New Genetic Trigger That Can Renew Cells Responsible For Smell Discovered�

According to a new study, neuroscientists from the University of California have discovered a genetic trigger that is able to stimulate the neurons from the nose that are responsible for smell to renew. With this study, the researchers believe that, in the future,�pharmaceutical companies will be able to develop new therapies for people who have loss their sens of smell due to old age or trauma.

This gene is sending a message to the olfactory stem cells from the nose to differentiate into mature sensory neurons which are able to detect odors and to transmit the sensation to the brain.

“Anosmia the absence of smell is a vastly underappreciated public health problem in our aging population. Many people lose the will to eat, which can lead to malnutrition, because the ability to taste depends on our sense of smell, which often declines with age,” said neuroscientist John Ngai, who is the leader of this research. He also added that one of the reasons that may lead to anosmia is represented by the fact that once with the aging process the olfactory stem cells lose their capacity to replace mature sensory cells or maybe this mature cells are depleted. With the finding of this gene they also found a way to promote active stem cells to renew the sensory cells and to maintain this way the olfactory function.

This study is very useful because in the future the scientists could harness stem cells that are found in others sensory organs and will be able to recover the functions of sensory organs which are affected by degenerative disease or are injured.

Smell Sence

Sensory neurons from the nose that are�responsible for smelling, live 30 day and then are replaced by new sensory neurons which are generated by the mature stem cells that are found in the olfactory epithelium.� The key question for the scientist is what is the mechanism that make the stem cells to divide into mature and functional sensory cells which are responsible for odor.

“These stem cells are capable of reconstituting the entire sensory epithelium of the nose following injury, so understanding how these stem cells work is important for understanding the regeneration process that goes on in the nose.” Nagi said.

The researchers found, after screening the epithelial cells of the nose for regulatory genes, that a gene called p63 which is also known as a transcription factor that is controlling the regulatory genes for stem cells that are found in the skin, in the prostate and in the airway lining. By inactivating p63 gene in mice, the scientist were able to demonstrate that nasal stem cells can differentiate into adult sensory neurons that are responsible for smelling.

The researcher said that this gene, called p63 can secrete a molecule which will make the stem cells in the nose not only to differentiate, but also to self-renew. If the action of this molecule is stopped, then the stem cells will go into differentiation.

The scientist hope that in the future will be able to create a drug the regulates or modulates the p63 gene in order to increase the production of nasal stem cells therefore the number of mature smell neurons.

The p63 gene can be normally found in a wide range of epithelial tissues meaning that these results could be transpolated to other stem cells found in the skin leading therefore to new treatment options that could replace not only nervous damaged tissues but other epithelial tissues as well.

Less Expensive HIV Treatment Monitoring Methods Just As Effective As Viral Load Testing

A group of international researchers discovered that�a far more affordable laboratory test that can help adjust�the HIV�anti-retroviral treatment may be just as useful as sophisticated traditional tests. This particular�finding may have major beneficial effects especially in rural Africa.

Although, the study results still must be confirmed by further clinical trials, the scientists state that viral load testing does not offer any greater benefit compared to�the cheaper testing method – CD4 +�T lymphocyte count.

No one had directly looked at this question in Africa before,� said James G. Kahn, MD, MPH, a professor of health policy, epidemiology, and global health at the University of California, San Francisco (UCSF) who led the economic aspect of the research. If it's true that you are not getting much clinical gain for the buck, maybe we should focus our attention on CD4+ testing.”

HIV attacks the type of immune cells called T-helper. These cells have�on their�surface a protein called CD4, which HIV uses to attach to the cell before entering it to multiply.�T-helper cells play an important role in the immune system by helping to coordinate all other cells in fighting an infection. A major reduction in the number of T-helper cells may have a serious�consequences on the immune system�proper functioning. HIV causes damage or destruction of the�T-helper cells. As a result, there are fewer�cells available to help the immune system to fight infection.

The test measures the number of CD4 T-helper cells in blood. The more cells per cubic millimeter a�person has, the immune system is stronger. . A low number of CD4 does not necessarily mean that person will get sick, but increases the probability of infections.

