NEW YORK/DETROIT (Reuters) - Johnson Controls Inc is exploring a potential sale of its automotive interiors unit, a move that would allow the diversified manufacturer to focus on higher-margin building controls and next-generation car batteries, three people familiar with the matter said on Wednesday.
Shares of Johnson Controls were up about 6 percent to $33.74 on the New York Stock Exchange, valuing the diversified conglomerate at around $23 billion.
Johnson Controls, the largest U.S. auto supplier with sales of more than $4 billion in car interiors for fiscal 2012, has grappled with industry-wide pressure on margins, low vehicle production in Europe and increased competition from China.
A successful sale of the interiors division, which competes with rivals such as Magna International Inc and Faurecia , would leave Johnson Controls with three other major business: automotive seating, building controls and car batteries.
The company also joins a growing number of diversified conglomerates looking to exit businesses that generate poor returns or do not fit with their core operations.
The Milwaukee, Wisconsin-based company is being advised by investment bank JPMorgan Chase on the potential interiors divestiture, two of the people said, asking not to be named because the discussions are private.
Johnson Controls posted revenue of $42 billion its last fiscal year. Automotive seating remains its largest segment with roughly $16 billion in sales for its fiscal 2012 that ended in September.
Johnson Controls and JPMorgan declined to comment.
In October, Johnson Controls separated its car seating from its interiors and electronics businesses, saying that economic and competitive characteristics between seating, interiors and electronics are "increasingly different."
"If you look at those businesses, the business models, capital intensity, the manufacturing footprint requirements are very, very different. And we also wanted to bring more focus to each of those segments," Chief Executive Steve Roell said at that time.
The diversified manufacturer, along with the rest of the industry, has been battling to improve poor margins in car interiors over the past few years. Visteon Corp is also trying to exit its auto interiors business.
The company's fiscal 2013 year outlook called for electronics and interiors business margins of between 1.9 percent and 2.1 percent, and its mid-term outlook through 2017 called for those margins to rise to 6 percent to 7 percent.
In comparison, Johnson Controls' power solutions business - the world's largest provider of advanced batteries for vehicles - expects margins between 14.6 percent to 14.8 percent in its 2013 fiscal year and improvement in margins by 2 percentage points in its outlook to 2017.
Its building efficiency business expects 2013 margins of 6.4 percent to 6.5 percent.
(Reporting by Soyoung Kim in New York and Bernie Woodall in Detroit; editing by Carol Bishopric)
WASHINGTON (AP) ? Congressman Peter King of New York is lacing up his boxing gloves for a fight that has nothing to do with budget cuts.
The 68-year-old Republican is known more for his bare-knuckle politics than his pugilistic skills. He plans to step into the ring Saturday for a two-round exhibition bout against a New York state light heavyweight kickboxing champion, "Irish" John Foley, at a pub in Wantagh, N.Y.
King says he weighs in at about 230 pounds and has been training for about nine years.
The congressman jokes that while he plans to throw real punches, Foley will probably throw "sort-of-real punches."
King says that back in 1991 he boxed with former pro Seamus McDonagh in an exhibition bout on the 20th anniversary of the first Joe Frazier-Muhammad Ali fight.
Mar. 5, 2013 ? A JDRF-funded study out of Switzerland has shown that a single gene called SIRT1 may be involved in the development of type 1 diabetes (T1D) and other autoimmune diseases. The study, "Identification of a SIRT1 Mutation in a Family with Type 1 Diabetes," was published March 5 in Cell Metabolism and represents the first demonstration of a monogenetic defect leading to the onset of T1D.
The research began when Marc Donath, M.D., endocrinologist and researcher at the University Hospital Basel in Switzerland, discovered an interesting pattern of autoimmune disease within the family of one of his patients, a 26-year-old male who had recently been diagnosed with T1D. The patient showed an uncommonly strong family history of T1D; his sister, father, and paternal cousin had also been diagnosed earlier in their lives. Additionally, another family member had developed ulcerative colitis, also an autoimmune disease.
