Credit constraints and investment behavior in Mexico's rural economy

This paper uses two recently completed surveys of individual entrepreneurs (farmers and microentrepreneurs) and registered enterprises (agricultural and nonagricultural) operating in Mexico’s rural sector to provide new evidence about the factors influencing the incidence of credit constraints and investment behavior. To measure the incidence of credit constraints, the authors use self-reported information on whether economic agents have a demand for loans, separating formal and informal markets. They define credit constraints as a situation where rural agents report an unsatisfied demand for loans (formal or informal), which originates from rural agents having projects that are too risky or from impediments hindering the ability of rural agents and lenders to reduce information asymmetries. The authors find that the self-reported demand for loans is low. Nevertheless, the incidence of credit constraints is pervasive, especially among individual entrepreneurs. The low use of loans has consequences for the amount of investments that occur in the rural economy, posing a major obstacle to Mexico’s convergence towards its NAFTA partners. The empirical analysis, which includes proxies of business prospects and creditworthiness, shows that improving the availability of loans to credit constrained agents would increase the number of agents making investments and their investment to capital ratios.Access to Finance,,Debt Markets,Bankruptcy and Resolution of Financial Distress,Banks&Banking Reform

Foreign bank entry - experience, implications for developing countries, and agenda for further research

In recent years, foreign bank participation has increased tremendously in several developing countries. In Argentina, Chile, the Czech Republic, Hungary and Poland, for example, more than fifty percent of banking assets are now in foreign-controlled banks. In Asia, Africa, The Middle East, and the former Soviet Union, the rate of entry by foreign banks has been slower, but the trend is similar. Although the number of countries welcoming foreign banks is growing, many questions about foreign bank entry are still being debated, including: 1) What draws foreign banks to a country? 2) Which banks expand abroad? 3) What do foreign banks do once they arrive? 4) How does the mode of a bank's entry - for example, as a branch of its parent, or as an independent subsidiary company - affect its behavior? The authors summarize current knowledge on these issues. In addition, since the existing literature focuses heavily on industrial countries, they put forth an agenda for further study of the effects of foreign bank entry in developing countries.Financial Intermediation,Banks&Banking Reform,Payment Systems&Infrastructure,Financial Crisis Management&Restructuring,Banking Law,Banks&Banking Reform,Financial Intermediation,Financial Crisis Management&Restructuring,Banking Law,Municipal Financial Management

Bank lending to small businesses in Latin America : does Bank origin matter?

In recent years foreign bank participation has increased tremendously in Latin America. Some observers argue that foreign bank entry will benefit Latin American banking systems by reducing the volatility of loans and deposits and increasing efficiency. Others are concerned that foreign banks might choose to extend credit only to certain customers, leaving some sectors-such as small businesses-unserved. The authors examine this issue. Using bank-level data for Argentina, Chile, Colombia, and Peru during the mid-1990s, they empirically investigate whether bank origin affects the share and growth rate of bank lending to small businesses. They find that although foreign banks generally lent less to small businesses (as share of total lending) than private domestic banks, the difference is due primarily to the behavior of small foreign banks. The difference was considerably smaller for large and medium-sized banks. And in Chile and Colombia, large foreign banks might actually lend slightly more (as share of total lending) than large domestic banks.Financial Intermediation,Banks&Banking Reform,Financial Crisis Management&Restructuring,Payment Systems&Infrastructure,Economic Theory&Research,Banks&Banking Reform,Financial Intermediation,Financial Crisis Management&Restructuring,Economic Theory&Research,Banking Law

Editorial: natural compounds in food safety and preservation

Research Areas: Nutrition & Dieteticsinfo:eu-repo/semantics/publishedVersio

Size-Controlled Water-Soluble Ag Nanoparticles

Ag nanoparticles of two different sizes (1 and 4 nm) were prepared within an apoferritin cavity by using an Ag+-loaded apoferritin as a nanoconfined environment for their construction. The initial amount of Ag' ions injected in the apoferritin cavity dictates the size of the final Ag particles. The protein shell prevents bulk aggregation of the metal particles, which renders them water soluble and extremely stable

Early Universe Constraints on Time Variation of Fundamental Constants

We study the time variation of fundamental constants in the early Universe. Using data from primordial light nuclei abundances, CMB and the 2dFGRS power spectrum, we put constraints on the time variation of the fine structure constant $\alpha$, and the Higgs vacuum expectation value $$without assuming any theoretical framework. A variation in$$ leads to a variation in the electron mass, among other effects. Along the same line, we study the variation of $\alpha$ and the electron mass $m_e$. In a purely phenomenological fashion, we derive a relationship between both variations.Comment: 18 pages, 12 figures, accepted for publication in Physical Review

