Hope you guessed Right!!!

File:Mikroglej 1.jpg

Microglia – ramified form from rat cortex before traumatic brain injury.

I am a microglial cell in the brain of the common house mouse, Mus musculus.

I am able to undergo a variety of structural changes based on my location and role at one particular point in time.

I may begin as a ramified (inactive) form in the absence of cell debris. In this “resting” form I comprise of long branching processes and a small cellular body remaining fairly motionless, while my branches examine the surrounding area. At this stage, I am unable to perform phagocytosis and display little or no immunomolecules.

Following this state, I can enter into intermediate form called the activated, non-phagocytic stage. Once activated,  I experience several morphological changes including the thickening and the retraction of my branches. I eventually begin the uptake of MHC class I/II proteins, secretion of cytotoxic factors, expression of immunomolecules and even secrete pro-inflammatory signaling molecules. Here I can finally undergo proliferation increasing my numbers for any immune defense. As an activated non-phagocytic microglia cell I become visible as a “bushy rod,” or small amoeboid structure moving by means of pseudopodia.

My next stage is as an activated phagocytic microglia cell. Here, I have a large amoeboid shape in general and possess antigen presenting, and inflammatory mediating signaling devices. My ability in phagocytosis now kicks in.

References

http://physrev.physiology.org/content/91/2/461.full

http://www.ncbi.nlm.nih.gov/books/NBK28217/

http://www.bionity.com/en/encyclopedia/Microglia.html

http://www.biomedcentral.com/1471-2121/12/35

http://images.search.yahoo.com/images/view

https://www.google.tt/search?

About me…..the “special” cell.

Hello!

See if you can figure out the type of cell I am.

I am present in the brain of a very common  model organism.

I differentiated from hematopoietic stem cells in the bone marrow, the myeloid progenitor cells, during a process called hematopoiesis, some of these “originator” cells differentiated into monocytes and traveled from the bone marrow to the brain. There, they further differentiated until I resulted.

Diagram showing the location of bone marrow within a bone.

My tasks are mainly within the Central Nervous System and are related to immune response. They include, phagocytosis, cytotoxicity, scavenging, antigen-presenting and promotion of brain tissue repair after injury. I also assist in maintaining homeostasis in regions that are not infected and promote inflammation in infected tissue via extracellular signaling of molecules which allow me to communicate with my kind and my neighbor.

When I grow up, instead of being replaced with myeloid progenitor cells I intend to proliferate. Eventually, I will become a Gitter cell after engulfing a great amount unwanted material.

If you are still clueless…here’s an additional hint, I exist in the neuroglia, (the web of connective tissue that surround and support neuron cells).

What cell am I?

References

http://www.britannica.com/EBchecked/topic/380412/microglia

http://www.bionity.com/en/encyclopedia/Microglia.html

http://images.search.yahoo.com/images/view

Model Organisms

Have you ever heard about model organisms?

This you must know!

Model organisms are species used enormously in scientific research usually of human disease. They are utilized mainly because human experimentation is impracticable in many instances and are considered unethical.  Model organisms are very easy to maintain and can be breed in a laboratory setting hence, they generally have certain experimental advantages. Models possess a wealth of biological data and over the years, much  data about these organisms have been accumulated.

Model organisms are chiefly chosen once they possess particular characteristics such as:

  • A short life cycle,
  • Can be genetically manipulated
  • Practical size,
  • Easy accessibility
  • Potential economic benefit.

Examples of model organisms include:

  1. The bacterium, Escherichia Coli (present in the human digestive system)
  2. The fruit fly, Drosophila melanogaster
  3. The  nematode worm, Caenorhabditis elegans
  4. The African clawed frog, Xenopus laevis
  5. The tomato plant, Solanum lycopersicum
  6. The House Mouse, Mus musculus

 

Drosophila melanogaster- fruit fly.

The common house mouse

Just to name a few.

There are many other organisms used from a wide assortment of lineages.

 References

http://eol.org/info/466

http://genome.wellcome.ac.uk/doc_WTD020803.html

http://wormclassroom.org/teaching-model-organisms

http://images.search.yahoo.com/images/view

Missed me???

Hey Readers!!! I’m back

Did you all miss me???

So now I am in the second year of my degree and enjoying the new courses. One of the many interesting and captivating courses I am doing this semester is called, CELL DEVELOPMENTAL BIOLOGY. As the name suggests, it deals with everything that pertains to CELLS. THE BUILDING BLOCKS OF LIFE!!!

