulates PDGFR-alpha signaling and growth in human and mouse malignant glioma
AUTHOR CONTACT:
Joanna J. Phillips
University of California, San Francisco, San Francisco, California, USA.
Phone: 415.514.4929; Fax: 415.514.9792; E-mail: joanna.phillips@ucsf.edu.
Zena Werb,
University of California, San Francisco, San Francisco, California, USA.
Phone: 415.476.4622; Fax: 415.476.4565; E-mail: zena.werb@ucsf.edu.
View this article at: http://www.jci.org/articles/view/58215?key=7d9ee1ebe13cc1c6c025
ONCOLOGY: Answers to age-old questions surrounding fat cell cancer
Myxoid round cell liposarcoma (MRCLS) is a cancerous tumor that typically arises in deep fat tissues of the limbs or abdomen. It was shown almost 20 years ago to be characterized by a chromosomal change that generates a fusion protein known as TLS:CHOP. Despite this, neither the cell from which MRCLS arise nor the mechanism(s) by which TLS:CHOP induces tumor formation have been definitively determined. A team of researchers led by Igor Matushansky, at Columbia University, New York, has now provided some answers to these questions; in doing so, they identified a potential new combination therapy for the treatment of MRCLS.
A compound isolated from the sea squirt Ecteinascidia turbinate, ET-743, is a highly effective therapy for patients with MRCLS, but how it works has not been determined. Using a new mouse model of MRCLS that they developed, Matushansky and colleagues found that expression of TLS:CHOP in endogenous mesenchymal stem cells led to the in vivo development of MRCLS and that ET-743 worked by decreasing expression of TLS:CHOP. Moreover, combining ET-743 treatment with administration of agonists of the protein PPAR-gamma improved survival of the mice. Matushansky and colleagues therefore suggest that ET-743 plus PPAR-gamma agonist could provide a rational combination for treating MRCLS.
TITLE: PPAR-gamma agonists enhance ET-743induced adipogenic differentiation in a transgenic mouse model of myxoid round cell liposarcoma
AUTHOR CONTACT:
Igor Matushansky
Columbia University, New York, New York, USA.
Phone: 212.851.4556; Fax: 212.851.4784; E-mail: im17@columbia.edu.
View this article at: http://www.jci.org/articles/view/60015?key=ace2cdfd6a47aee95dac
TUMOR IMMUNOLOGY: Access denied: dense matrix blocks immune cell path to cancer cells
An individual's immune system does respond to a tumor. However, in individuals diagnosed with cancer, the antitumor response was obviously inadequate to clear the tumor. It is hoped that understanding how tumors escape the antitumor immune response will identify candidate therapeutic approaches, with the rationale being that if the escape mechanism can be blunted then an individual's immune system will be able to destroy the tumor. In this context, a team of researchers led by Emmanuel Donnadieu, at Institut Cochin, France, has determined that in human lung tumors, immune cells known as T cells are rarely found in the clusters of cancer cells. Rather, they accumulate in the stromal region of the tumors (that is, the tissue that surrounds and supports the cancer cells). Moreover, Donnadieu and colleagues found that the T cells could not enter the cancer cell regions because a dense matrix that the T cells could not penetrate surrounded these regions. Treating human lung tumor slices with matrix-degrading compounds increased the ability of T cells to enter the cancer cell clusters. Donnadieu and colleagues hope that future studies will increase understanding of the mechanisms by which the dense matrix is generated and thereby identify potential new therapeutic approaches.
TITLE: Matrix architecture defines the preferential localization and migration of T cells into the stroma of human lung tumors
View this article at: http://www.jci.org/articles/view/45817?key=3f332821bf27bc9a78d3
VIROLOGY: Finally, experimental transformation of a primary cell into a tumor cell by the cancer-causing virus KSHV
Kaposi sarcoma herpesvirus (KSHV) is the causative agent of several cancers that arise most commonly in individuals with HIV/AIDS. Developing therapeutic approaches to treat individuals with these cancers is hampered by a lack of understanding of the mechanisms by which KSHV transforms normal cells into cancerous cells. This is poorly understood in part because researchers have been unable to experimentally infect a primary cell with KSHV and turn it into a cancer cell. However, Shou-Jiang Gao and colleagues, at the University of Texas Health Science Center at San Antonio, San Antonio, have now done just that.
