cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.1241552.v2
title: Histone H3 K27 acetylation marks a potent enhancer element on the adipogenic master regulator gene Pparg2

description: PPARγ2 is expressed almost exclusively in adipose tissue and plays a central role in adipogenesis. Despite intensive studies over the last 2 decades, the mechanism regulating the expression of the Pparg2 gene, especially the role of cis-regulatory elements, is still not completely understood. Here, we report a comprehensive investigation of the enhancer elements within the murine Pparg2 gene. Utilizing the combined techniques of sequence conservation analysis and chromatin marker examination, we identified a potent enhancer element that augmented the expression of a reporter gene under the control of the Pparg2 promoter by 20-fold. This enhancer element was first identified as highly conserved non-coding sequence 10 (CNS10) and was later shown to be enriched with the enhancer marker H3 K27 acetylation. Further studies identified a binding site for p300 as the essential enhancer element in CNS10. Moreover, p300 physically binds to CNS10 and is required for the enhancer activity of CNS10. The depletion of p300 by siRNA resulted in significantly impaired activation of Pparg2 at the early stages of 3T3-L1 adipogenesis. In summary, our study identified a novel enhancer element on the murine Pparg2 gene and suggested a novel mechanism for the regulation of Pparg2 expression by p300 in 3T3-L1 adipogenesis.
DOI: 10.6084/m9.figshare.1241552.v1
title: Histone H3 K27 acetylation marks a potent enhancer element on the adipogenic master regulator gene Pparg2

description: PPARγ2 is expressed almost exclusively in adipose tissue and plays a central role in adipogenesis. Despite intensive studies over the last 2 decades, the mechanism regulating the expression of the Pparg2 gene, especially the role of cis-regulatory elements, is still not completely understood. Here, we report a comprehensive investigation of the enhancer elements within the murine Pparg2 gene. Utilizing the combined techniques of sequence conservation analysis and chromatin marker examination, we identified a potent enhancer element that augmented the expression of a reporter gene under the control of the Pparg2 promoter by 20-fold. This enhancer element was first identified as highly conserved non-coding sequence 10 (CNS10) and was later shown to be enriched with the enhancer marker H3 K27 acetylation. Further studies identified a binding site for p300 as the essential enhancer element in CNS10. Moreover, p300 physically binds to CNS10 and is required for the enhancer activity of CNS10. The depletion of p300 by siRNA resulted in significantly impaired activation of Pparg2 at the early stages of 3T3-L1 adipogenesis. In summary, our study identified a novel enhancer element on the murine Pparg2 gene and suggested a novel mechanism for the regulation of Pparg2 expression by p300 in 3T3-L1 adipogenesis.
DOI: 10.6084/m9.figshare.1241553
title: A novel crosstalk between BRCA1 and poly (ADP-ribose) polymerase 1 in breast cancer

description: BRCA mutations are the main known hereditary factor for breast cancer. Notably, poly (ADP-ribose) polymerase 1 (PARP1) expression status plays a critical role in breast cancer progression and the clinical development of PARP1 inhibitors to treat BRCA-mutated breast cancer has advanced rapidly. However, dynamic crosstalk between BRCA1 and PARP1 remains largely unknown. Here, we showed that: (i) BRCA1 inactivation events (mutation, promoter methylation, or knockdown) were accompanied by increased PARP1 and nicotinamide adenine dinucleotide (NAD) levels, and a subsequent increase in NAD-dependent PARP1 activity in MDA-MB-231 and primary breast cancer cells; (ii) the overexpression of BRCA1 resulted in decreased PARP1 and NAD levels, and a subsequent impairment in NAD-dependent PARP1 activity in MDA-MB-231 and primary breast cancer cells; and (iii) intracellular NAD levels were largely responsible for regulating PARP1 activity in breast cancer cells, and NAD levels were positively correlated with PARP1 activity in human breast cancer specimens (R = 0.647, <i>P</i> &lt; 0.001). Interestingly, the high efficiency of PARP1 triggered by BRCA1 inactivation may further inhibit BRCA1 transcription by NAD depletion. These results highlight a novel interaction between BRCA1 and PARP1, which may be beneficial for the dynamic balance between BRCA1 and PARP1-related biologic processes, especially for maintaining stable DNA repair ability. All of this may improve our understanding of the basic molecular mechanism underlying BRCA1- and PARP1-related breast cancer progression.
DOI: 10.6084/m9.figshare.1241553.v1
title: A novel crosstalk between BRCA1 and poly (ADP-ribose) polymerase 1 in breast cancer

