We describe a comprehensive algorithm for the management of ingested rare-earth magnets in children. These newer and smaller neodymium magnets sold as adult toys are much stronger than the traditional magnets, and can attract each other with formidable forces. If >1 magnet is swallowed at the same time, or a magnet is co-ingested with another metallic object, the loops of intestine can be squeezed between them resulting in bowel damage including perforations. An algorithm that uses the number of magnets ingested, location of magnets, and the timing of ingestion before intervention helps to delineate the roles of the pediatric gastroenterologists and surgeons in the management of these cases.

Toxicity challenges by antifungal arsenals and emergence of multidrug resistance scenario has posed a serious threat to global community. To cope up with this alarming situation, phytoactive molecules are richest, safest, and most effective source of broad spectrum antimicrobial compounds. In the present investigation, six phytoactive molecules [cinnamaldehyde (CIN), epigallocatechin, vanillin, eugenol (EUG), furanone, and epigallocatechin gallate] were studied against Candida glabrata and its clinical isolates. Among these, CIN and EUG which are active components of cinnamon and clove essential oils, respectively, exhibited maximum inhibition against planktonic growth of C. glabrata at a concentration of 64 and 128 μg mL –1 , respectively. These two molecules effectively inhibited and eradicated approximately 80% biofilm of C. glabrata and its clinical isolates from biomaterials. CIN and EUG increased reactive oxygen species generation, cell lysis, and ergosterol content in plasma membrane and reduced virulence attributes (phospholipase and proteinase) as well as catalase activity of C. glabrata cells. Reduction of mitochondrial membrane potential with increased release of cytochrome c from mitochondria to cytosol indicated initiation of early apoptosis in CIN- and EUG-treated C. glabrata cells. Transcriptional analysis showed that multidrug transporter ( CDR1 ) and ergosterol biosynthesis genes were downregulated in the presence of CIN, while getting upregulated in EUG-treated cells. Interestingly, genes such as 1,3-β-glucan synthase ( FKS1 ), GPI-anchored protein ( KRE1 ), and sterol importer ( AUS1 ) were downregulated upon treatment of CIN/EUG. These results provided molecular-level insights about the antifungal mechanism of CIN and EUG against C. glabrata including its resistant clinical isolate. The current data established that CIN and EUG can be potentially formulated in new antifungal strategies.

Background: Urolithiasis is a chronic disease of mankind, which has enormous public health importance and it accounts for a substantial economic burden on our society. Hence, it becomes all the more important to formulate cheaper and easier means for treating this condition. The past few years have seen a number of drugs being introduced and successfully used in the medical expulsion therapy of small, uncomplicated ureteral calculi, with each drug claiming to provide better results than the others. Ours is perhaps the first study which has compared the efficacy of tamsulosin and silodosin in the medical expulsion therapy for ureteral calculi. Aims:To compare the efficacy of tamsulosin (0.4mg) vs silodosin (8mg), both in terms of the stone expulsion rate and the time to stone expulsion. Settings and Design:A prospective and a randomized controlled study was conducted in the Department of Urology, Regional Institute of Medical Sciences (RIMS), Imphal, Manipur, India. Material and Methods:From February to August 2012, 100 patients who were between the age group of 18-50 years, who had unilateral, uncomplicated middle or lower ureteral stones

Piracetam, a nootropic drug that has been clinically used for decades but remains enigmatic due to no distinct understanding of its mechanism of action. The present study aimed to investigate the role of caspase independent pathway in piracetam mediated neuroprotection. LPS administration caused significant alterations in oxidative stress related parameters like glutathione, glutathione reductase and increased lipid peroxidation. LPS administration also caused augmented expression of inflammatory cytokines and astrocytes activation. Piracetam treatment offered significant protection against LPS induced oxidative and inflammatory parameters and inhibited astrocytes activation. LPS administration caused augmented level of reactive oxygen species and depleted mitochondrial membrane potential which were attenuated with piracetam treatment. This study for the first time demonstrates the role of caspase independent death factors in piracetam induced neuroprotective effects in rat brain. Translocation of mitochondrial resident apoptosis inducing factor and endonuclease G to nucleus through cytosol after LPS administration was significantly blocked with piracetam treatment. Further, LPS induced DNA fragmentation along with up regulated Poly [ADP-ribose] polymerase 1 (PARP1) levels were also inhibited with piracetam treatment. Apoptotic death was confirmed by the cleavage of caspase 3 as well as histological alteration in rat brain regions. LPS administration caused significantly increased level of cleaved caspase 3, altered neuronal morphology and decreased neuronal density which were restored with piracetam treatment. Collectively our findings indicate that piracetam offered protection against LPS induced inflammatory responses and cellular death including its antioxidative antiapoptotic activity with its attenuation against mitochondria mediated caspase independent pathway.