The CD4+ count of�HIV infected patients usually raises after antiretroviral therapy, thus reducing the risk of infection.�Physicians have adapted the antiretroviral treatment for HIV using the CD4+ cell count since the early 1990s. Lately the standard method�that guides the treatment�in most developed countries, including the US�relies on�more sophisticated and far more expensive tests, that measure the blood�viral load. CD4+ cell count is still a routine test but the viral load�test is�used to guide treatment decisions, as reducing the number of viral replicas is considered to be�the main treatment objective.

The clinical trial included three types of patients �from Uganda�whose antiretroviral treatment was guided�by: viral load testing, CD4+ counts and patients under antiretroviral treatment�not guided by any�laboratory test. The results were then extrapolated�to life expectancy and treatment costs.�Patients that were included in the study were visited and tested over the course of one year.

The researchers discovered that�the�treatment for�patients that were monitored by any kind of laboratory test was higher. Monitoring the CD4+ count costs were substantially lower ($5 per test, compared to $3 per test for viral load). Further analysis proved that viral load testing does not necessarily provide extra clinical benefit compared to monitoring the CD4 + T lymphocyte count alone. In the end they concluded that�monitoring the CD4 + T lymphocyte count alone could provide substantial benefit at a lower cost.

Viral load testing�is very expensive if we think of the frequency with which�the test�should be performed.�A better approach would be�to spend the money saved from using less expensive monitoring�methods on antiretroviral drugs, extending�therefore the life expectancy of patients with limited financial possibilities.

Should The Dutch Scientist Publish His Super-Influenza Virus Research? Future Epidemics Could Be Prevented With The Risk Of Killing Millions

As many of you well know, a�Dutch scientist named Ron Fouchier managed to create a super deadly variant of H5N1 virus�. He presented his work at a�conference dedicated to influenza�this September.�The�Dutch scientist now wants to publish his findings and�different sources perceived this�move as a global threat, that could lead to the loss�of countless�lives.�But could the scientific�community�also benefit from the publication�of�such a�study?

The first thing probably�everybody was thinking at,�after reading that article probably was�terrorism. A terrorist�that could be�able�to reproduce the results of this study. This would�result in�a devastating scenario. We do not�want terrorists starting to think that�biological agents are a viable and effective weapon, when�counter terrorist organizations hardly started to�be�experienced�in combating conventional terrorist methods.�There are rare cases when terrorism�has regarded a disease�as a�viable�weapon.� A microbial or viral agent is very�ineffective�without an appropriate way to disperse it. But Fouchier’s�new H5N1�virus is highly contagious. One hundred�infected terrorists�could enter�the�New York City subway system�leading to�devastating consequences.�Human to human�transmission would be in this case the simplest “dispersal device”. And it became quite clear lately that�terrorist resources are not limited to this.

On the other hand�the US�could be regarded as�trying�to�prevent the discovery of antidote for the deadly�influenza-virus.

The new virus is so deadly and contagious�because it hosts�five�new mutations compared to the former influenza virus. The research evidentiated that all these�five mutations can be found�in nature but not combined in a single microorganism. But what if the virus naturally acquires all five mutations leading to an unstoppable global pandemic?�The collection of mutations exists separately�in nature. This does not necessarily�mean that they will�be someday found combined�in a single strain. It�is a matter of probability.�Can mankind assume this risk?�Individual�mutation of a�pathogen happens very�often in nature, but�what most people do not know�is that�that certain�strain evolution is very�rare.

Those that support the idea of�publishing the paper�actually think that it could�enable the scientific community to anticipate, therefore better react to a possible future scenario�if a highly contagious outbreak occurs.

In the end you can not�have it both ways. In order for a�vaccine and�a protective measure to be discovered�the research�should be published. But what�about the risks?

Second-Hand Pacemakers Give Hope To Indian Patients

On first sight, there is nothing new about using pacemakers in patients suffering from different heart rate abnormalities�as a very common�medical procedure. What is really unusual is that this particular�pacemaker was used by another patient in the past.

The�sixty one year-old patient from Mumbai instead of a new pacemaker,�received for free a�reconditioned device, that was used by a patient who passed away�in the U.S.

Pawar is one of�the many�patients from India�who received a free pacemaker, thanks to a colaboration between the United States and�the Holy Family Hospital in Mumbai. The Mumbai�hospital runs a�program dedicated to helping its poorest patients.

