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Biomedical subjects

J P Vaillancourt

Publications and source records attributed to J P Vaillancourt.

At least 19 recordsLinked to original sources
PubMed2000

A dark, firm dry-like condition in turkeys condemned for cyanosis.

A case-control study (n = 130) was conducted on toms condemned for cyanosis. Color (CIE L*a*b*), pH, and physical characteristics were measured on the Pectoralis major at slaughter and after 24 h. Meat from carcasses condemned for cyanosis had dark, firm, dry-like traits. It was darker and redder and showed higher water-holding capacity, lower cooking loss, and higher gel strength than did controls. Perimortem pH was negatively correlated with the lightness (L*) of meat at the time of slaughter (r = -0.58) and at 24 h postmortem (r = -0.64), positively correlated with water-holding capacity (r = 0.73) and gel strength (r = 0.43) and negatively correlated with cooking loss (r = -0.50). Ultimate pH was negatively correlated with lightness (L*) of meat at slaughter time (r = -0.62) and at 24 h postmortem (r = 0.79) was positively correlated with water-holding capacity (r = 0.87) and gel strength (r = 0.61) and negatively correlated with cooking loss (r = -0.52). Tests based on pH and L* of the P. major were also assessed; tests based on pH had a sensitivity in the range of 0.79 to 0.89 and specificity (Sp) of 0.60 to 0.94. Tests based on L* showed sensitivity of 0.75 to 0.92, and specificity of 0.79 to 0.97. The repeatability of measurements varied from good (L*: rho = 0.6) to excellent (pH: rho = 0.92). Overall, turkey breast condemned for cyanosis showed dark, firm, dry-like traits. Tests based on color and pH are described as a means of identifying turkeys condemned for cyanosis.

Animals↗
PubMed2000

Spatial distribution of cannibalism mortalities in commercial laying hens.

The distribution of cannibalism cases in a flock of 19,776 Babcock White Leghorns was monitored from 21 to 54 wk of age. The hens were kept in a single-floor house consisting of four banks of two-deck stair-step cages. Each of the 4,944 cages held four hens at a density of 152 cm(2) (60 inches(2)) per hen. Each cage was assigned a number from 1 to 4,944, and each dead bird was tagged according to its cage of origin. Dead birds were collected daily, kept in a freezer, and necropsied weekly. Farm personnel routinely transferred a live hen from an end cage to a cage where a mortality had occurred. The cause of death, age, cage number, and cage location were recorded for each dead hen. Of the 1,173 hens that died during the study period, 253 (21.6%) died from egg peritonitis, 184 (15.7%) from hypocalcemia, 167 (14.1%) from cannibalism, 164 (14%) from neoplastic disease, and the rest from various other causes. Cannibalism cases were analyzed statistically for clustering. Cannibalism was defined as death from tissue trauma and hemorrhage inflicted by cage mates. A spatial analysis showed that cannibalism is not a random event but one that occurs in clusters. The incidence of cannibalism was also found to be significantly higher on the top rows of cages as compared with the bottom rows.

Age Factors↗
PubMed2000

Risk factors for abattoir condemnation of turkey carcasses due to cyanosis in southern Ontario.

Cyanosis is a category of condemnation for poultry, as defined by Agriculture and Agrifood Canada. A retrospective study to examine the seasonal patterns and trends for turkey cyanosis condemnation was conducted for the years 1987 to 1995 with the use of condemnation records made available by a single abattoir in Ontario. Condemnation for cyanosis had a significant seasonal pattern, with major losses occurring in the colder months (October to March). A prospective longitudinal study was conducted during January to March and October to December 1996 in the same abattoir and the 75 turkey farms that contracted to process their birds through it and all the 913 truckloads of turkeys processed in these two 3-mo periods. The data from this prospective study were used for multivariate modeling of the effects of potential risk factors on the incidence of cyanosis. Risk factors (at P < or = 0.05) included bird type (broiler age turkeys, mature toms, and mature hens compared to toms and hens), ambient temperature (cold: -9.9 to 0.0 C and very cold: < or =-10.0 C compared to mild: >0.0 C), clean-out lot (the last shipped from a poultry house), shipping time > or =8 h, and emaciation (proportion of turkeys in the lot condemned for insufficient muscle mass). The crate density was a sparing factor, and an increase in turkey density during shipping resulted in a lower incidence of cyanosis. This study suggested that the number of turkeys condemned for cyanosis was associated with cold, shipping stress, and subclinical syndromes.