"This pattern of inheritance was indicative of dominant genetic mutation, and we therefore decided to attempt to identify it," Dr. Donath said.
Four years of analysis using three different genotyping and sequencing techniques pointed to a mutation on the SIRT1 gene as the common indicator of autoimmune disease within the family. The SIRT1 gene plays a role in regulating metabolism and protecting against age-related disease. To gain more understanding of how this genetic change in SIRT1 leads to T1D, Dr. Donath and his team performed additional studies with animal models of T1D. When the mutant SIRT1 gene found in the families was expressed in beta cells, those beta cells generated more mediators that were destructive to them. Furthermore, knocking out the normal SIRT1 gene in mice resulted in their becoming more susceptible to diabetes with greatly increased islet destruction. Dr. Donath speculates that the beta cell impairment and death due to the SIRT1 mutation subsequently activates the immune system toward T1D.
"The identification of a gene leading to type 1 diabetes could allow us to understand the mechanism responsible for the disease and may open up new treatment options," Dr. Donath explained.
Patricia Kilian, Ph.D., director of the Beta Cell Regeneration Program at JDRF, concurred, and said that the development is exciting for many reasons: "While the change in the genetic makeup within this family with type 1 diabetes is rare, the discovery of the role of the SIRT1 pathway in affecting beta cells could help scientists find ways to enhance beta cell survival and function in more common forms of the disease. This study also reinforces increasing evidence that abnormal beta cell function has a role in the development of type 1 diabetes, and that blocking or reversing early stages of beta cell dysfunction may help prevent or significantly delay the disease's onset. Drug companies are already in the process of developing SIRT1 activators, which could eventually speed our ability to translate these new research findings into meaningful therapies for patients."
JDRF is continuing to fund research by Dr. Donath that builds off of these latest findings.
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Journal Reference:
Anna Biason-Lauber, Marianne B?ni-Schnetzler, Basil?P. Hubbard, Karim Bouzakri, Andrea Brunner, Claudia Cavelti-Weder, Cornelia Keller, Monika Meyer-B?ni, Daniel?T. Meier, Caroline Brorsson, Katharina Timper, Gil Leibowitz, Andrea Patrignani, Remy Bruggmann, Gino Boily, Henryk Zulewski, Andreas Geier, Jennifer?M. Cermak, Peter Elliott, James?L. Ellis, Christoph Westphal, Urs Knobel, Jyrki?J. Eloranta, Julie Kerr-Conte, Fran?ois Pattou, Daniel Konrad, Christian?M. Matter, Adriano Fontana, Gerhard Rogler, Ralph Schlapbach, Camille Regairaz, Jos??M. Carballido, Benjamin Glaser, Michael?W. McBurney, Flemming Pociot, David?A. Sinclair, Marc?Y. Donath. Identification of a SIRT1 Mutation in a Family with Type 1 Diabetes. Cell Metabolism, 2013; 17 (3): 448 DOI: 10.1016/j.cmet.2013.02.001
Note: If no author is given, the source is cited instead.
Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.
Improper protein digestion in neurons identified as a cause of familial Parkinson'sPublic release date: 5-Mar-2013 [ | E-mail | Share ]
Contact: Karin Eskenazi ket2116@columbia.edu 212-342-0508 Columbia University Medical Center
Findings point to potential targets for preventing or treating the neurodegenerative disease
NEW YORK, NY (March 5, 2013) Researchers at Columbia University Medical Center (CUMC), with collaborators at the Albert Einstein College of Medicine of Yeshiva University, have discovered how the most common genetic mutations in familial Parkinson's disease damage brain cells. The mutations block an intracellular system that normally prevents a protein called alpha-synuclein from reaching toxic levels in dopamine-producing neurons. The findings suggest that interventions aimed at enhancing this digestive system, or preventing its disruption, may prove valuable in the prevention or treatment of Parkinson's. The study was published March 3 in the online edition of the journal Nature Neuroscience.