Gao and colleagues found that KSHV efficiently infects primary rat embryonic metanephric mesenchymal precursor cells and transforms them into cells that form tumors when injected into mice. They hope to use this model to study the molecular mechanisms by which KSHV transforms normal cells into cancerous cells, although they caution that additional analysis would be required to determine whether mechanisms uncovered using transformed rat cells are relevant to human cancers caused by KSHV.
TITLE: Direct and efficient cellular transformation of primary rat mesenchymal precursor cells by KSHV
AUTHOR CONTACT:
Shou-Jiang Gao
University of Southern California, Keck School of Medicine, Los Angeles, California, USA.
Phone: 323.442.8028; Fax: 323.442.1721; E-mail: shoujiag@usc.edu.
View this article at: http://www.jci.org/articles/view/58530?key=b593e40b17636db485f1
ONCOLOGY: Taking on features of cancer cells
The protein p27Kip1 has a role in suppressing tumor development and progression. It does so by inhibiting the activity of protein complexes that promote cell proliferation (cyclincyclin-dependent kinase complexes). In contrast, mutant forms of p27Kip1 that cannot inhibit cyclincyclin-dependent kinase complexes promote tumor development in mice. Now, a team of researchers led by Arnaud Besson, at INSERM UMR1037, France, has identified a mechanism by which mutant forms of p27Kip1 that cannot inhibit cyclincyclin-dependent kinase complexes promote cells to take on features of cancer cells. Future studies will determine whether normal p27Kip1 protein can regulate the same mechanism if mislocalized, as it often is in human tumors.
TITLE: p27Kip1 controls cytokinesis via the regulation of citron kinase activation
AUTHOR CONTACT:
Arnaud Besson
INSERM UMR1037, Cancer Research Center of Toulouse, Toulouse, France.
Phone: 33.561556435; Fax: 33.561558109; E-mail: arnaud.besson@inserm.fr.
View this article at: http://www.jci.org/articles/view/60376?key=2721832273bd35b1e9f0
###
[ | E-mail | Share ]
?
AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.
JCI online early table of contents: Feb. 1, 2012Public release date: 1-Feb-2012 [ | E-mail | Share ]
Contact: Karen Honey press_releases@the-jci.org 734-546-5242 Journal of Clinical Investigation
EDITOR'S PICK: A thought-provoking new therapeutic target for brain cancer?
Glioblastoma multiforme (GBM) is the most common of all malignant brain tumors that originate in the brain. Patients with GBM have a poor prognosis because it is a highly aggressive form of cancer that is commonly resistant to current therapies. New therapeutic approaches are therefore much needed. Joanna Phillips, Zena Werb, and colleagues, at the University of California, San Francisco, have now identified a potential new therapeutic target for the treatment of GBM.
A substantial proportion of GBMs show evidence of abnormal activation of signaling pathways triggered by a cell surface protein known as PDGFR-alpha, and this is thought to drive the tumor. PDGFR-alpha triggers activation of signaling pathways when it binds the growth factor PDGF. Phillips, Werb, and colleagues found that the protein SULF2, which is known to regulate the availability of growth factors such as PDGF, was expressed in primary human GBM tumors and cell lines. Moreover, GBMs characterized by abnormal activation of signaling pathways downstream of PDGFR-alpha showed the strongest SULF2 expression. Importantly, knocking down expression of SULF2 in human GBM cell lines decreased the growth of these cells upon transplantation into mice. Phillips, Werb, and colleagues therefore suggest that SULF2 is a candidate therapeutic target for the treatment of GBM and that assessing its levels could identify tumors dependent on growth factors such as PDGF. The latter is important as PDGFR-alpha and other molecules to which growth factors bind are themselves good therapeutic targets.
TITLE: Heparan sulfate sulfatase SULF2 regulates PDGFR-alpha signaling and growth in human and mouse malignant glioma
AUTHOR CONTACT:
Joanna J. Phillips
University of California, San Francisco, San Francisco, California, USA.
Phone: 415.514.4929; Fax: 415.514.9792; E-mail: joanna.phillips@ucsf.edu.
