Quantcast
Channel: Biotechnology Forums - All Forums
Viewing all 2695 articles
Browse latest View live

Genetic engineering doomsday scenarios?

0
0
Hi. I'm writing a sci-fi novel in which I am trying to define an easily-understood genetic engineering disaster that leads to a permanent ban against engineering of humans.

Please let me know if the following scenario even makes sense:

Humans are confronted with an ebola-like pandemic that's sweeping around the world like wildfire. A vaccine is hurriedly engineered that seems to work and, as a result, most of the population is eventually vaccinated. All seems well. However, the vaccine has resulted in genetic damage. All vaccinated humans are now carrying a recessive gene that can cause sterility. That leads to approximately 25% of the next generation with two faulty copies of the gene. Billions of genetic dead ends.

Since the above is almost certainly flawed logic, I'd appreciate any ideas on how to do something like this correctly. Ultimately, I'm looking for an excuse why humans have not been engineered into supermen 2000 years from now. It has to be a real shock to the system that humanity will never forget, resulting in a permanent ban.

Thanks
Dirk

Business developer Preclinical CRO Sweden/Denmark

0
0
Pharmaseed is Israel's largest GLP-certified pre-clinical CRO specialized in preclinical and translational studies in several domains: oncology, CNS, medical devices, inflammation, cardiovascular diseases, cell therapy and infectious diseases (http://www.pharmaseedltd.com).

PharmaSeed is looking for a Business Developer who will be responsible for new business development in Northern Europe countries, especially Sweden, Finland and Denmark, prospecting new leads and managing customer relations. Job position will be in Sweden or Denmark.

PharmaSeed has all the necessities for NCE, biologics and medical-device development to first-in-man trials such as safety and efficacy evaluation in various animal models as well as complementary in-vitro/ex-vivo models and on-site human anatomy services. Our clients are mostly small and medium enterprises and startups operating in the biotechnology and pharmaceutical sector, as well as technology transfer departments, incubators and research institutes. We provide our partners with the preclinical R&D studies required to develop technologies in the preclinical maturation phase.

What You Will Be Doing
- Active prospection of new leads and implementation of sales strategies and new business opportunities in Northern Europe countries (mainly Sweden, Denmark, Finland)
- Working in close contact with management to establish strategic direction for sales
- Managing marketing strategies to increase visibility and business opportunities
- Participation to local conferences and setting of face-to-face meetings with possible clients

What You Need for this Position
- You are fluent in English, oral and written
- Speaking Swedish and/or Danish is very appreciated
- You have excellent communication skills, written and verbal, as well as a convincing, persuasive personality
- You are proactive and multi-tasking
- You can work in a competitive environment and can adapt your working strategies depending on the situations
- You have background studies in scientific domains (Biology, Biotechnology, Pharmacology or Medical Sciences)
- A previous experience in sales or business development in the biomedical sector is appreciated but not strictly required

Salary – fixed salary + commission.

If you are interested in this position, please send me a cover letter and CV in English.

Training/Workshop@SCFBio, IIT Delhi in July, 2015

0
0
SCFBIO, IIT Delhi intends to start training/Workshop Programmes in Bioinformatics and Computational  Biology from 1st July, 2015. The training Programme will be divided into two batches with 10 days allocated for each batch.
1) Topics for the training/Workshop Programme are proposed to be covered with hands–on 
      training/Workshop in the following four modules:– 


  1. Genome analysis (First Three days of each batch)
  2. Protein Folding ( Fourth, Fifth, Sixth day of each batch)
  3. Drug Design (Seventh, Eighth, Ninth day of each batch)
  4. High performance computing in Bioinformatics.(Last day of each batch)

2) Duration of Training/Workshop:- 

      The training/Workshop programme for each module is proposed to be conducted for three days 
     (approx) and the entire set of modules mentioned above will be completed in 10 days time(from 
     9 am to 5 pm everyday). Participants can opt for any number of modules.

      Following are the tentative schedule for the batches
  • 1st  batch: 1st July, 2015 to 10th July, 2015
  • 2nd batch: 14th July, 2015 to 23rd July, 2015
    3) Eligibility :-       B.Sc/B.Tech./M.Sc./M.Tech./Ph.D Students and professionals from Biotech and Pharma industries.4) Maximum no of students :- 25 per batch 5) Fee :- Rs 3000 per module. (Rs 8000/- for three or more modules) 
visit the link
https://www.scfbio-iitd.res.in/training/training.html

Biometrics in Education – A Growing Demand

0
0
Biometric technology is becoming increasingly more powerful and cost-effective, and it has been making inroads into education sector. Educational institutions recognize the threat of insecurity to their children and are starting to adopt biometric identification systems to protect the students under their care. A growing trend is that biometric access control devices are being used to grant access to classrooms, colleges, universities and other service areas like canteens, dormitories and recreational facilities.

Biometric technology can provide many benefits in terms of convenience, safety and security. One of the most popular applications of biometrics in school is “cashless catering system” for school meals. In particular, individual pupils can be identified at the till by an automated biometric recognition mechanism and pay for the meal with the cost of their lunch being automatically deducted from the credit paid in advance by the parents. Besides, another well-known application is using biometrics for tracking the attendance of students and teachers. In details, an automated biometric system for recording attendance will be installed at the school gate or in class to identify the students and teachers for every roll-call. Once biometrics is being used successfully in one part of a school, the technology is usually embraced in other areas as well .Schools can then use the same biometric database to identify students for other applications such as online learning, library, media service, school trip and tours . Schools even can use biometrics for student identification at athletic events and dances to keep out other students who don’t belong.

