The Paraprofessional Conundrum: Why We Need Alternative Support Strategies

This four-page article describes a conundrum facing schools utilizing paraprofessionals to support students receiving special education. It considers three factors: (a) asked to engage in teacher-type instructional roles, (b) trained and supervised for teacher-type instructional roles, and (c) compensation commensurate with teacher-type instructional roles across six combinations. Regardless of whether or not the factors are present or not it often leads to series of undesirable outcomes. The article suggest a series of alternatives

Guidelines for Selecting Alternatives to Overreliance on Paraprofessionals

The Guidelines for Selecting Alternatives to Overreliance on Paraprofessionals is a field-tested schhol-based planning process. Support for the preparation of this article was provided by the United States Department of Education, Office of Special Education and Rehabilitative Services under the funding category, Model Demonstration Projects for Children and Youth with Disabilities, CFDA 84.324M (H324M02007), awarded to the Center on Disability and Community Inclusion at the University of Vermont. The contents of this document reflect the ideas and positions of the authors and do not necessarily reflect the ideas or positions of the U.S. Department of Education; therefore, no official endorsement should be inferred

Alternatives to Overreliance or Inappropriate Utilization of Paraprofessionals in Special Education

This article describes 12 alternatives to overreliance or Inappropriate utilization of paraprofessionals in special education based utilization in American schools. Support for the preparation of this article was provided by the United States Department of Education, Office of Special Education Programs, under the funding category, Model Demonstration Projects for Children and Youth with Disabilities, CFDA 84.324M (Project EVOLVE, H324M02007), awarded to the Center on Disability and Community Inclusion at the University of Vermont. The contents of this paper reflect the ideas and positions of the authors and do not necessarily reflect the ideas or positions of the U.S. Department of Education; therefore, no official endorsement should be inferred

A Guide to Schoolwide Planning for Paraeducator Supports

A Guide to Schoolwide Planning for Paraeducator Supports is a field-tested, schoolwide planning tool designed to improve the quality of paraprofessional supports offered in public schools to supports students with disabilities and other identified support needs. Support for the preparation of this article was provided by the United States Department of Education, Office of Special Education and Rehabilitative Services under the funding category, Model Demonstration Projects for Children and Youth with Disabilities, CFDA 84.324M (H324M980229), awarded to the Center on Disability and Community Inclusion at the University of Vermont. The contents of this paper reflect the ideas and positions of the authors and do not necessarily reflect the ideas or positions of the U.S. Department of Education; therefore, no official endorsement should be inferred

Cell migration leads to spatially distinct but clonally related airway cancer precursors

Background Squamous cell carcinoma of the lung is a common cancer with 95% mortality at 5 years. These cancers arise from preinvasive lesions, which have a natural history of development progressing through increasing severity of dysplasia to carcinoma in situ (CIS), and in some cases, ending in transformation to invasive carcinoma. Synchronous preinvasive lesions identified at autopsy have been previously shown to be clonally related. Methods Using autofluorescence bronchoscopy that allows visual observation of preinvasive lesions within the upper airways, together with molecular profiling of biopsies using gene sequencing and loss-of-heterozygosity analysis from both preinvasive lesions and from intervening normal tissue, we have monitored individual lesions longitudinally and documented their visual, histological and molecular relationship. Results We demonstrate that rather than forming a contiguous field of abnormal tissue, clonal CIS lesions can develop at multiple anatomically discrete sites over time. Further, we demonstrate that patients with CIS in the trachea have invariably had previous lesions that have migrated proximally, and in one case, into the other lung over a period of 12 years. Conclusions Molecular information from these unique biopsies provides for the first time evidence that field cancerisation of the upper airways can occur through cell migration rather than via local contiguous cellular expansion as previously thought. Our findings urge a clinical strategy of ablating high-grade premalignant airway lesions with subsequent attentive surveillance for recurrence in the bronchial tree

Pediatric Systemic Multi-Inflammatory Diseases in Italy During Sars-Cov-2 Epidemic: From Kawasaki Disease To Kawacovid

Introduction: Italy was affected by the SARS-CoV-2 epidemic after its outbreak in China. With a 4-weeks delay after the peak in adults, we observed an abnormal number of patients with characteristics of a multi-inflammatory disease and similarities with Kawasaki Disease (KD). Others reported similar cases, defined PIMS-TS or MIS-C.1,2 Objectives: To better characterize clinical features and treatment response of PIMS-TS and to explore its relationship with KD. Methods: We conducted an observational, retrospective, multicenter study. On April 24th-2020 the Rheumatology Study Group of the Italian Pediatric Society launched a national online survey, to enroll patients diagnosed with KD or with a multisystem inflammatory disease between February 1st 2020 and May 31st. The population was then divided into two different groups: 1) Classical and incomplete KD, named Kawasaki Disease Group (KDG); 2) KD-like multi-inflammatory syndrome, named KawaCOVID (KCG). An expert panel of pediatric rheumatologists re-analyzed every single patient to ensure appropriate classification. Data were collected with an online database. Results: 149 cases were studied, 96 with KDG and 53 with KCG. The two population significantly differed for clinical characteristics (see table 1). Lymphopenia, higher CRP levels, elevated Ferritin and Troponin-T characterized KCG such as lower WBC and platelets (all p values<0,05). KDG received more frequently immunoglobulins (IVIG) and acetylsalicylic acid (ASA) (81,3% vs 66%; p=0.04 and 71,9% vs 43,4%; p=0.001 respectively) as KCG more often received glucocorticoids (56,6% vs 14,6%; p<0.0001). SARS-CoV-2 assay more often resulted positive in KCG than in KDG (75,5% vs 20%; p<0.0001). Short-term follow data on KCG showed minor complications while on KDG a majority of patients had persistence of CAA. Comparing KDG with a KD-Historical Italian cohort (598 patients), no statistical difference was found in terms of clinical manifestations and laboratory data between the two groups Conclusion: Our study would suggest that SARS-CoV-2 infection might determine two distinct inflammatory diseases in children: KD, possibly triggered by SARS-CoV-2, and PIMS-TS. Older age at onset and clinical peculiarities, like the occurrence of myocarditis, characterize this multiinflammatory syndrome. Our patients had an optimal response to treatments and a good outcome, with few complications and no deaths