Zena Werb,
University of California, San Francisco, San Francisco, California, USA.
Phone: 415.476.4622; Fax: 415.476.4565; E-mail: zena.werb@ucsf.edu.
View this article at: http://www.jci.org/articles/view/58215?key=7d9ee1ebe13cc1c6c025
ONCOLOGY: Answers to age-old questions surrounding fat cell cancer
Myxoid round cell liposarcoma (MRCLS) is a cancerous tumor that typically arises in deep fat tissues of the limbs or abdomen. It was shown almost 20 years ago to be characterized by a chromosomal change that generates a fusion protein known as TLS:CHOP. Despite this, neither the cell from which MRCLS arise nor the mechanism(s) by which TLS:CHOP induces tumor formation have been definitively determined. A team of researchers led by Igor Matushansky, at Columbia University, New York, has now provided some answers to these questions; in doing so, they identified a potential new combination therapy for the treatment of MRCLS.
A compound isolated from the sea squirt Ecteinascidia turbinate, ET-743, is a highly effective therapy for patients with MRCLS, but how it works has not been determined. Using a new mouse model of MRCLS that they developed, Matushansky and colleagues found that expression of TLS:CHOP in endogenous mesenchymal stem cells led to the in vivo development of MRCLS and that ET-743 worked by decreasing expression of TLS:CHOP. Moreover, combining ET-743 treatment with administration of agonists of the protein PPAR-gamma improved survival of the mice. Matushansky and colleagues therefore suggest that ET-743 plus PPAR-gamma agonist could provide a rational combination for treating MRCLS.
TITLE: PPAR-gamma agonists enhance ET-743induced adipogenic differentiation in a transgenic mouse model of myxoid round cell liposarcoma
AUTHOR CONTACT:
Igor Matushansky
Columbia University, New York, New York, USA.
Phone: 212.851.4556; Fax: 212.851.4784; E-mail: im17@columbia.edu.
View this article at: http://www.jci.org/articles/view/60015?key=ace2cdfd6a47aee95dac
TUMOR IMMUNOLOGY: Access denied: dense matrix blocks immune cell path to cancer cells
An individual's immune system does respond to a tumor. However, in individuals diagnosed with cancer, the antitumor response was obviously inadequate to clear the tumor. It is hoped that understanding how tumors escape the antitumor immune response will identify candidate therapeutic approaches, with the rationale being that if the escape mechanism can be blunted then an individual's immune system will be able to destroy the tumor. In this context, a team of researchers led by Emmanuel Donnadieu, at Institut Cochin, France, has determined that in human lung tumors, immune cells known as T cells are rarely found in the clusters of cancer cells. Rather, they accumulate in the stromal region of the tumors (that is, the tissue that surrounds and supports the cancer cells). Moreover, Donnadieu and colleagues found that the T cells could not enter the cancer cell regions because a dense matrix that the T cells could not penetrate surrounded these regions. Treating human lung tumor slices with matrix-degrading compounds increased the ability of T cells to enter the cancer cell clusters. Donnadieu and colleagues hope that future studies will increase understanding of the mechanisms by which the dense matrix is generated and thereby identify potential new therapeutic approaches.
TITLE: Matrix architecture defines the preferential localization and migration of T cells into the stroma of human lung tumors
View this article at: http://www.jci.org/articles/view/45817?key=3f332821bf27bc9a78d3
VIROLOGY: Finally, experimental transformation of a primary cell into a tumor cell by the cancer-causing virus KSHV
Kaposi sarcoma herpesvirus (KSHV) is the causative agent of several cancers that arise most commonly in individuals with HIV/AIDS. Developing therapeutic approaches to treat individuals with these cancers is hampered by a lack of understanding of the mechanisms by which KSHV transforms normal cells into cancerous cells. This is poorly understood in part because researchers have been unable to experimentally infect a primary cell with KSHV and turn it into a cancer cell. However, Shou-Jiang Gao and colleagues, at the University of Texas Health Science Center at San Antonio, San Antonio, have now done just that.
Gao and colleagues found that KSHV efficiently infects primary rat embryonic metanephric mesenchymal precursor cells and transforms them into cells that form tumors when injected into mice. They hope to use this model to study the molecular mechanisms by which KSHV transforms normal cells into cancerous cells, although they caution that additional analysis would be required to determine whether mechanisms uncovered using transformed rat cells are relevant to human cancers caused by KSHV.
