Compared with the HIV-uninfected men in our sample, HIV-infected men were younger, with lower body mass index (BMI) and more often Black. HIV-infected men had lower FT (age-adjusted FT 88.7 ng/dL vs. 101.7 ng/dL in HIV-uninfected men; P = 0.0004); however, FT was not associated with CAC,

log carotid IMT, or the presence of carotid lesions. HIV status was not associated with CAC presence or log carotid IMT, but was associated with carotid lesion presence (adjusted odds ratio 1.69; 95% confidence interval 1.06, 2.71) in HIV-infected men compared with HIV-uninfected men. Compared with HIV-uninfected men, HIV-infected men had lower FT, as well as more prevalent carotid lesions. In both groups, FT was not associated with CAC presence, log carotid IMT, or carotid

lesion presence, suggesting that FT does not influence subclinical CVD in www.selleckchem.com/products/PLX-4032.html this population of men with and at risk Z-VAD-FMK clinical trial for HIV infection. Increased rates of myocardial infarction and accelerated cardiovascular disease (CVD) progression have been observed among HIV-infected individuals [1], particularly among those taking antiretroviral therapy [2, 3]. Identifying modifiable CVD risk factors among individuals with HIV infection is important to decrease CVD risk. Several population-based studies have shown that low serum testosterone (T) is associated with increased all-cause mortality [4] and CVD-related

death [5] in men. Low serum T may be a risk factor for CVD by several mechanisms, including increased visceral adiposity (leading to glucose intolerance and diabetes mellitus), inflammation, and a more direct effect on the vasculature [6-8]. There is an increased prevalence of hypogonadism in HIV-infected men [9] and hypogonadism may persist despite effective antiretroviral therapy [10]. Although CVD in HIV-infected men may be a consequence of underlying viral mechanisms or antiretroviral therapy, it is crucial to investigate other clinically reversible factors such as low T that might result in an increased susceptibility to atherosclerotic disease. To our Mannose-binding protein-associated serine protease knowledge, this is the first investigation of the potential role of T in the pathogenesis of CVD in HIV-infected individuals. The aim of our study was to examine the relationship between free testosterone (FT) and early stages of CVD and to explore nontraditional risk factors for CVD in an HIV-infected population, using an HIV-uninfected comparison group. We used data from a subpopulation of the Multicenter AIDS Cohort Study (MACS; see Appendix) to assess the relationship between FT and coronary artery calcium (CAC) presence, carotid intima-media thickness (IMT), and carotid lesion presence among men with and at risk from HIV infection.

Compared with the HIV-uninfected men in our sample, HIV-infected men were younger, with lower body mass index (BMI) and more often Black. HIV-infected men had lower FT (age-adjusted FT 88.7 ng/dL vs. 101.7 ng/dL in HIV-uninfected men; P = 0.0004); however, FT was not associated with CAC,

log carotid IMT, or the presence of carotid lesions. HIV status was not associated with CAC presence or log carotid IMT, but was associated with carotid lesion presence (adjusted odds ratio 1.69; 95% confidence interval 1.06, 2.71) in HIV-infected men compared with HIV-uninfected men. Compared with HIV-uninfected men, HIV-infected men had lower FT, as well as more prevalent carotid lesions. In both groups, FT was not associated with CAC presence, log carotid IMT, or carotid

lesion presence, suggesting that FT does not influence subclinical CVD in selleck this population of men with and at risk IWR-1 mouse for HIV infection. Increased rates of myocardial infarction and accelerated cardiovascular disease (CVD) progression have been observed among HIV-infected individuals [1], particularly among those taking antiretroviral therapy [2, 3]. Identifying modifiable CVD risk factors among individuals with HIV infection is important to decrease CVD risk. Several population-based studies have shown that low serum testosterone (T) is associated with increased all-cause mortality [4] and CVD-related

death [5] in men. Low serum T may be a risk factor for CVD by several mechanisms, including increased visceral adiposity (leading to glucose intolerance and diabetes mellitus), inflammation, and a more direct effect on the vasculature [6-8]. There is an increased prevalence of hypogonadism in HIV-infected men [9] and hypogonadism may persist despite effective antiretroviral therapy [10]. Although CVD in HIV-infected men may be a consequence of underlying viral mechanisms or antiretroviral therapy, it is crucial to investigate other clinically reversible factors such as low T that might result in an increased susceptibility to atherosclerotic disease. To our Osimertinib knowledge, this is the first investigation of the potential role of T in the pathogenesis of CVD in HIV-infected individuals. The aim of our study was to examine the relationship between free testosterone (FT) and early stages of CVD and to explore nontraditional risk factors for CVD in an HIV-infected population, using an HIV-uninfected comparison group. We used data from a subpopulation of the Multicenter AIDS Cohort Study (MACS; see Appendix) to assess the relationship between FT and coronary artery calcium (CAC) presence, carotid intima-media thickness (IMT), and carotid lesion presence among men with and at risk from HIV infection.

