Urine Albumin and Albumin/Creatinine Ratio

Published in Biochemistry
Friday, 29 April 2016 03:04
The urine albumin test or albumin/creatinine ratio (ACR) is used to screen people with chronic conditions, such as diabetes and high blood pressure (hypertension) that put them at an increased risk of developing kidney disease. Studies have shown that identifying individuals in the very early stages of kidney disease helps people and healthcare providers adjust treatment. Controlling diabetes and hypertension by maintaining tight glycemic control and reducing blood pressure delay or prevent the progression of kidney disease.
 
Albumin is a protein that is present in high concentrations in the blood. Virtually no albumin is present in the urine when the kidneys are functioning properly. However, albumin may be detected in the urine even in the early stages of kidney disease. (See the "What is being tested?" section for more.)
 
If albumin is detected in a urine sample collected at random, over 4 hours, or overnight, the test may be repeated and/or confirmed with urine that is collected over a 24-hour period (24-hour urine).
 
Most of the time, both albumin and creatinine are measured in a random urine sample and an albumin/creatinine ratio (ACR) is calculated. This may be done to more accurately determine how much albumin is escaping from the kidneys into the urine. The concentration (or dilution) of urine varies throughout the day with more or less liquid being released in addition to the body's waste products. Thus, the concentration of albumin in the urine may also vary.
 
Creatinine, a byproduct of muscle metabolism, is normally released into the urine at a constant rate and its level in the urine is an indication of the urine concentration. This property of creatinine allows its measurement to be used to correct for urine concentration in a random urine sample. The American Diabetes Association has stated a preference for the ACR for screening for albuminuria indicating early kidney disease. Since the amount of albumin in the urine can vary considerably, an elevated ACR should be repeated twice within 3 to 6 months to confirm the diagnosis.
 
When is it ordered?
According to the American Diabetes Association and National Kidney Foundation, everyone with type 1 diabetes should get tested annually, starting 5 years after onset of the disease, and all those with type 2 diabetes should get tested annually, starting at the time of diagnosis. If albumin in the urine (albuminuria) is detected, it should be confirmed by retesting twice within a 3-6 month period. People with hypertension may be tested at regular intervals, with the frequency determined by their healthcare provider.
 
What does the test result mean?
Moderately increased albumin levels found in both initial and repeat urine tests indicate that a person is likely to have early kidney disease. Very high levels are an indication that kidney disease is present in a more severe form. Undetectable levels are an indication that kidney function is normal.
 
The presence of blood in the urine, a urinary tract infection, vigorous exercise, and other acute illnesses may cause a positive test result that is not related to kidney disease. Testing should be repeated after these conditions have resolved.
 
Is there anything else I should know?
Studies have shown that elevated levels of urinary albumin in people with diabetes or hypertension are associated with increased risk of developing cardiovascular disease (CVD). More recently, research has been focused on trying to determine if increased levels of albumin in the urine are also indicative of CVD risk in those who do not have diabetes or high blood pressure.

Cholinesterase Tests

Published in Immunology
Friday, 29 April 2016 02:55
Cholinesterase testing has two main uses:
  • It can be used to detect and diagnose organophosphate pesticide exposure and/or poisoning. It may also be used to monitor those who may be at increased risk of exposure to organophosphate compounds, such as those who work in agricultural and chemical industries, and to monitor those who are being treated for exposure. Typically, tests for red blood cell acetylcholinesterase (AChE) and serum pseudocholinesterase (PChE) are used for this purpose.
  • It can be used several days prior to a surgical procedure to determine if someone with a history of or family history of post-operative paralysis following the use of succinylcholine, a common muscle relaxant used for anesthesia, is at risk of having this reaction. In these cases, the test for pseudocholinesterase is usually used. A second test, referred to as a dibucaine inhibition test, may be done to help determine the extent to which the activity of the enzyme is decreased.
 