Other medical equimpemet such as coronary stents or�implantable defibrilators were also�provided by�Daniel Mascarenhas Indian-born cardiologist who�runs the program. All�these medical devices donated to the Mumbai Holy Family Hospital were either pre-used by patients and removed after their�death or were�past their expiry dates.

Mascaras and his colegues from Texas Health Science Center presented their scheme in the American Journal of Cardiology in Octomber.

Pacemaker Device

From 2004 , a total of 53�sterilised�and reconditioned�devices were shipped from the U.S funeral�homes and have been used to help poor patients in India. Thirty four patients received their first device while sixteen required a�replacement. There were no infection cases�follwing these procedures and no device malfunction was reported proving this procedure risk-free.

On the other hand this scheme bring into light the precarious situation�of the health system in India where nearly 1,2 billion people are relying on a�exhaused public health system with hospitals overcowded by patients. Indian families with low incomes are still foreced to�borrow money from�banks�in order to�cover different medical fees.

A�brand new pacemaker in India�costs about 150.000 rupess (that is about 3.000 US Dollars) and has an utilization period of ten years, making it impossible to afford for most people. The need�for these devices�is overwhelming and many patiens actually�face a high morbidity due to costs and�lack of equiment.

Human Organs Could Be Grown By Scientists Using Pigs

Thanks to stem cells, human organs can�now be grown in pigs bodies to be�then�used in transplants,�according to�a new study. Researchers created chimeras animals, which can bear organs from other species by injecting stem cells in�the embryo stage of the animal.

Scientists have injected rat stem cells into a mouse embryo that was genetically modified so that it can not create its own organs. So they created mice that have rats organs.

The technique may allow pigs to form organs created from human stem cells, organs that can be transplanted later. By using stem cells of patients, the risk for a transplant to be rejected might be reduced and in the same time this technique can represent an abundant source of organs donors. Today, the shortage of organs for transplantation is leading to a long waiting lists.

Professor Hiromitsu Nakauchi, director of the Center for Stem Cell Biology and Regenerative Medicine at the University of Tokyo in Japan, said that “our ultimate goal is to generate functional organs from induced pluripotent stem cells”.

“The technique, known as blastocyst complementation, can offer a new approach for the supply of organs. I tried this technique successfully between mice and rats. We are confident in generating functional human organs using this approach.”

Stem Cells For Human Organs

Professor Nakauchi and his team of researchers, who presented the study at the annual conference of the European Society of Human Genetics, used a type of adult stem cells known as induced pluripotent stem cells that can be taken from tissue such as skin, which can develop into any cell type found in the body.

Researchers� injected cells taken from rat tissues into mouse embryos that could not grow their own pancreas, a organ that produces important hormones in the body, such as insulin. When mice reached adulthood, they showed no signs of diabetes and had a pancreas which was almost entirely formed of stem cells of the rat.

If this technique would use human stem cells, it could represent a way to treat patients with diabetes, providing a way to replace their own pancreas.� Professor Nakauchi hopes to test the growth techniques of other organs and he hopes to receive permission to use human stem cells. They have managed to produce pigs able to generate human blood by injecting human stem cells in pig fetuses.

Professor Chris Mason from the Department of Regenerative Medicine from the College London University, said that “there is no doubt that cure diabetes is a challenge, but to support this technique are required sustainable resources and a series of major funding for testing and development. “

New Protein Named Oncostatin M, Demonstrates Its Beneficial Effects After Miocardial Infarction

Even if even if there are many methods of reperfusion�after a heart attack, cardiac muscle dysfunction occurs in most cases, as myocytes�do not regenerate. In vertebrates, for example salamanders, a mechanism of regeneration of myocardium based on a process called dedifferentiation�was discovered, allowing healthy cells to regress to embryonic stage, divide and the differentiate to myocytes, thus restoring myocardial function. In humans, cardiac stem cells have been identified, but their exact role in restoring myocardium functionality after a heart attack is not yet established.

The research group from the Max Planck Institute, led by Dr. T. Braun, discovered that the molecule which appears to be responsible for� cardiomyocyte�dedifferentiation�process is a protein called oncostatin�M. The study started from the fact that human myocardial tissue contains higher concentrations of oncostatin�M after a heart attack. The researchers designed a study to see if oncostatin�M has the same benefits in mammals. Two groups of mice, a normal one and a genetically modified mice group�so that oncostatin�M could not have any effect.��The scientists then�induced a heart attack to all mice. In the normal mice group, the oncostatin M demonstrated its effects.