Parkinson's disease is characterized by the formation of Lewy bodies (which are largely composed of alpha-synuclein) in dopamine neurons. In 1997, scientists discovered that a mutation in alpha-synuclein can lead to Lewy body formation. "But alpha-synuclein mutations occur in only a tiny percentage of Parkinson's patients," said co-lead author David L. Sulzer, PhD, professor of neurology, pharmacology, and psychiatry at CUMC. "This meant that there must be something else that interfered with alpha-synuclein in people with Parkinson's."
Dr. Sulzer and his colleagues suspected that a gene called leucine-rich repeat kinase-2 (LRRK2) might be involved. LRRK2 mutations are the most common mutations to have been linked to Parkinson's. The current study aimed to determine how these mutations might lead to the accumulation of alpha-synuclein.
"We found that abnormal forms of LRRK2 protein disrupt a critical protein-degradation process in cells called chaperone-mediated autophagy," said Dr. Sulzer. "One of the proteins affected by this disruption is alpha-synuclein. As this protein starts to accumulate, it becomes toxic to neurons." Delving deeper, the researchers found that LRRK2 mutations interfere with LAMP-2A, a lysosome membrane receptor that plays a key role in lysosome function.
(Chaperone-mediated autophagy, or CMA, is responsible for transporting old or damaged proteins from the cell body to the lysosomes, where they are digested into amino acids and then recycled. In 2004, Dr. Sulzer and the current paper's other co-lead author, Ana Maria Cuervo, MD, PhD, professor of developmental & molecular biology, of anatomy & structural biology, and of medicine at Albert Einstein College of Medicine of Yeshiva University, showed that alpha-synuclein is degraded by the CMA pathway.)
"Now that we know this step that may be causing the disease in many patients, we can begin to develop drug treatments or genetic treatments that can enhance the digestion of these disease-triggering proteins, alpha-synuclein and LRRK2, or that remove alpha-synuclein," said Dr. Sulzer.
While LRRK2 mutations are the most common genetic cause of Parkinson's, it is too early to tell whether these findings, and therapies that might stem from them, would apply to patients with non-familial Parkinson's, the more common form of the disease. "Right now, all we can say is that it looks as though we've found a fundamental pathway that causes the buildup of alpha-synuclein in people with LRRK2 mutations and links these mutations to a common cause of the disease. We suspect that this pathway may be involved in many other Parkinson's patients," said Dr. Sulzer.
The study involved mouse neurons in tissue culture from four different animal models, neurons from the brains of patients with Parkinson's with LRRK2 mutations, and neurons derived from the skin cells of Parkinson's patients via induced pluripotent stem (iPS) cell technology. All the lines of research confirmed the researchers' discovery.
###
The paper is titled "Interplay of LRRK2 with chaperone-mediated autophagy." The other contributors are Samantha J. Orenstein (Einstein), Sheng-Han Kuo (CUMC), Inmaculada Tasset (Einstein), Esperanza Arias (Einstein), Hiroshi Koga (Einstein), Irene Fernandez-Carasa (University of Barcelona, Barcelona Spain), Etty Cortes (CUMC), Lawrence S. Honig (CUMC), William Dauer (University of Michigan, Ann Arbor, MI), Antonella Consiglio (University of Barcelona and University of Brescia, Brescia, Italy), and Angel Raya (Insitucio Catalana de Recerca I Estudies Avancas and Center for Networked Biomedical Research on Bioengineering, Biomaterials and Nanomedicine, Barcelona, Spain).
