Women\u27s Rights: Reframing the Issues for the Future

Good morning and welcome, everyone, to our panel on Women\u27s Rights: Refraining the Issues for the Future. I am Kathy Rodgers. I\u27m from the class of 1973 of Columbia Law School, and I\u27m looking around this room – this is not what room A and B looked like back then! Everybody has a microphone, which is great, because we hope to have some good interactive discussion with all of you this morning. I am also, in addition to being a Columbia Law alum, the president of NOW Legal Defense and Education Fund here in New York. For over thirty-two years, NOW Legal Defense has used the power of the law to define and defend women\u27s rights. I am particularly pleased to be here today with Columbia Law School alumnae because Columbia women have been a substantial part of our team throughout these thirty-two years as members of our staff, as academic partners, a s student interns (including some young men), as part of our volunteer leadership, as pro bono attorneys, and as supporters. So with all of these connections, it really is a matter of personal pride to be back here celebrating the women of Columbia Law School

RELASI ANTAR ANGGOTA FRAKSI PARTAI DEMOKRAT PERIODE 2014-2019 DPRD KAB. PARIGI MOUTONG TERHADAP PENGAMBILAN KEPUTUSAN

This research is about the relations between DPRD members and the Democratic Party fraction for the 2014–2019 period in Parigi Moutong Regency. The purpose of this study was to find out and analyze how the relations between members of the Democratic Party faction for the period 2014–2019  affected decision-making.  Relations between members of the Democrat party faction in the Parigi Moutong district DPRD at the start of Mr. Haris Lasimpara's replacement as chairman of the DPC had an impact on discordant communication between faction members. As a result, channelling people's aspirations is hampered, particularly for Democratic party constituents in each faction member's constituency. After the 2018 Parigi Moutong district head election, the regent who was elected was no longer a supporter of the Democratic Party. As a result, the Democratic Party is not adequately accommodated by the elected regent in channelling some of its aspirations, particularly in constituent areas

Nanoscale plasmonic phenomena in CVD-grown MoS2 monolayer revealed by ultra- broadband synchrotron radiation based nano-FTIR spectroscopy and near-field microscopy

Nanoscale plasmonic phenomena observed in single and bi-layers of molybdenum disulfide (MoS2) on silicon dioxide (SiO2) are reported. A scattering type scanning near-field optical microscope (s-SNOM) with a broadband synchrotron radiation (SR) infrared source was used. We also present complementary optical mapping using tunable CO2-laser radiation. Specifically, there is a correlation of the topography of well-defined MoS2 islands grown by chemical vapor deposition, as determined by atomic force microscopy, with the infrared (IR) signature of MoS2. The influence of MoS2 islands on the SiO2 phonon resonance is discussed. The results reveal the plasmonic character of the MoS2 structures and their interaction with the SiO2 phonons leading to an enhancement of the hybridized surface plasmon-phonon mode. A theoretical analysis shows that, in the case of monolayer islands, the coupling of the MoS2 optical plasmon mode to the SiO2 surface phonons does not affect the infrared spectrum significantly. For two-layer MoS2, the coupling of the extra inter-plane acoustic plasmon mode with the SiO2 surface transverse phonon leads to a remarkable increase of the surface phonon peak at 794 cm−1. This is in agreement with the experimental data. These results show the capability of the s-SNOM technique to study local multiple excitations in complex non- homogeneous structures

Interaction of amisulpride with GLUT1 at the blood-brain barrier. Relevance to Alzheimer’s disease

