he primordial digestive tube, consisting of the fore-, mid-, and hindgut.

DIVISION ARTERY VEIN LYMPHATICS SYMPATHETIC PARASYMPATHETIC FOREGUT: Oesophagus Stomach Proximal half of duodenum (up to common bile duct (CBD)) Liver Pancreas CELIAC ARETERY PORTAL VEIN,Spleenic vein,Gastric vein, CELIAC NODES CELIAC,GANGLIA VAGUS MIDGUT: Distal half of duodenum Jejunum Ileum Appendix Cecum Ascending colon Right 3/4 of transverse colon SUPERIOR MESENTERIC ARTERY ,SUPERIOR MESENTERIC VEIN, SUPERIOR MESENTERIC NODES ,SUPERIOR MESENTERIC GANGLIA, VAGUS HINDGUT: Left 1/4 of transverse colon Descending colon All of rectum down to ano-rectal line INFERIOR MESENTERIC ARTERY, INFERIOR MESENTERIC VEIN, INFERIOR MESENTERIC NODES GANGLIA,HYPOGASTRIC PLEXUS, PELVIC SPLANCHNIC NERVES Fee-for-service is a standard business model where services are unbundled and paid for separately.

In Health insurance and the health care industry fee-for-service involves when doctors and other health care providers receive a fee for each service such as an office visit, test, procedure, or other health care service[1]. Fee-forservice health insurance plans typically allow patients to obtain care from doctors or hospitals of their choosing[1], but in return for this flexibility they may pay higher copayments or deductibles[2]. Patients frequently pay providers directly for services, then submit claims to their insurance company for reimbursement[2]. A health maintenance organization (HMO) is a type of managed care organization (MCO) that provides a form of health care coverage in the United States that is fulfilled through hospitals, doctors, and other providers with which the HMO has a contract. The Health Maintenance Organization Act of 1973 required employers with 25 or more employees to offer federally certified HMO options.[1] Unlike traditional indemnity insurance, an HMO covers only care rendered by those doctors and other professionals who have agreed to treat patients in accordance with the HMO's guidelines and restrictions in exchange for a steady stream of customers. Point of Service Health Plans Point of service plans or POS insurance policies are similar to HMOs but offer more flexibility.

The tax expenditure for health

benefits is the amount of revenues that the federal government forgoes by exempting health benefits and spending from the federal income and Social Security taxes, including (1) employer health benefit contributions for workers and retirees, (2) health benefit deductions for the self-employed, (3) health spending under flexible spending plans, and (4) the tax deduction for health expenses. We estimate that this expenditure will be $188.5 billion in 2004.

In health insurance, a preferred provider organization (or "PPO", sometimes referred to as a participating provider organization) is a managed care organization of medical doctors, hospitals, and other health care providers who have covenanted with an insurer or a third-party administrator to provide health care at reduced rates to the insurer's or administrator's clients. The idea of a preferred provider organization is that the providers will provide the insured members of the group a substantial discount below their regularly-charged rates. This will be mutually beneficial in theory, as the insurer will be billed at a reduced rate when its insured utilize the services of the "preferred" provider and the provider will see an increase in its business as almost all insureds in the organization will use only providers who are members. Even the insured should benefit, as lower costs to the insurer should result in lower rates of increase in premiums. Preferred provider organizations themselves earn money by charging an access fee to the insurance company for the use of their network. They negotiate

with providers to set fee schedules, and handle disputes between insurers and providers. PPOs can also contract with one another to strengthen their position in certain geographic areas without forming new relationships directly with providers. Filgrastim is a granulocyte colonystimulating factor (G-CSF) analog used to stimulate the proliferation and differentiation of granulocytes. Filgrastim is used to treat neutropenia, stimulating the bone marrow to increase production of neutrophils. Causes of neutropenia include chemotherapy and bone marrow transplantation. Filgrastim is also used to increase the number of hematopoietic stem cells in the blood before collection by leukapheresis for use in hematopoietic stem cell transplantatio The most commonly observed adverse effect is mild-to-moderate bone pain after repeated administration and local skin reactions at the site of injection.Filgrastim generally has been well tolerated Persons with sickle cell disorders may suffer sickle cell crisis after receiving Filgrastim(Neupogen).Other adverse effects include spleen rupture, serious allergic reactions (including a rash over the whole body, shortness of breath, wheezing, dizziness, swelling around the mouth or eyes, fast pulse, and sweating), alveolar hemorrhage, acute respiratory distress syndrome (ARDS), and hemoptysis.

