AUROC, area under the receiver operating characteristics; DDLT, deceased donor liver transplantation; F, fibrosis stage; HCV, hepatitis C virus; HVPG, hepatic venous pressure gradient; LDLT, living donor liver transplantation; LR+, likelihood ratio positive; LR−, likelihood ratio negative; LSM, liver stiffness measurements; LT, liver transplantation; MMRM, mixed model for repeated measurements; NIA, necroinflammatory activity; NPV, negative predictive value; PPV, positive predictive value; S, sensitivity; Sp, specificity. From August 2004 to January 2008, 132 consecutive patients with HCV recurrence after LT out of a total of 293 patients who underwent transplantation in our click here institution

were considered for the study. Exclusion criteria were: graft or patient survival shorter than 12 months after LT (n = 17); combined kidney and liver transplantation (n = 4); hepatitis B virus or human immunodeficiency virus coinfection (n = 3); presence of ascites (n = 6), body mass index > 33 (n = 2), chronic graft rejection (n = 5), biliary tract complications (n = 8), veno-occlusive disease 5-Fluoracil clinical trial (n = 1), de novo autoimmune hepatitis (n = 1) and recurrence of hepatocellular carcinoma (n = 1) during the first year after LT. Therefore, the final number

of HCV-infected LT recipients included was 84 (64%). Another 19 patients who underwent LT for other etiologies were included as the control group. Patients were managed according to previously published protocols.28 Induction immunosuppression was cyclosporine A or tacrolimus and prednisone. Mycophenolate mofetil was added in patients who required cyclosporine or tacrolimus dose reduction or discontinuation. Immunosuppression therapy was recorded throughout the study. Acute rejection episodes were documented by liver histologic analysis and treated with steroid boluses if moderate or severe. After discharge,

patients were visited at the outpatient clinic, monthly for the first 3 months with complete recording of clinical and analytical variables, and every 2 or 3 months thereafter. A total of 73 HCV-infected LT recipients underwent repeated LSM at 3, 6, 9, and 12 months and a liver Farnesyltransferase biopsy 1 year after LT (median = 12.3 months). An HVPG measurement was available in 65 patients at the same time. The remaining 11 patients had cholestatic hepatitis.29 In these patients, liver biopsy (n = 11) and HVPG (n = 9) were performed when the clinical diagnosis was suspected (median = 6.7 months). LSM before initiation of antiviral treatment were available at 3 and 6 months in eight patients and at months 3, 6, and 9 in three. Another five non–HCV-infected patients with elevated alanine aminotransferase (≥ 40 IU/L) underwent a liver biopsy 1 year after LT (median = 13.4 months). The study was previously approved by the Investigation and Ethics Committee of the Hospital Clinic of Barcelona following the ethical guidelines of the 1975 Declaration of Helsinki.

53 Further work is needed to clarify the relative contributions of HIF1α and HIF21α to hepatocyte lipid accumulation. Iron accumulation has

a role in the pathogenesis of several hepatic diseases, including alcoholic liver disease and hereditary hemochromatosis. Macrophage iron increased the severity of alcoholic liver disease in a rodent find more model.72 In conditions of chronic iron deficiency, iron export is limited by production of hepcidin, which in turn degrades the iron efflux protein ferroportin. Using a model of hepatocyte-specific HIF1α deletion, Peyssonnaux et al.73 demonstrated that functional HIF1α is partially responsible for the down-regulation of hepcidin in chronic iron deficiency. In support of this, endothelial-cell ARNT-knockout mice, which are selleck chemicals llc completely defective in HIF signaling, accumulated high levels of iron.74 HIFs have been implicated in gut iron absorption, where some recent data showed that deletion of HIF2α, but not HIF1α, in intestinal cells resulted in down-regulation of serum iron and intestinal expression of the divalent metal ion transporter-1 (DMT1).75 A similar effect of HIF1α expression on DMT1 was observed in vitro

in HEPG2 cells.76 Recent evidence indicates a profound effect of HIF1α on cholestatic liver injury. Moon et al.77 recently described the effect of HIF1α deletion in bile-duct ligated mice, a model of cholestatic liver injury. Mice with a floxed HIF1α exon were mated to Mx-Cre mice, enabling near total excision of floxed genetic elements in cells of the immune system and the liver and partial deletion in other body tissues following serial injections of poly-I:C. Deletion of HIF1α was followed with bile duct ligation (BDL) or sham ligation. In WT mice, an increase of pimonidazole-stained areas and accumulation of HIF1α NADPH-cytochrome-c2 reductase was observed as early as 3 days following BDL, indicating hypoxia. Both HIF1αflox/MxCre and WT mice displayed similar increases in ALT, AST, and serum bile acids, but HIF1αflox/MxCre mice were protected from increases in collagen synthesis

