Basu called the decision a historic blunder. But, he was not one to split hairs over what could have been. He never contested the Lok Sabha polls, but continued to influence national politics till the very end. 

    Born into privilege (his father was a US-trained doctor ) and educated in elite institutions (St Xavier’s School and Presidency College), few would have expected Basu to grow into one of the most important Communist leaders of his time. His family had connections with revolutionaries fighting for India’s freedom, but it was during his trip to the UK in 1935 to become a barrister that he became influenced by the Communist movement. He started frequenting study circles, where he was initiated into Marxism by Communist leaders like Rajani Palme Dutt. His father had sent him to England to try and get into the ICS, but he returned in 1940 to become a Communist Party of India card holder. 

    In 1944, CPI leaders sent him to work with trade unions, first among port and dock workers and then among railway employees. His career as a legislator spanning 55 years started in 1946 when the electoral college comprising railway employees voted him to the Bengal Assembly. One of his main achievements was securing the release of political prisoners in 1946 from the Suhrawardi government. He was himself repeatedly arrested after the Communist Party was banned shortly afterIndependence in 1948, his first arrest coming on March 16 that year. 

    The general election in 1952 saw the emergence of Basu as one of the ablest parliamentarians of the country. Elected to the West Bengal assembly from the Baranagar constituency, he, along with fellow MLA Ratanlal Brahman, emerged as the main opposition to the Bidhan Chandra Roy government. Basu was recognized as the leader of the opposition. 

    The period till the split in the Communist Party and the formation of the CPM in 1965 saw the consolidation of Basu’s position both in the party and also as opposition leader. In 1953, he was unanimously elected the state secretary of the party. Among the major agitations in which he participated in this period was one against tram fare rise in Kolkata, an agitation by teachers in 1954 for higher pay, the proposed post and telegraph strike and the food movement in 1959. 

    The general election in 1967 paved the way for the short-lived first United Front government in West Bengal. Basu — as deputy CM — took up the reins of the government for the first time. This period also saw his maturity in coalition politics, which saw fruition in 1977 when the Left Front government was formed. For the next 23 years, he successfully headed a coalition of likeminded parties before relinquishing voluntarily the post of chief minister, continuing in active politics only as politburo member of CPM. 

    The 13-month-long second United Front government was voted to power in 1969. Ajoy Mukherjee became the chief minister for the second time and Basu his deputy. He was also given the home portfolio. During this period, Basu demonstrated his personal courage by facing alone a large group of armed policemen who stormed the assembly premises to protest the death of a colleague in a clash with SUCI supporters. 

    The fall of the second UF government over differences between Basu and Mukherjee and two years of political turmoil that followed led to an election in 1972. Alleging massive rigging by Congress, Basu withdrew from the contest at Baranagar. CPM and a number of other Left parties decided to boycott the assembly. 

    The Emergency in 1975 and the general election in 1977 saw the beginning of a new phase in Bengal. As leader of the Left Front (then sans CPI), Basu romped home and became CM. Thereafter, he went on to create history by leading for almost a quarter of a century a Marxist government within the ambits of a capitalist structure, using parliamentary methods. It has been a unique experiment in the history of communism itself, which continues even after Basu’s retirement. 

    Under Basu’s rule, the twin measure of operation barga and panchayat election changed the face of rural Bengal. Eviction of sharecroppers was stopped and their share in the crop ensured by recording their names. Ceiling surplus land was vested and distributed to the rural poor. Democracy was introduced at the grassroots by holding panchayat election. The rural poor became the beneficiaries of government projects. 

    But he wasn’t an unqualified success. Basu’s tenure as CM saw Bengal sink into precipitous economic decline. The state which was once India’s most industrialized witnessed an exodus of industry as trade unions ran riot. Towards the end of his tenure, Basu attempted to reverse this trend, but Bengal has still not been able to undo the damage. 

    He also failed to prevent abolition of English from the primary level in government and aided schools in the state, which contributed to a mass migration of several middle-class families out of the state. The resignations of two senior cabinet colleagues — Buddhadeb Bhattacharjee and Benoy Chowdhury — alleging corruption in the government and nexus with contractors were major embarrassments for him. 

    Still, Basu went from strength to strength, acquiring a pivotal role in national politics. It began with the CPM’s association with Jayaprakash Narayan’s movement during Emergency. Prior to the Lok Sabha election in 1989 that brought V P Singh to power, West Bengal had become a focal point of opposition politics, hosting meetings and conclaves. As the years went by, there was talk of his focus shifting from the state to the national scene. 

    With BJP coming to power at the Centre in 1998, the staunch secularist was quick to identify communal forces as a major threat and felt the Left should face the saffron challenge along with other secular forces, including Congress, its political opponent in West Bengal, Kerala and Tripura. It wasn’t an easy task though. Basu and former CPM general secretary Harkishen Singh Surjeet took the lead in bringing about a change in the party’s mindset towards Congress that finally culminated in the Left-UPA combination six years later in 2004. 

    The longest serving chief minister, Basu handed down his mantle to Buddhadeb Bhattacharjee in 2000. Since then, he had been acting as the guardian of the party and the Left Front. 