The collaboration of Sulzer and Cuervo was supported by a Udall Center of Excellence for Research in Parkinson's Disease of the NIH National Institute of Neurological Disorders and Stroke. This work was further supported by grants from the JPB Foundation, the National Institute on Aging (AG031782 and AG08702); the Rainwater Foundation; the Beatrice and Roy Backus Foundation; the Parkinson's Disease Foundation; Fondazione Guido Berlucchi; and Centers for Networked Biomedical Research, Ministry of Economy and Competitiveness and by a Hirschl/Weill-Caulier Career Scientist Award and a gift from Robert and Renee Belfer.
The authors declare no financial or other conflicts of interest.
Columbia University Medical Center provides international leadership in basic, pre-clinical, and clinical research; medical and health sciences education; and patient care. The medical center trains future leaders and includes the dedicated work of many physicians, scientists, public health professionals, dentists, and nurses at the College of Physicians and Surgeons, the Mailman School of Public Health, the College of Dental Medicine, the School of Nursing, the biomedical departments of the Graduate School of Arts and Sciences, and allied research centers and institutions. Established in 1767, Columbia's College of Physicians and Surgeons was the first institution in the country to grant the MD degree and is among the most selective medical schools in the country. Columbia University Medical Center is home to the largest medical research enterprise in New York City and State and one of the largest in the United States. Its physicians treat patients at multiple locations throughout the tri-state area, including the NewYork-Presbyterian/Columbia campus in Washington Heights, the new ColumbiaDoctors Midtown location at 51 W. 51st St. in Manhattan, and the new ColumbiaDoctors Riverdale practice. For more information, visit http://www.cumc.columbia.edu or http://www.columbiadoctors.org
[ | E-mail | Share ]
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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.
Improper protein digestion in neurons identified as a cause of familial Parkinson'sPublic release date: 5-Mar-2013 [ | E-mail | Share ]
Contact: Karin Eskenazi ket2116@columbia.edu 212-342-0508 Columbia University Medical Center
Findings point to potential targets for preventing or treating the neurodegenerative disease
NEW YORK, NY (March 5, 2013) Researchers at Columbia University Medical Center (CUMC), with collaborators at the Albert Einstein College of Medicine of Yeshiva University, have discovered how the most common genetic mutations in familial Parkinson's disease damage brain cells. The mutations block an intracellular system that normally prevents a protein called alpha-synuclein from reaching toxic levels in dopamine-producing neurons. The findings suggest that interventions aimed at enhancing this digestive system, or preventing its disruption, may prove valuable in the prevention or treatment of Parkinson's. The study was published March 3 in the online edition of the journal Nature Neuroscience.
Parkinson's disease is characterized by the formation of Lewy bodies (which are largely composed of alpha-synuclein) in dopamine neurons. In 1997, scientists discovered that a mutation in alpha-synuclein can lead to Lewy body formation. "But alpha-synuclein mutations occur in only a tiny percentage of Parkinson's patients," said co-lead author David L. Sulzer, PhD, professor of neurology, pharmacology, and psychiatry at CUMC. "This meant that there must be something else that interfered with alpha-synuclein in people with Parkinson's."
Dr. Sulzer and his colleagues suspected that a gene called leucine-rich repeat kinase-2 (LRRK2) might be involved. LRRK2 mutations are the most common mutations to have been linked to Parkinson's. The current study aimed to determine how these mutations might lead to the accumulation of alpha-synuclein.
"We found that abnormal forms of LRRK2 protein disrupt a critical protein-degradation process in cells called chaperone-mediated autophagy," said Dr. Sulzer. "One of the proteins affected by this disruption is alpha-synuclein. As this protein starts to accumulate, it becomes toxic to neurons." Delving deeper, the researchers found that LRRK2 mutations interfere with LAMP-2A, a lysosome membrane receptor that plays a key role in lysosome function.
(Chaperone-mediated autophagy, or CMA, is responsible for transporting old or damaged proteins from the cell body to the lysosomes, where they are digested into amino acids and then recycled. In 2004, Dr. Sulzer and the current paper's other co-lead author, Ana Maria Cuervo, MD, PhD, professor of developmental & molecular biology, of anatomy & structural biology, and of medicine at Albert Einstein College of Medicine of Yeshiva University, showed that alpha-synuclein is degraded by the CMA pathway.)