In reality, the first reported use of biometric systems in school was at Minnesota's Eagan High School in US in March 1997. Eagan High School, a testing ground for education technology since it opened, allowed willing students to use fingerprint readers to speed up the borrowing of library books. The use of biometric technology continued widening to the UK and first introduced in 2002. Fast-forward to 2014, reports indicated that 1.28 million British students attended biometric secondary schools & academies. Nowadays, the use of this technology in schools has become wider spread in other countries in Europe (Belgium, Sweden, France, Italy, etc.), Asia (China, Hong Kong, etc.), and Australia and recently in Middle East (United Arab Emirates, Saudi Arabia, etc.) and Africa (South Africa, Kenya, etc.). In 2012, The Bill & Melinda Gates Foundation, which has poured more than $4 billion into efforts to transform public education in the US, is pushing to develop an "engagement pedometer” which is a biometric bracelet enabling teachers to see, in real time, which kids are tuned in and zoned out. The foundation has given $1.4 million in grants to several university researchers to begin testing the devices in middle-school classrooms. In 2013, Sunderland brought in fingerprint-scanning devices for lectures on its London campus, replacing traditional paper registers. Ruth Davison, student relations and compliance manager at Sunderland, said the system had been installed because the site was “entirely international” and the Home Office required that all attendance be monitored. In 2015, Saudi Arabia’s Ministry of Education is launching a tender process for a fingerprint attendance and leave system for 45 education departments. Besides, within the year, Henan University of Technology in Henan Province and Minjiang University in Fujian Province of China have deployed facial recognition systems to track student attendance.

Education market is having a growing demand in many biometric applications. With the use of biometrics, it can address many problems occurring from elementary to university such as class attendance, library books borrowing, cashless canteen systems, vending machines, school trips and tours, and bus journeys. Schools will be capable of monitoring teacher performance on class, in school and allow them to have limited authorization to access different resources and report accurately the teaching status. The increase in demand of biometrics for education forces many biometric companies to adopt and develop the technologies to meet the market demand and provide children the best secure and convenient education environment.

M.Tech Bioinformatics at MNIT Bhopal

0
0
i have got m.tech bioinformatics@Mnit bhopla, is it good to join mnit bhopal ? do we have better plcements for m.tech bioinformatics at mnit bhopal  ? Please give me ur suggestion sir

Cancer Research for Higher Studies!

0
0
Hey!
I have completed my 3rd year B.Tech in Biotechnology.
I am planning to pursue cancer research for my higher studies.
Could anyone guide me on whats better in regards of cancer research - an M.Tech(India) or an MS (USA ? or Europe ?)
If anyone has or is pursuing it currently?

Thanks in advance! Smile

a career in stem cells

0
0
hello sir,
 i am curently pursuing my btech biotechnology(will be starting 5th semester) from manipal institute of technology. i wish to make a career in stem cells and regenerative medicine. i dont have any prior strong background in it. i have just participated in an international conference where i prsented a review poster on cancer stem cells. i have the following queries:

1.) how do i chart my career after btech? what all courses should i opt for and exams should i appear for?
2.) i am also interested in getting enrolled at nus. when should i apply for it? in which department? for masters or for phd?also how is the nus mba phd dual degree program? should i go for it after btech or should i do an msc in india and go for a phd , gain post doc experience and then go for an mba seperately?


really confused.please help




Huh

Epilepsy

0
0
INTRODUCTION

Epilepsy is one of the oldest disorders known to medical history. The term is derived from the Greek for seizing, possessing or afflicting, and gave rise also to the characteristic term seizure for its cardinal manifestation. The first clinical description of a recognizable generalized convulsion was written in Akkadian, one of the Semitic languages of Mesopotamia, in about 2000 BCE. This initial described attack, prophetically, was ascribed to the deleterious influence of the moon god and was treated by exorcism. About 200 years later, the Code of Hammurabi identified epilepsy as one of the reasons that a purchased slave could be returned for a full refund. In contrast, the Edwin Smith Papyrus from Egypt, dated to about the same period, contains a description of tonic-clonic seizures in the aftermath of head injury and prescribes methods of trephining of the skull for relief of convulsions and other symptoms of what can now be recognized as increased intracranial pressure after trauma [1].

Clinical descriptions of epilepsy over the next millennium or so are both interesting and poignant, as they are highly accurate as to symptoms and outcome but, lacking any understanding of the pathophysiology of the events, ascribe seizures and their sequelae to diabolical agencies and call for their treatment by largely magical means. The Saikikku, a Babylonian cuneiform medical text from about a millennium BCE, contains the first classification of convulsive and non-convulsive seizures, and seizures manifested largely or entirely by altered consciousness (absence or psychomotor epilepsy) were recognized by physicians in the Indian Ayurvedic tradition over the next 500 or so years [2].

Whether because of a higher incidence, better case ascertainment or an especial interest in these disorders by the priests and priestesses of Selene and Artemis, ancient Greek physicians were particularly attuned to epilepsy and its manifestations, and the writings of Hippocrates and his disciples remain today the basis of much clinical epileptology. Although thought at first to be visited by the gods on those who displeased them, epilepsy was understood in many quarters of classical Greek medicine as a brain disorder. Previously called the “sacred disease”, it was rechristened by Hippocrates himself the “great disease”, from which the term grand mal is derived, and was ascribed to hereditary influences and was to be treated by natural medicines and diet as well as the induction of sleep in the temple of Asclepius and the analysis of patient dreams by the temple priests, which is essentially the state of epilepsy treatment at the start of the 20th century.

In the subsequent centuries, epilepsy tended to be classed with mental disorders, and epileptics were benignly treated when and where the mentally ill were humanely managed and were incarcerated and scourged when and where the mentally ill were persecuted or prosecuted. A small percentage of epileptics with usually post-traumatic seizures were managed with surprising success by the neurosurgical techniques then available, and the animal-, vegetable- and mineral-based pharmacopoeia of the time was not always unsuccessful, in particular identifying some anodynes and adaptogens that are still used in holistic medicine today. The development of first church-related and then private hospitals for the chronically ill allowed the inpatient treatment of some patients with epilepsy as well as those later recognized to have “hysterical” seizures.

Modern pharmacological treatment of seizures began around 1857, in the belief that hysterical or psychogenic convulsions were caused by excessive masturbation and therefore that impotence-inducing potassium bromide would relieve them. In fact, bromide proved an effective if often toxic anticonvulsant and was the mainstay of treatment until the introduction of phenobarbital in 1912. The targeted development of phenytoin as a protectant against electroshock-induced seizures in animals and clinical trials attempting to separate the antiepileptic effects of the drug from its sedative properties introduced a new paradigm to the treatment of epilepsy that continues to operate to this day. The establishment by the National Institutes of Health of an ongoing program to screen drugs for antiepileptic effects and to institute trials of agents found to be potentially effective has led to three generations of anticonvulsants in widespread clinical use, and now a fourth generation of antiepileptic drugs, modification of existing anticonvulsants and prodrugs for more effective delivery of therapeutic effects is emerging.