description: BRCA mutations are the main known hereditary factor for breast cancer. Notably, poly (ADP-ribose) polymerase 1 (PARP1) expression status plays a critical role in breast cancer progression and the clinical development of PARP1 inhibitors to treat BRCA-mutated breast cancer has advanced rapidly. However, dynamic crosstalk between BRCA1 and PARP1 remains largely unknown. Here, we showed that: (i) BRCA1 inactivation events (mutation, promoter methylation, or knockdown) were accompanied by increased PARP1 and nicotinamide adenine dinucleotide (NAD) levels, and a subsequent increase in NAD-dependent PARP1 activity in MDA-MB-231 and primary breast cancer cells; (ii) the overexpression of BRCA1 resulted in decreased PARP1 and NAD levels, and a subsequent impairment in NAD-dependent PARP1 activity in MDA-MB-231 and primary breast cancer cells; and (iii) intracellular NAD levels were largely responsible for regulating PARP1 activity in breast cancer cells, and NAD levels were positively correlated with PARP1 activity in human breast cancer specimens (R = 0.647, <i>P</i> &lt; 0.001). Interestingly, the high efficiency of PARP1 triggered by BRCA1 inactivation may further inhibit BRCA1 transcription by NAD depletion. These results highlight a novel interaction between BRCA1 and PARP1, which may be beneficial for the dynamic balance between BRCA1 and PARP1-related biologic processes, especially for maintaining stable DNA repair ability. All of this may improve our understanding of the basic molecular mechanism underlying BRCA1- and PARP1-related breast cancer progression.
DOI: 10.6084/m9.figshare.1241553.v2
title: A novel crosstalk between BRCA1 and poly (ADP-ribose) polymerase 1 in breast cancer

description: BRCA mutations are the main known hereditary factor for breast cancer. Notably, poly (ADP-ribose) polymerase 1 (PARP1) expression status plays a critical role in breast cancer progression and the clinical development of PARP1 inhibitors to treat BRCA-mutated breast cancer has advanced rapidly. However, dynamic crosstalk between BRCA1 and PARP1 remains largely unknown. Here, we showed that: (i) BRCA1 inactivation events (mutation, promoter methylation, or knockdown) were accompanied by increased PARP1 and nicotinamide adenine dinucleotide (NAD) levels, and a subsequent increase in NAD-dependent PARP1 activity in MDA-MB-231 and primary breast cancer cells; (ii) the overexpression of BRCA1 resulted in decreased PARP1 and NAD levels, and a subsequent impairment in NAD-dependent PARP1 activity in MDA-MB-231 and primary breast cancer cells; and (iii) intracellular NAD levels were largely responsible for regulating PARP1 activity in breast cancer cells, and NAD levels were positively correlated with PARP1 activity in human breast cancer specimens (R = 0.647, <i>P</i> &lt; 0.001). Interestingly, the high efficiency of PARP1 triggered by BRCA1 inactivation may further inhibit BRCA1 transcription by NAD depletion. These results highlight a novel interaction between BRCA1 and PARP1, which may be beneficial for the dynamic balance between BRCA1 and PARP1-related biologic processes, especially for maintaining stable DNA repair ability. All of this may improve our understanding of the basic molecular mechanism underlying BRCA1- and PARP1-related breast cancer progression.
DOI: 10.6084/m9.figshare.1248945
title: Are Nonprofit Antipoverty Organizations Located Where They Are Needed? A Spatial Analysis of the Greater Hartford Region

