Deterioration of the flavor of sterilized concentrated milk (SCM) is recognized as the principal limiting factor to commercial acceptance of this product. Although a number of volatile compounds have been identified in SCM, quantitative information on these compounds is lacking. It is therefore difficult to ascertain the significance of these compounds. The purpose of this investigation was to determine the identity of additional flavor compounds of stored SCM and to determine the concentrations of the major flavor compounds. Vacuum steam distillation was utilized to recover volatile flavor compounds from samples of SCM. The distillates were extracted with ethyl ether, and components of the ethereal flavor concentrates were separated by gas-liquid chromatography (GLC). Major components whose identity was unknown were collected from the GLC effluent, and were analyzed by capillary column GLC and mass spectrometry. A system for transferring trapped components directly onto a capillary GLC column was developed. 2-Furfural, which had not previously been identified in SCM, and 2-furfurol, which had not been identified as a component of any stored milk product, were identified in stored SCM. Commercial samples of SCM were placed in controlled storage, and subjected to flavor panel evaluation and a number of quantitative determinations at selected intervals of storage. The concentration of the odd-numbered n-methyl ketones, C₃-C₁₁, and of o-aminoacetophenone were determined by measuring the absorbance of their respective 2, 4-dinitrophenylhydrazone derivatives. The concentration of 2-furfurol was determined by a gas entrainment, on-column trapping GLC technique. Acid degree values were obtained by titration of SCM milk fat. Hydroxymethylfurfural (HMF) values were determined by measuring the absorbance of the HMF thiobarbituric acid reaction product. The methyl ketones and o-aminoacetophenone were found to exceed their flavor threshold concentrations after 13 weeks storage of SCM at 27°C. The concentration of 2-furfurol exceeded its threshold concentration after 26 weeks at 27°C, but not after 13 weeks. Acid degree values increased slowly, but did not reach significant levels through 26 weeks at 27°C. Hydroxymethylfurfural values increased slowly through the first 13 weeks at 27°C storage, followed by a marked increase during the second 13 weeks. Heat degradation of thiamine was studied as a possible source of volatile flavor compounds. Heating of thiamine solutions in phosphate buffer at pH 6.7 resulted in the production of volatile components of potential flavor significance. The identity of these components was studied by gas entrainment, on-column trapping GLC, collection of components, and capillary column GLC in conjunction with mass spectrometry. The system developed for the transfer of trapped components directly onto the capillary GLC column was utilized. Hydrogen sulfide, 2-methyl furan, 2-methyl thiophene and a compound which appeared to be a dihydro-2-methyl thiophene were identified as volatile heat degradation products of thiamine. / Graduation date: 1968

Thesis (M.S.)--Ohio State University, 1963. / Include bibliographical references (leaves 97-115). Available online via OhioLINK's ETD Center

No description available.

No description available.

The control of milk protein production was investigated utilising two different approaches. The first model is one of intravenous infusion of atropine. Atropine, which decreases milk protein yield, has been theorised to act either by decreasing blood somatotropin (ST) concentration or by decreasing blood amino acid (AA) concentration. Thus, the first experiment was designed to test which mechanism, or both, is responsible for the effects on milk protein yield. Five lactating dairy cows were assigned to the following treatments which were administered intravenously: Saline (CONT), atropine (ATR), ATR + ST, ATR + AAs, and ATR + ST + AAs. Atropine treatment failed to decrease plasma ST concentration but did decrease plasma alpha-amino nitrogen concentration. Atropine treatment decreased milk protein yield but neither ST, AAs, nor ST + AAs were able to maintain milk protein yield at the CONT level when infused with ATR. It is clear that the treatments tested are not directly responsible for the decrease in milk protein yield due to ATR. Therefore, neither ST, AAs, nor ST + AAs appear to have direct control of milk protein production. Plasma insulin (INS) concentration was decreased and plasma IGF-I concentration was not decreased by ATR treatment. Insulin, therefore, presents itself as a candidate for direct control over milk protein synthesis. The second model is one of monitoring endocrine response to abomasal infusion of AAs mimicking the profile of milk protein with selective deletion of certain AAs. Six lactating dairy cows were subjected to the following treatments: Saline (negative control, NC), AAs (positive control, PC), PC minus methionine (PC-Met), PC minus lysine (PC-Lys), PC minus histidine (PC-His), and PC minus the branched-chain AAs (PC-BCAAs). All endocrine factors studied (ST, INS, glucagon & IGF-I) were affected by treatment. Plasma IGF-I concentration responded similarly, except for the PC-Met treatment, to milk protein yield (Weekes and Cant, 200

