Bionic Eye & Lanes

Bionic Eye & Lanes

Introduction

Bionic eye is a bio-electronic eye. Bionic eye replaces the functionality of a part or whole of the eye. An external camera is worn on a pair of dark glasses which sends the images in digital form to the radio receiver placed in the eye. The radio receiver is attached to the implant chip on the retina. The implantation is of two types, epiretinal implant and subretinal implant, based on whether the implant is placed on or behind the retina. In our proposed method of bionic eye, a small and a powerful camera powered by nanogenerator, is implanted inside the patient’s eye rather than worn on a pair of glasses. The camera is small and consumes very low power.

*The Human eye

Structure and function The Human eyes operate on the same principle as that of a camera. The Human eye is an organ that reacts to light for several purposes. The Human eye ball is roughly spherical in shape. The important part of the eye responsible for the vision is the retina. The retina is a light sensitive tissue lining the inner surface of the eye. Light falling on the eye is focused on to a sheet of light sensitive cells. The photosensitive ganglion cells in the retina that receive the light signals affect the adjustment of the size of the pupil. The ganglion cells are connected to the rods and the cone cells in the retina. The cone cells are responsible for colour recognition of the image viewed and the rod cells distinguish the movement and the contrast of the image on the retina. The retina is connected to a nerve called the optic nerve that connects the brain and the eye. The eye ball is placed in a protective cone shaped cavity in the skull called the orbit or the socket and measures approximately one inch in diameter.

Fig. 1 shows interior structure of the human eye in its basic form. The light signals enter the eye through the cornea. The cornea focuses the rays of light falling on eye. The light then passes the pupil and the lens of eye, which leads to the formation of an inverted image on the retina of the eyeball. The retina sends electrical signals to the brain through the optic nerve. The brain interprets the signals sent from the retina and forms the image.

*Basic Eye Disorders

The Eye disorders dealt here are listed below:

• Retinitis Pigmentosa

• Macular Degeneration

Retinitis Pigmentosa

Retinitis Pigmentosa (RP) is the name given to a group of hereditary diseases of the retina of the eye. RP is a progressive blinding disorder of the outer retina which involves degeneration of neurons . RP may be caused by a breakdown in the function of the rods or the cones in some part of the retina. The retina is so complex that, breakdowns may occur in a variety of ways and so RP is not a single disorder but a great number of disorders. The breakdown of cone function may be called Macular Degeneration.

Macular Degeneration

Macular Degeneration is a medical condition which usually affects older adults. Macular Degeneration is mainly due to the breakdown of the cones in the retina. The cone cells are responsible for distinguishing the colours of the image formed on the retina. In macular degeneration, a layer beneath the retina, called the retinal pigment epithelium (RPE), gradually wears out from its lifelong duties of disposing of retinal waste products. A large proportion of macular degeneration cases are age- related and it can make it difficult to read or recognize faces, although enough peripheral vision remains to allow other activities of daily life. Age related Macular Degeneration (AMD) usually affects people over the age of 50 and there are two distinct types - wet AMD and dry AMD. Wet AMD results from the growth of new blood vessels in the choroids, causing an accumulation of fluid in the macula which leads to retinal damage. Dry AMD represents at least 80% of all AMD cases and results in atrophy of the Retina. Usually yellowish-white round spots called drusen first appear in a scattered pattern deep in the macula.

To be continue…………..

New antibiotic - Texiobactin

New antibiotic in 30 years discovered in major breakthrough(Texiobactin)

Introduction

The first new antibiotic to be discovered in nearly 30 years has been hailed as a ‘paradigm shift’ in the fight against the growing resistance to drugs.

teixobactin has been discovered by scientists who claim it appears to be as good, or even better, than many existing drugs with the potential to work against a broad range of fatal infections such as pneumonia and tuberculosis.

Teixobactin has been found to treat many common bacterial infections such as tuberculosis, septicaemia and C. diff, and could be available within five years.

But more importantly it could pave the way for a new generation of antibiotics because of the way it was discovered.

Chemical Structure

Scientists have always believed that the soil was teeming with new and potent antibiotics because bacteria have developed novel ways to fight off other microbes.

Laboratory tests have shown the new antibiotic, called teixobactin, can kill some bacteria as quickly as established antibiotics and can cure laboratory mice suffering from bacterial infections with no toxic side-effects.

Studies have also revealed the prototype drug works against harmful bacteria in a unique way that is highly unlikely to lead to drug-resistance – one of the biggest stumbling blocks in developing new antibiotics.

Such a development would represent a huge boost for medicine because of growing fears that the world is running out of effective antibiotics given the rapid rise of drug-resistant strains of superbugs and the spread of these diseases around the globe.

Last year David Cameron warned that medicine could be cast back to the “dark ages” when people died of relatively trivial infections, especially following routine hospital operations, because of the lack of effective antibiotics.

Professor Kim Lewis of Northeastern University in Boston – who led the research and is working with NovoBiotic Pharmaceuticals, based in Cambridge, Massachusetts, which owns the patents on teixobactin – said that the first clinical trials on humans could begin in two years and, if successful, the drug could be in widespread use in 10 years.