    Call it a coincidence, but Basu turned 95 the day CPM decided to pull out of the UPA government in the Centre over the Indo-US nuclear deal. When Left Front leaders called on his residence that day, the veteran leader stressed the need for the Front partners to stick together. An emotional Basu told a crowd at his residence, “I have no idea how long I will live now but it is my wish to see the Left Front gets a chance to finish another term.’’

Source

Source

Surgery Will Allow Sufferers To Come Off Medication Completely

What is Quadriplegia?

Quadriplegia (kwod-rih-PLEE-jah) is a type of spinal cord injury (SCI) that also may be called tetraplegia (tet-ruh-PLEE-jah). You may become paralyzed (PER-e-liz-ed) if your spinal cord is injured or if you have certain diseases. The spinal cord is part of the central nervous system, which allows your brain to communicate with your body. The spine is made up of bones called vertebrae (VER-te-bray) that are stacked on top of each other. The spinal cord runs from the brain down through the center of the vertebrae. Tough fibrous discs separate the vertebrae, acting as cushions or shock absorbers.

• Quadriplegia means that the part of the spinal cord inside your neck has been injured. This injury causes loss of feeling and movement in your arms, legs, and trunk (center of your body). Spinal cord injuries are described by where on the spinal cord they have happened. Caregivers use letters and numbers to describe where your spinal cord is injured. The letter “C” stands for cervical (SER-vi-kl) or neck. There are eight cervical, 12 thoracic, five lumbar, and four sacral bones. If you have a C3 spinal cord injury, the damage is at the level of the third cervical spinal cord section.
• Spinal cord injuries are also described as complete or incomplete. This refers to how much function (movement and feeling) is left after you have healed from the injury. A complete SCI means that you have lost total (all) movement and feeling below the injured level. An incomplete SCI does not cause total loss of movement or feeling.

Symptoms

Although the most obvious symptom is impairment to the limbs, functioning is also impaired in the torso. This can mean a loss or impairment in controlling bowel and bladder, sexual function, digestion, breathing, and other autonomic functions. Furthermore, sensation is usually impaired in affected areas. This can manifest as numbness, reduced sensation, or burning neuropathic pain.
Secondarily, because of their depressed functioning and immobility, quadriplegics are often more vulnerable to pressure sores, osteoporosis and fractures, frozen joints, spasticity, respiratory complications and infections, autonomic dysreflexia, deep vein thrombosis, and cardiovascular disease.
Severity depends on both the level at which the spinal cord is injured and the extent of the injury.
An individual with an injury at C1 (the highest cervical vertebra, at the base of the skull) will likely lose function from the neck down and be ventilator-dependent. An individual with a C7 injury may lose function from the chest down but still retain use of the arms and much of the hands.
The extent of the injury is also important. A complete severing of the spinal cord will result in complete loss of function from that vertebra down. A partial severing or even bruising of the spinal cord results in varying degrees of mixed function and paralysis. For example, there are quadriplegics who have impairment in all four limbs but can still walk and use their hands due to the relatively minor extent of their injury. Others cannot walk but are able to maintain control of bladder, bowel, and sexual function.
It is common to have partial use of some limbs, such as the ability to move the arms but not the hands, or to be able to use the fingers but not have enough grip strength to lift objects. Furthermore, the deficit in the limbs may not be the same on both sides of the body; the left or right side may be more affected, depending on the location of the lesion on the spinal cord.

Prognosis

Delayed diagnosis of cervical spine injury has grave consequences for the victim. About one in twenty cervical fractures are missed, and about two-thirds of these patients have further spinal-cord damage as a result. About 30% of cases of delayed diagnosis of cervical spine injury develop permanent neurological deficits. In high-level cervical injuries, total paralysis from the neck can result. High-level quadriplegics (C5 and above) will likely need constant care and assistance in things such as getting dressed, eating, and bowel and bladder help. Low-level quadriplegics (C6-C7) can often live independently.
Even with “complete” injuries, in some rare cases, through intensive rehabilitation, slight movement can be regained through “rewiring” neural connections, as in the case of the late actor Christopher Reeve.

Tests

Tests help caregivers find out more about your spinal cord injury. They may also help caregivers plan your treatment. You may need one or more of the following tests.

• Neurologic (nu-roh-LAH-jik) tests: Caregivers may ask you questions and do other tests to learn what area of your spinal cord is injured.
• X-rays: X-rays help caregivers see the part of the spine that is damaged.
• CT scan: This test is also called a “CAT” scan. A special x-ray machine uses a computer to take pictures of your neck and spine. Your caregivers look at the pictures to see areas that might be injured.
• MRI: This test is also called magnetic resonance (REZ-oh-nans) imaging. This test may be done to show where and how much damage has occurred. You may need an MRI if you are having pain or muscle spasms.

