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Purpose: To assess the frequency of retinopathy and vision loss in patients with insulin-dependent diabetes mellitus and their relations to potentially modifiable risk factors. Methods: The authors conducted a multicenter cross-sectional study of diabetic complications and their risk factors using standardized methods of assessment. The sample was comprised of 3250 insulin-dependent diabetic patients (1668 men, 1582 women) aged 15 to 60 years with mean (standard deviation) duration of diabetes of 14.7 (9.3) years from 31 European diabetes centers; 2991 of the patients were eligible for retinal photography. Visual acuity was measured using the Snellen chart. Retinopathy was evaluated by retinal photographs (two fields per eye) graded at a central facility. Glycated hemoglobin (HbA,c), cholesterol, triglyceride, fibrinogen, von Willebrand factor, and urinary albumin excretion rate were assessed at a single location. Results: Corrected visual acuity was greater than or equal to 1.0 in both eyes in 69.7% of patients and less than or equal to 0.1 in the best eye in 2.3%. Factors significantly related to vision loss were age, duration of diabetes, glycated hemoglobin (HbA 1c ), and level of retinopathy. Mild nonproliferative retinopathy was found in 25.8% of the patients, moderate-severe nonproliferative retinopathy in 9.8% of the patients, and proliferative retinopathy in 10.6% of the patients. After adjustment for age, duration of diabetes, HbA 1c , and albumin excretion rate, significant risk factors for moderate-severe nonproliferative retinopathy were blood pressure and triglyceride, and risk factors for proliferative retinopathy were triglyceride and fibrinogen. Conclusion: Vision loss is a common complication of patients with insulin-dependent diabetes, with diabetic retinopathy an important cause. Apart from poor glycemic control, several other potentially modifiable risk factors for retinopathy may be important, including elevated blood pressure, plasma triglyceride, and fibrinogen. In view of the possible barriers to the full implementation of strict glycemic control in this type of diabetes, additional strategies for the prevention and slowing of progression of retinopathy should be investigated, such as blood pressure and lipid lowering therapies.

We report the first demonstration of a 40 MHz four-port all-fiber frequency shifter operating at a wavelength of 1.55 /spl mu/m. The device has a high-conversion efficiency and low-drive power consumption, and is made from standard telecommunications fiber.

The brains of six patients dying in diabetic ketoacidotic coma were examined histologically. Intravascular deposition of fibrin accompanied by ischaemic tissue damage was prominent in many vessels within the brain and other organs. Fibrinolytic and coagulation mechanisms were extensively studied in two patients before death and the results accorded with a major defect of these mechanisms. It is suggested that intravascular coagulation within the brain plays a major part in the production of coma in such patients and may well contribute to the mortality in this dangerous condition.

beta-Thromboglobulin levels and platelet-aggregate ratios were determined in blood-samples from healthy control subjects and from diabetic patients with and without microangiopathic complications. Patients with diabetic microangiopathy had significantly elevated beta-thromboglobulin levels and also reversible platelet aggregates. In nine newly treated diabetics blood-glucose control was associated with a significant fall in plasma beta-thromboglobulin. Since beta-thromboglobulin is a platelet-specific protein the results indicate that diabetic microangiopathy is associated with evidence of platelet activation and that this may be influenced by the degree of biochemical control.

Platelets from diabetics with microvascular complications were shown to have lowered aggregation thresholds to ADP, epinephrine and collagen. They also produced more malonyl dialdehyde (MDA) than normal controls. In eight diabetic subjects, administration of dipyridamole (100mg tds)raised platelet aggregation thresholds and increased cyclic AMP levels, presumably as a result of inhibition of phosphodiesterase activity. It also caused a slight reduction of MDA production. This latter effect could be due to the rise in cyclic AMP, although we have found an apparently direct inhibitory effect to dipyridamole on MDA and thromboxane B2 production by intact platelets and platelet microsomes in vitro. On withdrawal of the drug, platelet cyclic AMP and MDA levels and aggregation thresholds returned toward pre-treatment levels. The administration of aspirin (120) plus dipyridamole markedly inhibited platelet aggregation, particularly in response to arachidonic acid and collagen and strongly inhibited MDA production. However, the rise in platelet cyclic AMP levels produced by dipyridamole alone was not present when aspirin and dipyridamole were given together, Aspirin may influence platelet cyclic AMP metabolism directly or by inhibiting prostacyclin formation. Thus, under appropriate conditions, basal platelet cyclic AMP may provide an index of PGI2 production in vivo.