Milk, preheated at 82°C for 30 minutes, was heated to 146°C for four seconds (UHT-treated) and cooled to 5°C in a tubular heat exchanger. Immediately after heat treatment, 20 gallons of heated milk were vacuum distilled at 30°C in a semi-continuous, reduced pressure glass apparatus. Twenty gallons of non-heated milk were distilled in a similar manner to serve as a control. Continuous liquid-liquid ethyl ether extractions were employed to recover the compounds from the aqueous distillates. Gas chromatography, mass spectrometry, infrared spectrophotometry and odor confirmation were used to characterize the compounds in the flavor concentrates. A technique for collecting and transferring packed column gas chromatographic fractions to capillary columns for mass spectral analysis was developed. The following compounds were identified in UHT-treated milk (the underlined compounds appeared to result from the heat treatment): the C₃, ₄, ₅, ₇, ₈, ₉, ₁₀, ₁₁, ₁₃ n-methyl ketones, the C₈, ₁₀, ₁₂ delta-lactones, acetaldehyde, hexanal, benzaldehyde, furfural, phenylactaldehyde, vanillin, the C₆, ₈, ₁₀ n-alkanoic acids, ethanol, oct-1-en-3-ol, n-heptanol, 2-butoxyethanol, diacetyl, maltol, acetophenone, ethyl acetate, benzothiazole, toluene, naphthalene, a dichlorobenzene, a trichlorobenzene, methyl iodide, benzonitrile and chloroform. The following compounds were identified in non-heated milk: C₃, ₄, ₅, ₇, ₉ n-methyl ketones, C₁₀, ₁₂ delta-lactones, hexanal, benzaldehyde, C₆, ₈, ₁₀ n-alkanoic acids, ethanol, diacetyl, ethyl acetate, methyl palmitate, diethyl phthalate, a dichlorobenzene, a trichlorobenze and methyl iodide. The concentration of diacetyl in UHT-treated and non-heated milk was determined by a modified gas entrainment, on-column trapping GLC technique. The amount of diacetyl in non-heated milk was 3 ppb while the amount in the UHT-treated was 38 ppb. The diacetyl concentration of UHT-treated milk decreased approximately 40% over 16 days storage at 4°C. The average flavor threshold for diacetyl in milk was found to be 12 ppb. It seems therefore that the UHT-treatment increased the diacetyl concentration from a subthreshold level to above the average flavor threshold. It is suggested that diacetyl contributes to the "rich", "heated" note in the flavor of heated milk. / Graduation date: 1968

Milk protein content of cows in subtropical Queensland declines from the beginning of winter to the end summer and is a repeatable consistent observation across years. The genesis of such an event is hypothesised to lie in the nutritional and environmental changes that occur over this period with a change in forage type from the temperate species to the tropical species, a change in cereal grain supplementation and a reduction in intake associated with heat stress causing a change in the nutritional supply to the animal. A series of experiments examined the effect of high levels of ammonia absorption on milk production and milk components in dairy cows. The experiments used extensive, grazing trials with supplements of urea to increase ammonia absorption, and intensive, infusion of ammonia into cows indoors. Feeding urea in the supplement of cows grazing ryegrass increased milk protein significantly by 0.05 percentage units but had no effect on milk volume. Infusing ammonia intra-venously reduced milk volume (~ 20%) and milk protein content (<0.1 percentage units). The primary finding of these experiments was that infusion of high ammonia levels into dairy cows will depress milk protein production and content. However, the levels of ammonia absorption experienced under usual strip grazing conditions in Queensland over winter are not high enough to affect milk protein production and content. The effect of altering substrate supply and pattern associated with the shift in feed supply from winter to summer was examined by infusing different amino acid patterns and acetate into cows by a close arterial infusion method. Infusate was delivered to the external iliac artery, allowing the mammary gland first pass use of the nutrients. Supplying amino acids by infusion increased milk protein yield 18.7 vs 19.7 g/h (5.3 %) for infused half of the udder. Milk protein yield was increased more (19.2 vs 20.2 g/h for infused half of the udder) by infusion of a milk amino acid profile compared to a microbial amino acid profile. Infusing acetate has no effect on milk protein yield but decreased milk yield for infused half of the udder (560 vs 510 g/h). It may be concluded, that under the practical levels of crude protein and ammonia supply which arise from different agronomic practices (N fertiliser) and grazing management (stage of growth, strip grazing), that any practical increase in ammonia supply per se to the liver does not explain the depression in milk protein percentage seen in Queensland dairy herds.

Thesis (M.Sc.(Agric.))--University of Western Australia, 2005.

Thesis (M.P.H.)--University of Michigan, 1946.

Thesis (M.S.P.H.)--University of Michigan, 1941.