When is it ordered?
People who work with organophosphate compounds in the farming or chemical industries may be routinely monitored to assess any adverse exposure, once baseline levels have been established. Cholinesterase testing can also be used to assess any acute exposure to these compounds, which can cause neuromuscular damage. Toxicity can follow a rapid absorption of the compound in the lungs, skin, or gastrointestinal tract. The symptoms of toxicity are varied depending on the compound, quantity, and the site of exposure. Early symptoms may include:
  • Headache, dizziness
  • Nausea
  • Excessive tearing in the eyes, sweating and/or salivation
 
As the effects of the poisoning worsen, some additional symptoms may appear:
  • Vomiting, diarrhea
  • Dark or blurred vision due to constricted pupils
  • Muscle weakness, twitching, lack of coordination
  • Slowed breathing leading to respiratory failure, requiring lifesaving ventilation
  • In serious cases, seizures, coma, and death
 
Pre-operative screening for pseudocholinesterase activity is advised if a person or a close relative has experienced prolonged paralysis and apnea after the use of succinylcholine for anesthesia during an operation.
 
What does the test result mean?
In monitoring for occupational pesticide exposure
Following exposure to organophosphate compounds, AChE and PChE activity can fall to about 80% of normal before any symptoms occur and drop to 40% of normal before the symptoms become severe. Those who are regularly exposed to these compounds may be monitored for toxic exposure by establishing a baseline activity level and then testing on a regular basis to watch for a significant reduction on activity of acetylcholinesterase or pseudocholinesterase.
 
In testing for acute pesticide exposure/poisoning
Significantly decreased cholinesterase activity levels usually indicate excessive absorption of organophosphate compounds. Pseudocholinesterase and RBC acetylcholinesterase activity are usually decreased within a few minutes to hours after exposure. Pseudocholinesterase activity may regenerate in a few days to weeks, while acetylcholinesterase activity will remain low for as long as one to three months. Both plasma and RBC activities are immediately affected by pesticide exposure but, upon removal from exposure, AChE and PChE regenerate at different rates since AChE is produced in blood cells, which have a lifespan of 120 days, whereas PChE is produced in the liver, with a half-life of about two weeks.
 
In testing for succinylcholine sensitivity
About 3% of people have low activity levels of pseudocholinesterase due to an inherited deficiency and will have prolonged effects from the muscle relaxant succinylcholine. Total quantitative pseudocholinesterase levels will be evaluated prior to surgery for patients with a history or family history of prolonged apnea after use of this drug. Low activity levels of pseudocholinesterase levels indicate that these people may be at increased risk of experiencing prolonged effects of the muscle relaxant. A second test, the dibucaine inhibition test, may also be performed to help characterize the degree of a person's sensitivity to the drug. The lower the result from a dibucaine inhibition test, the greater the risk of drug sensitivity.
Reduced cholinesterase levels can also be caused by chronic liver disease and malnutrition. Total cholinesterase activity can be lowered in a number of other conditions, including pregnancy, renal disease, shock, and some cancers.
 
Is there anything else I should know?
If someone unexpectedly has prolonged apnea after surgery, testing for succinylcholine sensitivity may be performed; however, the sample should be obtained after 24 to 48 hours have elapsed following the surgery to avoid interference by any drugs given during the surgery that could affect the results. Drugs called cholinesterase inhibitors may have a moderate benefit in those with early diagnosed Alzheimer's disease.

Platelets Count

Published in Microbiology
Friday, 29 April 2016 02:26
Platelets

Platelets, also called "thrombocytes", are blood cells whose function (along with the coagulation factors) is to stop bleeding. Platelets have no nucleus: they are fragments of cytoplasm which are derived from the megakaryocytes of the bone marrow, and then enter the circulation. These unactivated platelets are biconvex discoid (lens-shaped) structures, 2–3 µm in greatest diameter. Platelets are found only in mammals, whereas in other animals (e.g. birds, amphibians) thrombocytes circulate as intact mononuclear cells. There are two methods for estimation of erythrocyte count:
•    Manual or microscopic method
•    Automated method
 