and alpha-smooth muscle actin staining, both markers for tissue fibrosis, as well as profibrotic mediators including PAI-1 and platelet-derived growth factor (PDGF)-A and PDGF-B.77 In a series of in vitro experiments, the same group reported that production of profibrotic mediators was induced by culturing mouse hepatocytes in 1% oxygen. Using an siRNA approach, the authors demonstrated that the production of profibrotic mediators was completely prevented in ARNT-null cells, but only partially prevented in HIF1α-null cells, suggesting that other HIF isoforms (particularly HIF2) play a role.78 These data in support of a role for HIF in liver fibrosis are rendered more compelling by evidence in other models of liver fibrosis.

Mean age of the patients in the study was 47 ± 13.4 years. Rheumatoid factor (RF) was positive in 63%, anticyclic citrullinated peptide antibody (anti-CCP) in 71% and both of them were positive in 49% of cases. A very small group of patients had greater than six tender joints (6%) and swollen joints (9%); moreover there was no significant differences in number

of tender and swollen joint counts across different populations. Mean DAS28 erythrocyte sedimentation rate (ESR) was 2.91 ± 1.02 and there were no statistically R788 clinical trial significant differences between the study groups. Almost half of the patients (49%) were in remission (DAS28 < 2.6) and one-third (36%) were in active disease (DAS28 > 3.2). However, a minority of patients Vorinostat datasheet (15%) were in low disease activity (DAS28 2.6–3.2). The mean HAQ score was 1.02 (± 0.60). X-rays of hand and feet were performed on 65% of patients, of whom 11% were found to have erosions. Sixty-six percent of our patients were on

one synthetic DMARD in the last 2 months before being involved in the study, 27% were on two synthetic DMARDs and 7% were not on synthetic DMARDs. Synthetic DMARDs were mostly used in the Asian group (74.8%). Methotrexate was the most commonly used DMARD (75%). It was used alone in 31% or in combination with other synthetic or biologic DMARDs (44%). Biologic DMARDs were used in 29%: 11% on rituximab, 8% on tocilizumab, 9% on anti-tumor necrosis factor and one patient was on abatacept. Use of biologics was more in the Qatari population (65.2%) and least in Asians (15.3%). Glucocorticoids were used in 51% of patients with dose range of 5–10 mg\day. In this cross-sectional study we described the characteristics

of RA in Qatar managed on an outpatient base and analyzed the severity and activity of the disease. Our study showed that the majority of patients was female (67%) and they were more frequently Qataris (91.3%) compared with Asians (52.5%) which reflects see more the pattern of the Qatar population (most Asians are male). Among all patients, RF was positive in 63%, anti-CCP in 71% and both were positive in 49% which is close to that reported from Kuwait 60%.[4] A comparative study of RA in British and Malaysian patients showed that RF was positive in 65% in each group of patients which is similar to our study.[7] In our study 64% of patients were either in remission (49% with DAS28 < 2.6) or in low disease activity (15% with DAS28 < 3.2) while mean DAS28-ESR was 2.85 ± 1.047. This is in contrast to a UAE study which showed that only a few patients (15%) were in low disease activity and most of them had high disease activity with mean DAS of 5.2.[6] However, 36% of our patients had moderate to high disease activity with DAS28 > 3.2. The majority of our patients (93%) were being treated with DMARDs over the last 2 months before enrolment in the study, 66% on one synthetic DMARD and 27% on two.

Mean age of the patients in the study was 47 ± 13.4 years. Rheumatoid factor (RF) was positive in 63%, anticyclic citrullinated peptide antibody (anti-CCP) in 71% and both of them were positive in 49% of cases. A very small group of patients had greater than six tender joints (6%) and swollen joints (9%); moreover there was no significant differences in number

of tender and swollen joint counts across different populations. Mean DAS28 erythrocyte sedimentation rate (ESR) was 2.91 ± 1.02 and there were no statistically click here significant differences between the study groups. Almost half of the patients (49%) were in remission (DAS28 < 2.6) and one-third (36%) were in active disease (DAS28 > 3.2). However, a minority of patients Roscovitine ic50 (15%) were in low disease activity (DAS28 2.6–3.2). The mean HAQ score was 1.02 (± 0.60). X-rays of hand and feet were performed on 65% of patients, of whom 11% were found to have erosions. Sixty-six percent of our patients were on