Now, I am on a new and improved mission. From this blog forth, I will be posting information about a special cell in the first person of course.

The cell will not necessarily be that of a human but, it is an organism that plays a very significant role in scientific research and discoveries in the biological and medical fields.

Interested to know what this organism is and what that special cell will be?

You just might find out in the upcoming posts……

Published Paper Review- “Recruitment of Brown Adipose Tissue as a Therapy for Obesity-Associated Diseases”.

Reference

Boss, Olivier and Stephen R. Farmer 2012. “Recruitment of Brown Adipose Tissue as a Therapy for Obesity-Associated Diseases” US National Library of Medicine: National Institute of Health. Accessed  April 10, 2013. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3356088/

http://ksj.mit.edu/sites/default/files/images/tracker/2009/brownadiposetissue.jp                                   http://www.nature.com/ncb/journal/v14/n12/images/ncb2642-f1.jpg

The article, “Recruitment of Brown Adipose Tissue as a Therapy for Obesity-Associated Diseases” was well informing as it sought to present data on the effective use of brown adipose  tissue in obesity and related diseases.

                       What is Brown adipose tissue?

According to the authors of the article, brown adipose tissue is a flexible tissue that can be recruited by stimuli, and deteriorates in the absence of a stimulus. Its has a major contribution in cold-induced non-shivering thermogenesis and body weight homeostasis in animals ana is closely related to UCP1.

https://i0.wp.com/ksj.mit.edu/sites/default/files/images/tracker/2009/brownadiposetissue.jpg

What is UCP1?                                                                                                                                                                                                       Thermogenin or uncoupling protein 1 ( UCP1) is an uncoupling protein found in the mitochondria of brown adipose tissue (BAT). It is used to generate heat by non-shivering thermogenesis. Non-shivering thermogenesis is the primary means of heat generation in hibernating mammals and in human infants.

The efficacy of increasing brown adipose tissue (BAT) recruitment (BAT mass and expression of UCP1) as a therapeutic approach for obesity and type 2 diabetes has been researched by many groups throughout the past 20 years.

Studies with rat specimens showed that agents which increase brown adipose tissue recruitment can effectively treat obesity and diabetes. In lean animals with normal brown adipose tissue amounts, enhancement of BAT recruitment or activity by drugs or cold exposure has no effect on body weight. While in obese animals, enhancement of energy spending by BAT recruitment is effective in decreasing body weight and improving metabolic status. Earlier results showed that over expression of UCP1 in white adipose tissue (WAT) of mice can prevent the development of obesity in genetic as well as dietary forms of diabetes. In contrast, lack of BAT or UCP1 stimulates obesity and diabetes in mice.

Some drugs were tested and it was revealed that induction of brown adipocyte formation with drugs in humans, in order to enhance or restore healthy levels of BAT recruitment, is possible to enhance energy expenditure.

                                 https://i0.wp.com/www.proteanservices.com/wp-content/uploads/2010/05/458839a-f1.2-292x300.jpg
Brown adipose tissue and white adipose tissue.

Studied also showed that primary preadipocytes isolated from white and brown adipose depots demonstrate in vitro (in an artificial environment outside the living organism) differentiation  into white and brown adipocytes. There were many hypotheses that showed in WAT depots, brown adipocytes can emerge from differentiation of brown adipocyte precursors or preadipocytes or by transdifferentiation of the existing white adipocytes. It was shown that hyperleptinemia in rats induces the transformation of white adipocytes into so-called post-adipocytes (or fat-oxidizing machines), which have the phenotype of brown adipocytes. Several other effectors enhance brown adipocyte recruitment in white depots like synthetic PPARγ ligands. Brown adipocytes within the interscapular BAT depot of mice share an origin with skeletal myocytes that arise from the dermomyotome.

https://i0.wp.com/www.nature.com/ncb/journal/v14/n12/images/ncb2642-f1.jpg

It is conceivable; therefore, that recruitment of WAT brown adipocytes is due to a selective activation of mural cells to progress along a brown lineage in response to effectors that are activated by the recruitment-associated stimulus. Possible effectors include BMP7, which has been shown to induce the conversion of mesenchymal stem cells to brown adipocytes in culture and is required for BAT formation in mice.

Infrared thermography provided data and proved that adult humans possess functional BAT that is activated by ephedrine.

