Marijuana Use May Increase The Risk of Testicular Cancer

According to a study conducted at the University of Southern California (USC) and published in the Cancer Journal, marijuana increases the risk of testicular cancer. These findings draw an alarm signal regarding marijuana use for both therapeutic and recreational purposes. Studies on the link between marijuana and testicular cancer have been also conducted in the past, and the discovery made by researchers at the University of Southern California confirms this connection.

Testicular cancer compared with other cancer types, has a� good prognosis, but it seems that marijuana leads to a more agressive subtype of testicular cancer. Testicular cancer occurs in people aged between 20 and 40 years and it seems that environmental factors play a key role. To see if marijuana has any role in causing this type of cancer, Victoria Cortessis and other researchers at the Keck School of Medicine of USC in Los Angeles, investigated 163 young men who had been diagnosed with testicular cancer. They were compared with a control group consisting of 292 healthy men. The two groups compared were�of the same race and same age. Researchers found that those who used marijuana had a higher risk of developing two specific types of testicular cancer associated with a worse prognosis (with non-seminoma�and mixed germ cell tumors).

Marijuana

Although it is unknown exactly how marijuana cause cancer, Cortessis�believes that marijuana induces carcinogenesis�through�the endocannabinoid system. What is even more interesting is that scientists found that those who used cocaine had lower risk of developing these two types of testicular cancer (non-seminoma�germ cell tumors and mixed). It looks like cocaine destroys sperm-producing cells of the testis, an effect shown in laboratory animal experiments. So cocaine induces infertility. However, Cortessis noted that epidemiological studies are needed to verify this hypothesis.

“We do not know what marijuana triggers in the testis that may lead to carcinogenesis, although we speculate that it may be acting through the endocannabinoid system�the cellular network that responds to the active ingredient in marijuana�since this system has been shown to be important in the formation of sperm,” said Cortessis.

New Accurate Non-Invasive Method For Diagnosing Epilepsy Discovered By Scientists

A team of�biomedical engineers� from University of Minnesota and researches at Mayo Clinic have discovered a new non-invasive method for the diagnosis of epilepsy. This is an innovative method that can diagnose epilepsy�immediately after a seizure, unlike current diagnosis methods that are used during seizures. The research, which was�published in the Brain, the international journal of neurology, can�represent a step forward�for future treatment of epilepsy.

Epilepsy is a neurological disease that is manifested by seizures.� Epilepsy seizures are recurrent and spontaneous seizures that are typically unprovoked and unpredictable. However,� seizures have several trigger factors, such as flash lights, reading, febrile illness, stress, sleep deprivation and others. Epilepsy seizures may also occur after brain surgery and also exist forms of epilepsy that occur only in childhood. Epilepsy symptoms can not be cured, only controlled by drugs.

According to The International Classification of Seizures, epilepsy seizures are divided into partial seizures ( focal or localization-related seizures) and generalized seizures. Partial seizures are subdivided into simple partial seizures in which there is no loss of consciousness and into complex partial seizures which are always associated with loss of consciousness. Generalized seizures are the result of a paroxysmal discharge that probably begins in thalamus and then spreads to other brain structures, but on electroencephalographic (EEG) recordings, they appear to start simultaneously in both cerebral hemispheres. Generalized seizures are always associated with loss of consciousness and generalized symptoms are divided into tonic-clonic, tonic, clonic, myoclonic, atonic and absence (petit mal) seizures.

Epilepsy Seizures

It is important to control epilepsy symptoms because may� have various consequences, such as falling or complications during childbirth. There is a fatal complication, which occur very rare, called sudden unexplained death in epilepsy (SUDEP) and occurs mostly in patients with frequent uncontrolled tonico-clonic seizures.

Epilepsy diagnosis is not easy and requires medical history, EEG tests, blood tests and imaging tests. The biggest challenge for medical researchers is to locate the part of the brain involved� seizures occurrence, in order to determine new possible treatments. In the past, most scientists studying patients while they were having a seizure (in ictal phase) and some of these studies involved invasive methods in order to collect data.

In this research,�biomedical engineers� from University of Minnesota and scientists from Mayo Clinic used a novel method for studying the brains of 28 patients immediately after seizures (in postictal phase). This method is represented by a specialized type of non-invasive EEG with 76 electrodes attached to the scalp for gathering data in contrast to most previous research that used 32 electrodes. The researchers also used specialized imaging technology to gather data about the exact part of the brain which is causing seizures. Researchers found that, in severe form of epilepsy, most frequently seizures originated in the frontal lobe. They also found that adults have seizures that originate in the temporal lobe. The findings may lead in the future to innovative non-invasive methods of locating the brain regions responsible for seizures.