Abnormal platelet function has been demonstrated in 20 patients with diabetic peripheral neuropathy. The results are compared to those obtained from 19 matched diabetic patients with no clinical evidence of complications and 20 matched normal control subjects. Platelets from patients with diabetic neuropathy showed an increased sensitivity to the aggregating agents adenosine diphosphate and adrenaline. Spontaneous platelet aggregation was demonstrated in both groups of diabetic patients.

We report a case of intraspinal subdural hematoma following trauma - a rare entity - with a review of the literature. The location of the hematoma in the cervical spine as described in this report is even more uncommon and was reported only once before. The pathophysiology of this entity is discussed, and the myelographic features are emphasized to facilitate the preoperative diagnosis.

Peripheral neuropathy is a serious complication of Diabetes Mellitus, The precise pathogenesis is unknown. Histological examination of biopsy material obtained from patients with diabetic neuropathy has revealed intravascular fibrin in vessels supplying the sural nerve in 10 out of 25 cases. This finding prompted us to study platelet function in this same group of patients.Blood samples were obtained from fifteen patients. After preparation of platelet-rich plasma, platelet aggregation was measured following the addition of various concentrations of ADP, collagen and adrenaline. The responses were assessed photoelectrically in a temperature-controlled, constantly stirred, non-glass system. In addition the samples were tested for spontaneous platelet aggregation.Spontaneous platelet aggregation was detected in one-third of samples studied, but in none of the controls. Enhanced ADP-induced aggregation was observed in 53% of samples and enhanced adrenaline-induced aggregation in 50%. Similar results were obtained with collagen.The data supports the view that enhanced platelet aggregation and intravascular thrombosis is of considerable importance in the pathogenesis of diabetic neuropathy.

A variety of platelet function tests have been performed in a series of IS diahetics (B male, 7 female). All had clinical evidence of peripheral neuropathy and some also had diabetic retinopathy. The following were measured a) Platelet survival as determined using 51Cr-labelled platelets;b) Plasma β-thromboglobulin;c) Platelet aggregate ratio;d) Malonyldialdehyde(MDA) production following the addition of thrombin or arachidonic acid to platelet-rich plasma.The tests showed widespread evidence of altered platelet function. Six patients had a reduced platelet survival time (No correlation was found between any of the tests in individual patients.These studies confirm that there is a widespread alteration in platelet function in diabetics with complications, but suggest that no single test may be used as an acceptable screening procedure.

Summary Many of the diabetic neuropathic syndromes are characterized by painful symptoms with a sensation of burning and associated with troublesome hyperaesthesia. It is important to distinguish between the acute and chronic forms of peripheral sensory neuropathy; while the former carries an excellent prognosis for symptomatic improvement within one year, the latter may cause persistent symptoms for many years. In contrast to the acute form, in which symptoms are particularly severe but abnormal neurological signs are minimal, patchy stocking and glove sensory loss together with peripheral small muscle wasting are often present in chronic sensorimotor neuropathy. Peripheral polyneuropathies are more common in patients with poor metabolic control, although recent evidence implicates blood glucose flux as a possible contributory factor to neuropathic pain. It is possible that blood glucose flux or altered peripheral blood flow leads to increased spontaneous activity in nociceptive afferent fibres which are present in the axonal sprouts that characterize small fibre neuropathy. In the diagnosis of the neuropathies, exclusion of other aetiological factors is of paramount importance as there is no specific diagnostic test for diabetic nerve damage. If there is no symptomatic improvement after a period of stable and optimal metabolic control together with simple analgesics, then the tricyclic drugs should be regarded as first line therapy. The rapid effect of these drugs suggests a peripheral rather than central mode of action.

