The Application of a Laboratory Induction Furnace to the Selective Smelting of a Montana Chromite Concentrate

The purpose of this experimental work was to determine with the utilization of a laboratory sized induction furnace a method whereby a high-iron Montana chromite concentrate could be successfully smelted to yield a product suitable for the subsequent production of standard ferrochrome.

Induction Furnace Smelting of Montana Chromite

In 1939 the total world production of crude chromite was approximately 1,167,000 metric tons; of which the United States produced only 3,672 metric tons and imported over 317,500 metric tons. Imports came mostly from the Philippine Islands, Cuba, South Africa, and Rhodesia.

Refining of Low Grade Zinc-Gold Precipitates

The purpose of this investigation was to ascertain if advantage could be taken of the copper in the precipitates as a collecting agent of the precious metals in the direct smelting furnace.The products produced to be low grade anode bullion and a slag low in precious metals, high in zinc and lead.

Flotation Concentration of a Montana Lead-Zinc-Silver-Ore

The Mike Horse mine, in the Huddelston mining district, is fifty-two miles northwest of Helena, Montana. The mine was discovered in 1898 by Joseph Heitmiller. There was only minor production from the date of discovery until 1915; the main drawback being lack of good road.

A Study of the Differential Seperation of Galena and Sphalerite

The smelting of complex lead ores is a difficult operation, especially when they contain considerable amounts of iron and zinc. When these ores are smelted, all of the zinc, which is valuable and well worth recovering, goes into the slag. With the advent of the flotation processes, and the ability of these processes to concentrate the lead and zinc minerals into separate products, the smelting of complex lead ores was to a great extent simplified.

Benefication of an Oxidized Lead Ore from the Franklin Mine Lewis and Clark County

This thesis is concerned with the beneficiation of an oxidized lead ore. Emphasis was placed upon concentration by flotation rather than by gravity methods, although some investigation was made with the Wilfley shaking table. The concentration of lead minerals received most consideration in the problem, but wherever possible attempts were made to increase the silver and gold concentration along with the lead.

Liraglutide once a day versus exenatide twice a day for type 2 diabetes: a 26-week randomised, parallel-group, multinational, open-label trial (LEAD-6)

BACKGROUND: Unlike most antihyperglycaemic drugs, glucagon-like peptide-1 (GLP-1) receptor agonists have a glucose-dependent action and promote weight loss. We compared the efficacy and safety of liraglutide, a human GLP-1 analogue, with exenatide, an exendin-based GLP-1 receptor agonist. METHODS: Adults with inadequately controlled type 2 diabetes on maximally tolerated doses of metformin, sulphonylurea, or both, were stratified by previous oral antidiabetic therapy and randomly assigned to receive additional liraglutide 1.8 mg once a day (n=233) or exenatide 10 microg twice a day (n=231) in a 26-week open-label, parallel-group, multinational (15 countries) study. The primary outcome was change in glycosylated haemoglobin (HbA(1c)). Efficacy analyses were by intention to treat. The trial is registered with ClinicalTrials.gov, number NCT00518882. FINDINGS: Mean baseline HbA(1c) for the study population was 8.2%. Liraglutide reduced mean HbA(1c) significantly more than did exenatide (-1.12% [SE 0.08] vs -0.79% [0.08]; estimated treatment difference -0.33; 95% CI -0.47 to -0.18; p<0.0001) and more patients achieved a HbA(1c) value of less than 7% (54%vs 43%, respectively; odds ratio 2.02; 95% CI 1.31 to 3.11; p=0.0015). Liraglutide reduced mean fasting plasma glucose more than did exenatide (-1.61 mmol/L [SE 0.20] vs -0.60 mmol/L [0.20]; estimated treatment difference -1.01 mmol/L; 95% CI -1.37 to -0.65; p<0.0001) but postprandial glucose control was less effective after breakfast and dinner. Both drugs promoted similar weight losses (liraglutide -3.24 kg vs exenatide -2.87 kg). Both drugs were well tolerated, but nausea was less persistent (estimated treatment rate ratio 0.448, p<0.0001) and minor hypoglycaemia less frequent with liraglutide than with exenatide (1.93 vs 2.60 events per patient per year; rate ratio 0.55; 95% CI 0.34 to 0.88; p=0.0131; 25.5%vs 33.6% had minor hypoglycaemia). Two patients taking both exenatide and a sulphonylurea had a major hypoglycaemic episode. INTERPRETATION: Liraglutide once a day provided significantly greater improvements in glycaemic control than did exenatide twice a day, and was generally better tolerated. The results suggest that liraglutide might be a treatment option for type 2 diabetes, especially when weight loss and risk of hypoglycaemia are major considerations.

Mutations in SDHD lead to autosomal recessive encephalomyopathy and isolated mitochondrial complex II deficiency

BACKGROUND Defects of the mitochondrial respiratory chain complex II (succinate dehydrogenase (SDH) complex) are extremely rare. Of the four nuclear encoded proteins composing complex II, only mutations in the 70 kDa flavoprotein (SDHA) and the recently identified complex II assembly factor (SDHAF1) have been found to be causative for mitochondrial respiratory chain diseases. Mutations in the other three subunits (SDHB, SDHC, SDHD) and the second assembly factor (SDHAF2) have so far only been associated with hereditary paragangliomas and phaeochromocytomas. Recessive germline mutations in SDHB have recently been associated with complex II deficiency and leukodystrophy in one patient. METHODS AND RESULTS We present the clinical and molecular investigations of the first patient with biochemical evidence of a severe isolated complex II deficiency due to compound heterozygous SDHD gene mutations. The patient presented with early progressive encephalomyopathy due to compound heterozygous p.E69 K and p.*164Lext*3 SDHD mutations. Native polyacrylamide gel electrophoresis and western blotting demonstrated an impaired complex II assembly. Complementation of a patient cell line additionally supported the pathogenicity of the novel identified mutations in SDHD. CONCLUSIONS This report describes the first case of isolated complex II deficiency due to recessive SDHD germline mutations. We therefore recommend screening for all SDH genes in isolated complex II deficiencies. It further emphasises the importance of appropriate genetic counselling to the family with regard to SDHD mutations and their role in tumorigenesis.