"Now that we know this step that may be causing the disease in many patients, we can begin to develop drug treatments or genetic treatments that can enhance the digestion of these disease-triggering proteins, alpha-synuclein and LRRK2, or that remove alpha-synuclein," said Dr. Sulzer.
While LRRK2 mutations are the most common genetic cause of Parkinson's, it is too early to tell whether these findings, and therapies that might stem from them, would apply to patients with non-familial Parkinson's, the more common form of the disease. "Right now, all we can say is that it looks as though we've found a fundamental pathway that causes the buildup of alpha-synuclein in people with LRRK2 mutations and links these mutations to a common cause of the disease. We suspect that this pathway may be involved in many other Parkinson's patients," said Dr. Sulzer.
The study involved mouse neurons in tissue culture from four different animal models, neurons from the brains of patients with Parkinson's with LRRK2 mutations, and neurons derived from the skin cells of Parkinson's patients via induced pluripotent stem (iPS) cell technology. All the lines of research confirmed the researchers' discovery.
###
The paper is titled "Interplay of LRRK2 with chaperone-mediated autophagy." The other contributors are Samantha J. Orenstein (Einstein), Sheng-Han Kuo (CUMC), Inmaculada Tasset (Einstein), Esperanza Arias (Einstein), Hiroshi Koga (Einstein), Irene Fernandez-Carasa (University of Barcelona, Barcelona Spain), Etty Cortes (CUMC), Lawrence S. Honig (CUMC), William Dauer (University of Michigan, Ann Arbor, MI), Antonella Consiglio (University of Barcelona and University of Brescia, Brescia, Italy), and Angel Raya (Insitucio Catalana de Recerca I Estudies Avancas and Center for Networked Biomedical Research on Bioengineering, Biomaterials and Nanomedicine, Barcelona, Spain).
The collaboration of Sulzer and Cuervo was supported by a Udall Center of Excellence for Research in Parkinson's Disease of the NIH National Institute of Neurological Disorders and Stroke. This work was further supported by grants from the JPB Foundation, the National Institute on Aging (AG031782 and AG08702); the Rainwater Foundation; the Beatrice and Roy Backus Foundation; the Parkinson's Disease Foundation; Fondazione Guido Berlucchi; and Centers for Networked Biomedical Research, Ministry of Economy and Competitiveness and by a Hirschl/Weill-Caulier Career Scientist Award and a gift from Robert and Renee Belfer.
The authors declare no financial or other conflicts of interest.
Columbia University Medical Center provides international leadership in basic, pre-clinical, and clinical research; medical and health sciences education; and patient care. The medical center trains future leaders and includes the dedicated work of many physicians, scientists, public health professionals, dentists, and nurses at the College of Physicians and Surgeons, the Mailman School of Public Health, the College of Dental Medicine, the School of Nursing, the biomedical departments of the Graduate School of Arts and Sciences, and allied research centers and institutions. Established in 1767, Columbia's College of Physicians and Surgeons was the first institution in the country to grant the MD degree and is among the most selective medical schools in the country. Columbia University Medical Center is home to the largest medical research enterprise in New York City and State and one of the largest in the United States. Its physicians treat patients at multiple locations throughout the tri-state area, including the NewYork-Presbyterian/Columbia campus in Washington Heights, the new ColumbiaDoctors Midtown location at 51 W. 51st St. in Manhattan, and the new ColumbiaDoctors Riverdale practice. For more information, visit http://www.cumc.columbia.edu or http://www.columbiadoctors.org
[ | 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.
MEXICO CITY (Reuters) - Mexico must give greater priority to economic cooperation and education in relations with the United States rather than allowing the fight against organized crime to take center stage, a senior Mexican official said on Monday.