Molecular pathways driving omeprazole nephrotoxicity

Omeprazole, a proton pump inhibitor used to treat peptic ulcer and gastroesophageal reflux disease, has been associated to chronic kidney disease and acute interstitial nephritis. However, whether omeprazole is toxic to renal cells is unknown. Omeprazole has a lethal effect over some cancer cells, and cell death is a key process in kidney disease. Thus, we evaluated the potential lethal effect of omeprazole over tubular cells. Omeprazole induced dose-dependent cell death in human and murine proximal tubular cell lines and in human primary proximal tubular cell cultures. Increased cell death was observed at the high concentrations used in cancer cell studies and also at lower concentrations similar to those in peptic ulcer patient serum. Cell death induced by omeprazole had features of necrosis such as annexin V/7-AAD staining, LDH release, vacuolization and irregular chromatin condensation. Weak activation of caspase-3 was observed but inhibitors of caspases (zVAD), necroptosis (Necrostatin-1) or ferroptosis (Ferrostatin-1) did not prevent omeprazole-induced death. However, omeprazole promoted a strong oxidative stress response affecting mitochondria and lysosomes and the antioxidant N-acetyl-cysteine reduced oxidative stress and cell death. By contrast, iron overload increased cell death. An adaptive increase in the antiapoptotic protein BclxL failed to protect cells. In mice, parenteral omeprazole increased tubular cell death and the expression of NGAL and HO-1, markers of renal injury and oxidative stress, respectively. In conclusion, omeprazole nephrotoxicity may be related to induction of oxidative stress and renal tubular cell deathSupported by FIS CP12/03262, CP14/00133, PI16/02057, PI16/ 01900, PI18/01366, PI19/00588, PI19/00815, DTS18/00032, ERAPerMed-JTC2018 (KIDNEY ATTACK AC18/00064 and PERSTIGAN AC18/00071, ISCIII-RETIC REDinREN RD016/0009 FEDER funds, Sociedad Española de Nefrología, Fundacion Renal Iñigo Álvarez de Toledo (FRIAT), ISCIII Miguel Servet (ABS, MDS-N), ISCIII Sara Borrell (JMM-M), Comunidad de Madrid CIFRA2 B2017/BMD-3686 (MF-B and DM-S

Urinary cyclophilin A as marker of tubular cell death and kidney injury

Background: Despite the term acute kidney injury (AKI), clinical biomarkers for AKI re-flect function rather than injury and independent markers of injury are needed. Tubular cell death, including necroptotic cell death, is a key feature of AKI. Cyclophilin A (CypA) is an intracellular protein that has been reported to be released during necroptosis. We have now explored CypA as a potential marker for kidney injury in cultured tubular cells and in clinical settings of ischemia-reperfusion injury (IRI), characterized by limitations of current diagnostic criteria for AKI. Meth-ods: CypA was analyzed in cultured human and murine proximal tubular epithelial cells exposed to chemical hypoxia, hypoxia/reoxygenation (H/R) or other cell death (apoptosis, necroptosis, fer-roptosis) inducers. Urinary levels of CypA (uCypA) were analyzed in patients after nephron sparing surgery (NSS) in which the contralateral kidney is not disturbed and kidney grafts with initial function. Results: Intracellular CypA remained unchanged while supernatant CypA increased in parallel to cell death induction. uCypA levels were higher in NSS patients with renal artery clamping (that is, with NSS-IRI) than in no clamping (NSS-no IRI), and in kidney transplantation (KT) recipients (KT-IRI) even in the presence of preserved or improving kidney function, while this was not the case for urinary Neutrophil gelatinase-associated lipocalin (NGAL). Furthermore, higher uCypA levels in NSS patients were associated with longer surgery duration and the incidence of AKI increased from 10% when using serum creatinine (sCr) or urinary output criteria to 36% when using high uCypA levels in NNS clamping patients. Conclusions: CypA is released by kidney tubular cells during different forms of cell death, and uCypA increased during IRI-induced clinical kidney injury independently from kidney function parameters. Thus, uCypA is a potential bi-omarker of kidney injury, which is independent from decreased kidney functionResearch by the authors was funded by FIS/ FEDER funds (PI17/00257, PI18/01386, PI19/00588, PI19/00815, DTS18/00032, ERA-PerMed-JTC2018 (KIDNEY ATTACK AC18/00064 and PERSTIGAN AC18/00071, ISCIII-RETIC REDinREN RD016/0009), Sociedad Española de Nefrología, FRIAT, Comunidad de Madrid en Biomedicina B2017/BMD-3686 CIFRA2-CM. Salary support: ISCIII Miguel Servet to A.B.S., MICIN Ramon y Cajal to M.D.S.-N., REDinREN RD016/0009 to M.F.-B.,SENEFRO to D.M.-S. and Consejería de Educación, Juventud y Deporte (Comunidad de Madrid/FSE) to A.M.L.-