Operative treatment of seizures, particularly resulting from brain injury, was at times carried out with substantial success even in antiquity. Trephination had been performed on more than 100 epileptic patients in the United States between 1828 and the 1860s, and surgical attempts to treat brain tumors causing seizures were made in Britain in the two following decades. In 1886 resection of functionally abnormal epileptogenic brain tissue was pioneered by Horsley on the basis of clinical observations by Hughlings Jackson and brain stimulation by Ferrier and Beevor. Resective surgery for epilepsy was subsequently advanced by the support of Charcot and Osler, and by the work of Krause in Germany, Armour in Britain and Harvey Cushing in the United States [3].

The formation of the International League Against Epilepsy in 1909 ushered in a century of clinical and research advances, including the development of neuroimaging and electroencephalography and subsequent advances in functional brain imaging, neuropsychology and psychiatric diagnosis and treatment. The mechanisms by which seizures arise and propagate have been largely obscure up until the present, and until recently a stigma was often attached to epilepsy that was disproportionate in comparison to other neurological diseases. The role of skull fracture and brain injury in causing seizures was appreciated in ancient times, and focal seizures were recognized in the 19th century to result from cerebral cortical irritation and later confirmed to be related to scar formation. Circulatory disturbance and particularly cortical hyperemia was also thought to be responsible for some seizures, and an early surgical treatment of epilepsy involved ligature of the vertebral arteries [4].

The importance of aberrant connections to and from an epileptogenic focus was shown in the first half of the 20th century when Penfield and others applied the histological techniques developed by Golgi and Cajal to resected brain tissue, and demonstrated the processes by which scar formation and pathological sprouting of damaged axons contribute to an epileptogenic focus. The identification by Gibbs and coworkers of characteristic EEG manifestations of absence or petit mal seizures and of the temporal lobe spike focus commonly present in psychomotor or complex partial epilepsy directed attention to the imbalance between excitation and inhibition in these disorders. The development of invasive techniques for neurophysiological recording in animal models and later in patients with has elucidated normal brain physiology and its possible derangement in epilepsy. These methods have also permitted the therapeutic application to clinical epilepsy of some types of brain stimulation formerly used in its study. Although as many as one third of patients with seizures are still refractory to treatment, advances in pharmacology and biotechnology are bearing out the observation in Wilder Penfield’s penultimate book that “epilepsy, though she wears the frightening mask of tragedy in her approach to each patient, takes the mask off at times before the physician who has the wit to stop and ponder her riddles” [5].

CLINICAL FEATURES AND CLASSIFICATION

The disease of epilepsy was defined by the ILAE in 2005 as “a disorder of the brain characterized by an enduring predisposition to generate epileptic seizures and by the neurobiologic, cognitive, psychological, and social consequences of this condition. The definition of epilepsy requires the occurrence of at least one epileptic seizure [6]. This distinction between disease and disorder was thought to be important to make as a disease may have more serious implications, and the possibility that a seizure disorder can be outgrown or placed in remission by effective treatment does not predict the likelihood or its further recurrence [7].

A recent redefinition of epilepsy specifies the occurrence at least 24 hours apart of two or more seizures. Persons who have two unprovoked seizures and over followup for the next 10 years demonstrate a risk of seizure recurrence of 60 per cent or more are also considered retrospectively the have epilepsy. The recognition of an epilepsy syndrome combining clinical features and EEG or imaging findings also allows the diagnosis of epilepsy to be made. Epilepsy is considered to have remitted in individuals who have been seizure-free for more than 10 years and off of anticonvulsant medications for at least 5 years, or who had an age-dependent epilepsy syndrome but are now beyond the age group in which such seizures characteristically occur [8].

The classification of seizures has been repeatedly attempted and revised. The traditional distinction has been made for centuries between grand mal or convulsive and petit mal or nonconvulsive seizures, but it has long been recognized that many if not most convulsive seizures begin focally rather than generally, and from the 19th century onward clinicians have differentiated between absence seizures and seizures of partial origin that primarily involve consciousness and behavior. Convulsive seizures are the most common, representing about 60 per cent of cases but affecting both cerebral hemispheres at onset in only about a third of cases, the other two-thirds of generalized seizures beginning focally in one hemisphere. The other 40 per cent of seizures are nonconvulsive, epitomized by absence attacks [9].

Partial seizures may start with a sensory, motor, autonomic or psychic aura, and may spread physiologically to adjacent cortical areas and clinically to adjacent muscle groups (Jacksonian march). Automatisms, repetitive movements ranging from lip smacking to more complex unconscious actions, may occur at this time also. Convulsive or tonic-clonic seizures begin with 10 to 30 seconds muscle contraction, arching of the back and a cry caused by chest muscle contraction, followed by a longer period of rhythmic muscle contraction, sometimes with incontinence and tongue-biting and then post-ictal obtundation for up to 30 minutes. Tonic contractions may predominate with cyanosis from cessation of breathing [10].

Primary generalized seizures involving both cerebral hemispheres from the onset include tonic-clonic, tonic, clonic, myoclonic, absence, and atonic seizures. These all involve loss of consciousness, usually without warning. Myoclonic seizures involve either localized, often extremity, muscle spasms or are generalized and principally trunkal. Atonic seizures are characterized by loss of muscle tone for one second or more, and may result in falls and injuries. The classical petit mal or absence seizures do not cause falling during unconsciousness, and consciousness returns without sequel after several seconds [11]. Six per cent of seizures are triggered only by specific stimuli, particularly visual or auditory (reflex seizures) [12].