TITLE: Direct and efficient cellular transformation of primary rat mesenchymal precursor cells by KSHV
AUTHOR CONTACT:
Shou-Jiang Gao
University of Southern California, Keck School of Medicine, Los Angeles, California, USA.
Phone: 323.442.8028; Fax: 323.442.1721; E-mail: shoujiag@usc.edu.
View this article at: http://www.jci.org/articles/view/58530?key=b593e40b17636db485f1
ONCOLOGY: Taking on features of cancer cells
The protein p27Kip1 has a role in suppressing tumor development and progression. It does so by inhibiting the activity of protein complexes that promote cell proliferation (cyclincyclin-dependent kinase complexes). In contrast, mutant forms of p27Kip1 that cannot inhibit cyclincyclin-dependent kinase complexes promote tumor development in mice. Now, a team of researchers led by Arnaud Besson, at INSERM UMR1037, France, has identified a mechanism by which mutant forms of p27Kip1 that cannot inhibit cyclincyclin-dependent kinase complexes promote cells to take on features of cancer cells. Future studies will determine whether normal p27Kip1 protein can regulate the same mechanism if mislocalized, as it often is in human tumors.
TITLE: p27Kip1 controls cytokinesis via the regulation of citron kinase activation
AUTHOR CONTACT:
Arnaud Besson
INSERM UMR1037, Cancer Research Center of Toulouse, Toulouse, France.
Phone: 33.561556435; Fax: 33.561558109; E-mail: arnaud.besson@inserm.fr.
View this article at: http://www.jci.org/articles/view/60376?key=2721832273bd35b1e9f0
###
[ | E-mail | Share ]
?
AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.
As invasive snakes expand territory, some mammal populations drop by more than 90 percent
Web edition : Monday, January 30th, 2012
Giant snakes are eating their way through the Everglades, leaving a drastically changed ecosystem in their wake, a new study shows.
The snakes, many of which measure 10 to 16 feet, are called Burmese pythons. But make no mistake: Virtually all of the roughly 30,000 living in southern Florida were born in the Everglades. Ecologists now report that populations of mammals have begun plummeting throughout the pythons? expanding range. And the timing of these mammal losses matches the geographic spread of the snakes, which federal officials believe were initially released into the wild by snake fanciers, probably 15 to 30 years ago.
Raccoons, opossums, deer and other mammals, along with birds and gators, have all turned up in the stomachs of captured pythons, testifying to the snakes? varied appetite, notes ecologist Michael Dorcas of Davidson College in North Carolina. ?But until now, there hadn?t been any indication that the snakes were altering the ecosystem,? says Dorcas, who led the study.
The new data ?make a persuasive case for cause and effect,? says herpetologist J. Whitfield Gibbons of the Savannah River Ecology Lab in Aiken, S.C., who was not affiliated with the new analysis. ?The investigators take a convincing position that introduced predatory pythons are responsible for the decline in numbers of large- and medium-size mammals in the Everglades.?
With much of the roughly 6,000-square-kilometer Everglades National Park virtually inaccessible, the team of 11 university and federal scientists took an indirect approach to surveying the region?s mammal populations. Between 2003 and 2011, researchers cruised roads on 313 nights and compared the number of individuals in each species they saw per 100 kilometers traveled to rates witnessed along the same roadways over 51 nights in the 1990s ? before pythons had established local breeding populations.
As in the earlier survey, raccoons and Virginia opossums were the most commonly observed mammals, although sightings of each were down by more than 98 percent in the most recent survey. Counts were 94 percent lower for white-tail deer and bobcat sightings were down 87 percent. And in contrast to the earlier survey, scientists saw no rabbits or foxes. Rabbits had been among the most common mammals witnessed in the 90s.
Roadside sightings of these species remained unchanged between the two periods in areas outside the python range. In spots of recent python migration, mammal sightings were also down somewhat from a decade earlier, drops ranging from 20 to 80 percent, Dorcas? team reports online the week of January 30 in the Proceedings of the National Academy of Sciences.