capsulatus Raf inhibitor Bath (Kao et al., 2004; Karlsen et al., 2005a). The extensive physiological changes in lifestyle were efficiently demonstrated with ICAT (isotope-coded affinity tag)-labelling of high- and low-copper grown cells combined with downstream LC-MS/MS, revealing more than 500 differentially expressed proteins (Kao et al., 2004). However, these cultures represented the extremes of copper concentrations in the growth medium, and much less is known regarding gene expression over the copper concentration

range where the switch in lifestyle actually takes place. Proteins of the outer membrane are part of the interface between the bacterium and its environment, and are essential for cells in their response to its habitat. These proteins must be diverse in function, including protection against environmental challenges, uptake of growth factors, and bacterial interaction (Navarre & Schneewind, 1999; Hancock & Brinkman, 2002; Borges-Walmsley et al., 2003; Odenbreit, 2005; Scott, 2006). We have recently described both the outer

membrane proteome (integral- and outer membrane associated proteins exposed to the periplasm FK228 or cell exterior) and the surfaceome (proteins associated to the cellular surface) of M. capsulatus Bath, and how the composition of the surfaceome significantly changes with only minor changes in the availability of copper during growth (Table 1) (Berven et al., 2003; Karlsen et al., 2008). In the following sections, we will review some of the findings on the M. capsulatus Bath surface-exposed proteins, their copper dependent expression, and the intriguing enrichment of c-type heme proteins on the cell surface. MopE was originally identified as one of five abundant proteins (MopA-E) present in the outer membrane of M. capsulatus Bath (Fjellbirkeland et al., 1997). The cellular localization of MopE was further determined by immunogold-conjugated buy ZD1839 antibody labelling

and NaCl-extraction of whole cells, demonstrating that MopE is surface exposed and noncovalently associated to the cell surface (Fjellbirkeland et al., 2001; Karlsen et al., 2005b). Furthermore, an N-terminal truncated form of MopE (MopE*) is secreted in significant amounts to the growth medium (Fjellbirkeland et al., 2001). The exact mechanisms of the cellular translocation of MopE, and how the processing of MopE to MopE* occurs is still unknown. However, MopE is synthesized with an N-terminal leader sequence, indicating a sec-dependent translocation of the protein across the Gram-negative inner membrane. The expression of mopE is induced when copper becomes limited, starting before the copper-switch and is highest in sMMO-expressing cells (Karlsen et al., 2003). In sMMO-expressing cells, MopE is the most prominent protein in the M. capsulatus Bath surfaceome (Table 1) (Karlsen et al., 2008), and MopE* is now also abundant in the growth medium (Karlsen et al., 2003).

monocytogenes would be anticipated to encounter periods of sustained nutrient

deprivation. The development of the GASP phenotype is marked by the ability of bacteria from an aged culture to outcompete bacteria from a younger culture during long-term selleck kinase inhibitor stationary phase growth (Finkel, 2006). GASP thus requires that a bacterial strain be capable of surviving for an extended period of time following its inoculation into growth medium. To measure the survival of L. monocytogenes during nutrient starvation, bacteria grown in nutrient-rich broth (BHI) were assessed for viability following incubation for 12 days at 37 °C. Cultures exhibited a characteristic lag, logarithmic, and stationary growth phase during the first 24 h of growth

