Biology

Do something that you love and youll never have to work a day in your life (Wilson, Blumenthal 87), said Mark Mackay once. I knew when I saw how a chiropractor works that it was the career I wanted to pursue and excel on for the rest of my life. I knew if I become a chiropractor, that Ill love every single day of my professional career.

Healing people has been my calling from the very beginning it just took me quite a long while to figure it out. Every day, I think of the littlest ways to help the people all around me. For instance, I volunteered with Big Brothers Big Sisters and adopted a little brother for a year to do my share for the community. I also have made sack lunches with my church and handed these out to homeless people in my hometown of Little Rock, Arizona. I did all of these because theres this unquenchable inner yearning in me to ease and, hopefully, cure the suffering in my own little corner of the world.
   
Being a chiropractor is the next step toward my lifes mission of using myself as a tool of overall wellness and health. The journey though, has not been easy and is in fact filled with various challenges. For instance, my academic performance used to suffer because I decided to put work before school, thinking that if I worked hard, it would soon pay-off. Thus, I excelled in the workforce but I failed to display my full academic potential. I gathered a lot of valuable experiences in the workforce, but still, I dont hesitate to admit that Ive learned my lesson.
   
Learning continues throughout life and since I graduated college, I have matured tremendously. The major turning point in my life was witnessing the birth of my 6 month old daughter.  It was then that I realized that I have not been living to my full potential. With the precious life now in my hands, I underwent a major shift in philosophy. Now, all I want is to position myself in such a way that I am able to provide for my daughter and ensure a bright future for her. I truly feel that being a chiropractor, practicing a profession that I would love to do forever, will help me achieve this goal.
   
My fascination with the bodys natural ability to heal itself began when I was just in elementary and I learned how a scab forms to help repair torn skin. I saw this natural way of healing in its most beautiful and practical form in chiropractic healthcare. I fell in love with the profession when I saw a local chiropractor about a lower back pain. I was absolutely amazed with the amount of time he spent interacting and getting to know his patients. Medical doctors that I have seen in the past never seem to spend time doing the same. It seemed as if they were more concerned with taking your money and getting you out of their office as fast as possible.
   
More and more, I began to see the great contrast between the natural healing techniques of chiropractic healthcare and the normal medical profession were used to. The medical profession believes that disease causes a lack of health, while chiropractic healthcare believes that a lack of health is expressed as disease. As a result, medicine treats the symptoms of sick people while chiropractics address and treat the root cause, which lead to symptoms.
   
By becoming a chiropractor, I would enjoy a rewarding career that would give me the ability to educate others about their potential for true health and well-being. I would help people decrease their pain, improve their quality of life and help gain and maintain optimal health with safe and effective care. Becoming a chiropractor would be the pinnacle of my mission to help cure this world of suffering.

Cholesterol is a waxy substance that a human body makes and uses to guard nerves, make cell tissues and create hormones. There are mainly two types of cholesterol low density lipoprotein (LDL) and high density lipoprotein (HDL). LDL cholesterol is also called as bad cholesterol, which is the main source of cholesterol buildup and blockage in the arteries. HDL cholesterol is also called as good cholesterol and helps in protecting the arteries from plaque buildup.

When there is excess cholesterol in the blood, it builds up in the arteries walls. Eventually, this buildup of cholesterol causes hardening of the arteries, which makes the arteries narrowed. With narrowed arteries, flow of blood to the heart is slowed down or obstructed. Oxygen is carried to the heart by blood, and if sufficient oxygen and blood cannot reach the heart, the person may suffer from chest pain. If the supply of blood to a part of the heart is totally cut off by obstruction, the outcome is a heart disease (National Heart, Lung, and Blood Institute 2001).

Cholesterol and Heart Disease
From the past four years, the facts have been gathered that cholesterol is associated with cardiovascular disease, mainly heart attacks and angina. Various studies show that higher the persons average cholesterol level, higher the occurrence of heart disease in that person.There are also indications with animal studies. When rabbits were fed cholesterol, it showed that some of the dietary cholesterol got settled in the arteries. This results in hardening of arteries and narrowing of arteries, which is known as atherosclerosis or arteriosclerosis. This results in reduced flow of blood to the muscles of the heart, which can lead to pain in the chest while exercising or during other stresses and heart attacks (Frohlich 2007). Another relation between cholesterol and cardiovascular disease is noticed in persons with cholesterol inherited disorders like familial hypercholesterolemia. Persons with familial hypercholesterolemia develop cardiovascular disease sooner in life. For example, if the person is inherited with two genes of this order, wide narrowing of arteries can take place as sooner as 5 to 6 years of age. Cardiac problems such as heart attack and angina have been significantly reduced with clinical trials utilising cholesterol lowering regimes like drugs or diet. In the Lipid Research Clinic Study, for every one percent reduction in blood cholesterol, there was two percent reduction in the possibility of a heart attack. In a person, who had angina or had a heart attack, reducing of LDL cholesterol not only reduced the occurrence of succeeding events but also improved the overall survival (Frohlich 2007).

High Cholesterol Levels in Childhood Cardiovascular Disease Risk Factors
The strongest risk factors of cardiovascular disease include increased low density lipoprotein (LDL) or bad cholesterol, reduced high density lipoprotein (HDL) or good cholesterol, type 1 or type 2 diabetes, obesity, high blood pressure and cigarette smoking. A few of these risk factors may be noticed at adolescent ages. Research has revealed that these risk factors should be tackled early. Kids and youngsters are becoming more and more fat and obese. According to a recent study, the occurrence of obesity in children of 12 to 19 years old is 15.5 percent.