Sargramostim....GMCSF...inc.granulocytes and macrophages s/E Bone pain flu-like" syndrome that has included symptoms of headache, low-grade fever, myalgias, arthralgias, and malaise. nausea, vomiting, and diarrhea clot formation thrombosis Exacerbation of psoriasis,rheumatoid arthritis, thyroiditis, and vasculitis may occur. Metabolic side effects have included edema, ascites, hypoalbuminemia, fluid retention resulting in pericardial/pleural effusions, and capillary-leak syndrome. The risk of occurrence is greater at higher dosages. pleural effusions and pleuritis. reversible, transient supraventricular arrhythmias. increased plasma creatinine concentrations have occurred in patients with existing renal dysfunction. elevated plasma bilirubin and liver enzyme concentrations have been reported in patients with existing liver dysfunction. Oncologic side effects, primarily myeloid malignancies, may result due to the action of sargramostim as a growth factor for tumors with myeloid characteristics. A first dose effect may occur, which is characterized by an increased heart rate, feeling faint, low blood pressure and reddening of the face. This tends to only happen on the first dose of sargramostim Diarrhea or stomach upset Swelling, pain, redness, tenderness at the site of injection Flu-like symptoms that may

include fever, headache, achiness or pain, weakness and fatigue Bone pain Swelling of feet or hand 48.CC Addisons disease : chronic endocrine disorder where in the adrenal glands produce insufficient steroid hormones (glucocorticoids and often mineralocorticoid s) Because primary hypocortisolism is manifested as a deficiency in glucocorticoid release from the adrenal cortex, increased ACTH will be released by the pituitary in order to trigger release of the absent glucocorticoid; it is because of this overstimulation of ACTH that bronzing of the skin occurs. In secondary or tertiary hypocortisolism, there is a deficiency of either CRH or ACTH release by the hypothalamus or

pituitary gland, respectively. Diagnosis: Hypercalcemia Hypoglycemia, low blood sugar (worse in children due to loss of glucocorticoid's glucogenic effects) Hyponatraemia (low blood sodium levels), due both to a deficiency in Aldosterone (a mineralocorticoid ) dependant Sodium retention and also the effect of Corticotropinreleasing hormone to stimulate secretion of ADH Hyperkalemia (raised blood potassium levels), due to loss of production of the hormone aldosterone Eosinophilia and lymphocytosis (increased number of eosinophils or lymphocytes, two types of white blood cells) Metabolic acidosis

(increased blood acidity), also due to loss of the hormone aldosterone because sodium reabsorption in the distal tubule is linked with acid/hydrogen ion (H+) secretion. Low levels of aldosterone stimulation of the renal distal tubule leads to sodium wasting in the urine and H+ retention in the serum.

Many intraerythrocytic hemoparasites survive the host immune system through rapid antigenic variation. Among babesial parasites antigenic variation has been demonstrated convincingly only for Babesia bovis and Babesia rodhaini. The molecular basis for antigenic variation in babesial parasites and its possible connection with cytoadherence and sequestration are discussed Structural glycoproteins are encoded for by HIV-1 env. gene,viral eversion of humoral immunity is more likely to occur secoundary to a mutation of the env gene.

It is a genomic imprinting......means genes are either expressed only from the allele inherited from the mother , or in other instances from the allele inherited from the father. so in this case,, father has......... aa.....bd..... mother has........ bc ....bf......

2 affected kids have received their..... bd...... from their father and....bf ....from their mother both kids have identical bd that come from their father, so it means these 2 allels are expressed as a disease ,and the healthy child who received her... aa from father ,...bf from mother. shows no sign of disease.......means the inherited allels are expressed normal and (this kids also does not have bd.) so genes are expressed only from the allele inherited (bd) from the father. Genomic imprinting is an epigenetic process that involves methylation and histone modifications in order to achieve monoallelic gene expression without altering the genetic sequence. These epigenetic marks are established in the germline and are maintained throughout all somatic cells of an organism. please clarify my answer and add your opinion.TY Posted by Sarim: one thing i wanted to clarify that the expression of the disease in genomic imprinting is because the specific genes are "NOT EXPRESSED" cz either got methylated or deleted. aa, bd, bc bf are the "Markers" on DNA fragments. those who recieved the "bd marker" , got the disease, which is coming from father side...and which means genes next to these markers either deleted or got methylated and not expressed.

1.protein syntheis starts on the free ribosomes in the cytoplasm and continues in the ER 2-Almost all proteins that are transported to the endoplasmic reticulum have a sequence consisting of 5-10 hydrophobic amino acids on the N-terminus 3-The protein is guided to the ER by a signal-recognition particle (SRP), which moves between the ER and the cytoplasm 4- The N-terminus (one end) of a polypeptide chain (i.e., a protein) contains a few amino acids that work as an address tag, which are removed when the polypeptide reaches its destination

the N terminus corresponds to the 5' end.....as the carboxy terminus is for the 3' end Multiple polymorphism:( aka Genetic Variation or Genetic polymorphism) -SNPs (Single Nucleotide Polymorphism) is the most common