This new discovery is a step forward not only in the diagnosis of epilepsy, but possibly in the treatment of this neurological disease. The imaging technology that we developed here at the University of Minnesota allowed us to tackle this research and gather several thousand data points that helped us determine our findings,� said Bin He,� the senior author of the study.

Iphone 5 Release Date: How The Apps And Keyboard Look Like

We are all aware about Apple’s� rumored decision for their new iPhone 5 – to use a thinner and more advanced screen, which allows the new handset to lose� 1.7 mm of thickness when compared with the iPhone 4S. This being said I think there are a lot of folks out there very curious regarding how exactly will the new screen perform and scale our day-to-day apps. Actually, there are a couple of days now since we first found out that the iOS 6 application simulator is able to run applications at 1136 x 640, resolution which we will probably see on the new 4 inch screen iPhone 5. Now we discover that Apple has already implemented a system that can scale applications. Basically some applications already have the needed native graphics required to run in this mode, the system applications are displayed correct and correspondingly and Springboard knows it� needs to list several applications.� All are being prepared for the release date of� the new iPhone 5.

Iphone 5

Iphone 5

Iphone 5 Springboard

Iphone 5 App

iPhone Keyboard

For the applications� we skip to the IOS keyboard because it will be changed in the new iPhone 5, but changes will occur only when talking about the landscape keyboard version. The landscape keyboard is longer than normal, but in portrait mode it is not modified at all considering that the portrait resolution was not changed.

Are Vitamin D And Calcium Supplements Really Effective?

According to an article published in the July issue of the journal The oncologist, vitamin D and calcium supplements do not prevent bone loss, as was believed. Epidemiologists from at Wake Forest Baptist Medical Center have studied 12 clinical trials and the guidelines that recommend supplements of vitamin D and calcium and found that they did not bring any benefit. Moreover, it seems these supplements are harmful as they�increase the�cardiovascular and prostate cancer risk.

Vitamin D and calcium supplements have been widely recommended for patients who have followed �androgen deprivation therapy (ADT). Androgen deprivation therapy is indicated for patients with advanced prostate cancer to stop tumor growth. To combat one of the adverse effects of androgen deprivation therapy,�that is�osteoporosis, patients are prescribed calcium and vitamin D supplements. Mridul�Datta, Ph.D., co-author of the study and a postdoctoral fellow who works with Schwartz at Wake Forest Baptist, noted that in this context prescribing these supplements seemed so logical that no one questioned their effectiveness.

After carefully analyzing the clinical trials and guidelines, epidemiologists have realized that the 500 to 1000 mg of calcium and 200 to 500 IU�of vitamin D per day did not prevent bone loss in men. Moreover, the fact that some studies have found an association between high calcium intake and risk of heart disease and prostate cancer is alarming. Gary G. Schwartz, Ph.D., who is a nationally-recognized prostate cancer epidemiologist at Wake Forest Baptist and lead author of the study, pointed out that these findings must be verified by further studies. Furthermore, Schwartz believes that scientists�should do a study to compare not only the potential benefits of calcium and vitamin D supplements but also potential risks, such as cardiovascular risk and risk of prostate cancer.

The role of vitamin D supplements in different situations is, however, �unclear. Low levels of vitamin D vitamin is associated with several diseases such as osteoporosis, multiple sclerosis, tuberculosis and cancer. However, it seems that supplements are not useful in patients with these diseases. Regarding the role of vitamin D supplements in cancer, there is still no significant�evidence to justify their use.
As for calcium, there have been studies that have suggested that calcium supplements, with or without vitamin D, increase cardiovascular risk, especially risk of myocardial infarction. It seems that high levels of calcium�stimulates�vascular calcification and increases mortality among those with kidney failure.

Exposure To Molds May Raise Children’s Asthma Risk

New discoveries on the triggers of asthma in children have been made by researchers at the University of Cincinnati (UC). They found that� children exposure to certain types of mold (Aspergillus ochraceus, Aspergillus unguis�and Penicillium variabile) is an important risk factor for developing asthma in children.

