Tuesday, December 24, 2013

Cancer cell: behaving as an organism defying death

Cell is a
structural and functional unit of life,

that we all know from our high school classes..

Cell specializing in to
tissue, tissue system, organ, organ system;

that is the pattern we find in
simple to complex evolutionary pattern in all life forms.

Amoeba always reminds us
the hidden potentiality of a cell..

where many functions like growth and reproduction been discarded

for the sake of
ultimate cooperation of multicellularity.

When a cell in our body rebels to cooperate,

go on dividing and growing by itself,

defying natural process of cell death called apoptosis,

that becomes cancerous..

Cell is still a mystery..

As and when it behaves of it's own,

as selfishly competing organism in itself,

for the reasons unknown..!!

Cell as we all know about:
Cell is a structural and functional unit of life, that's what our study revealed.

Basic structures were the same as for the animal cell ..

Basic structures were the same as for the plant cell too..

Similar work lead similar specialization of cells
and that lead to formation of Tissue and Tissue System.
Further advancement lead to Organ and Organ System formation
in most evolved animals and plants of today..

Today we have a world of lives,

where..

1. Amoeba, which is a single cell organism, acellular better suits a name..

2. Plants evolved at Organ System level, but cell physiology is still the same at the cellular level..

where..

2. Animals evolved at Organ System level, but cell physiology is still the same at the cellular level..

Cell as it still remains to be known:

Cancer cells have amazed us by behaving as an organism defying death:

Cancer is ultimately the result of cells that uncontrollably grow and do not die.

Normal cells in the body follow an orderly path of growth, division, and death.

Programmed cell death is called apoptosis, and when this process breaks down, cancer begins to form. Unlike regular cells, cancer cells do not experience programmatic death and instead continue to grow and divide. This leads to a mass of abnormal cells that grows out of control.

Reality of multicellularity (One Cell in Multicellular Organization): “Multicellularity is the ultimate in cooperation,” said Travisano, who wants to understand how cooperation emerges in selfishly competing organisms. “Multiple cells make up an individual that cooperates for the benefit of the whole. Sometimes cells give up their ability to reproduce for the benefit of close kin.”

The Paramount Factor: The new study suggests that environmental conditions are paramount: Give single-celled organisms reason to go multicellular, and they will.
(evolutionary biologist Michael Travisano of the University of Minnesota, co-author of a study Jan. 17 in the Proceedings of the National Academy of Sciences.)

Study of viruses may reveal the molecular evolutionary history of cell and tendencies hidden: It has been suggested that DNA and DNA replication machineries first originated in the viral world (Forterre 1999; Villarreal and DeFilippis 2000; Forterre 2002), that virus-induced transition of cells with RNA genomes into cells with DNA genomes triggered the emergence of the three cellular domains (Forterre 2006), that the nucleus of eukaryotic cells originated from a large DNA virus (Takemura 2001; Bell 2001), or even that the selection pressure to prevent the entry of virions promoted the evolution of cell walls (Jalasvuori and Bamford 2008). All these hypotheses are not easily testable, but recent findings make them reasonable. Indeed, it has been shown that cellular proteins playing very important roles in modern organisms may have a viral origin. For instance, phylogenetic analyses have revealed that the RNA polymerase, DNA polymerase and DNA helicase that transcribe and replicate DNA in modern mitochondria were recruited from a virus that was originally integrated into the genome of the bacterium at the origin of the mitochondria (Filée and Forterre 2005). More recently, it has been shown that placentation in mammals is initiated by a protein, syncitin, encoded by a retrovirus integrated in mammalian chromosomes (De Parseval and Heidmann 2005; Prudhomme et al. 2005). There are many other examples of the role that viruses have played in recent cellular evolution (for reviews, see Ryan 2007; Brosius 2003; Villarreal 2005). Brosius wrote, for instance, that “the interaction of hosts with retroviruses, retrotransposons and retroelements is one of the eternal conflicts that drive the evolution of life” (Brosius 2003). Prangishvili and myself have recently extended his argument, concluding that the conflict between cells and viruses has been (and still is) the major engine of life evolution (Forterre and Prangishvili 2009).

