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Otomycosis is a common condition encountered in a general otolaryngology clinic setting and has typically been described as fungal infection of the external auditory canal with frequent complications involving the middle ear. Although rarely life threatening, the disease is a challenging and frustrating entity for both pa-tients and otolaryngologists as it frequently requires long-term treatment and follow-up. Despite this, there could be recurrences. Karnasrava is a disease mentioned by Acharya Sushruta in the chapter of Karnaroga Vigyaniya under twenty-eight Karnarogas. Karnasrava is the condition characterized by discharge from Karna and occurs mainly due to Avarana of Vata Dosha. Otomycosis being one of the causes of Karnasrava was selected for the study. Treatment of Karnasrava is explained by Sushruta i.e. Karnadoopana, Karnapoorana, Prakshaalana etc. Case Study: This is a case report of 50-year-old female patient who had complains of pain in right ear since 1 month associated with watery discharge from right ear. The subject is a known case of diabetic mellitus since 1year. The Otoscopic examination of bilateral ear, confirmed that, diagnosis of right ear was Otomycosis associated with otitis media. Materials and Method: The subject who approached Shalakya tantra OPD of GAMC with symptoms of right ear pain associated with on and off watery discharge was systematically reviewed. Intervention was planned for Doshic component involved in Karnasrava. Result: The subject showed considerable improvement in right ear. Discussion: Karnasrava is the condition characterized by Srava from Karna and occurs mainly due to Av-arana of Vata Dosha. Otomycosis is a fungal infection of external auditory canal and one of the causes for Karnasrava. This study sheds light on holistic treatment like Karnadoopana told in the Ayurvedic clas-sics.

Vitamin E is important in maintaining normal neurological structure and function. In this study, 100 children with protein-energy malnutrition (PEM) were studied and compared to a suitably age-matched control group. Posterior column deficits, cerebellar deficits, and problems with fine motor coordination were present to a significant degree in the PEM subjects. The presence of neurological signs was correlated with various parameters of vitamin E deficiency, including low serum alpha-tocopherol levels and a low tocopherol/total lipid ratio which was present in 92 per cent of subjects. There was good concordance between vitamin E levels and vitamin E to serum lipid ratio in assessing vitamin E deficiency. We conclude that vitamin E deficiency is prevalent, to a hitherto unsuspected degree, in children with PEM and that these malnourished children have significant neurological deficits attributable to low vitamin E levels. This observation is of clinical significance as the neurological deficits are potentially reversible with vitamin E supplementation.

Neurological signs including posterior column, spinocerebellar, retinal, and peripheral nerve deficits are being increasingly recognized in vitamin E deficiency states. Children suffering from protein-energy malnutrition (PEM) revealed significantly reduced serum alpha-tocopherol levels compared to age-matched normal children, the deficient subjects also exhibited the widely recognized signs of tocopherol deficiency. In this prospective therapeutic intervention study moderate PEM subjects were administered aqueous oral vitamin E supplementation for 6 weeks and compared with control PEM subjects. The parameters studied included pre- and post-therapy serum alpha-tocopherol levels, alpha-tocopherol lipid ratio, lipid profile, creatine phosphokinase levels, and electroneurophysiological studies. Vitamin E supplementation normalized serum alpha-tocopherol levels (p < 0.001), alpha-tocopherol lipid ratio (p < 0.001), reduced creatine phosphokinase levels (p < 0.01), and reduced neurological signs in PEM subjects (p < 0.001). The observed improvement in neurological dysfunction among PEM subjects is of great interest, especially in developing countries. While larger studies are recommended, the importance of vitamin E administration in PEM is being reported.

Background— Life-threatening disorders of heart rhythm may arise during infancy and can result in the sudden and tragic death of a child. We performed exome sequencing on 2 unrelated infants presenting with recurrent cardiac arrest to discover a genetic cause. Methods and Results— We ascertained 2 unrelated infants (probands) with recurrent cardiac arrest and dramatically prolonged QTc interval who were both born to healthy parents. The 2 parent-child trios were investigated with the use of exome sequencing to search for de novo genetic variants. We then performed follow-up candidate gene screening on an independent cohort of 82 subjects with congenital long-QT syndrome without an identified genetic cause. Biochemical studies were performed to determine the functional consequences of mutations discovered in 2 genes encoding calmodulin. We discovered 3 heterozygous de novo mutations in either CALM1 or CALM2 , 2 of the 3 human genes encoding calmodulin, in the 2 probands and in 2 additional subjects with recurrent cardiac arrest. All mutation carriers were infants who exhibited life-threatening ventricular arrhythmias combined variably with epilepsy and delayed neurodevelopment. Mutations altered residues in or adjacent to critical calcium binding loops in the calmodulin carboxyl-terminal domain. Recombinant mutant calmodulins exhibited several-fold reductions in calcium binding affinity. Conclusions— Human calmodulin mutations disrupt calcium ion binding to the protein and are associated with a life-threatening condition in early infancy. Defects in calmodulin function will disrupt important calcium signaling events in heart, affecting membrane ion channels, a plausible molecular mechanism for potentially deadly disturbances in heart rhythm during infancy.