(Fig. 2a). After remaining in stationary phase for 1–2 days, L. monocytogenes entered a death phase during which an approximate 90% loss of cell viability was observed over 24 h. The subsequent bacterial population then maintained a stable cell density representative of a long-term stationary growth phase that persisted for the remaining days (Fig. 2a). The ability of L. monocytogenes to express the GASP phenotype was next assessed. As E. coli cultures need to be at least 8 days old (when cultured in LB under aerobic conditions) to express the GASP phenotype (Zambrano et al., 1993; Finkel, 2006), we aged L. monocytogenes cultures for 12 days prior to the assessment for GASP as an arbitrary staring point. Bacteria from a L. monocytogenes 12-day-old culture were

added to a 1-day-old culture at a ratio of 1 : 100 (Fig. 1). Bacteria from the 12-day-old culture outcompeted bacteria ABC294640 of the 1-day-old culture over 10 days, such that the ratio at day 10 was 10 : 1 of 12-day-old cells to 1-day-old cells (Fig. 2b). In contrast, when bacteria from a 1-day-old culture of L. monocytogenes were added to another 1-day-old culture at a ratio of 1 : 100, no change in this ratio was observed over 10 days (Fig. 2b). The competitive advantage exhibited by the bacteria from a 12-day-old culture was thus reflective of culture age, and indicated that L. monocytogenes is capable of expressing GASP. To determine if the Carnitine dehydrogenase L. monocytogenes GASP phenotype was the result of a stable genetic change, bacteria from a 12-day-old culture were grown in BHI to a high cell density, diluted 1 : 100 into fresh media, and once again grown to high cell density. This process was repeated every 24 h for a total of 12 cycles of dilution and outgrowth or passages (Fig. 1b). Bacteria from the passaged 12-day-old culture were then added to a 1-day-old culture of wild-type L. monocytogenes at a ratio of 1 : 100. Just as with bacteria from a non-passaged 12-day-old culture, bacteria from the passaged 12-day-old culture outcompeted bacteria of the 1-day-old culture over 10 days (Fig. 2b), thus indicating that L. monocytogenes GASP resulted from a stable genetic change.

In order to validate the accuracy of the reason for discontinuation determined by the clinician, we repeated the analysis with the immunovirological and clinical endpoint,

defining discontinuation as a consequence of failure on the basis of the following: discontinuation Ibrutinib purchase of ≥1 drug in the original regimen concomitant with (i) a single viral load >500 HIV-1 RNA copies/mL, or (ii) an increase in CD4 cell count <10% from the patient's pre-therapy value, or (iii) the occurrence of an AIDS-defining illness. A total of 3291 patients were included in the study: 28.2% were female and 39.9% were HCV antibody-positive; their median age was 36 years [interquartile range (IQR) 32–41 years]. Median

CD4 cell count at HAART initiation was 263 cells/μL (IQR 114–402 cells/μL), and median HIV RNA was 4.8 log10 copies/mL (IQR 4.2–5.3 log10 copies/mL). One hundred and thirty-eight patients (4.2%) initiated therapy with three NRTIs (of whom 117 initiated regimens including abacavir and 21 initiated regimens including tenofovir as the third drug), Nutlin-3a cell line 894 (27.2%) with an NNRTI-based regimen, 366 (11.1%) with a boosted PI, 1786 (54.3%) with a single PI, five (0.1%) with a combination of three other drugs (one NRTI+two PIs) and 102 (3.1%) with CYTH4 four or more drugs. Most patients

(52.6%) started HAART in the early period (1997–1999), 925 (28.1%) in the intermediate period (2000–2002) and 635 (19.3%) in the recent period (2003–2007) (Table 1). The median time of follow-up of patients was 12 (IQR 3–12) months; 288 patients (8.7% of the population) dropped out during the first year of follow-up; 14 of these died. During the first 12 months, 1189 (36.1%) patients discontinued ≥1 drug in their initial HAART. The main causes of discontinuation were intolerance/toxicity (696 of 1189 patients; 58.5%) and poor adherence (285 of 1189 patients; 24%); 126 patients (10.6%) discontinued because of immunovirological or clinical failure and 62 (5.2%) because of simplification strategies. Twenty patients (1.7%) interrupted temporarily or permanently all the ongoing drugs by clinician choice or patient wish. The Kaplan–Meier estimates of drug discontinuation for any reason in the first year were 39.5% (95% CI 37.1–41.9%) in those who initiated in 1997–1999, 35.6% (95% CI 32.3–38.9%) in those who initiated in 2000–2002, and 41.2% (95% CI 37.1–45.3%) in those who initiated in 2003–2007 (log-rank test P=0.06) (Fig. 1).