Due to the outbreak of childhood obesity, the requirement for pediatric health care specialists to become more familiar about the risk factors for cardiovascular disease and to start employing lifestyle modifications in patients has increased (Cook 2009). With the rise in childhood obesity, there is an increased occurrence of pediatric metabolic syndrome, which is another risk factor for cardiovascular disease. Metabolic syndrome is a collection of risk factors for diabetes and cardiovascular disease that appear to be connected to insulin resistance and obesity. Obesity and metabolic syndrome are connected strongly to abnormalities of lipid metabolism. According to the research, overweight school children, between 2.4 and 7.1 times, are more possibly to have high LDL cholesterol, total cholesterol and triglyceride levels than normal weight children. More number of mechanisms are present, by which insulin resistance can result in dyslipidemias. Hepatic synthesis of VLDL cholesterol, which leads to augmented LDL cholesterol and triglycerides, is increased with overloaded insulin presence in blood.Effects of insulin on lipoprotein lipase, an enzyme that helps in breaking down lipoproteins, increases the levels of LDL cholesterol and triglycerides. Sometimes, HDL cholesterol is degraded more quickly in patients who have metabolic syndrome.

Even, obesity obviously adds to dyslipidemias and cardiovascular disease, a significant genetic component is also added to the risk. If any of the family members is having cardiovascular disease, there is an increased risk for children or youngsters to develop the disease at some phase of their life. The family member can include a parent or a grandparent of age less than 55 who have cerebrovascular disease, peripheral vascular disease, coronary atherosclerosis, or myocardial infarction, coronary artery procedure or unexpected cardiac death. Children, who have high cholesterol levels or their parents with high cholesterol levels, are believed to be at risk. Diagnosis is suggested for them (Cook 2009).
Cook, W. B. (2009) High Cholesterol in Childhood Risk Factors for Cardiovascular Disease. Medscape Today online 34, (3) 27-32.

Statins, Cholesterol Levels, and Coronary Heart Disease Prevention
Statin is one of the most commonly prescribed drugs in the world. Before 20 years back, patients with high serum cholesterol levels, and those who had earlier experienced a heart attack, were not given any cholesterol lowering drugs. At that period, most of the Americans did not even hear about LDL and HDL cholesterols and very few have gone for measurements of cholesterol levels. With the innovation and progress of the statins, the obstruction was demolished, which blocked extensive cholesterol lowering treatment. Several studies regarding statins were published in the early and late 1900s. Those studies revealed that these drugs can decrease cardiovascular disease death and heart attack rates by 20 to 50 percent, based on the initial blood cholesterol levels and existence or non-existence of heart disease risk factors. The drug, statin, was shown to work effectively in women and men, middle aged people and old, and in patients with or without pre-existing diabetes or heart disease (Freeman 2006). After the beginning of 21st century, the atherosclerosis problem is not solved, however. Statin therapy noticeably decreases future cardiovascular events in people who have had an earlier heart attack, but it is short of providing ultimate cure.

The science advancement from the past twenty years have demonstrated a significant task of the immune system, mainly the macrophage and T lymphocyte, in encouraging the progress and coronary plaque catastrophic rupture that results in heart attacks or unexpected coronary death. The immunological responses look to be started by high cholesterol levels penetrating into the artery wall. But, once the procedure has started, even remarkable decrease in blood cholesterol appears to be incompetent of totally stopping it. HDL cholesterol has been exposed to alter immune responses and to take part in a path that is intended to eliminate cholesterol from the walls of the artery. According to the animal data, we can efficiently and cleverly interrupt immune processes straightly, or through the improvement of HDL functioning, but if we would have extra, important therapeutic methods in preventing cardiovascular disease. These approaches when combined with statins could radically decrease the atherosclerosis. We do not have enough tools to reduce the cholesterol levels, but those tools and their demonstration are possibly followed in the coming decade (Freeman 2006).

Freeman, M. W. (2006) Statins, Cholesterol, and the Prevention of Coronary Heart Disease. The FASEB Journal online 20, (2) 200-201. Available from httpwww.fasebj.orgcgicontentfull202200 2006
Importance of Cholesterol, Blood Pressure and Smoking for Coronary Heart Disease
Epidemiological studies conducted over the last five decades have shown that increased blood pressure, dyslipidemia, and cigarette smoking raise cardiovascular disease risks and randomised experiments have shown that reducing cholesterol and blood pressure prevents cardiovascular disease risks. However, there are popular fallacies about the significance of these traditional risk factors, including the extensively held belief that these risk factors account for only half of all coronary heart diseases. The Population Attributable Risk Fractions (PARF) method is a helpful way of measuring the combined impact of cholesterol, smoking and blood pressure for ischemic heart disease (IHD) mortality, but it emphasises the restrictions of using threshold values to decide the risk. Epidemiological studies have showed the log-linear relations between total cholesterol and ischemic heart disease risk, so that for each change in cholesterol unit, there is similar proportional modification in risk, in spite of early cholesterol levels  with no noticeable value of threshold below which lesser total cholesterol value is not related to lesser IHD risk (Lewington 2003).

The Heart Protection Study showed that statin therapy use to reduce levels of total cholesterol is linked to a like proportional decrease in cardiovascular disease risk, in spite of whether the previous total cholesterol treatment level is above or below 5.5mmoll.The Prospective studies meta-analysis demonstrated that the relations of general systolic blood pressure with IHD and stroke mortality are log-linear below to at least 11575 mmHG. Generally, a 200mmHg variation in normal systolic blood pressure is related to a two-fold variation in cardiovascular risk. However, there is a threat that results could be misunderstood to support the significance of 5.5mmoll as a value of threshold for total cholesterol. An even enhanced method to evaluate the significance of these identified vital risk factors can be to estimate the impact on risk of ending smoking and of modest and practical decline in blood pressure and cholesterol that could be attained, for example, by lessening the intake of salt in processed food and promoting the substitution of saturated fat in cooking with monounsaturated fats or polyunsaturated fats (Lewington 2003).

Lewington, S. (2003) The Importance of Cholesterol, Blood Pressure and Smoking for Coronary Heart Disease. European Heart Journal online 24, (19) 1703-1704.

Patients awareness of cholesterol, cardiovascular disease risk, and risk communication strategies
In spite of some latest developments in familiarity about cholesterol in U.S., patient obedience to cholesterol treatment suggestions are below the optimum level.

