further validation. There is much to be routinely done to improve secondary psychopathology in patients affected by this disease. The need for mental status screening at diagnosis should be emphasized to identify secondary mental illnesses to improve QoL with its treatment.

It has been suggested that repeated activation of the adrenergic system during antecedent episodes of hypoglycaemia contributes to the development of counterregulatory failure. We previously reported that treatment with carvedilol, a non-specific β-blocker, prevented the development of counterregulatory failure and improved hypoglycaemia awareness in recurrently hypoglycaemic non-diabetic rats. The current study investigated whether carvedilol has similar benefits in diabetic rats.

Recurrently hypoglycaemic streptozotocin-diabetic rats (STZ+RH) were treated with carvedilol for one week prior to undergoing a hypoglycaemic clamp. Hypoglycaemia awareness was evaluated in streptozotocin-diabetic rats made hypoglycaemia unaware using repeated injections of 2-deoxyglucose.

Compared to hypoglycaemia-naïve STZ-diabetic controls, exogenous glucose requirements were more than doubled in the STZ+RH animals and this was associated with a 49% reduction in the epinephrine response to hypoglycaemia. Treating STZ+RH animals with carvedilol improved the epinephrine response to hypoglycaemia. Of note, neither recurrent hypoglycaemia nor carvedilol treatment affected the glucagon response in diabetic animals. Additionally, carvedilol treatment improved the feeding response to insulin-induced hypoglycaemia in diabetic animals made ‘hypoglycaemia unaware’ using repeated injections of 2-deoxyglucose, suggesting the treatment improved awareness of hypoglycaemia as well.

Our data suggest that carvedilol may be useful in preventing impairments of the sympathoadrenal response and the development of hypoglycaemia unawareness during recurring episodes of hypoglycaemia in diabetic animals.

Our data suggest that carvedilol may be useful in preventing impairments of the sympathoadrenal response and the development of hypoglycaemia unawareness during recurring episodes of hypoglycaemia in diabetic animals.

The most frequently prescribed empirical antibiotic agents for mild and moderate diabetic foot infections (DFIs) are amino-penicillins and second-generation cephalosporins that do not cover

spp. Many clinicians believe they can predict the involvement of

in a DFI by visual and/or olfactory clues, but no data support this assertion.

In this prospective observational study, we separately asked 13 experienced (median 11years) healthcare workers whether they thought the

spp. IU1 cost would be implicated in the DFI. Their predictions were compared with the results of cultures of deep/intraoperative specimens and/or the clinical remission of DFI achieved with antibiotic agents that did not cover

.

Among 221 DFI episodes in 88 individual patients, intraoperative tissue cultures grew

in 22 cases (10%, including six bone samples). The presence of

was correctly predicted with a sensitivity of 0.32, specificity of 0.84, positive predictive value of 0.18 and negative predictive value 0.92. Despite two feedbacks of the interim results and a 2-year period, the clinicians’ predictive performance did not improve.

The combined visual and olfactory performance of experienced clinicians in predicting the presence of

in a DFI was moderate, with better specificity than sensitivity, and did not improve over time. Further investigations are needed to determine whether clinicians should use a negative prediction of the presence of

in a DFI, especially in settings with a high prevalence of pseudomonal DFIs.

The combined visual and olfactory performance of experienced clinicians in predicting the presence of Pseudomonas in a DFI was moderate, with better specificity than sensitivity, and did not improve over time. Further investigations are needed to determine whether clinicians should use a negative prediction of the presence of Pseudomonas in a DFI, especially in settings with a high prevalence of pseudomonal DFIs.

We sought to determine whether chromogranin A-positive hormone-negative (CPHN) endocrine cells are increased in the pancreas of pregnant women, offering potential evidence in support of neogenesis.

Autopsy pancreata from pregnant women (

=14) and age-matched non-pregnant control women (

=9) were obtained. Staining of pancreatic sections for chromogranin A, insulin and a cocktail of glucagon, somatostatin, pancreatic polypeptide and ghrelin was undertaken, with subsequent evaluation for CPHN cell frequency.

The frequency of clustered β-cells was increased in pregnant compared to non-pregnant subjects (46.6±5.0 vs. 31.8±5.0% clustered β-cells of total clustered endocrine cells, pregnant vs. non-pregnant,

<.05). Frequency of endocrine cocktail cells was lower in pregnant women than non-pregnant women (36.2±4.0 vs. 57.0±6.8% clustered endocrine cocktail cells of total clustered endocrine cells, pregnant vs. non-pregnant,

<.01). No difference in frequency of CPHN cells was found in islets, nor inh decreased frequency of other endocrine cells in clusters, suggesting a compensatory shift from other pancreatic endocrine cell types to β-cells as a mechanism to meet the increased insulin demands of pregnancy.

We evaluated the efficacy and safety of teneligliptin compared with placebo when added to metformin therapy in Chinese patients with type 2 diabetes inadequately controlled with metformin monotherapy.

This multicentre, randomized, double-blind, placebo-controlled, parallel-group study enrolled type 2 diabetes patients with glycosylated haemoglobin (HbA1c) 7.0%-<10.0% and fasting plasma glucose (FPG) <270mg/dl, receiving a stable metformin dose ≥1000mg/day. Teneligliptin 20mg or placebo was administered orally once daily (qd) before breakfast for 24weeks. The primary efficacy end-point was change in HbA1c from baseline to Week 24. Safety end-points included the incidence of adverse events (AEs).

The least square mean (LSM) change from baseline (standard error [SE]) was -0.72 (0.07) (95% confidence intervals [CI], -0.87, -0.58) for teneligliptin and -0.01 (0.07) (95% CI, -0.16, 0.13) for placebo. The differences (LSM ± SE) between the placebo and teneligliptin groups in HbA1c and FPG were -0.71%±0.11% (

<.