In addition to classification of types or seizures, classification of epilepsies has been attempted. The ILAE proposed in 1989 a scheme that differentiated localization-related epilepsies and syndromes, generalized epilepsies, undifferentiated syndromes and special syndromes. Localization-related epilepsies could be of unknown cause, arise from an identifiable lesion or injury (symptomatic) or have no discernible cause (cryptogenic). Generalized epilepsies could arise from identifiable insults, have no discernible causative lesion although the result of brain disorder or arise from an unknown cause. Some syndromes, particularly arising during sleep, could not be classified as partial or generalized, and special syndromes involved seizures of specific types or that occurred only under specific circumstances [13].

This classification was subsequently revised because it did not differentiate between underlying causes of epilepsy, such as brain tumor or inherited disorder, and these are important determinants of prognosis and response to therapy. The ILAE subsequently divided epilepsies into three categories of causation (genetic, structural or metabolic and unknown), and there were further subdivided. Epilepsies of unknown cause, mostly of genetic origin, were divided into subcategories of single-gene inheritance and complex inheritance. Symptomatic epilepsy, usually associated with obvious anatomical or identifiable pathological abnormalities of the brain, were subdivided into disorders of genetic or developmental origin and those acquired through brain injury. Two other categories were recognized: provoked epilepsies, in which specific events or factors brought on seizures, and cryptogenic epilepsies, in which the cause could not be determined despite appropriate evaluation [14].

PATHOPHYSIOLOGY OF EPILEPSY

The physiological basis of epilepsy is not known, but current evidence suggests that in susceptible individuals the normal asynchronous neuronal activity of the brain can become excessively synchronized. Brain injury or developmental abnormality may give rise to areas or regions in which the normal resistance of cerebral neurons to repetitive firing is diminished, which is the basis of the seizure focus sought in epilepsy evaluation. Excitatory neuronal circuits may be up-regulated or increased in activity or inhibitory circuits may be decreased in effect (down-regulated) in the region of a seizure focus in partial epilepsy or in the brain generally in generalized epilepsy. Disturbance of the blood-brain barrier by brain injuries or lesions may also allow toxic substances to enter the brain and affect excitation or inhibition [15].

The transition from the apparently normal (interictal) state to the ictal state (a seizure) is characterized by increasingly and excessively synchronous neuronal firing. This causes a marked shift in the neuronal membrane potential known as the paroxysmal depolarizing shift (PDS). The PDS consists of a period of depolarization mediated by calcium, on which are superimposed a burst of action potentials due to the opening of voltage-gated sodium channels, followed by a period of hyperpolarization due either to chloride ion influx mediated by the inhibitory transmitter GABA, the opening of calcium-dependent potassium channels or both. Excitatory neurons are ordinarily resistant to firing after a period of depolarization, but neurons manifesting the PDS continue to fire with undue ease [16].

CAUSES OF EPILEPSY

About 40 per cent of seizure disorders can be ascribed to some cause, while in the rest the cause is not apparent. Most cases in young people are the result of genetic disorders, congenital abnormality or developmental disturbance, while structural causes such as brain tumor or stroke predominate in older patients. Acute symptomatic seizures are those which occur in close association with brain injuries or lesions, and these are sometimes classified as seizure-related disorders rather than epilepsy [17].

There is clearly a genetic component to epilepsy, but only 1 or 2 per cent of cases are due to an identifiable single gene abnormality, of which several hundred have been described. Most of the gene mutations connected with epilepsy involve ones coding for the proteins of ion channels in the neuronal membrane, receptors for gamma-aminobuytric acid (GABA) or glutamate, receptors on the cell membrane involved in transduction (G-coupled or G-linked receptors) or enzymes responsible for neurotransmitter metabolism. The risk of developing seizures for the identical twin of a patient with epilepsy is 50 to 60 per cent, while the risk for fraternal twins is about 15 per cent. Twins with seizures will both have the same type of epilepsy syndrome 80 to 90 per cent of the time, while other first-degree relatives of patients with epilepsy have about a five-fold increase in risk. The generalized epilepsies are more closely associated with inheritance than are partial seizures, which are more often acquired [18].

Acquired seizures can result from a variety of brain lesions and injuries. Parasitic infections, chiefly tapeworm (neurocysticercosis), is responsible for half of the incidence of epilepsy in endemic areas. In other parts of the world the chief structural cause is brain tumors: 30 per cent of brain tumor patients have seizures, and they make up about 4 per cent of epilepsy cases. Vascular lesions such as malformations have a high likelihood of causing seizures (40 to 60 per cent); the overall risk of seizures after stroke is lower (2 to 4 per cent), but the incidence is greater in elderly patients (up to 30 per cent). Five to 20 per cent of patients with cerebral trauma develop seizures, more so after penetrating head wounds (50 per cent) than with closed head injury (twice to 7 times the risk for the general population, depending upon the severity of trauma). The risk of seizures with meningitis is around 10 per cent, but these occur in 50 per cent and subsequent chronic epilepsy in 25 per cent of patients with encephalitis. Alcohol abuse and dependence approximately increases the risk of developing seizures two- to three-fold [19].

EPIDEMIOLOGY AND PROGNOSIS

Epilepsy is one of the most common neurological disorders, affecting about 1 per cent of the pediatric and adolescent population and 3 per cent of elderly individuals. There is a slight female predominance and a preponderance in developing countries (80 per cent of cases). The incidence of epilepsy is about 50 cases per 100,000 in these countries and around 120 per 100,000 in developed ones. The incidence of seizure disorders is greater among impoverished residents of both developing and developed countries. It is increasing among children in the developing countries because of higher rates of infection or trauma there, while seizures are becoming more common among older patients in the developed countries because of improved survival after stroke [20].

The great majority of patients with convulsions, absence seizures and other forms of generalized epilepsy (80 percent) can achieve control with present treatments, but only about 50 per cent of those with partial seizures. A larger number of seizures in the first 6 months after seizure onset, resistance to first attempts at treatment, coexistence of partial and generalized seizures, family history of seizures, mental subnormality or psychiatric diagnosis in addition to epilepsy and generalized EEG abnormalities are associated with poorer prognosis [21]. Patients with epilepsy have a 2 to 4 times greater risk of death than the general population, and the risk of suicide is 2 to 6 times greater. Sudden expected death in epilepsy (SUDEP) represents about 15 per cent of deaths among seizure patients, and is associated with male sex, tonic-clonic seizures, lesional epilepsy, poor seizure control, noncompliance with therapy and substance abuse [22].