A study is conducted that discovered patients awareness of cholesterol and cardiovascular disease and their responses to three strategies for communicating cardiovascular disease risk. Researchers conducted seven focus groups in New England by means of open ended questions and visual threat communication prompts. The multidisciplinary study group carried out an in-depth analysis using immersioncrystallisation methods. The coded reports were analysed with the help of qualitative coding software NVivo (Goldman 2006).Participants from the groups were all conscious that high cholesterol levels negatively affect health. However, many participants had insufficient awareness about hypercholesterolemia and cardiovascular disease risk, and few were familiar with their cholesterol numbers. Many participants thought that their cholesterol levels were healthy, even if the doctor had not stated it. An approach that offers a cardiovascular risk adjusted age was estimated as apparent, impressive, appropriate, and potentially capable of inspiring people to formulate healthy changes. Few participants in every group were worried that a cardiovascular risk-adjusted age that was larger than chronological age would scare patients.

Difficult explanations about cholesterol levels and cardiovascular disease risk look to be inadequate for inspiring behaviour change. A cardiovascular risk-adjusted age calculator is a method that may keep patients in identifying their cardiovascular disease risk and, when combined by information about reduction of risk, it may be supportive in communicating cardiovascular disease risk to patients (Goldman 2006).
Goldman, R. E. et al. (2006) Patients Perceptions of Cholesterol, Cardiovascular Disease Risk, and Risk Communication Strategies.

Treating High Cholesterol
The main aim of the cholesterol treatment is to decrease the LDL cholesterol levels as much as necessary to decrease the risk of developing cardiovascular disease or heart attack. The greater the risk, the lesser the LDL cholesterol objective will be. There are two ways to reduce cholesterol levels Therapeutic Lifestyle Changes (TLC) TLC includes diet that lowers cholesterol, exercise, and weight management. TLC diet TLC diet is a low saturated fat and low cholesterol intake plan that contains less than seven percent of calories from saturated fat and less than 200 milligrams of dietary cholesterol per day. This diet suggests only sufficient calories to sustain a wanted weight and prevent weight gain (National Heart, Lung, and Blood Institute 2001). Weight management losing weight if a person is overweight can help decrease LDL cholesterol and it is particularly important for those with a group of risk factors that includes low HDL levels and high triglyceride levels and being obese with a large measurement of waist.Exercise Regular exercise is suggested for everyone. It helps in raising HDL levels and lowering LDL levels and is particularly important for those with low HDL levels and high triglyceride and being obese with a large measurement of waist. Drug treatment If drugs that reduce cholesterol are required, they are used with TLC treatment to lower the LDL cholesterol levels.

A. Manganous sulfate solution for 1000 mL
Dissolve one of the following in 1000 mL of distilled water
480 g MnSO4.4H2O or-
400 g MnSO4.2H2O or-
364 g MnSO4.H2O
B. Alkali-iodide (add azide if necessary) for 1000 mL
Dissolve in 1000 mL of distilled water
500 g NaOH or-            -AND-                135 g NaI or-
700 g KOH                                 150 g KI
Use azide while taking bacterial or nitrite laden samples
Dissolve 10 g NaN3 in 40 ml distilled water.
Add to 1 L of above solution.
C. Sulfuric acid (concentrated)
D. Starch for 100 mL
Dissolve 2 g soluble potato starch in 100 ml hot distilled water, stir.
(NOTE Add starch only to hot water as starch may take a little time to liquefy.)
E. Sodium thiosulfate for 1000 mL
In 1000 mL distilled water add 6.25 g Na2S2O3.5H2O
(NOTE As the solution is unpreserved, so must be freshly prepared.)

Materials
We require Test tubes with known volume or standard Biological Oxygen Demand water sampling bottles, few Beral Pipets, use Burets or preferably 10 mL syringes and Erlenmeyer Flasks

Methodology
In this Winkler Titration method, manganous sulfate was made to react with a potassium hydroxide-potassium iodide compound mixture to give out a white flocculent precipitate of bivalent manganese i.e. manganous hydroxide

MnSO4  2 KOH  Mn(OH)2  K2SO4
This precipitate was then made to react with dissolved oxygen in water to get tetravalent manganese

2 Mn(OH)2  O2  2 MnO(OH)2
Product formed, manganic basic oxide, is a brownish precipitate. Whereas if, a white precipitate comes out it indicates that no oxygen is present. Further, with acidification through sulfuric acid (or sulfamic acid, H3NSO3) the precipitate gets dissolved, forming out manganic sulfate

MnO(OH)2  2 H2SO4  Mn(SO4)  3 H2O
Formed manganic sulfate was made to react with potassium iodide yielding free iodine (I2), which gives out a brownish color. Iodine on the other side also tends to react with starch and bring into being a blue-black color which indicates the presence of iodine. This iodine can be titrated with sodium thiosulfate to give out sodium iodide, which will no further leave the brown color

2 Na2S2O3  I2  Na2S4O6  2 NaI
As a result we measured the amount of thiosulfate needed to eliminate all of the brown color, and helping in determination for total amount of I2 in the sample, and in a roundabout way giving us the amount of O2 present dissolved in

Cystic fibrosis is a secretory disease (including sweat and mucus glands) that is usually inherited. Inherited implies that it is passed on through genes of a parent to their children. To inherit cystic fibrosis, a person gets two faulty genes- each from both parents. The parents usually do not suffer from the disorder themselves. Cystic fibrosis is a multi-system infection, meaning that its infection involves several body organs in the lungs and the digestive system. Cystic fibrosis usually affects the liver, sinuses, lungs, intestines, pancreas and the human reproductive organs (Institute Of Health Sciences, 2009). Mucus refers to the substance which is made as a result of lining of certain body tissues. Usually, mucus is watery and slippery. The purpose of mucus in the body is to keep the linings of some organs moist so as to protect them from becoming dry or getting infected. However, for a person suffering from cystic fibrosis, their mucus usually becomes sticky and thick. This mucus eventually piles up in the lungs, blocking the airways. The building up of the mucus provides a suitable atmosphere for the growth of bacteria. This causes severe and serious infections which might completely damage the lungs (Medicine net, 2009).

