A Persian Adaptation of Medication Adherence Self-Efficacy Scale (MASES) in Hypertensive Patients: Psychometric Properties and Factor Structure

© 2015, Springer International Publishing Switzerland. Introduction: Poor adherence to anti-hypertensive treatment significantly contributes to the failure to achieve well-controlled blood pressure in patients with hypertension. Aim: To convert the original English version of Medication Adherence Self-efficacy Scale (MASES) into a Persian version for clinical application in hypertensive patients. Methods: The backward–forward translation method was used to produce the Persian version of the questionnaire. Then the internal consistency was assessed using Cronbach’s alpha. Exploratory Factor Analysis was applied to extract the components of the questionnaire. Correlation between blood pressures and drug adherence was then determined using the Persian MASES in hypertensive patients. Results: Cronbach’s alpha coefficient of the Persian version of MASES was >0.92, suggesting that it can yield consistent results. Exploratory Factor Analysis suggested an uni-dimensionality of the scale. Patients with uncontrolled hypertension showed poor adherence to hypertensive medications, therefore had significant lower self-efficacy scores than those with well-controlled blood pressure by medications. Conclusion: The Persian version of MASES is valid and reliable to assess self-efficacy of antihypertensive medication adherence in hypertensive patient, which is helpful to improve medication compliance in such patients in order to achieve better blood pressure controls

Plant glutathione S-transferase classification, structure and evolution

Glutathione S-transferases are multifunctional proteins involved in diverse intracellular events such as primary and secondary metabolisms, stress metabolism, herbicide detoxification and plant protection against ozone damages, heavy metals and xenobiotics. The plant glutathione S-transferase superfamily have been subdivided into eight classes. Phi, tau, zeta, theta, lambda, dehydroascorbate reductase and tetrachlorohydroquinone dehalogenase classes are soluble and one class is microsomal. Glutathione S-transferases are mostly soluble cytoplasmic enzymes. To date, the crystal structures of over 200 soluble glutathione S-transferases, present in plants, animals and bacteria have been resolved. The structures of glutathione S-transferase influence its function. Phylogenetic analysis suggests that all soluble glutathione S-transferases have arisen from an ancient progenitor gene, through both convergent and divergent pathways.Key words: Glutathione S-transferases (GST), classification, structure, evolution, phylogenetic analysis, xenobiotics

Systematic review of the role of high intensity focused ultrasound (HIFU) in treating malignant lesions of the hepatobiliary system

BACKGROUND: High Intensity Focused Ultrasound (HIFU) is an emerging non-invasive, targeted treatment of malignancy. The aim of this review was to assess the efficacy, safety and optimal technical parameters of HIFU to treat malignant lesions of the hepatobiliary system. METHODS: A systematic search of the English literature was performed until March 2020, interrogating Pubmed, Embase and Cochrane Library databases. The following key-words were input in various combinations: 'HIFU', 'High intensity focussed ultrasound', 'Hepatobiliary', 'Liver', 'Cancer' and 'Carcinoma'. Extracted content included: Application type, Exposure parameters, Patient demographics, and Treatment outcomes. RESULTS: Twenty-four articles reported on the clinical use of HIFU in 940 individuals to treat malignant liver lesions. Twenty-one studies detailed the use of HIFU to treat hepatocellular carcinoma only. Mean tumour size was 5.1 cm. Across all studies, HIFU resulted in complete tumour ablation in 55% of patients. Data on technical parameters and the procedural structure was very heterogeneous. Ten studies (n = 537 (57%) patients) described the use of HIFU alongside other modalities including TACE, RFA and PEI; 66% of which resulted in complete tumour ablation. Most common complications were skin burns (15%), local pain (5%) and fever (2%). CONCLUSION: HIFU has demonstrated benefit as a treatment modality for malignant lesions of the hepatobiliary system. Combining HIFU with other ablative therapies, particularly TACE, increases the efficacy without increasing complications. Future human clinical studies are required to determine the optimal treatment parameters, better define outcomes and explore the risks and benefits of combination therapies

