162 research outputs found

    ZIGBEE Protocol Based Low Power Health Care Monitoring System

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    ZigBee based health care system was a health care monitoring system which mainly measures the physical conditions of the patient. It was based on an LR-WPAN ad-hoc network known as ZigBee”. It was mainly utilized for the implementation of health care system with less cost and low Power usage. The key feature of this paper is that it less energy consumption, optimum bandwidth maintenance and appreciable compatible to the preexisting and newer technologies. This work is implementated in both hardware and software and it was compiled and simulated using MPLAB and Proteus simulation software

    Extensive local adaptation within the chemosensory system following Drosophila melanogaster's global expansion.

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    How organisms adapt to new environments is of fundamental biological interest, but poorly understood at the genetic level. Chemosensory systems provide attractive models to address this problem, because they lie between external environmental signals and internal physiological responses. To investigate how selection has shaped the well-characterized chemosensory system of Drosophila melanogaster, we have analysed genome-wide data from five diverse populations. By couching population genomic analyses of chemosensory protein families within parallel analyses of other large families, we demonstrate that chemosensory proteins are not outliers for adaptive divergence between species. However, chemosensory families often display the strongest genome-wide signals of recent selection within D. melanogaster. We show that recent adaptation has operated almost exclusively on standing variation, and that patterns of adaptive mutations predict diverse effects on protein function. Finally, we provide evidence that chemosensory proteins have experienced relaxed constraint, and argue that this has been important for their rapid adaptation over short timescales

    A retrospective observational study on effect of sperm morphology on embryo development after intracytoplasmic sperm injection

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    Background: The process of embryo development requires the contribution of both male and female gametes. However, abnormal sperm development can hinder the fertilization process, leading to infertility. To overcome these male fertility issues, intracytoplasmic sperm injection (ICSI) was developed. This technique has proven to be effective, resulting in about 80% of live births in ICSI cycles. Methods: It is a retrospective cohort study was conducted in department of reproductive medicine, Komali fertility centre a unit of Dr. Ramesh Cardiac and multispeciality hospital P Ltd, Guntur, Andhra Pradesh, India. The study was conducted during period of January 2022 to December 2022. Total 120 subjects were included based on our inclusion and exclusion criteria. Results: This study used the chi-square test and Pearson's correlation to evaluate the relationship between sperm morphology and various parameters, revealing that poor sperm morphology may contribute to low fertilization, cleavage, and pregnancy outcomes. Individuals with 3% sperm morphology exhibited higher mean fertility rates and lower negative pregnancy rates compared to those with 2% and 1% morphology, highlighting the importance of good sperm morphology for successful fertilization and pregnancy outcomes. Conclusions: In summary, the study highlights a strong correlation between sperm morphology, fertilization and cleavage rates, while a weak and no correlation was observed between sperm morphology and pregnancy outcome after ICSI. The findings suggest that an improvement in sperm morphology leads to increased fertilization and cleavage rates

    Transcription Inhibition by DRB Potentiates Recombinational Repair of UV Lesions in Mammalian Cells

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    Homologous recombination (HR) is intricately associated with replication, transcription and DNA repair in all organisms studied. However, the interplay between all these processes occurring simultaneously on the same DNA molecule is still poorly understood. Here, we study the interplay between transcription and HR during ultraviolet light (UV)-induced DNA damage in mammalian cells. Our results show that inhibition of transcription with 5,6-dichloro-1-beta-D-ribofuranosylbenzimidazole (DRB) increases the number of UV-induced DNA lesions (ÎłH2AX, 53BP1 foci formation), which correlates with a decrease in the survival of wild type or nucleotide excision repair defective cells. Furthermore, we observe an increase in RAD51 foci formation, suggesting HR is triggered in response to an increase in UV-induced DSBs, while inhibiting transcription. Unexpectedly, we observe that DRB fails to sensitise HR defective cells to UV treatment. Thus, increased RAD51 foci formation correlates with increased cell death, suggesting the existence of a futile HR repair of UV-induced DSBs which is linked to transcription inhibition

    Human Monocytes Undergo Excessive Apoptosis following Temozolomide Activating the ATM/ATR Pathway While Dendritic Cells and Macrophages Are Resistant