Latest findings in viral studies compels to coin new definition of life and organism:

Life: Mode of existence of ribosomes encoding organisms (cells) and capsid encoding organisms (viruses) and their ancestors.

Organism: An ensemble of integrated organs (molecular and cellular) producing individuals evolving through natural selection.
(shared from:Defining life: The virus viewpoint by Patrick Forterre in NCBI article: Published online 2010 March 3)

#some related blogpost links:
cancer cases in india
cellular chemistry of cancer cell
unruly behaviour of cell
viruses are cellular organism
vedic poetry of creation
cell multicellularity in new perspective
biological classification
origin of life in metaphysical perspective
mitochondria is a prokaryotic cyanobean symbiont

chloroplast is a prokaryotic cyanobean symbiont

Tuesday, December 17, 2013

Cancer: a non communicable disease on rise in India

New cancer case to rise 21% in 7 years.

India to have 1.32 million cancer patients by 2020.

Increase in incidence of cancers of lung, thyroid and brain tumor is rising among the young.

Gall bladder cancer in women seems to be rising
(apart from breast and uterine cancer)

as is kidney cancer in males.

(Decreasing cervical and increasing breast cancer is the trend in developed countries.)

"People are getting addicted to luxurious lifestyles and avoid physical work. There is hardly any space for exercise or walking in their daily schedules, but they have created a lot of space for liquor and tobacco,"

"India is a rare country in the sense that it imposes 11 to 20 percent customs duty on imported cancer medical equipment, while these items actually deserve to be given incentives. But we can't hope for a sensible decision from the country that spends roughly just one percent of its GDP on public health,"

thankfully shared from:http://wonderwoman.intoday.in/story/alarming-rise-in-cancer-in-india/1/97751.html

data thankfully shared from

http://fagoniacreticaforcancer.com/New-Cancer-cases-rise.aspx

The latest findings of National Registry Program (NRCP)
of the Indian Council of the Medical Research (ICMR) shows that
new cases growing at roughly 2.8% a year, leading to the projection of a 21% increase in the 7years. Estimated new cases stood at 1,086,783 in 2013, projected to 1,148,692 in 2015 and 1,320,928 in 2020.

Indian states most affected with following types of cancer:
National Center for Disease Informatics and Research ( a dedicated Government institute of India which collects cancer data) in their latest report from 2009 to 2011 says that Aizawal district in Mizoram shows the highest AAR (Age Adjusted Rate) in both males and females. All PBCRs (population Bases Cancer Registries) in Gujrat and Maharshtra and Bhopal PBCR have revealed mouth as leading site of cancer while cancer of Oesophagus leads in registries in Assam and Meghalaya. Stomach cancer is largest cancer in Sikkim and Mizoram while the cancer of the Nasopharynx is leading cancer in Nagaland.

The scientific advisory committee of the program has recommended making cancer a notifiable disease.

Press reports in Indian media about
increasing in incidence of cancer
Dainik Bhaskar/08.09.2013

At present only Punjab and Tripura states of India make reporting mandatory. The recommendation is under consideration.

Private medical colleges and hospitals in the country are planning to come up with a program to help the poor sections of society to face this menace of new uprising in these two non communicable diseases: Diabetes and Cancer.

On the initiatives of WHO, the health ministers of South East Asian nations are soon going to meet to discuss some common strategies to tackle these diseases.

(National News Network, New Delhi reports)

Tuesday, December 10, 2013

Cancer: deeper cellular chemistry and bioinformatics as the future line of treatment

Newer approach to understand cancer:

We now consider cancer as a systems biology disease, not just a disease of genetics. Depending on what numbers we use, 12 to 18 percent of cancers are familial or hereditary—which means the rest of them are not. They are somatic, in that the mutations that cause the cancer arise during a person's lifetime. So there's something about people’s biology that either predisposes them to cancer or keeps them healthy.

# At its root, cancer is a disease of the DNA. But to cure it, we need to move beyond genetics and work together to uncover cancer’s deeper cellular chemistry, says Ronnie Andrews, President, Genetic and Medical Sciences at Life Technologies. Scientific American spoke with Andrews* about this new approach to combat cancer in the 21st century.

