Miracle-dz/UniFAR-FTUs huggingface dataset:
California's Student Equity Policy: An unexploited opportunity among Hispanic-serving community colleges

This article examines California’s Student Equity Plan policy, which requires community colleges to identify inequities, develop activities, and create goals for achieving equitable outcomes in higher education. We provide an analysis of the Equity Plans submitted by a subset of HSI (Hispanic-serving institution) community colleges and focus on these questions: • In what ways do the Equity Plans of HSI community colleges address the success of Latina/o students? • Do the Equity Plans reflect the HSI status of the institution? • Do HSI’s Equity Plans focus on the most serious barriers to Latino/a success (e.g., developmental education and transfer)? Because HSI community colleges provide a majority of credentials and degrees and they represent a pathway to transfer, we see the potential for HSIs to reduce educational inequality through the Student Equity Plan process and funding ($530 million since 2014). Specifically, do HSIs take advantage of the Student Equity Plan process and funding as an opportunity to build their capacity to produce better and more equitable outcomes for Latinos/as? Or do they approach equity more broadly and generically? Our analysis sheds light on the ways in which HSIs address policy mandates strategically to build their capacity and strengthen their identity. 76 E. r. FElix, A. TrinidAd, C. d. Ching, And E. M. BEnsiMón
Migration with Pension Reform Expectations

Pension reforms, which imply a reduction in the generosity of pension benefits, are becoming widespread in response to the demographic transition. The scale, the timing, and the pace of these reforms vary across countries. In this theoretical article, authors analyse individual migration decisions, by adding a component linked to the expected old-age pension benefits in sending and receiving countries in two cases: when the pension system rules are known, and when there is a risk of the pension systems reforms. The results indicate that when individuals fail to take future pension wealth into account, they can make sub-optimal migration decisions.
Scleroderma fibroblasts promote migration of mononuclear leucocytes across endothelial cell monolayers

Perivascular infiltrates of inflammatory cells are a hallmark of lesional skin in scleroderma. We have explored the potential for scleroderma fibroblasts to modulate mononuclear leucocyte migration across endothelial cell monolayers in tissue culture, and to regulate expression of endothelial cell adhesion molecules. Fibroblasts were grown from skin biopsies of eight patients with active diffuse cutaneous scleroderma and from four healthy controls. Co‐culture and conditioned medium transfer experiments examined the effect of soluble fibroblast products on mononuclear leucocyte (U937) cell migration across endothelial cell (1E‐7) monolayers grown on tissue culture inserts. Co‐culture of scleroderma, but not control fibroblasts, promoted transendothelial migration of U937 cells. Scleroderma fibroblast‐conditioned medium had qualitatively similar effects and equivalent results were obtained using Jurkat‐6 (T lymphocyte) cells, and with peripheral blood mononuclear cells from a patient with diffuse cutaneous scleroderma. Promotion of leucocyte migration does not appear to result from increased endothelial adhesion molecule expression, since fibroblast‐conditioned medium did not up‐regulate endothelial cell expression of intercellular adhesion molecule‐1 (ICAM‐1), vascular cell adhesion molecule‐1 (VCAM‐1) or E‐selectin. Moreover, leucocyte migration across cytokine‐activated endothelial cell layers in co‐cuture with fibroblasts was less than across resting cells, although the selective effect of scleroderma fibroblast co‐culture persisted. Recombinant monocyte chemoattractant protein‐1 (MCP‐1) or IL‐8 increased passage of mononuclear leucocytes across endothelial cell monolayers, whilst anti‐MCP‐1, but not anti‐IL‐8 antibodies, significantly reduced the effect of fibroblast conditioned medium. These data suggest that systemic sclerosis (SSc) fibroblasts promote leucocyte migration across endothelial cell monolayers in tissue culture via an MCP‐1‐dependent mechanism. These findings may be relevant to the perivascular mononuclear leucocyte infiltrates characteristic of early SSc lesions.
On queueing delay in WSN with energy saving mechanism based on queued wake up