Myocardial infarction 4

Dr. Braun concluded that “We believe that oncostatin M has considerable potential for efficiently healing damaged heart muscle tissue. What we now need is to be able to pinpoint the precise window of application to prevent any possible negative effects.”

A potential disadvantage is that in coronary chronic diseases, oncostatin M can potentially exacerbate the prejudice caused by myocardial infarction.

Although�potential harmful effects of oncostatin M have been observed, �this new discovery could mean another step forward�towards� development of new therapies for myocardial infarction and�restoration of cardiac function after the occurrence of an injury.

Myocardial infarction (heart attack) is the result of coronary artery obstruction due to atherosclerosis, thrombus or vasospasm, which translates to decreased blood flow�to the myocardium, thus reducing the intake of oxygen and nutrients, leading to myocardial cell death.� Myocardial infarction is a common cause of mortality in older age groups. So far the area affected by infarction�can be reduced�by reperfusion�of myocardial tissue, in addition to early intervention with coronary vasodilators, antiplatelet agents, oxygen and other�medication but�there is�still�no satisfactory�therapy for large infarctions.

Computer Trained By Scientists To Evaluate Breast Cancer

Since the 20’s�the�way in which breast cancer is evaluated in terms of characteristics and breast cancer classification�have remained mostly unchanged. A doctor analyzes�a tissue sample under a microscope and writes down the diagnostic. Pathologists examine the�breast tissue sample and the scores the tumor according�to a classic scale that�has remained largely unchanged since�1928. These�scales are used to asses cancer severity�leading therefore�to a certain treatment option and also�establish the prognosis.

Computer�scientists and pathologists�from Standford School published a paper yesterday�in Science Translational Medicine to report their results in training�a computer evaluate and analyze�cancer microscopic images tissue samples . The computer results were more accurate than the�average�doctor analysis.

The computer model, named Computational Pathologist (C-Path), can learn how to analyze microscopic images of breast cancer tissues and determine the patient prognosis.

For C-path training, the research team used already known prognosis tissue samples, and trained the computer to measure and recognize different tumor structures and correlate�them with patient survival. Next the computer correlated�its results with the�known data and adapted its algorithms to better�predict survival. In time�the computer�figured out what cancer features influence more or less the patient’s�prognosis.

In simple terms, this computer is a learning student according to Daphne Kolle, PhD, paper senior author and computer science professor.

The medical world uses�three cancer cell key features to evaluate breast cancer:

1. Tube-like cells percentage of the tumor
2. The abnormal nuceli diversity in the periferic epithelial cells
3. Cell division rates

Breast Cancer tissue sample under the microscope

These three features are�determined subjectively using a microscope and�a score is calculated�that classifies the patient into a certain prognosis group.

Pathologists are usually trained to search, evaluate and score certain cellular abnormalities that are known for their clinical significance, but tumors present numerous additional characteristics, whose clinical importance has not been evaluated and correlated to�a certain prognosis according to�Andrew Beck, MD, paper’s first author.

The computer does exactly that and considers several factors in order to determine which can lead to a good or bad prognosis. In fact C-Path, examines and correlates about 6,642 cellular factors.�After training�the computer�on one group of patients, C-Path evaluated�breast cancer samples it had not seen before� �from new�patients. The C-Path results was then compared with the known data. The conclusion was that C-Path managed to statistically surpass acreage�pathologist evaluation.

The results of the Standofrd scientists team are�of major importance�as having a “smart and continuously learning” computer that can evaluate tumors will bring pathology accurate diagnosis to undeveloped countries, improving therefore the�cancer treatment and overall�survival rate.

Aplastic Anemia – Causes, Symptoms, Diagnosis, Evolution, Prognosis And Treatment

Apalstic anemia is a syndrome of bone marrow failure which is characterized by pancytopenia (a reduction in the number of red and white blood cells, as well as platelets) with markedly hypocellular marrow. Incidence of aplastic anemia� is 2 – 5 cases/million population/year. Criteria for diagnosis of severe aplastic anemia:

Aplastic Anemia Causes

The mechanism of pathogenesis in aplastic anemia is represented by:

• Intrinsic stem cell defect.
• �Failure of stromal microenvironment.
• Absence or deficiency of growth factors.
• Immune suppression of hemopoietic marrow.