Etiology
If ones lungs are healthy, there is normally a constant stream of mucus flowing across the surfaces of lungs and the air passages. The mucus serves to remove bacteria and debris. If one is suffering from cystic fibrosis, the mucus becomes extremely sticky and thick because of an altered water and salt balance in the lungs. Cystic fibrosis is a condition caused by an inherited faulty gene termed as Cystic Fibrosis Transmembrane Conductance Regulator (CFTR). Cystic fibrosis results when an individual has a pair of the faulty gene inherited from both parents. However, if one has only one cystic fibrosis gene, he or she cannot suffer from the disease but becomes a carrier and will also not be affected by the symptoms of cystic fibrosis. The illustration below describes how cystic fibrosis is inherited (BuPa, 2009).

From the above illustration, when both parents are cystic fibrosis carriers for every pregnancy there is one chance in a total of four of getting a cystic positive child, two out of four chances of getting a cystic carrier child and one in all the four chances of getting a cystic negative child -neither a carrier nor a victim of the disease (BuPa, 2009).
The most common physiological problems caused by Cystic Fibrosis
Since the disease is a multi-system infection, it results to quite a number of physiological problems which include CFTR Gene mutation, Chloridesodium channels, pancreatic problems, infertility, and enzyme. These problems are as discussed below.

CFTR gene mutation
Basically, gene mutation is an irreversible change in DNA sequence which makes up such a gene. Gene mutation occur through two different ways either through inheritance or can be acquired in the course of a persons lifetime. The CFTR gene mutation is an example of the inherited gene mutation case- it is a hereditary mutation (also referred to as germline mutation). There are over one thousand genetic mutations that are associated with varying degrees of the severity of cystic fibrosis disease. Majority among these mutations alter amino acids (the building blocks for proteins) in CFTR protein or else delete small amounts of DNA out of CFTR gene (Lurquin, Omoto, 2004). The most frequent mutation is called Delta F508 and results from the deletion of a single amino acid at 508 point in CFTR protein. This results to an abnormal channel in the CFTR protein. This abnormal channel eventually breaks down after a short while and as such, it cannot reach the cell membrane and transport the chloride ions. The disease forming mutations in CFTR gene changes the production, stability as well as structure of chloride ions. This causes the channel of chloride ions not to function properly thus affecting and destroying the transportation of chloride ions and the movement of water inside and outside the cells (Lurquin, Omoto, 2004).

Chloridesodium channels
Abnormalities of the functioning of the epithelial system in cystic fibrosis are linked to certain defects in the permeability of the cell membrane to sodium andor chloride ions. Recently, a certain class of chloride channels in the epithelial airways cells was reported to be lacking usual sensitivity for phosphorylation, through the camp dependent Kinase protein. This suggests that single genetic defaults in the chloride channels could be resulting to cystic fibrosis (Kakaz  Anthony, 2006).

Infertility
This condition affects the male and the female reproductive systems as a result of the faulty CFTR gene in the body. Mutations in CFTR gene disturb the functioning of chloride channel thus preventing natural flow of the chloride ions as well as water inside and outside the cells. As a result, the cells in male genital region generate mucus which is unusually sticky and thick. In men, this mucus then blocks the tubes carrying sperms from the vas deferens (testes) in a developing unborn male and the condition deteriorates before birth. With no vas deferens, sperms cannot be transferred from testes and part of the semen.  As a result, men having congenital bilateral lack of vas deferens cannot father children (are infertile) save for the use of modern reproductive technologies (Thomas  Schover, 2009). For women on the other hand, the condition results to the production of excessive mucus in the genital organs. This mucus builds up with time and eventually clogs the cervix. Once the cervix is blocked, it becomes impossible for the sperms to flow through the female virginal cannel to the oviduct where fertilization takes place. As a result, it becomes difficult for a woman to become pregnant until the condition is treated (Jacobs, 2007).

Pancreatic and Enzyme problems
The thick and sticky mucus clogs the ducts, tubes and the pancreases. Consequently, digestive enzymes which are responsible for production of the pancreas cannot be able to reach the small intestines. The digestive enzymes assist in the breaking down of food and without them the food is not properly broken down and consequently the small intestines cannot completely absorb proteins and fats. The end results are deficiency of vitamins in the body and malnutrition since the nutrients leave the body unused. In addition, it can result to intestinal gas, bulky stools, swollen bellies due to constipation or general discomfort and pain (Institute of Health Sciences, 2009).

Sinusitis, bronchietasis and pancreatitis
Sinuses refer to air filled gaps behind the nose, eyes and the forehead. They usually produce mucus and aides in keeping the lining of the nose moist. When the sinuses get swollen, they become clogged with mucus and are infected. The swelling of the sinuses has been reported to be as result of the faulty pair of gene present in cystic fibrosis infected people. Bronchietasis is a disease of the lungs whereby the bronchial tubes and the large airways in the lungs become enlarged, stretched out and flabby forming pockets (Davis, 1993). Mucus collects in these pockets causing infections in the lungs. Repeated infections in the lungs due to accumulating mucus create increasing damage to the bronchial tubes and eventually bronchietasis. If not treated, it can cause respiratory failure. The mucus that collects in the lung pockets comes from the excessive production of mucus in the body which is the necessary condition of cystic fibrosis. Pancreatitis refers to the painful inflammation in the pancreases. This painful inflammation of the pancreases is caused by a mal functioning pancreas (Davis, 1993).

Other problems which are related to cystic fibrosis include intestinal blockage episodes in newborns, nasal polyps (growth in the nose caused by the swelling of the sinuses) and clubbing (the widening and rounding of finger tips and toes). Clubbing develops because the lungs cannot function properly and hence they are not able to purify enough blood and consequently, oxygen in the blood stream is not sufficient. Cystic fibrosis also causes Pneumothorax, which is the collapsed lung, and Rectal Prolpse. Rectal prolapsed is frequent coughing and difficulties in passing stool. This condition causes the rectal tissue in the body to pop out from the rectum (Davis, 1993).

