Synchronisation schemes for two dimensional discrete systems

In this work we consider two models of two dimensional discrete systems subjected to three different types of coupling and analyse systematically the performance of each in realising synchronised states.We find that linear coupling effectively introduce control of chaos along with synchronisation,while synchronised chaotic states are possible with an additive parametric coupling scheme both being equally relevant for specific applications.The basin leading to synchronisationin the initial value plane and the choice of parameter values for synchronisation in the parameter plane are isolatedin each case.Comment: 17 pages 8 figures. submitted to physica script

Dietary iron intake in the first 4 months of infancy and the development of type 1 diabetes: a pilot study

<p>Abstract</p> <p>Aims</p> <p>To investigate the impact of iron intake on the development of type 1 diabetes (T1DM).</p> <p>Methods</p> <p>Case-control study with self-administered questionnaire among families of children with T1DM who were less than 10 years old at the time of the survey and developed diabetes between age 1 and 6 years. Data on the types of infant feeding in the first 4 months of life was collected from parents of children with T1DM (n = 128) and controls (n = 67) <10 years old. Because some cases had sibling controls, we used conditional logistic regression models to analyze the data in two ways. First we performed a case-control analysis of all 128 cases and 67 controls. Next, we performed a case-control analysis restricted to cases (n = 59) that had a sibling without diabetes (n = 59). Total iron intake was modeled as one standard deviation (SD) increase in iron intake. The SD for iron intake was 540 mg in the total sample and 539 mg in the restricted sample as defined above.</p> <p>Results</p> <p>The median (min, max) total iron intake in the first 4 months of life was 1159 (50, 2399) mg in T1DM cases and 466 (50, 1224) mg among controls (<it>P </it>< 0.001). For each one standard deviation increase in iron intake, the odds ratio (95% confidence interval) for type 1 diabetes was 2.01 (1.183, 3.41) among all participants (128 cases and 67 controls) while it was 2.26 (1.27, 4.03) in a restricted sample of T1 D cases with a control sibling (59 cases and 59 controls) in models adjusted for birth weight, age at the time of the survey, and birth order.</p> <p>Conclusion</p> <p>In this pilot study, high iron intake in the first 4 months of infancy is associated with T1DM. Whether iron intake is causal or a marker of another risk factor warrants further investigation.</p

Single-step removal of Hexavalent chromium and phenol using meso zerovalent iron

Novel meso-zero valent iron (mZVI) was investigated for treating complex wastewater containing toxic heavy metal Cr6+ and organic compound phenol. This study is first of its kind illustrating coupled removal in single-step with H2O2 playing a major role as an oxidant and reductant. The mechanism involved was electron transfer from Fe0/2+ to Cr6+ resulting in Fe2+/3+ which in turn was consumed for phenol oxidation returning as Fe2+ into the system for further Cr6+ reduction. While comparing, single-step simultaneous removal of Cr6+ and phenol showed better performance in terms of pollutant removal, Fe2+/3+ recurrent reaction and precipitation generation, double-tep sequential removal performed better in iron active-corrosion time. It was also observed that the entire redox cycle of Cr6+-Cr3+-Cr6+ was reusable for co-contaminant phenol degradation at all pH with the recurrence of Fe2+-Fe3+-Fe2+. The proposed technique was checked for its viability in a single batch reactor and the complex chemistry of the reactions are unfolded by conducting chemical speciation and mass balance study at every stage of reaction. The unique functioning of mZVI was proven with micro-analysis of ZVI's surface and compared with granular ZVI, cZVI. The results obtained from this study open the door for a safer and cleaner single treatment system in removing both toxic heavy metals and organic compounds from contaminated surface water, groundwater and many such industrial effluents

Survival motor neuron protein reduction deregulates autophagy in spinal cord motoneurons in vitro

