The paperless partograph: can it be effective to replace the WHO modified partograph

Background: The partograph is a graphical representation of the various events of labour plotted against time. The main aim was to determine whether the paperless partograph can replace the WHO partograph to monitor labour and aid in decision making.Methods: It is a hospital based prospective analytical study. The course of labour in 400 women with term singleton uncomplicated pregnancies were studied by using either partographs. 12 resident doctors were included to assess the user friendliness and asked to fill 240 separate partographs (120 each of WHO Modified and Paperless partograph).Results: The maternal and perinatal outcome was comparable between both the partographs. The Paperless partograph was however more user-friendly than the WHO partograph (p<0.0001).Conclusions: The Paperless partograph was found to be as effective as the WHO partograph in the effective management of labour. It is more user-friendly and has promising prospects to replace the WHO partograph

Estrogen-Mediated Upregulation of Noxa Is Associated with Cell Cycle Progression in Estrogen Receptor-Positive Breast Cancer Cells

Noxa is a Bcl-2-homology domain (BH3)-only protein reported to be a proapoptotic member of the Bcl-2 family. Estrogen has been well documented to stimulate cell growth and inhibit apoptosis in estrogen receptor (ER)-positive breast cancer cells. Intriguingly, recent reports have shown that 17β-estradiol (E2) induces Noxa expression, although the mechanisms underlying E2-mediated induction of Noxa and its functional significance are unknown. Using MCF7 human breast cancer cells as an experimental model, we show that Noxa is upregulated by E2 via p53-independent processes that involve c-Myc and ERα. Experiments using small interfering ribonucleic acids (siRNA) to specifically knock down p53, c-Myc, and ERα demonstrated that c-Myc and ERα, but not p53, are involved in the transcriptional upregulation of Noxa following E2 treatment. Furthermore, while E2 promoted the recruitment of c-Myc and ERα to the NOXA promoter in chromatin immunoprecipitation (ChIP) assays, E2 did not induce p53 recruitment. Interestingly, E2-mediated upregulation of Noxa was not associated with apoptosis. However, siRNA-mediated knockdown of Noxa resulted in cell cycle arrest in G0/G1-phase and significantly delayed the G1-to-S-phase transition following E2 treatment, indicating that Noxa expression is required for cell cycle progression in ER-positive breast cancer cells

VarSaw: Application-tailored Measurement Error Mitigation for Variational Quantum Algorithms

For potential quantum advantage, Variational Quantum Algorithms (VQAs) need high accuracy beyond the capability of today's NISQ devices, and thus will benefit from error mitigation. In this work we are interested in mitigating measurement errors which occur during qubit measurements after circuit execution and tend to be the most error-prone operations, especially detrimental to VQAs. Prior work, JigSaw, has shown that measuring only small subsets of circuit qubits at a time and collecting results across all such subset circuits can reduce measurement errors. Then, running the entire (global) original circuit and extracting the qubit-qubit measurement correlations can be used in conjunction with the subsets to construct a high-fidelity output distribution of the original circuit. Unfortunately, the execution cost of JigSaw scales polynomially in the number of qubits in the circuit, and when compounded by the number of circuits and iterations in VQAs, the resulting execution cost quickly turns insurmountable. To combat this, we propose VarSaw, which improves JigSaw in an application-tailored manner, by identifying considerable redundancy in the JigSaw approach for VQAs: spatial redundancy across subsets from different VQA circuits and temporal redundancy across globals from different VQA iterations. VarSaw then eliminates these forms of redundancy by commuting the subset circuits and selectively executing the global circuits, reducing computational cost (in terms of the number of circuits executed) over naive JigSaw for VQA by 25x on average and up to 1000x, for the same VQA accuracy. Further, it can recover, on average, 45% of the infidelity from measurement errors in the noisy VQA baseline. Finally, it improves fidelity by 55%, on average, over JigSaw for a fixed computational budget. VarSaw can be accessed here: https://github.com/siddharthdangwal/VarSaw.Comment: Appears at the International Conference on Architectural Support for Programming Languages and Operating Systems (ASPLOS) 2024. First two authors contributed equall

HDAC 1 and 6 modulate cell invasion and migration in clear cell renal cell carcinoma

