Huntington’s Chorea « Coolmristuff

Huntington’s Chorea « Coolmristuff

The disease was Huntington’s Chorea, which is an inherited, degenerative disorder of the Central Nervous System, caused by a dominant gene. This means that everyone who inherits the gene from one of his/her parents WILL develop the disease, and the likelihood of doing so is therefore 50%.

Huntington’s Chorea is a particularly devastating disease because symptoms normally do not occur until after the age of 35, but can onset later (the earlier the onset, the more severe the disease tends to be). It is principally a movement disorder, with the first observable symptoms manifesting themselves as ‘clumsiness’, but as the disease progresses the movements become uncontrollable. These movements appear to be very bizarre and include odd bodily postures. Other symptoms are also apparent including forgetfulness and irritability or withdrawing (in the early stages) progressing to dementia with severe memory loss and lack of reasoning.

Patients suffering from Huntington’s Chorea show degenerative changes in the basal ganglia structures, which ultimately result in a severely shrunken brain and enlarged ventricles. The caudate and putamen brain structures are particularly affected as they shrink up to half their normal size.

The symptoms of the disease are caused by a significant reduction (volume and activity) of two principal neurotransmitters (naturally occurring chemicals in the brain) – namely Acetylcholine and GABA, in turn affecting the activity of the neurotransmitter Dopamine, which becomes hyperactive. Huntington’s Chorea is therefore the ‘flip side of the coin’ to another movement disorder - Parkinson’s Disease where there is dopamine under activity.

Huntington’s Chorea is principally characterized by hyperkinesias – abnormal, purposeless, involuntary motor movements that can occur spontaneously or only when the patient is trying to do something. These movements may be repetitive or non-repetitive.

Drug therapies can ease the symptoms of the disease (including the use of dopamine antagonists or neuroleptics) but there may be severe side effects with these drugs. Unfortunately, there is no cure for Huntington’s Chorea. However, new techniques involving neural grafting (implanting healthy fetal brain cells into the damaged areas) may offer hope for sufferers in the near future.

http://en.wikipedia.org/wiki/Huntington’s_disease

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Huntington's Symptoms
Learn about the symptoms of HD Chorea and how to take action.
www.ChoreaMatters.com

multiple myeloma & mri

Multiple myeloma (MM) is an incurable clonal B-cell malignancy with terminally differentiated plasma cells. It afflicts approximately 55,000 people in the United States. Over the past 5 years, significant progress has been made in the diagnosis and assessment of patients with MM.  For the first time in decades, major therapeutic advances have been implemented in the treatment of MM patients. These include 2 new classes of agent: immunomodulatory drugs and proteosome inhibitors. In addition, clinical trials have solidified the role of hematopoietic stem cell transplant and established the benefits of post-transplant maintenance therapy. Finally, a number of new agents are in development that specifically target the myeloma cells and/or the bone marrow microenvironment. These advances have resulted in expanded treatment options, prolonged disease control and survival, and improved quality of life for patients with MM.

Because many organs can be affected by myeloma, the symptoms and signs vary greatly. A mnemonic sometimes used to remember the common tetrad of multiple myeloma is CRAB – C = Calcium (elevated), R = Renal failure, A = Anemia, B = Bone lesions.[

The presence of unexplained anemia, kidney dysfunction, a high erythrocyte sedimentation rate (ESR) and a high serum protein (especially raisedimmunoglobulin) may prompt further testing. A doctor will request protein electrophoresis of the blood and urine, which might show the presence of aparaprotein (monoclonal protein, or M protein) band, with or without reduction of the other (normal) immunoglobulins (known as immune paresis). One type of paraprotein is the Bence Jones protein which is a urinary paraprotein composed of free light chains (see below). Quantitative measurements of the paraprotein are necessary to establish a diagnosis and to monitor the disease. The paraprotein is an abnormal immunoglobulinproduced by the tumor clone. Very rarely, the myeloma is nonsecretory (not producing immunoglobulins).

