Cyclic Loading on Composite Repair of Corroded Steel Pipelines

The study aims to determine how cyclic loading affects the structural integrity and lifespan of composite repair systems used to restore corroded steel pipelines. As specified in Annexure C of the ISO 24817 repair code, pipe specimens are machined to produce flaws with 80% wall loss. Testing under static and cyclic pressure loading is done as per ASTM D2992 and ASTM D2143. Static pressure loading is accomplished by continually pressurizing the pipe specimen, and burst pressure is assessed. Various Rc-ratios or levels of cyclic loading severity are used in cyclic pressure loading tests. Each case's number of cycles before failure is determined experimentally, and the service de-rating factor is assessed in accordance with ISO 24817. The 235 bar pressure was sustained by the static-loaded repaired pipe specimens with 80% wall loss, and the failure was catastrophic. At around 7000 cycles, the cyclically loaded repaired samples with 80% wall loss failed, and the failure manifests as debonding or a leak

Performance assessment on manufacturing of unfired bricks using industrial wastes

This paper presents eco-friendly unburnt bricks made up of fly ash, waste plastic powder, waste glass powder, lime, gypsum and crusher sand as alternatives to conventional burnt clay bricks for sustainable development. The research focuses on the maximum utilization of industrial waste in eco-friendly unburnt brick production. Materials are characterized according to their chemical and geotechnical properties. In this research, we use a milled waste glass powder of size less than 600μm and plastic powder obtained from plastic waste of size less than 600μm are added along with crushed sand, gypsum, lime and fly ash with various mix proportions concerning FaL-G mix concept. All the proportions were taken on a weight basis. Compressive strength, water absorption, and efflorescence are the key parameters chosen for comparing the innovative brick with conventional fly ash brick. There are five different mixes (Type A, B, C, D & E) are made in this research. The plastic and glass powders are replaced by crusher sand at the increased rate of 2% in every mix whereas 2%,4%,6%,8%, and 10%. It was found that the type B bricks have 17.63% strength was increased when compared to base mix. From the test results, type B bricks have enhanced mechanical performance when compared to all other mixes

Phenotypic Heterogeneity Drives Differential Disease Outcome in Triple Negative Breast Cancer

The triple-negative breast cancer (TNBC) subtype is one of the most aggressive forms of breast cancer that has poor clinical outcome and still remains as an unmet clinical challenge. Accumulating evidence suggests that intratumoral heterogeneity or the presence of phenotypically heterogeneous cell populations within a tumor plays a crucial role in chemoresistance, tumor progression and metastasis. Increased understanding of the molecular regulators of intratumoral heterogeneity will enable the development of effective therapeutic strategies in TNBC. We have identified a molecular mediator involved in intratumoral heterogeneity in breast cancer using an unbiased approach. We isolated two heterogeneous tumor cell populations from the 4T1 TNBC tumor model and phenotypic characterization revealed that the cells are distinct in terms of their morphology, proliferation and self-renewal ability in vitro; as well as primary tumor formation and metastatic potential in vivo. Further, RNA sequencing on both cell populations was performed to identify the molecular mediators underlying this heterogeneity. Bioinformatic analysis performed on the differentially expressed genes along with the Kaplan-Meier survival analysis in TNBC patients identified Metastasis associated colon cancer 1 (Macc1) as the top candidate gene mediating the aggressive phenotype. The role of Macc1 in regulating the proliferative phenotype was validated using siRNA mediated gene knockdown. The role of Macc1 in the aggressive cancer cell phenotypes and disease progression is being studied further using a small molecule transcriptional inhibitor of Macc1 in cell line and animal models, thus increasing our understanding of the molecular underpinnings of intratumoral heterogeneity in breast cancer that is critical to the improvement in the treatment of women currently living with the highly aggressive TNBC subtype.</jats:p

Performance assessment on manufacturing of unfired bricks using industrial wastes

This paper presents eco-friendly unburnt bricks made up of fly ash, waste plastic powder, waste glass powder, lime, gypsum and crusher sand as alternatives to conventional burnt clay bricks for sustainable development. The research focuses on the maximum utilization of industrial waste in eco-friendly unburnt brick production. Materials are characterized according to their chemical and geotechnical properties. In this research, we use a milled waste glass powder of size less than 600μm and plastic powder obtained from plastic waste of size less than 600μm are added along with crushed sand, gypsum, lime and fly ash with various mix proportions concerning FaL-G mix concept. All the proportions were taken on a weight basis. Compressive strength, water absorption, and efflorescence are the key parameters chosen for comparing the innovative brick with conventional fly ash brick. There are five different mixes (Type A, B, C, D & E) are made in this research. The plastic and glass powders are replaced by crusher sand at the increased rate of 2% in every mix whereas 2%,4%,6%,8%, and 10%. It was found that the type B bricks have 17.63% strength was increased when compared to base mix. From the test results, type B bricks have enhanced mechanical performance when compared to all other mixes

DataSheet_1_Phenotypic heterogeneity drives differential disease outcome in a mouse model of triple negative breast cancer.docx