The symptoms of cystic fibrosis
The signs and symptoms usually vary over time and from one person to another. Some people will develop serious digestive and lung problems while others suffer from mild illness that does not show up till they become adolescents or even when they are adults. Sometimes, a person suffering from cystic fibrosis will show mild symptoms which begin to become more severe as the disease worsens (Lewis, 1993).
For instance, in most people, the functioning of the lungs begins to decline at early childhood and with time the lungs become permanently damaged resulting to serious problems in breathing. Consequently, breathing problems advance to respiratory failure which is the most common cause of deaths among people suffering from cystic fibrosis. If someone has cystic fibrosis, the enzymes that are produced by the pancreas do not reach the gut since the flow is clogged. Without the digestive enzymes, the patient cannot get enough nutrients especially fats and proteins. Such a person shows the signs of malnutrition and gross loss of weight even when they are observing proper and hygienic feeding manners. Again, the stool of such people contains excess fats which make it to appear oily, sticky and hard to flush away. The basic symptoms of the disease are as a result of thick and sticky mucus. The most frequent signs and symptoms of cystic fibrosis include frequent coughing which causes thick sputum and phlem as well as frequent bouts of the bronchitis that can lead to inflammation or permanent damage to the lungs (Lewis, 1993).

Cystic fibrosis causes salty tasting skin which is as a result of dehydration Dehydration is caused by the failure of the intestines to absorb enough water. Further, it causes unending diarrhea, infertility, huge appetite accompanied by poor growth and weight gain- this is referred to as failure to thrive.  A person suffering from cystic fibrosis should exhibit at least more than fifty percent of the symptoms mentioned above at the same time or on recurring and consecutive basis since other disorders might also result to several of the signs and symptoms mentioned above (Lewis, 1993).

The diagnosis of cystic fibrosis
To diagnose cystic fibrosis, the doctor first obtains a detailed family and medical history of the patient and then conducts a thorough objective examination. To confirm the diagnosis, the doctor also performs a number of laboratory tests, for the purposes of accuracy. The most accurate test for diagnosing cystic fibrosis is the sweat test. The sweat test is used to measure the level of salt in the sweat. To conduct this test, doctors usually rub some little amount of a testing chemical substance called Pilocarpine on the arm or the leg of the patient. Next, they attach an electrode on that spot. The electrode is used to provide an electric mild current which produces sweat (this could cause a feeling of intense warmth or tingling depending on the patient). After that, the doctors cover that area using a filter paper or gauze pad and wrap up with plastic. They leave the test to rest for thirty or forty minutes and then remove the plastic so that the sweat collected on the filter paper or gauze pad can be taken for analyzing. To provide accurate diagnosis, the test is usually done twice. High levels of salt in the body indicate the presence of cystic fibrosis (Jacobs, 2007).

However, there are also other tests which can be used to diagnose the disease. Such include blood tests to investigate the presence of the abnormal CFTR gene or any other blood test indicative of cystic fibrosis. Also a chest x ray which takes the picture of patients lungs to test whether there is scarring resulting from lung inflammation or a sinus x ray to test for the presence of sinusitis in the patient. Finally the sputum test is also used by doctors to test the bacteria growing in the sputum (Lewis, 1993).

Other tests used to diagnose cystic fibrosis are done for the pregnant women to test the fetus in the womb. For the pregnant women, the prenatal genetic testing will normally find out whether the developing baby is cystic fibrosis positive. Such tests include the Amniocentesis. For this test, the doctor will insert a hollow sterilized needle through the abdominal wall into the uterus and obtains cells from amniotic fluid. This fluid is then tested to find out if the pair CFTR genes of the fetus are normal. The final test done on the fetus is called the chorionic villus biopsy where the doctors use ultrasound that guides a thin tube via the virginal cannel and the cervix and into the uterus to remove small pieces of placenta for biopsy. The placental cells are then tested for cystic fibrosis (Andrews, 2001)

Treatments for the clogged mucus (lungs, sinuses, human reproductive organs)
Treatment for cystic fibrosis lung problems includes antibiotics for airways infections, physical therapy for the chest and exercises. Antibiotics are the principal treatment for cystic fibrosis serous cases. The choice of the antibiotics administered depends on seriousness of the condition, the level of bacterial strains involved and the patients history of antibiotic use. The antibiotics can be oral, inhaled or intravenous. For cystic fibrosis PCT (physical chest therapy), the back and chest are pounded repeatedly so as to dislodge mucus from the lungs and facilitate coughing up the accumulated mucus (Andrews, 2001). Cystic fibrosis CPT ought to be done three to four times on a daily basis. CPT is as well frequently called postural drainage. This is because it involves lying or sitting on ones stomach with the head down. This permits gravity to aid in draining mucus from the lungs. Since CPT is difficult and uncomfortable, a number of devices have been invented recently that are less tasking to operate. These devices include the electronic chest clapper (mechanical percussor), PEP (positive expiratory pressure) which creates vibrations for breaking mucus loose in the airways, and an inflatable therapy vest which utilizes high frequency waves of the air to force the mucus outside the lungs. PCT also uses the flutter device. This is a small device which is hand-held and it is used by breathing through it, an action which generates a wave of vibrations for dislodging mucus.  The final method for treating lung problems of cystic fibrosis involves aerobic exercises. Aerobic exercise helps in loosening the thick mucus, encouraging coughing to clear out the mucus and generally improving the physical condition (Andrews, 2001).

Treating the digestive system problems (the intestines, pancreases and live)
Nutritional therapy is important for improving growth and development as well as exercise, strength and tolerance. It may also make a cystic positive individual to become strong enough and develop immunity against the lung problems. This therapy involves high calorie diets and well balanced low fat- high protein content foods. Doctors usually recommend oral pancreatic enzymes for the facilitation of the digestion of proteins and fats and the absorption of adequate vitamins. The oral enzymes are administered as capsules which are taken before meals. Vitamin supplements of vitamins K, A, E and D are also prescribed by doctors to replace fat-soluble vitamins that the intestines are not able to absorb. Finally, the use of feeding tubes, the T- tubes that adds calories during the night is a probable treatment for cystic fibrosis. The tube is usually paced on ones stomach and a bottle containing nutritional solution is attached at the entrance of the T-tube (Davis, 1993).