Treatment

You will need to stay in the hospital right after the injury. Soon after, you may be moved to a rehabilitation (ree-hah-bil-ih-TAY-shun) center. The goal of rehabilitation is to help you learn to take care of yourself as much as possible. You may have one or more of the following treatments during rehabilitation:

• Bowel and bladder programs: Being paralyzed makes you unable to control when you urinate or have a BM. Caregivers will teach you how to manage your bowels and bladder.
• Braces: You may need a halo brace or a Philadelphia collar if the bones or ligaments that support your spine are injured. Another type of brace may be used if the injury is in your chest or lower back area. These braces include a clamshell (plastic body jacket) or a plaster or plastic body cast.
• Medications: Caregivers will teach you what medicines you need, why you need them, and how to take them. You may need one or more of the following medicines:
  • Steroids: This medicine is used to prevent and reduce spinal cord swelling and improve blood flow.
  • Osmotic diuretics: An osmotic (oz-MAH-tik) diuretic (deye-yoo-RET-ik) is medicine that may help decrease and prevent spinal cord swelling.
  • Blood pressure medicine: This medicine may be given to lower your blood pressure. Keeping your blood pressure under control protects your heart, lungs, brain, kidneys, and other organs.

• Mental health therapy: Being quadriplegic can cause you and your family to be depressed or sad. Mental health therapists help you and your family learn to cope with your spinal cord injury.
• Occupational therapy: Occupational (ok-u-PAY-shun-al) therapists (OT) teach you how to use special equipment so that you can care for yourself. They help you relearn how to perform your activities of daily living. This means learning how to eat, get dressed, and care for yourself. Your OT also teaches you work-related skills.
• Physical therapy: Physical (FIZ-i-kal) therapists (PT) teach you how to keep your muscles strong. They also help your joints stay limber (able to move easily) and teach you how to stay active. This therapy includes learning how to use a wheelchair. Caregivers teach you how to move from your bed to the chair and to the commode (toilet).
• Recreational therapy: Recreational therapists continue your skills training so that you can be active in your community. You may also learn fun activities.
• Respiratory care: Depending on how high on the spinal cord your injury is, you may have trouble breathing. You may need a machine called a ventilator (VEN-ti-lay-ter) to breathe for you. Respiratory (RES-pir-ah-tohr-ee) therapists make sure that your respiratory system (breathing system) stays healthy.
• Skin care: Being paralyzed puts your skin at risk for getting decubitus (de-KU-bi-tus) ulcers (sores). These also are called pressure sores. Caregivers help you learn how to keep your skin healthy, and what to do if you develop skin problems.

Surgeries

The injury to your spinal cord cannot be repaired, even with surgery.

• You may need surgery to stabilize (support) the bones in your spine. Pieces of vertebra or disc may be pressing on the spinal cord or nerve roots coming out of the spinal cord. You may need surgery to remove these pieces of bone or disc. Surgery also can be done to line up the bony spinal column. Caregivers may use bone from your hip or metal rods and screws to support your spine.
• You may be able to have surgery or use pieces of equipment to help you move better. Some of these procedures are called muscle tendon transfer, or functional electrical stimulation (FES). These procedures may be done about a year after your spinal cord injury. This will allow you to recover as much as possible.
• If your injury is high up on your spinal cord, you may need a ventilator to help you breathe. You may be able to have a phrenic (FREH-nik) nerve pacer. This surgery is expensive, but has some advantages over a ventilator. Talk to your caregiver about a phrenic nerve pacer.

Advice

Although this condition is very limiting, today’s tetraplegics still enjoy a better quality and duration of life than ever before. Technological breakthroughs have increased patient mobility, functionality and communicative abilities. Portable support systems have given all but the most dire of patients some measure of independence and autonomy.
Preventative and maintenance care is crucial for keeping up good health. There are far too many opportunistic conditions which might seriously affect a tetraplegic at any point in life… Make sure to see your doctor regularly and get checked out if you even suspect that something might be wrong. Keeping a positive mental state will help improve both the quality of life and your remaining physical functionality. Remember that the mind is still important to protect the remaining functions of the physical body. Life is a gift and there is no reason why even a high level quadriplegic can not find joy and peace while still living with their considerable hardships

Source

• Wikipedia
• Times of India
• Spinal Injury.Net
• Disease Condition.com
• Origins of Cerebral Plasy.Com
  

Gestational diabetes (or gestational diabetes mellitus, GDM) is a condition in which women without previously diagnosed diabetes exhibit high blood glucose levels during pregnancy.

Gestational diabetes generally has few symptoms and it is most commonly diagnosed by screening during pregnancy. Diagnostic tests detect inappropriately high levels of glucose in blood samples. Gestational diabetes affects 3-10% of pregnancies, depending on the population studied.No specific cause has been identified, but it is believed that the hormones produced during pregnancy increase a woman’s resistance to insulin, resulting in impaired glucose tolerance.

Babies born to mothers with gestational diabetes are at increased risk of problems typically such as being large for gestastional age (which may lead to delivery complications), low blood sugar, and jaundice. Gestational diabetes is a treatable condition and women who have adequate control of glucose levels can effectively decrease these risks.

Women with gestational diabetes are at increased risk of developing type 2 diabetes mellitus after pregnancy, while their offspring are prone to developing childhood obesity, with type 2 diabetes later in life. Most patients are treated only with diet modification and moderate exercise but some take anti-diabetic drugs, including insulin.

