pinecone/core-2020-05-10-deduplication huggingface dataset:
Using magnetic resonance imaging to quantify the inflammatory response following allergen challenge in allergic rhinitis

Current rhinometric and flow assessments measure nasal patency and are often poorly correlated with rhinitis symptoms. To evaluate magnetic resonance imaging (MRI) as a new method to measure inflammatory changes in nasal and sinus mucosa following nasal allergen challenge. A pilot study (n = 6) determined the optimal technical settings for MRI to measure inflammatory change which were then adopted for the main study. This study was a single blind, placebo-controlled, three-way crossover trial in 14 subjects with seasonal allergic rhinitis. Effects of cetirizine, cetirizine and pseudoephedrine (Cet+PE), or placebo on total nasal symptom scores (TNSS), peak nasal inspiratory flow (PNIF), nasal nitric oxide (nNO), acoustic rhinometry, and MRI end points following nasal intranasal allergen challenge were measured. There were significant changes in all parameters after allergen challenge (P < 0.01), except for nNO. MRI end points were less variable and more consistent than PNIF and acoustic rhinometry in detecting changes after allergen challenge. Total nasal airspace volume was the most sensitive and reproducible MRI measurement, with a mean reduction from -5.37 cm(3) (95%CI -7.35, -3.38; P < 0.001), which was maximal 60 min after allergen challenge. A change of one in TNSS corresponded to a change in MRI volume of -0.57 cm(3). There was an improvement in all parameters (except nNO) in subjects taking Cet+PE compared with placebo, however this did not achieve significance probably because of the small study size (overall analysis P > 0.07; comparison of active versus placebo P > 0.09). MRI provides novel insights into the anatomical inflammatory changes post allergen challenge and provides a new method for assessment of nasal patency and objective measurement of inflammatory responses
Cross-border insolvency and legal transnationalisation

The last twenty years have seen an explosion of approaches for dealing with an inevitable consequence of globalised markets, that of cross-border insolvencies. This article places phenomena such as the United Nations Commission on International Trade Law (UNCITRAL) Model Law on Cross-border Insolvency and Cross-border Insolvency Agreements (also known as Protocols) within the context of developing laws on international commercial transactions. First it briefly describes the evolution of the international commercial law (sometimes known as the law merchant) to provide a context to understanding the international commercial responses to the problems created by cross-border insolvencies. Next, it outlines the range of approaches being adopted by States and multilateral bodies in recent decades to resolve cross-border insolvency issues. Finally it draws some preliminary conclusions on the potential implication of this transnationalisation process and broader international commercial law perspective, in particular on the capacity of Cross-Border Insolvency Agreements to address cross-border insolvency issues
A comparative analysis of Anglo-Australian pre-packs :\ud
can the means be made to justify the ends?

Pre-packaged administrations have been prevalent in the UK for years.  However, Australia's voluntary administration regime has been more restrictive of the practice. This article analyses the evolution of UK pre-packs, why they are not prevalent in Australia and the challenges for UK and Australian lawmakers in striking the right balance with pre-packs in their respective administration regimes. The article proposes a mechanism that might make ‘connected-party’ pre-pack business sales work more fairly for stakeholders — that is, by obligating a connected-party purchaser to make a future-income contribution in favour of the insolvent company whose business has been ‘rescued’ by a pre-packaged sale in administration
Perspectives on the South African responsible lending regime and the duty to conduct pre-agreement assessment as a responsible lending practice