DIAGNOSIS

The EEG has been a crucial diagnostic tool for epilepsy since the 1930s. Abnormality of EEG background rhythms, focal or generalized slow waves, and paroxysmal or epileptiform discharges are reasonably specific for the presence of epilepsy, with correlations ranging from 70 to 98 per cent. Sensitivity to the diagnosis in asymptomatic patients is less, about 25 to 56 per cent, due to limitations of spatial sampling in recordings from scalp electrodes and temporal sampling during between-seizure or interictal studies. Only 0.5 per cent of normal subjects and 2 to 4 per cent of healthy children and nonepileptic patients had paroxysmal EEG abnormalities, while these are found in 10 to 30 per cent of patients with brain disorders but not epilepsy. Patients with monthly or more frequent seizures or temporal lobe seizure foci were more likely in several studies to have epileptiform EEG activity than those with seizures less often or foci in basal or mesial regions of cerebral cortex. EEGs recorded within 24 hours of a seizure showed abnormalities about 50 per cent of the time, while these were found in only a third of EEGs recorded at a later time. The recording of up to 4 EEGs, EEG recordings including sleep and possibly sleep deprivation as well will produce a yield of 80 per cent, and prolonged EEG monitoring will increase the yield of EEG abnormality by about 25 per cent [23].

Neuroimaging, chiefly MRI, shows abnormalities in 12 to 14 per cent of patients with first-time seizures and as many as 85 per cent of cases of intractable epilepsy. Fluid-attenuated inversion recovery (FLAIR) MRI shows hippocampal atrophy in up to 95 per cent of patients with temporal lobe seizure foci, and has shown abnormalities in other areas in addition to the temporal lobe in 15 to 20 per cent. About 20 per cent of patients with intractable seizures being evaluated for surgical treatment were found on MRI to have causative neoplasms. The yield of imaging procedures is further increased by diffusion tensor imaging, which is sensitive to the magnitude and dimension of water movement, and by computerized tomography of single-photon (SPECT) or positron (PET) emission after the infusion of radiopharmaceuticals [24].

TREATMENT

A very large pharmacopeia now exists for epilepsy, although a century after its introduction phenobarbital is still first-line pharmacotherapy in the developing world. Other available antiepileptic drugs include blockers of repetitive activation of sodium channels (phenytoin, carbamazepine, oxcarbazepine, lamotrigine and topiramate), agents that enhance the slow inactivation of sodium channels (lacosamide and rufinamide), agonists of GABAA receptor (phenobarbital, benzodiazepines and clobazam), antagonists of the N-methyl-D-aspartate (NMDA) receptor (felbamate), blockers of the alpha-amino-3-hydroxy-5-methyl-4-isoxazole priopionic acid (AMPA) receptor (perampenel, topiramate), blockers of N- and L-calcium channels (lamotrigine, topiramate, zonisamide and valproate), T-calcium channel blockers (ethosuximide, valproate), drugs that modulate the pacemaking H-current in the neuronal membrane (gabapentin and lamotrigine), inhibitors of carbonic anhydrase (topiramate, zonisamide), a drug which causes the neuronal KCNQ (Kv7) potassium channel to open (ezogabine) and two agents which bind to their own specific membrane receptors (gabapentin, levetiracetam) [25].

Most studies indicate that most anticonvulsants are about equal in efficacy. Certain antiepileptic drugs appear to work better for certain types of seizures or patients. Ethosuximide is optimally effective for absence seizures alone, with valproate, lamotrigine or topiramate preferable for absence accompanied by other seizure types. The latter are also often preferred for generalized tonic-clonic seizures, with leveteracitam recently approved and broad-spectrum agents such as felbamate or newer anticonvulsants such as rufinamide or clobazam recommended for refractory cases. Carbamazepine and valproate had the best combination of tolerability and efficacy in the VA Coöperative Studies of partial seizures, with lamotrigine and gabapentin best tolerated by older patients and lamotrigine and topiramate having the broadest spectrums of action. More recent European studies have suggested that the newer antiepileptic drugs have the same efficacy but fewer adverse effects than carbamazepine [26],[27].

Children and women of childbearing age may be differently affected by anticonvulsant drugs, as may elderly and immunocompromised patients. Neonates and children metabolize antiepileptic drugs more rapidly and older patients metabolize them more slowly, with resultant differences in dose requirement and tolerance. Anticonvulsants that induce hepatic enzymes may decrease the efficacy of contraceptives, and higher doses of estrogen and progesterone or a second method of contraception may be needed to prevent inadvertent pregnancy. Many anticonvulsants antagonize folic acid, so folic acid supplementation is wodely recommended, particularly in pregnant women with seizures, and polypharmacy should be avoided due to a higher risk of malformations. Certain antiepileptic drugs, particularly valproate, have been associated with fetal malformation. Amniocentesis is often recommended in pregnancy complicated by anticonvulsant therapy [28].



Liver and kidney function may also be determinants of anticonvulsant effect and selection. Phenyoin, carbamazepine, valproate and felbamate have been associated with liver injury, and there has been particular concern about phenytoin because of the complexity of its metabolism and interactions, while felbamate is now rarely used because of concerns about hepatic toxicity. Monitoring of liver function is recommended during use of the other anticonvulsants. Some of the drugs are dependent upon renal clearance (gabapentin, pregabalin, levetiracetam and lacosamide) and dose adjustment may be required in renal insufficiency. These drugs and lamotrigine, which is metabolized by the process of glucuronidation, may be used effectively in the presence of liver dysfunction [29].