Hypervariable DNA----- region within the DNA where there are Base pairs of "Nucleotide Repeats" and most of the time they are located in the Non-coding region(spacer DNA).They are used as "MARKERS".Variablity of these Repeats help us in RFLP, paternity testing, Forensic and linkage analysis. .Lack of oxygen causes the neuron's normal process for making ATP for energy to fail. 2.The cell switches to anaerobic

metabolism, producing lactic acid. 3.ATP-reliant ion transport pumps fail, causing the cell to become depolarized, allowing ions, including calcium (Ca++), to flow into the cell. 4.The ion pumps can no longer transport calcium out of the cell, and intracellular calcium levels get too high. 5.The presence of calcium triggers the release of the excitatory amino acid neurotransmitter glutamate. 6.Glutamate stimulates AMPA receptors and Ca++-permeable NMDA receptors, which open to allow more calcium into cells. 7.Excess calcium entry overexcites cells and causes the generation of harmful chemicals like free radicals, reactive oxygen species and calcium-dependent enzymes such as calpain, endonucleases, ATPases, and phospholipases in a process called excitotoxicity. ] Calcium can also cause the release of more glutamate. 8.As the cell's membrane is broken down by phospholipases, it becomes more permeable, and more ions and harmful chemicals flow into the cell. 9.Mitochondria break down, releasing toxins and apoptotic factors into the cell. 10.The caspase-dependent apoptosis cascade is initiated, causing cells to "commit suicide." 11.If the cell dies through necrosis, it releases glutamate and toxic chemicals into the environment around it. Toxins poison nearby neurons, and glutamate can overexcite them. 12.If and when the brain is reperfused, a number of factors lead to reperfusion injury. 13.An inflammatory response is mounted, and phagocytic cells

engulf damaged but still viable tissue. 14.Harmful chemicals damage the blood brain barrier. 15.Cerebral edema (swelling of the brain) occurs due to leakage of large molecules like albumins from blood vessels through the damaged blood brain barrier. These large molecules pull water into the brain tissue after them by osmosis. This "vasogenic edema" causes compression of and damag AMPA The -amino-3-hydroxy-5-methyl-4isoxazolepropionic acid receptor (also known as AMPA receptor) is a non-NMDA-type ionotropic transmembrane receptor for glutamate that mediates fast synaptic transmission in the central nervous system (CNS). .....NMDA (N-methyl D-aspartate) The NMDAR is a specific type of ionotropic glutamate receptor. Papilledema (or papilloedema) is optic disc swelling that is caused by increased intracranial pressure. The swelling is usually bilateral and can occur over a period of hours to weeks. Unilateral presentation is extremely rare. Papilledema may be asymptomatic or present with headache in the early stages. However it may progress to enlargement of the blind spot, blurring of vision, visual obscurations (inability to see in a particular part of the visual field for a period of time) and ultimately total loss of vision may occur. The signs of papilledema that are seen using an ophthalmoscope include:

venous engorgement (usually the first signs) loss of venous pulsation hemorrhages over and / or adjacent to the optic disc blurring of optic margins elevation of optic disc Paton's lines = radial retinal lines cascading from the optic disc Checking the eyes for signs of papilledema should be carried out whenever there is a clinical suspicion of raised intracranial pressure, and is recommended in newly onset headaches. This may be done by ophthalmoscopy or slit lamp examination. Causes: Raised intracranial pressure: brain tumor, pseudotumor cerebri or cerebral venous sinus thrombosis, Intracerebral hemorrhage Respiratory failure[1] Hypotonia Accutane (Isotretinoin), which is a powerful derivative of Vitamin A, rarely causes Papilledema. Hypervitaminosis A, in some people who take megadoses of nutritional supplements and vitamins. Hyperammonemia, elevated level of ammonia in blood (including cerebral edema/intracranial pressure) Guillain-Barr syndrome due to elevated protein levels Foster Kennedy syndrome (FKS) Chiari Malformation Tumors of the frontal lobe Acute Mountain Sickness and High Altitude Cerebral Oedema Lyme disease (Lyme meningitis specifically, when the bacterial infection is in the central nervous system, causing increased intracranial pressure).

Malignant Hypertension Medulloblastoma Pathophysiology: As the optic nerve sheath is continuous with the subarachnoid space of the brain (and is regarded as an extension of the central nervous system), increased pressure is transmitted through to the optic nerve. The brain itself is relatively spared from pathological consequences of high pressure. However, the anterior end of the optic nerve stops abruptly at the eye. Hence the pressure is asymmetrical and this causes a pinching and protrusion of the optic nerve at its head. The fibers of the retinal ganglion cells of the optic disc become engorged and bulge anteriorly. Persistent and extensive optic nerve head swelling, or optic disc edema, can lead to loss of these fibers and permanent visual impairment