Definition

Gestational diabetes is formally defined as “any degree of glucose intolerance with onset or first recognition during pregnancy”. This definition acknowledges the possibility that patients may have previously undiagnosed diabetes mellitus, or may have developed diabetes coincidentally with pregnancy. Whether symptoms subside after pregnancy is also irrelevant to the diagnosis .

How gestational diabetes can affect the baby?

Gestational diabetes affects the mother in late pregnancy, after the baby’s body has been formed, but while the baby is busy growing. Because of this, gestational diabetes does not cause the kinds of birth defects sometimes seen in babies whose mothers had diabetes before pregnancy.

However, untreated or poorly controlled gestational diabetes can hurt your baby. When you have gestational diabetes, your pancreas works overtime to produce insulin, but the insulin does not lower your blood glucose levels. Although insulin does not cross the placenta, glucose and other nutrients do. So extra blood glucose goes through the placenta, giving the baby high blood glucose levels. This causes the baby’s pancreas to make extra insulin to get rid of the blood glucose. Since the baby is getting more energy than it needs to grow and develop, the extra energy is stored as fat.

This can lead to macrosomia, or a “fat” baby. Babies with macrosomia face health problems of their own, including damage to their shoulders during birth. Because of the extra insulin made by the baby’s pancreas, newborns may have very low blood glucose levels at birth and are also at higher risk for breathing problems. Babies with excess insulin become children who are at risk for obesity and adults who are at risk for type 2 diabetes.

Classification

The White classification, named after Priscilla Whitewho pioneered in research on the effect of diabetes types on perinatal outcome, is widely used to assess maternal and fetal risk. It distinguishes between gestational diabetes (type A) and diabetes that existed prior to pregnancy (pregestational diabetes). These two groups are further subdivided according to their associated risks and management.[54]

There are 2 subtypes of gestational diabetes (diabetes which began during pregnancy):

• Type A1: abnormal oral glucose tolerance test (OGTT) but normal blood glucose levels during fasting and 2 hours after meals; diet modification is sufficient to control glucose levels
• Type A2: abnormal OGTT compounded by abnormal glucose levels during fasting and/or after meals; additional therapy with insulin or other medications is required

The second group of diabetes which existed prior to pregnancy is also split up into several subtypes.

Treatment

The goal of treatment is to reduce the risks of GDM for mother and child. Scientific evidence is beginning to show that controlling glucose levels can result in less serious fetal complications (such as macrosomia) and increased maternal quality of life. Unfortunately, treatment of GDM is also accompanied by more infants admitted to neonatal wards and more inductions of labour, with no proven decrease in cesarean section rates or perinatal mortality. These findings are still recent and controversial.

Counselling before pregnancy (for example, about preventive folic acid supplements) and multidisciplinary management are important for good pregnancy outcomes.[58] Most women can manage their GDM with dietary changes and exercise. Self monitoring of blood glucose levels can guide therapy. Some women will need antidiabetic drugs, most commonly insulin therapy.

Any diet needs to provide sufficient calories for pregnancy, typically 2,000 – 2,500 kcal with the exclusion of simple carbohydrates. The main goal of dietary modifications is to avoid peaks in blood sugar levels. This can be done by spreading carbohydrate intake over meals and snacks throughout the day, and using slow-release carbohydrate sources. Since insulin resistance is highest in mornings, breakfast carbohydrates need to be restricted more.

Regular moderately intense physical exercise is advised, although there is no consensus on the specific structure of exercise programs for GDM.

Self monitoring can be accomplished using a handheld capillary glucose dosage system. Compliance with these glucometer systems can be low.Target ranges advised by the Australasian Diabetes in Pregnancy Society are as follows:

• fasting capillary blood glucose levels <5.5 mmol/L
• 1 hour postprandial capillary blood glucose levels <8.0 mmol/L
• 2 hour postprandial blood glucose levels <6.7 mmol/L

Regular blood samples can be used to determine HbA1c levels, which give an idea of glucose control over a longer time period.

If monitoring reveals failing control of glucose levels with these measures, or if there is evidence of complications like excessive fetal growth, treatment with insulin might become necessary. The most common therapeutic regime involves premeal fast-acting insulin to blunt sharp glucose rises after meals.Care needs to be taken to avoid low blood sugar levels (hypoglycemia) due to excessive insulin injections. Insulin therapy can be normal or very tight; more injections can result in better control but requires more effort, and there is no consensus that it has large benefits.

There is some evidence that certain oral glycemic agents might be safe in pregnancy, or at least, are significantly less dangerous to the developing fetus than poorly controlled diabetes. However, few studies have been performed as of this time and this is not a generally accepted treatment. These agents may be used in research settings, or if the patient needs intervention but refuses insulin therapy, and is aware of the risks.Glyburide, a second generation sulfonylurea, has been shown to be an effective alternative to insulin therapy.In one study, 4% of women needed supplemental insulin to reach blood sugar targets.