REFRACTORY EPILEPSY

With the proliferation of antiepileptic drugs, much attention has been given to how many agents need to be tried before a patient is considered medically refractory and evaluated for seizure surgery or other alternative treatments. Failure on three or more drugs has been the usual criterion, but recent studies have suggested that inability to control seizures with adequate trials of two anticonvulsants appropriately taken and without limiting adverse effect is highly predictive of medical intractability in both pediatric and adult patients [30]. In addition to consideration of surgical therapy and new options for neurostimulation, immunotherapy has been suggested in patients who have seizures and autoimmune disorders, or who are found to have antibodies to various neural antigens. Intravenous corticosteroids, intravenous immunomodulatory agents or plasmapheresis followed by a prolonged course of oral corticosteroids, has been found to bring about a seizure reduction of 20 to 50 per cent in up to 75 per cent of medically refractory patients [31].

Nonpharmacologic treatment has attracted increasing attention. The ketogenic diet, high in fat and very low in carbohydrate while adequate for protein needs, maintains the brain in a state of ketosis that for still unclear reasons retards epileptogenesis; the diet reduces seizures by half in about 40 per cent of treated children and is effective for some adults, but long-term adherence is as low as 10 per cent, intestinal symptoms are common, carbohydrates must be rigorously avoided and there are long-term cardiovascular concerns. A more palatable version of the ketogenic diet (Atkins diet) developed for weight loss has produced as much as 50 per cent seizure reduction in children, with positive anecdotal evidence in adult patients [32]. There is physiological reason to believe that aerobic exercise could improve seizure control through induction of neural plasticity, enhanced production of neurotrophic factors and improved learning and memory; preliminary clinical data suggest benefit, although refractory epilepsy sometimes limits exercise [33]. Many other alternative and complementary therapies for refractory seizures, including nutritional supplements and vitamins, herbal preparations, dietary readjustment of glucose dysregulation, yoga and meditation and some homeopathic remedies have received anecdotal support but have not been demonstrated to be effective in clinical trials[34].

Surgical removal of lesions causing seizures has been attempted for centuries and was widely done in the 19th century, while resection of epileptogenic cerebral cortex was first attempted at the turn of the 20th. Up to 85 per cent of patients with unilateral temporal lobe epilepsy and unilateral hippocampal sclerosis can be rendered seizure-free by temporal lobe resection. Controlled trials of resective surgery for persistent seizures have suggested a seizure-free outcome after 1 or 2 years of 60 per cent versus about 8 per cent for continued attempts at anticonvulsant treatment, with significantly better quality of life. MRI-guided laser ablation is as effective as traditional resection, and has markedly better results with respect to memory improvement. Identification by three-dimensional EEG, invasive EEG recordings, SPECT scan or PET imaging of focal epileptogenic areas may permit their isolated resection, and has similar efficacy to standard surgery but much less cognitive and developmental effect in children with refractory epilepsy. Recent studies in which respective surgery was undertaken after only two years of unsuccessful drug treatment rather than as a last resort have suggested that nearly 75 per cent of such patients may be rendered seizure-free. In intractable generalized epilepsy, surgical division of the corpus callosum, or less commonly multiple resections of subcortical pathways involved in seizure propagation, reduce the number of seizures but are not curative [35].

Advances in biotechnology have had a major effect on epilepsy treatment. The surgical implantation, usually in the chest, of a cybernetic device that periodically stimulates the vagus nerve (VNS) and can also be activated by the patient at times of increased seizures of auras, has been feasible since the end of the 20th century. Current guidelines support VNS for patients older than 12 years with medically intractable partial seizures who are not candidates for potentially curative surgical resections, and for adjunctive long-term treatment of depression in patients older than 18 years with major depressive episodes not adequately relieved by 4 or more antidepressant treatments. VNS may have gradually increasing efficacy with time, and is now also considered for adjunctive treatment of epilepsy in children and improving mood in adults with epilepsy. About 50 per cent of patients have 50 per cent or more reduction in seizures, particularly with post-traumatic epilepsy, but fewer than 10 per cent become seizure-free and approximately one quarter of patients do not respond [36].

Deep brain stimulation (DBS) with implanted electrodes, usually in the centromedian nuclei of the thalamus, developed from earlier work on brain stimulation for movement disorders, pain and psychiatric conditions. DBS has been undertaken in patients with refractory generalized epilepsy in whom a resectable focus cannot be identified, as well as seizures of frontal lobe origin that are not amenable to respective surgery. Almost all reported generalized epilepsy patients have had 50 per cent or more improvement with some becoming seizure-free and a small number remaining seizure-free for up to 4 years without stimulation; approximately half of patients with seizures of frontal lobe origin had 50 per cent improvement [37].

Another recent biotechnology advance is an implanted device in which subdural electrodes record the cerebral cortical EEG and detect the development of pathological symmetry that is the hallmark of a developing seizure. The device then delivers short trains of current pulses to interrupt the transition to a seizure. The system was approved for clinical use in 2013, based on a clinical trials in which patients in whom the system was implanted and activated had significantly greater seizure reduction than those with devices that were implanted but not turned on. Patients treated with stimulation had improvement in memory and few adverse effects, but the rate of sudden death from SUDEP remained elevated. This and the small number of cases reported to date has prompted continuing study of the efficacy and safety of cybernetic means for seizure detection and prevention [38].

REFERENCES

1. Magiorkinis E, Sidriopoulou K, Diamantis A (2010). Hallmarks in the history of epilepsy: Epilepsy in antiquity. Epil & Behavior, 17(1): 103-108.

2. Temkin O (1994). The Falling Sickness, ed. 2 (revised). Baltimore, Johns Hopkins University Press.

3. Girvin JP (2014). History of epilepsy surgery. In, Operative Techniques in Epilepsy. New York, Springer International.

4. Feindel W, Leblanc R, Nogueira de Almeida A (2009). Epilepsy Surgery: 1909-2009. Epilepsia, 50 (suppl 3): 131-151.

5. Penfield W (1975). The Mystery of the Mind. Princeton, Princeton University Press.

6. Fisher RS, van Emde Boas W, Blume W, Elger C, Genton P, Lee P, Engel J Jr (2005). Epileptic seizures and epilepsy: Definitions proposed by the International League Against Epilepsy (ILAE) and the International Bureau for Epilepsy (IBE). Epilepsia, 46(4): 470-472.

7. Panayiotopoulos CP (2011). The new ILAE report on terminology and concepts for organization of epileptic seizures: A clinician’s critical view and contribution. Epilepsia, 52(12): 2155-2160.