Mexico has spent the past six years locked in a bloody fight with powerful drug cartels whose killings, kidnappings and extortion have marred the country's image, particularly in the United States, where it ships nearly 80 percent of its exports.
President Enrique Pena Nieto is keen to rewrite the script, focusing his efforts on the economy, which has grown at a faster pace than the United States' in the last three years.
Pena Nieto's conservative predecessor, Felipe Calderon, staked his name on crushing the gangs, but by the time he left office at the end of November nearly 70,000 people had died in the violence, and his efforts were widely condemned as a failure.
Sergio Alcocer, Mexico's deputy foreign minister responsible for the United States and Canada, said the focus on tackling the cartels and border security meant many of the benefits of Mexico's ties with the United States had been ignored.
"The U.S. population needs to see Mexico is an important part of daily life," he said in an interview with Reuters.
"We're not just a geographical accident, we're not a source of problems, on the contrary. We're an area of opportunity and a source of how problems can be resolved."
Too often, cross-border debates on security and immigration had obscured the valuable contribution made by Mexican migrants to the United States, while Mexico had not made the most of its northern neighbor in modernizing its economy, Alcocer said.
Calderon spent much of his time issuing warnings about the dangers of organized crime in Mexico, and frequently berated the United States for failing to reduce its appetite for illicit drugs - or cut the supply of illegal weapons heading south.
Pena Nieto has pledged to keep up the fight against organized crime, but has focused far less on the drug war in public than his predecessor, helping to create the impression that the violence in Latin America's second biggest economy is easing.
A monthly survey conducted since April 2009 on Mexicans' perception of public security rose to its most positive level in December, Pena Nieto's first full month in office - although homicides in the country hit a three month high that month.
STUDENT BLUES
Alcocer said the government wanted to find ways of stepping up cooperation with the United States to make North America more competitive, pointing to industries like carmaking, aerospace and energy. He noted that U.S. know-how in exploiting shale oil and gas would be particularly useful for Mexico.
There would also be a push to increase the number of Mexicans studying in the United States, and vice versa, he said.
In the 2011/2012 academic year, there were some 13,900 Mexicans studying at U.S. universities, according to the U.S.-based Institute of International Education.
That put Mexico in ninth place in the list of countries sending students there - behind nations like Vietnam, Taiwan and Saudi Arabia.
The latest Mexican figure was a drop from 14,850 students in the United States in 2008/2009, and occurred in a period during which the number of Mexicans receiving a university degree or higher has risen rapidly. The total has almost doubled from 6.8 million in 2000 to more than 12.9 million in 2010.
Pena Nieto's government aims to change the picture.
"Mexico could easily have around 30,000 to 40,000 in the United States, double what we have now," said Alcocer.
This was the target the government was working toward and to achieve it Mexico must improve English teaching and devote more funds to grants and scholarships, he said.
Attracting U.S. students to Mexico seems a bigger challenge, and the numbers have fallen sharply during the drug war.
Between the 2010/11 and 2009/10 academic years - the latest figures available - the number of Americans attending Mexican universities fell by more than 40 percent. At 4,167, the 2011 total was the lowest since the end of the 1980s.
"In large measures this is due to the widespread perception in the United States that our country is a violent country," said Alcocer.
(Reporting by Dave Graham; editing by Christopher Wilson)
Social Media Insights is a daily newsletter from Business Insider that collects and delivers the top social media news first thing every morning. You can sign up to receive Social Media Insightshere or at the bottom of this post.
Who Are These Social Media Users? (Pew Research) Pew Research Center took a demographic portrait of users of various social media services. This is what they found:
Twitter:?The percentage of Internet users who are on Twitter has doubled since November 2010, currently standing at 16 percent. Those under 50, and especially those 18-29, are the most likely to use Twitter. Urban dwellers are significantly more likely than both suburban and rural residents to be on Twitter.