Asthma�is a respiratory disease characterized by chronic airway inflammation. Asthma has several features in addition to chronic inflammation: bronchospasm, reversible airway obstruction, bronchial hyperreactivity. It is worth mentioning that�asthma occurs in vulnerable�persons or�people�with a�positive family history for allergies.

Researchers at the University of Cincinnati (UC), U.S. Environmental Protection Agency (EPA) and Cincinnati Children’s Hospital Medical Center, conducted a study with 300 patients. They have�followed the children not only in the first�4 years of life and then at the age of 7 years, but also the living conditions (home allergens and mold). Also, in the study �there were enrolled only children whose parents had allergies. What researchers found was that a quarter of children developed asthma�in the first seven years of life. It is known that asthma�has an important allergic component. There are incriminated occupational allergens, drugs, air pollutants (pollen, fungus, beetles, mites, etc.).

Molds

According to the researchers, mold exposure is a risk factor for developing asthma in children. They used the relative moldiness�environmental index (ERMI) in order�to determine that exposure to certain species of mold causes asthma. Pr.Reponen, professor in the UC College of Medicine’s Environmental Health department, pointed out�previous studies lacked of information about what species of mold were implied in development of asthma. What was known was that mold exposure worsens asthma symptoms. He also added that� knowledge of etiological factors of asthma�may be�a step forward to the �development of �new therapeutic targets to control the disease. “This is strong evidence that indoor mold contributed to asthma development and this stresses the urgent need for remediating�water damage in homes, particularly in lower-income, urban areas where this is a common issue,”�mentioned Reponen.

It is important to known that there are two type of asthma: allergic� and non-allergenic�asthma. Also, allergic asthma�has two�categories: atopic asthma and nonatopic�asthma. Atopic asthma�means that there is a predisposition to develop this disease, it has onset in childhood and is characterized by high levels of IgE. There are many factors involved in the development of asthma. Air pollutants, viral respiratory infections, stress,�exercise are only a few risk factors for asthma. Also, maternal smoking during pregnancy or after delivery is considered an important risk factor.

Research Finds New Brain Cancer Treatment

Researchers have discovered a new target for the�treatment of aggressive forms of cancer, glioblatoma�multiforme. Glioblastoma�multiforme�is one of the most severe forms of cancer which arise from glial cells of the�brain tissues. Although associated�with a poor prognosis, glioblastoma�multiforme is rare,� it represents on average only 20% of intracranial tumors.

The most common glioblastomas�develop in the cerebral hemispheres, but in children can occur in brainstem. There are glioblastomas�that�arise�from malignant transformation of an astrocytoma, but there are also glioblastomas�which occur sporadically. There are several genomic abnormalities�described� that cause glioblastomas: p53�gene mutation ( suppressor tumor gene), overexpression�of epidermal growth factor receptor (EGFR), gene amplification of platelet-derived growth factor-alpha (PDGF-alpha) gene, etc.

Brain Cancer

Glioblastoma�multiforme�is manifested by symptoms of intracranial hypertension such as headaches, vomiting and nausea. Also, these symptoms may be accompanied by paresis or other neurological impairment. Of course, the symptoms also depend on location of the�tumor. The most common glioblastoma�multiforme�has a fronto-temporal�location. Therefore,� symptoms such as impaired memory, personality and neurological deficit can occur. Treatment for glioblastoma�multiforme�consists of chemotherapy, radiotherapy and surgery. Unfortunately, treatment is often symptomatic, not curative because many tumors become�resistance to treatment. In addition, many drugs used in chemotherapy can not pass a blood-brain barrier to destroy the tumor. It is worth to note that symptomatic treatment�refers to reducing headaches or�seizures. Therefore,� corticosteroids or anticonvulsants are given to patients suffering from glioblastoma.

According to the National Cancer Institute, the average survival rate�of patients with glioblastoma�multiforme�is approximately 15 months. Because it is an incurable disease and also a�rapidly growing one, finding new targets�for treating this disease is extremely valuable. Dr. Luis Parada, chairman of developmental biology and director of the Kent Waldrep�Center for Basic Research on Nerve Growth and Regeneration, said that the disease is difficult to treat because the treatment is aimed especially at cancer cells that replicate quickly. Instead temozolomide, the drug used to stop tumor growth,� does not act on cells that replicate slowly and those are the�ones�responsible for relapses.