*thankfully shared from a blog by Ronnie Andrews - 11/11/13 : file:///E:/cancer-reconceptualized.html

Finding a cure means:

Let's say the blueprint for a cancer is developed in a downtown Los Angeles architectural firm. But the cell doesn’t become cancerous unless the blueprint makes it to a manufacturing facility located in Newport Beach. So the architects give their blueprint to a courier who drives to Newport Beach and can get there one of many different ways—if a road is blocked off somewhere, he can take a different route. After the Human Genome Project, pharmaceutical companies realized that they may not be able to change the blueprint for cancer—as in, the genetic instructions for it—but they could potentially block the highway system so that the courier couldn’t get to the manufacturing center and deliver these instructions. By this we mean that it might be possible to keep the cancer genome from being transcribed—to prevent the "bad" proteins that create massive cell production from ever being made.

Treating individual patient:

Let's say you get a biopsy of a person’s tumor and identify a handful of cells of interest in that tumor. Then you do a whole genome sequence analysis of those cells and see all of the multiple potential mutational drivers of the cancer. At the same time, there are new proteomic tools coming out that will show us in real great detail and quantification not only what proteins are being produced, but where they’re being produced in the cell.

Once we have all this information, what do we do? Let's go back to our analogy. What we want to do is make a Google map of the patient's cancer cells. Then a doctor could figure out where the courier is at any point in time and pick drugs that stop the courier today by disrupting a particular biochemical pathway. And, after identifying future off-ramps that the courier might take, doctors could also prescribe drugs that would thwart the cancer in the future.

http://ncip.nci.nih.gov/blog/bioinformatics/

Role of bioinformatics:

To find this perfect cocktail, you can imagine that a doctor would flip open an iPad, log on to a portal and pull down his patient’s information, which is password and HIPAA protected. Then he would relate the data from his patient to outcomes from similar patients from the past, whose details have been kept, anonymously, in a centralized database. He'll be able to query the database and say, "show me 50 patients around the world that look like my patient at the genome and protein level, and now show me the top protocols that have allowed for the best survival rates for that patient." This is the power of bioinformatics that we’re now all chasing. (*thankfully shared from a blog by Ronnie Andrews - 11/11/13 : file:///E:/cancer-reconceptualized.html)

Tuesday, December 3, 2013

Cancer: reasons behind unruly behaviour of a single cell

Cancers are primarily an environmental disease
with 90–95% of cases attributed to environmental factors
and 5–10% due to genetics.

Cancer is ultimately the result of cells that uncontrollably grow and do not die.
Normal cells in the body follow an orderly path of growth, division, and death.
Programmed cell death is called apoptosis, and when this process breaks down, cancer begins to form. Unlike regular cells, cancer cells do not experience programmatic death and instead continue to grow and divide. This leads to a mass of abnormal cells that grows out of control.

Cancer cells can spread through the body in a process known as metastasis. This cancer cell is moving down a pore in a filter. The image was taken at Cancer Research UK, where the spread of cancer is studied in the hope of finding a cure. (©Anne Weston )

Carcinogenesis or oncogenesis or tumorigenesis is literally the creation of cancer.

It is a process by which normal cells are transformed into cancer cells.
It is characterized by a progression of changes at the cellular, genetic and epigenetic level
that ultimately reprogram a cell to undergo uncontrolled cell division, thus forming a malignant mass.

Cancers are caused by a series of mutations.

Each mutation alters

the behavior of the

cell somewhat.

image credit:http://en.wikipedia.org

There are five broad groups that are used to classify cancer.

Carcinomas are characterized by cells that cover internal and external parts of the body such as lung, breast, and colon cancer.
Sarcomas are characterized by cells that are located in bone, cartilage, fat, connective tissue, muscle, and other supportive tissues.
Lymphomas are cancers that begin in the lymph nodes and immune system tissues.
Leukemias are cancers that begin in the bone marrow and often accumulate in the bloodstream.
Adenomas are cancers that arise in the thyroid, the pituitary gland, the adrenal gland, and other glandular tissues.