In theory, multiple myeloma can produce all classes of immunoglobulin, but IgG paraproteins are most common, followed by IgA and IgM. IgD and IgE myeloma are very rare. In addition, light and or heavy chains (the building blocks of antibodies) may be secreted in isolation: κ- or λ-light chains or any of the five types of heavy chains (α-, γ-, δ-, ε- or μ-heavy chains).

Additional findings include: a raised calcium (when osteoclasts are breaking down bone, releasing calcium into the bloodstream), raised serum creatinine due to reduced renal function, which may be due to paraprotein deposition in the kidney.

MRI is potentially useful for imaging multiple myeloma because of this modality's superior soft-tissue resolution. The typical MRI appearance of a myeloma deposit is a round, low signal intensity (relative to muscle) focus on T1-weighted images, which becomes high in signal intensity on T2-weighted sequences. Images 5-7 demonstrate the appearance of a typical myeloma lesion in the proximal humerus. Myeloma lesions tend to enhance somewhat with gadolinium administration. In addition, diffuse areas of replacement of the normal fatty marrow may be seen, resulting in large regions of low T1-weighted signal.

Gadolinium-based contrast agents (gadopentetate dimeglumine [Magnevist], gadobenate dimeglumine [MultiHance], gadodiamide [Omniscan], gadoversetamide [OptiMARK], gadoteridol [ProHance]) have recently been linked to the development of nephrogenic systemic fibrosis (NSF) or nephrogenic fibrosing dermopathy (NFD). For more information, see the eMedicine topic Nephrogenic Fibrosing Dermopathy. The disease has occurred in patients with moderate to end-stage renal disease after being given a gadolinium-based contrast agent to enhance MRI or MRA scans. As of late December 2006, the FDA had received reports of 90 such cases. Worldwide, over 200 cases have been reported, according to the FDA. NSF/NFD is a debilitating and sometimes fatal disease. Characteristics include red or dark patches on the skin; burning, itching, swelling, hardening, and tightening of the skin; yellow spots on the whites of the eyes; joint stiffness with trouble moving  or straightening the arms, hands, legs, or feet; pain deep in the hip bones or ribs; and muscle weakness. For more information, see the FDA Public Health Advisory or Medscape.

Degree of Confidence

Unfortunately, almost any musculoskeletal tumor has the same signal-intensity profile and enhancement pattern as myeloma. MRI, although sensitive to the presence of disease, is not disease specific. Additional tests must be employed to diagnose myeloma, such as measurement of gamma-globulin levels and direct aspiration of bone marrow to assess for plasmacytosis. Because of this, MRI may understage or overstage patients with myeloma.

In patients with extraosseous lesions, MRI may be useful to define the degree of involvement and to evaluate for cord compression.

The workup of suspected multiple myeloma includes a skeletal survey. This is a series of X-rays of the skull, axial skeleton and proximal long bones. Myeloma activity sometimes appear as “lytic lesions” (with local disappearance of normal bone due to resorption), and on the skull X-ray as “punched-out lesions” (pepper pot skull). Magnetic resonance imaging (MRI) is more sensitive than simple X-ray in the detection of lytic lesions, and may supersede skeletal survey, especially when vertebral disease is suspected. Occasionally a CT scan is performed to measure the size of soft tissue plasmacytomas. Bone scans are typically not of any additional value in the workup of myeloma patients.

Treatment for multiple myeloma is focused on disease containment and suppression. If the disease is completely asymptomatic (i.e. there is a paraprotein and an abnormal bone marrow population but no end-organ damage), treatment may be deferred.

In addition to direct treatment of the plasma cell proliferation,bisphosphonates (e.g. pamidronate or zoledronic acid) are routinely administered to prevent fractures and erythropoietin to treat anemia.

