What is the evidence of the impact of microfinance on the well-being of poor people?

The concept of microcredit was first introduced in Bangladesh by Nobel Peace Prize winner Muhammad Yunus. Professor Yunus started Grameen Bank (GB) more than 30 years ago with the aim of reducing poverty by providing small loans to the country’s rural poor (Yunus 1999). Microcredit has evolved over the years and does not only provide credit to the poor, but also now spans a myriad of other services including savings, insurance, remittances and non-financial services such as financial literacy training and skills development programmes; microcredit is now referred to as microfinance (Armendáriz de Aghion and Morduch 2005, 2010). A key feature of microfinance has been the targeting of women on the grounds that, compared to men, they perform better as clients of microfinance institutions and that their participation has more desirable development outcomes (Pitt and Khandker 1998). Despite the apparent success and popularity of microfinance, no clear evidence yet exists that microfinance programmes have positive impacts (Armendáriz de Aghion and Morduch 2005, 2010; and many others). There have been four major reviews examining impacts of microfinance (Sebstad and Chen, 1996; Gaile and Foster 1996, Goldberg 2005, Odell 2010, see also Orso 2011). These reviews concluded that, while anecdotes and other inspiring stories (such as Todd 1996) purported to show that microfinance can make a real difference in the lives of those served, rigorous quantitative evidence on the nature, magnitude and balance of microfinance impact is still scarce and inconclusive (Armendáriz de Aghion and Morduch 2005, 2010). Overall, it is widely acknowledged that no well-known study robustly shows any strong impacts of microfinance (Armendáriz de Aghion and Morduch 2005, p199-230). Because of the growth of the microfinance industry and the attention the sector has received from policy makers, donors and private investors in recent years, existing microfinance impact evaluations need to be re-investigated; the robustness of claims that microfinance successfully alleviates poverty and empowers women must be scrutinised more carefully. Hence, this review revisits the evidence of microfinance evaluations focusing on the technical challenges of conducting rigorous microfinance impact evaluations

GITR expression on T-cell receptor-stimulated human CD8+ T cell in a JNK-dependent pathway

Glucocorticoid-induced tumor necrosis factor receptor (TNFR) (GITR) family-related gene is a member of the TNFR super family. GITR works as one of the immunoregulatory molecule on CD4+ regulatory T cells and has an important role on cell survival or cell death in CD4+ T cells. Little is known about the expression of GITR on human CD8+ T cells on antigen-specific and non-specific activation. Here, we report that expression of GITR on human CD8+ T cells on T-cell receptor (TCR) (anti-CD3)-mediated stimulation is dependent on the JNK pathway. The activation of CD8+ T cells was measured by the expression of IL-2 receptor-\u3b1 (CD25), GITR and by IFN-\u3b3 production upon re-stimulation with anti-CD3 antibody. We studied the signaling pathway of such inducible expression of GITR on CD8+ T cells. We found that a known JNK-specific inhibitor, SP600125, significantly down-regulates GITR expression on anti-CD3 antibody-mediated activated CD8+ T cells by limiting JNK phosphorylation. Subsequently, after stimulation of the CD8+ cells, we tested for the production of IFN-\u3b3 by the activated cells following restimulation with the same stimulus. It appears that the expression of GITR on activated human CD8+ T cells might also be regulated through the JNK pathway when the activation is through TCR stimulation. Therefore, GITR serves as an activation marker on activated CD8+ cells and interference with JNK phosphorylation, partially or completely, by varying the doses of SP600125 might have implications in CD8+ cytotoxic T cell response in translational research

Identification of the Microlens in Event MACHO-LMC-20

We report on the identification of the lens responsible for microlensing event MACHO-LMC-20. As part of a \textit{Spitzer}/IRAC program conducting mid-infrared follow-up of the MACHO Large Magellanic Cloud microlensing fields, we discovered a significant flux excess at the position of the source star for this event. These data, in combination with high resolution near-infrared \textit{Magellan}/PANIC data has allowed us to classify the lens as an early M dwarf in the thick disk of the Milky Way, at a distance of $\sim 2$ kpc. This is only the second microlens to have been identified, the first also being a M dwarf star in the disk. Together, these two events are still consistent with the expected frequency of nearby stars in the Milky Way thin and thick disks acting as lenses.Comment: 6 pages, 4 figures, submitted to ApJ Letter

Community perspectives on HIV, violence and health surveillance in rural South Africa : a participatory pilot study

Acknowledgements: The authors would like to acknowledge the study participants who contributed time and information and made significant contributions to the analysis, and the staff at the MRC/Wits Rural Public Health and Health Transitions Research Unit (Agincourt), School of Public Health, Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, South Africa. Funding: The analysis presented in this paper is supported by Health Systems Research Initiative Development Grant from DFID/MRC/Wellcome Trust/ESRC (MR/N005597/1). The fieldwork was completed with the Umeå Centre for Global Health Research, with support from FORTE: Swedish Council for Health, Working Life and Welfare (grant No. 2006–1512). The Agincourt HDSS is supported by the School of Public Health, University of the Witwatersrand, South African Medical Research Council and the Wellcome Trust, UK (Grants 058893/Z/99/A; 069683/Z/02/Z; 085477/Z/08/Z; 085477/B/08/Z)Peer reviewedPublisher PD

Synthesis of some potential antimycobacterial agents

This article does not have an abstract

Examining the initial usability, acceptability and feasibility of a digital mental health intervention for college students in India

