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PUBLISH PAPER REVIEW-SYSTEMIC LUPUS ERYTHEMATOSUS

SYSTEMIC LUPUS ERYTHEMATOSUS

My publish paper review is based on Systemic Lupus Erythematous. You can feel free to read this article at  http://www.jle.com/en/revues/medecine/ejd/e-docs/00/01/88/56/article.phtml.

Systemic Lupus Erythematous is a chronic auto immune inflammatory disease that has protean manifestations and follows a relapsing and remitting course.. This affects more woman than men and is considered one of the most dramatic, frightening and lonely terminal diseases. Lupus is neither infectious nor contagious but sadly there is no cure. It is characterized by an autoantibody response to nuclear and cytoplasmic antigens.  This disease causes pain and swelling. It can affect the skin, ,joints, ,kidneys, lungs, nervous system and other organs of the body. Lupus flares vary from mild to serious.

The immune system in the body’s defense system. When healthy, it protects the body by making antibodies that attack germs and cancers. With lupus, the immune system misfires. Instead of providing protective antibodies, an autoimmune disease begins and makes “autoantibodies,” which attack the patient’s own tissues. As the attack goes on, other immune cells join the fight. This then leads to inflammation and abnormal blood vessels. These antibodies then end up in cells in organs, where they damage those tissues. People with lupus may also have an impaired process for clearing old and damaged cells from the body, which causes an abnormal immune response.

The  specific cause of SLE is unknown but multiple factors are associated with the development of the disease, including genetic, epigenetic, ethnic, immunoregulatory, hormonal, and environmental factors.

T cells play a central role in SLE pathogenesis, and T cells from patients with lupus show defects in both signaling and effector function. These T cells secrete less interleukin (IL)-2, and one defect in signaling seems to be linked to an increase in calcium influx. The following seem to be adversely affected in T cells from patients with SLE: effector activity such as CD8 cytotoxicity; T-regulatory, B-cell help; migration; and adhesion. However, the method by which each of these deficits contributes to the exact clinical syndrome seen in an individual patient is still unknown.

Immune complexes form in the microvasculature, leading to complement activation and inflammation. furthermore, antibody-antigen complexes deposit on the basement membranes of skin and kidneys. In active SLE, this process has been confirmed by demonstration of complexes of nuclear antigens such as DNA, immunoglobulins, and complement proteins at these sites. Autoantibodies have been found to be biomarkers for future neuropsychiatric events in SLE. Serum antinuclear antibodies (ANAs) are found in nearly all individuals with active SLE. Antibodies to native double-stranded DNA are relatively specific for the diagnosis of SLE.

Lupus affects most people in their 20s and 30s. it occurs more often in women than men. This disease is more common in some ethnic groups, mainly blacks and Asians, and tends to be worst in these groups. There are certain countries in which the disease appears to be more prevalent, for instance the Caribbean, the far east, and China. Ultraviolet light stimulates keratinocytes, which leads not only to overexpression of nuclear ribonucleoproteins (snRNPs) on their cell surfaces but also to the secretion of cytokines that simulate increased autoantibody production. Photosensitivity is clearly a precipitant of skin disease. Silica dust and cigarette smoking may increase the risk of developing SLE. Administration of estrogen to postmenopausal women appears to increase the risk of developing SLE. Estrogen can raise the risk of blood clots. Breastfeeding is associated with a decreased risk of developing SLE.

Lupus has many symptoms. Some common ones are

  • Joint pain or swelling
  • Muscle pain
  • Fever with no known cause
  • Fatigue
  • Red rashes, often on the face (also called the “butterfly rash”)
  • Anaemia
  • Kidney involvement
  • Hair loss
  • Seizures
  • Abnormal blood clotting
  • Arthritis

References

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Video

GLYCOLYSIS

Fun way to learn the long process of glycolysis. Helps in remembering the words..

PUBLISH PAPER REVIEW- ALCOHOL ALERT

My review is based on alcohol metabolism in the body and the effects it has on the body. This article (http://pubs.niaaa.nih.gov/publications/AA72/AA72.htm) was posted by the National Institutes of Health/ National Institute on Alcohol Abuse and Alcoholism.

As you all know many university students lean towards alcohol when stressed. Many people drink alcohol for the effect that alcohol has on the central nervous system. It is both a depressant and a stimulant, and drinking can result in feelings of euphoria, disorientation or a pleasurable release of tension. So let’s learn about what happens to the alcohol in the body and the reasons why we feel the way we do.

WHAT IS ALCOHOL?

There are many types of alcohol in the chemical world, but the one we consume the most is ethanol. Ethanol is a molecule made up of two carbon atoms, six hydrogen atoms, and one oxygen atom.  Being water soluble and fat soluble makes it enter the blood stream easily and also cell membranes. Some health consequences include alcoholism, liver damage, and various cancers. The effects of alcohol depends on the person. Their ability to metabolise alcohol which is controlled by genetic factors and environmental factors.

WHAT HAPPENS TO ALCOHOL WHEN CONSUMED?

Alcohol metabolism mostly takes place in the liver or sometimes in the pancreas and the brain, which can cause damage to cells and tissues. Alcohol is metabolised by the enzymes alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH). The ADH metabolizes alcohol to acetaldehyde, a carcinogen, then the acetaldehyde is further broken down to acetate. The acetate is broken down to water and carbon dioxide for elimination. The enzymes cytochrome P450 2E1 (CYP2E1) and catalase also break down alcohol to acetaldehyde. CYP2E1 is only used in persons who consume large amounts of alcohol. Acetaldehyde is short lived in the body but has the most effect on the body. Researchers believe that this product is responsible for the behavioural and psychological effects of alcohol. It causes memory impairment, sleepiness, and in-coordination.

