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Review | Open | Published: 29 July 2016
Screening for coeliac disease in adult patients with type 1 diabetes mellitus: myths, facts and controversy
Sjoerd F. Bakker1,
Maarten E. Tushuizen1,
Boudewina M. E. von Blomberg2,
Hetty J. Bontkes2,
Chris J. Mulder1 &
Suat Simsek3,4
This review aims at summarizing the present knowledge on the clinical consequences of concomitant coeliac disease (CD) in adult patients with type 1 diabetes mellitus (T1DM). The cause of the increased prevalence of CD in T1DM patients is a combination of genetic and environmental factors. Current screening guidelines for CD in adult T1DM patients are not uniform. Based on the current evidence of effects of CD on bone mineral density, diabetic complications, quality of life, morbidity and mortality in patients with T1DM, we advise periodic screening for CD in adult T1DM patients to prevent delay in CD diagnosis and subsequent CD and/or T1DM related complications.
Coeliac disease (CD) is a permanent intolerance to ingested gluten resulting in immune mediated inflammatory damage to the small intestinal mucosa and a subsequent malabsorption syndrome [1]. Diagnosis of CD requires duodenal biopsy when the patient is on a gluten-containing diet and for the vast majority of adult patients also positive serology [2]. CD is one of the commonest lifelong disorders encountered in Western countries with a prevalence of about 0.6 % in the general population [3] and is, in particular in genetically susceptible individuals, associated with other autoimmune disorders including type 1 diabetes mellitus (T1DM) and autoimmune thyroiditis [4]. T1DM is characterized by T-cell mediated destruction of the insulin-producing β-cells in the pancreas leading to hyperglycaemia and diabetic ketoacidosis [5]. Diabetes is diagnosed based on 1) plasma glucose criteria, either the fasting plasma glucose (FPG) or the 2-h plasma glucose (2-h PG) value after a 75-g oral glucose tolerance test (OGTT) or 2) on a glycated haemoglobin (HbA1c) value of >6.5 % [6]. Long term diabetic complications consist of micro- and macrovascular disease, which account for the major morbidity and mortality associated with T1DM [7]. Up to one-third of patients with T1DM have thyroid antibodies, and half of these patients may progress to clinical autoimmune thyroid disease [8]. The need for annual screening for thyroid disease in T1DM patients has therefore been recommended.
The over all prevalence of CD in T1DM patients is about 6 % [9]. The association between CD and T1DM was first noted over 40 years ago in children [10]. Therefore, screening in paediatric T1DM patients is advocated. However, international paediatric consensus based guidelines differ in the need and frequency of screening for CD [11]. Some recommend an annual screening interval by testing antibodies against tissue transglutaminase 2 (TG2A), others advice to perform these tests in the presence of typical CD symptoms only [11]. However, despite the high prevalence of CD in T1DM patients there is no consensus on screening adult T1DM patients for CD.
In this review it is discussed whether screening for CD should be performed in adult T1DM patients and at which interval. For this purpose, the current literature was screened with respect to the clinical features of patients with both diseases as compared to patients with T1DM alone.
Association between CD and T1DM
T1DM and CD are auto-immune, inflammatory diseases for which the major genetic contribution arises from the major histocompatibility complex [12]. These so-called HLA-DQ heterodimers enable the presentation of peptides that are derived from otherwise innocuous self- or non-self antigens (proteins from insulin producing beta cells in T1DM, gliadins in CD) and activate pathogenic effector T-cells [13]. Besides the genetic overlap in the major histocompatibility complex, genome wide association studies (GWAS) in these two diseases have revealed a large number of well validated, non-HLA genetic risk loci providing an opportunity to explore the possibility of overlapping susceptibility between them [12].
Thus, genetic overlap exists between CD and T1DM consisting of both HLA and non-HLA genes [14–16]. Both disorders are associated with the major histocompatibility complex (MHC) class 2 antigen DQ encoded by the alleles DQA1*05 with DQB1*02 (DQ2.5) and DQA1*03 with DQB1*03:02 (DQ8) [1, 17].
In patients with CD, individuals who are HLA-DQ 2.5 homozygous have a greater risk of developing CD and the gluten specific T-cell response is more vigorous when gluten peptides are presented by antigen presenting cells homozygous for HLA-DQ 2.5 [18, 19]. In European Caucasian populations, more than 90 % of CD patients carry the HLA-DQ 2.5 heterodimer and the majority of CD patients who do not carry this HLA-DQ 2.5 heterodimer are HLA-DQ8 or HLA-DQ2.2 positive [20].
The main determinant of risk of developing T1DM is HLA-DQ8 and to a lesser extent HLA-DQ 2.5 [21, 22]. In a recent study, we compared the frequency of HLA-DQ haplotypes between 2472 T1DM patients versus 483 T1DM + CD patients [16]. In patients with T1DM, the HLA-DQ 2.5 haplotype showed a significant association and provided the highest risk for developing double autoimmunity (OR = 1.44, p-value = 0.0003, Table 1). As expected, the absence of the haplotypes HLA-DQ 2.5, DQ8 and DQ 2.2 (which is classified as "other" which is present in about 25 % of T1DM patients), showed the strongest protection (OR = 0.66, p = 0.0001, Table 1). Therefore, an HLA-DQ 2.5 negative T1DM patient does not require monitoring for CD.
Table 1 Haplotype and genotype HLA association and frequency comparison between double autoimmunity versus type 1 diabetes-only [16]
In addition to the overlap between T1DM and CD in HLA genes, it was revealed that non-HLA genes overlap as well [12, 16]. CTLA-4 and IL2RA loci are more strongly associated with double autoimmunity than with either T1DM or CD alone [16]. The combination of HLA and non-HLA variants might improve risk prediction for potential CD [23].
Several environmental factors have been investigated as precipitating factors for the development of T1DM or CD. A popular theory, based on possible molecular mimicry, is the association between autoimmune diseases and viral infections. Prime viral candidates that have been shown to cause precipitation to T1DM are enteroviruses, more specifically Coxsackie viruses [24]. Moreover, rotavirus infection increases the risk for developing T1DM and an association between rotavirus and increased risk for CD has been described as well [25, 26]. Furthermore, an altered composition of bacteria in the gut, altered gut permeability and intestinal inflammation seem to be factors that contribute to the development of T1DM [27]. Exposure to cereals has been described as a risk factor for the development of both T1DM and CD related autoantibodies. However, these studies show conflicting results [28–30].