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/156228/2/ijop12640_am.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/156228/1/ijop12640.pd

Maternal Anti-Dengue IgG Fucosylation Predicts Susceptibility to Dengue Disease in Infants

Infant mortality from dengue disease is a devastating global health burden that could be minimized with the ability to identify susceptibility for severe disease prior to infection. Although most primary infant dengue infections are asymptomatic, maternally derived anti-dengue immunoglobulin G (IgGs) present during infection can trigger progression to severe disease through antibody-dependent enhancement mechanisms. Importantly, specific characteristics of maternal IgGs that herald progression to severe infant dengue are unknown. Here, we define \u3e /=10% afucosylation of maternal anti-dengue IgGs as a risk factor for susceptibility of infants to symptomatic dengue infections. Mechanistic experiments show that afucosylation of anti-dengue IgGs promotes FcgammaRIIIa signaling during infection, in turn enhancing dengue virus replication in FcgammaRIIIa(+) monocytes. These studies identify a post-translational modification of anti-dengue IgGs that correlates with risk for symptomatic infant dengue infections and define a mechanism by which afucosylated antibodies and FcgammaRIIIa enhance dengue infections

CD4⁺CD25⁻ T Cells Transduced to Express MHC Class I-Restricted Epitope-Specific TCR Synthesize Th1 Cytokines and Exhibit MHC Class I-Restricted Cytolytic Effector Function in a Human Melanoma Model

Cytolytic T cell-centric active specific and adoptive immunotherapeutic approaches might benefit from the simultaneous engagement of CD4⁺ T cells. Considering the difficulties in simultaneously engagingCD4⁺ and CD8⁺ T cells in tumor immunotherapy, especially in an Ag-specific manner, redirecting CD4⁺ T cells to MHC class I-restricted epitopes through engineered expression of MHC class I-restricted epitope-specific TCRs in CD4⁺ T cells has emerged as a strategic consideration. Such TCR-engineered CD4⁺ T cells have been shown to be capable of synthesizing cytokines as well as lysing target cells. We have conducted a critical examination of functional characteristics of CD4⁺ T cells engineered to express the α- and β-chains of a high functional avidity TCR specific for the melanoma epitope, MART-1, as a prototypic human tumor Ag system. We found that unpolarized CD4⁺CD25⁻ T cells engineered to express the MART-1 TCR selectively synthesize Th1 cytokines and exhibit a potent Ag-specific lytic granule exocytosis-mediated cytolytic effector function of comparable efficacy to that of CD8⁺ CTL. Such TCR engineered CD4⁺ T cells, therefore, might be useful in clinical immunotherapy

A randomized phase 2 study of trastuzumab and pertuzumab (TP) compared to cetuximab and irinotecan (CETIRI) in advanced/metastatic colorectal cancer (mCRC) with HER2 amplification: SWOG S1613

Background: HER2 (ERBB2) over-expression and amplification (HER2+) is seen in a small but distinct subset (2-3%) of mCRC and is enriched in RAS/BRAF wild type (WT) tumors. This subset is characterized by a limited response to anti-epidermal growth factor receptor monoclonal antibodybased (anti-EGFR) therapy and a promising response to dual-HER2 inhibition. Methods: In this multicenter, open label, randomized, phase 2 trial, we enrolled 54 patients with RAS/BRAF WT HER2+ mCRC who had had disease progression after 1 or 2 previous therapies. HER2 status was confirmed centrally with immunohistochemistry (IHC) and in-situ hybridization (ISH). HER2+ was defined as IHC 3+ or 2+ and ISH amplified (dual-probe HER2/CEP17 ratio \u3e 2.0). Patients were then randomly assigned in a 1:1 ratio to receive either TP (trastuzumab [loading 8 mg/kg then 6 mg/kg] + pertuzumab [loading 840 mg then 420 mg] every 3 weeks) or CETIRI (cetuximab 500 mg/m2 + irinotecan 180 mg/m2 every 2 weeks). Crossover was allowed for patients on CETIRI arm to TP (cTP) after progression. Restaging (per RECIST v1.1) was performed at 6 and 12 weeks and then every 8 weeks until progression. The primary endpoint was progression-free survival (PFS). Key secondary endpoints were overall response rate (ORR), overall survival (OS) and safety. Results: A total of 54 (out of planned 62 due to low accrual) patients were randomized to TP (26) and CETIRI (28) between 10/2017 and 12/2021. By 8/18/2022, 20 patients had crossed over to cTP arm. One CETIRI patient was not analyzable. The results for key endpoints by protocol defined stratification factors, prior irinotecan (Piri) (yes or no) and HER2/CEP17 ratio (HCR) (\u3e5 or ≤5), are summarized as of data cut-off of 9/6/2022. PFS did not vary significantly by treatment: medians 4.4 (95%CI: 1.9 - 7.6) months in TP group and 3.7 (95%CI: 1.6 - 6.7) months in CETIRI group (p = 0.35). Grade≥3 adverse events occurred in 23%, 46% and 40% of patients in TP, CETIRI and cTP groups. Conclusions: Dual-HER2 inhibition with TP appears to be a safe and effective treatment option for patients with RAS/BRAF WT HER2+ mCRC with a promising response rate of31%.Higher level of HER2 amplification may provide a greater degree of clinical benefit from TP compared to CETIRI. Future correlative efforts will explore biomarkers of response/resistance with this strategy