Lung adenocarcinoma originates from retrovirus infection of proliferating type 2 pneumocytes during pulmonary post-natal development or tissue repair

Jaagsiekte sheep retrovirus (JSRV) is a unique oncogenic virus with distinctive biological properties. JSRV is the only virus causing a naturally occurring lung cancer (ovine pulmonary adenocarcinoma, OPA) and possessing a major structural protein that functions as a dominant oncoprotein. Lung cancer is the major cause of death among cancer patients. OPA can be an extremely useful animal model in order to identify the cells originating lung adenocarcinoma and to study the early events of pulmonary carcinogenesis. In this study, we demonstrated that lung adenocarcinoma in sheep originates from infection and transformation of proliferating type 2 pneumocytes (termed here lung alveolar proliferating cells, LAPCs). We excluded that OPA originates from a bronchioalveolar stem cell, or from mature post-mitotic type 2 pneumocytes or from either proliferating or non-proliferating Clara cells. We show that young animals possess abundant LAPCs and are highly susceptible to JSRV infection and transformation. On the contrary, healthy adult sheep, which are normally resistant to experimental OPA induction, exhibit a relatively low number of LAPCs and are resistant to JSRV infection of the respiratory epithelium. Importantly, induction of lung injury increased dramatically the number of LAPCs in adult sheep and rendered these animals fully susceptible to JSRV infection and transformation. Furthermore, we show that JSRV preferentially infects actively dividing cell in vitro. Overall, our study provides unique insights into pulmonary biology and carcinogenesis and suggests that JSRV and its host have reached an evolutionary equilibrium in which productive infection (and transformation) can occur only in cells that are scarce for most of the lifespan of the sheep. Our data also indicate that, at least in this model, inflammation can predispose to retroviral infection and cancer

CADM1 inhibits squamous cell carcinoma progression by reducing STAT3 activity.

Although squamous cell carcinomas (SqCCs) of the lungs, head and neck, oesophagus, and cervix account for up to 30% of cancer deaths, the mechanisms that regulate disease progression remain incompletely understood. Here, we use gene transduction and human tumor xenograft assays to establish that the tumour suppressor Cell adhesion molecule 1 (CADM1) inhibits SqCC proliferation and invasion, processes fundamental to disease progression. We determine that the extracellular domain of CADM1 mediates these effects by forming a complex with HER2 and integrin α6β4 at the cell surface that disrupts downstream STAT3 activity. We subsequently show that treating CADM1 null tumours with the JAK/STAT inhibitor ruxolitinib mimics CADM1 gene restoration in preventing SqCC growth and metastases. Overall, this study identifies a novel mechanism by which CADM1 prevents SqCC progression and suggests that screening tumours for loss of CADM1 expression will help identify those patients most likely to benefit from JAK/STAT targeted chemotherapies

On String S-matrix, Bound States and TBA

The study of finite J effects for the light-cone AdS superstring by means of the Thermodynamic Bethe Ansatz requires an understanding of a companion 2d theory which we call the mirror model. It is obtained from the original string model by the double Wick rotation. The S-matrices describing the scattering of physical excitations in the string and mirror models are related to each other by an analytic continuation. We show that the unitarity requirement for the mirror S-matrix fixes the S-matrices of both theories essentially uniquely. The resulting string S-matrix S(z_1,z_2) satisfies the generalized unitarity condition and, up to a scalar factor, is a meromorphic function on the elliptic curve associated to each variable z. The double Wick rotation is then accomplished by shifting the variables z by quarter of the imaginary period of the torus. We discuss the apparent bound states of the string and mirror models, and show that depending on a choice of the physical region there are one, two or 2^{M-1} solutions of the M-particle bound state equations sharing the same conserved charges. For very large but finite values of J, most of these solutions, however, exhibit various signs of pathological behavior. In particular, they might receive a finite J correction to their energy which is complex, or the energy correction might exceed corrections arising due to finite J modifications of the Bethe equations thus making the asymptotic Bethe ansatz inapplicable.Comment: 77 pages, 6 figures, v2: the statement about the periodicity condition for mirror fermions corrected; typos corrected; references added, v3: misprints correcte