Temozolomide is an alkylating agent that passes the blood brain barrier and proved useful in combination with radiotherapy. After experiments conducted on laboratory animals, researchers found that tumor cells behave like stem cells. Stem cells are undifferentiated cells that can divide and specialize in different type of cells� in the body. Discussion on the existence of stem cells in solid tumors has generated a great�controversy among researchers.

Parkinson Disease

Parkinson disease is one of the most common progressive, degenerative neurologic disorders and is affecting approximately 1% of individuals older than 60 years. Anatomopathologic, Parkinson disease present two major findings: the loss of pigmented dopaminergic neurons in the substantia nigra (pars compacta) and the presence of Lewy bodies. The exact cause of Parkinson disease is still unknown and is believed that the disease appear due to a combination of genetic and environmental factors, but until now, no environmental cause of Parkinson disease has yet been proven. A known genetic mutation can be identified in approximately 10% of cases and in these cases the average age of onset is 50 years old.

Parkinson Disease Symptoms

Onset is often nonspecific, accompanied by depression and fatigue. 20% of patients experience an initial upper limb clumsiness. Typical onset of Parkinson disease is characterized by the appearance of a postural asymmetric tremor, which most commonly affects the upper limb.

Parkinson disease is characterized by three cardinal symptoms: akinesia or bradykinesia, tremor and extrapyramidal hypertonicity. Postural instability, which is the fourth cardinal symptom, occurs later, after several years of disease evolution.

Parkinson Disease

Akinesia or bradykinesia means a slowness in movements or a lack of initiative in motor movements, loss of associated movements, such as the lack of upper limb swing during walking, the lack of gesticulation during speech. Akinesia is characterized by rapid fatigue in alternative or repetitive movements. Facial bradykinesia is characterized by decreased facial expression (hypomimia), like a mask and blinking rate is decreased. Bradykinesia also includes speech impairments (bradylalia), voice is becoming softer, less distinct or more monotonal. Patient may also present difficulties in swallowing. Bradykinesia can be suppressed by strong excitant factors, situation in which the patient presents paradoxical kinesia (is moving very fast). Another paradoxical aspect of Parkinson disease is represented by akathisia (characterized by unpleasant sensations of inner restlessness that manifests itself with an inability to sit still or remain motionless).

Hypokinesia differentiates itself from paralysis by the fact that is characterized by amplitude and speed redaction of movements, and not by muscle weakness. Hypokinesia develops slowly, being long time unnoticed and refers to the a slow execution of voluntary (for example, to lift an object), and automatic movements (for example, blinking, upper limb balance while walking). When is quite advanced, hypokinesia leads to functional disability, patient realize that has a motor problem and is possible to describe it as a paresis instead of describing the slow and low amplitude of its movements. Hypokinesia, as a manifestation of the motor system abnormalities, is dangerous only in advanced forms, when it may lead to severe�immobilization of patient, with possibility of complications such as pneumonitis or pulmonary embolism.

Clinical manifestations of hypokinesia are the result of the combination of speed, frequency and amplitude reduction of spontaneous and automatic movements:

• Hypomimia: a reduced degree of facial expression, expressionless facies and decreased blink rate;
• Reduction of automatic movements:� reduction of head movements and gesticulation during conversation, decreased amplitude of upper limb balance while walking, arms may remain fixed in semiflexion during walking;
• Impairments in repetitive movements: repetitive movements become slower and successive movement amplitude decreases (for example, micrographia – as patient is writing the letters become increasingly smaller);
• Difficulty in initiating movements: the ability to arise from a chair is affected or hesitation at the first step when the patient is initiating gait. Some patients with Parkinson disease have difficulty in performing two simultaneously motor acts (for example, to lift and move the hands);
• Motor blockage or freezing phenomenon is a sudden interruption of motor act, usually occurs while walking,being a characteristic for basal ganglia dysfunction. Freezing phenomenon may occur spontaneously or may be caused by certain circumstances such as the need to move through a crowded space or in patient attempt to navigate doorways. Emotional stimuli as anger and fear can also trigger the freezing phenomenon;
• Hypophonia�is characterized by lower amplitude and inflection of voice. In severe cases difficult articulation of words results in a suppressed speech. Monotone voice, vocal tremor, poor articulation, variable speech rate,�trouble with the initiation of speech, and stuttering-like qualities are all characteristic for Parkinson disease and sometimes may lead to an unintelligible speech.