In the 2001 INSOL International Consumer Debt Report: Report of Findings
and Recommendations, the view was held that the solution to overspending and
over-indebtedness is inter alia to be found in the idea that prevention is better than
cure. Ex ante responsible lending practices as preventative measures to avoid
reckless credit granting and over-indebtedness are arguably more important tools
in establishing a healthy credit market than ex post measures. The focus of this
contribution, is therefore, to provide a detailed overview of the South African
reckless credit regime as a debt- prevention measure aimed at promoting responsible
lending, with specific focus on the aspect of pre-agreement assessment as a
core mechanism to avoid reckless credit granting and over-indebtedness. The
main features of the reckless credit regime are highlighted, and afterwards, a
detailed exposition of the evolution and extensive recent development of the
pre-agreement assessment component in South Africa is undertaken. Finally,
observations are made regarding the South African reckless regime in general
and with regard to affordability assessment specifically and its ability,
benchmarked against the essential features of a responsible lending regime as
advocated by Wilson in the book ‘International responses to issues of credit and
over-indebtedness in the wake of crisis’, to promote responsible lending. The conclusion
is reached that benchmarked against the four characteristics of an effective
responsible lending regime as identified by Wilson, it is apparent that the South
African reckless lending regime is no ‘toothless tiger’, and that it attaches the necessary
amount of significance to the credit provider’s duty to take reasonable steps
to do a proper pre-agreement assessment in order to avoid reckless credit
granting.http://onlinelibrary.wiley.com/journal/10.1002/(ISSN)1099-11072016-04-30hb201
Rwanda legal framework on insolvency : problems and proposals for reform

The purpose of this article is to explore some key insolvency issues, which will be
highly selective for this article, and to identify the weaknesses and inconsistencies
in the existing framework on insolvency. Rwanda does not have an efficient and
effective framework on insolvency, and the article argues that there is a need for
an improved insolvency law regime. In view of the weaknesses and inconsistencies,
it is vital to consider international best practices such as the United Nations
Commission on International Trade Law (UNCITRAL) Legislative Guide on
Insolvency and the UNCITRAL Model Law on Cross-border Insolvency as the
basis needed to deal with different aspects or elements of the Rwanda insolvency
law. The value of this article lies in the insights it offers into the current framework
on insolvency and the opportunity given to address the inconsistencies, weaknesses
and uncertainties that invariably arise from the law.http://onlinelibrary.wiley.com/journal/10.1002/(ISSN)1099-11072016-05-26hb201
Various aspects to consider with regard to special insolvency rules for small and medium-sized enterprises in South Africa

The notion of special insolvency rules for small and medium-sized enterprises
(SMEs) has attracted attention in international spheres, and within the ambit of
some international and comparative approaches, same is considered in this article
with particular focus on the South African position. In particular, we show that the
South African insolvency regime does not, at present, cater for financially distressed
small businesses in a specific and viable manner. In South Africa, although
attention has been paid to the development and support of small businesses, similar
considerations have not been observed with regard to the insolvency side of small
business concerns. No comprehensive and focused process of dealing with financially
distressed small businesses exists in the South African insolvency framework.
This scenario prevails, notwithstanding that there are existing foreign and international
policy guidelines, rules and regimes in developed jurisdictions that can serve
as pointers in this regard. The purpose of this article is to first highlight the need
for special treatment of small businesses by focusing on the shortcomings in the
South African system, and, as a natural sequential development, policy proposals
as unavoidable foundations to address these shortcomings. In the premises, the focus
is on the principles and policies that are relevant to any discussion regarding
insolvent businesses that fall within the scope of the SME category. Therefore, this
paper deals with the concept of the small business, the South African insolvency
regime and the international position pertaining to small businesses. In particular, the need for special treatment of SMEs under insolvent circumstances is discussed,
consideration is given to the existing South African mechanisms available to small
businesses in distress and the lack of suitable contextual provisions for small businesses
in distress is noted. A core component of this article is the position in South
Africa viewed against the backdrop of some international developments, international
documents and principles that are relevant to an insolvency and rescue/rehabilitation
regime within the context of the small business. As a logical conclusion,
recommendations for reform of the South African regime are made.http://onlinelibrary.wiley.com/journal/10.1002/(ISSN)1099-11072016-10-31hb201
The Costs and Benefits of Regulating the Market for Corporate Insolvency Practitioner Remuneration

