Experimental study on heat transfer from rectangular fins in combined convection

Combined natural and forced convective heat transfer arise in many transport processes in engineering devices and in nature, which is frequently encountered in industrial and technical processes, including electronic devices cooled by fans, heat exchangers placed in a low-velocity environment, and solar receivers exposed to winds. In this study, the effects of design parameters have been experimentally investigated for the air-side thermal performance under combined (natural and forced)convection of the rectangular plate heat sinks, and the values of optimum design parameters were sought. Many ideas for improving cooling methods have been proposed, one of which is the heat sink. In this work, the average Nusselt number (Nu) and thermal resistance of a simple base rectangular plate and five vertical rectangular plate heat sinks with different numbers of fins under natural and combined convection were experimentally investigated to obtain the maximum average Nu and minimum thermal resistance for various Reynolds numbers (Re) from 2300 to 40000, Rayleigh numbers (Ra) from 1300000 to 13000000, and Richardson numbers (Ri) from 0.4 to 3. Also, in this experiment, fin spacing (P) was varied from 2.8 mm to 14.6 mm and the dimensionless P/H ratio was varied from 0.1 to 0.49. The flow velocity varied in the range of 2 to 8 m/s under combined convection. Based on the effects of Ri and Re, two empirical equations for natural and also for combined convection heat transfer were derived to calculate the average Nu. The average deviation for these two equations is about 7%.The outcomes of this research can be beneficial for engineers who work on electronics cooling systems

Effectiveness of Lesson Study on Teachers Professional Skills in Hamadan Province Exceptional Education

The purpose of this study was to determine the effectiveness of the lesson study on professional skills in Hamadan province Exceptional Education Teachers’. Research method was ex-post facto. The population was all of exceptional teachers’ in Hamadan Province in 2013-2014 academic year. Through stratified random sampling method, 320 teachers were selected as sample. Data gathering tools included questionnaires of providing learning opportunities, interest in increasing knowledge and job skills, class organization and management, and observation forms included applying learning theories, use of teaching aids and education supplies, use of correct methods of assessment, encourage students to work in groups and test of familiar with theories of learning. Results showed that lesson study groups and other have significant differences in variables of providing learning opportunities (t=2.23;

Percutaneous device closure for secundum-type atrial septal defect: Short and intermediate-term results

BACKGROUND: Device closure of an isolated secundum type atrial septal defect (ASD) has been used as an alternative method for open surgical closure with comparable success and lower morbidity. In this study we evaluated the procedural success and mid-term follow-up results of percutaneous closure of secundum ASD with an Amplatzer�Septal Occluder(ASO) device or a Figula ASD occluder device. METHODS: From June 2001 to January 2009, 74 consecutive patients were scheduled for percutaneous device closure in two centers in Tehran, Iran. All patients had a stretched defect diameter of 30mm or less. After using a sizing balloon to measure the stop-flow diameter, device implantation was performed under the guidance of a trans-esophageal echocardiography (TEE).The size was generally 1 - 2 mm larger than the stretched diameter. Patients were followed for an average of 11 ±4 months. RESULTS: The median stretched diameter of the defect was 20.7±4.8 mm (range: 8 - 30 mm).A total of 73 devices were used in this study. Device closure was successful in 72 (97.2) out of 74 patients. Repositioning of the device was required in one patient. Major complications(including significant residual shunt and device embolization) occurred in 3 (4) patients.There was no procedure-related mortality in our patients. Mild-to-moderate residual shunt was detectable in 10 (13.7) patients immediately following the procedure and in 5 (6.7) patients 24 hours after the procedure. None had residual flow across the device at the end of the follow-up period. CONCLUSION: Device closure of ASD has a safety profile comparable to open surgical repair and can effectively close the defect with excellent procedural and mid-term results

Urinary tract infections in children after renal transplantation

Urinary tract infections (UTI) after pediatric kidney transplantation (KTX) are an important clinical problem and occur in 15–33% of patients. Febrile UTI, whether occurring in the transplanted kidney or the native kidney, should be differentiated from afebrile UTI. The latter may cause significant morbidity and is usually associated with acute graft dysfunction. Risk factors for (febrile) UTI include anatomical, functional, and demographic factors as well as baseline immunosuppression and foreign material, such as catheters and stents. Meticulous surveillance, diagnosis, and treatment of UTI is important to minimize acute morbidity and compromise of long-term graft function. In febrile UTI, parenteral antibiotics are usually indicated, although controlled data are not available. As most data concerning UTI have been accumulated retrospectively, future prospective studies have to be performed to clarify pathogenetic mechanisms and risk factors, improve prophylaxis and treatment, and ultimately optimize long-term renal graft survival

An ancestral 10-bp repeat expansion in VWA1 causes recessive hereditary motor neuropathy