MANUAL METHOD
 
Principle
Free-flowing capillary or well-mixed anticoagulated venous blood is added to a diluent at a specific volume in the Unopette reservoir.  The diluents (1% ammonium oxalate) lyses the erythrocytes but preserves leukocytes and platelets.  A 20 µL pipette is used with 1.98 ml of diluents to make a 1:100 dilution. The diluted blood is added to the hemacytometer chamber.  Cells are allowed to settle for 10 minutes before leukocytes and platelets are counted. (Always refer to the manufacturer’s instructions for the procedure.)
 
Equipment
Hemocytometer with cover glass, compound microscope. Unopette capillary pipette, lint-free wipe, alcohol pads,  hand counter, petri dish with moist filter paper.
 
Reagent
Ammonium oxalate: 11.45 gm
Sorensen’s phosphate buffer: 1.0 gm
Thimerosal: 0.1 gm
Distilled water: 1000 ml
 
Specimen
EDTA-anticoagulated blood or capillary blood is preferred.
 
Method
(1) Using the protective shield on the capillary pipette, puncture diaphragm of  Unopette reservoir.    
(2) Remove shield from pipette assembly by twisting. Holding pipette almost horizontally, touch tip of pipette to blood.  Pipette will fill by capillary action. Filling will cease automatically when the blood reaches the end of the capillary bore in the neck of the pipette.
(3) Wipe the outside of the capillary pipette to remove excess blood that would interfere with the dilution factor.
(4) Squeeze reservoir slightly to force out some air while simultaneously maintaining pressure on reservoir.
(5) Cover opening of overflow chamber of pipette with index finger and seat pipet securely in reservoir neck.
(6) Release pressure on reservoir. Then remove finger from pipette opening. At this  time negative pressure will draw blood into reservoir.
(7) Squeeze reservoir gently two or three times to rinse capillary bore forcing diluent up int, but not out of, overflow chamber, releasing pressure each time to return mixture to reservoir.
(8) Place index finger over upper opening and gently invert several times to thoroughly mix blood with diuent.
(9) Cover overflow chamber with pipette shield and incubate at room temperature for 10 minutes before charging the hemacytometer.
(10) Meticulously clean the hemacytometer with alcohol or other cleaning solution. This is important because dust particles and other debris can be mistaken for platelets especially on a light microscope. Allow to dry completely before charging with diluted specimen.
(11) To charge the hemacyto-meter, convert to dropper assembly by withdrawing pipette from reservoir and reseating securely in reverse position.
(12) Invert reservoir and discard the first 3 or 4 drops of mixture.
(13) Carefully charge hemacyto-meter with diluted blood by gently squeezing sides of reservoir to expel contents until chamber is properly filled.
(14) Place hemacytometer in moist Petri dish for 10 minutes to allow platelets to settle.  (Moistened filter paper retains evaporation of diluted specimen while standing.)
(15) Mount the hemacytometer on the microscope and lower its condenser.
(16) Procedure for counting platelets:

• Under 40x magnification, scan to ensure even distribution.  Platelets are counted in all twenty-five small squares within the large center square. Platelets appear greenish, not refractile.
• Count cells starting in the upper left of the large middle square.  Continue counting to the right hand square, drop down to the next row; continue counting in this fashion until the total area in that middle square (all 25 squares) have been counted.
• Count all cells that touch any of the upper and left lines, do not count any  cell that touches a lower or right line.
• Count both sides of the hemocyt-ometer and take the average.
 
Calculation
 
cells/mm3 =      Tc x Rd     
                    Ns x As x Ds
 
     Where Tc is the number of cells counted, Rd is the reciprocal of dilution, Ns is the number of squares counted, As area of each square and Ds is the depth of the solution.
 