Demographic characteristics
Many studies have investigated the prevalence of CD in paediatric and adult T1DM patients by different serological screening methods (gliadin, anti endomysium (EMA), anti tissue transglutaminase (TG2A) and anti reticulin antibodies). The prevalence of CD in T1DM patients (children and/or adults) is reported to vary between 0.8 % and 16.4 % with a mean prevalence of 6 % [4, 9, 31]. A large meta-analysis identified 27 studies, which included in total 26 605 individuals with T1DM [9]. Seventeen studies were performed in Europe, 4 in North America, 1 in South America, 1 in Australia, 3 in the Middle East and 1 in India (Fig. 1) [9]. A remarkable high prevalence of CD in T1DM patients is seen in studies performed in Algeria (16.4 %), India (11.1 %) and Saudi Arabia (11.3 %) [32–34]. The relatively high frequency of HLA-DQ 2.5 in the Middle East and India possibly contributes to the high prevalence of CD in T1DM [35]. Furthermore, these countries have a per capita wheat consumption that ranks among the highest in the world [35]. This high prevalence still needs to be confirmed in additional studies. Data from East-Asian and African T1DM cohorts and CD screening are lacking in current literature.
Mean prevalence of screen detected coeliac disease (CD) in children and adults with type 1 diabetes mellitus (T1DM) around the world. Mean prevalence is calculated from studies with at least 100 patients with T1DM [9]. N indicates the number of screening studies performed on each continent
The clinical presentation of CD in T1DM patients resembles that in non-T1DM patients and consists of gastrointestinal complaints (diarrhoea, constipation, vomiting, abdominal distension, anorexia) or extra-intestinal complaints such as growth failure, anaemia, decreased bone mass or osteoporosis, and dental enamel defects [4]. However, CD patients might also be asymptomatic and may have subtle complaints indicative of CD and may only be recognized in retrospect following the benefits of a GFD [36]. Previous studies have reported that 45–60 % of patients with T1DM and CD did not have any complaints of CD indicating a diagnostic challenge [37, 38].
Furthermore, gastrointestinal complaints are common in T1DM patients and a broad differential diagnosis exists for these patients (Table 2) [39, 40]. Furthermore, the fact that a large part of patients presents only with mild symptoms or seem to be asymptomatic provides difficulties for detecting CD [41]. Often, a reduced health is only recognized retrospectively, following the benefits conferred to a GFD [36].
Table 2 Differential diagnosis of gastrointestinal complaints in T1DM patients [39, 40, 105, 106]
It has been demonstrated that the risk of CD in T1DM patients is associated with age of onset of T1DM. Children with age of onset of T1DM younger than 4 years are at higher risk to develop CD than those with older age of onset [42]. Regarding clinical practice, we observed two peaks in the age of CD diagnosis in T1DM patients: around 10 and 45 years of age [41]. T1DM diagnosis precedes CD diagnosis in about 90 % of patients and females with T1DM have a higher risk of the additional diagnosis of CD than males [41, 42].
A new syndrome of gluten intolerance, non coeliac gluten sensitivity (NCGS), has been described. NCGS can be diagnosed in those patients with gluten intolerance who do not develop antibodies that are typical neither of CD nor of wheat allergy and who do not suffer from lesions in the duodenal mucosa [43]. Although disease characteristics of NCGS are overlapping with irritable bowel syndrome (IBS), a recent study observed that an associated autoimmune disease was present in 14 % of patients with NCGS, which was mainly autoimmune thyroiditis and sporadically T1DM [44].
Adherence to a GFD
Nutrition therapy is an important issue in the management of T1DM and the cornerstone of treatment in patients with CD [6, 45].
In T1DM, dietary interventions aim to maintain blood glucose, blood pressure, lipid levels and body mass index in the normal range [46]. A GFD together with an insulin therapy integrated into an individual's dietary and physical activity pattern imposes practical limitations and leads to restrictions in the lifestyle of a child or adolescent. Therefore, it may not be surprising that non adherence to a GFD in T1DM patients with CD is more common than in CD patients [47, 48]. Another problem that arises is the availability of gluten free food. In 5 different US states it was found to be significantly less available than food containing gluten [49]. The increased cost of GFD products may have an impact on compliance in T1DM patients with CD as well [49]. Therefore, we advise that patients with both conditions are guided by a skilled dietitian.
Clinical consequences of CD in adult patients with T1DM
So far, studies addressing the consequences of CD in adult T1DM patients differ in methodology, study size and prospective/retrospective design. Therefore, these results are difficult to compare and interpret. An overview of these results is given in Table 3.
Table 3 Clinical consequences of coeliac disease (CD) in adult Type 1 Diabetes Mellitus (T1DM) patients as compared to T1DM without CD
Glycaemic control
In adult patients with T1DM, no significant change of HbA1c levels was found, when comparing before CD diagnosis, at CD diagnosis and after treatment of CD by a GFD [50, 51]. This data is confirmed in a recent population based cohort study which found that having a diagnosis of CD does not influence the risk of hospital admission due to hypoglycaemia, keto-acidosis or coma in T1DM patients [52].
Lipid profile
Undetected CD in the general population is associated with lower cholesterol levels, which is thought to contribute to a favourable cardiovascular risk profile in untreated CD patients [53]. Accordingly, lower levels of cholesterol and triglycerides were found in newly detected, untreated CD patients with T1DM [54]. The assumed mechanism that may contribute to the lower cholesterol levels in undetected CD patients is malabsorption.
Microvascular complications