one synthetic DMARD in the last 2 months before being involved in the study, 27% were on two synthetic DMARDs and 7% were not on synthetic DMARDs. Synthetic DMARDs were mostly used in the Asian group (74.8%). Methotrexate was the most commonly used DMARD (75%). It was used alone in 31% or in combination with other synthetic or biologic DMARDs (44%). Biologic DMARDs were used in 29%: 11% on rituximab, 8% on tocilizumab, 9% on anti-tumor necrosis factor and one patient was on abatacept. Use of biologics was more in the Qatari population (65.2%) and least in Asians (15.3%). Glucocorticoids were used in 51% of patients with dose range of 5–10 mg\day. In this cross-sectional study we described the characteristics

of RA in Qatar managed on an outpatient base and analyzed the severity and activity of the disease. Our study showed that the majority of patients was female (67%) and they were more frequently Qataris (91.3%) compared with Asians (52.5%) which reflects Atorvastatin the pattern of the Qatar population (most Asians are male). Among all patients, RF was positive in 63%, anti-CCP in 71% and both were positive in 49% which is close to that reported from Kuwait 60%.[4] A comparative study of RA in British and Malaysian patients showed that RF was positive in 65% in each group of patients which is similar to our study.[7] In our study 64% of patients were either in remission (49% with DAS28 < 2.6) or in low disease activity (15% with DAS28 < 3.2) while mean DAS28-ESR was 2.85 ± 1.047. This is in contrast to a UAE study which showed that only a few patients (15%) were in low disease activity and most of them had high disease activity with mean DAS of 5.2.[6] However, 36% of our patients had moderate to high disease activity with DAS28 > 3.2. The majority of our patients (93%) were being treated with DMARDs over the last 2 months before enrolment in the study, 66% on one synthetic DMARD and 27% on two.

For example, the gene aziU3 shows sequence similarity only to hypothetical proteins of unknown functions in different bacterial species. The involvement of aziU3 in the azinomycin B biosynthesis is yet to be determined. Using our optimized Ibrutinib genetic manipulation systems described above that enables easier transfer of foreign DNA into S. sahachiroi, we investigated whether this gene is essential for azinomycin B biosynthesis by in-frame

deletion. A 1.73-kb upstream region and a 1.77-kb downstream region of aziU3 were cloned into pOJ260 to yield pMSB-WS09. This plasmid was classified as a suicide plasmid because of the absence of a Streptomyces replicon and the genes for site-specific integration. After introduction into Streptomyces, the plasmid could propagate only if integrated into LY2109761 mouse the chromosome via the first crossover event between either pair of homologous regions to yield conjugants/transformants. In general, introduction of suicide plasmids into wild-type streptomycete is more difficult than the site-specific integrative or autoreplicative plasmids (Kieser et al., 2000). Nevertheless, conjugal transfer of our pMSB-WS09 from E. coli to S. sahachiroi was achieved at an unexpected high efficiency (10−5 conjugants per recipient). The gene aziU3 was deleted after the second crossover event between another pair of homologous regions to yield the mutant strain ΔaziU3 (Fig. 2 and Fig. S7). Bioassay

and HPLC-MS analyses demonstrated that the azinomycin B biosynthesis

was abolished when aziU3 was absent from the azi cluster (Figs 3 and 4). To rule out possible polar effects caused by gene replacement, complementation of aziU3 was performed in trans using an integrative plasmid pMSB-WS38 with aziU3 located downstream of the promoter PermE*, which is from the erythromycin biosynthetic gene cluster of Saccharopolyspora erythraea. This plasmid was introduced into the deletion mutant ΔaziU3 by intergeneric conjugation to yield the complementation strain ΔaziU3::aziU3 (Fig. 2 and Fig. S7). Production of azinomycin B in the complementation strain was not only restored but also increased 24% compared with the wild-type strain. These results indubitably indicated that AziU3 was involved in the azinomycin B biosynthesis. In addition, it also showed that the promoter PermE* Tau-protein kinase from S. erythraea worked as a strong constitutive promoter in S. sahachiroi, which is not observed in every Streptomyces species. It was speculated that ΔaziU3::aziU3 produces higher amounts of azinomycin B than the wild-type strain because of increased aziU3 expression regulated by the strong promoter PermE*. To further increase the expression level of this gene, the plasmid pMSB-WS38 carrying one copy of aziU3 was introduced into wild-type S. sahachiroi by protoplast transformation, yielding WT::aziU3. As expected, production of azinomycin B increased further (Fig.