description: The geographic distribution of nonprofit antipoverty organizations has important implications for economic development, social services, public health, and policy efforts. With counts of antipoverty nonprofits at the census tract level in Greater Hartford, Connecticut, we examine whether these organizations are located in areas with high levels of poverty with a spatial zero-inflated-Poisson model. Covariates that measure need, resources, urban structure, and demographic characteristics are incorporated into both the zero-inflation component and the Poisson component of the model. Variation not explained by the covariates is captured by the combination of a spatial random effect and an unstructured random effect. Statistical inferences are done within the Bayesian framework. Model comparison with the conditional predictive ordinate suggests that the random effects and the zero-inflation are both important components in fitting the data. All three need measures—proportion of people below the poverty line, unemployment rate, and rental occupancy—are found to have significantly positive effect on the mean of the count, providing evidence that antipoverty nonprofits tend to locate where they are needed. The dataset and R/OpenBUGS code are available in supplementary materials online.
DOI: 10.6084/m9.figshare.1248945.v1
title: Are Nonprofit Antipoverty Organizations Located Where They Are Needed? A Spatial Analysis of the Greater Hartford Region

description: The geographic distribution of nonprofit antipoverty organizations has important implications for economic development, social services, public health, and policy efforts. With counts of antipoverty nonprofits at the census tract level in Greater Hartford, Connecticut, we examine whether these organizations are located in areas with high levels of poverty with a spatial zero-inflated-Poisson model. Covariates that measure need, resources, urban structure, and demographic characteristics are incorporated into both the zero-inflation component and the Poisson component of the model. Variation not explained by the covariates is captured by the combination of a spatial random effect and an unstructured random effect. Statistical inferences are done within the Bayesian framework. Model comparison with the conditional predictive ordinate suggests that the random effects and the zero-inflation are both important components in fitting the data. All three need measures—proportion of people below the poverty line, unemployment rate, and rental occupancy—are found to have significantly positive effect on the mean of the count, providing evidence that antipoverty nonprofits tend to locate where they are needed. The dataset and R/OpenBUGS code are available in supplementary materials online.
DOI: 10.6084/m9.figshare.1250831
title: Synthesis, Crystal Structure, and DNA-Binding Studies of a Cadmium(II) Complex With Bis(<i>N</i>-benzylbenzimidazol-2-ylmethyl)aniline

description: A complex of cadmium (II) picrate (pic) with Bis(<i>N</i>-benzylbenzimidazol-2-ylmethyl)aniline (Bebba), with composition [Cd(Bebba)<sub>2</sub>](pic)<sub>2</sub>, was synthesized and characterized by elemental analysis, electrical conductivity and IR and UV/Vis spectral measurements. The crystal structure of the cadmium(II) complex has been determined by single-crystal X-ray diffraction. The cadmium(II) cation is bonded to two Bebba ligands through four benzimidazole nitrogen, resulting in a distorted octahedron geometry. The DNA-binding properties of the cadmium(II) complex were investigated by electronic absorption, fluorescence spectra and viscosity measurements. The experimental results suggest that the cadmium(II) complex binds to DNA in an intercalation mode.
DOI: 10.6084/m9.figshare.1250831.v1
title: Synthesis, Crystal Structure and DNA-Binding Studies of a Cadmium(II) Complex with the Bis(<i>N</i>-benzylbenzimidazol-2-ylmethyl)aniline

description: A complex of cadmium (II) picrate (pic) with Bis<b>(</b><i>N</i><b>-</b>benzylbenzimidazol-2-ylmethyl)aniline (Bebba), with composition [Cd(Bebba)<sub>2</sub>](pic)<sub>2</sub>, was synthesized and characterized by elemental analysis, electrical conductivity and IR and UV/Vis spectral measurements. The crystal structure of the cadmium(II) complex has been determined by single-crystal X-ray diffraction. The cadmium(II) cation is bonded to two Bebba ligands through four benzimidazole nitrogen, resulting in a distorted octahedron geometry. The DNA-binding properties of the cadmium(II) complex were investigated by electronic absorption, fluorescence spectra and viscosity measurements. The experimental results suggest that the cadmium(II) complex binds to DNA in an intercalation mode.
DOI: 10.6084/m9.figshare.1250831.v2
title: Synthesis, Crystal Structure, and DNA-Binding Studies of a Cadmium(II) Complex With Bis(<i>N</i>-benzylbenzimidazol-2-ylmethyl)aniline

