Listening to food workers: Factors that impact proper health and hygiene practice in food service

Background

Foodborne disease is a significant problem worldwide. Research exploring sources of outbreaks indicates a pronounced role for food workers'' improper health and hygiene practice.

Objective

To investigate food workers'' perceptions of factors that impact proper food safety practice.

Method

Interviews with food service workers in Baltimore, MD, USA discussing food safety practices and factors that impact implementation in the workplace. A social ecological model organizes multiple levels of influence on health and hygiene behavior.

Results

Issues raised by interviewees include factors across the five levels of the social ecological model, and confirm findings from previous work. Interviews also reveal many factors not highlighted in prior work, including issues with food service policies and procedures, working conditions (e.g., pay and benefits), community resources, and state and federal policies.

Conclusion

Food safety interventions should adopt an ecological orientation that accounts for factors at multiple levels, including workers'' social and structural context, that impact food safety practice.     

The role of cumulative growth hormone exposure in determining mortality and morbidity in acromegaly: a single centre study

Purpose

Acromegaly has traditionally been associated with significant mortality and cardiovascular morbidity. The aim of this study was to assess the overall mortality and improvement in mortality and morbidity in acromegaly and correlate these with cumulative growth hormone exposure.

Methods

All patients treated for acromegaly at our centre until 2012 were analysed in this retrospective observational study. Baseline demographic details such as age at diagnoses, radiological features and pituitary status were obtained on these 167 patients. Cumulative GH levels (GHy) were calculated as a sum of average of GH readings in consecutive years. Mortality rates and development of new diabetes, hypertension and cardiovascular events (stroke, congestive cardiac failure and ischaemic heart disease) were assessed.

Results

The SMR for overall cohort was 1.6. There has been a significant improvement in SMR over the past two decades (SMR until 1992 2.5; SMR since 1992 1.0). Cumulative GH exposure was significantly high in patients who died (35.2 vs 24.1, p < 0.01) and in those with incident metabolic or vascular events during follow up (51.6 vs 24.4, p = 0.0001). The cardiovascular event rate of the ‘new’ cohort was significantly better than the ‘old’ cohort (8.0 vs. 29.1 %, p < 0.001).

Conclusion

There has been significant improvement in mortality and morbidity associated with acromegaly, in the setting of routine care in a specialized endocrine unit. Early and effective treatment to ‘control’ acromegaly could reduce GH exposure and hence vascular comorbidities.

     

Growth hormone and pituitary radiotherapy, but not serum insulin-like growth factor-I concentrations, predict excess mortality in patients with acromegaly

Increased mortality in patients with acromegaly has been confirmed in a number of retrospective studies, but causative factors and relationship to serum IGF-I remain uncertain. The West Midlands Pituitary database contains details of 419 patients (241 female) with acromegaly. Serum IGF-I data from the Regional Endocrine Laboratory were available for 360 patients (86%). At diagnosis, mean age was 47 yr (range, 12-84) and mean duration of follow-up was 13 yr (0.5-48). Sixty-one percent were treated by surgery and 39% by nonsurgical means. Radiotherapy was used alone or as adjuvant therapy in 50%. All patients were registered with the Office of National Statistics to obtain information on deaths. At the date of analysis (31 December 2001), 95 of the 419 patients had died (43 males), giving a standardized mortality ratio of 1.26 [confidence interval (CI), 1.03-1.54; P = 0.046]. After controlling for age and sex, data indicated that mortality was increased in subjects with posttreatment GH levels more than 2 micro g/liter, compared with those with levels less than 2 micro g/liter [ratio of mortality rates (RR), 1.55 (range, 0.97-2.50); P = 0.068]. By contrast, a much smaller increase was observed for subjects with elevated posttreatment IGF-I levels compared with those with normal levels [RR, 1.20 (range, 0.71-2.03); P = 0.50]. Treatment with radiotherapy was associated with increased mortality [RR, 1.67 (range, 1.09-2.56); P = 0.018], with cerebrovascular disease the predominant cause of death [standardized mortality ratio, 4.42 (range, 2.71-7.22); P = 0.005]. These results confirm the increased mortality in acromegaly and suggest that reduction of GH levels to less than 2 micro g/liter is beneficial in terms of improving long-term outcome. The sole use of IGF-I as a marker for effective treatment of acromegaly is not justified by this data. This study also highlights the potential deleterious effect of radiotherapy.     