Metformin has shown promising results. Treatment of polycystic ovarian syndrome with metformin during pregnancy has been noted to decrease GDM levels.A recent randomized controlled trial of metformin versus insulin showed that women preferred metformin tablets to insulin injections, and that metformin is safe and equally effective as insulin. Severe neonatal hypoglycemia was less common in insulin-treated women, but preterm delivery was more common. Almost half of patients did not reach sufficient control with metformin alone and needed supplemental therapy with insulin; compared to those treated with insulin alone, they required less insulin, and they gained less weight.There remains a possibility of long-term complications from metformin therapy, although follow-up at the age of 18 months of children born to women with polycystic ovarian syndrome and treated with metformin revealed no developmental abnormalities.

If diet, exercise, and oral medication are inadequate to control glucose levels, insulin therapy may become necessary.

The development of macrosomia can be evaluated during pregnancy by using sonography. Women who use insulin, with a history of stillbirth, or with hypertension are managed like women with ouvert diabetes.

Research suggests a possible benefit of breastfeeding to reduce the risk of diabetes and related risks for both mother and child.

A repeat OGTT should be carried out 2-4 months after delivery, to confirm the diabetes has disappeared. Afterwards, regular screening for type 2 diabetes is advised.

Source

Wikipedia

American Diabetes Association

Definition

Situs inversus is a condition in which the organs of the chest and abdomen are arranged in a perfect mirror image reversal of the normal positioning.

Description

Normal human development results in an asymmetrical arrangement of the organs within the chest and abdomen. Typically, the heart lies on the left side of the body (levocardia), the liver and spleen lie on the right, and the lung on the left has two lobes while the lung on the right has three lobes. This normal arrangement is known as situs solitus.
However, in about 1 in 8,500 people, the organs of the chest and abdomen are arranged in the exact opposite position: the heart is on the right (dextrocardia), as is the two-lobed lung, and the liver, spleen, and three-lobed lung are on the left. Yet because this arrangement, called situs inversus, is a perfect mirror image, the relationship between the organs is not changed, so functional problems rarely occur.

Causes and Symptoms

Early in the normal development of an embryo, the tube-like structure that becomes the heart forms a loop toward the left, identifying the left/right axis along which the other organs should be positioned. Although the mechanism that causes the heart loop to go left is not fully understood, at least one gene has been identified to have a role in this process. However, it is thought that many factors may be involved in causing situs inversus. Rarely, situs inversus can run in families, but most often it is an isolated and accidental event occurring in an individual for the first time in the family.
Most people with situs inversus have no medical symptoms or complications resulting from the condition. Although only 3-5% of people with situs inversus have any type of functional heart defect, this is higher than the rate of heart defects in the general population, which is less than 1%.
It is estimated that about 25% of people with situs inversus have an underlying condition called primary ciliary dyskinesia (PCD). PCD, also known as Kartagener’s syndrome, is characterized as situs inversus, chronic sinus infections, increased mucous secretions from the lungs, and increased susceptibility to respiratory infections. PCD is caused by a defect in the cilia that impairs their normal movements.

Diagnosis

Situs inversus should detected by a thorough physical examination. It is often picked up when a physician, using a stethoscope, hears otherwise normal heart sounds on the right side of the body instead of the left. To confirm the a suspected diagnosis of situs inversus, imaging studies such as MRI, CT, or ultrasound may be ordered, and a referral may be made to a cardiologist or internist for completeness. Imaging studies will also rule out the possibility of random arrangement of the organs, or heterotaxy, which has a much higher risk for serious medical complications.

Treatment

There is no treatment for situs inversus. In the unlikely case that a heart defect is present, it should be treated accordingly by a cardiologist.
Individuals who have situs inversus should be sure to inform all physicians involved in their medical care. In addition to preventing unnecessary confusion, this will reduce the risk of missing a crucial diagnosis that presents with location-specific symptoms (such as appendicitis).

Alternative Treatment

Not applicable.

Prognosis

The prognosis for an individual with situs inversus is good, and in the absence of a heart defect or other underlying diagnosis, life expectancy is normal.

Prevention

There is no known method of preventing situs inversus.

Significance

Situs inversus has an autosomal recessive pattern of inheritance.
Situs inversus is generally an autosomal recessive genetic condition, although it can be X-linked or found in identical “mirror” twins.
In the absence of congenital heart defects, individuals with situs inversus are phenotypically unimpaired, and can lead normal healthy lives, without any complications related to their medical condition. There is a 5-10% prevalence of congenital heart disease in individuals with situs inversus totalis, most commonly transposition of the great vessels. The incidence of congenital heart disease is 95% in situs inversus with levocardia.
Many people with situs inversus totalis are unaware of their unusual anatomy until they seek medical attention for an unrelated condition. The reversal of the organs may then lead to some confusion, as many signs and symptoms will be on the ‘wrong’ side. For example, if an individual with situs inversus develops appendicitis, they will present to the physician with left lower abdominal pain, since that is where their appendix lies. Thus, in the event of a medical problem, the knowledge that the individual has situs inversus can expedite diagnosis. People with this rare condition should inform their physicians before an examination, so they may redirect their search for heart sounds and other signs.
Situs inversus also complicates organ transplantation operations as donor organs will almost certainly come from situs solitus donors. As hearts and livers are chiral, geometric problems arise placing an organ into a cavity shaped in the mirror image. For example, a person with situs inversus who requires a heart transplant needs all the vessels to the transplant donor heart reattached to their existing ones. However, the orientation of these vessels in a person with situs inversus is reversed, necessitating steps so that the blood vessels join properly.