Spinal muscular atrophy (SMA) is a genetic disorder characterized by degeneration of spinal cord motoneurons (MNs), resulting in muscular atrophy and weakness. SMA is caused by mutations in the Survival Motor Neuron 1 (SMN1) gene and decreased SMN protein. SMN is ubiquitously expressed and has a general role in the assembly of small nuclear ribonucleoproteins and pre-mRNA splicing requirements. SMN reduction causes neurite degeneration and cell death without classical apoptotic features, but the direct events leading to SMN degeneration in SMA are still unknown. Autophagy is a conserved lysosomal protein degradation pathway whose precise roles in neurodegenerative diseases remain largely unknown. In particular, it is unclear whether autophagosome accumulation is protective or destructive, but the accumulation of autophagosomes in the neuritic beadings observed in several neurite degeneration models suggests a close relationship between the autophagic process and neurite collapse. In the present work, we describe an increase in the levels of the autophagy markers including autophagosomes, Beclin1 and light chain (LC)3-II proteins in cultured mouse spinal cord MNs from two SMA cellular models, suggesting an upregulation of the autophagy process in Smn (murine survival motor neuron protein)-reduced MNs. Overexpression of Bcl-xL counteracts LC3-II increase, contributing to the hypothesis that the protective role of Bcl-xL observed in some SMA models may be mediated by its role in autophagy inhibition. Our in vitro experimental data indicate an upregulation in the autophagy process and autophagosome accumulation in the pathogenesis of SMA, thus providing a valuable clue in understanding the mechanisms of axonal degeneration and a possible therapeutic target in the treatment of SMA

Retina Clinic,

Background: Post-operative endophthalmitis remains one of the most visually devastating complications of cataract surgery. Cluster endophthalmitis is defined as five or more cases of endophthalmitis occurring on a particular day in a single operating room in one centre. Excessive inflammation, particularly in the early post-operative phase, should be regarded as infective endophthalmitis. Early diagnosis and immediate intervention in such case, lead to salvage of eye as well as better visual outcome. Objective: To find out the causative organisms and visual outcome after an outbreak of post-operative endophthalmitis in high volume cataract surgical centre. Materials and methods: Retrospective, interventional case series of 19 patients with acute post-operative endophthalmitis after manual small incision cataract surgery in a single day, underwent vitreous tap and received intravitreal Vancomycin, amikacin and Dexamethasone. Subconjunctival vancomycin was given at the end of the procedure. Vitreous samples were stained using Grams stain, Giemsa stain and KOH mount. Samples were sent to the hospital’s microbiology laboratory for culture and sensitivity testing. All patients received intravenous ciprofloxacin for 3 days and oral ciprofloxacin for 7 days. Topical Prednisolone acetate, Ofloxacin, Gentamycin and atropine were given to all patients. Patients were followed up till 6 weeks

Autophagy modulators regulate survival motor neuron protein stability in motoneurons

SpinalMuscular Atrophy (SMA), a neurodegenerative disorder primarily affecting motoneurons (MNs), is caused by the loss of the Survival Motor Neuron 1 (SMN1) gene and reduced levels of full-length survival motor neuron (SMN) protein. The exact cellular/molecular mechanisms involved in SMN-induced MN degeneration are under study. Autophagy is a degradation pathway whose precise roles in neurodegeneration remain largely unknown, but abnormal autophagy has a central role in some neurodegenerative diseases, including MN disorders. The analysis of the autophagy response in SMA and its role in the development of the disease could be essential to understand the disease. In the present work, we describe an increase of autophagosomes and LC3-II protein in spinal cord MNs of severe SMA mouse model. A time-course experiment demonstrated increased LC3-II levels fromembryonic to postnatal stage, suggesting a deregulation of the autophagy process as the disease progressed. Using an in vitro model ofMN culture, we analyzed the effect of autophagy modulators on Smn (murine survival motor neuron) protein level. Results suggest that the inhibitors of the autophagy flux cause reduction ofSmn protein, whereas autophagy inducers increase the level of Smn protein inMNs. In order to evaluate other proteolytic systems involved to SMN degradation,we also studied the effect of the inhibition of the calcium-dependent protease, calpain, on Smn protein level. Our results demonstrate that calpain reduction increases Smn and LC3-II level in cultured MNs. Collectively, these results provide new insight into the role of autophagy and its modulation in SMN protein regulation