Abattoirs↗
PubMed2000

Roaster breast meat condemned for cyanosis: a dark firm dry-like condition?

A case-control study (n = 68) of roaster chickens condemned for cyanosis was conducted. Color (CIE L*a*b*) and pH were measured at slaughter, and after 24 h aging on ice, at four predetermined sites of the Pectoralis major. Cyanotic carcasses (dark) had a higher pH than controls at the time of slaughter and at 24 h postmortem (P < 0.01). Perimortem pH was significantly correlated with pH at 24 h postmortem (r = 0.64) and also was correlated with lightness (L*) perimortem and postmortem (24 h; r = -0.36 and -0.50, respectively). Perimortem pH was not correlated with meat redness (a*) at slaughter time and after 24 h. Ultimate pH and lightness at 24 h postmortem were also correlated. Tests based on pH, L*, and a* of the P. major were assessed: the sensitivity and specificity at various cut-off points were, respectively, pH(6.3) = 76.47 and 88.24%, L*(41) = 91.18 and 79.41%, and a*(3) = 76.47 and 97.06%. The repeatability (p) of pH and color measurements was excellent and ranged from 0.87 to 0.98. Breast meat from roasters condemned for cyanosis had dark, firm, and dry (DFD)-like traits, and accurate tests based on color and pH could be described as a means of identifying chickens condemned for cyanosis.

Animals↗
PubMed2000

Bacteriological and histological profile of turkeys condemned for cyanosis.

Canadian Food Inspection Agency (CFIA) has adopted the term cyanosis to describe a category of condemnation for poultry that is dark but has no other condemnable lesions. Two case-control studies (n = 30 pairs; n = 65 pairs) of 18-wk-old tom turkeys were conducted. A case was defined as a carcass condemned by the veterinary inspector for cyanosis, and a control carcass was one that passed inspection. Microbiological tests were conducted on samples of Pectoralis major and Gastrocnemius lacteralis. A modified Rappaport Vassiliadis medium was used for Salmonella, and a Petrifilm method was used to assess aerobic counts, coliform counts, and Escherichia coli. The Salmonella (qualitative) test was negative for all cases and controls, and there were no significant differences between the aerobic counts, coliform counts, and E. coli counts of case and control carcasses. Two pathologists conducted a blind histopathological study: there were no lesions compatible with those of septicemia-toxemia, as defined by CFIA and the USDA, nor any significant histopathological differences between the skin, P. major, G. lateralis, kidney, liver, spleen, small intestine, pancreas, lung, and heart of cases and controls. The inter-rater agreement between pathologists ranged from good to excellent (Kappa = 0.7 to 1.0). In the absence of important lesions and microbial contamination, carcasses with this color change alone should be suitable for human consumption.

Animals↗
PubMed2000

Poult enteritis complex.

