Green functions for generalized point interactions in 1D: A scattering approach

Recently, general point interactions in one dimension has been used to model a large number of different phenomena in quantum mechanics. Such potentials, however, requires some sort of regularization to lead to meaningful results. The usual ways to do so rely on technicalities which may hide important physical aspects of the problem. In this work we present a new method to calculate the exact Green functions for general point interactions in 1D. Our approach differs from previous ones because it is based only on physical quantities, namely, the scattering coefficients, $R$ and $T$, to construct $G$. Renormalization or particular mathematical prescriptions are not invoked. The simple formulation of the method makes it easy to extend to more general contexts, such as for lattices of $N$ general point interactions; on a line; on a half-line; under periodic boundary conditions; and confined in a box.Comment: Revtex, 9 pages, 3 EPS figures. To be published in PR

Expression of insulin-like growth factor I by activated hepatic stellate cells reduces fibrogenesis and enhances regeneration after liver injury

BACKGROUND/AIM: Hepatic stellate cells (HSCs) express alpha-smooth muscle actin (alphaSMA) and acquire a profibrogenic phenotype upon activation by noxious stimuli. Insulin-like growth I (IGF-I) has been shown to stimulate HSCs proliferation in vitro, but it has been reported to reduce liver damage and fibrogenesis when given to cirrhotic rats. METHODS: The authors used transgenic mice (SMP8-IGF-I) expressing IGF-I under control of alphaSMA promoter to study the influence of IGF-I synthesised by activated HSCs on the recovery from liver injury. RESULTS: The transgene was expressed by HSCs from SMP8-IGF-I mice upon activation in culture and in the livers of these animals after CCl4 challenge. Twenty four hours after administration of CCl4 both transgenic and wild type mice showed similar extensive necrosis and increased levels of serum transaminases. However at 72 hours SMP8-IGF-I mice exhibited lower serum transaminases, reduced hepatic expression of alphaSMA, and improved liver morphology compared with wild type littermates. Remarkably, at this time all eight CCl4 treated wild type mice manifested histological signs of liver necrosis that was severe in six of them, while six out of eight transgenic animals had virtually no necrosis. In SMP8-IGF-I mice robust DNA synthesis occurred earlier than in wild type animals and this was associated with enhanced production of HGF and lower TGFbeta1 mRNA expression in the SMP8-IGF-I group. Moreover, Colalpha1(I) mRNA abundance at 72 hours was reduced in SMP8-IGF-I mice compared with wild type controls. CONCLUSIONS: Targeted overexpression of IGF-I by activated HSCs restricts their activation, attenuates fibrogenesis, and accelerates liver regeneration. These effects appear to be mediated in part by upregulation of HGF and downregulation of TGFbeta1. The data indicate that IGF-I can modulate the cytokine response to liver injury facilitating regeneration and reducing fibrosis

Loss of Dystroglycan Drives Cellular Senescence via Defective Mitosis-Mediated Genomic Instability

Nuclear β-dystroglycan (β-DG) is involved in the maintenance of nuclear architecture and function. Nonetheless, its relevance in defined nuclear processes remains to be determined. In this study we generated a C2C12 cell-based DG-null model using CRISPR-Cas9 technology to provide insights into the role of β-DG on nuclear processes. Since DG-null cells exhibited decreased levels of lamin B1, we aimed to elucidate the contribution of DG to senescence, owing to the central role of lamin B1 in this pathway. Remarkably, the lack of DG enables C2C12 cells to acquire senescent features, including cell-cycle arrest, increased senescence-associated-β-galactosidase activity, heterochromatin loss, aberrant nuclear morphology and nucleolar disruption. We demonstrated that genomic instability is one driving cause of the senescent phenotype in DG-null cells via the activation of a DNA-damage response associated with mitotic failure, as shown by the presence of multipolar mitotic spindles, which in turn induced the formation of micronuclei and γH2AX foci (DNA-damage marker), telomere shortening and p53/p21 upregulation. Altogether, these events might ultimately lead to premature senescence, impeding the replication of the damaged genome. In summary, we present evidence supporting a role for DG in protecting against senescence, through the maintenance of proper lamin B1 expression/localization and proper mitotic spindle organization

Effect of temperature on behavior, glycogen content, and mortality in Limnoperna fortunei (Dunker, 1857) (Bivalvia: Mytilidae)

