Prevalence of and risk factors for acute laminitis in horses treated with corticosteroids

A retrospective treated versus untreated study (study 1) and multicentre prospective cohort study (study 2) were undertaken to determine the prevalence of, and risk factors associated with, acute laminitis in horses treated with corticosteroids. All old treated with corticosteroids January–December 2014 (study 1) and January 2015–February 2017 (study 2) by two first opinion and referral hospitals in UK were included. Additionally, an untreated animal was identified for each treated animal (study one). Signalment, body condition (study 2 only), relevant medical history, primary condition, corticosteroid therapy prescribed and occurrence of acute laminitis during or within 14 days of cessation of corticosteroid treatment were recorded.For study 1, 205 cases and 205 controls were identified; two animals within each group (1 per cent) developed laminitis. In total, 1565 animals were included in study 2; laminitis period prevalence was 0.6 per cent (95 per cent CI 0.4 per cent to 1.2 per cent), with 10 cases in 1565 treated animals. There were significant associations between laminitis and breed (pony vs horse; p=0.01; univariable analysis only), the presence of a laminitis risk factor (history of laminitis or an underlying endocrinopathy; p<0.001; OR (95 per cent CI) 18.23 (5.05 to 65.87)) and body condition (overweight/obese vs not; p=0.04; OR (95 per cent CI) 4.0 (1.09 to 14.75)).

Research on preparation of phosphate-modified animal glue binder for foundry use

In this paper, three phosphates were used as modifiers to modify animal glue binder. The structural characteristics and thermal properties of animal glue binder treated with phosphates were studied by Fourier transform-infrared spectroscopy, gel permeation chromatography and derivative thermogravimetric analysis. The results showed that the modified animal glue binder had better sand tensile strength and lower viscosity than untreated animal glue binder. The best modification process was as follows: the optimal amount of sodium carbonate was 4 wt% to animal glue; the optimal weight ratio of the modifiers was sodium pyrophosphate : sodium tripolyphosphate : sodium hexametaphosphate : animal glue = 3 : 3 : 4 : 100, and the optimal reaction should be performed at 80°C for a reaction time of 120 min. A final tensile strength of approximately 3.20 MPa was achieved and the viscosity value was approximately 880 mPa s.

Acid-Base Relationships in the Blood of the Toad, Bufo Marinus: I. The Effects of Environmental CO2

An abrupt increase in ambient CO2, resulted in a marked respiratory acidosis which took place within 30 min. During this time there was a considerable reduction in the PCO2. difference between arterial blood and inspired gas caused by an increase in ventilations. Prolonged CO2 exposure (24 h) showed that there was some compensation for the acidosis in that plasma bicarbonate concentrations increased substantially. At the same time, however, the PCO2 of arterial blood always rose so that the net result was usually only a small increase in pH. Upon return to air, the blood was backtitrated along a buffer line elevated above and parallel to that seen during the initial response to hypercapnia. The fall in arterial blood PCO2, during the early stages of recovery often led to pH values higher than those seen in the untreated animal. After 48 h in air, recovery had gone further with PCO2 pH and [HCO3-] levels approaching but rarely reaching the pre-exposure values.

Whole body response of the peripheral circulation following hemorrhage in the rat

Changes in mean circulatory filling pressure (MCFP) after hemorrhage reflect the whole-body response of the peripheral circulation to restore the driving force for venous return. In this study, changes in MCFP were measured for 15 min following a rapid 8 ml/kg hemorrhage. Three groups of rats were studied: 1) conscious, untreated; 2) conscious, ganglion blocked; and 3) pentobarbital anesthetized. In all three groups, hemorrhage decreased MCFP approximately 2.6 mmHg immediately after hemorrhage. In the conscious untreated rat, MCFP recovered 1.3 mmHg in 15 min; 83% of this recovery was complete within 2 min, and over 50% was complete by 30 s posthemorrhage. With ganglionic blockade, recovery was slowed to about 70% of that in the conscious, untreated animal during the first 5 min after hemorrhage. MCFP recovery was substantially depressed by pentobarbital, averaging only 42% of that in the untreated animal 5 min after hemorrhage. The results demonstrate that peripheral changes can quickly restore nearly 50% of the MCFP decrease occurring immediately after mild hemorrhage and that about one-third of this response is mediated by the sympathetic nervous system. Pentobarbital anesthesia greatly inhibits recovery, although its repressive mechanism is not known.

INDUCTION OF OVULATION IN THE GUINEA-PIG

SUMMARY Ovulation has been induced in the cyclic guinea-pig at a time when the ovaries contain mature follicles, by a single injection of purified luteinizing hormone (LH), follicle-stimulating hormone or guinea-pig gonadotrophins from homogenates of female guinea-pig anterior pituitaries. An injection of any one of the substances given too early only caused follicular luteinization and the ova were retained, even with increased dosage. A single injection of LH in mid-dioestrus caused 'LH effects' on the follicles (destruction of the growing follicles), giving a histological picture similar to that which obtains at the time of ovulation in the untreated animal. Homogenates of anterior pituitaries taken from donor guinea-pigs 1–2 days before ovulation was due (but not at any other time in the cycle) when injected into recipients at middioestrus had similar effects on the follicles. Donor anterior pituitaries taken from guinea-pigs in which ovulation had been inhibited by daily injections of progesterone, caused ovulation in recipients with mature ovarian follicles or 'LH effects' in those in mid-dioestrus. It is suggested that in the guinea-pig there is a basal secretion of gonadotrophins during most of the cycle. A day or two before ovulation occurs and when the ovaries already contain ripe follicles, there is a marked increase in the synthesis of LH which is then released from the anterior pituitary gland and rupture of the follicles occurs.

Cadmium enhancement of proximal tubular sodium reabsorption

Stop-flow studies were performed to localize the site of cadmium action on renal sodium reabsorption. In the untreated dog undergoing mannitol diuresis, a maximal lumen:plasma sodium gradient was established across the proximal tubule during free flow with no further lowering of luminal concentration during ureteral occlusion, Naprox/NaFF = 1.02 ± .05. During occlusions after cadmium, sodium concentrations in proximally trapped fluid were reduced below free-flow values, Naprox/NaFF = 0.85 ± .08. This difference between treated and untreated animals was statistically significant ( P = < .001) and indicates that cadmium enhances proximal sodium reabsorption. Although distal sodium patterns were unaltered by cadmium, it was not possible to rule out a possible distal site since distal sodium reabsorption is already virtually complete during occlusion in the untreated animal. Cadmium, given intravenously as Cd115, was not excreted in the urine.

THE EFFECT OF INORGANIC SALTS ON THE CHEMICAL CHANGES IN THE BLOOD OF THE DOG AFTER OBSTRUCTION OF THE DUODENUM

The chemical changes in the blood of dogs treated with various inorganic salts after obstruction of the duodenum are reported. Two dogs treated with sodium chloride survived approximately six times as long as the average untreated animal, one living 22 days, the other 24 days. Ammonium chloride was found to produce an acidosis. The administration of potassium chloride, calcium chloride, and magnesium chloride did not prevent the usual rise in non-protein nitrogen and fall in chlorides, and the fatal outcome. Iodides seemingly hasten the toxic process. Sodium bromide appears to have an inhibitory action upon it, but much less than that of sodium chloride. Sodium sulfate, magnesium sulfate, sodium citrate, monosodium phosphate, and disodium phosphate failed to alter the course of the intoxication. Atropine and pilocarpine were without therapeutic value in preventing the changes characteristic of intestinal obstruction.