Poult enteritis complex (PEC) is a general term that encompasses the infectious intestinal diseases of young turkeys. Some diseases, such as coronaviral enteritis and stunting syndrome, are relatively well characterised, while others, such as transmissible viral enteritis, poult growth depression and poult enteritis mortality syndrome, remain ill-defined. All forms of PEC are multifactorial, transmissible and infectious. Salient clinical features include stunting and poor feed utilisation that result from enteritis. In the more severe forms, runting, immune dysfunction and mortality are reported. Gross and microscopic lesions of enteritis are present in all forms but tend to be non-specific. Other lesions may be present, depending on the agents involved. The basic pathogenesis involves the following: a) alteration of the intestinal mucosa, generally by one or more viruses infecting enterocytes; b) inflammation; c) proliferation of secondary agents, usually bacteria. Non-infectious factors interplay with infectious agents to modulate the course and severity of disease. Diarrhoea is believed to be primarily osmotic because of maldigestion and malabsorption, but may also have a secretory component. Transmission is primarily faecal-oral. No public health significance is recognised or suspected. Prevention is based on eliminating the infectious agents from contaminated premises and preventing introduction into flocks. This is accomplished by an effective cleaning, disinfection and biosecurity programme. All-in/all-out production or separate brooding and finishing units are helpful. Control may require regional co-ordination among all companies producing turkeys, especially if the production is highly concentrated, and a quarantine programme for more severe forms of PEC. No vaccines or specific measures for controlling the organisms involved in PEC are available. Treatment is supportive for the viral component, while antibiotics, especially those with efficacy against Gram positive bacteria, may help to reduce the impact to bacterial infections. Evidence suggests that PEC occurs wherever turkeys are raised commercially, but this is not well documented and distribution of the various organisms that have been associated with PEC is largely unknown. The disease causes enormous economic loss, mostly from failure of the turkey to reach its genetic potential.

Animals↗
PubMed1999

Involvement of caspases in proteolytic cleavage of Alzheimer's amyloid-beta precursor protein and amyloidogenic A beta peptide formation.

The amyloid-beta precursor protein (APP) is directly and efficiently cleaved by caspases during apoptosis, resulting in elevated amyloid-beta (A beta) peptide formation. The predominant site of caspase-mediated proteolysis is within the cytoplasmic tail of APP, and cleavage at this site occurs in hippocampal neurons in vivo following acute excitotoxic or ischemic brain injury. Caspase-3 is the predominant caspase involved in APP cleavage, consistent with its marked elevation in dying neurons of Alzheimer's disease brains and colocalization of its APP cleavage product with A beta in senile plaques. Caspases thus appear to play a dual role in proteolytic processing of APP and the resulting propensity for A beta peptide formation, as well as in the ultimate apoptotic death of neurons in Alzheimer's disease.

Acute Disease↗
PubMed1999

Purification and catalytic properties of human caspase family members.

Members of the caspase family of cysteine proteases are known to be key mediators of mammalian inflammation and apoptosis. To better understand the catalytic properties of these enzymes, and to facilitate the identification of selective inhibitors, we have systematically purified and biochemically characterized ten homologues of human origin (caspases 1 - 10). The method used for production of most of these enzymes involves folding of active enzymes from their constituent subunits which are expressed separately in E. coli, followed by ion exchange chromatography. In cases where it was not possible to use this method (caspase-6 and -10), the enzymes were instead expressed as soluble proteins in E. coli, and partially purified by ion exchange chromatography. Based on the optimal tetrapeptide recognition motif for each enzyme, substrates with the general structure Ac-XEXD-AMC were used to develop continuous fluorometric assays. In some cases, enzymes with virtually identical tetrapeptide specificities have kcat/Km values for fluorogenic substrates that differ by more than 1000-fold. Using these assays, we have investigated the effects of a variety of environmental factors (e.g. pH, NaCl, Ca2+) on the activities of these enzymes. Some of these variables have a profound effect on the rate of catalysis, a finding that may have important biological implications.

Apoptosis↗
PubMed1998

Cell death attenuation by 'Usurpin', a mammalian DED-caspase homologue that precludes caspase-8 recruitment and activation by the CD-95 (Fas, APO-1) receptor complex.