Initial therapy

Initial treatment of multiple myeloma depends on the patient’s age and comorbidities. In recent years, high-dose chemotherapy with hematopoietic stem-cell transplantation has become the preferred treatment for patients under the age of 65. Prior to stem-cell transplantation, these patients receive an initial course of induction chemotherapy. The most common induction regimens used today are thalidomide–dexamethasone, bortezomib based regimens, and lenalidomide–dexamethasone. [7] Autologous stem cell transplantation, the transplantation of a patient’s own stem cells after chemotherapy, is the most common type of stem cell transplantation for multiple myeloma. It is not curative, but does prolong overall survival.Allogeneic stem cell transplantation, the transplantation of a healthy person’s stem cells into the affected patient, has the potential for a cure, but is only available to a small percentage of patients. Furthermore, there is a 5-10% treatment-associated mortality rate.

Patients over age 65 and patients with significant concurrent illness often cannot tolerate stem cell transplantation. For these patients, the standard of care has been chemotherapy with melphalan and prednisone. Recent studies among this population. suggest improved outcomes with new chemotherapy regimens. Treatment with bortezomib, melphalan and prednisone had an estimated overall survival of 83% at 30 months, lenalidomide plus low-dose dexamethasone an 82% survival at 2 years and melphalan, prednisone and lenalidomide had a 90% survival at 2 years. Head-to-head studies comparing these regimens have not been performed.

External links

• Myeloma UK

• International Myeloma Foundation

• Online Myeloma ISS scoring tool

• Multiple Myeloma Research Foundation

• MM Support Network

• Myeloma Euronet – European Network of Myeloma Patient Groups

• The Leukemia & Lymphoma Society’s Myeloma Page

• Overview at Mayo Clinic

• Risk Adapted Approach to Myeloma Therapy

Soucre

http://en.wikipedia.org/wiki/Multiple_myeloma

http://www.emedicine.com/Radio/topic460.htm

http://radiology.rsnajnls.org/cgi/reprint/201/1/243

http://www.ncbi.nlm.nih.gov/pubmed/1110582?dopt=Citation

http://caonline.amcancersoc.org/cgi/content/full/57/5/301

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Sickle Cell Disease The Silent Crisis

  

  

  

These patients are too young. That is always my first thought when  see the History and Physical. Sickle Cell Disease can be so destuctive to some patients. It can be a challanging managing these patients, since acurate diagnosis can be tricky with this disease. Sickle cell disease is a genetically transmitted autosomal recessive disorder in red blood cells. Instability of the hemoglobin molecule in the deoxygenated state, cuases red blood cells to change from the usual biconcave disc shape to an irregular sickled shape. The abnormal shape of these red blood cells and their propensity to adhere to the walls of blood vessels can occlude the vessels, preventing normal blood flow and decreasing the delivery of oxygen to organs and tissues, a condition known as crisis. The sickled cells are also extremely susceptible to hemolysis, causing individuals with sickle cell disease to have chronic anemia.  sickle cell anemia – support group.

Vaso-occlusive episodes are associated with dehydration, acidosis, and fever. Cold and systemic illnesses (eg, infections) commonly precipitate sickle cell crises. Sudden changes in altitude and travel in nonpressurized aircraft sometimes precede onset of a vasoocclusive crisis.

The skeletal manifestations of sickle cell disease are the result of changes inbone and bone marrow caused by the chronic tissue hypoxia that is exacerbated by episodic occlusion of the microcirculation by the abnormal sickle cells. The main processes that lead to bone and joint destruction in sickle cell disease are infarction of bone and bone marrow, compensatory bone marrow hyperplasia, secondary osteomyelitis, and secondary growth defects.

When the rigid erythrocytes jam in the arterial and venous sinusoids of skeletal tissue the resultant effect is intravascular thrombosis, which leads to infarction of bone and bone marrow. Repeated episodes of these crises eventually lead to irreversible bone infarcts and osteonecrosis especially in weight bearing areas. These areas of osteonecrosis (avascular necrosis/aseptic necrosis) become radiographically visible as sclerosis of bone with secondary reparative reaction and eventually result in degenerative bone and joint destruction.

