Discovery of Insulin by 
Banting & Best in 1921
Ever since the discovery by Oscar Minkowski (1858-1931) in 1889 that removal of pancreas caused diabetes mellitus. The race was on for the substance that can regulate blood glucose. The race was won by Banting in 1921, an orthopaedic surgeon turned researcher.
Frederick Grant Banting (1891-1941) 
& his co-worker Charles Herbert Best (1899-1978) & their dog Marjory. The stamp shows a page from Banting's research note-book which read 'Diabetus. Ligate pancreatic ducts of dog. Keep dogs alive till acini degenerate leaving islets. Try to isolate the internal secretion of these to relieve glycosurea. (The word diabetes was misspelt).
75th Anniversary of the Discovery 
of Insulin.(1921-1996) Banting 
and Best. Extraction from the islets 
which they called Isletin (insulin)
control the blood glucose of dogs 
rendered diabetic through removal 
of their pancreases. The first person
to receive Isletin was a 14 year old
boy Leonard Thompson with IDDM.
He lived for 13 years and died from
severe diabetic ketoacidosis.
50th Anniversary of the Discovery 
of Insulin. Laboratory equipment 
from Banting and Best's laboratory 
at the University of Toronto.
50th Anniversary of the Discovery 
of Insulin. Banting was awarded the
Nobel Prize in Medicine & Physiology
in 1924. He initially refused the 
prize as his co-worker Best was not 
included. He later accepted the prize 
money and shared it with Best. 
Two other people who contributed 
greatly in the discovery of insulin
were John Macleod (1879-1935) 
Head of Physiology at the University 
of Toronto and joined winner of the 
Nobel Prize and James Collip 
(1892-1965) a biochemist who help
to isolate insulins. However, the 
four fell out with each other at the 
end in the scramble to gain recognition.
50th Anniversary of the Discovery
of Insulin by Banting and Best.. 
Section 6 Management of New Vessels of the Disc 
(for a larger view of the retina, click the picture for a popu-up)
The use of lasers to treat diabetic retinopathy is an invasive and destructive 
procedure and it is essential to obtain informed consent for each new 
treatment course as for any surgical procedure.
6.1 Definition
NVD are defined as any abnormal collection of leaking vessels occurring on 
the optic disc or within one disc diameter of the optic disc. They may be 
distinguished from collateral vessels by the presence of dye leakage on 
fluorescent angiography.
6.2 Treatment
Treatment of NVD (and NVE, see section 7) is by pan-retinal laser photo-
coagulation (PRP). The risk of severe visual loss in high risk patients is 
reduced by 50% at 2 and 5 years by this therapy and by up to 70% in 
moderate risk patients. PRP should be given with fully informed consent 
(see below under counselling) and can be tailored to the nature fo the 
NVD in order to minimize effects on the visual field.
6.2.1 Early NVD
Newly developing flat ‘early’ new vessel usually respond well to a basic 
PRP comprising 15000-2000, 200-500 micron laser burns applied pre- and 
post-equatorially outside the vascular arcades (Figure 23a, b). Lesions 
should normally be applied leaving lesion-wide (ie 200-500 micron) 
intervals throughout the fundus to preserve visual field. Some practitioners 
prefer routinely to use a smaller spot size such as 200 micron but a 
correspondingly larger number of burns is required to achieve an effect. 
In addition, spot size will vary with the lens used (see above). Sufficient 
energy should be applied to achieve ‘blanching’ (ie. a greyish white lesion) 
of the retina without producing visible necrosis. The amount of energy 
required will vary for each patient and also at different retinal locations 
in the same eye depending on factors such as retinal thickness, oedema 
and degree of melanisation of the retinal pigment epithelium (the main 
energy absorbing tissue in this procedure).
Figure 23 NVD (long arrow) and NVE (short arrows) before a) and after b) treatment with panretinal photocoagulation. 
6.2.2 Established NVD
‘ Established’ new vessels are those which have developed into mature 
branching and/or arcade formations, but are still ‘flat’ ie they lie on the 
retinal surface, and have not led to haemorrhage. Established NVD may 
require a full PRP (>2000 laser burns) applied over more than one session. 
The precise number of burns will depend on the response to treatment 
which should be monitored at 2-3 weekly intervals.
6.2.3 Florid NVD
NVD in young adolescents may progress rapidly to extensive sheets of 
vessels occupying a wide region of the peripapillary retina (Figure 15). 
Such vessels require urgent, aggressive management which should 
comprise a full PRP applied in a single session if possible. Laser lesions 
should be appropriately ‘ heavy ‘ in florid retinopathy. 
Further laser should be applied at weekly intervals until regression of 
vessels is achieved. If the neovascularization cannot be controlled, 
vitrectomy with endolaser may be required (see below).
6.2.4 Stable NVD
NVD respond to PROP either by regressing completely (especially in 
older subjects and if treated early) or by ‘maturing’ into non-leaking 
smaller vascular formations which do not progress. These can be 
described as ‘ stable’ NVD which require observation and monitoring, 
if necessary with fluorescent angiography, but probably do not require 
further photocoagulation.
6.2.5 Non-responding NVD
In a proportion of patients, NVD fail to regress and/or mature into an 
inactive stable state. Inadequate laser therapy is a frequent cause, 
often due to poor patient compliance with the PRP procedure. This 
may be improved by performing the laser with local (retrobulbar) or 
general anaesthetic. In the latter case, the laser may be applied via 
the indirect ophthalmoscope with good effect and a larger burn size. 
Older photocoagulation systems such as Xenon arc may also be useful 
in treating wider confluent areas of retina. Even if fully treed as 
described above, certain patients still fail to respond. Re-treating 
treated areas of the retina may then be performed, usually however 
at the expense of the visual field. This will affect the patient’s 
fitness to drive and appropriate counselling is essential. Recourse to 
vitrectomy may be necessary if the neovascularization cannot be 
controlled (see below).
6.2.6 Forward NVD
Patient may present with untreated ‘forward’ NVD or the NVD may 
project into the vitreous cavity during the course of treatment as a 
result of posterior vitreous detachment (PVD). In the absence of 
vitreous haemorrhage forward NVD should be treated urgently with a 
full PRP with the proviso that an overly aggressive PRP may induce 
too rapid a regression of he forward vessels and cause vitreous 
bleeding. In such circumstances vitrectomy and intra-operative 
endolaser therapy is likely to be the treatment of choice (see below).
6.2.7 NVD with vitreous haemorrhage
Treatment of NVD in the presence of small collection of subhyaloid 
or intra-gel blood should be aimed at performing a basic PRP (2000 
laser burns, 500 micron) followed by careful application of further 
brief laser applications (200-300 laser burns per session) until 
regression of the NVD is achieved. However, this may not be 
successful and vitrectomy with endolaser may be required. 
Epidemiology Clinical features Risk factors Screening
Lasers and lenses. NVD,, NVE.. Maculopathy
Vitrectomy. Cataract Special problems Counselling
References.. AAO guidelines Atlas of Retinopathy Contact lenses
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