Example:
Total number of cells= 230
Dilution 1:100
Number of squares counted: 1
Area of each square: 1 mm3
Depth of solution: 0.1mm

cells/mm3 =         230 x 100        
                  1 x 1 mm2 x 0.01 mm
               = 230,000/mm3 (µL)
               = 230 x 103/L
 
REFERENCE RANGES
• 150,000 - 450,000/µL
• 150 - 450 x 109/L
 
REFERENCES
1. Brown, B.A., Haemotology, Principles and Procedures, Lea & Febiger, U.S.A., 1976.
2. Hoffbrand, A. V. and Pettit, 1. E., Essential Haemotology, Blackwell Scientific Publication, U.S.A., 1980.
3. Kassirsky, I. and Alexeev, G., Clinical Haemotology, Mir Publishers, U.S.S.R., 1972.
4. Widmann, F.K., Clinical interpretation of Laboratory tests, F.A. Davis Company, U.S.A., 1985.
5. Kirk, C.J.C. et al, Basic Medical Laboratory Technology, Pitman Book Ltd., U.K. 1982.
6. Green, J.H., An Introduction to human Physiology, Oxford University Press, U.K., 1980.

Serum Angiotensin Converting Enzyme

Published in Immunology
Friday, 29 April 2016 02:18
Angiotensin-converting enzyme (ACE) is an enzyme that helps regulate blood pressure. An increased blood level of ACE is sometimes found in sarcoidosis, a systemic disorder of unknown cause that often affects the lungs but may also affect many other body organs, including the eyes, skin, nerves, liver, and heart., This test measures the amount of ACE in the blood.
 
A classic feature of sarcoidosis is the development of granulomas, small tumor-like masses of immune and inflammatory cells and fibrous tissue that form nodules under the skin and in organs throughout the body. Granulomas change the structure of the tissues around them and, in sufficient numbers, they can cause damage and inflammation and may interfere with normal functions. The cells found at the outside borders of granulomas can produce increased amounts of ACE. The level of ACE in the blood may increase when sarcoidosis-related granulomas develop.
 
The angiotensin-converting enzyme (ACE) test is primarily ordered to help diagnose and monitor sarcoidosis. It is often ordered as part of an investigation into the cause of a group of troubling chronic symptoms that are possibly due to sarcoidosis.
 
Sarcoidosis is a disorder in which small nodules called granulomas may form under the skin and in organs throughout the body. The cells surrounding granulomas can produce increased amounts of ACE and the blood level of ACE may increase when sarcoidosis is present.
 
The blood level of ACE tends to rise and fall with disease activity. If ACE is initially elevated in someone with sarcoidosis, the ACE test can be used to monitor the course of the disease and the effectiveness of corticosteroid treatment.
 
A health practitioner may order ACE along with other tests, such as AFB tests that detect mycobacterial infections or fungal tests. This may help to differentiate between sarcoidosis and another condition causing granuloma formation.
 
When is it ordered?
An ACE test is ordered when someone has signs or symptoms that may be due to sarcoidosis, such as:
  • Granulomas
  • A chronic cough or shortness of breath
  • Red, watery eyes
  • Joint pain
 
This is especially true if the person is between 20 and 40 years of age, when sarcoidosis is most frequently seen.
 
When someone has been diagnosed with sarcoidosis and initial ACE levels were elevated, a health practitioner may order ACE testing at regular intervals to monitor the change in ACE over time as a reflection of disease activity.
 
What does the test result mean?
An increased ACE level in a person who has clinical findings consistent with sarcoidosis means that it is likely that the person has an active case of sarcoidosis, if other diseases have been ruled out. ACE will be elevated in 50% to 80% of those with active sarcoidosis. The finding of a high ACE level helps to confirm the diagnosis.
 
A normal ACE level cannot be used to rule out sarcoidosis because sarcoidosis can be present without an elevated ACE level. Findings of normal ACE levels in sarcoidosis may occur if the disease is in an inactive state, may reflect early detection of sarcoidosis, or may be a case where the cells do not produce increased amounts of ACE. ACE levels are also less likely to be elevated in cases of chronic sarcoidosis.
 