Indexación: Web of ScienceBackground: Class I histone deacetylases (HDACs) have been reported to be overexpressed in clear cell renal cell carcinoma (ccRCC), whereas the expression of class II HDACs is unknown. Methods: Four isogenic cell lines C2/C2VHL and 786-O/786-OVHL with differential VHL expression are used in our studies. Cobalt chloride is used to mimic hypoxia in vitro. HIF-2 alpha knockdowns in C2 and 786-O cells is used to evaluate the effect on HDAC 1 expression and activity. Invasion and migration assays are used to investigate the role of HDAC 1 and HDAC 6 expression in ccRCC cells. Comparisons are made between experimental groups using the paired T-test, the two-sample Student's T-test or one-way ANOVA, as appropriate. ccRCC and the TCGA dataset are used to observe the clinical correlation between HDAC 1 and HDAC 6 overexpression and overall and progression free survival. Results: Our analysis of tumor and matched non-tumor tissues from radical nephrectomies showed overexpression of class I and II HDACs (HDAC6 only in a subset of patients). In vitro, both HDAC1 and HDAC6 over-expression increased cell invasion and motility, respectively, in ccRCC cells. HDAC1 regulated invasiveness by increasing matrix metalloproteinase (MMP) expression. Furthermore, hypoxia stimulation in VHL-reconstituted cell lines increased HIF isoforms and HDAC1 expression. Presence of hypoxia response elements in the HDAC1 promoter along with chromatin immunoprecipitation data suggests that HIF-2 alpha is a transcriptional regulator of HDAC1 gene. Conversely, HDAC6 and estrogen receptor alpha (ER alpha) were co-localized in cytoplasm of ccRCC cells and HDAC6 enhanced cell motility by decreasing acetylated alpha-tubulin expression, and this biological effect was attenuated by either biochemical or pharmacological inhibition. Finally, analysis of human ccRCC specimens revealed positive correlation between HIF isoforms and HDAC. HDAC1 mRNA upregulation was associated with worse overall survival in the TCGA dataset. Conclusions: Taking together, these results suggest that HDAC1 and HDAC6 may play a role in ccRCC biology and could represent rational therapeutic targets.http://bmccancer.biomedcentral.com/articles/10.1186/s12885-016-2604-

The total neutron production from the alpha induced reaction on natural Zirconium

A significant amount of alpha particles, upto $\sim$ 35 MeV are produced in the reactor environment. Alpha induced reaction on natural Zirconium, a reactor component, upto 40 MeV has been measured using stacked foil activation technique. The total neutron production cross section from all possible channels for $\alpha$ energies upto 35 MeV is also estimated using TALYS 1.96. The isomeric cross section ratio for the production of the radionuclide $^{95}Nb$ has been measured and reported for the first time

Alcohol Regulates Genes that Are Associated with Response to Endocrine Therapy and Attenuates the Actions of Tamoxifen in Breast Cancer Cells

Hereditary, hormonal, and behavioral factors contribute to the development of breast cancer. Alcohol consumption is a modifiable behavior that is linked to increased breast cancer risks and is associated with the development of hormone-dependent breast cancers as well as disease progression and recurrence following endocrine treatment. In this study we examined the molecular mechanisms of action of alcohol by applying molecular, genetic, and genomic approaches in characterizing its effects on estrogen receptor (ER)-positive breast cancer cells. Treatments with alcohol promoted cell proliferation, increased growth factor signaling, and up-regulated the transcription of the ER target gene GREB1 but not the canonical target TFF1/pS2. Microarray analysis following alcohol treatment identified a large number of alcohol-responsive genes, including those which function in apoptotic and cell proliferation pathways. Furthermore, expression profiles of the responsive gene sets in tumors were strongly associated with clinical outcomes in patients who received endocrine therapy. Correspondingly, alcohol treatment attenuated the anti-proliferative effects of the endocrine therapeutic drug tamoxifen in ER-positive breast cancer cells. To determine the contribution and functions of responsive genes, their differential expression in tumors were assessed between outcome groups. The proto-oncogene BRAF was identified as a novel alcohol- and estrogen-induced gene that showed higher expression in patients with poor outcomes. Knock-down of BRAF, moreover, prevented the proliferation of breast cancer cells. These findings not only highlight the mechanistic basis of the effects of alcohol on breast cancer cells and increased risks for disease incidents and recurrence, but may facilitate the discovery and characterization of novel oncogenic pathways and markers in breast cancer research and therapeutics