description: A complex of cadmium (II) picrate (pic) with Bis(<i>N</i>-benzylbenzimidazol-2-ylmethyl)aniline (Bebba), with composition [Cd(Bebba)<sub>2</sub>](pic)<sub>2</sub>, was synthesized and characterized by elemental analysis, electrical conductivity and IR and UV/Vis spectral measurements. The crystal structure of the cadmium(II) complex has been determined by single-crystal X-ray diffraction. The cadmium(II) cation is bonded to two Bebba ligands through four benzimidazole nitrogen, resulting in a distorted octahedron geometry. The DNA-binding properties of the cadmium(II) complex were investigated by electronic absorption, fluorescence spectra and viscosity measurements. The experimental results suggest that the cadmium(II) complex binds to DNA in an intercalation mode.
DOI: 10.6084/m9.figshare.1250831.v3
title: Synthesis, Crystal Structure, and DNA-Binding Studies of a Cadmium(II) Complex With Bis(<i>N</i>-benzylbenzimidazol-2-ylmethyl)aniline

description: A complex of cadmium (II) picrate (pic) with Bis(<i>N</i>-benzylbenzimidazol-2-ylmethyl)aniline (Bebba), with composition [Cd(Bebba)<sub>2</sub>](pic)<sub>2</sub>, was synthesized and characterized by elemental analysis, electrical conductivity and IR and UV/Vis spectral measurements. The crystal structure of the cadmium(II) complex has been determined by single-crystal X-ray diffraction. The cadmium(II) cation is bonded to two Bebba ligands through four benzimidazole nitrogen, resulting in a distorted octahedron geometry. The DNA-binding properties of the cadmium(II) complex were investigated by electronic absorption, fluorescence spectra and viscosity measurements. The experimental results suggest that the cadmium(II) complex binds to DNA in an intercalation mode.
DOI: 10.6084/m9.figshare.1254915
title: Effect of Dicarboxylate Ligands on the Construction of Cd(II) Complexes Based on a Flexible Bis-Triazole Ligand

description: In this work, two dicarboxylate ligands, 4,4′-oxybis(benzoic acid) (H<sub>2</sub>oba) and 4,4′-biphenyldicarboxylic acid (H<sub>2</sub>bpdc) were employed as coligands to perform a comparison on the structures of Cd(II)-btmx complexes (btmx = 1,4-bis(1,2,4-triazol-1-ylmethyl)-2,3,5,6-tetramethylbenzene) motifs. Two new complexes, {[Cd(btmx)(oba)]·H<sub>2</sub>O}<sub>n</sub> (1) and [Cd(btmx)(bpdc)]<sub>n</sub> (2), have been synthesized and characterized. Structural analyses show that 1 shows a 1D double-chain, while 2 displays an undulating 2D 4<sup>4</sup>-<i>sql</i> network with 2-fold interpenetration. The structural differences of the two complexes suggest that the dicarboxylate ligands have great impact on the formation of such coordination architectures. Furthermore, the photoluminescence properties of 1 and 2 have also been investigated.
DOI: 10.6084/m9.figshare.1254915.v2
title: Effect of Dicarboxylate Ligands on the Construction of Cd(II) Complexes Based on a Flexible Bis-Triazole Ligand

description: In this work, two dicarboxylate ligands, 4,4′-oxybis(benzoic acid) (H<sub>2</sub>oba) and 4,4′-biphenyldicarboxylic acid (H<sub>2</sub>bpdc) were employed as coligands to perform a comparison on the structures of Cd(II)-btmx complexes (btmx = 1,4-bis(1,2,4-triazol-1-ylmethyl)-2,3,5,6-tetramethylbenzene) motifs. Two new complexes, {[Cd(btmx)(oba)]·H<sub>2</sub>O}<sub>n</sub> (1) and [Cd(btmx)(bpdc)]<sub>n</sub> (2), have been synthesized and characterized. Structural analyses show that 1 shows a 1D double-chain, while 2 displays an undulating 2D 4<sup>4</sup>-<i>sql</i> network with 2-fold interpenetration. The structural differences of the two complexes suggest that the dicarboxylate ligands have great impact on the formation of such coordination architectures. Furthermore, the photoluminescence properties of 1 and 2 have also been investigated.
DOI: 10.6084/m9.figshare.1254915.v1
title: Effect of Dicarboxylate Ligands on the Construction of Cd(II) Complexes Based on a Flexible Bis-Triazole Ligand