When monitoring the course of the disease, an ACE level that is initially high and then decreases over time usually indicates spontaneous or therapy-induced remission and a favorable prognosis. A rising level of ACE, on the other hand, may indicate either an early disease process that is progressing or disease activity that is not responding to therapy.

Edible Fishes in Pakistan

Published in Zoology
Friday, 29 April 2016 02:02
About one thousand species of fishes are found in marine and fresh water in Pakistan. Majority of these are edible. And very few are examined for their nematode parasites.
 
Most of marine fishes are included among the group of edible fishes. Some of these including, Scomberomorus guttatus, Pomadasys olivaceum, Pomadasys maculatum, Pomadasys stridens, Otolithus ruber, Sphyraena forsteri, Sphyraena jello, Lates calcarifer and Sillago sihama are popular edible fishes in Pakistan, due to their delicious taste and are full of nourishment such as proteins and vitamins particularly vitamin E and vitamin D.

Total Leukocyte Count (TLC)

Published in Microbiology
Tuesday, 26 April 2016 07:00
Total Leukocyte Count (TLC)

Total leukocyte count (TLC) refers to the number of white blood cells in 1 μl of blood (or in 1 liter of blood if the result is expressed in SI units). There are two methods for estimation of TLC:
  • Manual or microscopic method
  • Automated method
     A differential leukocyte count should always be performed along with TLC to obtain the absolute cell counts.
     The purpose of carrying out TLC is to detect increase or decrease in the total number of white cells in blood, i.e. leukocytosis or leukopenia respectively. TLC is carried out in the investigation of infections, any fever, hematologic disorders, malignancy, and for follow-up of chemotherapy or radiotherapy.

MANUAL METHOD
 
Principle
A sample of whole blood is mixed with a diluent, which lyses red cells and stains nuclei of white blood cells. White blood cells are counted in a hemocytometer counting chamber under the microscope and the result is expressed as total number of leukocytes per μl of blood or per liter of blood.
 
Equipment
(1) Hemocytometer or counting chamber with coverglass: The recommended hemocytometer is one with improved Neubauer rulings and metallized surface. There are two ruled areas on the surface of the chamber. Each ruled area is 3 mm × 3 mm in size and consists of 9 large squares with each large square measuring 1 mm × 1 mm. When the special thick coverglass is placed over the ruled area, the volume occupied by the diluted blood in each large square is 0.1 ml. In the improved Neubauer chamber, the central large square is divided into 25 squares, each of which is further subdivided into 16 small squares. A group of 16 small squares is separated by closely ruled triple lines. Metallized surface makes background rulings and cells easily visible. The 4 large corner squares are used for counting leukocytes, while the central large square is used for counting platelets and red blood cells. Only special coverglass, which is intended for use with hemocytometer, should be used. It should be thick and optically flat. When the special coverglass is placed on the surface of the chamber, a volumetric chamber with constant depth and volume throughout its entire area is formed. Ordinary cover slips should never be employed since they do not provide constant depth to the underlying chamber due to bowing.
     When the special cover glass is placed over the ruled area of the chamber and pressed, Newton’s rings (colored refraction or rainbow colored rings) appear between the two glass surfaces; their formation indicates the correct placement of the cover glass.
(2) Pipette calibrated to deliver 20 μl (0.02 ml, 20 cmm): WBC bulb pipettes, which have a bulb for dilution and mixing (Thoma pipettes) are no longer recommended. This is because blood and diluting fluid cannot be mixed adequately inside the bulb of the pipette. Bulb pipettes are also difficult to calibrate, costly, and charging of counting chamber is difficult. Tips of pipettes often chip easily and unnecessarily small volume of blood needs to be used.
(3) Graduated pipette, 1 ml.
(4) Pasteur pipette
(5) Test tube (75 × 12 mm).
 