Intensive insulin therapy to normalize blood glucose levels effectively delays the onset and slows the progression of microvascular complications including diabetic retinopathy, nephropathy and neuropathy in T1DM patients [55–57]. Several studies investigated the influence of (newly diagnosed) CD with or without treatment by a GFD on long term diabetic complications and found CD to be either protective [51, 54, 58] or aggravating [59–61]. A recent large nationwide study in Sweden revealed that the duration of CD is important for the eventual effect [60]. They showed that individuals with T1DM and CD were at a lower risk of diabetic retinopathy in the first 5 years after CD diagnosis (adjusted hazard ratio (HR) 0.57 [95 % CI 0.36–0.91]), followed by a neutral risk in years 5 to <10 years (1.03 [0.68–1.57]). With longer follow-up, coexisting CD was a risk factor for diabetic retinopathy (10 to <15 years of follow-up, adjusted HR 2.83 [95 % CI 1.95–4.11]; ≥15 years of follow-up, 3.01 [1.43–6.32]) [60]. They ascribe the protective effect in the first 5 years to lower cholesterol levels and lower body mass index (BMI). However, this study lacks individual-based information on GFD adherence.
In a study of our group we found less diabetic retinopathy in a T1DM population with a mean CD duration of 3 years+ treatment by GFD compared to T1DM patients without CD [51]. Also, a previous study by Pitocco et al. showed more subclinical atherosclerosis in T1DM patients with a mean duration of treated CD of 9.9 years [61]. These studies suggest that a short duration of CD is protective and a longer duration of CD may aggravate diabetic complications [51, 60].
CD is associated with a higher risk of end-stage renal disease (ESRD) with a Hazard Ratio (HR) for ESRD of 2.87 (95 % CI 2.22 to 3.71, p < 0.001) [62]. The cumulative prevalence of end-stage renal disease in T1DM patients without CD, is 2.2 % at 20 years and 7.7 % at 30 years [63]. Interestingly, in T1DM patients with CD it was found that non-adherence to a GFD was associated with early elevation of albumin excretion in urine, a recognized factor for diabetic nephropathy [64]. Skovbjerg et al. found that there was a higher prevalence of CD in T1DM patients with nephropathy (2.6 %) than in T1DM patients without nephropathy (1 %) [65]. A recent study found a positive association between longstanding CD in T1DM patients and chronic renal disease in T1DM [66]. For chronic renal disease, this excess risk was present after more than 10 years of CD (HR 2.03, 95 % CI 1.08, 3.79) [66]. However, data about GFD adherence was lacking. These studies suggest that concomitant CD in T1DM patients might lead to more nephropathy in case of longstanding CD, in particular in case of poor adherence to a GFD [64]. The underlying mechanisms need, however, to be elucidated.
Bone mineral density
Decreased bone mineral density (BMD) is observed both in T1DM patients [67] and in CD patients [68]. In the latter group of patients, this is especially related to the intestinal malabsorption of vitamin D, necessary for healthy bone metabolism [68]. Reports have shown that bone mineral density is lower in paediatric T1DM patients with undiagnosed CD than in T1DM patients without CD [69, 70]. As expected, also in adults with both T1DM and active CD, a decreased BMD was found, but whether CD or T1DM was the cause remains unclear [71]. A study by Sategna-Guidetti showed that treatment by a GFD results in an improvement of lumbar spine BMD in adults with CD [72].
In summary, BMD in T1DM + CD patients is generally decreased and follow-up of BMD with possible treatment is warranted. Besides maintaining a GFD, data is scarce whether calcium and vitamin D supplementation in CD patients is mandatory [68]. Lifestyle changes as regular exercise and smoking cessation should be advised, and in the case of osteoporosis, calcium, vitamin D and bisphosphonates should be prescribed [68].
Both T1DM and CD are chronic illnesses which influence the quality of life (QOL) since the treatments are burdensome and the complications can be debilitating and life threatening. T1DM patients have a diminished QOL which is partly caused by the development of vascular complications [73]. The lower QOL in CD patients is reported especially in the social aspects of life and in those with symptoms, women being mostly affected [74]. In adult T1DM patients with both T1DM and treated CD, we described a compromised QOL particularly in women and both social functioning and general health perception was affected [75]. This is of importance since patients with T1DM are at increased risk of depression [76]. The additional diagnosis of CD further increases the risk of depression, and this should be taken into account in the clinical support of these patients [77].
Comorbidity and mortality
T1DM is, beside CD, associated with autoimmune thyroid diseases (Hashimoto's or Graves' disease) (AIT), autoimmune gastritis, Addison's disease, and vitiligo [8]. The presence of a third autoimmune disease in T1DM + CD patients is frequently found. A study by Kaspers et al. found a higher incidence of AIT in patients with T1DM and CD (6.3 %) when compared to those with CD alone (2.3 %) [78]. Our clinical practice study in adults revealed that 28 % of T1DM + CD patients were diagnosed with a third autoimmune disease, mainly autoimmune thyroiditis (22 %) [79].
A small group of patients with CD fail to improve clinically and histologically upon elimination of dietary gluten and this complication is referred to as refractory coeliac disease (RCD) [80]. RCD imposes a serious risk of developing enteropathy-associated T-cell lymphoma (EATL). The prevalence of RCD and EATL in the general population is very rare and studies investigating the risk of developing RCD or malignancy in T1DM + CD patients are currently lacking [81].
The question whether CD influences the mortality in T1DM patients was recently investigated in Sweden [82]. These authors described that having a CD diagnosis for more than 15 years was associated with a 2.8-fold increased risk of death in individuals with T1DM [82]. They hypothesized that the excess mortality was caused by persistent low grade inflammation due to CD or poor adherence to a GFD while using insulin therapy.
Rationale for screening for CD in adult T1DM patients
