Minerals and functional groups present in the jackfruit seed: a spectroscopic investigation

In this work, emission and Fourier transform infrared spectra of the jackfruit seed, in powdered form, are recorded. Analysis of the emission spectrum confirms the presence of two hitherto undetected elements, manganese and magnesium. The Fourier transform infrared spectrum reveals the presence of some specific functional groups, attributed to the different bands present in the spectrum.     

Patient Health Questionnaire-9 as an Effective Tool for Screening of Depression Among Indian Adolescents

PurposeDetection of depression among adolescents in the primary care setting is of paramount importance, especially in resource-constrained countries such as India. This article discusses the diagnostic accuracy, reliability, and validity of the Patient Health Questionnaire–9 (PHQ-9) when pediatricians use it among Indian adolescents.MethodsPediatricians administered the PHQ-9 to 233 adolescent students aged 14–18 years, along with the Beck Depression Inventory. Our psychologist clinically diagnosed depression based on an International Classification of Diseases, 10th Revision, interview of participants. One month later, the PHQ-9 was readministered among students. We conducted appropriate analyses for validity and diagnostic accuracy.ResultsA total of 31 students (13.3%) had a form of depression on psychiatric interview. A PHQ-9 score of ≥5 was ideal for screening (sensitivity, 87.1%; specificity, 79.7%). In addition to good content validity, PHQ-9 had good 1-month test–retest reliability (r = .875) and internal consistency (Cronbach's α = .835). There was high convergent validity with the Beck Depression Inventory (r = .76; p = .001). The concordance rate between the PHQ-9 threshold score of ≥10 and the International Classification of Diseases, 10th Revision based diagnosis was good (Cohen's κ = .62). The area under the receiver operating characteristic curve for PHQ-9 was .939.ConclusionsThe PHQ-9 is a psychometrically sound screening tool for use by pediatricians in a primary care setting in India. Because it is a short, simple, easy to administer questionnaire, the PHQ-9 has tremendous potential in helping to tackle the growing problem of depression among adolescents in developing countries.     

Investigating the effects of tropomyosin mutations on its flexibility and interactions with filamentous actin using molecular dynamics simulation

Tropomyosin (Tpm) is a two-chained α-helical coiled-coil protein that binds to filamentous actin (F-actin), and regulates its interactions with myosin by occupying three average positions on F-actin (blocked, closed, and open). Mutations in the Tpm are linked to heart diseases including hypertrophic cardiomyopathy (HCM) and dilated cardiomyopathy (DCM). To elucidate the molecular mechanisms of Tpm mutations (including DCM mutation E54K, HCM mutations E62Q, A63V, K70T, V95A, D175N, E180G, L185R, E192K, and a designed synthetic mutation D137L) in terms of their effects on Tpm flexibility and its interactions with F-actin, we conducted extensive molecular dynamics simulations for the wild-type and mutant Tpm in complex with F-actin (total simulation time 160 ns per mutant). The mutants exhibited distinct changes (i.e., increase or decrease) in the overall and local flexibility of the Tpm coiled-coil, with each mutation causing both local and long-range modifications of the Tpm flexibility. In addition, our binding calculations revealed weakened Tpm–F-actin interactions (except for L185R, D137L and A63V) involving five periods of Tpm, which correlate with elevated fluctuation of Tpm relative to the blocked position on F-actin that may lead to easier activation and increased Ca²⁺-sensitivity. We also simulated the αβ/βα-Tpm heterodimer in comparison with the αα-Tpm homodimer, which revealed greater flexibility and weaker actin binding in the heterodimer. Our findings are consistent with a complex mechanism underlying how different Tpm mutations perturb the Tpm function in distinct ways (e.g., by affecting specific sites of Tpm), which bear no simple links to the disease phenotypes (e.g., HCM vs. DCM).     

Prophylactic probiotics for prevention of necrotizing enterocolitis in very low birth weight newborns

Our study showed that enteral administration of prophylactic probiotics in neonatal intensive care setup could significantly reduce morbidity due to necrotising enterocolitis in very low birth weight newborn. It also helps in establishing early full enteral feeding and reduces hospital stay.     