Reagent
WBC diluting fluid (Turk’s fluid) consists of a weak acid solution (which hemolyzes red cells) and gentian violet (which stains leucocyte nuclei deep violet). Diluting fluid also suspends and disperses the cells and facilitates counting. Its composition is as follows:
• Acetic acid, glacial 2 ml
• Gentian violet, 1% aqueous 1 ml
• Distilled water to make 100 ml
 
Specimen
EDTA anticoagulated venous blood or blood obtained by skin puncture is used. (Heparin should not be used since it causes leukocyte clumping). While collecting capillary blood from the finger, excess squeezing should be avoided so as not to dilute blood with tissue fluid.
 
Method
(1) Dilution of blood: Take 0.38 ml of diluting fluid in a test tube. To this, add exactly 20 μl of blood and mix. This produces 1:20 dilution. Alternatively, 0.1 ml of blood can be added to 1.9 ml of diluting fluid to get the same dilution.
(2) Charging the counting chamber: Place a coverglass over the hemocytometer. Draw some of the diluted blood in a Pasteur pipette. Holding the Pasteur pipette at an angle of 45° and placing its tip between the coverglass and the chamber, fill one of the ruled areas of the hemocytometer with the sample. The sample should cover the entire ruled area, should not contain air bubbles, and should not flow into the side channels. Allow 2 minutes for settling of cells.
(3) Counting the cells: Place the charged hemocytometer on the microscope stage. With the illumination reduced to give sufficient contrast, bring the rulings and the white cells under the focus of the low power objective (× 10). White cells appear as small black dots. Count the number of white cells in four large corner squares. (To reduce the error of distribution, counting of cells in all the nine squares is preferable). To correct for the random distribution of cells lying on the margins of the square, cells which are touching the left hand lines or upper lines of the square are included in the count, while cells touching the lower and right margins are excluded.
 
(a) Calculation of TLC:
TLC/μl = Nw x Cd x Cv
                    NLS
          = Nw x 20 x  10
                      4
          = Nw x 50
                    
     Where Nw is the number of WBCs counted,  Cd is the correction of dilution, Cv is the correction of volume and NLS is the number of large squares counted.
(b) TLC/L = Number of WBCs counted × 50 × 106 (106 is the correction factor to convert count in 1 μl to count in 1 liter). Example: If 200 WBCs are counted in 4 large squares, TLC/μl will be 10,000/μl and TLC/liter will be 10.0 × 109/liter.
     If TLC is more than 50,000/ml, then dilution of blood should be increased to 1:40 to increase the accuracy of the result.
     If TLC is less than 2,000/ml then lesser dilution should be used.
Expression of TLC: Conventionally, TLC is expressed as cells/μl or cells/cmm or cells/mm3. In SI units, TLC is expressed as cells × 109/liter. Conversion factors for conventional to SI units is 0.001 and SI to conventional units is 1000.
 
Correction of TLC for nucleated red cells: The diluting fluid does not lyse nucleated red cells or erythroblasts. Therefore, they are counted as leukocytes in hemocytometer. If erythroblasts are markedly increased in the blood sample, overestimation of TLC can occur. To avoid this if erythroblasts are greater than 10 per 100 leukocytes as seen on blood film, TLC should be corrected for nucleated red cells by the following formula:
CTLC =    TLC x 100 
             NRBC + 100
 
     Where CTLC is the Corrected TLC/μl, TLC is the Total Leukocyte Count and NRBC is the Nucleated RBCs per 100 WBCs.
 
REFERENCE RANGES
• Adults: 4000-11,000/μl
• At birth: 10,000-26000/μl
• 1 year: 6,000-16,000/μl
• 6-12 years: 5,000-13,000/μl
• Pregnancy: up to 15,000/μl
 
CRITICAL VALUES
TLC < 2000/μl or > 50000/μl.
 