Approximately thirty thousand people living in the United States of America have cystic fibrosis. Cystic fibrosis affects both the males and the females regardless of ethnic and racial backgrounds. However, the disease is more prevalent among the Caucasians and less common amongst the African Americans. Cystic fibrosis is one among the major inherited conditions among the Americans. Statistics show that one out of every three thousand babies conceived in the US, suffers from cystic fibrosis. Furthermore, approximately twelve million Americans are living carriers of the abnormal CFTR and ninety percent of them do not know that they have the faulty gene. Cystic fibrosis is therefore among the major threats to human beings and more attention to prevent and cure the condition is not only necessary but also urgent.

The designated web page is the official National Cancer Institutes page on Cancer, including statistics from the American Cancer Society on cancer incidence.
I was startled to realize that the commonest types of cancer were types that I had not previously heard of, like non melanoma skin cancer. I was really interested to read more about this cancer that represents half of all cancers diagnosed in the USA. Fortunately, this is a treatable type that results in less than 1000 deaths in over 100000 affected.

The most frequent cancer types are in order of appearance, apart from non melanoma skin cancer lung cancer (including bronchus), breast, prostate, colorectal, bladder, melanoma skin cancer, non-Hodgkin lymphoma, kidney, leukemia, endometrial, pancreatic and last thyroid cancer.

A very interesting observation had to do with the relatively low appearance of male breast cancer, a fact attributed to the effect female hormones have on breast cancer (breast cancer is hormone-dependent). However, when researching deeply one finds that male breast cancer results in relatively more deaths than female ones. I couldnt help but wonder for this phenomenon, and I realized that male breast cancer happens at a much older age, when predisposing factors have already settled in (obesity is one of them). Moreover, male patients report to their physician much later, when the cancer has already progressed in stage (see table reprinted from Fentiman).

Table 1 TNM stage at presentation of male breast cancer (Fentiman 597)

One realizes immediately that thrombophlebitis is a blood clotting disease that occurs after long periods of staying still or from other predisposing conditions. The worst thing that can happen after thrombophlebitis has settled would be to have a blood clot travel in the heart or the lungs causing embolism.
When searching more carefully, we realize that thrombophlebitis can also be the result of a type of cancer, particularly pancreatic cancer, which causes the blood to clot more easily due to the production of coagulation factors. It then can be manifestated as migratory thrombophlebitis (Thayalasekaran) (positive Trousseau sign) and even be the first sign of disease leading to the cancer diagnosis. A lot of risk factors apart from cancer predispose to this condition, such as pregnancy, pace makers, catheterization, hormone replacement therapy or genetic factors (Appleby).

Treatment is with medications, but a lot of supporting prevention measures can help aid the prognosis of the disease such as support stockings, filters in major veins but most of all self care measures such as elevation daily, heat on superficial clots and over the counter drugs

Writing is a field that is as broad as it is complicated, and to complicate matters more, scientific writing even has specific demands that make writing even more complex.  Initially, it is best to consider the major parts of a scientific essay, regardless of the field that one is writing on.  These major parts are the title page, the abstract, the introduction, the review of literature, the methodology, the results, the discussion, the conclusion, and the literature cited.  (Cordova)  The title page is where the title of the paper is shown, to include details such as the name of the researcher, the college or university where the researcher is at, as well as other details like sub-titles or study rationales.  The abstract is a summary of the study, with the primary emphasis on results and conclusions. (Cordova)  The introduction is where the researcher should express the study problem or the thesis of the research, the hypothesis, the objectives of the research, the significance and limitations of the research.  This has to be followed with the review of literature which is the section where the researcher discusses previously published papers, journals, or researches related to, are the basis for, or influence the study at hand.  Then, when this is complete, the researcher should explain all the methods and processes involved in conducting the study in the research methodology, after which, all the results have to be stated to include tables, illustrations, computations and the like.  After presenting the results, the researcher should proceed to discuss the significance of these results in relation to the study problem, and finally, a conclusion should be made based on the hypothesis.  These basic parts of the scientific research should also be considered in writing a simple essay or journal.  The format may be different, because heading would no longer be necessary, but the sequence of sections has to follow the scientific method.  It has to be remembered that when writing a scientific paper, the results, whether negative or positive, (CUL) have to be included, because these results are the reason for the conduction or the research or the writing of the paper. 

The conclusion, which is often the problem, should also not just be a simple re-stating of the thesis rather, it should relate the thesis to all the other sections of the paper such as the results and the methodology. 
   
With the important sections of the scientific paper now out of the way, it is important to know how to choose a topic.  The very first consideration in choosing a research topic is feasibility, which is determined by how concise and how narrow the research topic is.  For instance, a researcher will not do research on the effects of pollution on the propagation of trees.  This topic needs to be narrowed down and made more concise. 

This is done by introducing more specific variables, so with these variables the topic would more likely become, the negative effects of air pollution from smoke belchers on the propagation of eucalyptus trees in southern Australian highways.  Here now, the topic has become more specific and easier to research because it has more direction and more variables to consider.  In perusing or analyzing a research question, certain elements need to be considered these are time, science involved, and significance.  Hence, if the question is, What are the effects of blue coloured algae on the growth of kelp, the question may be broken down as follows  where does kelp grow  In what particular annual season do they grow  Where is blue algae found  What season do they grow in abundance  What filed of science is involved here (Marine biologybotany)  What effects will the research have on the community at large and what will the results do to the existing body of knowledge on algae and kelp
   
When the analysis of the research question or problem is done, the next step is to do the actual research.  However, where and how does one start doing the research  Initially, the researcher has to do what is called synthesis reading or the perusal of various other researches and studies related to or having and impact on the research at hand.  In determining which of these information sources should be used in the context of relevance and significance to the research topic, a few things have to be considered first, the author, then the date of publication, and finally, the content of the source.  The author has to be an authority in the field being researched, the date should be within the period in which the research at hand is being conducted or the paper is being written, and the content has to support or complement the research problem or thesis being researched.  Then, one has to consider the types of sources being used, (KYVL) for this, a helpful matrix is one obtained from the KY Virtual Library which is pasted here as follows

The immune system functions as a defence against opportunistic microbes. It as well necessitates the capability of detecting between self and non-self molecules to make sure that an immune response is not raised against the organisms own tissues. This discrimination is partly realized by the identification of a pathogens chemical motifs by the host receptors. As a result, latent, potential, or probable pathogens have tailored various ways to overcome the immune systems of the host, while the host responds with a novel defence (Grennan 2006, p. 810). PAMPs or pathogen associated molecular patterns are molecules associated with groups of pathogens, which are identified by cells of innate immune system. These molecules can as well be referred to as minute molecular motifs conserved in a class of microbes. Pathogen associated molecular patterns are recognized by Toll-like receptors (TLRs) as well as other pattern recognition receptors referred to as pathogen recognition receptors(PRRs) in both animals and plants (Ausubel 2005, p. 975).