Cancers are often referred to by terms that contain a prefix related to the cell type in which the cancer originated and a suffix such as -sarcoma, -carcinoma, or just -oma. Common prefixes include:

Adeno- = gland
Chondro- = cartilage
Erythro- = red blood cell
Hemangio- = blood vessels
Hepato- = liver
Lipo- = fat
Lympho- = white blood cell
Melano- = pigment cell
Myelo- = bone marrow
Myo- = muscle
Osteo- = bone
Uro- = bladder
Retino- = eye
Neuro- = brain

A protein that can mean life or death for cells: Sep. 17, 2013 — Each cell in an organism has a sensor that measures the health of its "internal" environment. This "alarm" is found in the endoplasmic reticulum (ER), which is able to sense cellular stress and trigger either rescue responses or the death of the cell. A team from the Institute for Research in Biomedicine (IRB), in Barcelona, has discovered that the protein Mitofusin 2 (Mfn2) plays a crucial role in correctly measuring stress levels, and also makes sure the pathways of cell repair or cell death are effective. The researchers reveal some of the molecular mechanisms that connect Mfn2 to endoplasmic reticulum stress in the latest edition of the scientific journal, EMBO Journal, from the Nature Group, published by the European Molecular Biology Organization.

In the image, the ER of a

cell with the Mfn2 protein (left)

and without it. On the right,

the ER form vesicles which

indicates that the organelle is

completely disorganized and

unable to respond correctly

to cellular stress.

(Credit: JP Muñoz)

When the scientists removed Mfn2 from the cell under conditions of cell stress, the endoplasmic reticulum responded by over-activating the repair pathways. By doing so, it contradictorily functioned worse, reducing the capacity of cells to overcome the stress insult and promoting to a lesser degree apoptotic cell death. "When Mfn2 is removed, the cellular stress response pathways are completely disrupted," says Antonio Zorzano, coordinator of IRB's Molecular Medicine Programme and leader of the group "Heterogenic and polygenic diseases."

"The fact that we can modulate cell damage response with Mfn2 opens a wide window of possible therapeutic avenues for further study," says Muñoz. The Chilean scientist at IRB explains that tumour cells don't activate cell death properly and proliferate uncontrolled. "Cancer cells have already been noted to have low Mfn2 levels, and if we could increase such levels, we would be able to promote apoptosis," he continues. According to this, other research teams have already published work indicating that the overexpression of Mfn2 induce apoptosis.

Professor Per Hall. (Credit: Gustav Mårtensson)

Genetic 'Spelling Mistakes' that increase risk of common cancers determined:

Mar. 27, 2013

More than 80 'genetic mistakes' that can increase the risk of breast, prostate and ovarian cancer have found in a large, international research study within the framework of the EU network COGS. For the first time, researchers also have a relatively clear picture of the total number of genetic alternations that can be linked to these cancers. Ultimately the researchers hope to be able to calculate the individual risk of cancer, to better understand how these cancers develop and and to be able to generate new treatments.

The scientists performed genetic analyses on all study participants. The composition of nitrogen bases A, G, C and T was studied on 200,000 selected sections of the DNA strand. When cancer patients had significantly different compositions compared to healthy control subjects, the difference were considered to be relevant to risk of disease. The alternations can be described as a genetic 'spelling mistake', where A, G, C or T have been replaced with another letter. This spelling mistake is called Single Nucleotide Polymorphis, (SNP) - pronounced 'snip'. "COGS is the largest genotyping project in the world targeting identification of alterations that influence the risk of common cancers. The collaborative efforts have been tremendous and key to success," says COGS coordinator Per Hall.

Decoded: Molecular messages that tell prostate and breast cancers to spread:

Apr. 30, 2013

Cancer cells are wily, well-traveled adversaries, constantly side-stepping treatments to stop their spread. But for the first time scientists at the University of Michigan have decoded the molecular chatter that ramps certain cancer cells into overdrive and can cause tumors to metastasize throughout the body.

Russell Taichman, a professor at the U-M School of dentistry and research associate Younghun Jung lookes at prostate and breast tumors. Their study, "Recruitment of mesenchymal stem cells into prostate tumors promotes metastasis," appears April 30 in the online journal Nature Communications.