8. Fisher RS, Acevedo C, Arzimanoglu A, Bogacz A, Cross H, Elger CE, Engel J Jr, Forsgren L, French JA, Glynn M, Hesdorffer DC, Lee BI, Mathern GW, Moshé SL, Perucca E, Scheffer IE, Tomson T, Watanabe M, Wiebe S (2014). A practical clinical definition of epilepsy. Epilepsia, 55(4): 475-482.

9. Lomen-Hoerth C, Messing RO (2010). Nervous system disorders. In McPhee SD, Hammer GD (eds). Pathophysiology of Disease: An Introduction to Clinical Medicine. New York, McGraw-Hill.

10. Holmes GL, Browne TR (2008). Handbook of Epilepsy, ed. 4. Philadelphia, Lippincott Williams & Wilkins.

11. Hughes JR (2009). Absence seizures: a review of recent reports with new concepts. Epil & Behavior, 15(4): 404-412.

12. Xue LY, Ritaccio AL (2006). Reflex seizures and reflex epilepsy. Amer J Electroneurodiag Tech, 46(1): 39-48.

13. Commission on Classification and Terminology of the International League Against Epilepsy (1989). Proposal for revised classification of epilepsies and epileptic syndromes. Epilepsia, 30(4): 389-399.

14. Shorvon SD (2011). The etiologic classification of epilepsy. Epilepsia, 52(6): 1052-1057.

15. Goldberg EM, Coulter DA (2013). Mechanisms of epileptogenesus: a convergence on neural circuit dysfunction. Nat Rev Neurosci, 14(5): 337-349.

16. Somjen GG (2004). Ions in the Brain: Normal Function, Seizures and Stroke. New York, Oxford University Press.

17. Nelligan A, Hauser WA, Sander JW (2012). The epidemiology of the epilepsies. Handbook Clin Neurol, 107: 113-133.

18. Pandolfo M (2011). Genetics of epilepsy. Semin Neurol, 31(5): 506-518.

19. Bhalla D, Godet B, Druet-Cabanac M, Preux PM (2011). Etiologies of epilepsy: a comprehensive review. Exp Rev Neurother, 11(6): 861-876.

20. Newton CR, Garcia HH (2012). Epilepsy in poor regions of the world. Lancet, 380(9848): 1193-1201.

21. Eadie MJ (2012). Shortcomings in the current treatment of epilepsy. Exp Rev Neurother, 12(12): 1419-1427.

22. Rivlin P, Nashef L, Tomson T (2013). Prevention of sudden unexpected death in epilepsy: a realistic goal? Epilepsia, 54(suppl 2): 23-28.

23. Smith SJM (2005). EEG in the diagnosis, classification and management of patients with epilepsy. J Neurol Neurosurg Psychiat, 76: ii2-ii7.

24. Friedman E (2014). Epilepsy imaging in adults: getting it right. Amer J Radiol, 203(5): 1093-1103.

25. Schmidt D, Schachter SC (2014). Drug treatment of epilepsy in adults. Brit Med J, 348: g254.

26. French JA, Kanner AM, Bautista J, et al, for the Therapeutics and Technology Assessment Subcommittee of the AAN, Quality Standards Subcommittee of the AAN and AES (2004). Efficacy and tolerability of the new antiepileptic drugs I: treatment of new onset epilepsy: report of the Therapeutics and Technology Assessment Subcommittee and Quality Standards Subcommittee of the American Academy of Neurology and the American Epilepsy Society. Neurology,62(8):1252-60.

27. Marson AG, Al-Kharusi AM, Alwaidh M, et al, for the SANAD Study Group (2007). The SANAD study of effectiveness of carbamazepine, gabapentin, lamotrigine, oxcarbazepine, or topiramate for treatment of partial epilepsy: an unblinded randomised controlled trial. Lancet, 369(9566):1000-15.

28. Harden CL, Meador KJ, Pennell PB, et al, for the AAN and AES (2009). Management issues for women with epilepsy-Focus on pregnancy (an evidence-based review): II. Teratogenesis and perinatal outcomes: Report of the Quality Standards Subcommittee and Therapeutics and Technology Subcommittee of the American Academy of Neurology and the American Epilepsy Society. Epilepsia, 50(5):1237-46.

29. Asconape JJ (2014). Use of antiepileptic drugs in hepatic and renal disease. Handbook Clin Neurol, 119: 417-432.

30. Ramos-Lizana J, Rodriguez-Lucenilla MI, Aguilera-López P, Aguirre-Rodríguez J, Cassinello-García E (2012). A study of drug-resistant childhood epilepsy testing the new ILAE criteria. Seizure, 21(4):266-72.

31. Quek AM, Britton JW, McKeon A, So E, Lennon VA, Shin C, Klein C, Watson RE Jr, Kotsenas AL, Lagerlund TD, Cascino GD, Worrell GA, Wirrell EC, Nickels KC, Aksamit AJ, Noe KH, Pittock SJ (2012). Autoimmune epilepsy: clinical characteristics and response to immunotherapy. Arch Neurol. 69(5): 582-593.

32. Levy RG, Cooper PN, Giri P (2012). Ketogenic diet and other dietary treatments for epilepsy. Cochrane Database Syst Rev, 3:CD001903.

33. Arida RM, Scorza FA, Scorza CA, Cavalheiro EA (2009). Is physical activity beneficial for recovery in temporal lobe epilepsy? Evidences from animal studies. Neurosci Biobehav Rev, 33(3):422-31.

34. Gaby AR (2007). Natural approaches to epilepsy. Altern Med Rev, 12(1): 9-24.

35. Health Quality Ontario (2012). Epilepsy Surgery: An evidence survey. Ont Health Tech Assess Ser, 12(17): 1-28.

36. Morris GL III, Gloss D, Buchhalter J, Mack KJ, Nickels K, Harden C (2013). Evidence-based guideline update: Vagus nerve stimulation for the treatment of epilepsy - Report of the Guideline Development Subcommittee of the American Academy of Neurology. Neurology, 10.1212/WNL.0b013e3182a393d1.