description: In this work, two dicarboxylate ligands, 4,4′-oxybis(benzoic acid) (H<sub>2</sub>oba) and 4,4′-biphenyldicarboxylic acid (H<sub>2</sub>bpdc) were employed as coligands to perform a comparison on the structures of Cd(II)-btmx complexes (btmx = 1,4-bis(1,2,4-triazol-1-ylmethyl)-2,3,5,6-tetramethylbenzene) motifs. Two new complexes, {[Cd(btmx)(oba)]·H<sub>2</sub>O}<sub>n</sub> (1) and [Cd(btmx)(bpdc)]<sub>n</sub> (2), have been synthesized and characterized. Structural analyses show that 1 shows a 1D double-chain, while 2 displays an undulating 2D 4<sup>4</sup>-<i>sql</i> network with 2-fold interpenetration. The structural differences of the two complexes suggest that the dicarboxylate ligands have great impact on the formation of such coordination architectures. Furthermore, the photoluminescence properties of 1 and 2 have also been investigated.
DOI: 10.6084/m9.figshare.1254974
title: Effects of Data Sparsity and Spatiotemporal Variability on Hazard Maps of Workplace Noise

description: Personal sampling, considered a state-of-the-art technique to assess worker exposures to occupational hazards, is often conducted for the duration of a work shift so that time-weighted average (TWA) exposures may be evaluated relative to published occupational exposure limits (OELs). Such cross-shift measurements, however, provide little information on the spatial variability of exposures, except after a very large number of samples. Hazard maps, contour plots (or similar depiction) of hazard intensity throughout the workplace, have gained popularity as a way to locate sources and to visualize spatial variability of physical and chemical hazards within a facility. However, these maps are often generated from short duration measures and have little ability to assess temporal variability. To assess the potential bias that results from the use of short-duration measurements to represent the TWA in a hazard map, noise intensity measurements were collected at high spatial and temporal resolution in two facilities. Static monitors were distributed throughout the facility and used to capture the temporal variability at these locations. Roving monitors (typical of the hazard mapping process) captured spatial variability over multiple traverses through the facility. The differences in hazards maps generated with different sampling techniques were evaluated. Hazard maps produced from sparse, roving monitor data were in good agreement with the TWA hazard maps at the facility with low temporal variability. Estimated values were within 5 dB of the TWA over approximately 90% of the facility. However, at the facility with higher temporal variability, large differences between hazard maps were observed for different traverses through the facility. On the second day of sampling, estimates were at least 5 dB different than the TWA for more than half of the locations within the facility. The temporal variability of noise was found to have a greater influence on map accuracy than the spatial sampling resolution.
DOI: 10.6084/m9.figshare.1254974.v1
title: Effects of Data Sparsity and Spatiotemporal Variability on Hazard Maps of Workplace Noise

description: ABSTRACTPersonal sampling, considered a state-of-the-art technique to assess worker exposures to occupational hazards, is often conducted for the duration of a workshift so that time-weighted average (TWA) exposures may be evaluated relative to published occupational exposure limits. Such cross-shift measurements, however, provide little information on the spatial variability of exposures, except after a very large number of samples. Hazard maps, contour plots (or similar depiction) of hazard intensity throughout the workplace, have gained popularity as a way to locate sources and to visualize spatial variability of physical and chemical hazards within a facility. However, these maps are often generated from short duration measures and have little ability to assess temporal variability. To assess the potential bias that results from the use of short-duration measurements to represent the TWA in a hazard map, noise intensity measurements were collected at high spatial and temporal resolution in two facilities. Static monitors were distributed throughout the facility and used to capture the temporal variability at these locations. Roving monitors (typical of the hazard mapping process) captured spatial variability over multiple traverses through the facility. The differences in hazards maps generated with different sampling techniques were evaluated. Hazard maps produced from sparse, roving monitor data were in good agreement with the TWA hazard maps at the facility with low temporal variability. Estimated values were within 5 dB of the TWA over approximately 90% of the facility. However, at the facility with higher temporal variability, large differences between hazard maps were observed for different traverses through the facility. On the second day of sampling, estimates were at least 5 dB different than the TWA for more than half of the locations within the facility. The temporal variability of noise was found to have a greater influence on map accuracy than the spatial sampling resolution.