The main causes of aplastic anemia are:

• Chemicals (benzene and related compounds).
• Drugs ( chloramphenicol, gold salts, D-peniciline, phenylbutazone, carbamazepine, hydantoin and derived drugs, antineoplastic drugs and acetazolamide).
• Radiation.
• Viruses� (hepatitic C virus,� parvovirus� B19, Epstein-Barr virus, cytomegalovirus).
• Fanconi anemia.
• Dyskeratosis� congenita� may� evolve� into� aplastic anemia.
• Schwachmann – Diamond syndrome (congenital granulocyte aplasia) may evolve into aplastic anemia.
• Idiopathic (in above 65% of cases).
• Other (connective tissue diseases, pregnancy).

Aplastic Anemia

Aplastic Anemia Symptoms

Patients with aplastic anemia will experience symptoms which are related to the decrease in bone marrow production of blood cells. The onset of this disease is insidious and the initial symptom can be represented by bleeding or by anemia, infections and fever can also represent symptoms of aplastic anemia.

The main symptoms are represented by fatigue, headaches, loss of apetite, weight loss, dyspneea, palpitations, bleeding (epistaxis, gingival bleeding, metrorrhagia, purpura, ecchymoses after minor trauma), recurrent infections which are secondary to cytopenias.

Physical examination is generally unrevealing.

Aplastic Anemia Diagnosis

Peripheral blood

• Pancytopenia.
• Low reticulocyte count and possible macrocytosis.
• Low absolute� neutrophil count (if <200/ul, prognosis is extremely poor).
• Negative sucrose hemolysis test and HAM test (absence of hemolysis), to rule out paroxysmal nocturnal hemoglobinuria.
• Positive HAM test (hemolysis of patients erithrocytes by normal acidified serum) and sucrose hemolysis test associated with presence of hemosiderinuria are diagnostic findings for paroxysmal nocturnal hemoglobinuria in aplastic crisis.

Bone marrow

• Markedly hypocellular marrow, due to replacement of hemopoietic marrow by adipous tissue (not fibrosis or neoplastic cells).
• Presence of cytogenetic abnormalities suggests hypoplastic myelodysplastic syndrome rather than aplastic anemia.

Aplastic Anemia – Bone Marrow Biopsy

Positive diagnosis of aplastic anemia is sustained by the following criteria:

Bone marrow (one of the following criteria):

• Marrow cellularity less than 25% from normal or
• Marrow cellulatity less than 50% from normal with less than 30% hemopoietic cells.

Peripheral blood (at least two of the following criteria):

• Absolute neutrophil count less than 500/ul.
• Platelet count less than 20,000/ul.
• Anemia with corrected reticulocyte index of less than 1.

Aplastic Anemia Evolution And Prognosis

Median survival of untreated severe aplastic anemia is 3 to 6 months (20% survive longer than 1 year).

Aplastic anemia is having a poor prognosis, death will occur due to complications:

• Acute

1. Infectious: respiratory (Gramm negative microorganisms), cutaneous.
2. Hemorrhagic: epistaxis, purpura, metrorrhagia, gastrointestinal bleeding, bleeding into the central nervous system.
3. Malignant: acute leukemia and myelodysplastic syndrome.

• Chronic

1. Hemochromatosis due to repeated transfusion with its consequences: liver cirrhosis and diabetes.

Aplastic Anemia Treatment

Bone marrow transplantation represents the only curative option:

• Major indication in patients less than 40 years of age.
• Only one-third of patients have a HLA-identical or 1 antigen mismatched donor.
• With an appropiate donor cure is achieved in 75% – 85% of previously untransfused patients, whereas only 55-60% of multiply transfused patients achive cure.

Immunosuppressive therapy is not a curative option and is represented by:

• Antithymocyte globulin (ATG)
• Cyclosporine A (CSP-A)

Androgen hormones in the treatment of moderate or severe aplastic ane is controversed because recent studies showed no efficacy as primray therapy.