37. Valentín A, García Navarrete E, Chelvarajah R, Torres C, Navas M, Vico L, Torres N, Pastor J, Selway R, Sola RG, Alarcón G (2013). Deep brain stimulation of the centromedian thalamic nucleus for the treatment of generalized and frontal epilepsies. Epilepsia, 54(10):1823-33.

38. Sprengers M, Vonck K, Carrette E, Marson AG, Boon P. Deep brain and cortical stimulation for epilepsy. Cochrane Database Syst Rev, 6:CD008497.

Why is DY Patil Vidyapeeth so reputed?

0
0
Hey everyone,

A lot of people seem to think very highly of DY Patil's biotech program, I don't understand why. It is after all a deemed university.
I'm still college hunting, I've applied for Amity Mumbai and Noida, and DY Patil. Unfortunately I can't appear for both DY Patil and Amity Noida, but I definitely prefer studying in Noida. I don't see why Amity gets a bad rep either, a lot of its faculty comes from institutes most students worship.

Thanks in advance for your answers.

Supreme Court Quashes AIPMT | All India Pre-Medical Test for MBBS to be Reconducted

0
0
The very recent verdict of Supreme Court over the alleged cheating in AIPMT-2015 has given blow to CBSE, as the latter has been asked to freshly conduct the exam within 4 weeks!.

CBSE, which was about to declare the results of the exam (in which over 6 lakh students appeared), to decide the fate of the aspirants for a prospective career in MBBS, has been given strict directions to conduct the exam and that too promptly, without wasting any time.

There are two aspects and consequences of this verdict:

a) It has prevented the alleged cheaters to get admission in top notch hospitals/institutes and later on emerge as crook doctors (expected to spoil the sacred profession).

b) It has given a hard blow to the hard-work and sleepless nights of those who shined in the AIPMT through their own effort. They will have to make that best effort again.

Let's hope the re-conduct is conducted neatly!

The discussion is open to opinions and views.

Thanks

Blood Groups - Different protein structure?

0
0
Do different Blood Groups have a different protein make - up?
i.e. the protein profile of each blood group would be different?

Top Biotech College rankings in India

0
0
hi 

please tell me the top ranking for m.tech biotech.
and order of preference iitg,nit all , bits pilani,  dtu 
which wil be better

Now Detergent in Mother Dairy Milk !!

0
0
Nestle's Maggi was already under fire that now Mother Dairy's packaged Milk has come under scrutiny over alleged presence of Detergents in the product! The incidence has come into light once again in Uttar Pradesh (this time in Agra). Though Mother Dairy has categorically denied any sort of adulteration, the findings have indeed raised an alarm amongst the urban population who have been totally dependent upon packaged products of various kinds for their day to day activities/living.
[Image: 4%20%282%29.png]

Mother Dairy is a wholly-owned subsidiary of the National Dairy Development Board.

Source: NDTV and ZeeNews

Following is a short clipping of the news piece:



Bio-engineering in *fiction* - need help verifying information for my novel

0
0
Hi. I have written a scene  for a novel. In this scene, characters discuss bio-engineering - specifically designer humans and how they will be developed. Processes such as cloning are included. I would appreciate any help verifying how realistic the explanations I provide the reader with are. I welcome any suggestions on how to improve this part of the book. 

If you would like to proof-read the text, please let me know. I promise to include your name (if you like) in the dedication and hopefully a copy of the book.

Thanks. Look forward to getting expert eyes on the text.

Difference between biotech and biochem

0
0
I have biotech, biochem and chem as my subjects (bsc biotech 2nd year. Nagpur University). The syllabus for both the subjects is almost same then what is the difference?

Dengue | I got it Twice! | My Story

0
0
Till my high school, I was quite a healthy guy. I would dance, I would race, I would trek (I would do everything which a young enthusiast could do). But the moment I entered my college, I don't know how and why, I became vulnerable to plethora of diseases! You name one, I would have that! It started with IBS, followed by tonsilitis, then Herpes and then Dengue!!!

Whereas other diseases weren't that shaking/life threatening, Dengue just shook the wits of mine! I was at 'Death Bed'! And worst so, I confronted Dengue TWICE in my Life!

So here's my story of facing DENGUE TWICE in LIFE! And just for your knowledge- I'm just 25.


DENGUE - The Disease that took me to Death Bed (Twice)


I will start with the (cute) picture of the tiny creature that did all the havoc in my life:
[Image: Aedes_aegypti_CDC-Gathany.jpg]
Aedes aegypti: The vector for transmitting several types of tropical fevers (Dengue being a common one). Image courtesy wikimedia
Now let's see the image of the 'core culprit' - The Virus that resides in this vector and causes the disease to the infected person.
[Image: Dengue.jpg]
 Dengue virus virions (the cluster of dark dots) in this TEM micrograph. Image courtesy: wikimedia.


About the Dengue Virus

Dengue virus is named by the disease itself, DENV: Dengue Fever Virus. It's an RNA virus belonging to the family Flaviviridae (with a broad range of arsenals in it's kitty - epaciviruses known for causing hepatitis. flaviviruses known for dengue hemorrhagic fever, encephalitis. pestiviruses the culprits behind hemorrhagic syndromes, fatal mucosal disease and even abortions)

DENV has 5 serotypes or strains (the major cause behind multiple infections of this disease). Whereas the 5th strain has recently been reported in 2013, the first four are recognized as DENV-1, DENV-2, DENV-3 and DENV-4.

An infection by one strain gives life long immunity to that particular serotype, but not for other serotypes.


More Content to come | Will Update on next visit to this forum (and that will be very soon!)

jnu ceeb syllaus

0
0
please tell me the syllabus for msc entrance exam conducted by jnu

Fingerprinting in Tissue Culture

0
0
How can one use finger printing in tissue culture to ensure genomic consistency, for a commercial lab that is?

Thought for the Day :)

0
0
Don't be satisfied with stories, 

How things have gone with others. 



Unfold your own myth..


                                                                                                                 --- Rumi

Putative ebola vaccine

0
0
What are the steps involved in the production of a putative ebola vaccine using recombinant technology?
Viewing all 2695 articles
Browse latest View live




Latest Images