Tumor cells secrete signals that
call in wound healing cells to
the tumor site. In the process,
the normal wound healing cells
make the tumor cells more
aggressive and able to metastasize.
(Credit: Image courtesy of University of Michigan)

Consider that a tumor is a wound that won't heal. To that end, both cancerous and benign tumors emit distress signals and messages to recruit healing-type cells, called mesenchymal stem cells, or MSCs, Taichman said.

"Now we know what messages (tumors) send to recruit and alter those healing cells, and we can take steps to block those messages," said Taichman, the study's principal investigator. To that end,

Taichman said he was surprised at the large role played by the protein CXCL16 in altering the healing type cells in such a way that they revved the cancer cells into overdrive.

Life style changes may lengthen telomeres a measure of cell aging: Sep. 16, 2013 — A small pilot study shows for the first time that changes in diet, exercise, stress management and social support may result in longer telomeres, the parts of chromosomes that affect aging. The study will be published online on Sept. 16, 2013 in The Lancet Oncology.

Three-dimensional representation

of the molecular structure of a

telomere (G-quadruplex).

picture credit:http://en.wikipedia.org


The greenish-yellow tips on this human chromosome (No. 16) are telomeres. Scientists claim they have evidence that explains why lifestyle changes known to be good for you — low-fat diets, exercise, reducing stress — can lengthen your life. picture credit: http://www.npr.org

Telomeres are the protective caps on the ends of Telomeres are the protective caps on the ends of chromosomes that affect how quickly cells age. They are combinations of DNA and protein that protect the ends of chromosomes and help them remain stable. As they become shorter, and as their structural integrity weakens, the cells age and die quicker.

In recent years, shorter telomeres have become associated with a broad range of aging-related diseases, including many forms of cancer, stroke, vascular dementia, cardiovascular disease, obesity, osteoporosis and diabetes.

For five years, the researchers followed 35 men with localized, early-stage prostate cancer to explore the relationship between comprehensive lifestyle changes, and telomere length and telomerase activity. All the men were engaged in active surveillance, which involves closely monitoring a patient's condition through screening and biopsies.

Ten of the patients embarked on lifestyle changes that included: a plant-based diet (high in fruits, vegetables and unrefined grains, and low in fat and refined carbohydrates); moderate exercise (walking 30 minutes a day, six days a week); stress reduction (gentle yoga-based stretching, breathing, meditation). They also participated in weekly group support.

They were compared to the other 25 study participants who were not asked to make major lifestyle changes.

The group that made the lifestyle changes experienced a "significant" increase in telomere length of approximately 10 percent. Further, the more people changed their behavior by adhering to the recommended lifestyle program, the more dramatic their improvements in telomere length, the scientists learned.

Telomere nucleotide sequences for human and mouse is TTAGGG, i.e.Telomeric repeat (5' to 3' toward the end).

#consulted & shared thankfully from: http://www.sciencedaily.com, http://www.npr.org , http://en.wikipedia.org, http://www.medicalnewstoday.com

Notes on Carcinogens:

Procarcinogen

A procarcinogen is a precursor to a carcinogen. One example is nitrites when taken in by the diet. They are not carcinogenic themselves, but turn into nitrosamines in the body, which are carcinogenic.

Common carcinogens

Occupational carcinogens

Occupational carcinogens are agents that pose a risk of cancer in several specific work-locations:

