Learning and Serving: Pro Bono Legal Services by Law Students

All lawyers\u27 codes of professional ethics in the United States expect members of the bar to perform legal services for low-income persons. In practice, as we all know, many lawyers perform a great deal of such service while others do little or none. By much the same token, the accreditation rules of the American Bar Association urge all law schools to provide students with opportunities to do pro bono legal work; by much the same token, some schools in the United States have extensive programs for their students but many do not. In 1998, the Association of American Law Schools created a Commission on Pro Bono and Public Service Opportunities to help law schools improve their pro bono programs. The Commission began its work by reviewing available research and by surveying all law schools to learn the current extent of pro bono services by law students. The Commission learned that nearly all law schools offer clinical programs through which students can eam credit for providing legal services to low-income clients, but that schools were much more varying in the extent to which they gave students the opportunity to provide voluntary services without credit

Learning and Serving: Pro Bono Legal Services by Law Students

All lawyers\u27 codes of professional ethics in the United States expect members of the bar to perform legal services for low-income persons. In practice, as we all know, many lawyers perform a great deal of such service while others do little or none. By much the same token, the accreditation rules of the American Bar Association urge all law schools to provide students with opportunities to do pro bono legal work; by much the same token, some schools in the United States have extensive programs for their students but many do not. In 1998, the Association of American Law Schools created a Commission on Pro Bono and Public Service Opportunities to help law schools improve their pro bono programs. The Commission began its work by reviewing available research and by surveying all law schools to learn the current extent of pro bono services by law students. The Commission learned that nearly all law schools offer clinical programs through which students can eam credit for providing legal services to low-income clients, but that schools were much more varying in the extent to which they gave students the opportunity to provide voluntary services without credit

Analyzing the Impact of Changes in Trade and Domestic Policies: The Case of the Soybean Complex

This study analyzes the impacts of domestic and trade policy changes on the soybean complex using a Stochastic Equilibrium Displacement Model (SEDM). Three different policies, Loan Deficiency Payments (LDP), transportation costs and export taxes are considered in the analysis. The results indicate that Brazil benefits from a reduction in transportation costs and becomes more competitive in the global soybean market. Brazilian exports of soybeans increase due to relatively lower export prices. However, Brazil gains little improvement in the export competitiveness of the soybean joint products, soybean meal and oil. A lower U.S. LDP rate results in the loss of competitiveness for the United States in the world soybean market. Furthermore, the results show that an Argentine export tax reduction increases soybean exports from Argentina, but it reduces the global supply of soybean meal and soybean oil.International Trade, Loan Deficiency Payment, Soybean, Soybean Joint Products, Stochastic Equilibrium Displacement Model, Transportation Costs, Agricultural and Food Policy, International Relations/Trade,

Dexamethasone induces apoptosis in pulmonary arterial smooth muscle cells

BACKGROUND: Dexamethasone suppressed inflammation and haemodynamic changes in an animal model of pulmonary arterial hypertension (PAH). A major target for dexamethasone actions is NF-κB, which is activated in pulmonary vascular cells and perivascular inflammatory cells in PAH. Reverse remodelling is an important concept in PAH disease therapy, and further to its anti-proliferative effects, we sought to explore whether dexamethasone augments pulmonary arterial smooth muscle cell (PASMC) apoptosis. METHODS: Analysis of apoptosis markers (caspase 3, in-situ DNA fragmentation) and NF-κB (p65 and phospho-IKK-α/β) activation was performed on lung tissue from rats with monocrotaline (MCT)-induced pulmonary hypertension (PH), before and after day 14–28 treatment with dexamethasone (5 mg/kg/day). PASMC were cultured from this rat PH model and from normal human lung following lung cancer surgery. Following stimulation with TNF-α (10 ng/ml), the effects of dexamethasone (10(−8)–10(−6) M) and IKK2 (NF-κB) inhibition (AS602868, 0–3 μM (0-3×10(−6) M) on IL-6 and CXCL8 release and apoptosis was determined by ELISA and by Hoechst staining. NF-κB activation was measured by TransAm assay. RESULTS: Dexamethasone treatment of rats with MCT-induced PH in vivo led to PASMC apoptosis as displayed by increased caspase 3 expression and DNA fragmentation. A similar effect was seen in vitro using TNF-α-simulated human and rat PASMC following both dexamethasone and IKK2 inhibition. Increased apoptosis was associated with a reduction in NF-κB activation and in IL-6 and CXCL8 release from PASMC. CONCLUSIONS: Dexamethasone exerted reverse-remodelling effects by augmenting apoptosis and reversing inflammation in PASMC possibly via inhibition of NF-κB. Future PAH therapies may involve targeting these important inflammatory pathways