Blood-brain barrier (BBB) dysfunction may be involved in the increased sensitivity of Alzheimer's disease (AD) patients to antipsychotics, including amisulpride. Studies indicate that antipsychotics interact with facilitated glucose transporters (GLUT), including GLUT1, and that GLUT1 BBB expression decreases in AD. We tested the hypotheses that amisulpride (charge: +1) interacts with GLUT1, and that BBB transport of amisulpride is compromised in AD. GLUT1 substrates, GLUT1 inhibitors and GLUT-interacting antipsychotics were identified by literature review and their physicochemical characteristics summarised. Interactions between amisulpride and GLUT1 were studied using in silico approaches and the human cerebral endothelial cell line, hCMEC/D3. Brain distribution of [3H]amisulpride was determined using in situ perfusion in wild type (WT) and 5xFamilial AD (5xFAD) mice. With transmission electron microscopy (TEM) we investigated brain capillary degeneration in WT mice, 5xFAD mice and human samples. Western blots determined BBB transporter expression in mouse and human. Literature review revealed that, although D-glucose has no charge, charged molecules can interact with GLUT1. GLUT1 substrates are smaller (184.95±6.45g/mol) than inhibitors (325.50±14.40g/mol) and GLUT-interacting antipsychotics (369.38±16.04). Molecular docking showed beta-D-glucose (free energy binding: -15.39kcal/mol) and amisulpride (-29.04kcal/mol) interact with GLUT1. Amisulpride did not affect [14C]D-glucose hCMEC/D3 accumulation. [3H]amisulpride uptake into the brain (except supernatant) of 5xFAD mice compared to WT remained unchanged. TEM revealed brain capillary degeneration in human AD. There was no difference in GLUT1 or P-glycoprotein BBB expression between WT and 5xFAD mice. In contrast, caudate P-glycoprotein, but not GLUT1, expression was decreased in human AD capillaries versus controls. This study provides new details about the BBB transport of amisulpride, evidence that amisulpride interacts with GLUT1 and that BBB transporter expression is altered in AD. This suggests that antipsychotics could potentially exacerbate the cerebral hypometabolism in AD. Further research into the mechanism of amisulpride transport by GLUT1 is important for improving antipsychotics safety

Genomic analyses in Cornelia de Lange Syndrome and related diagnoses: Novel candidate genes, <scp>genotype–phenotype</scp> correlations and common mechanisms

Cornelia de Lange Syndrome (CdLS) is a rare, dominantly inherited multisystem developmental disorder characterized by highly variable manifestations of growth and developmental delays, upper limb involvement, hypertrichosis, cardiac, gastrointestinal, craniofacial, and other systemic features. Pathogenic variants in genes encoding cohesin complex structural subunits and regulatory proteins (NIPBL, SMC1A, SMC3, HDAC8, and RAD21) are the major pathogenic contributors to CdLS. Heterozygous or hemizygous variants in the genes encoding these five proteins have been found to be contributory to CdLS, with variants in NIPBL accounting for the majority (&gt;60%) of cases, and the only gene identified to date that results in the severe or classic form of CdLS when mutated. Pathogenic variants in cohesin genes other than NIPBL tend to result in a less severe phenotype. Causative variants in additional genes, such as ANKRD11, EP300, AFF4, TAF1, and BRD4, can cause a CdLS‐like phenotype. The common role that these genes, and others, play as critical regulators of developmental transcriptional control has led to the conditions they cause being referred to as disorders of transcriptional regulation (or “DTRs”). Here, we report the results of a comprehensive molecular analysis in a cohort of 716 probands with typical and atypical CdLS in order to delineate the genetic contribution of causative variants in cohesin complex genes as well as novel candidate genes, genotype–phenotype correlations, and the utility of genome sequencing in understanding the mutational landscape in this population