For example, the gene aziU3 shows sequence similarity only to hypothetical proteins of unknown functions in different bacterial species. The involvement of aziU3 in the azinomycin B biosynthesis is yet to be determined. Using our optimized learn more genetic manipulation systems described above that enables easier transfer of foreign DNA into S. sahachiroi, we investigated whether this gene is essential for azinomycin B biosynthesis by in-frame

deletion. A 1.73-kb upstream region and a 1.77-kb downstream region of aziU3 were cloned into pOJ260 to yield pMSB-WS09. This plasmid was classified as a suicide plasmid because of the absence of a Streptomyces replicon and the genes for site-specific integration. After introduction into Streptomyces, the plasmid could propagate only if integrated into NVP-LDE225 price the chromosome via the first crossover event between either pair of homologous regions to yield conjugants/transformants. In general, introduction of suicide plasmids into wild-type streptomycete is more difficult than the site-specific integrative or autoreplicative plasmids (Kieser et al., 2000). Nevertheless, conjugal transfer of our pMSB-WS09 from E. coli to S. sahachiroi was achieved at an unexpected high efficiency (10−5 conjugants per recipient). The gene aziU3 was deleted after the second crossover event between another pair of homologous regions to yield the mutant strain ΔaziU3 (Fig. 2 and Fig. S7). Bioassay

and HPLC-MS analyses demonstrated that the azinomycin B biosynthesis

was abolished when aziU3 was absent from the azi cluster (Figs 3 and 4). To rule out possible polar effects caused by gene replacement, complementation of aziU3 was performed in trans using an integrative plasmid pMSB-WS38 with aziU3 located downstream of the promoter PermE*, which is from the erythromycin biosynthetic gene cluster of Saccharopolyspora erythraea. This plasmid was introduced into the deletion mutant ΔaziU3 by intergeneric conjugation to yield the complementation strain ΔaziU3::aziU3 (Fig. 2 and Fig. S7). Production of azinomycin B in the complementation strain was not only restored but also increased 24% compared with the wild-type strain. These results indubitably indicated that AziU3 was involved in the azinomycin B biosynthesis. In addition, it also showed that the promoter PermE* Janus kinase (JAK) from S. erythraea worked as a strong constitutive promoter in S. sahachiroi, which is not observed in every Streptomyces species. It was speculated that ΔaziU3::aziU3 produces higher amounts of azinomycin B than the wild-type strain because of increased aziU3 expression regulated by the strong promoter PermE*. To further increase the expression level of this gene, the plasmid pMSB-WS38 carrying one copy of aziU3 was introduced into wild-type S. sahachiroi by protoplast transformation, yielding WT::aziU3. As expected, production of azinomycin B increased further (Fig.

The qRT-PCR and relative transcription

of genes were analyzed as described previously (Wang et al., 2009). Brucella melitensis strains were grown overnight in TSB medium with aeration at 37 °C. For each strain, three 1-mL aliquots of cultures in TSB medium (initial OD600 nm 0.05) were incubated at 37 °C with shaking in a 24-well plate containing an insert plate with a porous membrane (diameter, 1.0 μm) (BD Falcon). After 24 h, bacteria were fixed for 20 min with 4% paraformaldehyde, and plates were centrifuged for 10 min at 1500 g. Membranes were cut and dehydrated for 5 min in 25%, 50%, 75%, 95% and 100% ethanol at room temperature. They were finally prepared by critical-point drying, mounted on an aluminum stub and covered with a thin layer of gold (20–30 nm). Examination PI3K inhibitor was carried out with a scanning electron microscope (Hitachi S450). Exopolysaccharide was stained as follows: bacteria in a middle logarithmic-phase culture (OD600 nm 1.0) were fixed with 4% paraformaldehyde for 20 min before staining. For detection of polysaccharides, 1 mL of 0.05% calcofluor white (fluorescent whitener 28; Sigma) was added to 0.1 mL of paraformaldehyde-fixed cells. Visualization was accomplished using an epifluorescence microscope (Olympus