Limnoperna fortunei (Dunker 1857) is a freshwater mussel with physiological tolerance to different environmental conditions, which may explain its success as an invasive species. The role of abiotic factors in its establishment, abundance and projections of risk of further spread into several areas has been studied. These mussels may respond to multiple environmental stressors, such as temperature, through physiological mechanisms, behavioral responses, mortality or some combination of these. The aim of this study was to investigate the behavioral responses (valve closing), glycogen concentrations and mortality of L. fortunei under four different temperatures (5°C, 10°C, 20°C and 30° C) during a chronic test (30 days). Two-way analysis of variance (ANOVA) was used to compare glycogen concentrations across days of the experiment and at the different temperatures. Differences in valve-closing behavior and mortality among temperatures were tested using repeated-measures ANOVA. We observed that most of the mussels maintained at 5°C closed their valves (74.7 ± 15.3%), indicating that they remain inactive at low temperatures. The glycogen levels significantly differed among the temperatures tested. These differences occurred mainly due to the high glycogen values observed in mussels exposed to 10°C. Stability in glycogen concentrations was observed within each particular temperature. The cumulative mortality was higher at extreme temperatures (5°C and 30°C). The ideal temperature for laboratory maintenance and tests is approximately 20°C. Our data also show that L. fortunei can survive and maintain their energy reserves (glycogen) for several days at 5°C, an important feature related to its invasion success

Perinatal Factors Associated With Early Deaths Of Preterm Infants Born In Brazilian Network On Neonatal Research Centers [fatores Perinatais Associados Ao óbito Precoce Em Prematuros Nascidos Nos Centros Da Rede Brasileira De Pesquisas Neonatais]