The triple negative breast cancer (TNBC) subtype is one of the most aggressive forms of breast cancer that has poor clinical outcome and is an unmet clinical challenge. Accumulating evidence suggests that intratumoral heterogeneity or the presence of phenotypically distinct cell populations within a tumor play a crucial role in chemoresistance, tumor progression and metastasis. An increased understanding of the molecular regulators of intratumoral heterogeneity is crucial to the development of effective therapeutic strategies in TNBC. To this end, we used an unbiased approach to identify a molecular mediator of intratumoral heterogeneity in breast cancer by isolating two tumor cell populations (T1 and T2) from the 4T1 TNBC model. Phenotypic characterization revealed that the cells are different in terms of their morphology, proliferation and self-renewal ability in vitro as well as primary tumor formation and metastatic potential in vivo. Bioinformatic analysis followed by Kaplan Meier survival analysis in TNBC patients identified Metastasis associated colon cancer 1 (Macc1) as one of the top candidate genes mediating the aggressive phenotype in the T1 tumor cells. The role of Macc1 in regulating the proliferative phenotype was validated and taken forward in a therapeutic context with Lovastatin, a small molecule transcriptional inhibitor of Macc1 to target the T1 cell population. This study increases our understanding of the molecular underpinnings of intratumoral heterogeneity in breast cancer that is critical to improve the treatment of women currently living with the highly aggressive TNBC subtype.</p

Targeting the Id1-Kif11 Axis in Triple-Negative Breast Cancer Using Combination Therapy

The basic helix-loop-helix (bHLH) transcription factors inhibitor of differentiation 1 (Id1) and inhibitor of differentiation 3 (Id3) (referred to as Id) have an important role in maintaining the cancer stem cell (CSC) phenotype in the triple-negative breast cancer (TNBC) subtype. In this study, we aimed to understand the molecular mechanism underlying Id control of CSC phenotype and exploit it for therapeutic purposes. We used two different TNBC tumor models marked by either Id depletion or Id1 expression in order to identify Id targets using a combinatorial analysis of RNA sequencing and microarray data. Phenotypically, Id protein depletion leads to cell cycle arrest in the G0/G1 phase, which we demonstrate is reversible. In order to understand the molecular underpinning of Id proteins on the cell cycle phenotype, we carried out a large-scale small interfering RNA (siRNA) screen of 61 putative targets identified by using genomic analysis of two Id TNBC tumor models. Kinesin Family Member 11 (Kif11) and Aurora Kinase A (Aurka), which are critical cell cycle regulators, were further validated as Id targets. Interestingly, unlike in Id depletion conditions, Kif11 and Aurka knockdown leads to a G2/M arrest, suggesting a novel Id cell cycle mechanism, which we will explore in further studies. Therapeutic targeting of Kif11 to block the Id1–Kif11 axis was carried out using small molecular inhibitor ispinesib. We finally leveraged our findings to target the Id/Kif11 pathway using the small molecule inhibitor ispinesib in the Id+ CSC results combined with chemotherapy for better response in TNBC subtypes. This work opens up exciting new possibilities of targeting Id targets such as Kif11 in the TNBC subtype, which is currently refractory to chemotherapy. Targeting the Id1–Kif11 molecular pathway in the Id1+ CSCs in combination with chemotherapy and small molecular inhibitor results in more effective debulking of TNBC.</jats:p

Targeting the Id1-Kif11 Axis in Triple-Negative Breast Cancer Using Combination Therapy

The basic helix-loop-helix (bHLH) transcription factors inhibitor of differentiation 1 (Id1) and inhibitor of differentiation 3 (Id3) (referred to as Id) have an important role in maintaining the cancer stem cell (CSC) phenotype in the triple-negative breast cancer (TNBC) subtype. In this study, we aimed to understand the molecular mechanism underlying Id control of CSC phenotype and exploit it for therapeutic purposes. We used two different TNBC tumor models marked by either Id depletion or Id1 expression in order to identify Id targets using a combinatorial analysis of RNA sequencing and microarray data. Phenotypically, Id protein depletion leads to cell cycle arrest in the G0/G1 phase, which we demonstrate is reversible. In order to understand the molecular underpinning of Id proteins on the cell cycle phenotype, we carried out a large-scale small interfering RNA (siRNA) screen of 61 putative targets identified by using genomic analysis of two Id TNBC tumor models. Kinesin Family Member 11 (Kif11) and Aurora Kinase A (Aurka), which are critical cell cycle regulators, were further validated as Id targets. Interestingly, unlike in Id depletion conditions, Kif11 and Aurka knockdown leads to a G2/M arrest, suggesting a novel Id cell cycle mechanism, which we will explore in further studies. Therapeutic targeting of Kif11 to block the Id1&ndash;Kif11 axis was carried out using small molecular inhibitor ispinesib. We finally leveraged our findings to target the Id/Kif11 pathway using the small molecule inhibitor ispinesib in the Id+ CSC results combined with chemotherapy for better response in TNBC subtypes. This work opens up exciting new possibilities of targeting Id targets such as Kif11 in the TNBC subtype, which is currently refractory to chemotherapy. Targeting the Id1&ndash;Kif11 molecular pathway in the Id1+ CSCs in combination with chemotherapy and small molecular inhibitor results in more effective debulking of TNBC