CD fulfills many of the WHO criteria for screening in patients with T1DM but not all of them [83]. CD is common and well defined, screening tests are simple + safe + accurate, screening seems to be culturally acceptable, treatment is available and clinical detection of CD can be difficult. However, studies are lacking whether screening for CD in T1DM patients is cost effective and it is currently unknown whether screen detected asymptomatic CD patients benefit from starting with a GFD. The latter will be investigated by the CD-DIET study [84] which is designed as a prospective controlled trial in which asymptomatic screen detected CD patients will be treated with or without a GFD. The results of the efficacy and safety of a GFD in patients with T1DM with asymptomatic CD will add significant data to the discussion about screening for CD in T1DM patients [84].
Consequently, there is still no consensus on screening adult patients with T1DM for CD. International guidelines for adult CD and T1DM differ in their recommendations for screening of CD in T1DM patients [2, 6, 85–91] (Table 4). At present, a case-finding approach in adult T1DM patients is most acceptable, ethically and financially [2, 92]. However, a recent study in the United States and Canada underscores the need for an uniform screening program. This study revealed a high variability in testing for CD in T1DM patients together with an inconsistency of management of CD [93]. In addition, we have recently reported that approximately 20 % of patients with T1DM and CD reported to have had CD related complaints for at least 5 years before CD diagnosis was made [79]. The long term consequences of a diagnostic delay are currently unknown. The high prevalence of several complications as reported in Table 3 in T1DM + CD patients, together with improvement of BMD after start of a GFD provides a strong rationale for an uniform screening program together with careful monitoring. Further, a recent randomized study showed that screen-detected and apparently asymptomatic EmA-positive patients at risk for CD benefit from a GFD as measured by extensive clinical, serologic, and histologic parameters [94]. Hypothetically, this data might be extrapolated to asymptomatic CD in T1DM patients. Another argument for screening is the fact that the incidence of T1DM and CD is rising over time [95, 96].
Table 4 Clinical recommendations for screening of CD in T1DM patients in adult CD and T1DM guidelines
We propose the following screening algorithm (Fig. 2) for CD in adult T1DM patients. CD should be diagnosed by serology and duodenal biopsy with the patient on a gluten-containing diet [2]. Serology is by TG2A and if patients are IgA deficient, IgG-TG2A can be used. Villous atrophy (Marsh IIIa- IIIc) is required for diagnosis of CD [2]. Due to the high sensitivity and specificity of TG2A, this test is used for screening in T1DM patients [97]. In case of IgA deficient individuals, or in patients with high probability of CD, IgG TG2A should be tested as 2 % of CD patients are IgA deficient [2]. As T1DM patients might have transient elevations of TG2A, a confirmatory small intestinal biopsy is recommended [98, 99]. In case of a biopsy with Marsh I-II, a serological repetition in 5 year is recommended. Further, another differential diagnosis for intraepithelial lymphocytosis should be considered (e.g. Giardia, olmesartan induced, small intestinal bacterial overgrowth). So far, only retrospective data is available and prospective studies are needed to determine a screening interval for CD in T1DM patients. As proposed by DeMelo et al. [100], we suggest to repeat TG2A testing every 5 years in case of negative serology. A recent systematic review found that most cases of CD are diagnosed within 5 years of T1D diagnosis and they advise screening at T1D diagnosis and within 2 and 5 years thereafter [101]. Only the Australian Diabetes Society recommends screening for CD after 5 years of T1DM diagnosis (Table 4). As studies are lacking investigating the screening frequency in T1DM patients, we advocate continuing screening every 5 years for CD in T1DM patients. In the presence of CD a clinical work-up should be performed to evaluate and possibly treat bone mineral density and vitamin deficiencies (Fig. 2). Based on current data, this screening algorithm is not applicable to all countries as studies about prevalence of CD in T1DM patients are lacking from several countries (Fig. 1).
Proposed algorithm for the screening and follow-up of coeliac disease (CD) in asymptomatic patients with type 1 diabetes mellitus (T1DM). DXA dual X-ray absorptiometry, GFD gluten free diet, GDS gastroduodenoscopy, TG2A tissue transglutaminase 2 antibodies. 1 IgA TG2A should be evaluated first, in IgA deficient individuals or in patients with high probability of CD IgG TG2A should be performed
HLA-DQ typing
The European Society for Paediatric Gastroenterology, Hepatology and Nutrition (ESPGHAN) guidelines recommend assessing the HLA-DQ2.5/DQ8 genotype in patients with T1DM, as an initial approach for CD screening. A recent study investigated the clinical relevance and cost-effectiveness of human leukocyte antigen (HLA)-genotyping in T1DM patients as a screening tool [102]. They found that HLA-DQ typing in T1DM patients is neither distinctive nor cost-effective in screening for CD [102]. This might be due to the fact that only 25 % of T1DM patients is HLA-DQ 2.5 or DQ 8 negative [14, 16]. Thus, in our algorithm HLA-DQ typing is excluded.
According to recent guidelines for symptomatic children who have high antibody titres, a duodenal biopsy is not needed anymore for diagnosing CD [103]. Indeed, a recent study showed that none of the T1DM children with high TG2A titres would have needed a biopsy for diagnosis [104]. Whether this is also the case in symptomatic adult T1DM patients with high TG2A titres remains to be established.
CD fulfills many of the WHO criteria for screening as it is common, simple to diagnose, and treatment is available. Detection of CD in T1DM patients is important as morbidity and mortality is increased in patients with both T1DM and CD. Furthermore, several clinical consequences are present in both disorders as decreased BMD, nephropathy, retinopathy and decreased QOL which need careful follow-up. We propose an algorithm for periodic screening and advise a multidisciplinary approach for these complex patients.
AIT:
autoimmune thyroid diseases
BMI:
BMD:
DXA:
dual X-ray absorptiometry
EATL:
enteropathy-associated T cell lymphoma
EMA:
anti-endomysial antibody
ESPGHAN:
European Society for Paediatric Gastroenterology, Hepatology and Nutrition
ESRD:
end-stage renal disease
FPG:
fasting plasma glucose
GDS:
gastroduodenoscopy
GWAS:
genome wide association studies
HbA1c:
glycated haemoglobin
IBS:
NCGS:
non coeliac gluten sensitivity
OGTT:
oral glucose tolerance test
RCD:
refractory coeliac disease
TG2A:
tissue transglutaminase 2
T1DM:
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Pham-Short A, Donaghue C, Ambler G, et al. Early elevation of albumin excretion rate is associated with poor gluten-free diet adherence in young people with coeliac disease and diabetes. Diabet Med. 2014;31:208–12.
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Mollazadegan K, Fored M, Lundberg S, et al. Risk of renal disease in patients with both type 1 diabetes and coeliac disease. Diabetologia. 2014;57:1339–45.
Gunczler P, Lanes R, Paoli M, Martinis R, Villaroel O, Weisinger JR. Decreased bone mineral density and bone formation markers shortly after diagnosis of clinical type 1 diabetes mellitus. J Pediatr Endocrinol Metab. 2001;14:525–8.
Larussa T, Suraci E, Nazionale I, Abenavoli L, Imeneo M, Luzza F. Bone mineralization in celiac disease. Gastroenterol Res Pract. 2012;2012:198025.
Diniz-Santos DR, Brandao F, Adan L, Moreira A, Vicente EJ, Silva LR. Bone mineralization in young patients with type 1 diabetes mellitus and screening-identified evidence of celiac disease. Dig Dis Sci. 2008;53:1240–5.
Artz E, Warren-Ulanch J, Becker D, Greenspan S, Freemark M. Seropositivity to celiac antigens in asymptomatic children with type 1 diabetes mellitus: association with weight, height, and bone mineralization. Pediatr Diabetes. 2008;9:277–84.
Lunt H, Florkowski CM, Cook HB, Whitehead MR. Bone mineral density, type 1 diabetes, and celiac disease. Diabetes Care. 2001;24:791–2.
Sategna-Guidetti C, Grosso SB, Grosso S, et al. The effects of 1-year gluten withdrawal on bone mass, bone metabolism and nutritional status in newly-diagnosed adult coeliac disease patients. Aliment Pharmacol Ther. 2000;14:35–43.
Rubin RR, Peyrot M. Quality of life and diabetes. Diabetes Metab Res Rev. 1999;15:205–18.
Kurppa K, Collin P, Maki M, Kaukinen K. Celiac disease and health-related quality of life. Expert Rev Gastroenterol Hepatol. 2011;5:83–90.
Bakker SF, Pouwer F, Tushuizen ME, Hoogma RP, Mulder CJ, Simsek S. Compromised quality of life in patients with both Type 1 diabetes mellitus and coeliac disease. Diabet Med. 2013;30:835–9.
Anderson RJ, Freedland KE, Clouse RE, Lustman PJ. The prevalence of comorbid depression in adults with diabetes: a meta-analysis. Diabetes Care. 2001;24:1069–78.
Garud S, Leffler D, Dennis M, et al. Interaction between psychiatric and autoimmune disorders in coeliac disease patients in the Northeastern United States. Aliment Pharmacol Ther. 2009;29:898–905.
Kaspers S, Kordonouri O, Schober E, Grabert M, Hauffa BP, Holl RW. Anthropometry, metabolic control, and thyroid autoimmunity in type 1 diabetes with celiac disease: a multicenter survey. J Pediatr. 2004;145:790–5.
Tack GJ, Verbeek WH, Schreurs MW, Mulder CJ. The spectrum of celiac disease: epidemiology, clinical aspects and treatment. Nat Rev Gastroenterol Hepatol. 2010;7:204–13.
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Mollazadegan K, Sanders DS, Ludvigsson J, Ludvigsson JF. Long-term coeliac disease influences risk of death in patients with type 1 diabetes. J Intern Med. 2013;274:273–80.
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Bai JC, Fried M, Corazza GR, et al. World Gastroenterology Organisation global guidelines on celiac disease. J Clin Gastroenterol. 2013;47:121–6.
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Ludvigsson JF, Card TR, Kaukinen K, et al. Screening for celiac disease in the general population and in high-risk groups. United European Gastroenterol J. 2015;3:106–20.
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Dabelea D. The accelerating epidemic of childhood diabetes. Lancet. 2009;373:1999–2000.
Kang JY, Kang AH, Green A, Gwee KA, Ho KY. Systematic review: worldwide variation in the frequency of coeliac disease and changes over time. Aliment Pharmacol Ther. 2013;38:226–45.
Rostom A, Dube C, Cranney A, et al. The diagnostic accuracy of serologic tests for celiac disease: a systematic review. Gastroenterology. 2005;128:S38–46.
Barera G, Bonfanti R, Viscardi M, et al. Occurrence of celiac disease after onset of type 1 diabetes: a 6-year prospective longitudinal study. Pediatrics. 2002;109:833–8.
Husby S, Koletzko S, Korponay-Szabo IR, et al. European Society for Pediatric Gastroenterology, Hepatology, and Nutrition guidelines for the diagnosis of coeliac disease. J Pediatr Gastroenterol Nutr. 2012;54:136–60.
DeMelo EN, McDonald C, Saibil F, Marcon MA, Mahmud FH. Celiac disease and type 1 diabetes in adults: is this a high-risk group for screening? Can J Diabetes. 2015;39:513–9.
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Elias J, Hoorweg-Nijman JJ, Balemans WA. Clinical relevance and cost-effectiveness of HLA genotyping in children with Type 1 diabetes mellitus in screening for coeliac disease in the Netherlands. Diabet Med. 2015;32:834–8.
Popp A, Mihu M, Munteanu M, et al. Prospective antibody case finding of coeliac disease in type-1 diabetes children: need of biopsy revisited. Acta Paediatr. 2013;102:e102–6.
Samsom M, Akkermans LM, Jebbink RJ, van Isselt IH, vanBerge-Henegouwen GP, Smout AJ. Gastrointestinal motor mechanisms in hyperglycaemia induced delayed gastric emptying in type I diabetes mellitus. Gut. 1997;40:641–6.
Horowitz M, Fraser R. Disordered gastric motor function in diabetes mellitus. Diabetologia. 1994;37:543–51.
SB contributed to the design of the review, collected and analyzed the data and wrote the draft of the paper. MT participated in writing of the manuscript and critically reviewed the data of the articles. BB, HB and CM critically reviewed the intellectual content of the study. SS contributed to the concept and design of the study, performed acquisition of data and critically reviewed the paper. All authors read and approved the final manuscript.
SB is financially supported by the Coeliac Disease Consortium, The Netherlands.
Department of Gastroenterology and Hepatology, VU University Medical Centre, De Boelelaan 1117, 1081 HV, Amsterdam, The Netherlands
Sjoerd F. Bakker
, Maarten E. Tushuizen
& Chris J. Mulder
Department of Pathology, Unit Medical Immunology, VU University Medical Centre, Amsterdam, The Netherlands
Boudewina M. E. von Blomberg
& Hetty J. Bontkes
Department of Internal Medicine, North West Clinics, Alkmaar, The Netherlands
Suat Simsek
Department of Internal Medicine, VU University Medical Centre, Amsterdam, The Netherlands
Search for Sjoerd F. Bakker in:
Search for Maarten E. Tushuizen in:
Search for Boudewina M. E. von Blomberg in:
Search for Hetty J. Bontkes in:
Search for Chris J. Mulder in:
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Correspondence to Sjoerd F. Bakker.
Clinical characteristics
Tissue-transglutaminase antibodies
Complications and type 1 diabetes mellitus