Kartagener syndrome

About 25% of individuals with situs inversus have an underlying condition known as primary ciliary dyskinesia (PCD). PCD is a dysfunction of the cilia that manifests itself during the embryologic phase of development. Normally-functioning cilia determine the position of the internal organs during early embryological development, and so individuals with PCD have a 50% chance of developing situs inversus. If they do, they are said to have Kartagener syndrome, characterized by the triad of situs inversus, chronic sinusitis, and bronchiectasis. Cilia are also responsible for clearing mucus from the lung, and the dysfunction causes increased susceptibility to lung infections.

Notable persons with situs inversus

Notable individuals with documented cases of situs inversus include:

• Randy Foye, an American basketball player for the NBA’s Minnesota Timberwolves. He has suffered no discernible complications, and the condition is not expected to jeopardize his career as a professional athlete.
• Catherine O’Hara, the Canadian comedic actress has said in interviews that her organs are reversed and her heart is on the right side of her chest.
• Donny Osmond, whose appendicitis was initially dismissed as a less serious condition because nobody realized he had situs inversus. It was discovered when he was taken to hospital when on tour with his family in England.
• Enrique Iglesias, the Spanish singer told the press that he was born with situs inversus.

Fictional characters with situs inversus

• In the Ian Fleming novel Dr. No, Julius No explains to James Bond that he once survived a murder attempt because his heart is located on his right side, which his would-be-killers did not know when they stabbed the spot on the left where the heart of a normal human being would be.
• Souther, from the anime/manga Fist of the North Star, has situs inversus totalis, making him immune to standard pressure-points martial arts.
• In the webcomic It’s Walky!, anyone who goes through the Martian resurrection process ends up being completely reversed, with their organs mirrored within their bodies and their primary hand becoming the opposite of what it had been before. This process happens to several major characters throughout the comic’s run.
• In the WB series Jack & Jill, Simon Rex played a young man with situs inversus.
• Fortune, from Metal Gear Solid 2: Sons of Liberty. Revolver Ocelot points this out when he shoots Fortune on the left side of her chest, then remembers and states that her heart was on the right side.
• In Margaret Mahy’s novel The Tricksters, the character Hadfield is said to be an exact mirror image of his otherwise identical twin Felix, including having his vital organs in mirror-image layout.
• In the Lord Peter Wimsey short story The Image in the Mirror by Dorothy Sayers, a character with reversed organs has long been haunted by dreams of a doppelgänger and by fears that he himself might be only the reflection of someone else.
• In the Max Brooks novel World War Z, a character describes operating on a patient who had dextrocardia with situs inversus, and transplants a heart from someone with the same condition. Unbeknownst to him, the transplant heart is infected with the virus Solanum, thus turning the patient into a zombie.

Sources

• Wikipedia
• Health At OZ

Intelligent pill’ knows where to release drug

Dutch group Philips has developed an “intelligent pill” that contains a microprocessor, battery, wireless radio, pump and a drug reservoir to release medication in a specific area in the body. Philips, one of the world’s biggest hospital equipment makers, said on Tuesday that the “iPill” capsule, measures acidity with a sensor to determine its location in the gut, and can then release drugs where they are needed. Delivering drugs to treat digestive tract disorders such as Crohn’s disease directly to the location of the disease means doses can be lower, reducing side effects, Philips said. While capsules containing miniature cameras are already used as diagnostic tools, those lack the ability to deliver drugs, Philips said. The “iPill” can also measure the local temperature and report it wirelessly to an external receiver

The human body has two major areas of blood vessels that distribute from and return blood to the left and right heart. The portion of the circulation that distributes the blood from the left side of the heart, throughout the body, is referred to as systemic circulation. The portion of the circulation that distributes the blood from the right side of the heart, to the lungs, is referred to as the pulmonary (lung) circulation. When the doctor or a nurse measures the blood pressure on a person’s arm, it is the systemic blood pressure that is being measured. When these pressures are abnormally high, the person is diagnosed as having high blood pressure or hypertension.

The right ventricle pumps venous blood returning from the body into the arteries of the lungs to receive oxygen. The pressures in the lung arteries (pulmonary arteries) are normally lower than the pressures in the systemic circulation. When pressure in the pulmonary circulation becomes abnormally elevated, it is referred to as pulmonary hypertension.

What Causes Pulmonary Hypertension?

Pulmonary hypertension results from constriction, or tightening, of the blood vessels that supply blood to the lungs. Consequently it becomes difficult for blood to pass through the lungs. Consequently, it becomes difficult for the blood to pass through the lungs, making it harder for the heart to pump blood forward. This stress on the heart leads to enlargement of the heart and eventually fluid build up in the liver and tissues, such as in the legs. Affected patients can sometimes notice increasing shortness of breath and dizziness.