These receptors activate both the innate and acquired immune responses and thus protect the organism from infections, through recognition of some conserved non-self molecules. An endotoxin found on the cell wall of a bacterium (Lipopolysaccharide) is considered to be prototypical PAMP and is specifically identified by Toll-like receptor 4, an innate immune system recognition receptor. Apart from lipopolysaccharides, other PAMPs comprise of lipoteichoic acid, from gram positive bacteria, bacterial flagellin, and nucleic acid variants usually associated with viruses, such as double stranded RNA (dsRNA). Though the word PAMP is relatively novel, the idea that molecules resulting from microbes ought to be distinguished by receptors from multicellular organisms has been held for a number of decades, and references to an endotoxin receptor are available in much of the older literature (Ausubel 2005, p. 977).
Over the years, the term PAMP has been under criticism by some immunologists on the basis that a large number of microbes, not only pathogens, express the molecules detected. Therefore the term MAMP (microbe associated molecular pattern) has been suggested. A virulence signal which is able to bind to a pathogen receptor in combination with a MAMP has been suggested as one way to constitute a PAMP. In plant immunology, the terms PAMP and MAMP are often treated interchangeably, considering them as the very first step in plant immunity (Ausubel 2005, p. 979).
Mechanism of Immune Recognition
Immune recognition is a unique mechanism and is mediated between products encoded in dissimilar genomes. Besides, the selective advantage imposed through immune recognition on the host genome normally implies a selective disadvantage to the pathogen genome. This conflict of interests directs evolution of non specific immunity toward identification of invariant molecular components of the infectious agents (Janeway 1989, p.6). Molecular structures which are imperative for microbes survival are never subject to variability in the sense that mutations upsetting these structures are mortal, lethal, and deadly for microbes. Molecular structure conservation means that they are shared by groups of pathogens. For instance, the generic structure of lipopolysaccharide is shared by the entire class of gram negative bacteria (Janeway 1989, p.6).

A receptor which would identify the conserved lipid A of lipopolysaccharide would therefore be capable of detecting the presence of any gram negative bacteria. This example exemplifies another characteristic of innate immune recognition, where the targets of recognition mechanism represent molecular patterns called pathogen associated molecular patterns (PAMPs), rather than other particular structures (Janeway 1989, p.10). Host organisms have developed receptors which can specifically identify or recognize pathogen associated molecular patterns that include both pattern recognition receptors (PRRs) and Toll-like receptors (TLRs). This evolutionary strategy of host organisms not only prevents the generation of microbial escape mutants, but permits a limited number of germline encoded receptors to identify a great array of molecular structures linked to pathogens as well. Additionally, it ought to be emphasized that PAMPs recognition by Toll-like receptors and PRRs not only permits the adaptive immune response to discriminate between non-self and self, but also between pathogen associated non-self and innocuous non-self (Janeway 1989, p.10).

The Roles of TLRs in Innate and Acquired Immune Response
The defence of the host organism against the invading microbial pathogens is induced by the immune system that consists of two components acquired immunity and innate immunity. Both components recognize the microbial pathogens as non-self and hence trigger the immune system to eradicate them. Today, both innate and acquired components of immune system have been characterized independently and the major research interest in immunology has been restricted to acquired immunity. In this immunity, T and B lymphocytes use antigen receptors, such as T-cell receptors and immunoglobulins to recognize non-self (Takeda and Akira 2005, p. 1). The mechanisms through which these antigen receptors identify foreign antigens have been extensively analyzed and the main mechanisms like clonality, memory, and diversity have been well characterized. However, these receptors exist only in vertebrates and according, the mechanism for non-self recognition in less advanced organisms is not fully understood. In addition, the mammalian innate immune system has not been well researched on. Consequently, innate immune cells of mammals, such as dendritic cells and macrophages are known to be activated by microbial components like lipopolysaccharide from gram negative, a receptor liable for recognition remains unknown (Takeda and Akira 2005, p. 1).

Toll-like receptors are germline encoded type 1 transmembrane receptors that are expressed on various cell types comprising dendritic cells and macrophages. They function as pattern recognition receptors, activating innate immunity by recognizing PAMPs that are unique to microbes and imperative for their survival (Carpenter and ONeill 2007, p.1891). Therefore, TLRs provide both instantaneous protective responses against pathogens as well as the acquired response by stimulation of dendritic cells recruitment and maturations (Muzio et al 2000, p. 453). Toll-like receptor triggering leads to nuclear factor kappa B-mediated activation of inflammatory genes. More than ten TLRs have been demonstrated and described in humans and agonists have been defined for nine of them.  Toll-like receptors can function as heterodimers or homodimers, mounting the repertoire of specificities. TLR1, TLR2, and TLR6 are activated by any microbial product as well as peptidoglycan, TLR3 by double stranded RNA (dsRNA), TLR4 by LPS, TLR5 by flagellin, imidazoquinolines triggers both TLR7 and TLR8, and TLR9 is activated by CpG DNA (Campos et al 2001, p. 419).