The time-dependent queueing delay in wireless sen-sor network (WSN) with node radios being activated via the queued wake up mechanism is considered. The mathematical model of the system is based on the transient M/G/1/K-type queue with finite buffer and the N-policy, in which the server becomes active after the idle period if the fixed number N of packets are accumulated in the buffer queue. The closed-form representation for the Laplace transform of the queueing delay distribution at fixed time epoch is found. The approach is based on the idea of embedded Markov chain, total probability law, renewal theory and linear algebra. A numerical example is attached as well.
Improving the chance of recovery from the short‐ and long‐term consequences of depression

&NA; Major depressive disorder (MDD) is a common, chronic disorder that requires long‐term management. Although effective treatments are available, MDD frequently remains undiagnosed. Furthermore, once recognized, treatment duration and dosage are often inadequate and adherence to medication is often poor. However, adequate acute phase treatment of MDD is essential to reduce symptomatology, and improve quality of life and the clinical course. After remission, treatment should be continued for 4–9 months to consolidate the remission and prevent relapse. For patients who do not respond adequately to their initial antidepressant therapy, switching or augmentation of therapy may be necessary. Many patients suffer residual symptomatology, even when classified as being in remission. In addition to the suffering and impairment that this causes, residual symptomatology is associated with a high rate of relapse. Clinicians should strive to achieve asymptomatic recovery both in terms of core symptomatology and psychosocial disability. This requires appropriate treatment at therapeutic doses for a sufficient duration; education and support to promote patient compliance with treatment; and regular monitoring and prompt intervention for patients with symptoms that persist even at subsyndromal levels. In conclusion, there remains considerable scope for improving the identification, treatment and management of patients with MDD.
Differential Expression of Methicillin Resistance by Different Biofilm-Negative Staphylococcus epidermidis Transposon Mutant Classes

ABSTRACT Biofilm formation mediated by polysaccharide intercellular adhesin (PIA) is the major virulence factor of Staphylococcus epidermidis and is often associated with methicillin resistance. Transposon Tn917 insertions leading to a biofilm-negative phenotype in the biofilm-producing S. epidermidis strain 1457 (mecA-negative) were transferred into the methicillin-resistant, biofilm-producing S. epidermidis 1057 (mecA-positive) by transduction. According to their phenotypes and genotypes, the mutants could be separated into genetic classes I to IV (D. Mack, H. Rohde, S. Dobinsky, J. Riedewald, M. Nedelmann, J. K. M. Knobloch, H.-A. Elsner, and H. H. Feucht, Infect. Immun. 68:3799–3807, 2000). All transductants of S. epidermidis 1057 had phenotypes for biofilm formation similar to those of the corresponding mutants of S. epidermidis 1457. With a mecA-specific probe, identical hybridization patterns were observed for wild-type S. epidermidis 1057 and all the transductants. There were minor changes in oxacillin MICs for Class II and III transductants compared to those for wild-type S. epidermidis 1057. On population analysis, S. epidermidis 1057 displayed a heterogeneous expression type of resistance with an oxacillin MIC of ≥6 μg/ml for more than 90% of the cells. An almost identical profile was observed with biofilm-negative class I mutants, where the transposon insertions inactivate the icaADBC gene locus essential for PIA synthesis. In contrast, class III mutants were more sensitive to oxacillin with a MIC of ≤1 μg/ml for more than 90% of the cells. The class IV mutant displayed homogenous resistance with a MIC of ≥50 μg/ml for more than 90% of the cells. On oxacillin gradient plates, the class II mutant displayed decreased resistance. Apparently, different independent mutations leading to a biofilm-negative phenotype of S. epidermidis by influencing expression of icaADBC on the level of transcription significantly influence the expression of methicillin resistance. However, transcription of mecA was not significantly altered in the different transductants compared to the wild type, independent of mecA induction with oxacillin, indicating that other mechanisms influencing phenotypic expression of methicillin resistance are involved.
Political connections and misallocation of procurement contracts: evidence from Ecuador

This paper uses detailed ownership information of private firms in Ecuador and the identity of bureaucrats to document the effects of political connections on firm size and the allocation of government contracts. Reduced-form estimates show a significant positive effect of political connection on sales, assets, debt, and costs. Using contract-level data, we find that politically connected firms enjoy higher probability of winning discretionary contracts and charge higher prices for homogeneous goods and services than unconnected firms. Back-of-the-envelope calculations indicate a political connection premium of 475 million USD per year in overpricing. Further analysis from production function estimates suggest that politically connected firms are less efficient than unconnected ones. This translates into a 1.5 to 3.5 percent excess cost of provision.
Comparison of Offline and Online Algorithms for Fully-Dynamic Graph Connectivity