“
“Objectives  To explore how the use of digital media could affect how people view professional behaviour. Key findings  The growth in social networking sites has been phenomenal and they are now an extremely popular medium for interacting with others both commercially and privately. This as-yet-uncontrolled digital media provides ample opportunities for public and professional scrutiny for the unwary. Instances of employer screening and employee dismissal are already documented. All pharmacists who use digital media now need to be conscious that their virtual presence could be subject to regulator

investigation. Conclusions  It is important that individuals are aware of the risks associated with using digital media and that pharmacy organisations begin to provide clear leadership to help pharmacists know what is and is not acceptable. “
“Communication is a key issue in the delivery of healthcare BI 2536 solubility dmso services. In the pharmacy context, pharmacist–patient communication may vary from brief counselling episodes to extensive pharmaceutical care consultations. Many community pharmacies have

developed practices to facilitate the effective delivery of pharmacy care, in particular to chronic patients, although the nature and extent of the services differ widely from country to country. Diabetes-focused pharmaceutical care is an example highlighting both the opportunities and challenges associated with an expansion of pharmacy services Phospholipase D1 from product dispensing to pharmaceutical consultations. An area of particular challenge of such an expansion of pharmaceutical services

R788 is the development of expertise in the delivery of patient-centred pharmaceutical consultations. Although well known to medicine and nursing, patient-centredness has not been routinely incorporated into the training of pharmacists, evaluation of pharmacy practice or conduct of pharmacy-related research. There are few studies of the communication process based on analysis of an objective record such as an audio or video recording and the common perspective is largely a one-way information flow from pharmacist to patient. This has hampered the field’s ability to link pharmacy communication to outcomes, including patient adherence and satisfaction with services. An extensive body of communication research on physician–patient interaction, employing the Roter Interaction Analysis System (RIAS), exists and the system presents a potentially useful tool in the pharmacy context. The purpose of this essay is to explore the utility of the RIAS for analysis of pharmacist–patient interaction and its implication for improving patient care and optimizing pharmacy-specific outcomes. “
“Objectives The practice environment in Alberta has emerged as the most unique in North America, including access to laboratory values, a province-wide electronic health record and legislation to support additional prescribing authority for qualified pharmacists.

Methods  Four focus groups were conducted with 32 South Australian pharmacists: two groups included community pharmacists and pharmacy owners;

one included hospital pharmacists and another, consultant pharmacists. Key findings  Four themes emerged: (1) poor awareness of health care reform agenda; (2) strong adherence to the supply model; (3) lack of appreciation of alternative models; and (4) communication barriers. Conclusions  Participants’ low awareness of Australia’s health care reforms and their expressed beliefs and attitudes to their current role in the health system suggest that they are not well prepared for the potential future roles expected of health professionals in the health care reform agenda. “
“Objective  To make a case for why UK pharmacy selleck chemical must adapt to the increasing demands of professionalism in practice. Methods  A review based on evidence

from the literature and personal opinion. Key findings  Pharmacists, just as with other occupational groups, have over the years been developing and fine-tuning ways through which they can attain full professional status and therefore command the same level of recognition and respect as the main traditional professions, notably medicine and law. Many commentators, however, believe that this ambition is far from being realised. Their argument is that the path to professional status is not that easily available to all occupations. Although there is a professionalisation process that the traditional professions go learn more through, it has been argued that services provided by pharmacy, beyond dispensing, can also promote its level of professionalism; for example, extensive counseling, medication therapy management, health screening, compounding or provision of durable medical equipment. Conclusions  As UK pharmacy and the wider UK National Health Service undergo changes and reconfiguration it is hoped that the creation of the ID-8 new professional body for pharmacy (the Royal Pharmaceutical Society) will help pharmacy in the UK develop the ideals

of professionalism. The old regulator (the Royal Pharmaceutical Society of Great Britain) in July 2009 published two documents, the Code of conduct for pharmacy students and Fitness-to-practise procedures in schools of pharmacy,[1] to help instil professionalism among future pharmacists. The code of conduct sets out the expectations of students studying pharmacy in the UK and is based on seven principles, which are to make the care of patients your first concern, to exercise your professional judgement in the interests of patients and the public, to show respect for others, to encourage patients to participate in decisions about their care, to develop your professional knowledge and competence, to be honest and trustworthy and to take responsibility for your working practices.