TLRs Recognition of Microorganisms
Toll-like receptors being membrane bound molecules recognize microbial products within or on the surface of extracellular compartments of cells. Thus, intracellular recognition of invading microbial pathogens seems to involve a TLR independent system. Recent evidence shows that nucleotide binding oligomerization domain (NOD) family of proteins plays a substantial function in the recognition of pathogenic microbes. It has previously been indicated that TLR2 is capable of recognizing peptidoglycan (Takeuchi et al 1999, p. 443). However, peptidoglycan (PGN) contains a thick layer which is made up of overlapping lattice of 2 sugars that are cross linked by bridges of amino acids, and thus the exact structure of PGN which is recognized by TLR2 remains unknown. Nucleotide binding oligomerization was originally recognized as a molecule which is related to apotosis regulator, Apaf-1. It encompasses a caspase recruitment domain (CARD), a C-terminal domain, and a NOD domain.

Recent researches by a number of scientists have illustrated that over expression of NOD1 enables 293 cells to respond to peptidoglycan preparation (Girardin 2003, p. 1584). Therefore, NOD1 may play an essential role in sensing intracellular gram negative bacterial infections. Though, TLR2 has been reported to identify peptidoglycan, it is probable that TLR2 recognizes lipopeptide or lipoprotein contaminants trapped in the layers of PGN mesh. The viral identification is as well mediated by TLR dependent and independent mechanisms. TLR3 mediated recognition of dsRNA or viruses leads to TRIF dependent activation of interferon regulatory factor 3 (IRF-3) and nuclear factor kappa B. However, dsRNA or viruses are recognized in a TLR3 independent manner, as the impairment of responsiveness to dsRNA or viruses in TLR3 scarcity is only partial. RIG-1 is recognized as a molecule which is responsible for recognition of viruses and mediates 1RF-3 activation (Figure 1).

Figure 1 TLR Dependent  Independent Recognition of Microbial Constituents
(Yoneyama 2004 730)
TLRs and Phagocytosis
The process of phagocytosis is an essential step for defence of the host against microbial invaders, as it activates both degradation of pathogens and resultant presentation of pathogen derived peptide antigen. Recognition of pathogens by Toll-like receptors results in expression of genes, such as co-stimulatory molecules and inflammatory cytokines.  Phagocytosis mediated antigen when presented together with Toll-like receptor dependent gene expression of co-stimulatory molecule and inflammatory cytokines, instruct development of antigen-specific adaptive or acquired immunity (Figure 2). Thus, it is of great interest to characterize the correlation between TLRs and phagocytosis process. For instance, in absence of MyD88 (a common adaptor in TLR signalling) or TLR2TLR4, phagocytosis of bacteria comprising Salmonella typhimurium, Staphylococcus aureus, and Escherichia coli has been shown to be impaired because of impaired phagosome maturation. Several studies indicate that Toll-like receptor-mediated MyD88 dependent activation of p38 is needed for maturation of phagosome.

Figure 2 Adaptive  Innate Immunity
(Takeda  Akika 2000 8)
TLR Signalling Pathways
TLRs stimulation by microbial components or products triggers expression of a number of genes which are involved in the hosts immune responses (Takeuchi et al 2000, p. 113). The molecular mechanisms through which Toll-like receptors elicit gene expression are today being elucidated by analyses of TLR mediated signalling pathways. Microbial identification of TLRs assists dimerization of TLRs. Toll-like receptor 2 is shown to form a heterophilic dimer with either TLR1 or TLR6, but in other usual cases TLRS are alleged to form homodimers. TLRs dimerization triggers activation of signalling pathways that emanate from a cytoplasmic Toll Interleukin-1 Receptor domain (TIR). A TIR domain containing adaptor MyD88, was shown to be important for stimulation of inflammatory cytokines, such as Tumour necrosis facto-alpha (TNF-) and interleukin 12 (IL-12) through all Toll-like receptors (Takeuchi et al 2000, p. 113). However, specific TLRs activation results in slightly dissimilar patterns of gene expression profiles. For instance, activation of Toll-like receptor-3 and 4 signalling pathways leads to induction of type 1 interferons, but activation of TLR2 and TLR5 mediated pathways does not (Doyle 2002, p. 251). TLR7, TLR8, and TLR9 signalling pathways as well results in induction of type 1 interferons by mechanism distinct from TLR3 or 4 mediated induction. Therefore, its crystalline clear that Toll-like receptors activation leads to expression of several genes that are later involved in the immune response of the host (Figure 3).

Figure 3 Toll-like Receptor Signalling Pathways
(Hemmi et al 20033059 Beutler 2004 259)
Interaction between TLRs and Dendritic cells (DCs)

Dendritic cells express a collection of PRRs on the surface, which can specifically interact with pathogen associated molecular patterns, including mannose receptors, Toll-like receptors, and c-type lectins. Dissimilar DCs subsets could express different TLRs. For instance, mouse spleen CD8 DCs are indicated to express Toll-like-2, 3, 4, and 9 and encompass a greater Ag presentation ability than CD8- which express TLR-2, 3, 4, 5, 7, and 9 (Liu 2006, p.214 ). It has been discovered that DCs utilize a number of TLRs in detecting several characteristics of a pathogen at the same time and transmit the information regarding the nature of the microbial pathogens (danger signals) to direct an immune response tailored to the threat. Therefore, Toll-like receptor-induced signals could serve as one of the mechanisms of self or non-self discrimination (Figure 4). Triggering of distinct TLRs on DCs can induce dissimilar cytokine profiles leading to specific activation status of dendritic cells. For instance, TLR-associated molecule MyD88 signals are able to activate downstream TRAF6 stimulation, and this is followed by activation of nucleic factor kappa B (Liu 2006, p. 214). This may perhaps result in production of different sets of cytokines and render DCs with ability to promote generation of Th1, Th2 plus other T-helper cell subsets as well as cytotoxic T cells.

Figure 4 TLRs in Control of Self  Non-self Ag Presentation by DCs
(Liu 2006 215)

The major role of Toll-like receptors in the immune system is recognition of pathogen associated molecular patterns (PAMPs). The result of this pathogenic recognition is the killing and subsequent elimination of the pathogens by the acute inflammatory response as well as the presentation of antigens to adaptive immune system cells (Basset 2003, p. 21). Therefore, TLRs is very substantial in both components of immune system (innate immunity and acquired or adaptive immunity).