In the fully dynamic graph connectivity problem we are modifying a graph by inserting and deleting edges and answering queries if two vertices are connected by a path. For the offline case we are given all of the queries and modifications beforehand, while for the online we should respond without any knowledge for the future operations. In this paper we are going to compare implementation of the online algorithm by Holm, de Lichtenberg, and Thorup[1] which has running time of O(log n) per operation with an implementations of a modified version of Eppstein’s O(log n) offline algorithm for dynamic minimum spanning tree[2] adapted to solve dynamic connectivity.
Rhinovirus infections in myelosuppressed adult blood and marrow transplant recipients.

Scant data are available on the clinical significance of rhinovirus infections in immunocompromised patients. We reviewed the clinical courses of and outcomes for 22 myelosuppressed adult blood and marrow transplant recipients with rhinovirus infections who were hospitalized at the M.D. Anderson Cancer Center (Houston) from January 1992 to January 1997. In 15 patients (68%), illnesses remained confined to the upper respiratory tract. Seven patients (32%) developed fatal pneumonia. These patients had profound respiratory failure a mean of 12 days (range, 3-21 days) after the onset of symptoms. In six of these seven cases, rhinovirus was isolated before death from a bronchoalveolar lavage fluid specimen and/or an endotracheal aspirate. Five patients underwent autopsies, one of which revealed disseminated aspergillosis and four of which revealed interstitial pneumonitis and/or acute respiratory distress syndrome and no other organisms. In conclusion, rhinovirus infections may be associated with considerable pulmonary-related morbidity and mortality in severely myelosuppressed immunocompromised patients.
Furin regulates both the activation of Pseudomonas exotoxin A and the Quantity of the toxin receptor expressed on target cells

Pseudomonas exotoxin A (PE) binds and enters mammalian cells via the alpha 2-macroglobulin receptor/low density lipoprotein receptor-related protein (LRP). The toxin then requires proteolytic cleavage to generate an enzymatically active fragment with translocates to the cell cytosol and inhibits protein synthesis. To assess the role of furin in determining toxin susceptibility, CHO cells were transfected with a mouse furin gene (CHO+fur cells) and maintained under neomycin selection. Cells expressing the transfected gene were about two- to threefold more sensitive to PE than were cells expressing only a neomycin resistance gene (CHO+neo cells). Possible reasons for the increased toxin sensitivity include the cleavage of a greater number of PE molecules and/or the conversion of more single-chain LRP to the processed, two-chain form. Processing of LRP appears to be necessary to allow the surface display of this receptor. Results of ligand binding studies indicated that the CHO+fur cells displayed about twofold more surface-expressed LRP than did CHO+neo cells. In addition, the in vitro cleavage of PE by recombinant furin enhanced toxin potency about threefold for CHO+neo cells but enhanced it very little for CHO+fur cells. This suggested that CHO+fur cells were processing PE at close to the maximum usable rate. Together these findings suggest that furin is involved in at least two separate protein processing pathways that each contribute to the sensitivity of cells to PE.
Long-Term Environmental Enrichment Leads to Regional Increases in Neurotrophin Levels in Rat Brain

A number of studies have demonstrated that both morphological and biochemical indices in the brain undergo alterations in response to environmental influences. In previous work we have shown that rats raised in an enriched environmental condition (EC) perform better on a spatial memory task than rats raised in isolated conditions (IC). We have also found that EC rats have a higher density of immunoreactivity than IC rats for both low and high affinity nerve growth factor (NGF) receptors in the basal forebrain. In order to determine if these alterations were coupled with altered levels of neurotrophins in other brain regions as well, we measured neurotrophin levels in rats that were raised in EC or IC conditions. Rats were placed in the different environments at 2 months of age and 12 months later brain regions were dissected and analyzed for NGF, brain-derived neurotrophic factor (BDNF), and neurotrophin-3 (NT-3) levels using Promega ELISA kits. We found that NGF and BDNF levels were increased in the cerebral cortex, hippocampal formation, basal forebrain, and hindbrain in EC animals compared to age-matched IC animals. NT-3 was found to be increased in the basal forebrain and cerebral cortex of EC animals as well. These findings demonstrate significant alterations in NGF, BDNF, and NT-3 protein levels in several brain regions as a result of an enriched versus an isolated environment and thus provide a possible biochemical basis for behavioral and morphological alterations that have been found to occur with a shifting environmental stimulus.
Apoptosis Resistance in Barrett's Esophagus: Ex vivo Bioassay of Live Stressed Tissues