Alcohol Metabolizing Process

Drinkers suffer slow reactions, slurred speech and memory loss. This can be caused by ethanol attaching to glutamate receptors in your brain’s neural circuitry. These receptors now receives an ethanol molecule instead of chemical signals. This interrupt the flow of signals and slows the brain down. GABA (gamma-amino butyric acid) is an inhibitory neurotransmitter in the central nervous system. Ethanol also binds to these GABA receptors, and in turn slows down brain activity. Unlike glutamate receptors, ethanol actually makes GABA receptors more receptive, causing the brain to slow down even more. But alcohol isn’t only a depressant, it can also stimulate the production of dopamine and endorphins, chemicals that produce feelings of pleasure.

The body can only metabolise a certain amount of alcohol per hour no matter how much the individual drinks. Metabolism rate depends on liver size and body mass and also the variations of ADH and ALDH enzymes in the body. A fast ADH enzyme or a slow ALDH enzyme can cause acetaldehyde build up and causes nausea and rapid heart rate. Genetic differences in these enzymes explains why some ethnic groups have lower or higher rates of alcohol related problems.

The way alcohol is metabolised and eliminated can explain why some people can drink more than others. Also this can explain why some may develop serious health conditions due to alcohol. 

So Students drink because they think alcohol makes it easier to meet other people, relaxes their social inhibitions and helps them have more fun. But while you all are having with alcohol please remember the effects it has on the body. Excessive drinking may have serious health consequences.

DRINK RESPONSIBLY!!!

 

Reference:

QUIZ TIME

GLYCOLYSIS QUIZ 

(1)

Which of the structure below is α-L-glucose?

A) Image

B) Image

C) Image

D) Image

(2)

How many ATP is produced in the Glycolysis reaction?

A) 2

B) 6

C) 3

D) 4

E) 1

Select the correct multiple answer using ONE of the keys A, B, C, D or E as follows:

A. 1, 2 and 3 are correct

B. 1 and 3 are correct

C. 2 and 4 are correct

D. only 4 is correct

E. all are correct

(3)

What are the enzymes that are involved in substrate level phosphorylation in glycolysis?

1) pyruvate kinase

2) enolase

3) phosphoglycerate kinase

4) phosphofructokinase 1

 (4)

The cofactors in the TCA cycle are:

1) NAD+

2) TPP

3) lipoate

4) FAD

(5)

In the reaction involving the enzyme glyceraldehyde-3-phosphate dehydrogenase of gylcolysis, which of the following occurs?

1) 2ADP         2ATP

2) 2NAD+          2NADH + H+   

3) 1,3-bisphosphoglycerate            3-phosphoglycerate

4) Glyceraldehyde-3-phosphate              1,3-bisphosphoglycerate

ENZYME INHIBITION

Enzyme inhibitors are molecules which binds to the enzyme to decrease their activity. These can either be reversible or irreversible. The set we will look at today is the reversible inhibitors. reversible inhibitors binds to enzymes with non-covalent bonds such as hydrogen bonds, hydrophobic interactions and ionic bonds. Reversible inhibitors generally do not undergo chemical reactions when bound to the enzyme and can be easily removed by dilution or dialysis.

 

  Competitive inhibition Non-competitive inhibition Un-competitive inhibition Mixed inhibition
Does the inhibitor resemble the substrate? Yes- have similar shape to substrate No similarity in shape to substrate No No
Where does the inhibitor bind? • Inhibitor binds to Enzyme, not to ES• Substrate and inhibitor compete for the active site  • Inhibitor binds either to ES or to Enzyme and ES• Substrate and Inhibitor bind at different sites and the active site is unaffected by Inhibitor • I binds only to ES at a different site from the substrate active site • Binds at separate site from the substrate active site, to free enzyme or ES
What is the effect on Vmax  and Km? Vmax  unchanged and Kincreases. Vmax  reduced and Km unchanged Vmax  and Km are both reduced by same amount Vmax  reduced and Km may be increased or decreased
Line Weaver Burk plots  Image  Image  Image Image

Enzyme Nomenclature

There are six major classes in naming enzymes developed by the IUBMB.

EzyFamily

http://www.csbio.sjtu.edu.cn/bioinf/EzyPred/Readme.htm

OXIDOREDUCTASES

  • Oxidation/reduction reactions
  • Transfer of electrons (H) is involved
  • Coenzymes are usually required
  • Also called dehydrogenases

TRANFERASES

  • Transfer of a functional group from a donor to acceptor molecule
  • Groups transferred – contain C, N, P
  • Examples – phosphotranferases, methyl-transferases
  • Kinases – transfer phosphate from ATP

HYDROLASES

  • Hydrolytic reactions
  • Cleavage of bonds by addition of H2O
  • Bonds – C-C; C-O; C-N; P-O
  • Acid anhydride bonds are also cleaved

LYASES

  • Elimination reaction that splits one molecule into two without an additional acceptor.
  • Cleavage of C-C, C-S, and certain C-N bonds
  • Does not involve H2O (may be a product)
  • Addition of groups to double bonds

ISOMERASES

  • Conversion of one isomer to another
  • Geometric or structural changes within a molecule
  • Intramolecular rearrangement
  • Example- shift of a double bond- aldose to ketose

LIGASES

  • Joining of molecules
  • Bond formation- coupled to hydrolysis of a high-energy compound
  • ATP or other nucleoside tri-P involved
  • Bond formation –usually between C, O, S, N
Video

Enzyme basics

Digestive enzymes