The release by the Australian Treasury on Friday, 7 November, 2014 of the Insolvency Law Reform Bill (ILRB) 2014 throws the spotlight once again on corporate insolvency law reform in Australia. Significantly, the ILRB 2014 identifies amongst its purposes two objectives with respect to Corporate Insolvency Practitioner (CIP) remuneration reform.  Namely to: promote market competition on price and quality and improve the overall confidence in the professionalism and competence of insolvency practitioners. This paper considers whether the proposed CIP remuneration reforms outlined in the ILRB 2014 will effectively achieve these objectives. Where it is considered reforms are misdirected, further changes, informed by United Kingdom insolvency reform proposals, are considered.Full Tex
Differential production of angiostatin by concomitant antitumoral resistance-inducing cancer cells

The phenomenon by which tumor-bearing hosts are capable of inhibiting secondary tumor implants or metastases, known as concomitant antitumoral resistance (CAR), is presumably due to antiangiogenesis at places distant from the primary tumor. Although angiostatin, a potent inhibitor of angiogenesis, has been reported to be one of the factors responsible for suppressing the growth of secondary tumors in mice bearing previous tumors, it has not been definitively proven yet. With the aim of investigating whether CAR-inducing cancer cells display a differential angiostatin production and to support the role ascribed to that molecule concerning the inhibition of secondary tumor implants, 5 tumor models with different CAR-inducing capacities were studied herein. One of the 2 human lung cancer cell lines analyzed revealed a strong CAR against secondary s.c. tumor implants in nude mice, and 2 of 3 of the murine mammary tumors used exhibited inhibitory effect on secondary s.c. and i.v. tumor inoculations in syngeneic hosts. Since angiostatin is a proteolytic fragment from plasminogen, we examined by Western blot the ability of all conditioned media collected from the tumor cells studied to convert plasminogen to angiostatin. An association between in vivo generation of CAR and in vitro conversion of plasminogen into angiostatin was found. Since different enzymatic mechanisms were described to explain the generation of angiostatin, we also studied gelatinase and urokinase-type plasminogen activator secretion in conditioned media by zymography. The conversion of plasminogen into angiostatin by conditioned media was mainly inhibited by broad-spectrum serine proteinase inhibitors, suggesting a possible role for 1 or more enzymes of that group in the process. These findings suggest the existence of a differential angiostatin generation by CAR-inducing cancer cells, providing additional support to previous data obtained by other authors.Fil: Binda, María Mercedes. Fundación de Investigacián del Cáncer CEFYBO; Argentina.Fil: Matar, Pablo. Universidad Nacional de Rosario. Instituto de Genética Experimental; Facultad de Ciencias Médicas. Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET);Argentina.Fil: González, Alejandro D. Fundación de Investigacián del Cáncer CEFYBO; Argentina.Fil: Rozados, Viviana R. Universidad Nacional de Rosario. Instituto de Genética Experimental; Facultad de Ciencias Médicas. Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET);ArgentinaFil: Gervasoni, Silvia I. Universidad Nacional de Rosario. Instituto de Genética Experimental; Facultad de Ciencias Médicas; Argentina.Fil: Scharovsky, O. Graciela. Universidad Nacional de Rosario. Instituto de Genética Experimental; Facultad de Ciencias Médicas. Consejo Nacional de Investigaciones UNR; Argentina.Fil: Bonfil, R. Daniel. Departments of Urology and Pathology, Wayne State University School of Medicine, Detroit, MI; USA
Stage at diagnosis is a key explanation of differences in breast cancer survival across Europe