BACKGROUND AND AIMS:Barrett's esophagus (BE) is a premalignant lesion of the distal esophagus in which squamous epithelial cells are replaced by metaplastic intestinal-like columnar epithelium that contains goblet cells. The factors that contribute to the progression from normal squamous mucosa to BE, Barrett's dysplasia, and adenocarcinoma are not well understood at the molecular level. Since reflux of bile acids is associated with BE development, we speculate that cells with an apoptosis-resistant phenotype are selected after long-term repeated exposure to pulses of bile acids. This will result in the survival of cells with unrepaired DNA damage, and a consequent increase in genomic instability leading to cancer progression. The major goal of this study is to compare sensitivity to apoptosis induced by the bile acid, deoxycholate (DOC), a known inducer of apoptosis, in normal esophageal squamous epithelium, normal colon epithelium, and BE.METHODS:Thirteen patients with a confirmed diagnosis of BE and four patients who had undergone clinically indicated colectomy were included in the present study. Freshly obtained biopsies were incubated with control medium or medium supplemented with 1 mM DOC for 3 h and then evaluated for apoptotic changes using transmission electron microscopy and immunohistochemical staining for two apoptotic markers, cleaved caspase 3 and cleaved cytokeratin 18.RESULTS:Our results indicate that BE is resistant to apoptosis induced by DOC compared to esophageal squamous epithelium and normal colon epithelium. In addition, electron micrographs revealed mitochondrial swelling in squamous epithelial cells treated ex vivo with DOC, which was absent in epithelial cells of BE. Formation of swollen mitochondria is an early marker of apoptotic cell death. Altogether, the data indicate that reduced apoptosis capability in BE tissue may contribute to progression to esophageal adenocarcinoma.
ATP regulates muscarine‐sensitive potassium current in dissociated bull‐frog primary afferent neurones.

1. Bull‐frog dorsal root ganglion cells in primary culture were voltage clamped in the whole‐cell configuration. The pipette solution contained ATP (5 mM). 2. Step depolarizations (5‐70 mV, 0.1‐1 s) from a holding potential close to the resting potential (range, ‐64 to ‐79 mV) evoked a non‐inactivating potassium current with properties indistinguishable from those which have been reported for the M‐current of bull‐frog sympathetic neurones. 3. An unhydrolysable ATP analogue APP(NH)P (5 mM), substitute with ATP in the pipette solution, did not support the M‐current activation. 4. Bath application of ATP (30 nM‐30 microM) reduced the amplitude of the M‐current in a concentration‐dependent manner, congruent to 50% inhibition of the current occurring with 1 microM‐ATP. The main effect of ATP was to reduce the maximum M‐conductance without changing the activation and deactivation kinetics of the M‐current. 5. Essentially the same results were obtained with ADP (0.1‐30 microM) and alpha, beta‐methylene‐ATP (10‐30 microM). AMP (10‐100 microM) and adenosine (10‐30 microM) were without effect on the M‐current. 6. The ATP‐induced inhibition of the M‐current was irreversible when an unhydrolysable GTP analogue GTP‐gamma‐S (10‐30 microM) was present in the pipette solution. ATP (3 microM) reduced the amplitude of the M‐current only by about 10% when GDP‐beta‐S (100 microM) was present in the pipette solution. Pre‐treatment of the cells with pertussis toxin (IAP; 500 ng ml‐1) for 24 h at 24 degrees C did not prevent the ATP‐induced M‐current inhibition. 7. Phorbol 12‐myristate 13‐acetate (PMA; 1‐3 microM) reduced the amplitude of the M‐current to about 50%. A reduction in the M‐current amplitude by PMA (3 microM) and ATP (10 microM) was attenuated when staurosporine (200 nM) was present in the pipette solution. Forskolin (10 microM) was without effect on the M‐current. 8. It is concluded that ATP acting at P2 receptors, associated with an IAP‐insensitive GTP‐binding protein, inhibits the M‐current in amphibian primary afferent neurones.
Human papillomavirus (HPV) 16 E6 sensitizes cells to atractyloside‐induced apoptosis: Role of p53, ICE‐like proteases and the mitochondrial permeability transition