Parkinson Disease

Rigidity or extrapyramidal hypertonicity, is manifested by an increase in resistance to passive movements about a joint. Rigidity can be either smooth (lead pipe) or oscillating (cogwheeling).�This resistance contributes to the slowness of movements and to decreased amplitude of associated movements. Is usually distributed on all muscle groups, but with a slight predominance on trunk and limb flexors, leading to a flexion posture of the body, which seen from�lateral evokes the appearance of a question mark. Besides posture abnormalities, the patient loses compensatory reflexes necessary to restore balance. Posture influences walking, patients may take smaller steps and gait cadence is reduced.

Tremor in Parkinson disease is characterized by a rhythmic movements of the limbs and occurs when members are not engaged in voluntary action (resting tremor). Tremor is slowly and may be temporarily suspended or reduced by voluntary, active movements and reappears after a few seconds of rest. Typically, occurs when the patient is completely relaxed, first in one upper limb and then spreads slowly to the lower limbs and to the mandible. Very rarely, tremor may affect the head, but never affects the voice. Parkinsonian tremor amplitude is increased by stress, anxiety and fatigue. At the onset, tremor may be limited to one upper limb, later extending to the other hand and legs, and finally may include lips, jaw, tongue and very rarely the entire head.

Parkinson Disease

Secondary clinical signs of Parkinson disease are represented by respiratory and sphincter impairment and constipation. Cognitive impairment can lead to dementia in 30% of cases. Sleep disorders are represented by daytime sleepiness associated with sleep-wake rhythm reversal. 50% -70% of patients with Parkinson disease develop depression. Personality changes may occur, patients become surly and selfish. Autonomic disorders can cause salivation, seborrhea, hypotension, and sensory disorders can cause paresthesias and limb pain.

Parkinson Disease Diagnosis

Parkinson disease is diagnose by the three cardinal symptoms: bradykinesia, tremor and rigidity. No laboratory or imaging explorations are required in patients with typical presentation of the disease. This patients are aged 55 years or older and present a slowly progressive and asymmetric resting tremor, bradykinesia or rigidity. Patients who do not present tremor should generally be considered for MRI evaluation to exclude brain lesions such as stroke, tumor, or demyelination.

Rectal And Colon Cancer

According to The Cancer Genome Atlas (TCGA) project’s large-scale study of colon and rectal cancer tissue specimens, rectal cancer and colon cancer are based on the same genomic alterations. Researchers have realized this fact after they conducted a study�on 224 colorectal cancer specimens. The study, funded by the National Cancer Institute (NCI) and the National Human Genome Research Institute (NHGRI), provides a better understanding of the origin of colorectal cancer and may be the basis for new therapies to treat cancer. Harold E. Varmus, M.D., NCI director, said: “This genetic information unquestionably will be the springboard for determining what will be useful clinically against colorectal cancers.”

Genetic Cancer

Colorectal cancer is the most common digestive cancers and the fourth most common cancer in both men and women, after non-melanoma skin cancer, prostate cancer (breast) and lung. It is already known that colorectal cancer is based�on two important risk factors: genetic alterations and adenomatous�polyps. Adenomatous�polyps are considered premalignant�lesions and their malignant risk is even higher as the adenoma�is higher. In genetic terms, the three types of key genes involved in colorectal cancer are: protooncogenes, those that coordinate cell proliferation, tumor suppressor genes and genes involved in repairing mutations that occur during replication.

Researchers noted that several genetic errors are recurrent in colorectal cancer. It was also found that in colorectal cancer there is�a phenomenon of hypermutation. Because the mechanisms that should�repair mutations occurred during replication are deficient, the degree of mutation is high. The researchers also noticed that, of the 224 colorectal cancers analyzed, 24 gene mutations occur in a significant number of cases. In addition to mutations known from previous studies, there�have been found new ones (ARID1A, Sox9�and FAM123B/WTX).

As with other cancers, colorectal cancer involves the interaction of various factors such as genetic predisposition, individual predisposing conditions and environmental factors. Among environmental factors, it was found that high-fat diet is an important risk factor. Also, red meat intake, physical inactivity and obesity seems to predispose to colorectal cancer. In terms of individual predisposing conditions, age over 50 years, personal history of adenomas, history of inflammatory bowel disease (Crohn’s disease and ulcerative colitis), are risk factors for colorectal cancer. Regarding heredity, 25% of colorectal cancers have positive family history of disease. It is important to remember is that if detected early, colorectal cancer is curable. This is why colonoscopy� is recommended every 5 years among people aged over 50 years.