Carcinogen	Associated cancer sites or types	Occupational uses or sources
Arsenic and its compounds	Lung Skin Hemangiosarcoma	Smelting byproduct Component of: Alloys Electrical and semiconductor devices Medications (e.g. melarsoprol) Herbicides Fungicides Animal dips Drinking water from contaminated aquifers.
Asbestos	Lungs Asbestosis Gastrointestinal tract Pleural Mesothelioma Peritoneal Mesothelioma	Not in widespread use, but found in: Constructions Roofing papers Floor tiles Fire-resistant textiles Friction linings (only outside Europe) Replacement friction linings for automobiles still may contain asbestos
Benzene	Leukemia Hodgkin lymphoma	Light fuel oil Former use as solvent and fumigant Printing Lithography Paint Rubber Dry cleaning Adhesives Coatings Detergents
Beryllium and its compounds	Lung	Missile fuel Lightweight alloys Aerospace applications Nuclear reactors
Cadmium and its compounds	Prostate	Yellow pigments Phosphors Solders Batteries Metal paintings and coatings
Hexavalent chromium(VI) compounds	Lung	Paints Pigments Preservatives
IC engine exhaust gas	Lung Bladder	Exhaust gas from engines
Ethylene oxide	Leukemia	Ripening agent for fruits and nuts Rocket propellant Fumigant for foodstuffs and textiles Sterilant for hospital equipment
Nickel	Nose Lung	Nickel plating Ferrous alloys Ceramics Batteries Stainless-steel welding byproduct
Radon and its decay products	Lung	Uranium decay Quarries and mines Cellars and poorly ventilated places
Vinyl chloride	Hemangiosarcoma Liver	Refrigerant Production of polyvinyl chloride Adhesive for plastics Former use in pressurized containers
Shift work that involves circadian disruption	Breast
Involuntary smoking (Passive smoking)	Lung
Radium-226, Radium-224, Plutonium-238 , Plutonium-239 and other alpha particle emitters with high atomic weight	Bone (they are bone seekers) Liver	Nuclear fuel processing Radium dial manufacturing

Others

Gasoline (contains aromatics)
Lead and its compounds
Alkylating antineoplastic agents (e.g. mechlorethamine)
Other alkylating agents (e.g. dimethyl sulfate)
Ultraviolet radiation from the sun and UV lamps
Alcohol (causing head and neck cancers)
Other ionizing radiation (X-rays, gamma rays, etc.)

#consulted & shared thankfully from: http://www.sciencedaily.com, http://www.npr.org , http://en.wikipedia.org, http://www.medicalnewstoday.com

Tuesday, November 26, 2013

Antibiotic crisis and molecular medicine

Antibacterial/Antibiotic:

In 1928 that Alexander Fleming observed antibiosis against bacteria by a fungus of the genus Penicillium. Fleming postulated the effect was mediated by an antibacterial compound named penicillin, and that its antibacterial properties could be exploited for chemotherapy.

Sir Alexander Fleming, 1952
Photograph courtesy of Associated Press

The discovery of such a powerful antibiotic was unprecedented, and the development of penicillin led to renewed interest in the search for antibiotic compounds with similar efficacy and safety. These drugs were later renamed antibiotics by Selman Waksman, an American microbiologist, in 1942.

Antibiotics and World War 2:

Penicillin, the first natural antibiotic discovered by Alexander Fleming in 1928

1939 - coinciding with the start of world war 2,

commercially manufactured antibiotics universally and effectively used to treat wounds and ulcers during WW2.

As the first antibiotic discovered was penicillin. Penicillin was first widely used on large numbers of patients in World War II (1939–45).

The wonder drug:

Penicillin was first tested for military use in the spring of 1943, with pilot studies on soldiers with chronic bacterial infections in Bushnell General Hospital in Utah and Halloran General Hospital in New York. By autumn, doctors were using antibiotic in combat zones, where it was limited to American and Allied military and to patients with life-threatening infections.

The first U.S. wounded to directly benefit from the drug were the flight crews of the Eighth Air Force stationed in Britain. Rationing was necessary, as a single infection could require 2 million or more units of the drug (single ampoules sealed glass vessels holding solutions

for hypodermic injection contained 100,000 units). During the war, the armed forces received 85 percent of the nation's production, which amounted to 231 billion units in 1943. With the implementation of successful mass-production techniques, 1,633 billion units were produced in 1944 and 7,952 billion units in 1945. Penicillin became the war's "wonder drug," and its remarkable medical effects on infectious disease made World War II different from any previous war. (http://www.lib.niu.edu/2001/iht810139.html)

Antibiotic crisis:

Antibiotics, the wonder drug of the 20th century, may become irrelevant in the very near future and as so called Superbugs develops immunity to medication.

Overuse of antibiotics may lead to superbug epidemic much sooner than is commonly thought.

A crisis looms. In the very near rapidly approaching future, the wonder drugs of the 20th century, antibiotics, may cease to be useful.

Antibiotics become a thing of the past: revolutionary research:

Just this month, researchers have announced a new treatment that will combat antibiotic resistance. This new synthesis, called PPMO *, offers a fundamentally different attack on bacterial infections.

