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This study explores how community socioeconomic status (SES), geographical location, and administrator perspectives influence the implementation of exclusionary disciplinary policies. Using Geographical Information Systems mapping technology, in-depth interviewing, and document analysis, this study finds that schools located in high SES sectors have higher rates of exclusionary disciplinary practices, whereas schools located in low SES sectors have lower levels. The findings also indicate five normative values that influence leadership's decisions to exclude students more frequently. These guiding belief systems include productive efficiency, equality versus equity, the potential of legal liability, prescribing to a cultural deficit ideology, and the notion of strict surveillance. [ABSTRACT FROM AUTHOR]

The article discusses a research project which identified the most prominent gender-based concerns on the authors' university campus. Topics covered include how the challenges faced in the project have informed the researchers' identities as academics, feminists, and activists, emotions involved in the gender center project, and benefits of negotiating institutional structures and historically situated alliances.

Introduction: It is well known that neutrons are more effective treatments than photons to treat hypoxic tumors due to the interaction with the nucleus and the production of heavy particles. This study aimed to evaluate the suitability of Boron neutron capture therapy (BNCT) for the treatment of lung cancer. To this end, neutron dose distributions were calculated in lung tumor volume and peripheral organs at risk (OARs). Material and Methods: Dose distribution to treat lung cancer was calculated by MCNPX code. An elliptical tumor with a volume of 27cm3 was centered in the left lung of the ORNL phantom and was irradiated with neutron spectrums of Massachusetts Institute of Technology (MIT) and CNEA-MEC. The tumor was loaded with different concentrations of Boron 0, 10, 30, and 60 ppm to evaluate the delivered dose to OARs. Results: Neutron absorbed dose rates in the tumor were 2.2×10-3, 2.6×10-3, 3.4×10-3, and 4.7×10-3 Gy/s for boron concentrations of 0, 10, 30, and 60 ppm, respectively for MIT. Moreover, similar results for CNEAMEC were 1.2×10-3, 1.6×10-3, 2.5×10-3, and 3.7×10-3 Gy/s. The heart absorbed the maximum neutron dose rate of 1.7×10-4 and 1.6×10-4 Gy/s in MIT and CNEA, respectively. For all energy bins of spectrums, the neutrons flux is decreased as it penetrates the lung. Conclusion: An increase in boron concentrations in tumors increases the absorbed doses while deteriorates dose uniformity. The results show that the MIT source is well suited to treat deep lung tumors while maintaining the OARs' dose within the threshold dose. [ABSTRACT FROM AUTHOR]

Background: Leptin, an adipocyte-derived hormone, has a pivotal role in the regulation of body weight through acting on its specific leptin receptor (LEPR). The 223A/G polymorphism of the LEPR gene is one of the most common polymorphism in all populations. In this study, we aimed to investigate the impact of the 223A/G polymorphism of the LEPR gene on serum levels of leptin in type 2 diabetes mellitus(T2DM) in a sample of Iranian population. Materials and Methods: One hundred and forty-four T2DM patients were screened and compared to 147 healthy controls. The 223A/GLEPR polymorphism was genotyped using polymerase chain reaction (PCR) followed by restriction fragment length polymorphism (RFLP). The serum levels of leptin were measured. Results: The mean serum levels of leptin in T2DM patients were significantly higher than that of healthy control subjects; 22.90 ng/ml (95 % confidence interval [CI] = 20.79 - 25.23) vs. 8.70 ng/ml (95 % CI = 7.87 - 9.63). The genotypes (AA, AG, and GG) distributions of the 223A/G polymorphism were 55.5 %, 41 %, and 3.5 % in T2DM and 54.4 %, 42.2 %, and 3.4 % in healthy controls. The results showed no significant differences in the 223A/G LEPR genotype and allele frequencies between T2DM and control subjects (x2 = 0.043, P = 0.979 and x2 = 0.003, P = 0.957), respectively. In addition, the serum leptin levels were markedly higher in subjects with GG genotype than those with AG or GG genotype only in T2DM Conclusion: The 223A/G LEPR gene polymorphism is associated with markedly increased serum leptin levels in T2DM. However, no differences were determined in genotype and allele frequencies between T2DM patients and control subjects. [ABSTRACT FROM AUTHOR]

Background: Leptin, an adipocyte-derived hormone, has a pivotal role in the regulation of body weight through acting on its specific leptin receptor (LEPR). The 223A/G polymorphism of the LEPR gene is one of the most common polymorphism in all populations. In this study, we aimed to investigate the impact of the 223A/G polymorphism of the LEPR gene on serum levels of leptin in type 2 diabetes mellitus(T2DM) in a sample of Iranian population. Materials and Methods: One hundred and forty-four T2DM patients were screened and compared to 147 healthy controls. The 223A/GLEPR polymorphism was genotyped using polymerase chain reaction (PCR) followed by restriction fragment length polymorphism (RFLP). The serum levels of leptin were measured. Results: The mean serum levels of leptin in T2DM patients were significantly higher than that of healthy control subjects; 22.90 ng/ml (95 % confidence interval [CI] = 20.79 - 25.23) vs. 8.70 ng/ml (95 % CI = 7.87 - 9.63). The genotypes (AA, AG, and GG) distributions of the 223A/G polymorphism were 55.5 %, 41 %, and 3.5 % in T2DM and 54.4 %, 42.2 %, and 3.4 % in healthy controls. The results showed no significant differences in the 223A/G LEPR genotype and allele frequencies between T2DM and control subjects (x2 = 0.043, P = 0.979 and x2 = 0.003, P = 0.957), respectively. In addition, the serum leptin levels were markedly higher in subjects with GG genotype than those with AG or GG genotype only in T2DM Conclusion: The 223A/G LEPR gene polymorphism is associated with markedly increased serum leptin levels in T2DM. However, no differences were determined in genotype and allele frequencies between T2DM patients and control subjects. [ABSTRACT FROM AUTHOR]

To achieve malignancy, cancer cells convert numerous signaling pathways, with evasion from cell death being a characteristic hallmark. The cell death machinery represents an anti-cancer target demanding constant identification of tumor-specific signaling molecules. Control of mitochondrial radical formation, particularly superoxide interconnects cell death signals with appropriate mechanistic execution. Superoxide is potentially damaging, but also triggers mitochondrial cytochrome c release. While paraoxonase (PON) enzymes are known to protect against cardiovascular diseases, recent data revealed that PON2 attenuated mitochondrial radical formation and execution of cell death. Another family member, PON3, is poorly investigated. Using various cell culture systems and knockout mice, here we addressed its potential role in cancer. PON3 is found overexpressed in various human tumors and diminishes mitochondrial superoxide formation. It directly interacts with coenzyme Q10 and presumably acts by sequestering ubisemiquinone, leading to enhanced cell death resistance. Localized to the endoplasmic reticulum (ER) and mitochondria, PON3 abrogates apoptosis in response to DNA damage or intrinsic but not extrinsic stimulation. Moreover, PON3 impaired ER stress-induced apoptotic MAPK signaling and CHOP induction. Therefore, our study reveals the mechanism underlying PON3's anti-oxidative effect and demonstrates a previously unanticipated function in tumor cell development. We suggest PONs represent a novel class of enzymes crucially controlling mitochondrial radical generation and cell death. [ABSTRACT FROM AUTHOR]