 These painful crises, which occur in almost all patients at some point in their lives, can last hours to days, affecting the bones of the back, the long bones, and the chest. Some patients have one episode every few years, while others have many episodes per year. The crises can be severe enough to require admission to the hospital for pain control and intravenous fluids.

Repeated crises can cause damage to the kidneys, lungs, bones, eyes, andcentral nervous system.

 Infarction usually occurs in a segmental pattern that suggests damage to the large cerebral arteries. The most common abnormalities found on arteriography or magnetic resonance angiography (MRA) are marked narrowing or complete occlusion of the anterior cerebral arteries (ACA) and/or middle cerebral arteries (MCA). Multiple, bilateral vessel involvement is usual, even in patients who have unilateral neurologic signs. Vessel narrowing is the consequence of intimal and medial proliferation that is thought to be caused by endothelial damage from sickled red blood cells. The damaged, irregular endothelium can serve as a nidus for the adhesion of platelets and sickle cells, thereby resulting in thrombus formation. The stroke event occurs when narrowing is severe enough to compromise distal flow or the thrombus dislodges and causes distal embolization. Transient neurologic symptoms can result from vessel spasm. Intracranial hemorrhage can be intracerebral or subarachnoid and can result from rupture of an aneurysm of the circle of Willis. Intracerebral hemorrhage may also occur years later in patients who had prior cerebral infarction as a result of a rupture of fragile collateral vessels (moyamoya).

The SILENT STROKE

Silent Stroke Is Not Detected With a Standard Neurologic Examination. To evaluate the sensitivity and specificity of neurologic examinations for detecting silent stroke, a pediatric neurologist examined four groups of children: 1) children with stroke detected with MRI but without focal neurologic findings (silent stroke); 2) children with stroke detected with MRI with focal neurologic findings (overt stroke); 3) children with sickle cell disease but no evidence of stroke with MRI; and 4) normal sibling controls. The division found the neurologic examination was not a sensitive method to detect a silent stroke; 34% of children with stroke as defined by MRI exhibited no focal neurologic findings [Glauser, 1995]. All children with a silent stroke had abnormal neurocognitive scores [Glauser, 1995].Common symptoms include:

• Attacks of abdominal pain

• Bone pain

• Breathlessness

• Delayed growth and puberty

• Fatigue

• Fever

• Jaundice

• Paleness

• Rapid heart rate

• Susceptibility to infections

• Ulcers on the lower legs (in adolescents and adults)

MRI is the best method for detecting early signs of osteonecrosis in patients with sickle cell disease and for identifying episodes of osteomyelitis

Nuclear scanning can also be used to detect early avascular necrosis. This modality also plays a role in detecting osteomyelitis. Likewise, indium leukocyte scanning has an important role in diagnosing osteomyelitis.

Patients with acute bone pain crises usually present with fever, leukocytosis, and warmth and tenderness around the affected joints. This process tends to affect the knees and elbows, mimicking rheumatic fever and septic arthritis. In adolescence and adulthood, the most prominent complication is osteonecrosis of 1 or more epiphyses, usually of the femoral or humeral heads. Chronic pain is often associated with later stages of osteonecrosis, particularly in the femoral head. Pain due to avascular necrosis is most notable with weight bearing on the joint. Patients often have pain associated with functional limitation of the affected joint.

Patients with sickle cell disease are prone to infection of the bone and bone marrow, or osteomyelitis, in areas of infarction and necrosis. Although Staphylococcus aureus is the most common cause of osteomyelitis in the general population, studies have shown that in patients with sickle cell disease the relative incidence of Salmonella osteomyelitis is twice that of staphylococcal infection

Treatment

Bone marrow transplant offers the only potential cure for sickle cell anemia. But very few people have a suitable donor for transplant.