The new diminished mammal counts in python territory ?are pretty similar to what we found,? says Joshua Holbrook of Florida Atlantic University in Boca Raton. A more circumscribed road-sampling survey he coauthored in 2010 in Florida Scientist turned up nine mammals over four nights: seven deer, a possum and an unidentified small mammal. On five nights, he and his colleagues saw none. Meanwhile, beyond the python?s range in the nearby Corbett Wildlife Management Area, he and Thomas Chesnes of Palm Beach Atlantic University sighted 40 mammals over nine nights.
?This study paints a stark picture of the real damage that Burmese pythons are causing to native wildlife and the Florida economy,? says U.S. Interior Secretary Ken Salazar. His agency announced new rules on January 17 that will ban the importation and interstate transport of Burmese pythons, yellow anacondas and three other invasive constrictors sold in the pet trade. All have been found in Everglades National Park.
With so many invasive constrictors already breeding in South Florida, research is now focusing on ways to limit their spread and better understand the prey they threaten. Although Burmese pythons need freshwater to survive, a team of biologists with the U.S. Geological Survey led by Kristen Hart in its Davie, Fla., lab showed that the snakes can apparently derive much of their needed moisture from the tissue of prey animals.
The team?s experiments suggest that python hatchlings can?t survive more than two months with access to only saltwater. But a pair of hatchlings was still alive after 200 days with access to only brackish water. And a yearling snake with access to only saltwater survived 7 months ? holding open the prospect that these adept swimmers could, if motivated, enter the marine realm and migrate long distances through seawater, the team reports in the Feb. 10 Journal of Experimental Marine Biology and Ecology. In fact, Burmese pythons have already been found eating endangered wood rats on Key Largo, off the mainland coast.
(Reuters) ? Exxon Mobil Corp's (XOM.N) fourth-quarter profit narrowly beat Wall Street's expectations as rising crude oil prices offset falling margins for chemicals, engine lubricants and fuel.
The results sent Exxon Mobil's shares down 1 percent to $84.68 in premarket trading on Wall Street, where analysts and investors have come to expect results that widely beat expectations.
Production of natural gas and crude oil slipped during the period.
The company posted net income of $9.4 billion, or $1.97 per share, compared with $9.25 billion, or $1.85 per share, in the year-ago period.
Analysts expected earnings of $1.96 per share, according to Thomson Reuters I/B/E/S.
The quarterly profit was Exxon Mobil's lowest for 2011.
Total revenue rose 16 percent to $121.61 billion. Analysts expected $119.7 billion in revenue.
Oil companies around the world benefited from a jump in oil prices during the fourth quarter. Crude futures traded in New York jumped about 25 percent to end the quarter at $98.83 per barrel. Brent prices gained 5 percent during the quarter.
The price jump helped to lift Exxon Mobil's profit in the upstream unit, which produces oil and natural gas, by 18 percent. Land sales also lifted the results, the company said.
Still, the weak economy harmed Exxon Mobil's margins. Profit at Exxon Mobil's downstream unit, which makes engine lubricant, fell 13 percent. The chemical unit, which makes plastics and related products, saw profit drop 49 percent.
The Irving, Texas-based company spent $10 billion during the quarter on capital projects and exploration, in line with the same period in 2010.
(Reporting By Ernest Scheyder, editing by Dave Zimmerman)
One week from tonight the NBC show Smash premieres. However I am here to tell you that you don?t have to wait until next Monday to watch it. Nope you can check out the entire episode right here, sweet! I don?t know about you but I can?t wait for the new series Smash to debut and now well I don?t have to. See thanks to my pal Kelsey at NBC I can watch the entire first episode below. You read it correctly the entire thing right here and a whole week early too. In case you aren?t entirely sure what Smash is about, although I am not sure how that can be since the promos for it are literally everywhere but that being said let me give a little run down of the show. The show is a musical drama set on the back drop of a Broadway musical about the infamous Marilyn Monroe. It has a stellar cast that includes the lovely Debra Messing, Oscar Winner Anjelica Huston and American Idol alum Katharine McPhee, to name just a few. Plus the amazing Steven Spielberg is the executive producer so that is pretty cool. Anyway to me it sounds and [...]
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Public release date: 1-Feb-2012
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