Gaussian quantum computation with oracle-decision problems

We study a simple-harmonic-oscillator quantum computer solving oracle decision problems. We show that such computers can perform better by using nonorthogonal Gaussian wave functions rather than orthogonal top-hat wave functions as input to the information encoding process. Using the Deutsch-Jozsa problem as an example, we demonstrate that Gaussian modulation with optimized width parameter results in a lower error rate than for the top-hat encoding. We conclude that Gaussian modulation can allow for an improved trade-off between encoding, processing and measurement of the information.Comment: RevTeX4, 10 pages with 4 figure

Bromodomain and extra-terminal protein mimic JQ1 decreases inflammation in human vascular endothelial cells: Implications for pulmonary arterial hypertension

Background and objective Nuclear factor kappa B (NF-kB)-mediated inflammatory gene expression and vascular endothelial cell proliferation/remodelling are implicated in the pathophysiology of the fatal disease, pulmonary arterial hypertension (PAH). Bromodomain and extra-terminal (BET) proteins are essential for the expression of a subset of NF-kB-induced inflammatory genes. BET mimics including JQ1+ prevent binding of BETs to acetylated histones and down-regulate the expression of selected genes. Methods The effects of JQ1+ on the proliferation of primary human pulmonary microvascular endothelial cells (HPMECs) from healthy subjects were measured by bromodeoxyuridine (BrdU) incorporation. Cell cycle progression was assessed by flow cytometry; mRNA and protein levels of cyclin-dependent kinases (CDKs), inhibitors and cytokines were determined by reverse transcription-quantitative PCR (RT-qPCR), Western blotting or ELISA. Histone acetyltransferase (HAT) and deacetylase (HDAC) activities were determined in nuclear extracts from whole lung of PAH and control patients. Results JQ1+ significantly inhibited IL6 and IL8 (IL6 and CXCL8) mRNA and protein in HPMECs compared with its inactive enantiomer JQ1−. JQ1+ decreased NF-kB p65 recruitment to native IL6 and IL8 promoters. JQ1+ showed a concentration-dependent decrease in HPMEC proliferation compared with JQ1−-treated cells. JQ1+ induced G1 cell cycle arrest by increasing the expression of the CDK inhibitors (CDKN) 1A (p21cip) and CDKN2D (p19INK4D ) and decreasing that of CDK2, CDK4 and CDK6. JQ1+ also inhibited serum-stimulated migration of HPMECs. Finally, HAT activity was significantly increased in the lung of PAH patients. Conclusion Inhibition of BETs in primary HPMECs decreases inflammation and remodelling. BET proteins could be a target for future therapies for PAH

Is mitochondrial dysfunction a driving mechanism linking COPD to nonsmall cell lung carcinoma?

© ERS 2017. Chronic obstructive pulmonary disease (COPD) patients are at increased risk of developing nonsmall cell lung carcinoma, irrespective of their smoking history. Although the mechanisms behind this observation are not clear, established drivers of carcinogenesis in COPD include oxidative stress and sustained chronic inflammation. Mitochondria are critical in these two processes and recent evidence links increased oxidative stress in COPD patients to mitochondrial damage. We therefore postulate that mitochondrial damage in COPD patients leads to increased oxidative stress and chronic inflammation, thereby increasing the risk of carcinogenesis. The functional state of the mitochondrion is dependent on the balance between its biogenesis and degradation (mitophagy). Dysfunctional mitochondria are a source of oxidative stress and inflammasome activation. In COPD, there is impaired translocation of the ubiquitin-related degradation molecule Parkin following activation of the Pink1 mitophagy pathway, resulting in excessive dysfunctional mitochondria. We hypothesise that deranged pathways in mitochondrial biogenesis and mitophagy in COPD can account for the increased risk in carcinogenesis. To test this hypothesis, animal models exposed to cigarette smoke and developing emphysema and lung cancer should be developed. In the future, the use of mitochondria-based antioxidants should be studied as an adjunct with the aim of reducing the risk of COPD-associated cancer