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text:
Tag: Norma Ennis Musgrove Craig
Last summer, Aunt Mary Mae brought her collection of family pictures to the Musgrove reunion on Lake Texoma. She and I spent three days going through the collection, which included several unlabeled photographs from the early 1900s. As the oldest daughter of William (Bill) and Eva (Buckmaster) Musgrove, Mary Mae inherited their pictures, including some from Bill's parents and aunt Odessa (Pennington) Smith.
Pictures were scanned on my Flip-pal scanner, photographed and some originals Mary Mae gave to me to preserve for the next generations. All those photographs are now scanned into my computer and labeled. I've just finished making a CD with just over 200 pictures, many from Mary Mae's collection, but a few others collected from other sources. All pictures are used with the permission of the owners.
While I won't be able to attend the reunion this year, tomorrow twenty copies of that CD will go into the mail. I've already found two mistakes – a name misspelled and a DAR obit inadvertently included. My email address is on each CD to contact me with other errors.
Here's some pictures from the CD. Could the tall young man in the picture below be William (Bill) Musgrove Jr.-Nora's brother and Eva's future husband? And perhaps the boy in the front could be Kenneth Eugene Smith, Nora and Bill's younger cousin and Dessa's son? The ages fit. If anyone has these same photographs labeled or photographs of these people at about the same age, please contact me. If this is Eva, it's the earliest photograph I've seen.
The photo postcard below was in both the Mary Mae (Musgrove) Dollar collection and the Norma Ennis (Musgrove) Craig collection.
William Walker Musgrove is on the left in the picture below, but the man on the right was unknown, until I looked through the Norma Ennis (Musgrove) Craig's book. Benjamin Harrison Musgrove, William Walker's younger brother, is the man on the right.
Several of the other photographs are still unidentified, but not forgotten. I'll continue to post the rest of them on the blog and research other ways to identify the photographs.
Have fun at the lake!
Author Andrea Musgrove PerishoPosted on July 6, 2014 Categories Musgrove, PenningtonTags Benjamin Harrison Musgrove, Eva Buckmaster Musgrove, Kenneth Eugene Smith, Mary Mae (Musgrove) Dollar, Nora Musgrove, Norma Ennis Musgrove Craig, Odessa, old photographs, William (Bill) Musgrove16 Comments on Musgrove Family Reunion – CD of Family Pictures
Serendipity on the Research Trail
One of my primary goals on a recent genealogy research trip to Oklahoma and Texas was to find a book with the genealogy research of Norma Ennis Musgrove Craig, a first cousin 2X removed. Norma's book summarizes her 40+ years of genealogy research on our Musgrove/Musgrave family. I learned of the book, which contained childhood pictures of my grandfather, through a Google search and ordered the microfilm through the Family History Center. 1 I was able to make copies of each page, but the microfilm pictures weren't very clear. I wanted better copies of the pictures.
As part of preplanning for the trip, I had contacted everyone on Ancestry.com who seemed to have good sources for Norma or her sister Beulah, who wrote many of the charming family stories in the book. Beulah had passed away in 2003 and Norma in 2008. Only one person responded. Evidently when Beulah died, another family member got the house and the contents, including the genealogy research and the book. No one had seen any of materials since then.
I planned stops in Holdenville, Ada and the Oklahoma History Center, since Norma and Beulah had connections in each of those places. I researched each of those sites ahead of time to find the hours of operation, days open and any other pertinent information.
The Hughes County Historical Society in Holdenville was listed on-line, but with a disconnected phone number, no other contact information nor hours of operation.2 Since I had no idea what hours the HCHS would be open and since it was the direction I was traveling, that was my first stop. After a two and one half hour drive from Tulsa, I was standing in front of the closed doors of the dark HCHS building. My heart sank as I scanned the doors and windows finding no contact information nor hours of operation. As I turned to my car to rethink my next step, a man in a pickup truck stopped at the light called out "Are you trying to get in the museum?" When I answered yes, he continued with "Go to the business two doors down. They'll have the phone number to reach someone."
Two doors down, they did give me the name and seven digit phone number of the HCHS coordinator. Back in my car, I dialed the number using what I thought was the most likely area code. No luck, I reached someone in western OK. Next, I tried the other OK area code. Number out of service. Rats! Back to the business two doors down. They reminded me of the third OK area code, which I had forgotten in my sixteen years out of the state, and probably didn't even need to use any way to reach the number.
Then the woman asked what I was looking for. I told my story about the book, the sister from Holdenville, etc., etc. She stopped me asking "What was the sister's name?" When I gave her Beulah's name, she just looked at me and said "You should just talk to her son. He owns the business across the street."
Across the street, Beulah's son was busy with customers, but his daughter, who did not typically work with her father, was filling in for the day. After some discussion about the family, probably to confirm who I really was, the daughter told me the same story about a family member getting Beulah's house and no one having access to that research any more. Then she told me, Norma's daughter had all of Norma's records. She gave me Norma's daughter's name and address.3
After a conversation establishing who I was, a meeting with Norma's daughter was set up for the next Saturday morning. The records had been stored since Norma's death, with no one else in the family interested in them. Norma had some strokes before her death, but still tried to work with her research, getting it mixed up. It would take a few days for the daughter to get the records organized enough for us to review.
On Saturday morning, I was given an original copy of Norma's book, with the original picture of my grandfather and his two siblings along with much of Norma's original research on my family line, including pictures, marriage licenses, wills, etc. In addition, I was able to conduct about two hours of interviews of Norma's daughter, who remembered my 2nd great grandmother, Myzella Medcalf Musgrove. I was able to take pictures of a quilt made by Myzella. The quilt was registered with the Oklahoma Historical Society, as being over 100 years old.4
One of the stories during the interview was how Norma got some grief from family members with some of her research results. Norma's grandfather, William Tate Musgrove, my 2nd great grandfather, had evidently told the family he was Irish and had come to America on a ship.5 Norma's research showed a paper trail where William Tate, a Civil War veteran who fought with the 42nd Regiment, Indiana Volunteers was not only born in the United States, but his family had been here since 1747. Norma and Beulah both became DAR members through Samuel Musgrave, William Tate's great grandfather. I was able to share that my father's y-DNA test linked him to other descendants of Oswin Musgrave who arrived in Pennsylvania about 1682, confirming Norma's paper trail.6 By the way, in Norma's book, she included William Tate's nickname of Flannel Mouth, earned with the tall tales he was known for telling.7
All the information collected on these two trips will certainly keep me busy until my next genealogy field trip.
1. Craig, Norma Ennis Musgrove and Beulah Musgrove Berryman. Musgrave–Musgrove, 1747-1986, [Self published. Place of publication not indicated.], 1987. Microfilm of typescript (photocopy, 157, [8] leaves) at the Rockport Public Library, Rockport, Indiana. Family History Library, film 1502916 item 9; (https://familysearch.org/eng/library/fhlcatalog/mainframeset.asp:accessed 12 Aug 2013.)
2. Hughes County Historical Society, www.okgenweb.org/~okhughes/resources.htm. Currently open 9:30-1:00 on Saturdays, as of July 2013.
3. Names and identifying information of living persons have not been used to protect their privacy. If you have a specific need to know, please contact me at amperisho@gmail.com.
4. http://www.okhistory.org/research/folkquilt As of 12 Aug 2013, the Oklahoma History Center website shows a couple of examples of old quilts, but doesn't list pictures of all the quilts submitted. I'll post my pictures in a later blog.