Apoptotic cell suicide initiated by ligation of CD95 (Fas/APO-1) occurs through recruitment, oligomerization and autocatalytic activation of the cysteine protease, caspase-8 (MACH, FLICE, Mch5). An endogenous mammalian regulator of this process, named Usurpin, has been identified (aliases for Usurpin include CASH, Casper, CLARP, FLAME-1, FLIP, I-FLICE and MRIT). This protein is ubiquitously expressed and exists as at least three isoforms arising by alternative mRNA splicing. The Usurpin gene is comprised of 13 exons and is clustered within approximately 200 Kb with the caspase-8 and -10 genes on human chromosome 2q33-34. The Usurpin polypeptide has features in common with pro-caspase-8 and -10, including tandem 'death effector domains' on the N-terminus of a large subunit/small subunit caspase-like domain, but it lacks key residues that are necessary for caspase proteolytic activity, including the His and Cys which form the catalytic substrates diad, and residues that stabilize the P1 aspartic acid in substrates. Retro-mutation of these residues to functional caspase counterparts failed to restore proteolytic activity, indicating that other determinants also ensure the absence of catalytic potential. Usurpin heterodimerized with pro-caspase-8 in vitro and precluded pro-caspase-8 recruitment by the FADD/MORT1 adapter protein. Cell death induced by CD95 (Fas/APO-1) ligation was attenuated in cells transfected with Usurpin. In vivo, a Usurpin deficit was found in cardiac infarcts where TUNEL-positive myocytes and active caspase-3 expression were prominent following ischemia/reperfusion injury. In contrast, abundant Usurpin expression (and a caspase-3 deficit) occurred in surrounding unaffected cardiac tissue, suggesting reciprocal regulation of these pro- and anti-apoptotic molecules in vivo. Usurpin thus appears to be an endogenous modulator of apoptosis sensitivity in mammalian cells, including the susceptibility of cardiac myocytes to apoptotic death following ischemia/ reperfusion injury.

Alternative Splicing↗
PubMed1997

A combinatorial approach defines specificities of members of the caspase family and granzyme B. Functional relationships established for key mediators of apoptosis.

There is compelling evidence that members of the caspase (interleukin-1beta converting enzyme/CED-3) family of cysteine proteases and the cytotoxic lymphocyte-derived serine protease granzyme B play essential roles in mammalian apoptosis. Here we use a novel method employing a positional scanning substrate combinatorial library to rigorously define their individual specificities. The results divide these proteases into three distinct groups and suggest that several have redundant functions. The specificity of caspases 2, 3, and 7 and Caenorhabditis elegans CED-3 (DEXD) suggests that all of these enzymes function to incapacitate essential homeostatic pathways during the effector phase of apoptosis. In contrast, the optimal sequence for caspases 6, 8, and 9 and granzyme B ((I/L/V)EXD) resembles activation sites in effector caspase proenzymes, consistent with a role for these enzymes as upstream components in a proteolytic cascade that amplifies the death signal.

Amino Acid Sequence↗
PubMed1997

Intact cell evidence for the early synthesis, and subsequent late apopain-mediated suppression, of poly(ADP-ribose) during apoptosis.

Poly(ADP-ribose) polymerase (PARP), which is catalytically activated by DNA strand breaks, has been implicated in apoptosis, or programmed cell death. A protease (CPP32) responsible for the cleavage of PARP and necessary for apoptosis was recently purified and characterized. The coordinated sequence of events related to PARP activation and cleavage in apoptosis has now been examined in individual cells. Apoptosis was studied in a human osteosarcoma cell line that undergoes a slow (8 to 10 days), spontaneous, and reproducible death program in culture. Changes in the abundance of intact PARP, poly(ADP-ribose) (PAR), and a proteolytic cleavage product of PARP that contains the DNA-binding domain were examined during apoptosis in the context of individual, whole cells by immunofluorescence with specific antibodies. The synthesis of PAR from NAD increased early, within 2 days of cell plating for apoptosis, prior to the appearance of internucleosomal DNA cleavage and before the cells become irreversibly committed to apoptosis, since replating yields viable, nonapoptotic cells. Strong expression of full-length PARP was also detected, by immunofluorescence as well as by Western analysis, during this same time period. However, after approximately 4 days in culture, the abundance of both full-length PARP and PAR decreased markedly. After 6 days, a proteolytic cleavage product containing the DNA-binding domain of PARP was detected immunocytochemically and confirmed by Western analysis, both in the nuclei and in the cytoplasm of cells. A recombinant peptide spanning the DNA-binding domain of PARP was expressed, purified, and biotinylated, and was then used as a probe for DNA strand breaks. Fluorescence microscopy with this probe revealed extensive DNA fragmentation during the later stages of apoptosis. This is the first report, using individual, intact cells, demonstrating that poly(ADP-ribosyl)ation of nuclear proteins occurs prior to the commitment to apoptosis, that inactivation and cleavage of PARP begin shortly thereafter, and that very little PAR per se is present during the later stages of apoptosis, despite the presence of a very large number of DNA strand breaks. These results suggest a negative regulatory role for PARP during apoptosis, which in turn may reflect the requirement for adequate NAD and ATP during the later stages of programmed cell death.

