Objectives Corneal confocal microscopy ( CCM ) is a noninvasive ophthalmic technique that identifies corneal nerve degeneration in a range of peripheral neuropathies and in patients with multiple sclerosis, Parkinson's disease, and amyotrophic lateral sclerosis. We sought to determine whether there is any association of corneal nerve fiber measures with cognitive function and functional independence in patients with MCI and dementia. Methods In this study, 76 nondiabetic participants with MCI ( n = 30), dementia ( n = 26), and healthy age‐matched controls ( n = 20) underwent assessment of cognitive and physical function and CCM . Results There was a progressive reduction in corneal nerve fiber density ( CNFD ), branch density ( CNBD ), and fiber length ( CNFL ) ( P < 0.0001) in patients with MCI and dementia compared to healthy controls. Adjusted for confounders, all three corneal nerve fiber measures were significantly associated with cognitive function ( P < 0.05) and functional independence ( P < 0.01) in MCI and dementia. The area under the ROC curve to distinguish MCI with CNFD , CNBD , and CNFL was 69.1%, 73.2%, and 73.0% and for dementia it was 84.8%, 84.2%, and 86.2%, respectively. Interpretation CCM demonstrates corneal nerve fiber loss, which is associated with a decline in cognitive function and functional independence in patients with MCI and dementia.

There are potentially many ways of assessing diabetic peripheral neuropathy (DPN). However, they do not fulfill U.S. Food and Drug Administration (FDA) requirements in relation to their capacity to assess therapeutic benefit in clinical trials of DPN. Over the past several decades symptoms and signs, quantitative sensory and electrodiagnostic testing have been strongly endorsed, but have consistently failed as surrogate end points in clinical trials. Therefore, there is an unmet need for reliable biomarkers to capture the onset and progression and to facilitate drug discovery in DPN. Corneal confocal microscopy (CCM) is a non-invasive ophthalmic imaging modality for in vivo evaluation of sensory C-fibers. An increasing body of evidence from multiple centers worldwide suggests that CCM fulfills the FDA criteria as a surrogate endpoint of DPN.

Corneal confocal microscopy is a non-invasive ophthalmic imaging modality, which was initially used for the diagnosis and management of corneal diseases. However, over the last 20 years it has come to the forefront as a rapid, non-invasive, reiterative, cost-effective imaging biomarker for neurodegeneration. The human cornea is endowed with the densest network of sensory unmyelinated axons, anywhere in the body. A robust body of evidence shows that corneal confocal microscopy is a reliable and reproducible method to quantify corneal nerve morphology. Changes in corneal nerve morphology precede or relate to clinical manifestations of peripheral and central neurodegenerative conditions. Moreover, in clinical intervention trials, corneal nerve regeneration occurs early and predicts functional gains in trials of neuroprotection. In view of these findings, it is timely to summarise the knowledge in this area of research and to explain why the case for corneal confocal microscopy is sufficiently compelling to argue for its inclusion as a Food and Drug Administration endpoint in clinical trials of peripheral and central neurodegenerative conditions.

IntroductionTo assess the effect of exenatide and pioglitazone or basal-bolus insulin on diabetic peripheral neuropathy (DPN) in patients with poorly controlled type 2 diabetes (T2D).Research design and methodsThis is a substudy of the Qatar Study, an open-label, randomized controlled trial. 38 subjects with poorly controlled T2D were studied at baseline and 1-year follow-up and 18 control subjects were assessed at baseline only. A combination of exenatide (2 mg/week) and pioglitazone (30 mg/day) or glargine with aspart insulin were randomly assigned to patients to achieve an HbA1c <53 mmol/mol (<7%). DPN was assessed with corneal confocal microscopy (CCM), DN4, vibration perception and sudomotor function.ResultsSubjects with T2D had reduced corneal nerves, but other DPN measures were comparable with the control group. In the combination treatment arm (n=21), HbA1c decreased by 35.2 mmol/mol (3.8 %) (p<0.0001), body weight increased by 5.6 kg (p<0.0001), corneal nerve branch density increased (p<0.05), vibration perception worsened (p<0.05), and DN4 and sudomotor function showed no change. In the insulin treatment arm, HbA1c decreased by 28.7 mmol/mol (2.7 %) (p<0.0001), body weight increased by 4.6 kg (p<0.01), corneal nerve branch density and fiber length increased (p≤0.01), vibration perception improved (p<0.01), and DN4 and sudomotor function showed no change. There was no association between the change in CCM measures with change in HbA1c, weight or lipids.ConclusionsTreatment with exenatide and pioglitazone or basal-bolus insulin results in corneal nerve regeneration, but no change in neuropathic symptoms or sudomotor function over 1 year.