Analisis Faktor Risiko Kejadian Anemia pada Remaja Putri: Literatur Review

Anemia is an indicator of malnutrition that can affect a country's economic development. anemia is a global health problem in the world. The prevalence of anemia in 2019 globally is 29.9%, Southeast Asia is 41.9% and in Indonesia (ages 15-49 years) is 30.6%. There is an increase in the prevalence of anemia in adolescents; from 22.7% (Riskesdas 2013) increased to 32% in the 2018 Riskesdas survey. The purpose of this study was to determine various risk factors for anemia in young women in several countries. Research method with literature review, secondary data sources (google scholar, pubmed, Sciencedirect. Results: from the review of articles in this study, the prevalence of anemia ranged from 20% to 47.7%. Research in Utar Paradesh India was 20%, in Ethiopia was 29.4% and the highest in Pakistan (2019) of 47.9% consisting of mild anemia 47.7%, moderate anemia 51.7% and severe anemia 5.7%. In Jordan the prevalence of anemia is 4.9% in men, 19 .3% in non-pregnant women, and 27.4% in pregnant women. Conclusion: in this literature study it was found that the factors affecting anemia in female adolescents were higher in the late adolescent phase, those who lived in rural areas, parents' education, socioeconomic level low number of family members, menstrual disorders and low intake of nutrients (micronutrients).For this reason, increasing education-based health education in schools is effective in increasing knowledge, attitudes and behavior in preventing anemia yes ng can make a real contribution in overcoming priority public health problems.Anemia merupakan indikator kesehatan gizi buruk yang dapat mempengaruhi pembangunan ekonomi suatu negara, sehingga anemia dikatakan masalah kesehatan global dunia. Prevalensi anemia tahun 2019 secara global 29.9%, Asia tenggara 41,9% dan di Indonesia (Usia 15-49 tahun) sebesar 30.6%. Adanya peningkatan prevalensi anemia remaja; dari 22.7% (Riskesdas 2013) meningkat menjadi 32% pada survei Riskesdas 2018. Tujuan penelitian ini untuk mengetahui berbagai faktor risiko anemia pada remaja putri di beberapa negara. Metode penelitian dengan literatur riview, sumber data sekunder (google scholar,pubmed, Sciencedirect. Hasil: dari review artikel dalam penelitian ini didapatkan prevalensi anemia berkisar 20 % hingga 47.7%  Penelitian di Utar Paradesh India sebesar 20%, di Ethiopia sebesar 29.4% dan yang paling tinggi di Pakistan (2019) sebesar 47.9% yang terdiri dari anemia ringan 47.7%, anemia sedang 51.7% dan anemia berat 5.7%. Di Jordan prevalensi anemia 4,9% pada laki-laki, 19,3% pada wanita tidak hamil, dan 27,4% pada wanita hamil. Kesimpulan: pada penelitian literatur ini didapatkan bahwa faktor yang mempengaruhi anemia remaja putri lebih tinggi pada fase remaja akhir, mereka yang tinggal dipedesaan, pendidikan orang tua, tingkat sosial ekonomi rendah, jumlah anggota keluarga, gangguan menstruasi serta asupan rendah akan zat gizi (mikronutrien).Untuk itu peningkatan edukasi kesehatan berbasis pendidikan di sekolah efektif dalam meningkatkan pengetahuan, sikap dan perilaku dalam mencegah anemia yang dapat berkontribusi nyata dalam mengatasi prioritas masalah kesehatan masyarakat

Women\u27s Rights: Reframing the Issues for the Future

Good morning and welcome, everyone, to our panel on Women\u27s Rights: Refraining the Issues for the Future. I am Kathy Rodgers. I\u27m from the class of 1973 of Columbia Law School, and I\u27m looking around this room – this is not what room A and B looked like back then! Everybody has a microphone, which is great, because we hope to have some good interactive discussion with all of you this morning. I am also, in addition to being a Columbia Law alum, the president of NOW Legal Defense and Education Fund here in New York. For over thirty-two years, NOW Legal Defense has used the power of the law to define and defend women\u27s rights. I am particularly pleased to be here today with Columbia Law School alumnae because Columbia women have been a substantial part of our team throughout these thirty-two years as members of our staff, as academic partners, a s student interns (including some young men), as part of our volunteer leadership, as pro bono attorneys, and as supporters. So with all of these connections, it really is a matter of personal pride to be back here celebrating the women of Columbia Law School