Pulmonary hypertension can be caused by diseases of the heart and the lungs such as chronic obstructive pulmonary disease (COPD) or emphysema, failure of the left heart ventricle, recurrent pulmonary embolism (blood clots traveling from the legs or pelvic veins obstructing th epulmonary arteries), or underlying disease such as scleroderma. Pulmonary hypertension can also be caused by chronic low blood oxygen levels as in some patients with sleep apnea. If pulmonary hpertension is caused by other illnesses it is called secondary pulmonary hypertension.

When pulmonary hypertension occurs without underlying heart and lung disease or other illnesses, it is called primary pulmonary hypertension. Primary pulmonary hypertension is more common in young females.

History of the disease

The first reported case of primary pulmonary hypertension occured in 1891 with a published description of an autopsy that showed thickening of the deceased’s pulmonary artery, but with no indications of heart or lung disease. In 1951, when 39 cases were reported in the US, the disease got its name.

Between 1967 and 1973, an unexplained increase in primary pulmonary hypertension was reported in central Europe. The increase in the number of cases was eventually attributed to aminorex fumarate, an amphetamine like drug introduced in Europe in 1965 to control appetite. When aminorex was removed form the market, the incidence of primary pulmonary hypertension went down to normal levels.

Signs and Symptoms

Because symptoms may develop very gradually, patients may delay seeing a physician for years. A history usually reveals gradual onset of shortness of breath, fatigue, non productive cough, angina pectoris, fainting or syncope, peripheral edema (Swelling of the limbs, especially around the ankles and feet), and rarely hemoptysis (coughing up blood). Pulmonary arterial hypertension typically does not present with orthopnea or paroxysmal nocturnal dyspnea while pulmonary venous hypertension typically does.

In order to establish the cause, the physician will generally conduct a thorough medical history. A detailed family history is taken to determine whether the disease might be familial. A history of exposure to cocaine, methamphetamine, alcohol leading to cirrhosis, and smoking leading to emphysema are considered significant. A physical examination is performed to look for typical signs of pulmonary hypertension including a loud P₂ (pulmonic valve closure sound), (para)sternal heave, jugular venous distension, pedal edema, ascites hepatojugular reflux, clubbing etc. Evidence of tricuspid insufficiency is also sought and, if present is consistent with the presence of pulmonary hypertension.

Diagnosis

Because pulmonary hypertension can be of five major types, a series of tests must be performed to to distinguish pulmonary arterial hypertension from venous, hypoxic, thomboembolic or miscellaneous varieties. A physical examination is performed to look for typical signs of pulmonary hypertension. These include altered heart sounds, such as a widely split S₂ or second heart sound, a loud P₂ or pulmonic valve closure, (para)sternal heave, possible S₃ or third heart sound, and pulmonary regurgitation. Other signs include an elevated jugular venous pressure, pheripheral edema (swelling of the ankles and feet), ascites (abdominal swelling due to he accumulation of fluid), hepatojugular reflux, and clubbing.

Further procedures are required to confirm the presence of pulmonary hypertension and exclude other possible diagnoses. These generally include pulmonary function tests, blood tests to exclude HIV, autoimmune diseases and liver disease, ECG, arterial blood gas measurements, xrays of the chest (followed by high resolutiion CT Scanning if interstitial lung disease is suspected), and ventilation perfusion or V/Q scanning to exclude thromboembolic pulmonary hypertension. Biopsy of the lung is usually not indicated unless the pulmonary hypertension is thought to be due to an underlying interstitial lung disease. But lung biopsies are fraught with risks of bleeding due to the high intrapulmonary blood pressure. Clinical improvement is often measured by a six minute walk test, ie the distance a patient can walk in six minutes. Stability and improvement in this measurement correlate with better survival. Blood BNP level is also being used now to follow progress of patients with pulmonary hypertension.

Diagnosis of PAH requires the presence of pulmonary hypertension with two other conditions. Pulmonary artery occlusion pressure (PAOP OR PCWP) must be less than 15mm Hg (2000 Pa) and pulmonary vascular resistance (PVR) must be greater than 3 wood units (240 dyn*s*cm^-5 or 2.4 mN*s*cm^-5)

Although pulmonary arterial pressure can be estimated on the basis of echocardiography, pressure measurements with a Swan-Ganz catheter provides the most definite assessment. PAOP and PVR cannot be measured directly with echocardiography. Therefore diagnosis of PAH requires right-sided cardiac catheterization. A Swan-Ganz catheter can also measure the cardiac output, which is far more important in measuring disease severity than the pulmonary arterial pressure.
Normal pulmonary arterial pressure in a person living at sea level has a mean value of 12–16 mm Hg (1600–2100 Pa). Pulmonary hypertension is present when mean pulmonary artery pressure exceeds 25 mm Hg (3300 Pa) at rest or 30 mm Hg (4000 Pa) with exercise.
Mean pulmonary artery pressure (mPAP) should not be confused with systolic pulmonary artery pressure (sPAP), which is often reported on echocardiogram reports. A systolic pressure of 40 mm Hg typically implies a mean pressure more than 25 mm Hg. Roughly, mPAP = 0.61*sPAP + 2.