Motor conduction velocity (M.C.V.) was measured in the median and lateral popliteal nerves in thirty-nine newly diagnosed diabetics at diagnosis, during the first six weeks of treatment, and again after six months' treatment. The mean M.C.V. in the group at diagnosis was comparable with values previously reported in patients with established diabetes. The mean change in the M.C.V. during treatment was in the direction of improvement and was shown to differ significantly from zero. The mean M.C.V. after diabetic control was established was greater than at diagnosis, although still well below that for non-diabetic subjects. It is suggested that this improvement in electrical function indicates improvement in nerve structure and that early effective control of the diabetic state would lead to a reduction in the incidence of serious nerve damage.

The hyperglycemic effects of clopamide 30 mg/day, clorexolone 25 mg/day and hydrochlorothiazide 25 mg/day were compared in a double-blind trial. The subjects were 18 established diabetics with mild hypertension or diabetic retinopathy. In the 15 patients not receiving insulin, clopamide and clorexolone caused a considerable elevation of the mean blood glucose, but hydrochlorothiazide at the dose used had no significant effect. Clopamide, clorexolone and, to a lesser extent, hydrochlorothiazide lowered the plasma potassium, blood pressure and body weight, and raised the blood urea. In the three insulin-dependent patients the changes in blood glucose were small and not statistically significant, although the changes in most other variables were similar to those described for the remainder of the group. The clinical and metabolic implications of these findings are discussed.

Dogs, pigs, rabbits, guinea pigs, and mice were exposed to nuclear detonations in two open underground partitioned shelters. The shelters were of similar construction, and each was exposed to separate detonations. Each inner chamber filled through its own 'orifice'; thus four separate pressure environments were obtained. An aerodynamic mound was placed over the escape hatch of each structure to determine its effect on the pressure-curve shape inside the chamber. In one test a sieve plate bolted across the top of the mound was evaluated. Wind protective baffles of solid plate and of heavy wire screen were installed in the shelters to compare primary and tertiary blast effects on dogs. One dog was severely injured from tertiary blast effects associated with a maximal dynamic pressure (Q) of 10.5 psi, and one was undamaged with a maximal Q of 2 psi. Primary blast effects resulting from peak overpressures of 30.3, 25.5, 9.5, and 4.1 psi were minimal. The mortality was 19 per cent of the mice exposed to a peak pressure of 30.3 psi and 5 and 3 per cent of the guinea pigs and mice exposed to a peak pressure of 25.5 psi. Many of the rabbits, guinea pigs, and mice sustained slight lung hemorrhages at maximum pressures of 25.5 and 30.3 psi. Eardrum perforation data for all species, except mice, were recorded. Following shot 2, thermal effects were noted. Animals of the groups saved for observation have died from ionizing-radiation effects.

Publisher Summary This chapter presents a study of borderline diabetics. In the study, it was found that treatment of a group of mildly hyperglycemic diabetic individuals with tolbutamide appeared to protect them against the manifestations of arterial disease over a five-year period as compared to a closely similar group treated, double-blind, with an indistinguishable placebo. The 248 borderline diabetics involved in this study were newly detected in the Bedford population survey of 1962 and were defined as having capillary blood sugar values between 120 and 199 mg/100 ml 2 h after 50 gm of oral glucose. Shortly after their detection, the 248 subjects were randomly allocated to tolbutamide or placebo treatment groups, each of which was further randomly divided into approximately equal-sized carbohydrate-restricted and placebo diet subgroups.

Mice were used to assess biologically the inside environment of two designs of heavy concrete personnel structures subjected to nuclear blast. A sample consisted of 20 mice; one sample was used in each of l2 structures. Aside from two samples placed in unrealistic locations, there was no immediate mortality. By D+20 days two mice from the close-in shelters and seven from those further out had died. (auth)