Infection of cervical epithelial cells with certain high risk HPV genotypes is thought to play an etiologic role in the development of cervical cancer. In particular, HPV type 16 and 18 early protein 6 (E6) is thought to contribute to epithelial transformation by binding to the tumor suppressor protein p53, targeting it for rapid proteolysis, resulting in loss of its cell cycle arrest and apoptosis‐inducing activities. Recent data indicate that factors responsible for triggering apoptosis reside in the cytoplasm of cells, and not in the nucleus. In particular, the findings that mitochondria are required in certain cell‐free models for induction of apoptosis and that bcl‐2 is localized to mitochondria have focused attention on the role of the mitochondrial membrane permeability transition (MPT) in apoptosis. Here we present data to indicate that HPV 16 E6 expression sensitizes cells to MPT‐induced apoptosis. We also report that HPV 16 E6 sensitization of cells to MPT‐induced apoptosis occurs only in the presence of wildtype (wt) p53 expression. The extent of apoptosis induced by atractyloside (an inducer of the MPT) in normal, temperature‐sensitive (ts) p53, and HPV‐16 E6 transfected J2‐3T3 cells, and the HPV expressing cervical carcinoma cell lines SiHa, Hela and CaSki was determined. C33A cells, which express mutant p53 but not HPV, were also exposed to atractyloside in the presence or absence of HPV 16 E6 expression. Dose‐dependent apoptosis induced by atractyloside in normal J2‐3T3 cells and cervical carcinoma cells was measured by loss of cell viability, nuclear fragmentation and DNA laddering. The sensitivity of cells to atractyloside‐induced apoptosis was found to be: HPV 16 E6‐J2‐3T3 > CaSki > normal‐J2‐3T3 cells ≈ ts p53‐J2‐3T3 ≈ vector‐J2‐3T3 cells > Hela > SiHa > C33A ≈ C33A 16 E6. Cyclosporin A (CsA), an inhibitor of the MPT, and ICE‐I, a protease inhibitor, provided protection against atractyloside‐induced apoptosis. These findings indicate that: 1) high risk HPV 16 E6 protein is capable of sensitizing cells to apoptosis; 2) HPV 16 E6 sensitization of cells to atractyloside‐induced apoptosis occurs in a p53‐dependent fashion; 3) the target of HPV 16 E6 sensitization of cells to atractyloside‐induced apoptosis is the mitochondria; and 4) HPV 16 E6 sensitization of cells to atroctycoside‐induced apoptosis involves an ICE‐like protease‐sensitive mechanism, regulating the onset of the MPT. These findings constitute the first evidence that mitochondria play a role in HPV 16 E6 modulation of apoptosis. J. Cell. Biochem. 66:245‐255. © 1997 Wiley‐Liss, Inc.
Public health by stealth.

What does it take to light a fire to create cultural change about the way we do death, dying and bereavement in Australia? The GroundSwell Project set out to embark on a bold journey to create cultural change in the death and dying space in Australia. For 7 years we have delivered over 55 arts/health projects and have punched well above our weight. What have we learned about change and innovation? We've learned that we had to set up a fiercely independent organisation, drawing on short term funding so that we were never locked into delivering results that perpetuated 'systemic malaise'. We grew a network of activators across Health and Palliative care, community as well as other non-health related workplaces. We sought to find the right people, likening them to 'positive outliers' and engaged their head, heart and hands so they may influence others for a ripple effect. We work well with power or rank, a critical skill when leaning into complex social change. We've learned that we must engage leaders not just in health but ALL sectors, institutions, all walks of life.why not make it possible for any change to be truly 'social'? In this presentation, you will glean highlights from a range of our innovations and our approach to leadership, social research and collaboration. You'll have pause to reflect on how in your current role in the health system, you too can create change, by drawing on non-health specific discourse, using a stronger social lens. Wanting to engage all walks of life to improve public health is one thing, doing it and maintaining momentum is another! Join Jessie from the GroundSwell Project, Australia to learn about what they have gleaned from 7 years of being just a little too ahead of their time.