For aerobic and anaerobic growth experiments, all S. oneidensis strains were cultured in a defined salts medium (M1) supplemented with 20 mM lactate as carbon/energy source (Myers & Nealson, 1988). Vibrio parahaemolyticus and V. harveyi were tested for anaerobic metal reduction activity in marine broth (Difco) growth medium. Bacterial growth experiments were carried out in a B. Braun Biostat

B batch reactor with automatic feedback control of pH, temperature, and dissolved O2 concentration. Electron acceptors were synthesized as previously described (Saffarini et al., 1994; Blakeney et al., 2000; Taratus et al., 2000; Payne & DiChristina, see more 2006; Neal et al., 2007) and added at the following final concentrations: , 10 mM; , 2 mM; Fe(III) citrate, 50 mM; amorphous MnO2, 15 mM; trimethylamine-N-oxide (TMAO), 25 mM; , 10 mM; fumarate, 30 mM; and DMSO, 25 mM. Gentamycin was supplemented at 15 μg mL−1. PD98059 ic50 For the growth of E. coli β2155 λ pir, diaminopimelate was amended at 100 μg mL−1. Cell growth was monitored by direct cell counts via epifluorescence microscopy and by measuring terminal electron acceptor depletion or end product accumulation. Acridine

orange-stained cells were counted (Zeiss AxioImager Z1 Microscope) according to the previously described procedures (Burnes et al., 1998). Cell numbers at each time point were calculated as the average of 10 counts from two parallel yet independent anaerobic incubations. was measured spectrophotometrically with sulfanilic acid-N-1-naphthyl-ethylenediamine dihydrochloride solution (Montgomery & Dymock, 1962). Fe(III) reduction was monitored by measuring HCl-extractable Fe(II) production with ferrozine (Stookey, 1970). Mn(IV) concentration was Rapamycin cell line measured colorimetrically after reaction with benzidine hydrochloride as previously described (Burnes et al., 1998). Mn(III)-pyrophosphate concentration was measured colorimetrically as previously described (Kostka et al., 1995). concentrations were measured by cyanolysis as previously described

(Kelly & Wood, 1994). Growth on O2, TMAO, DMSO, and fumarate was monitored by measuring increases in cell density at 600 nm. Control experiments consisted of incubations with cells that were heat-killed at 80 °C for 30 min prior to inoculation. Genome sequence data for S. oneidensis MR-1, S. putrefaciens 200, S. putrefaciens CN32, S. putrefaciens W3-18-1, S. amazonensis SB2B, S. denitrificans OS217, S. baltica OS155, S. baltica OS195, S. baltica OS185, S. baltica OS223, S. frigidimarina NCIMB400, S. pealeana ATCC 700345, S. woodyi ATCC 51908, S. sp. ANA-3, S. sp. MR-4, S. sp. MR-7, S. loihica PV-4, S. halifaxens HAW-EB4, S. piezotolerans WP3, S. sediminis HAW-EB3, and S. benthica KT99 were obtained from the National Center for Biotechnology Information (NCBI, http://www.ncbi.nlm.nih.gov) or the Department of Energy Joint Genome Institute (DOE-JGI, http://jgi.doe.gov).

For aerobic and anaerobic growth experiments, all S. oneidensis strains were cultured in a defined salts medium (M1) supplemented with 20 mM lactate as carbon/energy source (Myers & Nealson, 1988). Vibrio parahaemolyticus and V. harveyi were tested for anaerobic metal reduction activity in marine broth (Difco) growth medium. Bacterial growth experiments were carried out in a B. Braun Biostat

B batch reactor with automatic feedback control of pH, temperature, and dissolved O2 concentration. Electron acceptors were synthesized as previously described (Saffarini et al., 1994; Blakeney et al., 2000; Taratus et al., 2000; Payne & DiChristina, MAPK inhibitor 2006; Neal et al., 2007) and added at the following final concentrations: , 10 mM; , 2 mM; Fe(III) citrate, 50 mM; amorphous MnO2, 15 mM; trimethylamine-N-oxide (TMAO), 25 mM; , 10 mM; fumarate, 30 mM; and DMSO, 25 mM. Gentamycin was supplemented at 15 μg mL−1. Dabrafenib ic50 For the growth of E. coli β2155 λ pir, diaminopimelate was amended at 100 μg mL−1. Cell growth was monitored by direct cell counts via epifluorescence microscopy and by measuring terminal electron acceptor depletion or end product accumulation. Acridine

orange-stained cells were counted (Zeiss AxioImager Z1 Microscope) according to the previously described procedures (Burnes et al., 1998). Cell numbers at each time point were calculated as the average of 10 counts from two parallel yet independent anaerobic incubations. was measured spectrophotometrically with sulfanilic acid-N-1-naphthyl-ethylenediamine dihydrochloride solution (Montgomery & Dymock, 1962). Fe(III) reduction was monitored by measuring HCl-extractable Fe(II) production with ferrozine (Stookey, 1970). Mn(IV) concentration was Tolmetin measured colorimetrically after reaction with benzidine hydrochloride as previously described (Burnes et al., 1998). Mn(III)-pyrophosphate concentration was measured colorimetrically as previously described (Kostka et al., 1995). concentrations were measured by cyanolysis as previously described

