Assessment of Tsunami Preparedness in East Coast of India through Mega Mock Tsunami Drill conducted on 24 November 2017

Though tsunamis are infrequent, the death toll from tsunamis is huge compared with other natural disasters. The 26 December 2004 Indian Ocean tsunami resulted in disastrous loss of life and property. The major challenge with tsunamis is that they are infrequent, which requires great persistence in sustaining the process of capacity building and preparedness. Because of this infrequency, instruction through tsunami mock drills is the best way to train coastal communities to prepare for devastating actual events. The situational awareness and ability to respond quickly is best achieved through pre-event education and mock drills. The Tsunami mock drills evaluates the ability of warning centre and disaster offices to respond to a tsunami. The drills also educate the public on: where they would receive the official warnings, by which means, what those warnings indicate, how to understand them, and what they need to do in response. INCOIS in collaboration with MHA and NDMA has conducted mega mock tsunami mock drill on 24 November, 2017 to East coast of India. Disaster Management Organisations of Andhra Pradesh, Odisha, Puducherry, Tamil Nadu and West Bengal participated in the drill. They took the drill to community level and executed evacuations at different villages. The average elapsed time achieved from time of receipt of warning to activating the public notification systems was 30 minutes. This is great achievement compared with previous mock drills as it has substantially improved, though the involvement of communities was at huge level. The Tsunami mock drill was very successful which enhanced the awareness and preparedness among the coastal people of East Coast of Indi

Antiinflammatory Therapy with Canakinumab for Atherosclerotic Disease

Background: Experimental and clinical data suggest that reducing inflammation without affecting lipid levels may reduce the risk of cardiovascular disease. Yet, the inflammatory hypothesis of atherothrombosis has remained unproved. Methods: We conducted a randomized, double-blind trial of canakinumab, a therapeutic monoclonal antibody targeting interleukin-1β, involving 10,061 patients with previous myocardial infarction and a high-sensitivity C-reactive protein level of 2 mg or more per liter. The trial compared three doses of canakinumab (50 mg, 150 mg, and 300 mg, administered subcutaneously every 3 months) with placebo. The primary efficacy end point was nonfatal myocardial infarction, nonfatal stroke, or cardiovascular death. RESULTS: At 48 months, the median reduction from baseline in the high-sensitivity C-reactive protein level was 26 percentage points greater in the group that received the 50-mg dose of canakinumab, 37 percentage points greater in the 150-mg group, and 41 percentage points greater in the 300-mg group than in the placebo group. Canakinumab did not reduce lipid levels from baseline. At a median follow-up of 3.7 years, the incidence rate for the primary end point was 4.50 events per 100 person-years in the placebo group, 4.11 events per 100 person-years in the 50-mg group, 3.86 events per 100 person-years in the 150-mg group, and 3.90 events per 100 person-years in the 300-mg group. The hazard ratios as compared with placebo were as follows: in the 50-mg group, 0.93 (95% confidence interval [CI], 0.80 to 1.07; P = 0.30); in the 150-mg group, 0.85 (95% CI, 0.74 to 0.98; P = 0.021); and in the 300-mg group, 0.86 (95% CI, 0.75 to 0.99; P = 0.031). The 150-mg dose, but not the other doses, met the prespecified multiplicity-adjusted threshold for statistical significance for the primary end point and the secondary end point that additionally included hospitalization for unstable angina that led to urgent revascularization (hazard ratio vs. placebo, 0.83; 95% CI, 0.73 to 0.95; P = 0.005). Canakinumab was associated with a higher incidence of fatal infection than was placebo. There was no significant difference in all-cause mortality (hazard ratio for all canakinumab doses vs. placebo, 0.94; 95% CI, 0.83 to 1.06; P = 0.31). Conclusions: Antiinflammatory therapy targeting the interleukin-1β innate immunity pathway with canakinumab at a dose of 150 mg every 3 months led to a significantly lower rate of recurrent cardiovascular events than placebo, independent of lipid-level lowering. (Funded by Novartis; CANTOS ClinicalTrials.gov number, NCT01327846.