The extracellular matrix comprises a network of macromolecules such as collagens, proteoglycans and glycoproteins. VWA1 (von Willebrand factor A domain containing 1) encodes a component of the extracellular matrix that interacts with perlecan/collagen VI, appears to be involved in stabilizing extracellular matrix structures, and demonstrates high expression levels in tibial nerve. Vwa1-deficient mice manifest with abnormal peripheral nerve structure/function; however, VWA1 variants have not previously been associated with human disease. By interrogating the genome sequences of 74 180 individuals from the 100K Genomes Project in combination with international gene-matching efforts and targeted sequencing, we identified 17 individuals from 15 families with an autosomal-recessive, non-length dependent, hereditary motor neuropathy and rare biallelic variants in VWA1. A single disease-associated allele p.(G25Rfs*74), a 10-bp repeat expansion, was observed in 14/15 families and was homozygous in 10/15. Given an allele frequency in European populations approaching 1/1000, the seven unrelated homozygote individuals ascertained from the 100K Genomes Project represents a substantial enrichment above expected. Haplotype analysis identified a shared 220 kb region suggesting that this founder mutation arose >7000 years ago. A wide age-range of patients (6–83 years) helped delineate the clinical phenotype over time. The commonest disease presentation in the cohort was an early-onset (mean 2.0 ± 1.4 years) non-length-dependent axonal hereditary motor neuropathy, confirmed on electrophysiology, which will have to be differentiated from other predominantly or pure motor neuropathies and neuronopathies. Because of slow disease progression, ambulation was largely preserved. Neurophysiology, muscle histopathology, and muscle MRI findings typically revealed clear neurogenic changes with single isolated cases displaying additional myopathic process. We speculate that a few findings of myopathic changes might be secondary to chronic denervation rather than indicating an additional myopathic disease process. Duplex reverse transcription polymerase chain reaction and immunoblotting using patient fibroblasts revealed that the founder allele results in partial nonsense mediated decay and an absence of detectable protein. CRISPR and morpholino vwa1 modelling in zebrafish demonstrated reductions in motor neuron axonal growth, synaptic formation in the skeletal muscles and locomotive behaviour. In summary, we estimate that biallelic variants in VWA1 may be responsible for up to 1% of unexplained hereditary motor neuropathy cases in Europeans. The detailed clinical characterization provided here will facilitate targeted testing on suitable patient cohorts. This novel disease gene may have previously evaded detection because of high GC content, consequential low coverage and computational difficulties associated with robustly detecting repeat-expansions. Reviewing previously unsolved exomes using lower QC filters may generate further diagnoses

An ancestral 10-bp repeat expansion in VWA1 causes recessive hereditary motor neuropathy.

The extracellular matrix comprises a network of macromolecules such as collagens, proteoglycans and glycoproteins. VWA1 (von Willebrand factor A domain containing 1) encodes a component of the extracellular matrix that interacts with perlecan/collagen VI, appears to be involved in stabilizing extracellular matrix structures, and demonstrates high expression levels in tibial nerve. Vwa1-deficient mice manifest with abnormal peripheral nerve structure/function; however, VWA1 variants have not previously been associated with human disease. By interrogating the genome sequences of 74 180 individuals from the 100K Genomes Project in combination with international gene-matching efforts and targeted sequencing, we identified 17 individuals from 15 families with an autosomal-recessive, non-length dependent, hereditary motor neuropathy and rare biallelic variants in VWA1. A single disease-associated allele p.(G25Rfs*74), a 10-bp repeat expansion, was observed in 14/15 families and was homozygous in 10/15. Given an allele frequency in European populations approaching 1/1000, the seven unrelated homozygote individuals ascertained from the 100K Genomes Project represents a substantial enrichment above expected. Haplotype analysis identified a shared 220 kb region suggesting that this founder mutation arose >7000 years ago. A wide age-range of patients (6-83 years) helped delineate the clinical phenotype over time. The commonest disease presentation in the cohort was an early-onset (mean 2.0 ± 1.4 years) non-length-dependent axonal hereditary motor neuropathy, confirmed on electrophysiology, which will have to be differentiated from other predominantly or pure motor neuropathies and neuronopathies. Because of slow disease progression, ambulation was largely preserved. Neurophysiology, muscle histopathology, and muscle MRI findings typically revealed clear neurogenic changes with single isolated cases displaying additional myopathic process. We speculate that a few findings of myopathic changes might be secondary to chronic denervation rather than indicating an additional myopathic disease process. Duplex reverse transcription polymerase chain reaction and immunoblotting using patient fibroblasts revealed that the founder allele results in partial nonsense mediated decay and an absence of detectable protein. CRISPR and morpholino vwa1 modelling in zebrafish demonstrated reductions in motor neuron axonal growth, synaptic formation in the skeletal muscles and locomotive behaviour. In summary, we estimate that biallelic variants in VWA1 may be responsible for up to 1% of unexplained hereditary motor neuropathy cases in Europeans. The detailed clinical characterization provided here will facilitate targeted testing on suitable patient cohorts. This novel disease gene may have previously evaded detection because of high GC content, consequential low coverage and computational difficulties associated with robustly detecting repeat-expansions. Reviewing previously unsolved exomes using lower QC filters may generate further diagnoses

An Expedient Synthesis, Acetylcholinesterase Inhibitory Activity, and Molecular Modeling Study of Highly Functionalized Hexahydro-1,6-naphthyridines

A series of hexahydro-1,6-naphthyridines were synthesized in good yields by the reaction of 3,5-bis[(E)-arylmethylidene]tetrahydro-4(1H)-pyridinones with cyanoacetamide in the presence of sodium ethoxide under simple mixing at ambient temperature for 6–10 minutes and were assayed for their acetylcholinesterase (AChE) inhibitory activity using colorimetric Ellman’s method. Compound 4e with methoxy substituent at ortho-position of the phenyl rings displayed the maximum inhibitory activity with IC50 value of 2.12 μM. Molecular modeling simulation of 4e was performed using three-dimensional structure of Torpedo californica AChE (TcAChE) enzyme to disclose binding interaction and orientation of this molecule into the active site gorge of the receptor