Audits and inspections are never enough: a critique to enhance food safety

Internal and external food safety audits are conducted to assess the safety and quality of food including on-farm production, manufacturing practices, sanitation, and hygiene. Some auditors are direct stakeholders that are employed by food establishments to conduct internal audits, while other auditors may represent the interests of a second party purchaser or a third-party auditing agency. Some buyers conduct their own audits or additional testing, while some buyers trust the results of third-party audits or inspections. Third-party auditors, however, use various food safety audit standards and most do not have a vested interest in the products being sold. Audits are conducted under a proprietary standard, while food safety inspections are generally conducted within a legal framework. There have been many foodborne illness outbreaks linked to food processors that have passed third-party audits and inspections, raising questions about the utility of both. Supporters argue third-party audits are a way to ensure food safety in an era of dwindling economic resources. Critics contend that while external audits and inspections can be a valuable tool to help ensure safe food, such activities represent only a snapshot in time. This paper identifies limitations of food safety inspections and audits and provides recommendations for strengthening the system, based on developing a strong food safety culture, including risk-based verification steps, throughout the food safety system

Isoaspartate, Carbamoyl phosphate synthase-1, and carbonic anhydrase-III as biomarkers of liver injury

We had previously shown that alcohol consumption can induce cellular isoaspartate protein damage via an impairment of the activity of protein isoaspartyl methyltransferase (PIMT), an enzyme that triggers repair of isoaspartate protein damage. To further investigate the mechanism of isoaspartate accumulation, hepatocytes cultured from control or 4-week ethanol-fed rats were incubated in vitro with tubercidin or adenosine. Both these agents, known to elevate intracellular S-adenosylhomocysteine levels, increased cellular isoaspartate damage over that recorded following ethanol consumption in vivo. Increased isoaspartate damage was attenuated by treatment with betaine. To characterize isoaspartate-damaged proteins that accumulate after ethanol administration, rat liver cytosolic proteins were methylated using exogenous PIMT and 3H-S- adenosylmethionine and proteins resolved by gel electrophoresis. Three major protein bands of ~75-80 kDa, ~95-100 kDa, and ~155-160 kDa were identified by autoradiography. Column chromatography used to enrich isoaspartate-damaged proteins indicated that damaged proteins from ethanol-fed rats were similar to those that accrued in the livers of PIMT knockout (KO) mice. Carbamoyl phosphate synthase-1 (CPS-1) was partially purified and identified as the ~160kDa protein target of PIMT in ethanol-fed rats and in PIMT KO mice. Analysis of the liver proteome of 4-week ethanol-fed rats and PIMT KO mice demonstrated elevated cytosolic CPS-1 and betaine homocysteine S-methyltransferase-1 when compared to their respective controls, and a significant reduction of carbonic anhydrase-III (CA-III) evident only in ethanol-fed rats. Ethanol feeding of rats for 8 weeks resulted in a larger (~2.3-fold) increase in CPS-1 levels compared to 4- week ethanol feeding indicating that CPS-1 accumulation correlated with the duration of ethanol consumption. Collectively, our results suggest that elevated isoaspartate and CPS-1, and reduced CA-III levels could serve as biomarkers of hepatocellular injury

Alcohol-related brain damage in humans

Chronic excessive alcohol intoxications evoke cumulative damage to tissues and organs. We examined prefrontal cortex (Brodmann’s area (BA) 9) from 20 human alcoholics and 20 age, gender, and postmortem delay matched control subjects. H & E staining and light microscopy of prefrontal cortex tissue revealed a reduction in the levels of cytoskeleton surrounding the nuclei of cortical and subcortical neurons, and a disruption of subcortical neuron patterning in alcoholic subjects. BA 9 tissue homogenisation and one dimensional polyacrylamide gel electrophoresis (PAGE) proteomics of cytosolic proteins identified dramatic reductions in the protein levels of spectrin β II, and α- and β-tubulins in alcoholics, and these were validated and quantitated by Western blotting. We detected a significant increase in α-tubulin acetylation in alcoholics, a non-significant increase in isoaspartate protein damage, but a significant increase in protein isoaspartyl methyltransferase protein levels, the enzyme that triggers isoaspartate damage repair in vivo. There was also a significant reduction in proteasome activity in alcoholics. One dimensional PAGE of membrane-enriched fractions detected a reduction in β-spectrin protein levels, and a significant increase in transmembranous α3 (catalytic) subunit of the Na+,K+-ATPase in alcoholic subjects. However, control subjects retained stable oligomeric forms of α-subunit that were diminished in alcoholics. In alcoholics, significant loss of cytosolic α- and β-tubulins were also seen in caudate nucleus, hippocampus and cerebellum, but to different levels, indicative of brain regional susceptibility to alcohol-related damage. Collectively, these protein changes provide a molecular basis for some of the neuronal and behavioural abnormalities attributed to alcoholics