Treatment

Treatment is determined by whether the PH is arterial, venous, hypoxic, thromboembolic, or miscellaneous. Since pulmonary venous hypertension is synonymous with congestive heart failure, the treatment is to optimize left ventricular function by the use of diuretics, beta blockers, ACE inhibitors, etc., or to repair/replace the mitral valve or aortic valve. In PAH, lifestyle changes, digoxin, diuretics, oral anticoagulants, and oxygen therapy are considered conventional therapy, but have never been proven to be beneficial in a randomized, prospective manner. High dose calcium channel blockers are useful in only 5% of IPAH patients who are vasoreactive by Swan-Ganz catheter. Unfortunately, calcium channel blockers have been largely misused, being prescribed to many patients with non-vasoreactive PAH, leading to excess morbidity and mortality. The criteria for vasoreactivity have changed. Only those patients whose mean pulmonary artery pressure falls by more than 10 mm Hg to less than 40 mm Hg with an unchanged or increased cardiac output when challenged with adenosine, epoprostenol, or nitric oxide are considered vasoreactive. Of these, only half of the patients are responsive to calcium channel blockers in the long term. A number of agents has recently been introduced for primary and secondary PAH. The trials supporting the use of these agents have been relatively small, and the only measure consistently used to compare their effectivity is the “6 minute walking test”. Many have no data on mortality benefit or time to progression.

Vascoactive Substances

Many pathways are involved in the abnormal proliferation and contraction of the smooth muscle cells of the pulmonary arteries in patients with pulmonary arterial hypertension. Three of these pathways are important since they have been targeted with drugs — endothelin receptor antagonists, phosphodiesterase type 5 inhibitors, and prostacyclin derivatives.
Because inexpensive generic drugs for this disease are not widely available, the World Health Organization does not include them in its model list of essential medicines.

Prostaglandins

Prostacyclin (prostaglandin I₂) is commonly considered the most effective treatment for PAH. Epoprostenol (synthetic prostacyclin, marketed as Flolan) is given via continuous infusion that requires a semi-permanent central venous catheter. This delivery system can cause sepsis and thrombosis. Flolan is unstable, and therefore has to be kept on ice during administration. Since it has a half-life of 3 to 5 minutes, the infusion has to be continuous (24/7), and interruption can be fatal. Other prostanoids have therefore been developed. Treprostinil (Remodulin) can be given intravenously or subcutaneously, but the subcutaneous form can be very painful. An increased risk of sepsis with intravenous Remodulin has been reported by the CDC. Iloprost (Ilomedin) is also used in Europe intravenously and has a longer half life. Iloprost (marketed as Ventavis) is the only inhaled form of prostacyclin approved for use in the US and Europe. This form of administration has the advantage of selective deposition in the lungs with less systemic side effects. Oral and inhaled forms of Remodulin are under development. Beraprost is an oral prostanoid available in Japan and South Korea.

Endothelin receptor antagonists

The dual (ET_A and ET_B) endothelin receptor antagonist bosentan (marketed as Tracleer) was approved in 2001. Sitaxsentan, a selective endothelin receptor antagonist that blocks only the action of ET_A, has been approved for use in Canada, Australia, and the European Union, to be marketed under the name Thelin. Sitaxsentan has not been approved for marketing by the US FDA. A new trial to address the FDA’s concerns will begin in 2008. A similar drug, ambrisentan is marketed as Letairis in U.S. by Gilead Sciences. In addition, another dual/nonselective endothelin antagonist, Actelion-1, from the makers of Tracleer, will enter clinical trials in 2008.

Phosphodiesterase type 5 inhibitors

Sildenafil, a selective inhibitor of cGMP specific phosphodiesterase type 5 (PDE5), was approved for the treatment of PAH in 2005. It is marketed for PAH as Revatio.

Surgical

Atrial septostomy is a surgical procedure that creates a communication between the right and left atria. It relieves pressure on the right side of the heart, but at the cost of lower oxygen levels in blood (hypoxia). It is best performed in experienced centers. Lung transplantation cures pulmonary arterial hypertension, but leaves the patient with the complications of transplantation, and a post-surgical median survival of just over five years
Pulmonary thromboendarterectomy (PTE) is a surgical procedure that is used for chronic thromboembolic pulmonary hypertension. It is the surgical removal of an organized thrombus (clot) along with the lining of the pulmonary artery; it is a very difficult, major procedure that is currently performed in a few select centers. Case series show remarkable success in most patients.
Treatment for hypoxic and miscellaneous varieties of pulmonary hypertension have not been established. However, studies of several agents are currently enrolling patients. Many physicians will treat these diseases with the same medications as for PAH, until better options become available. Such treatment is called off-label use.

Monitoring

Patients are normally monitored through commonly available tests such as:

• pulse oximetry,
• arterial blood gas tests,
• chest X-rays,
• serial ECG tests,
• serial echocardiography, and
• spirometry or more advanced lung function studies.

Sources

• American Heart Association

• Wikipedia

• Medicine Net.Com

• MediaFact.Com

• Ohio State University Medical Center