As a result, treatment for sickle cell anemia is usually aimed at avoiding crises, relieving symptoms and preventing complications. If you have sickle cell anemia, you’ll need to make regular visits to your doctor to check your red blood cell count and monitor your health. You may also require treatment from specialists at a hospital or sickle cell anemia clinic. Treatments may include medications to reduce pain and prevent complications, blood transfusions and supplemental oxygen, as well as bone marrow transplant.

Risks and benefits of allogeneic bone marrow transplantation in children with complications of sickle cell disease.

Additional treatments may include:

• Dialysis or kidney transplant for kidney disease

• Drug rehabilitation and counseling for the psychological complications

• Gallbladder removal (if there is significant gallstone disease)

• Hip replacement for avascular necrosis of the hip (death of the joint)

• Irrigation or surgery for priapism (persistent, painful erections)

• Partial exchange transfusion for acute chest syndrome

• Surgery for eye problems

• Transfusions or surgery for brain problems, such as strokes

• Wound care, zinc oxide, or surgery for leg ulcers

Medications

Medications used to treat sickle cell anemia include:

• Antibiotics. Children with sickle cell anemia usually begin taking the antibiotic penicillin when they’re about 2 months of age and continue until they’re 5 years old. Doing so helps prevent infections, such as pneumonia, which can be life-threatening to an infant or child with sickle cell anemia. Antibiotics may also help adults with sickle cell anemia fight certain infections.

• Pain-relieving medications. To relieve pain during a sickle crisis, your doctor may advise over-the-counter pain relievers and application of heat to the affected area. You may also need stronger prescription painkillers.

• Hydroxyurea (Droxia, Hydrea). This prescription drug, normally used to treat cancer, may be helpful for adults with severe disease. When taken daily, it reduces the frequency of painful crises and may reduce the need for blood transfusions. It seems to work by stimulating production of fetal hemoglobin — a type of hemoglobin found in newborns that helps prevent the formation of sickle cells. There is some concern about the possibility that long-term use of this drug may cause tumors or leukemia in certain people. Your doctor can help you determine if this drug may be beneficial for you.

Blood transfusions

In a red blood cell transfusion, red blood cells are removed from a supply of donated blood. These donated cells are then given intravenously to a person with sickle cell anemia.

Blood transfusions increase the number of normal red blood cells in circulation, helping to relieve anemia. In children with sickle cell anemia at high risk of stroke, regular blood transfusions can decrease their risk of stroke.

Blood transfusions carry some risk. Blood contains iron. Regular blood transfusions cause an excess amount of iron to build up in your body. Because excess iron can damage your heart, liver and other organs, people who undergo regular transfusions must often receive treatment to reduce iron levels. In 2005, the Food and Drug Administration approved deferasirox (Exjade), the first oral medication that can reduce excess iron levels, for use in people older than the age of 2.

GE’s new 3T MRI scanner MR750

Simply Powerful, Powerfully Simple It’s MR beyond boundaries, giving you every edge. Break free from traditional 3.0T scanning – powerfully, precisely, productively. Just for starters, we’re talking about a complete liver study in a 15-minute time slot, or the breast images you need in only two sequences. No more “what ifs” – it’s time for “right nows.”

The strongest whole-body gradients – the most powerful in the industry – and the new gold standard in body, breast and MSK imaging… now that’s powerfully simple MR.

 

 

Break the Bonds: Start from a Position of PowerThe Signa® MR750 3.0T’s stunning new technologies take 3.0T imaging to a new level. This remarkable technology allows you to focus on what’s most important – patients.

The most reliable 3.0T magnet, the Signa® MR750 3.0T is built around GE’s third-generation short-bore, superconducting 3.0T magnet – proven to deliver high homogeneity for excellent results…even in large or off-center FOV imaging, fat saturation techniques and high-performance applications such as cardiac, fMRI, diffusion tensor and spectroscopy. Other technical breakthroughs include:

• Sophisticated real-time SAR optimization.

• Unique heat extraction gradient architecture for faster acquisitions and fewer slowdowns.

• Exclusive OpTix optical RF technology for greater SNR.

• ARC, accelerated parallel imaging.