Apoptosis↗
PubMed1997

Validation of a poultry biosecurity survey.

A questionnaire for farm managers was designed, to obtain information regarding biosecurity on Ontario commercial broiler chicken and turkey operations, and then pre-tested. The questions that could be validated were verifiable by seeing the facility, by using farm records or by interviewing technical personnel other than the survey respondent. The survey was validated using a convenience sample of 24 farms from two companies. For 15 questions with dichotomous responses, the sensitivity ranged from 16.7 to 100%; the specificity ranged from 0 to 100%. For example, fences and gates seen during the farm visit were not accurately reported on the survey (poor sensitivity). Chance-corrected agreement was low (kappa < 0.4) for 34 questions, fair to good (0.4 < kappa < 0.8) for 25 questions, and excellent (kappa > 0.8) for seven questions. The percent agreement for questions where only one of the possible options was observed on validation ranged from 60.9 to 100%. Five questions with continuous numeric variables were analysed. A difference was observed (P < 0.1) between the survey and validation data for three questions regarding the number of birds, the bird sources and the downtime between flocks. In spite of pre-testing, the lack of clear wording and the absence of definitions for technical terms appeared to reduce validity. Response bias seems to be an issue with biosecurity surveys. The value of validating questionnaires before their use in epidemiologic research is confirmed.

Animal Husbandry↗
PubMed1996

Cleavage of huntingtin by apopain, a proapoptotic cysteine protease, is modulated by the polyglutamine tract.

Apoptosis has recently been recognized as a mode of cell death in Huntington disease (HD). Apopain, a human counterpart of the nematode cysteine protease death-gene product, CED-3, has a key role in proteolytic events leading to apoptosis. Here we show that apoptotic extracts and apopain itself specifically cleave the HD gene product, huntingtin. The rate of cleavage increases with the length of the huntingtin polyglutamine tract, providing an explanation for the gain-of-function associated with CAG expansion. Our results show that huntingtin is cleaved by cysteine proteases and suggest that HD might be a disorder of inappropriate apoptosis.

Animals↗
PubMed1996

The three-dimensional structure of apopain/CPP32, a key mediator of apoptosis.

Cysteine proteases related to mammalian interleukin-1 beta converting enzyme (ICE) and to its Caenorhabditis elegans homologue, CED-3, play a critical role in the biochemical events that culminate in apoptosis. We have determined the three-dimensional structure of a complex of the human CED-3 homologue CPP32/apopain with a potent tetrapeptide-aldehyde inhibitor. The protein resembles ICE in overall structure, but its S4 subsite is strikingly different in size and chemical composition. These differences account for the variation in specificity between the ICE- and CED-3-related proteases and enable the design of specific inhibitors that can probe the physiological functions of the proteins and disease states with which they are associated.

Amino Acid Sequence↗
PubMed1995

Identification and inhibition of the ICE/CED-3 protease necessary for mammalian apoptosis.

The protease responsible for the cleavage of poly(ADP-ribose) polymerase and necessary for apoptosis has been purified and characterized. This enzyme, named apopain, is composed of two subunits of relative molecular mass (M(r)) 17K and 12K that are derived from a common proenzyme identified as CPP32. This proenzyme is related to interleukin-1 beta-converting enzyme (ICE) and CED-3, the product of a gene required for programmed cell death in Caenorhabditis elegans. A potent peptide aldehyde inhibitor has been developed and shown to prevent apoptotic events in vitro, suggesting that apopain/CPP32 is important for the initiation of apoptotic cell death.

Amino Acid Sequence↗