Probing pre-supernova mass loss in double-peaked Type Ibc supernovae from the Zwicky Transient Facility

Eruptive mass loss of massive stars prior to supernova (SN) explosion is key to understanding their evolution and end fate. An observational signature of pre-SN mass loss is the detection of an early, short-lived peak prior to the radioactive-powered peak in the lightcurve of the SN. This is usually attributed to the SN shock passing through an extended envelope or circumstellar medium (CSM). Such an early peak is common for double-peaked Type IIb SNe with an extended Hydrogen envelope but is uncommon for normal Type Ibc SNe with very compact progenitors. In this paper, we systematically study a sample of 14 double-peaked Type Ibc SNe out of 475 Type Ibc SNe detected by the Zwicky Transient Facility. The rate of these events is ~ 3-9 % of Type Ibc SNe. A strong correlation is seen between the peak brightness of the first and the second peak. We perform a holistic analysis of this sample's photometric and spectroscopic properties. We find that six SNe have ejecta mass less than 1.5 Msun. Based on the nebular spectra and lightcurve properties, we estimate that the progenitor masses for these are less than ~ 12 Msun. The rest have an ejecta mass > 2.4 Msun and a higher progenitor mass. This sample suggests that the SNe with low progenitor masses undergo late-time binary mass transfer. Meanwhile, the SNe with higher progenitor masses are consistent with wave-driven mass loss or pulsation-pair instability-driven mass loss simulations.Comment: Submitted to ApJ. Comments are welcome. arXiv admin note: text overlap with arXiv:2210.0572

MicroRNA let-7c Is Downregulated in Prostate Cancer and Suppresses Prostate Cancer Growth

Prostate cancer (PCa) is characterized by deregulated expression of several tumor suppressor or oncogenic miRNAs. The objective of this study was the identification and characterization of miR-let-7c as a potential tumor suppressor in PCa.Levels of expression of miR-let-7c were examined in human PCa cell lines and tissues using qRT-PCR and in situ hybridization. Let-7c was overexpressed or suppressed to assess the effects on the growth of human PCa cell lines. Lentiviral-mediated re-expression of let-7c was utilized to assess the effects on human PCa xenografts.We identified miR-let-7c as a potential tumor suppressor in PCa. Expression of let-7c is downregulated in castration-resistant prostate cancer (CRPC) cells. Overexpression of let-7c decreased while downregulation of let-7c increased cell proliferation, clonogenicity and anchorage-independent growth of PCa cells in vitro. Suppression of let-7c expression enhanced the ability of androgen-sensitive PCa cells to grow in androgen-deprived conditions in vitro. Reconstitution of Let-7c by lentiviral-mediated intratumoral delivery significantly reduced tumor burden in xenografts of human PCa cells. Furthermore, let-7c expression is downregulated in clinical PCa specimens compared to their matched benign tissues, while the expression of Lin28, a master regulator of let-7 miRNA processing, is upregulated in clinical PCa specimens.These results demonstrate that microRNA let-7c is downregulated in PCa and functions as a tumor suppressor, and is a potential therapeutic target for PCa

Robust estimation of bacterial cell count from optical density

Optical density (OD) is widely used to estimate the density of cells in liquid culture, but cannot be compared between instruments without a standardized calibration protocol and is challenging to relate to actual cell count. We address this with an interlaboratory study comparing three simple, low-cost, and highly accessible OD calibration protocols across 244 laboratories, applied to eight strains of constitutive GFP-expressing E. coli. Based on our results, we recommend calibrating OD to estimated cell count using serial dilution of silica microspheres, which produces highly precise calibration (95.5% of residuals <1.2-fold), is easily assessed for quality control, also assesses instrument effective linear range, and can be combined with fluorescence calibration to obtain units of Molecules of Equivalent Fluorescein (MEFL) per cell, allowing direct comparison and data fusion with flow cytometry measurements: in our study, fluorescence per cell measurements showed only a 1.07-fold mean difference between plate reader and flow cytometry data