Gonadotropin-releasing hormone is required for enhanced luteinizing hormone subunit gene expression in vivo

Pre- and postcastration changes in LH beta and common alpha mRNAs were correlated with pituitary and serum LH levels in two different species after abolition of pituitary stimulation by GnRH. A GnRH antagonist (GnRH-ANT) was used to block gonadotroph GnRH receptors in male rats, and a GnRH antiserum (GnRH-AS) was used to inhibit GnRH stimulation of female and male mouse and male rat pituitaries. The postcastration increases in LH beta and common alpha mRNA levels (2- and 3.5-fold, respectively) were abolished in male rats after 7 days of continuous GnRH-ANT infusion. The postcastration increases in LH beta and common alpha mRNA in female (1.9- and 2.2-fold respectively) and male mice (1.4- and 3.6-fold, respectively) were also prevented after daily sc injection of GnRH-AS, as were the rises in LH beta (3-fold) and common alpha (4-fold) in castrated male rats. The pituitary LH content (postgonadectomy) was no different from intact control levels in all experimental animals regardless of treatment, while the increase in serum LH concentration in rats (7- and 8-fold) and in female (4.8-fold) and male mice (9.8-fold) was prevented by both GnRH-ANT and GnRH-AS administration. In intact rats treated with GnRH-ANT the LH beta mRNA level decreased (57%) while the common alpha mRNA level was unaffected after 7 days. Neither pituitary nor serum LH levels were altered in intact rats or mice after appropriate treatments. We conclude that endogenous GnRH is required for the postcastration rise of both LH beta and common alpha-subunit mRNA levels in rats and mice.     

Glucose and alanine metabolism during bacterial infections in rats and rhesus monkeys

To investigate the effects of bacterial infection on glucose and alanine metabolism, a variety of studies were carried out in rat and monkey models. These included glucose turnover by a pulse-dose technique in infected rats; alanine and glucose production and utilization in control and septic monkeys; in vivo measurement of gluconeogenesis in rats, with and without an alanine load; the in vitro rate of glucose formation from various substrates by isolated liver perfusion and hepatic cells; and in vivo rates of oxidation of glucose labeled with ¹⁴C at the 1 or 6 carbon position. In rats, glucose turnover was markedly accelerated 24 hr after inoculation of either 10⁴ or 10⁷Streptococcus pneumoniae. Glucose utilization and production were also accelerated during illness and early recovery from a pneumococcal infection in monkeys. The rates of gluconeogenesis as measured by either a pulse technique in rats or continuous infusion of labeled alanine in monkey were significantly elevated during pneumococcal septicemia. During the agonal stages (10⁷) of the pneumococcal infection in rat, an alanine load resulted in a decreased rate of labeled glucose production and an increase in plasma glucose when compared to values of fasted control rats. However, early illness caused similar or increased rates of glucose production from alanine in vivo. Similar reduced rates of glucose formation were observed when the isolated livers or hepatocytes from rats during the agonal stages of infection were perfused with excess quantities of gluconeogenic substrates. Thus, in the rat, gluconeogenic capacity (ability to form glucose from excess substrates) appears to decrease only during the agonal stages of pneumococcal infection. During acute pneumococcal sepsis in the rhesus monkey, alanine production and utilization were significantly elevated and it was estimated that over 90% of the newly produced alanine was utilized for glucose synthesis. When arterial-venous differences were measured across the hindquarters, significantly more alanine was released, presumably from skeletal muscle of the septic monkey, compared to the recovery period or in the control groups. Thus, the increase in glucose synthesis in both rat and monkey appears to be correlated with substrate availability and kinetic rate, rather than gluconeogenic capacity of the liver. The major increase in glucose utilization during both S. pneumoniae and Francisella tularensis live vaccine strain (LVS) infections in rat was a progressive elevation in the rate of oxidation via the pentose phosphate shunt in the rat. Further, the rate of oxidation appeared to be correlated with the magnitude of the bacteremia, which is an indication of the severity of the infection. Therefore, since glucose oxidation is necessary for a number of metabolic processes of various cells (such as phagocytosis and RNA synthesis), the increased glucose production during pneumococcal sepsis in the rat or rhesus monkey may not represent functional wastage to remove the excess alanine produced in skeletal muscle but a necessary process in the host defense mechanism against infectious disease.     