REFERENCES
1. Cheesbrough M. District laboratory practice in tropical countries. Part 1 and Part 2. Cambridge. Cambridge University Press, 1998.
2. Lewis SM, Bain BJ, Bates I. Dacie and Lewis Practical Haematology (9th Ed). London. Churchill Livingstone, 2001.
3. The Expert Panel on Cytometry of the International Council for Standardization in Haematology: Recommended methods for the visual determination of white blood cell count and platelet count. World Health Organization. WHO/DIL/00.3. 2000.
4. World Health Organization. Manual of Basic Techniques for a Health Laboratory (2nd Ed). Geneva: World Health Organization, 2003.

Acetylcholine Receptor (AChR) Antibody

Published in Immunology
Saturday, 23 April 2016 18:06
An acetylcholine receptor (AChR) antibody test is used to help diagnose myasthenia gravis (MG) and to distinguish it from other conditions that may cause similar symptoms, such as chronic muscle fatigue and weakness.
 
AchR antibodies hinder the action of acetylcholine, a chemical (neurotransmitter) that transmits messages between nerve cells. The antibodies do this in three major ways:
  • "Binding" antibodies attach to the acetylcholine receptors on nerve cells and may initiate an inflammatory reaction that destroys them.
  • "Blocking" antibodies may sit on the receptors, preventing acetylcholine from binding.
  • "Modulating" antibodies may cross-link the receptors, causing them to be taken up into the muscle cell and removed from the neuromuscular junction.
Three different types of tests are available to determine which of these may be the problem in a particular individual. However, the test that measures "binding" antibodies is most commonly used because it is generally rare for the other two tests to be positive without the "binding" test being positive as well. These other tests may be used when a doctor strongly suspects myasthenia gravis and the "binding" test is negative.
 
One or more of the AChR antibody tests may be ordered as part of a panel of tests that may also include a striated muscle antibody test to help establish a diagnosis. Depending upon results, an anti-MuSK (muscle-specific kinase) antibody test may also be ordered. The AChR antibody test may be ordered initially as a baseline test and then as indicated to evaluate MG disease activity and/or response to therapy.
 
People with MG often have an enlarged thymus gland and may have thymomas (typically benign tumors of the thymus). Located under the breastbone, the thymus is an active part of the immune system during childhood but normally becomes less active after puberty. If a thymoma is detected, such as during a chest computed tomography (CT) scan done for a different reason, then an AChR antibody test may sometimes be used to determine whether the person has developed these antibodies.
 
When is it ordered?
The AChR antibody test may be ordered when a person has symptoms that suggest MG, such as:
  • Drooping eyelid
  • Double vision
  • Decreased eye movement control
  • Difficulty swallowing, chewing, with choking, drooling and gagging
  • Slurred speech
  • Weak neck muscles
  • Trouble holding up head
  • Difficulty breathing
  • Difficulty walking and an altered gait
  • Specific muscle weakness but normal feelings/sensations
  • Muscle weakness that worsens with sustained effort and improves with rest
When a person has been diagnosed with MG, an AChR antibody test may be ordered occasionally to evaluate MG disease activity and/or response to therapy.
 
An AChR antibody test may sometimes be ordered when a thymoma is detected.
 
What does the test result mean?
AChR antibodies are not normally present in the blood. They are autoantibodies and their presence indicates an autoimmune response.
 
If a person has AChR antibodies and symptoms of MG, then it is likely that the person has this condition.
 
AChR antibodies may be seen with some thymomas, in people who are being treated with drugs such as penicillamine, with some small cell lung cancers, with autoimmune liver disease, and with Lambert-Eaton myasthenic syndrome (a condition associated with interference with the release of acetylcholine from the nerve ending).
 
A negative test result does not rule out MG. Up to 50% of those with ocular MG (affecting only eye-related muscles) and about 10-15% of those with generalized MG will be negative for AChR antibodies.
 
In general, the greater the quantity of AChR antibody, the more likely a person is to have significant symptoms, but the test results cannot be used to evaluate the severity of symptoms in a specific person.

