SPATIAL pH DISTRIBUTION DURING RIPENING OF CAMEMBERT CHEESE

2005 ◽  
Vol 48 (1) ◽  
pp. 279-285 ◽  
Author(s):  
S. Liu ◽  
V. M. Puri
2007 ◽  
Vol 43 (2-3) ◽  
pp. 425-435 ◽  
Author(s):  
Mitsuhisa Ichiyanagi ◽  
Yohei Sato ◽  
Koichi Hishida
Keyword(s):  

2017 ◽  
Vol 70 (2) ◽  
pp. 220-227 ◽  
Author(s):  
Qing Hong ◽  
Gang Wang ◽  
Qiuxiang Zhang ◽  
Fengwei Tian ◽  
Liu Xiao-Ming ◽  
...  

2017 ◽  
Vol 78 ◽  
pp. 60-63 ◽  
Author(s):  
J.A. Ramírez-Cano ◽  
L. Veleva ◽  
R.M. Souto ◽  
B.M. Fernández-Pérez

2017 ◽  
Vol 9 (2) ◽  
pp. 74-79 ◽  
Author(s):  
Jin Xiao ◽  
Anderson T Hara ◽  
Dongyeop Kim ◽  
Domenick T Zero ◽  
Hyun Koo ◽  
...  

2002 ◽  
Vol 68 (11) ◽  
pp. 5737-5740 ◽  
Author(s):  
Ariel Maoz ◽  
Ralf Mayr ◽  
Geraldine Bresolin ◽  
Klaus Neuhaus ◽  
Kevin P. Francis ◽  
...  

ABSTRACT Bioluminescent mutants of Yersinia enterocolitica were generated by transposon mutagenesis using a promoterless, complete lux operon (luxCDABE) derived from Photorhabdus luminescens, and their production of light in the cheese environment was monitored. Mutant B94, which had the lux cassette inserted into an open reading frame of unknown function was used for direct monitoring of Y. enterocolitica cells on cheeses stored at 10°C by quantifying bioluminescence using a photon-counting, intensified charge-coupled device camera. The detection limit on cheese was 200 CFU/cm2. Bioluminescence of the reporter mutant was significantly regulated by its environment (NaCl, temperature, and cheese), as well as by growth phase, via the promoter the lux operon had acquired upon transposition. At low temperatures, mutant B94 did not exhibit the often-reported decrease of photon emission in older cells. It was not necessary to include either antibiotics or aldehyde in the food matrix in order to gain quantitative, reproducible bioluminescence data. As far as we know, this is the first time a pathogen has been monitored in situ, in real time, in a “real-product” status, and at a low temperature.


1997 ◽  
Vol 35 (2) ◽  
pp. 195-197 ◽  
Author(s):  
P. Gilot ◽  
C. Hermans ◽  
M. Yde ◽  
J. Gigi ◽  
M. Janssens ◽  
...  

1987 ◽  
Vol 50 (5) ◽  
pp. 372-378 ◽  
Author(s):  
ELLIOT T. RYSER ◽  
ELMER H. MARTH

The ability of Listeria monocytogenes to survive the Camembert cheese-making process and grow during ripening of the cheese was examined. Pasteurized whole milk was inoculated to contain about 500 L. monocytogenes [strain Scott A, V7, California, (CA) or Ohio (OH)] CFU/ml and made into Camembert cheese according to standard procedures. All wheels of cheese were ripened at 6°C following 10 d of storage at 15–16°C to allow proper growth of Penicillium camemberti. Duplicate wedge (pie-shaped), surface and interior cheese samples were analyzed for numbers of L. monocytogenes by surface-plating appropriate dilutions made in Tryptose Broth (TB) on McBride Listeria Agar (MLA). Initial TB dilutions were stored at 3°C and surface-plated on MLA after 2, 4, 6 or 8 weeks if the organism was not quantitated in the original sample. Selected Listeria colonies from duplicate samples were confirmed biochemically. Results showed that numbers of Listeria in cheese increased 5- to 10-fold 24 h after its manufacture. Listeria counts for strains Scott A, CA and OH decreased to <10 to 100 CFU/g in all cheese samples taken during the first 18 d of ripening. In contrast, numbers of strain V7 remained unchanged during this period. All L. monocytogenes strains initiated growth in cheese after 18 d of ripening. Maximum Listeria counts of ca. 1 × 106 to 5 × 107 CFU/g were attained after 65 d of ripening. Generally, a 10- to 100-fold increase in numbers of Listeria occurred in wedge or surface as compared to interior cheese samples taken during the latter half of ripening. During this period, Listeria growth paralleled the increase in pH of the cheese during ripening.


2014 ◽  
Vol 11 (1) ◽  
pp. 943-974 ◽  
Author(s):  
V. M. C. Rérolle ◽  
M. Ribas-Ribas ◽  
V. Kitidis ◽  
I. Brown ◽  
D. C. E. Bakker ◽  
...  

Abstract. We present here a high resolution surface water pH dataset obtained in the Northwest European shelf seas in summer 2011. This is the first time that pH has been measured at such a high spatial resolution (10 measurements h–1) in this region. The aim of our paper is to investigate the carbonate chemistry dynamics of the surface water using pH and ancillary data. The main processes controlling the pH distribution along the ship's transect, and their relative importance, were determined using a statistical approach. The study highlights the impact of biological activity, temperature and riverine inputs on the carbonate chemistry dynamics of the shelf seas surface water. For this summer cruise, the biological activity formed the main control of the pH distribution along the cruise transect. Variations in chlorophyll and nutrients explained 29% of the pH variance along the full transect and as much as 68% in the northern part of the transect. In contrast, the temperature distribution explained ca. 50% of the pH variation in the Skagerrak region. Riverine inputs were evidenced by high dissolved organic carbon (DOC) levels in the Strait of Moyle (northern Irish Sea) and the southern North Sea with consequent remineralisation processes and a reduction in pH. The DOC distribution described 15% of the pH variance along the full transect. This study highlights the high spatial variability of the surface water pH in shelf seawaters where a range of processes simultaneously impacts the carbonate chemistry.


2011 ◽  
Vol 38 (9) ◽  
pp. 11804-11812 ◽  
Author(s):  
M. Sicard ◽  
C. Baudrit ◽  
M.N. Leclerc-Perlat ◽  
P.H. Wuillemin ◽  
N. Perrot

1994 ◽  
Vol 266 (2) ◽  
pp. R638-R645 ◽  
Author(s):  
R. A. Graham ◽  
A. H. Taylor ◽  
T. R. Brown

The true distribution of the pH in tissues can be determined from the in vivo 31P-nuclear magnetic resonance (NMR) spectrum by converting the parts per million (PPM) axis of the pH responsive resonance to pH using the Henderson-Hasselbalch equation. In addition, the intensity axis of the resonance must be divided by the derivative of the Henderson-Hasselbalch equation to correct for the nonlinear relationship between pH and PPM. This nonlinear relationship causes the apparent center of the resonance in PPM to be dependent not only on the center of the pH distribution but also on its width and distance from the pKa, where Ka is the association constant. Therefore, the pH determined from uncorrected spectra may be in significant error, particularly if the pH distribution is distant from the pKa and is broad. The method was applied to the isolated perfused Morris hepatoma 5123C to determine the distribution of intracellular pH (pHi) using resonances from two intracellular compounds. The two resonances did not report the same pHi unless the spectral data were properly corrected. The method should be of interest to anyone interested in pHi.


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