Chronic Inflammatory Demyelinating Polyradiculoneuropathy (CIDP) – Symptoms, Diagnosis And Treatment

Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) is characterized by a chronic, symmetric sensorimotor disorder with cytoalbuminologic dissociation and interstitial and perivascular endoneurial infiltration by lymphocytes and macrophages. This features make CIDP to be considered the chronic clinical equivalent of acute� inflammatory demyelinating polyradiculonevritis (Guillain-Barre syndrome). There are a variety of subtypes with different immunological and inflammatory aspects that can be framed in class of chronic acquired demyelinating neuropathies.

CIDP subtypes also include distal simetric disorders with predominantly sensory symptoms, with multifocal sensorimotor neuropathy or sensorimotor mononeuropathy multiplex with prominent conduction block (Lewis-Sumner neuropathy) and subtypes associated with other systemic disorders.

CIDP associated with immunoglobulin M paraproteins; with POEMS syndrome (polyneuropathy, organomegaly, endocrinopathy, monoclonal gammopathy and skin changes) and with anti�myelin-associated glycoprotein antibodies (MAG antibodies) are considered to be distinct forms of CIPD because they have a specific cause and respond differently to treatment than other subtypes of CIDP.

Chronic Inflammatory Demyelinating Polyradiculoneuropathy

Different from Guillain-Barre syndrome by evolution in time,� chronic inflammatory demyelinating polyradiculoneuropathy is an immune mediated neurological disease that can occur at all ages, between 2 and 70 years, with a slight predominance in males. Most commonly occurs between 50 and 60 years, and recurrent forms of the� disease are more common in young people.

CIDP can develop after acute respiratory infections, vaccinations, surgery and pregnancy. Similar manifestations to CIDP were observed in non-Hodgkin’s lymphoma, AIDS, malignant melanoma, myasthenia gravis, multiple sclerosis, chronic liver diseases and carcinomas.

The exact cause of the disease is unknown, but is assumed to be an immunologically mediated disease, characterized by segmental demyelination of peripheral nerves. There may be a genetic predisposition for this condition.

Chronic Inflammatory Demyelinating Polyradiculoneuropathy Symptoms

Typical symptomatology of� CIDP is charcaterized by symmetrical,�sensorimotor polyneuropathy with gradual development of motor deficits (sometimes deficits may exacerbate). Reflexes are depressed. Although some symptoms are similar to Guillain-Barre syndrome,�respectively aspect of cerebrospinal fluid and electrophysiological abnormalities (aspects of demyelinating polyneuropathy),� CIDP�differentiates from Guillain-Barre syndrome by the following aspects:

• Slow progression, lasting for a period of 2-3 months;
• A more reduced severity compared with the acute form;
• Fluctuations of disease severity and symptoms over the years;
• Higher levels of proteins in cerebrospinal fluid;
• A much lower nerve conduction velocity;
• Associated with systemic diseases like lupus or Hodgkin’s lymphoma.

CIDP debuts slowly, insidiously, with a evolution of months to its maximum intensity. Initial symptoms are present in the limbs, predominating motor impairments. The disease is characterized by progressive symmetric polyneuropathy with symmetrical paresis, proximal and distal, with early onset. Paresis are getting worsen after 6-9 weeks of evolution of the disease, are moderate or severe and are associated with depressed reflexes, decreased or normal muscle tone, muscle atrophy and fasciculations. Respiratory disturbances are rare, and when they occur assisted ventilation is required.

Chronic Inflammatory Demyelinating Polyradiculoneuropathy

Sensory disturbances are characterized by numbness in the fingers,which are not accompanied by pain. Proprioceptive and vibratory sense deficits are characteristic and gait is frequently abnormal. Type of gait depends on location of weakness and degree of proprioceptive loss, patients may present steppage gait or a slapping gait.

Autonomic nervous system impairments are characterized by orthostatic hypotension, cardiac disorders and sphincter disorders.

Cranial nerves are rarely affected. Impairment of facial nerve is leading to unilateral or bilateral facial paresis. In less than 15% of patients were found oro-pharyngeal muscle paralysis. Ophthalmoparesis may occur in 5% of patients and is unilateral or bilateral, symmetrical and accompanied by palpebral ptosis. Diplopia can occur and is produced by impairment of cranial nerves III, IV, or VI.