• Faster reconstructions.

• Anatomy-optimized RF coils and arrays.

• Easily scalable for future expansion.

 

 

Break Away: Routine Exams Faster, Advanced Exams Routine

As the most efficient scanner available, every scan is a study in speed. Conduct in-room patient set up in as little as 30 seconds and start scanning in just a few simple steps. The Signa® MR750 3.0T makes routine exams faster than the industry standard, and advanced exams routine.

 

The Signa® MR750 3.0T is designed around clinical workflow needs with a strong focus on improving productivity, such as:

• Automated clinical applications mean fewer steps to faster studies.

• A high-resolution color in-room operator console (iROC) equals quick exam set up.

• The Express Patient Table offers one-time patient transfer, comfort and operational efficiency. Two 32-channel surface coil connections integrated right into the table can simplify patient preparation outside the scanning room.

• With a simple, one-handed motion, the integrated arm boards can be optimally positioned to support the patient for injections and transport.

• Located to the left and right of the scanner bore, the dual-sided controls let you operate the scanner from either side of the patient table.

• Start scanning in just a few simple steps with IntelliTouch patient positioning.

• The system gives patients a quick, easy, and comfortable MR experience.

The strongest whole-body gradients – the most powerful in the industry – deliver incredible 50mT/m gradient field on each axis (X, Y and Z) simultaneously, plus a slew-rate of 200 T/m/s combined with OpTix – an exclusive optical RF technology. The result: higher accuracy and more reproducible scans. Additionally, you’ll experience up to 60% more anatomical coverage and resolution per unit time, 27% more SNR and faster reconstruction speeds. What’s more, enjoy the new gold standard in body, breast and MSK imaging.

Clinical Break Down: Fresh Vision, New Clarity

Thanks to unprecedented temporal system stability and high signal-to-noise, the subtle brain activation signal treats in the foreground and can be captured much more reliably. The Signa® MR750 3.0T delivers routine, accurate, repeatable fMRI studies with 60% more spatial resolution in the same scan time and with reduced number of paradigm repetitions.
Combining multiple series into one, VIBRANT – IDEAL helps reduce exam time and ensure “can’t miss” fat suppression in breast studies. With no need for shimming and ARC parallel imaging on the Signa® MR750 3.0T, your productivity benefits are substantial.

This system is ready for clinical prime time. Read about the details behind this remarkable technology.

• With Cube, you can more easily reformat sub-millimeter isotropic 3D volume image data from a single acquisition into any plane-axial, sagittal, coronal or oblique – with no gaps or loss of resolution. New, self-calibrated ARC parallel imaging engine speeds up the acquisition, while eliminating aliasing even in small FOV imaging.

• 3D MERGE: Generating excellent gray-white matter contrast in the spinal cord without sacrificing SNR, this high-definition, 3D application acquires 1 mm slices in a clinically relevant scan time, enabling reformats in different planes.

• Time of Flight imaging on the Signa® MR750 3.0T gives you more -more spatial resolution and more contrast between the flowing blood and the surrounding tissue- for more small vessel detail more confident diagnoses.

• Providing exceptionally uniform, consistent fat suppression across the entire image in a very large field of view, LAVA-IDEAL produces four contrasts in just one acquisition, for confident diagnoses and fewer repeat exams.

• Now delivering improved performance, which lets you more than double the slices or alternative to acquire more diffusion directions in the same scan time, DTI/FiberTrak lets you visualize white matter trajectories in the brain.