Facebook: Facebook remains the most-used social networking platform, as two-thirds of online adults say that they are Facebook users.? Women are more likely than men to be Facebook users, and Facebook use is especially common among younger adults.
Pew broke down demographics for Instagram, Pinterest and Tumblr as well. Read >>
Google+ Can Now Do Things Facebook Can't (The Huffington Post) For months, Google engineers have been hard at work improving Google+. Now Google+ is turning to outside developers for help super-charging its platform with the launch of Google+ Sign-In. It has the makings of a classic win-win. For developers, there's the potential for an app to "take off" when paired with Google+. For users, the more people who are developing for Google+ features and products, the better Google+ will be. For its part, Google has clearly explained how developers can get started and how this works. With Sign-In, Google brings a social identity system to apps with the ability to share data back-and-forth. But Facebook does that already, right? Facebook Connect? That may be true but Google is offering some things that Facebook doesn't.? Read >>
Quantifying Social Media (Social Media Today) Social Media marketers get absolutely obsessed with engagement figures, whether it?s the retweet count on Twitter or the number of +1?s your brand gets. However, likes and other engagement metrics are only half of the story.
Engagement is important, but it is not everything
Measurement is key
You can quantify return on investment from social media
Help is available
You need to be doing this
If you?re investing in social there?s simply no excuse to not be doing everything you can to track the return on investment from your activity. Read >>
Twitter Not A Reliable Indication Of Public Opinion (Pew Research via Mashable) Seemingly dozens of startups exist which try to make sense of Twitter sentiment, and Twitter itself has been trying hard to portray its sentiment data as an accurate reflection of public opinion. However, Pew Research Center ? among the gold standards of public research polling ? says it might be all for naught. Pew compared traditional public poll results with Twitter sentiment data around eight of the most significant political events over the last year, often finding significantly divergent results.? Read >>
Facebook Is One Step Closer To Killing The Carriers... (TechCrunch) Facebook will wage its war against your phone?s "phone" application on a new front with an update to Messenger For Android that adds VoIP calling for Canadians. It?s also improving group messaging. By combining voice-over-data calling with unified instant, asynchronous, and email messaging, Facebook could dominate communication in the developing world. Here?s why this war is worth it. Facebook?s mission to connect the world breaks down into two channels:
Public and semi-public posting to your profile and the news feed
Private communication.
It already hosts a lot of both of those stacks. The big parts that remain out of its grasp are serious email and short-form public publishing like Twitter, SMS and voice.? Read >>
...But Facebook Is Becoming Uncool (The Joy of Tech via All Things Digital) A little parental humor for the day.
Now what are you parents going to do? Read >>
How The Social Internet Changed The World (Best Communication Degrees via Ber|Art Visual Design) In these heady, modern times, and thanks to the rise of empowering social media platforms you can do anything you like on the Internet. All of which has led to global change, huge shifts in ideologies and an ongoing rethink in how we absorb and process information. Read >>
Nine months ago, Twitvid rebranded itself as Telly, as the company sought to help users find interesting videos based on things their friends were sharing. Since that rebranding, it?s launched a web app for video discovery, as well as mobile apps. The startup is updating its iPhone app, adding a few features that it hopes will improve the user experience and make it easier for viewers to share.
![[ Back to EurekAlert! ]](https://lh3.googleusercontent.com/blogger_img_proxy/AEn0k_svxPzyvk0BEMl4ljbW3gQsfVSthC0AX7AjmidraMwmaEheUVtlmylqY4IanCURxWiiD-qaVSXgkQxPUr3f0FqRUXpsEnrz7sv1b0wHVJU=s0-d){kind=small}
Public release date: 5-Mar-2013
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Nine months ago, Twitvid rebranded itself as Telly, as the company sought to help users find interesting videos based on things their friends were sharing. Since that rebranding, it?s launched a web app for video discovery, as well as mobile apps. The startup is updating its iPhone app, adding a few features that it hopes will improve the user experience and make it easier for viewers to share.