On the asymptotic formula for Goldbach numbers in short intervals

Let $R(k)=\sum\limits_{l+m=k}\Lambda(l)\Lambda(m)$, \Sing(k) = 2 \prod\limits_{p>2}\left(1-\frac{1}{(p-1)^2}\right) \prod\limits_{\substack{ p\mid k\\ p>2 }} \left(\frac{p-1}{p-2}\right) if $k$ is even and \Sing(k) =0 if $k$ is odd. It is known that R(k) \sim k\Sing(k) as $N\to \infty$ for almost all $k\in [N,2N]$ and that \sum_{k\in [n,n+H)}R(k) \sim \sum_{k\in [n,n+H)} k\Sing(k) \quad\hbox{for} \quad n\to \infty \eqno{(1)} uniformly for $H\geq n^{1/6+\epsilon}$. Here we prove, assuming $N^\epsilon\leq H\leq N^{1/6+\epsilon}$ and $N\to\infty$, that (1) holds for almost all $n\in [N,2N]$

High-throughput imaging of ATG9A distribution as a diagnostic functional assay for adaptor protein complex 4-associated hereditary spastic paraplegia

Adaptor protein complex 4-associated hereditary spastic paraplegia is caused by biallelic loss-of-function variants in AP4B1, AP4M1, AP4E1 or AP4S1, which constitute the four subunits of this obligate complex. While the diagnosis of adaptor protein complex 4-associated hereditary spastic paraplegia relies on molecular testing, the interpretation of novel missense variants remains challenging. Here, we address this diagnostic gap by using patient-derived fibroblasts to establish a functional assay that measures the subcellular localization of ATG9A, a transmembrane protein that is sorted by adaptor protein complex 4. Using automated high-throughput microscopy, we determine the ratio of the ATG9A fluorescence in the trans-Golgi-network versus cytoplasm and ascertain that this metric meets standards for screening assays (Z'-factor robust >0.3, strictly standardized mean difference >3). The 'ATG9A ratio' is increased in fibroblasts of 18 well-characterized adaptor protein complex 4-associated hereditary spastic paraplegia patients [mean: 1.54 ± 0.13 versus 1.21 ± 0.05 (standard deviation) in controls] and receiver-operating characteristic analysis demonstrates robust diagnostic power (area under the curve: 0.85, 95% confidence interval: 0.849-0.852). Using fibroblasts from two individuals with atypical clinical features and novel biallelic missense variants of unknown significance in AP4B1, we show that our assay can reliably detect adaptor protein complex 4 function. Our findings establish the 'ATG9A ratio' as a diagnostic marker of adaptor protein complex 4-associated hereditary spastic paraplegia

High-throughput imaging of ATG9A distribution as a diagnostic functional assay for adaptor protein complex 4-associated hereditary spastic paraplegia

Adaptor protein complex 4-associated hereditary spastic paraplegia is caused by biallelic loss-of-function variants in AP4B1, AP4M1, AP4E1 or AP4S1, which constitute the four subunits of this obligate complex. While the diagnosis of adaptor protein complex 4-associated hereditary spastic paraplegia relies on molecular testing, the interpretation of novel missense variants remains challenging. Here, we address this diagnostic gap by using patient-derived fibroblasts to establish a functional assay that measures the subcellular localization of ATG9A, a transmembrane protein that is sorted by adaptor protein complex 4. Using automated high-throughput microscopy, we determine the ratio of the ATG9A fluorescence in the trans-Golgi-network versus cytoplasm and ascertain that this metric meets standards for screening assays (Z'-factor robust >0.3, strictly standardized mean difference >3). The `ATG9A ratio' is increased in fibroblasts of 18 well-characterized adaptor protein complex 4-associated hereditary spastic paraplegia patients [mean: 1.54 +/- 0.13 versus 1.21 +/- 0.05 (standard deviation) in controls] and receiver-operating characteristic analysis demonstrates robust diagnostic power (area under the curve: 0.85, 95% confidence interval: 0.849-0.852). Using fibroblasts from two individuals with atypical clinical features and novel biallelic missense variants of unknown significance in AP4B1, we show that our assay can reliably detect adaptor protein complex 4 function. Our findings establish the 'ATG9A ratio' as a diagnostic marker of adaptor protein complex 4-associated hereditary spastic paraplegia