Treatment of chronic mucocutaneous candidosis with ketoconazole: a study of 12 cases

Twelve patients with chronic mucocutaneous candidosis were treated orally with ketoconazole (doses, 200-400 mg daily) for a mean period of six months. Seven of the patients had one of the following abnormalities: congenital endocrinopathy syndrome, an autosomal recessive or autosomal dominant defect in which candidosis is not associated with endocrinopathy, or the malabsorption syndrome. All patients had fungal infections of the mouth, and 11 had onychomycosis. Two patients were also infected with dermatophytes. At the end of treatment, 10 patients were cured of oral infection, and 11 with nail infections showed significant improvement. Marked improvement of hand and foot infections was also recorded. Patients infected with dermatophyte fungi had the poorest responses to therapy. The mean (+/- SD) MIC for isolates of Candida albicans from eight patients was 0.95 (+/- 0.78) microgram/ml. Clinical and biochemical monitoring showed no toxicity, and no resistant fungi emerged during treatment. Results of this initial study of ketoconazole for treatment of severe and recalcitrant superficial infections indicate the need for further assessment of this drug, which appears to offer a simple, nontoxic, and effective treatment of fungal infections.     

Gonadotropin-releasing hormone agonist analog-induced steroidogenic lesion in the neonatal rat testis: evidence for direct gonadal action

In this study we sought to determine whether a GnRH agonist analog (GnRH-A) could influence steroidogenesis by a direct effect on the neonatal rat testis. Five-day-old male rats were given a single sc injection of hCG (600 IU/kg BW), GnRH-A [D-Ser(tBu)6]des-Gly10-GnRH N-ethylamide (4 micrograms/kg BW), or their combination. Testicular testosterone (T) was increased (3-fold) only 6 h post-GnRH-A treatment, whereas after hCG administration testicular T remained elevated (3 to 6-fold) for 48 h. Testicular progesterone (P) increased by 40% 6-72 h after hCG treatment, but was not raised after GnRH-A injection. In vitro T production by testes from control and GnRH-A-treated (injection 24 h earlier) animals was stimulated 5 to 8-fold by hCG (7.9 nM) or 8-bromo-cAMP (8-Br-cAMP; 1 mM). hCG and 8-Br-cAMP did not further stimulate T production from testes of animals treated with hCG in vivo 24 h earlier. While hCG and 8-Br-cAMP had only a small stimulatory effect (1.5 to 2-fold) on in vitro P production by testes from control or hCG-treated animals, their stimulation of P production from testes of GnRH-A-treated animals was dramatic (20 to 30-fold). In vitro P production from testes of animals receiving combined treatment with hCG and GnRH-A in vivo reached a high hCG-stimulated rate similar to that found after GnRH-A treatment alone; the unstimulated values were also considerably elevated (5-fold) compared to those of untreated animals. The ability of GnRH-A treatment to stimulate testicular P production in the presence of a high concentration of hCG strongly suggests a direct gonadal action of the peptide. The possibility of such action was corroborated by the finding of abundant GnRH receptors in the neonatal testis. These results indicate that the steroidogenic lesion seen in adult rat testis after gonadotropic stimulation (blockade of C21 steroid side-chain cleavage with compensatory accumulation of P) can be reproduced in neonatal rat testes by a direct action of GnRH-A, but not by hCG.     

Supplementation of islet culture medium with insulin may have a beneficial effect on islet secretory function

Recent reports suggest that apoptosis resulting from the disruption of the normal cell-matrix relationship (anoikis) during islet isolation could lead to a loss of islet tissue in culture. Insulin is known to have a role in cell growth and survival, and this study was undertaken to assess any beneficial effect on islets by supplementing the islet culture medium with insulin. Human and porcine islets were cultured in medium supplemented with 0, 10, 100, and 1,000 ng x mL(-1) insulin. Secretory function was assessed by perifusion at days 1 and 8. The results demonstrated a significant variation in stimulation index between isolations for human islets, but there was no effect relating to the concentration of insulin in the medium or time in culture. For porcine islets, there was a significant (p < 0.001) improvement in secretory function for islets cultured in 10 and 100 ng x mL(-1) insulin, relative to 0 and 1,000 ng x mL(-1) insulin. There was no interisolation variation or effect of time in culture. In conclusion, the secretory function of porcine islets benefited from the addition of 10 to 100 ng x mL(-1) insulin to the culture medium, but interisolation variation in human islet secretory function did not allow any specific effect of the insulin to be determined.