PK course contents were perceived to lack depth and relevance to practice, and pharmacist had no experiential training that included aspects of PK. These, and other issues, result in poor application of PK in practice.

Background/aim: Genetic predisposition is implicated in the etiology of metabolic syndrome. This study aimed to investigate the association of vaspin rs2236242 and leptin rs7799039 polymorphisms with their serum levels and with the risk of developing metabolic syndrome in Egyptian women. Materials and methods:This case control study included 100 Egyptian women with metabolic syndrome and 100 without metabolic syndrome. The genotypes of vaspin rs2236242 and leptin rs7799039 were detected by a methodology based on PCR-RFLP. Serum vaspin and leptin levels were determined by ELISA. Results:The metabolic syndrome group was associated with higher serum vaspin and leptin levels when compared to the nonmetabolic syndrome group. The AA genotype of leptin rs7799039 was associated with metabolic syndrome and with higher serum leptin levels, while the different genotypes of vaspin rs2236242 were not associated with metabolic syndrome or different serum vaspin levels. Conclusion:The AA genotype of leptin rs7799039 was associated with metabolic syndrome and higher serum leptin levels. Serum leptin and vaspin can be used as diagnostic markers of metabolic syndrome.

ObjectivesTo explore knowledge and attitude of pharmacists in Qatar towards natural health products (NHPs).MethodsThe quantitative component of this study consisted of an anonymous, online, self-administered questionnaire to assess knowledge about NHPs among pharmacists in Qatar. Descriptive statistics and inferential analysis were conducted using Statistical Package of Social Sciences (SPSS®). Means and standard deviation were used to analyze descriptive data, and statistical significance was expressed as P-value, where P≤0.05 was considered statistically significant. Associations between variables were measured using Pearson correlation. The qualitative component utilized focus group (FG) meetings with a purposive sample of community pharmacists. Meetings were conducted until a point of saturation was reached. FG discussions were audio-taped and transcribed verbatim. Data were analyzed using a framework approach to sort the data according to emerging themes.ResultsThe majority of participants had average to poor knowledge about NHPs while only around 7% had good knowledge. In the FG meetings, participants considered the media, medical representatives, and old systems of natural health as major source of their knowledge. They criticized undergraduate pharmacy courses (for inadequately preparing pharmacists to deal with NHPs) and the pharmacy regulations (for being irrelevant). A perception of NHPs as being “safe” still exists among pharmacists.ConclusionsPharmacists’ ability to provide effective services associated with NHPs is limited by poor access to evidence-based information and poor knowledge. A perception of NHPs and CAM as ‘safe’ still exists among pharmacists, and regulations related to NHPs require addressing to follow best practice and ensure patient safety.

The current literature on the role of microRNA (miRNA) in tumour metabolism is growing, and a number of studies regularly confirm the impact miRNA can have in energy reprograming in tumours. However, there remains to be a lack of understanding of the larger perspective of the role of miRNA in the metabolism story. In the first part of this review, we provide a comprehensive and up-to-date description of the extensive role of miRNAs in tumour metabolism including glucose, lipid and amino acid metabolism. However, in the second part, we aim to provide a description of the multidimensional role miRNA can be playing in tumour metabolism. Of paramount importance is the role miRNA has in responding to metabolic cues and how it can alter cellular state and fate, including cancer stem cells, in response to such cues. In addition, exosomal miRNAs can provide means by which cells can communicate metabolic signals and messages with other cells within the tumour microenvironment, altering therefore the phenotype and functional capacity of these cells. With this expanding area of research better understanding of the role of miRNA in tumour metabolism in a mechanistic approach, and not only describing which miRNAs can effect which genes, can help to exploit the therapeutic implications behind the extensive role of miRNA in tumour metabolism.