5. While the 1880 census shows the father of William Tate Musgrove born in New Jersey and his mother born in Pennsylvania, the 1900 and 1910 schedules indicate his parents were born in Ireland.
1880 U. S. Census, Justice Precinct 3, Collin County, Texas, population schedule (1st enumeration), enumeration district (ED) 22, p. 32 (penned), line 25, dwelling 211, family 225, W. T. Musgrave; digital image, Ancestry.com (http://www.ancestry.com: accessed 12 Aug 2013); citing National Archives and Records Administration microfilm roll 1296, enumeration district (ED) 022, p. 135D; imaged from FHL microfilm 1255296.
1900 U. S. Census, Bates Township, Pottawatomie County, Oklahoma, population schedule (1st enumeration), enumeration district (ED) 192, p. 9A (penned), line 15, dwelling 186, family 186, William Musgrove; digital image, Ancestry.com (http://www.ancestry.com: accessed 12 Aug 2013); citing National Archives and Records Administration microfilm roll 1342, enumeration district (ED) 0192, p 9A; imaged from FHL microfilm 1241342.
1910 U. S. Census, Pottawatomie Township, Oklahoma County, Oklahoma, enumeration district 230, p. 6A (penned), line 3, dwelling 98, family 99, William T. Musgrave; digital image, Ancestry.com (http://www.ancestry.com: accessed 12 Aug 2013); citing National Archives and Records Administration microfilm roll T624_1265, enumeration district (ED) 0230, page 6A; imaged from FHL microfilm 1375278.
6. Musgrave, Duane and Marie Wilson Musgrave, A History of the Moses Musgrave Family, Quakers, Pennsylvania, Virginia, Tennessee, Kentucky, Illinois, Kansas, and Further West, Evansville Bindery Inc, Evansville, Indiana, 1998.
7. Craig and Berryman, Musgrave-Musgrove, 1747-1986, p. 43.
Author Andrea Musgrove PerishoPosted on August 12, 2013 Categories Musgrave, MusgroveTags A History of the Moses Musgrave Family, Hughes County Historical Society, Myzella Medcalf, Myzella Medcalf Musgrove, Norma Craig, Norma Ennis Musgrove Craig, Norma Musgrove Craig, Oswin Musgrave, Samuel Musgrave, William Tate Musgrave, William Tate Musgrove1 Comment on Serendipity on the Research Trail
Samuel Musgrave and Elizabeth Brand – Revolutionary War Service
Samuel Musgrave – Revolutionary War Patriot
Samuel was born in Lancaster County, Pennsylvania in 1747. He was one of eight children born to Moses Musgrove Jr. and Elizabeth, who's last name is unknown. He moved to Fayette County, PA., then to Muhlenburgh County, Kentucky, and finally, to Warwick County, Indiana. Samuel is the third generation of his family to live in what became the United States of America. His parents and grandparents were Quakers, who did not believe in war and fighting. So Samuel, as a soldier in the Revolutionary War, could not have participated in Quaker services, until reinstated to the Monthly Meeting, after confessing his sins. There is no evidence this ever happened.
"Samuel married Elizabeth Brand on September 10, 1767 in Pennsylvania." Most of the information we have on him is from his Revolutionary War pension applications. The information within the quotation marks has been summarized by Richard Graham Musgrove and Samuel's 5th great grand-daughter, Jennifer Berryman at the behest of her grandmother, Beulah Arlene Musgrove Berryman and great-aunt, Norma Ennis Musgrove Craig.
"Samuel began his military service as a Private in the Cumberland County militia. He was assigned to the 4th Battalion and served in the 8th Company. He refers to his immediate superior officer as "Captain Jack."His first day's march carried them toward Shippenstown, now named Shippensburg. A sixty mile march to the Susquehanna River carried them through Carlisle. He related that they "went on the river" to Lancaster County where they enjoyed a short few days of rest. Captain Jack took his men down the main road to Chester County and to Philadelphia. (When traveling through Lancaster and Chester Counties, he was traveling near the area where he was born and raised.) Crossing the Schuylkill River on a floating bridge, they arrived in Philadelphia and were given ten days rest after being assigned to barracks.
"They next traveled by sloop on the Delaware River to Trenton, New Jersey.
Revolutionary War Flag
With Long Island, New York, as their destination, they marched through Princeton and arrived in time for the battle on August 27, 1776. Approximately 3,500 colonists were under the command of Generals Washington, Sullivan, Putnam and Sterling. They suffered casualties of about 300 killed and 1,100 wounded or captured while facing a superior force of British troops. Using fog to cover their departure, the colonists crossed the East River in small boats. His unit returned to Philadelphia and, after a few days was verbally discharged and told to return to his home.
"He was welcomed with open arms by Elizabeth and four children, Huldah, Moses, Mary and Samuel Davies. During this break in his militia service, David was born. In July 1777, Samuel began another three months of service in the militia. He relates that his officers were William Duffle, George Crawford and John Cunningham who were under the command of Colonel Jonas McCoy. His company marched into Delaware and remained there a short time until General Washington moved his army back to New Port, Pennsylvania. Recrossing the Brandywine River, his company joined forces with a battalion of riflemen under a Colonel Erwin. As a part of a scouting party, Samuel was sent to Tron Hill to determine the size of the British force and their positions. (Battle of Brandywine.)
"He and others of his militia were sent to march with a group of Regulars to Chadd's Ford where they were positioned to the right of the army for the battle which occurred on September 11, 1777. This time the colonists were more evenly matched. About 11,000 men fought under General Washington. British Generals Howe, Cornwallis and Knyphausen led about 12,500 troops and suffered 90 killed and 480 wounded or captured.
"Following the battle, Samuel's unit returned to Philadelphia. He was ill and furloughed for two weeks. He stayed with his sister at Chadd's Ford. Upon return to his unit, he was still too ill to travel and, since his three months were up, was discharged.
"In 1782, he was drafted again to serve his country as an Indian scout (spy-from DAR records.)Leaving behind two more children, James and Elizabeth, he served two months. Scouting in groups of five, six or seven men, they were based in a stockade fort at Hannahtown, Pennsylvania (the town had been burned by Indians) and served under Lt. Robert Ritche.
Their remaining children were born following this last term of service to his country. Sarah, Jane and William were born in Fayette County, Pennsylvania and the youngest, Ann in Monongalia County, Virginia, now West Virginia.
Samuel and Elizabeth moved to Warrick County, Indiana."*
Samuel Musgrove was awarded a pension for his Revolutionary War Service receiving $26.66 per annum from March 4, 1821, issued December 9, 1833.
Samuel Musgrave, Revolutionary War Patriot Gravestone
Elizabeth Musgrove also applied for a pension on January 30, 1843, age 93, from Warwick County, Ind., as the widow of Samuel Musgrove, who had died on September 2, 1834. Bible records proving the birth dates of their children were filed: Huldah, b 10 June 1768; Moses, b 8 May 1770; Mary, b 22 June 1772; Samuel Davies, b 22 mar 1775; David, b 22 Nov 1776; Elizabeth, b 25 July 1781; Sarah, b 21 Nov 1783; William, b 19 May 1788; Margaret, b 17 June 1780 and Ann, b 19 Dec 1790. Their son, Moses, is our ancestor.
NOTE: In DAR records and in the National Genealogical Society Quarterly article, Samuel's last name is listed as MUSGROVE, though other records, including gravestone, say MUSGRAVE.
*Extensive quotes for Samuel, Moses and Enos Musgrave from "The American Family Musgrove," by Richard Graham Musgrove.
"National Genealogical Society Quarterly: Abstracts of Revolutionary War Pension Applications."
Samuel Musgrove – Pension Claim W9211, PA service, Indiana Agency.; Certificate 25203. Act 7 June 1832.
"Roster of Soldiers and Patriots of the American Revolution Buried in Indiana," Mrs. Roscoe O'Byrne, page 263 for Samuel Musgrave information.
Research of Jennifer Berryman, Beulah Arlene Musgrove Berryman and Norma Ennis Musgrove Craig.
Author Andrea Musgrove PerishoPosted on December 16, 2012 May 8, 2013 Categories Musgrave, Quakers, Revolutionary WarTags Battle of Princeton, Battlle of Brandywine, Chadd's Ford, Hannahtown, Jennifer Berryman, Musgrave, Musgrove, Norma Ennis Musgrove Craig, Quaker, Revolutionary War, Richard Graham Musgrove4 Comments on Samuel Musgrave and Elizabeth Brand – Revolutionary War Service