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    Immunodeficiency is a severe therapy-limiting side effect of anticancer chemotherapy resulting from sensitivity of immunocompetent cells to DNA damaging agents. A central role in the immune system is played by monocytes that differentiate into macrophages and dendritic cells (DCs). In this study we compared human monocytes isolated from peripheral blood and cytokine matured macrophages and DCs derived from them and assessed the mechanism of toxicity of the DNA methylating anticancer drug temozolomide (TMZ) in these cell populations. We observed that monocytes, but not DCs and macrophages, were highly sensitive to the killing effect of TMZ. Studies on DNA damage and repair revealed that the initial DNA incision was efficient in monocytes while the re-ligation step of base excision repair (BER) can not be accomplished, resulting in an accumulation of DNA single-strand breaks (SSBs). Furthermore, monocytes accumulated DNA double-strand breaks (DSBs) following TMZ treatment, while DCs and macrophages were able to repair DSBs. Monocytes lack the DNA repair proteins XRCC1, ligase IIIα and PARP-1 whose expression is restored during differentiation into macrophages and DCs following treatment with GM-CSF and GM-CSF plus IL-4, respectively. These proteins play a key role both in BER and DSB repair by B-NHEJ, which explains the accumulation of DNA breaks in monocytes following TMZ treatment. Although TMZ provoked an upregulation of XRCC1 and ligase IIIα, BER was not enhanced likely because PARP-1 was not upregulated. Accordingly, inhibition of PARP-1 did not sensitize monocytes, but monocyte-derived DCs in which strong PARP activation was observed. TMZ induced in monocytes the DNA damage response pathways ATM-Chk2 and ATR-Chk1 resulting in p53 activation. Finally, upon activation of the Fas-receptor and the mitochondrial pathway apoptosis was executed in a caspase-dependent manner. The downregulation of DNA repair in monocytes, resulting in their selective killing by TMZ, might impact on the immune response during cancer chemotherapy

    Genome Instability and Transcription Elongation Impairment in Human Cells Depleted of THO/TREX

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    THO/TREX connects transcription with genome integrity in yeast, but a role of mammalian THO in these processes is uncertain, which suggests a differential implication of mRNP biogenesis factors in genome integrity in yeast and humans. We show that human THO depletion impairs transcription elongation and mRNA export and increases instability associated with DNA breaks, leading to hyper-recombination and γH2AX and 53BP1 foci accumulation. This is accompanied by replication alteration as determined by DNA combing. Genome instability is R-loop–dependent, as deduced from the ability of the AID enzyme to increase DNA damage and of RNaseH to reduce it, or from the enhancement of R-loop–dependent class-switching caused by THOC1-depletion in CH12 murine cells. Therefore, mammalian THO prevents R-loop formation and has a role in genome dynamics and function consistent with an evolutionary conservation of the functional connection between these mRNP biogenesis factors and genome integrity that had not been anticipated

    Triple negative breast cancer: proposals for a pragmatic definition and implications for patient management and trial design.

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    In trials in triple negative breast cancer (TNBC), oestrogen and progesterone receptor negativity should be defined as < 1% positive cells. Negativity is a ratio of <2 between Her2 gene copy number and centromere of chromosome 17 or a copy number of 4 or less. In routine practice, immunohistochemistry is acceptable given stringent quality assurance. Triple negativity emerging after neoadjuvant treatment differs from primary TN and such patients should not enter TNBC trials. Patients relapsing with TN metastases should be eligible even if their primary was positive. Rare TN subtypes such as apocrine, adenoid-cystic and low-grade metaplastic tumours should be excluded. TN and basal-like (BL) signatures overlap but are not equivalent. Since the significance of basal cytokeratin or EGFR overexpression is not known and we lack validated assays, these features should not be used to subclassify TN tumours. Tissue collection in trials is mandatory so the effect on outcome of different tumour phenotypes and BRCA mutation can be explored. No prospective studies have established that TN tumours have particular sensitivity or resistance to any specific chemotherapy agent or radiation. TNBC patients should be treated according to tumour and clinical characteristics
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