The research showed that BAT can be recruited in humans just as in animals. Hence, brown adipose tissue could play an important role in human energy balance and body weight homeostasis and thus, has revived a concept that BAT is a therapeutic target for combating obesity-related metabolic disorders as there formerly existed a problem in identifying drug targets for brown adipocyte.

Studies found that stroma-vascular cell preparations from human BAT contained only very limited quantities of cells that can differentiate into brown adipocytes. Human brown adipocyte stem or progenitor cells, CD34+ are present in skeletal muscle and hMADs in subcutaneous WAT. These cells have self-renewal capability,  differentiate, in response to specific agents, into functional brown adipocytes and are rich in mitochondria. These cell types are thus quite distinct, and each have the potential of generating relevant cell models for studying human brown adipocyte biology as well as screening for anti-obesity therapeutics. Such screens could identify agents that induce the differentiation of the cells into brown adipocytes.

Analysis of several functional features of BAT include quantitative phenotypic cellular screens, PCR, western blot analysis of brown-selective genes and measurement of cell respiration to determine the degree of uncoupling of oxidative phosphorylation.

Authors found that defective recruitment or activity of brown adipose tissue may contribute to weight gain and insulin resistance. The metabolic activity and energy expenditure, thermogenesis, in humans is activated by cold. The amount of BAT inversely correlates to body weight and is independent of age.

Brown adipocyte stem cells are present in skeletal muscle and subcutaneous WAT of humans. This suggests that enhancing BAT recruitment to restore BAT mass to a healthy level, is practicable.

The investigations supported the contention that activation of BAT formation in obese individuals is therapeutically powerful. We also propose that enhancement of brown adipocyte functions in white adipose tissue (WAT) will also regulate energy balance as well as reduce insulin resistance in obesity-associated inflammation in WAT.

Investigations proved that resistance to obesity and other related disorders in various rodent models resulted from increased BAT mass and the number of brown adipocytes or UCP1 expression. Readily accessible brown adipocyte stem/progenitor cellsthrough biopsy of human tissues encourages the development of transplantation procedures to treat obese and diabetic patients. The implants in mice proved to advance the metabolic condition of obese, insulin resistant mice. In addition, brown adipocytes have beneficial effects on glucose metabolism, insulin sensitivity and overall energy balance. we looked at the  mechanism through which BAT affects the “adipostat.” BAT is quite different from WAT as BAT expresses significantly lower levels of resistin and other adipokines associated with insulin resistance.

https://i0.wp.com/c431376.r76.cf2.rackcdn.com/20466/fendo-03-00014-HTML/image_m/fendo-03-00014-g001.jpg

Diagram showing the recruitment of brown adipose tissue.

In simpler words…brown adipose tissue helps adults burn more calories than white adipose tissue!!!

The most promising strategy for developing therapeutics for obesity and specifically, type two diabetes is to increase BAT mass. This allows the development of effective drugs for obesity, diabetes, and the metabolic syndrome that have very little side effects.

       

Where did all the weeks go? :/

Today was my last tutorial for the semester….I am not sure if to be happy about it or sad. The semester is coming to an end!!!!!!!! Where did all the weeks go? Exams are approaching so quickly. So fellow students:

                                https://shels1biochemistinthemaking.wordpress.com/wp-content/uploads/2013/04/cpa-exam-quit-procrastinate-start-study.jpg

Anywhooos we were not marked our last tutorial so the nervousness was not there for this one. The class was sooo scarce. My final lab write up was also due today (after about a month of performing the lab). It was based on determining enzymatic activity in sweet potato extract, Irish potato extract and milk. Surprisingly….after all this extra time given students were still experiencing problems. I should talk….

                                                        Image.

My graph of substrate concentration against time was way off the origin and I did not know what to do!!!

Luckily, I asked sir and he indicated that marks would not be lost for that…phew. That’s a relief but hopefully I can obtain a better mark in this lab.

Glycolyis Wordle

Glycolysis means “splitting sugars”  and it  occurs in the cytosol of a living cell.

In glycolysis, glucose (a six carbon sugar) is split into two molecules of a three-carbon sugar, pyruvate. Glycolysis yields two molecules of ATP (free energy containing molecule), two molecules of pyruvic acid and two “high energy” electron carrying molecules of NADH.

Glycolysis can occur with or without oxygen (aerobic and anaerobic respectively). In the presence of oxygen, glycolysis is the first stage of cellular respiration. Without oxygen, glycolysis allows cells to make small amounts of ATP. This process is called fermentation.

Here is a wordle giving most of the keywords of the process.

Glycolysis wordle