Hitachi Oasis 1.2 Tesla open MRI

Hitachi Oasis 1.2 Tesla open MRI

OASIS™  featured on National Medical Report

OASIS™ provides maximum diagnostic performance and uncompromised patient comfort. Combining high-performance MR electronics of the best high-field equipment — fast gradients and multi-channel RF technology with Hitachi-designed Zenith RF coils — with Hitachi’s proprietary 1.2T open architecture vertical-field magnet, Oasis is a new generation of MR systems providing diagnostic confidence, patient comfort and investment value. Oasis supports demanding workflow, features Hitachi’s legendary reliability, is easy to learn and use, and provides powerful differentiating features for you MR imaging services. Anonymous said... Hi All, My workplace recently bought an Oasis. For the last 2.5 months I have been scanning on this machine. I have run 12 diffrent systems including an Aris I and II. This is a great magnet. Its a cross between an open and closed. Image quality rivals the Semiens 1.5 espree. Angios are beautiful, scan times run between 20-30 min for most apps. Pts seem to like it also. Biggest downer is the gradients are very loud, but it comes with the Magnacoustics music and the headphones are a big help in pt noise reduction. Even the most difficult Rads reluctantly agree image production is far superior than ANY open we have seen so far. With a windows based interface that uses some features of the old Aries system apps training took only a month and both techs were fast comming up to speed. I hope this helps.

Philips Panorama High Field Open

Philips Panorama High Field OpenHigh Field Performance comparable to 1.5T in a truly open configuration

• Solenoid Technology coils
  • Superb coverage and comfort
  • High SNR
  • Fully SENSE compatible
  • Excellent homogeneity
• 1.5T signal, 1.0T contrast for minimal susceptibility and distortion
• SmartExam – One click to consistent and reproducible MRI exams
  • One click for planning, scanning and processing
  • 100% consistency and reproducibility
  • Covers over 75% of examinations
  • Brain, Knee, Shoulder and Spine capabilities
• ExamCards automate the most complex studies
• Clinical performance in all applications

Preferred by Patients

• 72% of patients prefer the Panorama over any cylindrical system*
• Ambient Experience further boosts preference
• Preference represents value
• Ability to market your practice directly to the patient
• Source: GfK Panelservices Benelux

Comfortable, high field open MRI

Ipad and MRI

– Apple Inc. on Wednesday unveiled their latest creation at the Yerba Buena Center in San Francisco, California, the long-awaited tablet device, the iPad. Apple Inc.’s CEO and founder Steve Jobs announced Apple’s latest device, a thin-tablet device, similar to the iPhone. The device is .5 inches thin, 1.5 pounds, and features a fully capacitive multi-touch display 9.7 inch IPS display. It’s powered by Apple’s own silicon chip, the 1Ghz Apple A4 chip, with 16GB to 64GB of flash storage. Additionally, the iPad touts 10 hours of battery life, WiFi 802.11n, Bluetooth 2.1, a Microphone, and an accelerometer. The device can also run all iPhone apps unmodified out of the box from the app store, from which customers have downloaded 3 billion already. Apple developers noted that they rewrote all of their proprietary apps to take advantage of the iPad’s larger screen. The iPad will be released along a new app, an ebook reader. Pioneered by the Amazon Kindle, Apple has created their own version of an online book store, iBooks. It’s an online component similar to iTunes that will allow customers to buy books for their device, the store is partnered with Penguin, Macmillion, Simon & Shuster, and others to provide a wide-selection of material. In addition, Apple will release a new developers kit to that allows third party developers to take advantage of the device. “What this device does is extraordinary,” said Jobs. “You can browse the web with it. It’s the best web experience you’ve ever had.” Jobs said that the iPad has the best web browsing experience, stating that it’s “way better than a laptop, way better than a phone.” He demonstrated the tablet device which featured a single button to be used with the on-screen keyboard. More at : Apple unveils long-awaited tablet device “iPad”In the forefront of breaking technology,

CoActiv Medicalannounces newEXAM-PACStouch screen image viewing for the Apple iPad large-screen digital viewing and communications device. Based on the existingEXAM-PACSiPhone image viewing system, the new iPad system will support bi-directional data communication between aPACSand any iPad using the new device’s built-in WiFi capabilities. This version ofEXAM-PACSfor iPad will also be fully compatible with theApple iPad3G model scheduled for release in April. The updated 3G model will allow connectivity for anywhere, anytime image viewing.