IX71). The susceptibilities of Brucella strains to polymyxin B (Sigma) were determined 5-Fluoracil datasheet following a protocol described previously (Martinez de Tejada et al., 1995) with modifications. Brucella melitensis strains were cultured for 72 h on TSA. Then, bacterial suspensions of approximately 1 × 104 CFU mL−1 were prepared in phosphate-buffered saline and 100-μL aliquots were mixed with different concentrations of Adenosine 100 μL polymyxin B (the final concentrations in the wells were 2000, 1000, 500 and 250 μg mL−1, respectively) and cultured in 96-well plates. After a 1-h incubation at 37 °C in a 5% CO2 atmosphere, a 50-μL aliquot of each well was serially diluted and spread in triplicate on TSA plates for CFU

determination. The results were expressed as the mean±SD of three assays. All the results represent the averages from at least three separate experiments. The sensitivity of Brucella strains to hydrogen peroxide, high-salinity or high-osmolarity stresses was determined as follows: B. melitensis strains inoculated into TSB medium were grown to the early logarithmic phase (OD600 nm 0.6) at 37 °C. To determine the effect of high-salinity or high-osmolarity stress on B. melitensis, the log-phase cells were incubated at 37 °C for 20 min in the presence of NaCl (1.5 M) or sorbitol (1.5 M). To test the effect of oxidative stress, the cells were incubated for 30 min in 440 mM H2O2. After the treatment, the survival percent of the bacteria was determined as above. All the results represent the averages from at least three separate experiments. Previously, we compared proteome differences between BM and BMΔvirB in GEM4, a which strongly induces virB.

The qRT-PCR and relative transcription

of genes were analyzed as described previously (Wang et al., 2009). Brucella melitensis strains were grown overnight in TSB medium with aeration at 37 °C. For each strain, three 1-mL aliquots of cultures in TSB medium (initial OD600 nm 0.05) were incubated at 37 °C with shaking in a 24-well plate containing an insert plate with a porous membrane (diameter, 1.0 μm) (BD Falcon). After 24 h, bacteria were fixed for 20 min with 4% paraformaldehyde, and plates were centrifuged for 10 min at 1500 g. Membranes were cut and dehydrated for 5 min in 25%, 50%, 75%, 95% and 100% ethanol at room temperature. They were finally prepared by critical-point drying, mounted on an aluminum stub and covered with a thin layer of gold (20–30 nm). Examination Maraviroc supplier was carried out with a scanning electron microscope (Hitachi S450). Exopolysaccharide was stained as follows: bacteria in a middle logarithmic-phase culture (OD600 nm 1.0) were fixed with 4% paraformaldehyde for 20 min before staining. For detection of polysaccharides, 1 mL of 0.05% calcofluor white (fluorescent whitener 28; Sigma) was added to 0.1 mL of paraformaldehyde-fixed cells. Visualization was accomplished using an epifluorescence microscope (Olympus

IX71). The susceptibilities of Brucella strains to polymyxin B (Sigma) were determined selleck kinase inhibitor following a protocol described previously (Martinez de Tejada et al., 1995) with modifications. Brucella melitensis strains were cultured for 72 h on TSA. Then, bacterial suspensions of approximately 1 × 104 CFU mL−1 were prepared in phosphate-buffered saline and 100-μL aliquots were mixed with different concentrations of Avelestat (AZD9668) 100 μL polymyxin B (the final concentrations in the wells were 2000, 1000, 500 and 250 μg mL−1, respectively) and cultured in 96-well plates. After a 1-h incubation at 37 °C in a 5% CO2 atmosphere, a 50-μL aliquot of each well was serially diluted and spread in triplicate on TSA plates for CFU

determination. The results were expressed as the mean±SD of three assays. All the results represent the averages from at least three separate experiments. The sensitivity of Brucella strains to hydrogen peroxide, high-salinity or high-osmolarity stresses was determined as follows: B. melitensis strains inoculated into TSB medium were grown to the early logarithmic phase (OD600 nm 0.6) at 37 °C. To determine the effect of high-salinity or high-osmolarity stress on B. melitensis, the log-phase cells were incubated at 37 °C for 20 min in the presence of NaCl (1.5 M) or sorbitol (1.5 M). To test the effect of oxidative stress, the cells were incubated for 30 min in 440 mM H2O2. After the treatment, the survival percent of the bacteria was determined as above. All the results represent the averages from at least three separate experiments. Previously, we compared proteome differences between BM and BMΔvirB in GEM4, a which strongly induces virB.