“The problem is that pathogens are acquiring resistance faster than we can develop new antibiotics and this is causing a human health crisis. We now have some strains of tuberculosis that are resistant to all available antibiotics,” Professor Lewis said.

“Teixobactin is highly effective against tuberculosis and there is an opportunity to develop a single-drug treatment against tuberculosis based on teixobactin rather than a treatment regime based on administering three different antibiotics.”

Test-tube studies, published in the journal Nature, showed that teixobactin was able to kill bacteria as quickly as the antibiotics vancomycin and oxacillin.

Scientists at the University of Bonn in Germany have shown that teixobactin works in a unique way by binding to the fatty lipids that form the building blocks used by bacteria to manufacture their cell walls.

“This binding site represents a particular Achilles heel for antibiotic attack and this may also explain why resistance to teixobactin was not detected,” said Tanya Schneider of Bonn University.

Professor Lewis said that the failure to detect any signs of resistance to teixobactin establishes a new paradigm in the development of antibiotics, which had assumed resistance will eventually occur.

“Bacteria develop resistance by mutations in their proteins. The targets of teixobactin are not proteins, they are polymer precursors of cell wall building blocks so there is really nothing to mutate,” Professor Lewis said.

“We’ve been operating under the dogma that the development of resistance is inevitable and we need to focus on introducing antibiotics faster than pathogens can acquire resistance,” he said.

“Teixobactin gives us an example of how we can develop an alternative strategy on developing compounds where resistance is not going to rapidly develop,” he added.

About 25,000 people a year in Europe alone already die from infections that are resistant to antibiotics and the World Health Organisation has described the rise of antibiotic-resistance as one of the most significant global risks facing modern medicine.

Professor Mark Woolhouse, Professor of Infectious Disease Epidemiology at the University of Edinburgh, said: “Any report of a new antibiotic is auspicious, but what most excites me about [this research] is the tantalising prospect that this discovery is just the tip of the iceberg... It may be that we will find more, perhaps many more, antibiotics using these latest techniques. We should certainly be trying – the antibiotic pipeline has been drying up for many years now; we need to open it up again, and develop alternatives to antibiotics at the same time, if we are to avert a public health disaster.”

But Dr Angelika Gründling, Reader in Molecular Microbiology at Imperial College London, said: “It’s important to bear in mind that the new antibiotic only works against certain types of bacteria – such as MRSA and streptococcus, and not on other multi-drug resistant pathogens such as E. coli... And of course the new antibiotic described in the paper has yet to be tested in humans. It is possible that it might not be as effective as hoped and there could be unforeseen side-effects that might limit its use.”

Mechanism of action

Teixobactin is an inhibitor of cell wall synthesis that acts primarily by binding to lipid II, a fatty molecule which is a precursor to peptidoglycan. Lipid II is also targeted by the antibiotic vancomycin. Binding of teixobactin to lipid precursors inhibits production of the peptidoglycan layer, leading to lysis of vulnerable bacteria.

Biosynthesis and Spectrum

Teixobactin is synthesized in Eleftheria terrae by nonribosomal peptide synthetases Txo1 and Txo2 (Encoded by genes txo1 and txo2). It is potent in-vitro against most gram positive bacteria including S. aureus, Enterococci, M tuberculosis Clostridium difficile, Bacillus anthracis and also in vivo methicillin-resistant aureus (MRSA), streptococcal pneumonia.

It also shows good activity against strains of E. Coli with a defective outer membrane permeability barrier. It is more robust against mutation of the target pathogens because of its unusual antibiotic mechanism of binding to less mutable fatty molecules rather than binding to relatively mutable proteins in the bacterial cell. 

Pharmacodynamic Properties

Teixobactin inhibits bacterial cell wall synthesis primarily acting by binding to lipid II-precursor to peptidoglycan and lipid III–precursor of cell wall teichoic acid leading to lysis of vulnerable bacteria. So there is excellent bactericidal activity. This is similar to the mechanism of action of Vancomycin.

Teixobactin forms a complex by binding to lipid I, II,and III by and incubating 2 nmol of each purified precursor with 2 to 4 n mole of Teixobactin for 30 min at room temperature. Teixobactin and control compounds like vancomycin/ lassomycin were incubated with human liver microsome at 37°c to determine their effect on five major Cytochrome p450s.

Pharmacokinetic Properties

The mean plasma concentration of Teixobactin after a single iv injection of 20mg per kg Teixobactin. Few Pharmacokinetic parameters are highlighted as initial.

Con (27.2ug/ml); AUC to last (57.8ug-hr/ml); T1/2 (4.7hr) Total Cl (6.9ml/hr); Total Cl (5.8ml/min/kg); Vol. of distribution (47ml) Vss (9.7ml); Last time point (24hr); Oral route is preferred than parenteral route.

Adverse drug events and clinical uses

a)      Mammalian cytotoxicity; Haemolytic activity; Complex formation of Teixobactin.

b) Life threatening blood and lung infections with staphylococcus aureus and streptococcus pneumoniae ;infections of heart, prostate, urinary tract and abdomen with enterococcus; Infections with vancomycin resistance enterococcus(VRE); infections with MRSA.