What to consider when pseudohypoparathyroidism is ruled out: IPPSD and differential diagnosis

Background: Pseudohypoparathyroidism (PHP) is a rare disease whose phenotypic features are rather difficult to identify in some cases. Thus, although these patients may present with the Albright''s hereditary osteodystrophy (AHO) phenotype, which is characterized by small stature, obesity with a rounded face, subcutaneous ossifications, mental retardation and brachydactyly, its manifestations are somewhat variable. Indeed, some of them present with a complete phenotype, whereas others show only subtle manifestations. In addition, the features of the AHO phenotype are not specific to it and a similar phenotype is also commonly observed in other syndromes. Brachydactyly type E (BDE) is the most specific and objective feature of the AHO phenotype, and several genes have been associated with syndromic BDE in the past few years. Moreover, these syndromes have a skeletal and endocrinological phenotype that overlaps with AHO/PHP. In light of the above, we have developed an algorithm to aid in genetic testing of patients with clinical features of AHO but with no causative molecular defect at the GNAS locus. Starting with the feature of brachydactyly, this algorithm allows the differential diagnosis to be broadened and, with the addition of other clinical features, can guide genetic testing. Methods: We reviewed our series of patients (n = 23) with a clinical diagnosis of AHO and with brachydactyly type E or similar pattern, who were negative for GNAS anomalies, and classify them according to the diagnosis algorithm to finally propose and analyse the most probable gene(s) in each case. Results: A review of the clinical data for our series of patients, and subsequent analysis of the candidate gene(s), allowed detection of the underlying molecular defect in 12 out of 23 patients: five patients harboured a mutation in PRKAR1A, one in PDE4D, four in TRPS1 and two in PTHLH. Conclusions: This study confirmed that the screening of other genes implicated in syndromes with BDE and AHO or a similar phenotype is very helpful for establishing a correct genetic diagnosis for those patients who have been misdiagnosed with "AHO-like phenotype" with an unknown genetic cause, and also for better describing the characteristic and differential features of these less common syndromes

Failures in sprouts-related risk communication

Nutritional and perceived health benefits have contributed to the increasing popularity of raw sprouted seed products. In the past two decades, sprouted seeds have been a recurring food safety concern, with at least 55 documented foodborne outbreaks affecting more than 15,000 people. A compilation of selected publications was used to yield an analysis of the evolving safety and risk communication related to raw sprouts, including microbiological safety, efforts to improve production practices, and effectiveness of communication prior to, during, and after sprout-related outbreaks. Scientific investigation and media coverage of sprout-related outbreaks has led to improved production guidelines and public health enforcement actions, yet continued outbreaks call into question the effectiveness of risk management strategies and producer compliance. Raw sprouts remain a high-risk product and avoidance or thorough cooking are the only ways that consumers can reduce risk; even thorough cooking messages fail to acknowledge the risk of cross-contamination. Risk communication messages have been inconsistent over time with Canadian and U.S. governments finally aligning their messages in the past five years, telling consumers to avoid sprouts. Yet consumer and industry awareness of risk remains low. To minimize health risks linked to the consumption of sprout products, local and national public health agencies, restaurants, retailers and producers need validated, consistent and repeated risk messaging through a variety of sources

Evaluation of the endocannabinoid system in post-mortem human prefrontal cortex of alcoholic subjects

Trabajo presentado al "ECNP Workshop on Neuropsychopharmacology for Young Scientist in Europe" celebrado en Niza (Francia) del 4 al 7 de Marzo de 2010 y al "The 20th Annual Symposium on the Cannabinoids" celebrado en Suecia del 24 al 27 de julio de 2010.-- Trabajo publicado en la revista European Neuropsychopharmacology 20(Supl. 1): http://dx.doi.org/10.1016/S0924-977X(10)70011-0.-- et al.Peer reviewe