Hemopoietic growth factors have been used to treat neutropenia

• �Granulocyte-macrophage colony-stimulating factor (GM-CSF) and granulocyte colony-stimulating factor (G-CSF) resulted in temporary improvement in neutrophil counts in some patients treated with this cytokines.
• Interleukin-3 (IL-3) improved temporary the absolute neutrophil count in a few patients.
• Interleukin-1 (EL-l)was not effective in a study including a small group of patients.

Other therapeutic measures:

• HLA typing of patient and siblings (ideal is the existence of a normal twin) in order to identify a HLA matched donor, marrow transplantation beeing the therapy of choice in patients less than 40 years of age.
• Transfusions�� should be administered only when imperious needed. In potential transplant recipients there will� not be used family donors and under no circumstances the HLA matched donor.
• Platelet transfusions are used only on assessement of risk of life-threatening bleeding (not solely on platelet count). Platelet transfusions from a single donor should be used to minimize sensitization and subsequent refractoriness. When the patient has become refractory to platelet transfusions, only HLA matched donors canprovide efficient platelets.
• Red blood cells (RBC’s) transfusions are indicated when hemoglobin level is less than 7-8 g/dl. In order to reduce subsequent sesitization packed RBC’s (irradiated or washed) are to be transfused, or leukocyte-depleted blood products.
• In severe neutropenic, hospitalised patients, measures in order to reduce risk of infections shouldbe undertaken (isolation in aseptic room, no visits allowed, gloves and mask for the medical care personell).
• Prompt institution of broad spectrum antibiotics, intravenously for fever after the appropiate cultures have been obtained.

Acute Myeloid Leukemia – Causes, Syptoms And Diagnosis

Acute myeloid leukemia (AML) is a clonal malignancy of hemopoietic tissue characterised by anarhic proliferation of abnormal blast cells in the marrow and impaired production of normal blood cells resulting in anemia and thrombocytopenia. Acute myeloid leukemia occurs in seven morphologic types, each with characteristic
clinical and laboratory features.� Acute myeloid leukemia accounts for 80% of acute leukemias in adults and 15% -20% in children.

Acute Myeloid Lukemia Causes

Three environmental factors are certain causative agents:

• Ionizing radiation.
• Chronic benzene and organic chemicals exposure.
• Treatment with alkylating agents or other cytotoxic drugs.

Other possible involved factors are:

• Genetic� factors�� (Down� syndrome,� Bloom� syndrome, Fanconi anemia).
• Viral agents (HIV).
• Genetic alterations reflected in multiple chromosome abnormalities are frequent in acute myeloid leukemia patients, famillial aggregation beeing reported but its significance is unknown.
• Chronic myeloproliferative disorders and preleukemic syndromes ream progress to acute myeloid leukemia.

Acute Myelogenous Leukemia

Acute Myeloid Leukemia Symptoms

Acute myeloid leukemia onset frequent with symptoms and signs of:

• Anemia: pallor, fatigue, weakness, palpitations, dyspnea on exertion.
• Thrombocytopenia (low platelet count): bruising, petechiae, epistaxis, gingival bleeding, conjunctival hemorrhages, prolonged bleeding after minor cuts.
• Neutropenia (low neutrophil counts): infections (eg. cutaneous) with pyogenic Gram-negative microorganisms or systemic candidosis.
• Fever, anorexia and weight loss may be present. Hepatomegaly and splenomegaly occur in about 1/3 of acute myeloid leukemia patients.
• Lymph node enlargement� is� uncommon� except with the monocytic type.
• Leukemic cells may infiltrate any organ or tissue in the body, but organ dysfunction is unusual. Occasionally large aggregates of myeloblasts or monoblasts (granulocytic sarcomas) may develop.

Acute Myeloid Leukemia Diagnosis

Peripheral blood

• Anemia and thrombocytopenia are constant present.
• Leukopenia below 4.000/ul occurs in about 50% of patients, and neutropenia below 1.000/ul is encountered in over one half of patients at diagnosis. Mature neutrophils may be hyper- or hyposegmented and hypogranular.
• Myeloblasts comprise from 3 to 95% of the leukocytes and in one third of the patients up to 10% of the myeloblasts contain Auer rods (clumps of azurophilic granular material that form elongated needles seen in the cytoplasm of leukemic blasts. They are composed of fused lysosomes and contain peroxidase, lysosomal enzymes and large crystalline inclusions).
• In 5% of patients occurs extreme elevation of the leukocyte count which became symptomatic (leukostasis) at counts greater than�� 100.000/ul.�� Leukostasis�� occurs�� most� likely� in� the circulation�� of�� the�� central�� nervous�� system,�� leading�� to intracerebral hemorrhage, in the lungs, resulting in pulmonary insufficiency or in the penis, causing priapism (prolonged and painful erection).
• Hyperuricemia and elevated serum lactic dehydrogenase levels.
• �Patients with high leukocyte counts may have false hypoglycemia and hypoxia.
• Electrolyte abnormalities are infrequent but there may occur:

1. Hypercalcemia and hypophosphatemia.
2. �Severe hypokalemia or false hyperkalemia in patients with very high leucocyte counts.

Bone marrow

Is most often hyprecellular with� monomorphic blastic metaplasia. Blast cells are identified by the presence of Auer� rods, reactivity with cytochemical� stains (myeloperoxidase present in� myeloblasts,� chloracetate� esterase present in monoblasts) or rectivity with monoclonal antibodies to epitopes specific for myeloblasts. Cytogenetic abnormalities are present in about 50% of patients.

Acute Myelogenous Leukemia

Unusual Presentations Of Acute Myeloid Leukemia

• Hypoplastic leukemia: pancytopenia (a reduction in the number of red and white blood cells, as well as platelets) and hypoplastic marrow.
• Oligoblasticc leukemia: anemia and thrombocytopenia, a few blast cells in the blood and marrow (this type is often considered a myelodisplastic syndrome).
• Congenital or neonatal leukemia is 10 times more common in newborns with Down syndrome than in apparently normal babies.
• Hybrid (biphenotypic) leukemias are characterised by cells which have both myeloid and lymphoid markers (chimeric) or cells that have either myeloid or lymphoid markers but arise from the same clone (mosaic).
• Mixed leukemias have myeloid and lymphoid cells present simultaneously, each derived from a distinct clone.
• Coexistence of Acute myelogenous leukemia and mediastinal germ cell tumors has been reported, and there is evidence for a aclonal relationship between the neoplastic cells of the two diseases.

Study Spotlights HIV Starting The Infection Process

When transmitted by heterosexual contact from one person to another, the HIV virus faces a genetic bottleneck, as only one type of HIV virus from the�many genetic scrambled viruses will start the new infection.

Researchers from the New Emory Vaccine Center have demonstrated that a patient’s new HIV infection differs fundamentally from the HIV main strains that are found in his partner genital tract population. This result spotlights the process of HIV transmission, and�the bottleneck effect�that is not�happening by chance, or due to�the partner’s genital tract HIV�strains dominant population.

Researchers published their findings in�Proceedings of National Academy of Sciences, Early Edition, online this week.

If the new infection strain�was determined�by chance�it would be one strain�commonly found in the�donor’s genital tract, but this is not the case according to�Eric Hunter, PhD senior author, and pathology professor at the Emory university School Of Medicine. The results actually�suggest that the transmission method�selects certain strains.�The HIV virus that will start a new infection is a single variant, but�differs totally�for each�transmission event.

Hiv Infection

The first author of the paper is Debrah�Boeras, senior scientist, PhD.

Patient samples were a result of collaboration with the Emory’s HIV research programs from Rwanda and Zambia, through which the research team received vaginal swabs, blood, and semen from 8 consenting couples from Rwanda and Zambia, exactly when the couples were diagnosed positive to HIV. From the total of eight couples , in six cases, female to male transmission was reported.

Boreas and his team analyzed the DNA sequence that codes the env gene (encodes glycoproteins forming�the virus�envelope – external coat) and discovered that a single HIV genetic variant from the donor’s genital�tract�population lead to a new infection. These results could be a starting point for further study regarding the exact features of HIV variants that start a new infection.

The huge challenge�will probably�be detecting those particular infectious�features, identifying the strains and targeting them, in�order to protect more people from getting infected.

Other studies concluded that the “founder” HIV viruses , have envelope glycoproteins that are more dense, and have less spaces that can be modified with sugar, feature that may change the way in which these viruses interact with the genital mucosa of the healthy partner.

This aspect is currently�in the Hunter laboratory, and the results could help create a new but still elusive vaccine.