PPMO are synthetic analogs of DNA or RNA that have the ability to silence the expression of specific genes.

The mechanism that PPMOs use to kill bacteria is revolutionary,” said Bruce Geller, a professor of microbiology in the OSU College of Science and lead author on the study. “They can be synthesized to target almost any gene, and in that way avoid the development of antibiotic resistance and the negative impacts sometimes associated with broad-spectrum antibiotics.

“Molecular medicine,”# Geller said, “is the way of the future.” PPMOs specifically target the underlying genes of a bacterium, whereas conventional antibiotics disrupt its cellular function with broader, often unwanted consequences.

#(The molecular medicine perspective emphasizes cellular and molecular phenomena and interventions rather than the previous conceptual and observational focus on patients and their organs.)

*PPMO: peptide-conjugated phosphorodiamidate morpholino oligomer

The findings were published this month in the Journal of Infectious Diseases, by researchers from OSU, the University of Texas Southwestern Medical Center, and Sarepta, Inc., a Corvallis, Ore., firm.

Reference:1.Geller, Bruce L., Marshall-Batty, Kimberly, Schnell, Frederick J., Mcknight, Mattie M., Iversen, Patrick L. and David E. Greenberg. Gene-Silencing Antisense Oligomers Inhibit Acinetobacter Growth In Vitro and In Vivo. Journal of Infectious Diseases, October 2013

Thankfully consulted and shared above references from: http://nimblepixie.com/?p=8038 http://jid.oxfordjournals.org/content/early/2013/09/30/infdis.jit460.abstract http://www.lib.niu.edu/2001/iht810139.html http://en.wikipedia.org

Thursday, November 21, 2013

Links between culture, health and happiness

The Impact of Cultural Engagement and Sports Participation on Health and Satisfaction with Life

A survey in Scotland has found that people who engage in culture are more likely to report good health.

Flag of Scotland
picture credit:http://www.wikipedia.org

Participation in culture is significantly associated with good health and high life satisfaction in Scotland, according to the latest research. A detailed study by Scottish Government analysts of the impact on health of both culture and sport, based on data from the Scottish Household Survey 2011, confirms for the first time that participating in culture or attending cultural places or events has a positive impact on the nation’s health and life satisfaction.

The report, Healthy Attendance: The Impact of Cultural Engagement and Sports Participation on Health and Satisfaction with life in Scotland 2013, identifies a positive link with wellbeing even when other factors including age, economic status, income, area deprivation, education qualification, disability or long-standing illness and smoking are accounted for.

thankfully shared from

http://www.scotland.gov.uk/Publications/Recent

thankfully shared from

http://www.scotland.gov.uk/Publications/Recent

thankfully shared from

http://www.scotland.gov.uk/Publications/Recent

thankfully shared from

http://www.scotland.gov.uk/Publications/Recent

thankfully shared from

http://www.scotland.gov.uk/Publications/Recent

Key findings show:

Those who attended a cultural place or event in the previous 12 months were almost 60 per cent more likely to report good health compared to those who did not.
Those who participated in a creative or cultural activity in the previous 12 months were 38 per cent more likely to report good health compared to those who did not.
Those who visited a library and those who visited a museum were almost 20 per cent more likely to report good health than those who had not.
Those who visited a theatre were almost 25 per cent more likely to report good health than those who did not.
Those who participated in dance were 62 per cent more likely to report good health than those who did not.
Those who read for pleasure were 33 per cent more likely to report good health than those who did not.

The research follows data from the 2010 Scottish Household Survey that shows that people who are encouraged to participate in cultural activity as children are more likely to continue to do so into adulthood.

The survey involved nearly 10,000 respondents.