Retrospective study of pneumonia in non-racing horses in California

Pneumonia is a significant disease of horses. Although pneumonia has traditionally been studied in racehorses, little information is available for non-racing horses. Non-racing horses that died with pulmonary lesions (n = 156) were available from cases submitted for autopsy from January 2015 to June 2020. Bronchopneumonia (35%), interstitial pneumonia (29%), embolic pneumonia (21%), granulomatous pneumonia (13%), and pleuritis (2%) were observed in the examined horses. Seventy-four horses died or were euthanized because of pulmonary diseases, and 82 horses died or were euthanized because of non-pulmonary causes but had lung lesions. Of the horses that died from pulmonary causes, the most common finding was bronchopneumonia, with abscesses and/or necrosis in the cranioventral aspect of the lung. Bacteria isolated from cases of bronchopneumonia were Streptococcus equi subsp. zooepidemicus (48.5%), Klebsiella pneumoniae (12.1%), and Actinobacillus equuli subsp. haemolyticus (9.1%). The most common extrapulmonary lesions responsible for death in horses that also had lesions in the lung were mainly in the gastrointestinal system (30%), multiple systems (septicemia and/or toxemia; 27%), and musculoskeletal system (12%). The main postmortem findings in cases of bronchopneumonia of non-racing horses were similar to those reported previously in racehorses. However, some non-racing horses also had interstitial and granulomatous pneumonia, patterns not described previously in racehorses in California, likely as a result of the inclusion of extended age categories for non-racing horses. We also found that the equine lung was frequently affected in cases of sepsis and gastrointestinal problems of infectious origin

Interaction of amisulpride with GLUT1 at the blood-brain barrier. Relevance to Alzheimer's disease

Blood-brain barrier (BBB) dysfunction may be involved in the increased sensitivity of Alzheimer's disease (AD) patients to antipsychotics, including amisulpride. Studies indicate that antipsychotics interact with facilitated glucose transporters (GLUT), including GLUT1, and that GLUT1 BBB expression decreases in AD. We tested the hypotheses that amisulpride (charge: +1) interacts with GLUT1, and that BBB transport of amisulpride is compromised in AD. GLUT1 substrates, GLUT1 inhibitors and GLUT-interacting antipsychotics were identified by literature review and their physicochemical characteristics summarised. Interactions between amisulpride and GLUT1 were studied using in silico approaches and the human cerebral endothelial cell line, hCMEC/D3. Brain distribution of [3H]amisulpride was determined using in situ perfusion in wild type (WT) and 5xFamilial AD (5xFAD) mice. With transmission electron microscopy (TEM) we investigated brain capillary degeneration in WT mice, 5xFAD mice and human samples. Western blots determined BBB transporter expression in mouse and human. Literature review revealed that, although D-glucose has no charge, charged molecules can interact with GLUT1. GLUT1 substrates are smaller (184.95±6.45g/mol) than inhibitors (325.50±14.40g/mol) and GLUT-interacting antipsychotics (369.38±16.04). Molecular docking showed beta-D-glucose (free energy binding: -15.39kcal/mol) and amisulpride (-29.04kcal/mol) interact with GLUT1. Amisulpride did not affect [14C]D-glucose hCMEC/D3 accumulation. [3H]amisulpride uptake into the brain (except supernatant) of 5xFAD mice compared to WT remained unchanged. TEM revealed brain capillary degeneration in human AD. There was no difference in GLUT1 or P-glycoprotein BBB expression between WT and 5xFAD mice. In contrast, caudate P-glycoprotein, but not GLUT1, expression was decreased in human AD capillaries versus controls. This study provides new details about the BBB transport of amisulpride, evidence that amisulpride interacts with GLUT1 and that BBB transporter expression is altered in AD. This suggests that antipsychotics could potentially exacerbate the cerebral hypometabolism in AD. Further research into the mechanism of amisulpride transport by GLUT1 is important for improving antipsychotics safety