Sequential lending with dynamic joint liability in micro-finance

This paper develops a theory of sequential lending in groups in micro-finance that centers on the notion of dynamic incentives, in particular the simple idea that default incentives should be relatively uniformly distributed across time. In a framework that allows project returns to accrue over time, as well as strategic default, we show that sequential lending can help resolve problems arising out of coordinated default, thus improving project efficiency vis-a-vis individual lending. Inter alia, we also provide a justification for the use of frequent repayment schemes, as well as demonstrate that, depending on how it is manifested, social capital has implications for project efficiency and borrower default. We next examine the optimal choices for the MFI and derive conditions for the optimality of the group lending arrangement. Our framework also provides for some plausible hypotheses as to why there has been a recent transition from group to individual lending

Sequential lending with dynamic joint liability in micro-finance

This paper develops a theory of sequential lending in groups in micro-finance that centers on the notion of dynamic incentives, in particular the simple idea that default incentives should be relatively uniformly distributed across time. In a framework that allows project returns to accrue over time, as well as strategic default, we show that sequential lending can help resolve problems arising out of coordinated default, thus improving project efficiency vis-a-vis individual lending. Inter alia, we also provide a justification for the use of frequent repayment schemes, as well as demonstrate that, depending on how it is manifested, social capital has implications for project efficiency and borrower default. We next examine the optimal choices for the MFI and derive conditions for the optimality of the group lending arrangement. Our framework also provides for some plausible hypotheses as to why there has been a recent transition from group to individual lending

Spin dependent observable effect for free particles using the arrival time distribution

The mean arrival time of free particles is computed using the quantum probability current. This is uniquely determined in the non-relativistic limit of Dirac equation, although the Schroedinger probability current has an inherent non-uniqueness. Since the Dirac probability current involves a spin-dependent term, an arrival time distribution based on the probability current shows an observable spin-dependent effect, even for free particles. This arises essentially from relativistic quantum dynamics, but persists even in the non-relativistic regime.Comment: 5 Latex pages, 2.eps figures; discussions sharpened and references added; accepted for publication in Physical Review

Medulloblastoma Exome Sequencing Uncovers Subtype-Specific Somatic Mutations

Medulloblastomas are the most common malignant brain tumors in children1. Identifying and understanding the genetic events that drive these tumors is critical for the development of more effective diagnostic, prognostic and therapeutic strategies. Recently, our group and others described distinct molecular subtypes of medulloblastoma based on transcriptional and copy number profiles2–5. Here, we utilized whole exome hybrid capture and deep sequencing to identify somatic mutations across the coding regions of 92 primary medulloblastoma/normal pairs. Overall, medulloblastomas exhibit low mutation rates consistent with other pediatric tumors, with a median of 0.35 non-silent mutations per megabase. We identified twelve genes mutated at statistically significant frequencies, including previously known mutated genes in medulloblastoma such as CTNNB1, PTCH1, MLL2, SMARCA4 and TP53. Recurrent somatic mutations were identified in an RNA helicase gene, DDX3X, often concurrent with CTNNB1 mutations, and in the nuclear co-repressor (N-CoR) complex genes GPS2, BCOR, and LDB1, novel findings in medulloblastoma. We show that mutant DDX3X potentiates transactivation of a TCF promoter and enhances cell viability in combination with mutant but not wild type beta-catenin. Together, our study reveals the alteration of Wnt, Hedgehog, histone methyltransferase and now N-CoR pathways across medulloblastomas and within specific subtypes of this disease, and nominates the RNA helicase DDX3X as a component of pathogenic beta-catenin signaling in medulloblastoma

Kinetic and mechanistic studies on the interaction of thiosemicarbazide <span style="font-size:14.0pt;font-family:"Times New Roman";mso-fareast-font-family: "Times New Roman";mso-ansi-language:EN-US;mso-fareast-language:EN-US; mso-bidi-language:AR-SA">with <i>cis </i>- diaquaethylenediamine platinum (II) ion</span>

453-457Kinetics of interaction of thiosemicarbazide with [Pt(en)(H2O2)2+ has been studied spectrophotometrically as a function of [Pt(en)(H2O2)2+ , [thiosemicarbazide] and temperature at a particular pH(4.0) where the substrate complex exists predominantly as the diaqua species and the ligand thiosemicarbazide as a neutral molecule. Th<span style="font-size:14.0pt;font-family:HiddenHorzOCR; mso-bidi-font-family:HiddenHorzOCR">e interaction reaction shows distinct two step consecutive process, the first step is the ligand assisted anation and the second step is the chelation step. The activation parameters for both the steps are evaluated (ΔH1≠= 35 .69 ± 0.80 k J mol -1, ΔS1≠ = -166± 2.54 JK-1 mol -1 and ΔH2≠= 44.54 ± 1.32 k J mol -1 , ΔS2≠ = -182 ± 4. 18 JK-1 mol -1 ).</span

Selective cyanide sensing using a Fe(III) complex of pyridoxal-beta alanine Schiff base

Fluorogenic chemosensors using pyridoxal derivatized ligands as fluorophore is a rapidly growing field of research. Here we report a new Fe(III) complex, [Fe(HBala-pydx)(Bala-pydx)] (H2Bala-pydx is the Schiff base of pyridoxal with beta-alanine), which can serve as a sensitive and selective turn-on fluorescent sensor for the detection of cyanide(CN−) in micromolar concentrations (L.O.D. is 1.134 µM), via the ligand displacement approach, in aqueous-acetonitrile medium. The Fe(III) complex is adequately characterized by analytical and spectroscopic methods along with X-ray crystal structure determination

A Novel COMMD1 Mutation Thr174Met associated with Elevated Urinary Copper and Signs of Enhanced Apoptotic Cell death in a Wilson Disease patient

Wilson disease (WD) results from accumulation of copper and caused due to mutations in ATP7B, a copper transporting ATPase. Besides regular hepatic and neurological symptoms, WD patients occasionally manifest atypical symptoms due to unknown cause. To understand the molecular etiology of atypical WD manifestations, we screened COMMD1, a gene implicated in canine copper toxicosis, in 109 WD patients including those with atypical symptoms. In a patient showing apoptotic symptoms and high urinary copper surpassing normal WD levels, we identified a novel, putative mutation in COMMD1. Two other changes were also identified in the gene. We have examined genotypephenotype correlation between the detected changes and the atypical presentation of the WD patient