(Kelly & Wood, 1994). Growth on O2, TMAO, DMSO, and fumarate was monitored by measuring increases in cell density at 600 nm. Control experiments consisted of incubations with cells that were heat-killed at 80 °C for 30 min prior to inoculation. Genome sequence data for S. oneidensis MR-1, S. putrefaciens 200, S. putrefaciens CN32, S. putrefaciens W3-18-1, S. amazonensis SB2B, S. denitrificans OS217, S. baltica OS155, S. baltica OS195, S. baltica OS185, S. baltica OS223, S. frigidimarina NCIMB400, S. pealeana ATCC 700345, S. woodyi ATCC 51908, S. sp. ANA-3, S. sp. MR-4, S. sp. MR-7, S. loihica PV-4, S. halifaxens HAW-EB4, S. piezotolerans WP3, S. sediminis HAW-EB3, and S. benthica KT99 were obtained from the National Center for Biotechnology Information (NCBI, http://www.ncbi.nlm.nih.gov) or the Department of Energy Joint Genome Institute (DOE-JGI, http://jgi.doe.gov).

Urine and capillary ketone measurements, blood gas analysis and/or venous bicarbonate measurement were analysed together with the clinical outcome of either admission or discharge of the patient. Selleck p38 MAPK inhibitor Capillary β-hydroxybutyrate measurement gave a strong negative correlation (r -0.771; p<0.001) with serum bicarbonate concentration. Urine ketone measurement showed a weaker negative correlation (r -0.493; p<0.001) with bicarbonate levels.

There was no difference in the ability to predict hospital admission between blood ketone measurement and urine ketone measurement )positive predictive value 84.6% [95% confidence interval 73.2–95.9%] vs positive predictive value 75.0% [95% confidence interval 62.2–87.8%], respectively). The findings of this study suggest that blood ketone measurement is a better predictor of acid base status than urine ketone measurement. Copyright © 2010 John Wiley & Sons. “
“Anaemia is often an unrecognised complication of diabetes that has an adverse effect on the progression

of diabetes related complications. Anaemia predicts mortality in diabetes related chronic kidney disease (CKD). Contributors to its development include absolute and/or functional iron deficiency and erythropoietin insufficiency. This study aimed to look at the prevalence of anaemia and markers of iron deficiency in patients with diabetes related CKD. An analysis was done of the results from all patients (225 men, 93 women; mean age 70 years) attending joint Dipeptidyl peptidase diabetes–renal clinics over a 12-month period. Haemoglobin (Hb) was measured in 88%. The mean Hb was 12.6g/dl in men and 11.7g/dl in women. A total of 21.5% www.selleckchem.com/products/Deforolimus.html (11.5% men, 10% women) had Hb <11g/dl who should have anaemia management as per National Institute for Health and Clinical Excellence guidelines. Among the anaemic population, CKD stage 3 was present in 25% of men and in 8% of women, with CKD stage 4 present in 20% of men and in 32% of women. Fifty-three percent had absolute iron deficiency (serum ferritin <100μg/L) and 41% had inadequate iron stores (serum ferritin between 100 and 500μg/L). Functional iron deficiency defined

by serum ferritin >100μg/L and red cell hypochromasia ≥6% was noted in 21.6% of anaemic patients. Anaemia is a frequent finding in patients with diabetes related CKD. A significant proportion of patients had functional iron deficiency that required iron therapy for optimisation of their iron stores before starting erythropoiesis-stimulating agents. Measurement of red cell hypochromasia is a valuable tool to detect this group of patients. Copyright © 2010 John Wiley & Sons. “
“The aims of this study were to translate the Michigan Diabetes Knowledge Test (MDKT) into the Malaysian language, and to examine the psychometric properties of the Malaysian version. A standard translation procedure was used to create the Malaysian version of the MDKT from the original English version.