Timescales for pluton growth, magma-chamber formation and super-eruptions.

Generation of silicic magmas leads to emplacement of granite plutons, huge explosive volcanic eruptions and physical and chemical zoning of continental and arc crust1-7. Whereas timescales for silicic magma generation in the deep and middle crust are prolonged8, magma transfer into the upper crust followed by eruption is episodic and can be rapid9-12. Ages of inherited zircons and sanidines from four Miocene ignimbrites in the Central Andes indicate a gap of 4.6 Myr between initiation of pluton emplacement and onset of super-eruptions, with a 1-Myr cyclicity. We show that inherited zircons and sanidine crystals were stored at temperatures <470 °C in these plutons before incorporation in ignimbrite magmas. Our observations can be explained by silicic melt segregation in a middle-crustal hot zone with episodic melt ascent from an unstable layer at the top of the zone with a timescale governed by the rheology of the upper crust. After thermal incubation of growing plutons, large upper-crustal magma chambers can form in a few thousand years or less by dike transport from the hot-zone melt layer. Instability and disruption of earlier plutonic rock occurred in a few decades or less just before or during super-eruptions.

Corneal lipid deposition in Cuban tree frogs (Osteopilus septentrionalis) and its relationship to serum lipids: an experimental study.

To evaluate the association between corneal lipid infiltration (corneal arcus) and dietary cholesterol in Cuban tree frogs (Osteopilus septentrionalis), 47 wild-caught frogs were fed diets of either regular or high-cholesterol crickets containing 0.7% and 1.7% cholesterol dry matter, respectively. Serum total cholesterol and triglycerides were measured when the frogs were euthanized after 17 mo. In a subsample of frogs, serum lipoproteins were characterized using high-performance liquid chromatography. The first case of corneal lipid deposition occurred in a female frog after 13 mo on the high-cholesterol diet. In the subsequent 4 mo, 5/11 males and 11/35 females developed the disease. Four of these affected frogs were females on the regular diet. Frogs with corneal lipid deposition had elevated serum total cholesterol (27.3 +/- 19.8 mmol/L) and low-density lipoproteins (LDL, 17.8 +/- 18.9 mmol/L) compared with unaffected captive frogs (16.5 +/- 20.4 and 9.0 +/- 7.6 mmol/L, respectively). Corneal lipid deposition was more prevalent in frogs on the high-cholesterol diet, and this group had higher serum total cholesterol (34.1 +/- 15.2 mmol/L in females, 22.8 +/- 14.8 mmol/L in males) than did frogs on the diet of regular crickets (12.3 +/- 8.7 mmol/L in females, 10.4 +/- 3.1 mmol/L in males). Captive frogs on both diets had higher serum total cholesterol than did wild frogs (3.1 +/- 2.1 mmo/L in females, 5.3 +/- 2.6 mmo/L in males). This additional serum cholesterol was primarily carried on very low-density lipoproteins (VLDL) and LDL rather than high-density lipoproteins (HDL), as indicated by the significantly higher ratio of VLDL cholesterol and LDL cholesterol over HDL cholesterol in captive frogs compared with wild frogs. Elevation in this ratio was significantly higher in captive females than in captive males. There was no evidence that increased serum cholesterol in captive females was directly related to the process of vitellogenesis.

Effects of prostaglandin F2 alpha and leukotriene D4 on pupil size, intraocular pressure, and blood-aqueous barrier in dogs.

In each of 5 groups of dogs, 0.05 ml of 1 of the following solutions was injected into the anterior chamber of both eyes: phosphate-buffered saline solution, 0.001 microgram of prostaglandin F2 alpha (PGF2 alpha), 0.01 microgram of PGF2 alpha, 0.1 microgram of leukotriene D4 (LTD4), and 1 microgram of LTD4. A 10% solution of sodium fluorescein was injected IV (14 mg/kg of body weight) at the same time, and pupil size, intraocular pressure, and anterior chamber fluorescence were measured for 1 hour after injections. In a dose-dependent manner, PGF2 alpha was a potent miotic. A significant effect on intraocular pressure was not detected when the groups given PGF2 alpha were compared with the control group. When compared with LTD4, PGF2 alpha significantly (P less than 0.05) increased the breakdown of the blood-aqueous barrier, as evidenced by increased fluorescein leakage into the anterior chamber. Leukotriene D4 caused a decrease in pupil size only at 5 minutes, compared with that of the control group. Intraocular pressure was greater (but not significantly) in the group given 1 microgram of LTD4.

Inherited lysosomal storage disease in an English springer spaniel.

Alpha-L-fucosidosis was diagnosed in a 17-month-old English Springer Spaniel with a history of slow development and progressive visual impairment. Lymphocytes and mononuclear cells with vacuolated cytoplasm were seen in a blood smear and in CSF, respectively. A severe deficiency of alpha-L-fucosidase activities in plasma and leukocytes was determined. Histologic examination revealed vacuolation of neurons, macrophages, and epithelial cells in most organ tissues. Canine fucosidosis is a progressive and fatal lysosomal storage disease in English Springer Spaniels. Affected dogs develop a neurologic disorder characterized by progressive motor and mental deterioration. Visual impairment is an unusual primary sign in a dog with alpha-L-fucosidosis.

Use of phacofragmentation for cataract removal in horses: 12 cases (1985-1989).

The medical records of 12 horses that had cataracts removed by use of phacofragmentation were reviewed. Cataracts were removed from 16 eyes in horses ranging in age from 2 months to 15 years. Complications after surgery included corneal ulcers in 13 eyes, diffuse corneal edema in 5 eyes, and uncontrollable uveitis in 3 eyes. Follow-up information was obtained in all horses from 1 month to 3.5 years after surgery. Visual results were judged good by owners or veterinarians in 10 of the horses.

Hereditary deficiency of all vitamin K-dependent procoagulants and anticoagulants.

Hereditary combined deficiency of vitamin K-dependent factors is a rare entity. We report a 7-year-old girl of Arab origin with hereditary deficiency of the procoagulants factors II, VII, IX and X and the natural anticoagulants proteins C and S. The patient is the tenth offspring of a consanguinous marriage and presented at 6 weeks with spontaneous intracerebral haemorrhage. Symptoms improved following plasma infusion. A sibling died at 5 d from uncontrollable umbilical bleeding. Blood coagulation work-up at 6 years showed: factor II:C (activity) 12 U/dl, factor II:Ag (antigen) 40 U/dl; factor VII:C 12 U/dl; factor IX:C 36 U/dl, factor IX:Ag 57 U/dl; factor X:C 17 U/dl, factor X:Ag 54 U/dl; protein C activity 43 U/dl; protein C:Ag 45 U/dl; protein S:Ag 34 U/dl; levels of factors V:C and VIII:C were normal. Assays of coagulation factors in the parents and five of the siblings were within the normal range. Following acute infection and dilantin therapy procoagulant activity levels were reduced further and were partially increased after vitamin K infusion. Crossed immunoelectrophoresis of prothrombin in the presence of calcium lactate revealed a population of des-carboxyprothrombin. Serum vitamin K epoxide levels were undetectable. The data suggest that the defect in our patient stems from abnormal carboxylation of the vitamin K-dependent proteins and that the mode of inheritance is autosomal recessive.