Objective: To evaluate perinatal factors associated with early neonatal death in preterm infants with birth weights (BW) of 400-1,500 g. Methods: A multicenter prospective cohort study of all infants with BW of 400-1,500 g and 23-33 weeks of gestational age (GA), without malformations, who were born alive at eight public university tertiary hospitals in Brazil between June of 2004 and May of 2005. Infants who died within their first 6 days of life were compared with those who did not regarding maternal and neonatal characteristics and morbidity during the first 72 hours of life. Variables associated with the early deaths were identified by stepwise logistic regression. Results: A total of 579 live births met the inclusion criteria. Early deaths occurred in 92 (16%) cases, varying between centers from 5 to 31%, and these differences persisted after controlling for newborn illness severity and mortality risk score (SNAPPE-II). According to the multivariate analysis, the following factors were associated with early intrahospital neonatal deaths: gestational age of 23-27 weeks (odds ratio - OR = 5.0; 95%CI 2.7-9.4), absence of maternal hypertension (OR = 1.9; 95%CI 1.0-3.7), 5th minute Apgar 0-6 (OR = 2.8; 95%CI 1.4-5.4), presence of respiratory distress syndrome (OR=3.1;95%CI 1.4-6.6), and network center of birth. Conclusion: Important perinatal factors that are associated with early neonatal deaths in very low birth weight preterm infants can be modified by interventions such as improving fetal vitality at birth and reducing the incidence and severity of respiratory distress syndrome. The heterogeneity of early neonatal rates across the different centers studied indicates that best clinical practices should be identified and disseminated throughout the country. Copyright © 2008 by Sociedade Brasileira de Pediatria.844300307Joseph, K.S., Liston, R.M., Dodds, L., Dahlgren, L., Allen, A.C., Socioeconomic status and perinatal outcomes in a setting with universal access to essential health care services (2007) CMAJ, 177, pp. 583-590Mathews, T.J., MacDorman, M.F., Infant mortality statistics from the 2004 period linked birth/infant death data set (2007) Natl Vital Stat Rep, 55, pp. 1-32Kramer, M.S., Demissie, K., Yang, H., Platt, R.W., Sauve, R., Liston, R., The contribution of mild and moderate preterm birth to infant mortality. Fetal and Infant Health Study Group of the Canadian Perinatal Surveillance System (2000) JAMA, 284, pp. 843-849Ananth, C.V., Vintzileos, A.M., Epidemiology of preterm birth and its clinical subtypes (2006) J Matern Fetal Neonatal Med, 19, pp. 773-782Brasil. Ministério da Saúde. DATASUS. Informaç ões de Saúde-Estatísticas Vitais- Mortalidade e Nascidos Vivos: nascidos vivos desde 1994. http://tabnet.datasus.gov.br/cgi/deftohtm.exe? sinasc/cnv/nvuf.def. Acesso: 29.10.2007Brasil. Ministério da Saúde. DATASUS. Informaç ões de Saúde-Estatísticas Vitais- Mortalidade e Nascidos Vivos: óbitos infantis - desde 1979. http://tabnet.datasus.gov.br/cgi/ deftohtm.exe?sim/cnv/infuf.def. Acesso: 29.10.2007Barros, F.C., Diaz-Rossello, J.L., The quality of care of very low birth weight babies in Brazil (2007) J Pediatr (Rio J), 83, pp. 5-6Horbar, J.D., Badger, G.J., Carpenter, J.H., Fanaroff, A.A., Kilpatrick, S., LaCorte, M., Trends in mortality and morbidity for very low birth weight infants, 1991-1999 (2002) Pediatrics, 110, pp. 143-151Fanaroff AA, Stoll BJ, Wright LL, Carlo WA, Ehrenkranz RA, Stark AR, et al. Trends in neonatal morbidity and mortality for very low birth weight infants. Am J Obstet Gynecol. 2007;196:147.e1-8(2004) Infra-estrutura para atendimento integral ao recém-nascido, , http://www.sbp.com.br/show_item2.cfm?id_categoria=21&id_detalhe=1636&tipo_detalhe=s.Access:02.11.2007, Departamento de Neonatologia da Sociedade Brasileira de PediatriaBallard, J.L., Khoury, J.C., Wedig, K., Wang, L., Eilers-Walsman, B.L., Lipp, R., New Ballard Score, expanded to include extremely premature infants (1991) J Pediatr, 119, pp. 417-423Alexander, G.R., Himes, J.H., Kaufman, R.B., Mor, J., Kogan, M., A United States national reference for fetal growth (1996) Obstet Gynecol, 87, pp. 163-168Kattwinkel, J., (2000) Textbook of Neonatal Resuscitation, , 4th ed. Chicago, IL: American Academy of Pediatrics/American Heart Association;Richardson, D.K., Corcoran, J.D., Escobar, G.J., Lee, S.K., SNAP-II and SNAPPE-II: Simplified newborn illness severity and mortality risk scores (2001) J Pediatr, 138, pp. 92-100El-Metwally D, Vohr B, Tucker R. Survival and neonatal morbidity at the limits of viability in the mid 1990s: 22 to 25 weeks. J Pediatr. 2000;137:616-22Costeloe, K., Hennessy, E., Gibson, A.T., Marlow, N., Wilkinson, A.R., The EPICure study: Outcomes to discharge from hospital for infants born at the threshold of viability (2000) Pediatrics, 106, pp. 659-671MacDonald, H., American Academy of Pediatrics. Committee on Fetus and Newborn. Perinatal care at the threshold of viability (2002) Pediatrics, 110, pp. 1024-1027Jain, L., Raju, T.N., editors. Late preterm pregnancy and the newborn (2006) Clin Perinatol, 33, pp. 751-972de Kleine, M.J., den Ouden, A.L., Kollee, L.A., Ilsen, A., van Wassenaer, A.G., Brand, R., Lower mortality but higher neonatal morbidity over a decade in very preterm infants (2007) Paediatr Perinat Epidemiol, 21, pp. 15-25Moro, M., Figueras-Aloy, J., Fernández, C., Doménech, E., Jiménez, R., Pérez-Rodríguez, J., Mortality for newborns of birthweight less than 1,500 g in Spanish neonatal units (2002-2005) (2007) Am J Perinatol, 24, pp. 593-601Drumond Ede, F., Machado, C.J., Franca, E., Early neonatal mortality: An analysis of multiple causes of death by the Grade of Membership method (2007) Cad Saude Publica, 23, pp. 157-166Richardson, D.K., Shah, B.L., Frantz 3rd, I.D., Bednarek, F., Rubin, L.P., McCormick, M.C., Perinatal risk and severity of illness in newborns at 6 neonatal intensive care units (1999) Am J Public Health, 89, pp. 511-516Horbar, J.D., Rogowski, J., Plsek, P.E., Delmore, P., Edwards, W.H., Hocker, J., Collaborative quality improvement for neonatal intensive care. NIC/Q Project Investigators of the Vermont Oxford Network (2001) Pediatrics, 107, pp. 14-22Vohr, B.R., Wright, L.L., Dusick, A.M., Perritt, R., Poole, W.K., Tyson, J.E., Center differences and outcomes of extremely low birth weight infants (2004) Pediatrics, 113, pp. 781-789Horbar JD, Plsek PE, Leahy KNIC/Q 2000. NIC/Q 2000: establishing habits for improvement in neonatal intensive care units. Pediatrics. 2003;111:e397-410Evans, N., Hutchinson, J., Simpson, J.M., Donoghue, D., Darlow, B., Henderson-Smart, D., Prenatal predictors of mortality in very preterm infants cared for in the Australian and New Zealand Neonatal Network (2007) Arch Dis Child Fetal Neonatal Ed, 92, pp. F34-F40Walther, F.J., Withholding treatment, withdrawing treatment, and palliative care in the neonatal intensive care unit (2005) EarlyHumDev, 81, pp. 965-972von Dadelszen, P., Magee, L.A., Taylor, E.L., Muir, J.C., Stewart, S.D., Sherman, P., Maternal hypertension and neonatal outcome among small for gestational age infants (2005) Obstet Gynecol, 106, pp. 335-339Casey, B.M., McIntire, D.D., Leveno, K.J., The continuing value of the Apgar score for the assessment of newborn infants (2001) N Engl J Med, 344, pp. 467-471,308-31