Vitiligo: A part of a systemic autoimmune process

Background : Recent clinical and animal experimental studies postulate that the pathogenetic mechanisms of vitiligo could be of systemic origin as vitiligo is associated with ocular and auditory abnormalities as well as other autoimmune disorders.Hence, we studied genetic factors, systemic associations, ocular and auditory abnormalities of vitiligo. Methods: The study group included 150 new cases of various types of vitiligo. One hundred age- and sex-matched nonvitiligo cases were included as controls in the study. A complete family history was taken for all patients. Examination was carried out taking note of the type of vitiligo and approximate percentage of body surface involved. All relevant laboratory investigations, a thorough audiological examination including pure tone audiometry and a complete ophthalmologic examination were carried out in all patients and controls. Statistical analysis was done using the Chi square test. Results: Fifty-four vitiligo patients (36%) had a family history of vitiligo. Anemia was present in 30 (20%) vitiligo patients but only in five (5%) controls, a difference that was statistically significant (χ 2 = 15.8, P < 0.001). Diabetes mellitus was present in 24 (16%) vitiligo patients and only 2 (2%) of controls (Chi square, χ2 = 12.4, P < 0.001). Hypothyroidism and alopecia areata were present in 18 (12%) and 11 (7.4%) vitiligo patients respectively and none of the controls. Hypoacusis was seen in 30 (20%) vitiligo patients and two (2%) controls (χ2 = 8.19, P < 0.005). Twenty-four vitiligo patients (16%) and five controls (5%) had specific ocular abnormalities like uveitis, iris and retinal pigmentary abnormalities (c2 = 7.39, P < 0.001). Conclusion: This study demonstrates statistically significant clinical evidence confirming that vitiligo is a part of systemic autoimmune process

Synthesis of TiN, VN, and CrN from Ammonolysis of TiS2TiS_2, VS2VS_2, and Cr_2S_3\hspace{2mm}^1

A new route to synthesize pure TiN, VN, and CrN from the ammonolysis of $TiS_2$, $VS_2$, and $Cr_2S_3$ is described. Thermo-gravimetric analysis and temperature-programmed reaction (TPR) of $TiS_2$, $VS_2$, and $Cr_2S_3$ with ammonia are employed to understand the reaction pathway to nitride formation. X-ray photoelectron spectroscopic studies confirm the formation of pure nitride phases. Reactivity of these nitride powder toward oxidation was examined by TPR studies. Magnetic susceptibility measurements show that TiN is Pauli-paramagnetic and VN is weakly paramagnetic, whereas CrN shows a paramagnetic to antiferromagnetic transition at 280 K. Electrical conductivity measurements show TiN and VN are metallic, whereas CrN is semiconducting

The poorly membrane permeable antipsychotic drugs amisulpride and sulpiride are substrates of the organic cation transporters from the SLC22 family.

Variations in influx transport at the blood-brain barrier might affect the concentration of psychotropic drugs at their site of action and as a consequence might alter therapy response. Furthermore, influx transporters in organs such as the gut, liver and kidney may influence absorption, distribution, and elimination. Here, we analyzed 30 commonly used psychotropic drugs using a parallel artificial membrane permeability assay. Amisulpride and sulpiride showed the lowest membrane permeability (P e -6 cm/s) and will require influx transport to penetrate the blood-brain barrier and other physiological barriers. We then studied the uptake of amisulpride and sulpiride by the organic cation transporters of the SLC22 family OCT1, OCT2, OCT3, OCTN1, and OCTN2 Amisulpride was found to be transported by all five transporters studied. In contrast, sulpiride was only transported by OCT1 and OCT2. OCT1 showed the highest transport ability both for amisulpride (CLint = 1.9 ml/min/mg protein) and sulpiride (CLint = 4.2 ml/min/mg protein) and polymorphisms in OCT1 significantly reduced the uptake of both drugs. Furthermore, we observed carrier-mediated uptake that was inhibitable by known OCT inhibitors in the immortalized human brain microvascular endothelial cell line hCMEC/D3. In conclusion, this study demonstrates that amisulpride and sulpiride are substrates of organic cation transporters of the SLC22 family. SLC22 transporters may play an important role in the distribution of amisulpride and sulpiride, including their ability to penetrate the blood-brain barrier

Red spectral shift and enhanced quantum efficiency in phonon-free photoluminescence from silicon nanocrystals

Crystalline silicon is the most important semiconductor material in the electronics industry. However, silicon has poor optical properties because of its indirect bandgap, which prevents the efficient emission and absorption of light. The energy structure of silicon can be manipulated through quantum confinement effects, and the excitonic emission from silicon nanocrystals increases in intensity and shifts to shorter wavelengths (a blueshift) as the size of the nanocrystals is reduced. Here we report experimental evidence for a short-lived visible band in the photoluminescence spectrum of silicon nanocrystals that increases in intensity and shifts to longer wavelengths (a redshift) with smaller nanocrystal sizes. This higher intensity indicates an increased quantum efficiency, which for 2.5-nm-diameter nanocrystals is enhanced by three orders of magnitude compared to bulk silicon. We assign this band to the radiative recombination of non-equilibrium electron-hole pairs in a process that does not involve phonons. © 2010 Macmillan Publishers Limited. All rights reserved