We used multiple regression models to assess the influence of disease stage at diagnosis on the 5-year relative survival of 4,478 patients diagnosed with breast cancer in 1990-1992. The cases were representative samples from 17 population-based cancer registries in 6 European countries (Estonia, France, Italy, Netherlands, Spain and UK) that were combined into 9 regional groups based on similar survival. Five-year relative survival was 79% overall, varying from 98% for early, node-negative (T1N0M0) tumours; 87% for large, node-negative (T2-3N0M0) tumours; 76% for node-positive (T1-3N+M0) tumours and 55% for locally advanced (T4NxM0) tumours to 18% for metastatic (M1) tumours and 69% for tumours of unspecified stage. There was considerable variation across Europe in relative survival within each disease stage, but this was least marked for early nodenegative tumours. Overall 5-year relative survival was highest in the French group of Bas-Rhin, Côte d'Or, Hérault and Isère (86%), and lowest in Estonia (66%). These geographic groups were characterised by the highest and lowest percentages of women with early stage disease (T1N0M0: 39% and 9%, respectively). The French, Dutch and Italian groups had the highest percentage of operated cases. The number of axillary nodes examined, a factor influencing nodal status, was highest in Italy and Spain. After adjusting for TNM stage and the number of nodes examined, survival differences were greatly reduced, indicating that for these women, diagnosed with breast cancer in Europe during 1990-1992, the survival differences were mainly due to differences in stage at diagnosis. However, in 3 regional groups, the relative risks of death remained high even after these adjustments, suggesting less than optimal treatment. Screening for breast cancer did not seem to affect the survival patterns once stage had been taken into account
Restoration of endogenous wild-type p53 activity in a glioblastoma cell line with intrinsic temperature-sensitive p53 induces growth arrest but not apoptosis.

p53 protein is a transcription factor involved in multiple tumor-suppressor activities including cell cycle control and apoptosis. TP53 gene is frequently mutated in glioblastoma, suggesting the importance of inactivation of this gene product in gliomagenesis. Restoration of p53 function in glioblastoma cell lines deficient for p53 has shown that p53 induces growth arrest or apoptosis depending on the cell line and vector used to transduce wild-type TP53 alleles. Considering that astrocytes grow and express p53, it is not clear whether these results reflect physiologic responses or the result of p53 overexpression in combination with cellular responses to viral vector infection. Here, we reassessed this issue using a glioblastoma cell line (LN382) that expresses an endogenous temperature-sensitive mutant p53. This cell line expresses TP53 alleles (100% as determined by a p53 transcriptional assay in yeast) mutated at codon 197 GTG (Val) &amp;gt; CTG (Leu). We found that the p53 protein in these cells acted as an inactive mutant at 37 degrees C and as a functional wild-type p53 below 34 degrees C as demonstrated by several lines of evidence, including (i) restoration of transactivating ability in yeast, (ii) induction of p53-modulated genes such as CDKN1(p21) and transforming growth factor-alpha, (iii) disappearance of accumulated p53 protein in the nucleus and (iv) decrease in steady state p53 protein levels. This temperature switch allowed p53 levels, which were close to physiological levels to dramatically reduce LN382 cell proliferation by inducing a G(1)/S cell cycle block, but not to induce apoptosis. The lack of apoptosis was considered to be a result of the low level p53 expression, because increasing wild-type p53 levels by adenoviral-mediated gene transfer caused apoptosis in these cells. The LN382 cell line will be extremely useful for investigations into the roles of p53 in cellular responses to a variety of stimuli or damages
Peptidylglycine alpha-amidating monooxygenase- and proadrenomedullin-derived peptide-associated neuroendocrine differentiation are induced by androgen deprivation in the neoplastic prostate

Most PCs show NE differentiation. Several studies have tried to correlate NE expression with disease status, but the reported findings have been contradictory. Prostatic NE cells synthesize peptides with a wide spectrum of potential functions. Some of these active peptides, such as PAMP, are amidated. PAM is the only carboxy-terminal peptide-amidating enzyme identified. We studied expression of PAMP and PAM in normal prostate and prostatic tumors (clinical specimens and human xenograft models) with or without prior androgen-deprivation therapy and found a wide distribution of both molecules in NE subpopulations of all kinds. Although the correlation of either marker to tumor grade, clinical progression or disease prognosis did not reach statistical significance, PAMP- or PAM-immunoreactive cells were induced after androgen-blockade therapy. In the PC-310 and PC-295 androgen-dependent models, PAMP or PAM NE differentiation was induced after castration in different ways, being higher in PC-310, which might explain its long-term survival after androgen deprivation. We show induction of expression of 2 new NE markers in clinical specimens and xenografted PC after endocrine therapy
Arsenic trioxide induces apoptosis in human gastric cancer cells through up-regulation of p53 and activation of caspase-3