Optimization of autologous muscle stem cell survival in the denervated hemilarynx

Objective: Current treatments for vocal fold paralysis are suboptimal in that they fail to restore dynamic function. Autologous muscle stem cell (MSC) therapy is a promising potential therapy for vocal fold paralysis in that it can attenuate denervation‐induced muscle atrophy and provide a vehicle for delivery of neurotrophic factors, thereby potentially selectively guiding reinnervation. The goal of this project was to characterize optimal conditions for injected autologous MSC survival in the thyroarytenoid (TA) muscle following recurrent laryngeal nerve (RLN) injury by local administration of adjuvant factors. Study Design: Animal experiment. Methods: Unilateral RLN transection and sternocleidomastoid muscle (～1 g) biopsies were performed in 20 male Wistar rats. One month later, 10⁶ autologous MSCs labeled via retroviral‐enhanced green fluorescent protein (EGFP) transduction were injected into the denervated hemilarynx of each animal with one of four adjuvant therapies: cardiotoxin [(CTX) 10^?5 M], insulin‐like growth factor‐1 [(IGF‐ 1) 100 μg/mL], ciliary neurotrophic factor [(CNTF) 50 μg/mL], or saline. Animals were euthanized 1 month later and larynges harvested, sectioned, and analyzed for MSC survival. Results: All specimens demonstrate extensive MSC survival, with fusion of the MSCs with the denervated myofibers. Based on mean fluorescent intensity of the laryngeal specimens, IGF‐1 and CNTF had the greatest positive influence on MSC survival. Myofiber diameters demonstrated myofiber atrophy to be inversely related to MSC survival, with the least atrophy in the groups having the greatest MSC survival. Conclusions: Autologous MSC therapy may be a future treatment for vocal fold paralysis. These findings support a model whereby MSCs genetically engineered to secrete CNTF and/or IGF‐1 may not only promote neural regeneration, but also enhance MSC survival in an autocrine fashion.     

Tyrosinase and ocular diseases: some novel thoughts on the molecular basis of oculocutaneous albinism type 1

Tyrosinase (TYR) is a multifunctional copper-containing glycoenzyme (approximately 80 kDa), which plays a key role in the rate-limiting steps of the melanin biosynthetic pathway. This membrane-bound protein, possibly evolved by the fusion of two different copper-binding proteins, is mainly expressed in epidermal, ocular and follicular melanocytes. In the melanocytes, TYR functions as an integrated unit with other TYR-related proteins (TYRP1, TYRP2), lysosome-associated membrane protein 1 (LAMP1) and melanocyte-stimulating hormone receptors; thus forming a melanogenic complex. Mutations in the TYR gene (TYR, 11q14-21, MIM 606933) cause oculocutaneous albinism type 1 (OCA1, MIM 203100), a developmental disorder having an autosomal recessive mode of inheritance. In addition, TYR can act as a modifier locus for primary congenital glaucoma (PCG) and it also contributes significantly in the eye developmental process. Expression of TYR during neuroblast division helps in later pathfinding by retinal ganglion cells from retina to the dorsal lateral geniculate nucleus. However, mutation screening of TYR is complicated by the presence of a pseudogene-TYR like segment (TYRL, 11p11.2, MIM 191270), sharing approximately 98% sequence identity with the 3' region of TYR. Thus, in absence of a full-proof strategy, any nucleotide variants identified in the 3' region of TYR could actually be present in TYRL. Interestingly, despite extensive search, the second TYR mutation in 15% of the OCA1 cases remains unidentified. Several possible locations of these "uncharacterized mutations" (UCMs) have been speculated so far. Based on the structure of TYR gene, its sequence context and some experimental evidences, we propose two additional possibilities, which on further investigations might shed light on the molecular basis of UCMs in TYR of OCA1 patients; (i) partial deletion of the exons 4 and 5 region of TYR that is homologous with TYRL and (ii) variations in the polymorphic GA complex repeat located between distal and proximal elements of the human TYR promoter that can modulate the expression of the gene leading to disease pathogenesis.