A spreadsheet for calculation of ingredients for standardization of requeijão cremoso

The standardization of requeijão cheese quality characteristics is a processing stage which is directly influenced by the chemical composition of the raw material. Fat and water concentrations are the main factors that cause variation in quality properties of the requeijão and, when not thoroughly controlled, may cause a lack in standardization of the food. Calculations of ingredients for effective standardization must be made in relation to the final product through of iterative calculations, which makes the manual process unfeasible. Thus, the objective of the present study was to develop a spreadsheet for ingredient calculation, with restrictions being the different concentrations of fat and water in order to standardize the final products. The spreadsheet was developed using the Excel 2007® Solver function, with just four input data: quantity of mass, water and fat content of the mass and fat content of the cream. The optimal solution was that which maximizes the amount of final product while meeting the stipulated constraints of fat and water. Results obtained with the spreadsheet were validated by processing the requeijão cheeses and comparison of the theoretical and practical parameters using the t-test. There was no significant difference between fat and water contents (p>0.10) estimated and verified in practice. Therefore, the use of the spreadsheet proved to be efficient for standardization of requeijão formulations

Suplemento mineral aniônico para vacas no periparto: parâmetros sanguíneos, urinários e incidência de patologias de importância na bovinocultura leiteira

A fim de avaliar o efeito do suplemento mineral aniônico sobre parâmetros sanguíneos, urinários e incidência de hipocalcemia e retenção de placenta, dezoito vacas de aptidão leiteira com grau de sangue 7/8 Holandesa preta e branca, com 440-620 kg e 5-10 anos, foram divididas com delineamento em blocos em função da ordem de parto em dois grupos: controle (BCAD=46,38mEq/kg de MS) e tratamento (com adição de suplemento mineral aniônico e BCAD = -249,28mEq/kg de MS). Foram monitorados níveis de cálcio total e pH na urina e soro sanguíneo; TCO2, pCO2, HCO3, excesso de base, cálcio ionizado, Na, K, Se no sangue; escore de condição corporal, hematócrito e hemoglobina. Os dados sanguíneos, urinários e ECC foram submetidos ao Proc Means do SAS (2000) com análise de variância a 5% e teste de Tukey e a incidência de retenção de placenta analisada por Mann-Whitney (P<0,07) e a concentração sérica de Se por teste t de Student (P<0,05), ambos pelo GraphPad Prism 5.0. O suplemento mineral aniônico diminuiu os valores de TCO2, pCO2, HCO3 e EB no sangue com menor perda de peso, mas a variação de pH e cálcio foi restrita ao tempo. O suplemento mineral aniônico não provocou leve acidose metabólica desejada e, consequentemente, não preveniu a hipocalcemia. Contudo, por apresentar Se em sua composição, proporcionou maior concentração deste micronutriente no soro e contribuiu para menor retenção de placenta