Arsenic trioxide (As 2O 3) can induce clinical remission in patients suffering from acute promyelocytic leukemia, through induction of apoptosis and activation of caspases. We investigated the potential use of As 2O 3 in human gastric cancer and its possible mechanisms. Human gastric cancer cell lines AGS and MKN-28 were treated with various concentrations (0.1 to 100 μM of As 2O 3 for 24 to 72 hr. Apoptosis was determined by acridine orange staining, flow cytometry and DNA fragmentation. Protein levels of p53, p21 wafl/cipl, c-myc, bcl-2 and bax were detected by Western blotting. Effects of As 2O 3 on caspase-3 protease activity, its protein concentration and cleavage of poly(ADP)-ribose polymerase (PARP) were also studied. As 2O 3 inhibited cell growth and induced apoptosis in both cell lines, though AGS cells were more sensitive. As 2O 3 induced apoptosis in AGS cells in a concentration- and time-dependent manner. Treatment resulted in a marked increase in p53 protein levels as early as 4 hr. Co-incubation with p53 anti-sense oligo-nucleotide suppressed As 2O 3-induced intracellular p53 over-expression and apoptosis. As 2O 3 increased the activity of caspase-3, with appearance of its 17 kDa peptide fragment, and cleavage of PARP, with appearance of the 85 kDa cleavage product, both in parallel with the induction of apoptosis. Both the tripeptide caspase inhibitor zYAD-fmk and the specific caspase-3 inhibitor DEVD-fmk partially suppressed As 2O 3-induced caspase-3 activation and apoptosis. As 2O 3 inhibits cell growth and induces apoptosis in gastric cancer cells, involving p53 over-expression and activation of caspase-3. The potential use of this compound in the treatment of gastric cancer is worth further investigation. © 2001 Wiley-Liss, Inc.postprin
High frequency of loss of heterozygosity in vulval intraepithelial neoplasia (VIN) is associated with invasive vulval squamous cell carcinoma (VSCC)

Vulval intraepithelial neoplasia (VIN) is thought to be the premalignant phase of human papillomavirus (HPV)-associated vulval squamous cell carcinoma (VSCC). Various molecular events have been suggested as markers for progression from VIN to VSCC, but loss of heterozygosity (LOH) in vulval neoplasia has rarely been studied in this context. We performed LOH analysis by polymerase chain reaction (PCR) amplification of polymorphic microsatellite markers at 6 chromosomal loci (17p13-p53, 9p21-p16, 3p25, 4q21, 5p14 and 11p15). The presence of HPV was assessed using consensus PCR primers and DNA sequencing. To examine any association between LOH and the presence of invasive disease, we analyzed 43 cases of lone VIN III, 42 cases of lone VSCC and 21 cases of VIN with concurrent VSCC. HPV DNA was detected in 95% of lone VIN III samples and 71% of lone VSCC samples. Fractional regional allelic loss (FRL) in VIN associated with VSCC was higher than in lone VIN (mean FRL 0.43 vs. 0.21, p < 0.005). LOH at 3p25 occurred significantly more frequently in HPV-negative VSCC than in HPV-positive VSCC (58% vs. 22%, p < 0.04). These data suggest that genetic instability in VIN, reflected by LOH, may increase the risk of invasion. In addition, molecular events differ in HPV-positive and -negative VSCC and 3p25 may be the site of a tumor suppressor gene involved in HPV-independent vulval carcinogenesis