Bacterial Genetics

Published in Bacterial Genetics
Saturday, 23 April 2016 18:02
Bacterial genetics is the subfield of genetics devoted to the study of bacteria. Bacterial genetics are subtly different from eukaryotic genetics, however bacteria still serve as a good model for animal genetic studies. One of the major distinctions between bacterial and eukaryotic genetics stems from the bacteria's lack of membrane-bound organelles (this is true of all prokaryotes. While it is a fact that there are prokaryotic organelles, they are never bound by a lipid membrane, but by a shell of proteins), necessitating protein synthesis occur in the cytoplasm.
 
Like other organisms, bacteria also breed true and maintain their characteristics from generation to generation, yet at same time, exhibit variations in particular properties in a small proportion of their progeny. Though heritability and variations in bacteria had been noticed from the early days of bacteriology, it was not realised then that bacteria too obey the laws of genetics. Even the existence of a bacterial nucleus was a subject of controversy. The differences in morphology and other properties were attributed by Nageli in 1877, to bacterial pleomorphism, which postulated the existence of a single, a few species of bacteria, which possessed a protein capacity for a variation. With the development and application of precise methods of pure culture, it became apparent that different types of bacteria retained constant form and function through successive generations. This led to the concept of monomorphism.

Genetics

Published in Genetics
Saturday, 23 April 2016 17:54
Genetics is the study of genes, heredity, and genetic variation in living organisms. It is generally considered a field of biology, but it intersects frequently with many of the life sciences and is strongly linked with the study of information systems.
 
The father of genetics is Gregor Mendel, a late 19th-century scientist and Augustinian friar. Mendel studied 'trait inheritance', patterns in the way traits were handed down from parents to offspring. He observed that organisms (pea plants) inherit traits by way of discrete "units of inheritance". This term, still used today, is a somewhat ambiguous definition of what is referred to as a gene.
 
Trait inheritance and molecular inheritance mechanisms of genes are still a primary principle of genetics in the 21st century, but modern genetics has expanded beyond inheritance to studying the function and behavior of genes. Gene structure and function, variation, and distribution are studied within the context of the cell, the organism (e.g. dominance) and within the context of a population. Genetics has given rise to a number of sub-fields including epigenetics and population genetics. Organisms studied within the broad field span the domain of life, including bacteria, plants, animals, and humans.
 
Genetic processes work in combination with an organism's environment and experiences to influence development and behavior, often referred to as nature versus nurture. The intra- or extra-cellular environment of a cell or organism may switch gene transcription on or off. A classic example is two seeds of genetically identical corn, one placed in a temperate climate and one in an arid climate. While the average height of the two corn stalks may be genetically determined to be equal, the one in the arid climate only grows to half the height of the one in the temperate climate, due to lack of water and nutrients in its environment.
 
History
The observation that living things inherit traits from their parents has been used since prehistoric times to improve crop plants and animals through selective breeding. The modern science of genetics, seeking to understand this process, began with the work of Gregor Mendel in the mid-19th century.
 
Although the science of genetics began with the applied and theoretical work of Mendel, other theories of inheritance preceded his work. A popular theory during Mendel's time was the concept of blending inheritance: the idea that individuals inherit a smooth blend of traits from their parents. Mendel's work provided examples where traits were definitely not blended after hybridization, showing that traits are produced by combinations of distinct genes rather than a continuous blend. Blending of traits in the progeny is now explained by the action of multiple genes with quantitative effects. Another theory that had some support at that time was the inheritance of acquired characteristics: the belief that individuals inherit traits strengthened by their parents. This theory (commonly associated with Jean-Baptiste Lamarck) is now known to be wrong—the experiences of individuals do not affect the genes they pass to their children, although evidence in the field of epigenetics has revived some aspects of Lamarck's theory. Other theories included the pangenesis of Charles Darwin (which had both acquired and inherited aspects) and Francis Galton's reformulation of pangenesis as both particulate and inherited.
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