#some related blog post of the author:

http://sciencedoing.blogspot.in/2013/11/chronic-stress-alters-gene-activity-in.html

http://sciencedoing.blogspot.in/2013/05/oxidative-stress-strain-as-predisposing.html

http://sciencedoing.blogspot.in/2012/09/free-radicals-cause-and-concern.html

http://sciencedoing.blogspot.in/2011/12/oxygen-necessary-evil.html

http://sciencedoing.blogspot.in/2012/09/free-radicals-cause-and-concern.html

http://sciencedoing.blogspot.in/2013/05/dark-oxidants-super-oxides-in-depth-of.html

reference courtesy:

http://www.scotland.gov.uk/Resource/0043/00430649.pdf

http://www.enterprise-europe-scotland.com

http://www.scotland.gov.uk

http://www.heraldscotland.com

http://new.a-n.co.uk

http://www.modernghana.com

Monday, November 11, 2013

Chronic stress alters gene activity in immune cells and oxidative stress detection tools

Chronic stress' effects can be traced to your genes

Researchers say repeated stress that triggers the sympathetic nervous system can lead to inflammation that is linked to many health problems.

A bad boss can cripple your immune system
"So what this suggests is that if you're working for a really bad boss over a long period of time, that experience may play out at the level of gene expression in your immune system."

Last Updated: Wednesday, November 06, 2013, 16:02

(http://zeenews.india.com/news/health/health-news/chronic-stress-effects-can-be-traced-to-your-genes_24897.html)

http://www.health24.com/Mental-Health/

Stress/News/Effects-of-chronic-stress-can-

be-traced-to-genes-20131106

Washington: A new study has showed that chronic stress alters gene activity in immune cells
before they reach the bloodstream.

With these changes,
the cells are primed to fight an infection or trauma that doesn't actually exist,
leading to an overabundance of the inflammation that is linked to many health problems.

Ohio State University scientists made and their colleagues from other institutions, testing blood samples from humans living in poor socioeconomic conditions, found that similarly primed immune cells were present in these chronically stressed people as well.

Co-lead author John Sheridan, professor of oral biology in the College of Dentistry and associate director of Ohio State's Institute for Behavioral Medicine Research (IBMR),sa di that the cells share many of the same characteristics in terms of their response to stress.

He said that there is a stress-induced alteration in the bone marrow in both our mouse model and in chronically stressed humans that selects for a cell that's going to be pro-inflammatory.

Sheridan and colleagues have been studying the same mouse model for a decade to reveal how chronic stress - and specifically stress associated with social defeat - changes the brain and body in ways that affect behavior and health.

The mice are repeatedly subjected to stress that might resemble a person's response to persistent life stressors. In this model, male mice living together are given time to establish a hierarchy, and then an aggressive male is added to the group for two hours at a time.

This elicits a "fight or flight" response in the resident mice as they are repeatedly defeated by the intruder.

Under normal conditions, the bone marrow in animals and humans is making and releasing billions of red blood cells every day, as well as a variety of white blood cells that constitute the immune system.

In this work, the researchers compared cells circulating in the blood of mice that had experienced repeated social defeat to cells from control mice that were not stressed. The stressed mice had an average fourfold increase in the frequency of immune cells in their blood and spleen compared to the normal mice.

#The study has been published in the journal Proceedings of the National Academy of Sciences.

#This work was supported by the National Institutes of Health; the Mind, Body, Brain and Health Initiative of the John D. and Catherine T. MacArthur Foundation; the British Columbia Ministry of Child and Family Development via the Human Early Learning Partnership; and the Allergy, Genes and Environment Research Network.

Additional co-authors are Erica Sloan of UCLA and the Monash Institute of Pharmaceutical Sciences in Australia; Michael Bailey (associate professor of oral biology) and Brenda Reader of Ohio State's IBMR; Jesusa Arevalo of UCLA; Gregory Miller and Edith Chen of Northwestern University; and Michael Kobor of the University of British Columbia.(http://www.eurekalert.org/pub_releases/2013-11/osu-eoc110513.php)

Oxidative stress

is considered to be involved in

a multitude of pathogenic processes

and is also implicated in the process of aging.

Generation of reactive oxygen species (ROS) is inevitable for aerobic organisms and, in healthy cells, occurs at a controlled rate. Under conditions of oxidative stress, ROS production is dramatically increased, resulting in subsequent alteration of membrane lipids, proteins, and nucleic acids. Oxidative damage of these biomolecules is associated with aging as well as a variety of pathological events, including atherosclerosis, carcinogenesis, ischemia reperfusion injury, and neurodegenerative disorders.