redpajama_set_name: RedPajamaCommonCrawl


text:
Secondary/Double Glazing
Tilt and Turn
French / Patio Doors
Orangeries & Conservatories
Victorian Conservatories
Edwardian Conservatories
Lean-To Conservatories
P-Shape Conservatories
Living Room Systems
Roofing & Fascias
GRP Roofing
Cut Timber Roofing
Lead Roofing
Exterior Shelters
5 Reasons Your Home Needs a Bi-folding Door
Bi-Folding Doors - Why do you need them? Demand for home improvements has been growing for a number of years now, but one product that seems to have suddenly appeared everywhere and become hugely popular within the home improvements market is the elegant and beautiful Bi-folding Door. Their appeal is there for all to see. Effortlessly open up your property to a width of six or seven metres. Beautiful looks and a seamless transition between your house and garden are other desirable features...
Countrywide Windows Sponsor Team Rhino in support of The Bone Cancer Research Trust
Countrywide Windows, the professional, reliable and affordable double-glazing and conservatory installation company are sponsoring Team Rhino, who are participating in the Prudential Ride London 100 to raise money for The Bone Cancer Research Trust. Team Rhino consists of 6 members who have previously competed in the London Orbital. They are using their passion for riding and competing to raise money for a great cause. The Bone Cancer Research Trust is a charity that offers hope to peopl...
Why an Orangery Could Be the Perfect Addition to Your Home
What is an Orangery? An Orangery is extremely similar to a greenhouse, these extensions were originally used for growing citrus plants in a space that protected them from cold weather during the winter months. As time went on and fruits became cheaper and easier to buy, the orangery lost its purpose. Rather than fading away into the distance never to be seen again, the orangery evolved and modernised itself to become one of the most beautiful and worthwhile additions to your home. What's t...
Countrywide Windows gives Westfield Church a new look
Countrywide Windows has partnered with Westfield church to give it a new, modern look. Westfield Church, also based in Bridgwater had multiple renovations and installations; including structured glass screens and Smart Systems aluminium windows, as well as the installation of new fascias. Rachel Leach, Administrator at Westfield Church commented; "The work undertaken by Countrywide Windows was brilliant, it was a smooth process from quotation to completion and the church cafe looks great. T...
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Amazing Home Improvement Ideas for 2022
2022 is well underway and already new and exciting products and ideas are being thrown around the industry. There is so much choice available to every homeowner nowadays and this range is only going to get bigger and bigger giving you the opportunity to make your home even more unique and eye-catching. In this weeks blog we are going to look at some up and coming products for 2022 and some that already exist but are continually improving and evolving in order to meet the needs of the ever-chan...
Why Does Your Home Need a Roof Lantern?
2022 is here and hopefully this will be the year that we see the end of the pandemic and focus on the recovery of people and businesses around the world. It has been a hectic few years and no one could have predicted how long this would have gone on for or the fact that nearly two years later we are still fighting this terrible virus. However, we are starting to see light at the end of the tunnel and although Omicron has spread fast it is extremely positive that it is milder than strains such a...
Home Improvement Projects For 2022
With 2022 fast approaching it is time to reflect on what has been a hectic and crazy year for the entire world. The pandemic has shaken the world to its core and with hopefully the worst of it behind us, it is now time to look to the future as we try and exit this pandemic and get back to normality. Families, friends and businesses have all been greatly affected by Covid-19 and as we start to recover we can look at future plans and ideas that have perhaps been put on hold due to the lockdowns ...
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Course Comments: Arizona City Golf Course is one of the oldest golf courses in Arizona. Our claim to fame is our greens. Every year we have some of the best greens in the State. Being a traditional golf course in the desert it is unusual to have six holes where water comes into play with two fountains in our lakes on nine and seventeen.


Safe Work Australia Week commences today (21st October) and runs through to the 27th October, with the theme 'Safety begins with 'S' but starts with 'You".
Safety is an ongoing topic in any workplace but this week specifically encourages staff on all levels to contribute to their workplace health and safety. It is up to all of us to facilitate continuous improvement and ensure a safe working environment for everyone.
Nominations are also being called for the Safety Ambassador of the Year Award to highlight and reward the efforts of individuals who improve their workplace safety. The results will be announced at the end of the month on the Safe Work Australia website.
There is still time to invite and encourage your staff to participate in Safe Work Australia Week.
For more suggested activities and other information, visit the Safe Work Australia website.
The 2012 APPEA HSR & Safety Workforce Forum has been rescheduled for Monday 12th November.
It will still take place at the Perth Convention and Exhibition Centre.
The forum provides a unique opportunity for workforce representatives from right across the Australian oil and gas industry to come together in one place to network, develop skills and share workplace experiences, issues and solutions.
This day will assist HSRs and the workforce to perform their roles effectively and contribute to improved safety and health performance.
Registrations remain open for delegates wishing to register for this highly regarded event.
The 2012 Health and Safety Representative (HSR) of the Year Awards are also now open.
The HSR Awards recognize individuals in the Australian oil and gas industry who have contributed through leadership, dedication and initiative to the health and safety of their colleagues.
Recipients will be presented with their award at the HSR and Safety Workforce Forum.
This is an important opportunity to recognize the work of the HSRs in the oil and gas community.
If you know a health and safety representative who has demonstrated a commitment to workplace safety in the past year, nominate them for the 2012 HSR of the Year.
Nomination forms are available online at the APPEA website.


text:
package jdk.nashorn.internal.runtime;

import static jdk.nashorn.internal.codegen.Compiler.SCRIPTS_PACKAGE;
import static jdk.nashorn.internal.codegen.Compiler.binaryName;
import static jdk.nashorn.internal.codegen.CompilerConstants.JS_OBJECT_PREFIX;

import java.security.ProtectionDomain;
import jdk.nashorn.internal.codegen.ObjectClassGenerator;

/**
 * Responsible for on the fly construction of structure classes.
 */
final class StructureLoader extends NashornLoader {
    private static final String JS_OBJECT_PREFIX_EXTERNAL = binaryName(SCRIPTS_PACKAGE) + '.' + JS_OBJECT_PREFIX.symbolName();

    /**
     * Constructor.
     */
    StructureLoader(final ClassLoader parent) {
        super(parent);
    }

    static boolean isStructureClass(final String name) {
        return name.startsWith(JS_OBJECT_PREFIX_EXTERNAL);
    }

    @Override
    protected Class<?> findClass(final String name) throws ClassNotFoundException {
        if (isStructureClass(name)) {
            return generateClass(name, name.substring(JS_OBJECT_PREFIX_EXTERNAL.length()));
        }
        return super.findClass(name);
    }

    /**
     * Generate a layout class.
     * @param name       Name of class.
     * @param descriptor Layout descriptor.
     * @return Generated class.
     */
    private Class<?> generateClass(final String name, final String descriptor) {
        final Context context = Context.getContextTrusted();

        final byte[] code = new ObjectClassGenerator(context).generate(descriptor);
        return defineClass(name, code, 0, code.length, new ProtectionDomain(null, getPermissions(null)));
    }
}

redpajama_set_name: RedPajamaGithub


Check out this web site about microbes eating the oil in the Gulf of Mexico. Also check out Dr.Hewston's Bulletin Board on the 2nd floor of the NR Building.
I am a life-long resident of the North Coast.I worked in the timber indusry for 22 yrs. I am Environmental Resource Engineering Major. My intrests are municiple water systems, and waste water/storm run-off management.


text:
Home > Curious Traveler > Episode
Curious Traveler - Curious Stockholm
What did Alfred Nobel invent that led him to create the Nobel Prize? What is Gamla Stan? What's so important about the throne inside the Royal Palace of Stockholm? What is the Djurgarden Canal, and why was it only for the Royal Family? Why did the Swedes grow grass on their rooftops, and what...
STEREO | HD
About Curious Traveler
CURIOUS TRAVELER takes viewers on an enriching and entertaining "field trip for grown-ups" to some of the most intriguing European and North American cities in the world. Daytime Emmy- and Telly-winning travel, arts and entertainment journalist Christine Van Blokland brings her passion and genuine curiosity for the arts, quirky characters, storytelling, and lifelong learning to this new series. In each location, Christine explores the hidden histories in their art, architecture, museums, monuments, houses of worship and city parks. Each episode begins with Christine's list of "Curious Questions": Is the Mona Lisa really a prostitute? Is the Eiffel Tower really Egyptian? Why are there acorns all through Grand Central Terminal? Christine's previous television credits include: Let's Go!, Georgia Traveler, Let's Go! Georgiaand Better Destinations.