Chronic Inflammatory Demyelinating Polyradiculoneuropathy Diagnosis

Chronic inflammatory demyelinating polyradiculoneuropathy�is diagnosed based on symptoms and paraclinical examinations.

Lumbar puncture reveals a cerebrospinal fluid with normal pressure and acellular. The most important anomaly is represented by an increased protein concentration over 1000 mg / dl, but without a high cellularity. This anomaly is called�albuminocytological dissociation.

Sensory and motor nerve conduction velocity show demyelinating and axonal changes.

Nerve biopsy shows myelin degeneration in 40% of cases in the peripheral nerves and posterior roots of spinal nerves and interstitial and perivascular infiltration of the endoneurium with inflammatory T cells and macrophages with local edema. Evidence exists of segmental demyelination and remyelination with onion bulb formation, in10%-40% of cases.

Chronic Inflammatory Demyelinating Polyradiculoneuropathy

Chronic Inflammatory Demyelinating Polyradiculoneuropathy Treatment

Corticosteroid therapy has proven effective in treating CIDP, as well as intravenous administration of immunoglobulin. Plasmapheresis is useful in treating this disease, but not as useful as imunoglubuline therapy. Other therapies are represented by alpha-interferon, anti-D immunoglobulin and cyclosporin A.

Chronic inflammatory demyelinating polyradiculoneuropathy �is a slowly progressive disease with relapses and remissions. Mortality is between 5% -10% and most commonly occurs by intercurrent infections. Corticosteroid therapy associated with plasmapheresis confer a very good prognosis, even with full recovery.

Different Results From HIV Prophylaxis Studies

Multiple clinical trials that have been examining the effects of anti-retroviral drugs as a way to prevent HIV infections in healthy heterosexuals have recorded very different results.

Doctors said that the results from three large studies that took place in Africa, which were published in the�New England Journal of Medicine, are varied and questions about the groups what would receive the most benefit from these drugs have appeared.

The use of anti-retroviral drugs in HIV-negative patients is called pre-exposure prophylaxis (PrEP). This sort of approach is used in order to prevent healthy patients from contracting the virus during sex with HIV-positive partners.

One of the studies published in the journal included only heterosexual couples. One of the partners was HIV-positive whilst the other was HIV-negative. The study showed that the risk of an HIV infection was reduced with almost 75 percent for the HIV-negative partners that were taking the anti-retroviral drugs. 4,700 couples participated in the study, called�Partners PrEP, from 2008 to 2010, in Uganda and Kenya. Patients were randomly given tenofovir, tenofovir & emtricitabine or placebo on a daily basis. The conclusion of the study was that both treatments showed a good response for protecting both men and women. The authors of the study estimate that the patient’s adherence to the drugs was approximately 92 percent.

Truvada

Another study published in the same journal had to be stopped in April 2011 due to the fact that the group that was being given the anti-retroviral drugs had shown no improvement in the protection level, compared to the group that was receiving placebo pills. This study, known as�FEM-PrEP, was a randomized clinical trial that included 2,120 women from Tanzania, Kenya and South Africa. 33 women that were taking the anti-retroviral drugs became infected with HIV. 35 women that were taking placebo got infected as well.

Unlike the other study, authors report an adherence rate of only 40 percent, whilst also having patients reporting side effects such as vomiting and nausea, liver or kidney problems. According to the researchers, the women participated in the study considered themselves at low risk, thus the low overall adherence rate.

The results of the third study which was published, called TDF-2, have shown a 62% efficiency in pre-exposure prophylaxis. The study included 1,219 patients (men and women) from Botswana. All the patients participating in the study were sexually active heterosexuals.

The results shown in previous studies suggested that the risk of an HIV infection was reduced with 44 percent through the use of anti-retroviral drugs in HIV-negative patients. Higher rates were discovered in patients with higher adherence to the treatment scheme.

Professor Myron Cohen and Dr. Lindsey Baden stated in an editorial in the journal that the cause of these different results taken from different studies is still unknown. They also added that more studies concerning PrEP are necessary because of the general approval that in the near future, pre-exposure prophylaxis will be a part of the HIV prevention plan. Authors believe that a management plan is needed for future patient approach.

“The health care provider who recommends pre-exposure prophylaxis needs a management plan that recognizes the effects of the intervention on the patient’s sexual behavior, safety and well-being as well as the ramifications of the intervention for the health of the public”, wrote�Cohen and Baden.