The authors showed that half of British companies taking clients to remote high altitude destinations did not bring basic drugs to prevent or treat altitude illness. The study did not inquire about other important drugs, but they did discover that several of the companies did not carry group drugs because of fear of liability.

An international flight over the ocean is also a place remote from emergency medical care. Two decades ago, most international airlines did not carry emergency medications on their airplanes. Beyond the expense and logistics of keeping these kits stocked and up to date, there was a fear that flight crews could not be expected to utilize these first aid kits appropriately. After some high profile medical emergencies in the course of long flights, congressional hearings were held in the United States to analyze the issue.[3] It was discovered that almost every flight had AZD6244 order medical personnel on board as passengers who would volunteer to help in an emergency—if drugs and equipment were available. Since that time, virtually all airlines carry well-stocked first aid kits

and even automatic external defibrillators.[4] A similar situation exists in many this website adventure travel destinations—medical personnel can frequently be found in an emergency and could be effective if an expedition medical kit was available. The fear of being sued has clouded not only the issue of having drugs available on an expedition, but also who should be in charge of those drugs. If there is a problem as a result of offering medical care on a foreign expedition, the liability issue is more complicated than it might seem. If a physician was along on a trip as a regular client, whether he/she is construed as practicing medicine by helping a fellow client would depend on whether a doctor–patient relationship has been established, implicitly or explicitly. In many parts of the world, good-faith medical care in an emergency is protected by “Good Samaritan laws” that protect bystanders from being sued

for their efforts to help a stranger in an emergency, as long as their efforts are not grossly negligent, wanton, or willful. check details In these instances, a doctor–patient relationship is not considered to have occurred—mainly because of the absence of a preexisting duty to the victim or an intent to charge for the services. If, however, physicians have been offered a financial incentive or a discount to accompany a trek, legal advisors have argued that these physicians are no longer “bystanders,” but de facto employees of the adventure travel company with an implied or express contract to provide medical services, and therefore not protected under Good Samaritan laws. The decision as to whether the person who offered medical care was a Good Samaritan or an employee of the company would only be relevant if there was a law suit.

This observation may be used to grade more precisely the risk of ulceration in elderly diabetic patients. Copyright © 2013 John Wiley & Sons. “
“The objective of this observational case report was to present the first case consistent with the ‘dead in bed’ syndrome in which hypoglycaemia

has been documented by real-time glucose monitoring at the time of death. We report the case of a 41-year-old male with type 1 diabetes. Diagnosed at age 14, he had poor glycaemic control during his teen years and suffered from severe hypoglycaemia unawareness. His diabetes was complicated by nephropathy, find more neuropathy and retinopathy. He was last seen alive and well by the family seven days before he was found dead in bed with his insulin pump and sensor in situ. The last recorded interaction between the patient and the pump system was seven days previously with evidence of prolonged hypoglycaemia around the time. Post-mortem examination showed no specific cause of death. The findings in this case report are consistent with ABT-199 cost the hypothesis that hypoglycaemia is a precipitant of the ‘dead in bed’ syndrome in diabetes and indicate that the presence of low glucose alarms does not provide complete protection against such an event. Copyright © 2013 John Wiley & Sons. “
“The primary aim of this study

was to better understand patients’ experience of admission to hospital with diabetic ketoacidosis (DKA) and its psychological impact. The secondary aim was to improve our service Cell press provision for patients following an episode of DKA. Forty patients who had been admitted to hospital with DKA were invited to participate. Four patients agreed to take part (three female, one male; mean age 34 years, range 21–49 years). All participants had type 1 diabetes.

Participants completed a semi-structured interview and psychometric questionnaires. Descriptive statistics were generated for demographic and questionnaire data. Interview transcripts were qualitatively analysed using thematic analysis. The thematic analysis showed three important themes: Consequences of DKA; Recognising and Managing DKA; and Hospital Experience. The theme of Recognising and Managing DKA highlighted that only one participant recognised insufficient insulin as a trigger for DKA, and other people first recognised symptom severity in every case. The theme Hospital Experience seemed to support a number of studies that have found poor provision of care for those presenting with DKA. It is important to note that there were only four participants who contributed, which limited the conclusions that can be drawn. It appeared some patients lack understanding of what DKA is. It seems that better provision of information on DKA needs to be given to both the individual and their family members. There was some evidence that an admission for DKA is a marker for follow-up psychological assessment. Copyright © 2013 John Wiley & Sons. “
“Type 2 diabetes is the disease of our times.