Biomedical subjects

L Hollis

Publications and source records attributed to L Hollis.

4 recordsLinked to original sources

PubMed2005

Microbiological survey of prepackaged pâté and ham in New Zealand.

AIMS: To gauge the effectiveness of pâté and ham manufacturers' management of the microbial safety and quality of their products. METHODS AND RESULTS: A survey of 60 batches of prepackaged pâté showed that 41.7% of the batches had aerobic plate counts (APC) exceeding 10(5) CFU g(-1), one of pâté sample contained a Bacillus cereus count of >5000 CFU g(-1) and another contained 1700 CFU g(-1) of Listeria monocytogenes. No other pathogens were isolated from any of the samples. The survey of prepackaged ham showed that only 1% (1/104) of the ham samples were positive for L. monocytogenes (50 CFU g(-1)). CONCLUSIONS: The presence of microbial hazards in these foods has generally declined since the early 1990s in New Zealand. Noncomplying APC levels may be due to an over-estimation of product shelf life or poor food handling practices during manufacture. SIGNIFICANCE AND IMPACT OF THE STUDY: Few of the samples tested contained pathogens at significant levels. The prevalences of L. monocytogenes in pâté and ham were low. The presence of 1700 CFU g(-1) of L. monocytogenes in a pâté sample indicates that occasionally, the population can be exposed to levels of L. monocytogenes above the zero tolerance level set in New Zealand.

Bacillus cereus↗

PubMed2001

Tissue-specific cadmium accumulation, metallothionein induction, and tissue zinc and copper levels during chronic sublethal cadmium exposure in juvenile rainbow trout.

Juvenile rainbow trout, on 3% of body weight daily ration, were exposed to 0 (control) or 3 microg/L Cd (as Cd(NO3)2*4H2O) in moderately hard (140 mg/L as CaCO3), alkaline (95 mg/L as CaCO3, pH 8.0) water for 30 days. Particular attention focused on Cd burden in tissues (gills, liver, kidney, and whole body) and induction of metallothionein (MT) in gills, liver, and kidney during chronic Cd exposure. Mortality in Cd-exposed fish was minimal ( approximately 10%), and no growth effects occurred over the 30-day exposure. Cd accumulated in a time-dependent fashion to 9 times (gills), 3 times (liver), 20 times (kidney), 2 times (carcass), and 2 times (whole body) control levels by 30 days; absolute concentrations were in the order kidney > gill > liver > whole body > carcass. Tissue (gills, liver, and kidney) Zn and Cu burdens were not altered by chronic exposure to 3 microg/L Cd. MT concentrations in all tissues increased over the 30 days of Cd exposure, but the increases were much less than those of Cd on a molar binding site basis. Absolute MT concentrations were in the order liver > kidney > gill, but relative increases were greatest in kidney (fourfold), followed by gills (twofold) and liver (1.3-fold). MT levels were sufficient to bind all Cd in gill, liver, and kidney under control conditions, and after chronic Cd exposure remained sufficient in liver and kidney, but not in gills. Total metal levels (Cd + Zn + Cu) greatly exceeded MT binding capacity in all tissues under all conditions.

Animals↗

PubMed2000

Effects of long term sublethal Cd exposure in rainbow trout during soft water exposure: implications for biotic ligand modelling.

The objectives of the study were to determine the physiological and toxicological effects of chronic cadmium exposure on juvenile rainbow trout in soft water. Particular attention focused on acclimation, on comparison to an earlier hard water study, and on whether a gill surface binding model, originally developed in dilute soft water, could be applied in this water quality to fish chronically exposed to Cd. Juvenile rainbow trout, on 3% of body weight daily ration, were exposed to 0 (control), 0.07, and 0.11 microg l(-1) Cd [as Cd(NO(3))(2).4H(2)O] in synthetic soft water (hardness=20 mg l(-1) as CaCO(3), alkalinity=15 mg l(-1) as CaCO(3), pH 7.2) for 30 days. Mortality was minimal for all treatments (up to 14% for 0.11 microg l(-1) Cd). No significant effects of chronic Cd exposure were seen in growth rate, swimming performance (stamina), routine O(2) consumption, or whole body/plasma ion levels. In contrast to the hard water study, no acclimation occurred in either exposure group in soft water, with no significant increases in 96-h LC(50) values. Cadmium accumulated in a time-dependent fashion to twice the control levels in the gills and only marginally in the liver by 30 days. No significant Cd accumulation occurred in the gall bladder or whole body. Cadmium uptake/turnover tests were run using radioactive 109Cd for acute (3 h) exposures. Saturation of the gills occurred for control fish but not for Cd-exposed fish when exposed to up to 36 microg l(-1) Cd for 3 h. Cd-exposed trout accumulated less 'new' Cd in their gills compared to controls and they internalized less 109Cd than control fish. This effect of lowered Cd uptake by the gills of acclimated trout was earlier seen for the fish acclimated to 10 microg l(-1) Cd in hard water. The affinity of the gill for Cd was greater in hard water (logK(Cd-gill)=7.6) than in soft water (logK(Cd-gill)=7.3) but the number of binding sites (B(max)=0.20 microg g(-1) gill) was similar in both media. In addition, there was a shift in affinity of the gill for Cd (i.e. lowered logK(Cd-gill)) and increased B(max) with chronic Cd exposure in both soft water and hard water. We conclude that the present gill modelling approach (i.e. acute gill surface binding model or Biotic Ligand Model) does work for soft and hard water exposures but there are complications when applying the model to fish chronically exposed to cadmium.

Animals↗

PubMed1999

Menière's disease.

Menière's disease is an idiopathic condition classically described as a triad of vertigo, deafness and tinnitus. A wide differential diagnosis exists, but acoustic neuroma must be actively excluded. Various medical and surgical treatment options are available, although two-thirds of patients spontaneously resolve with time.

Humans↗