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The highly conductive property of Titanium Carbide MXene (Ti3C2Tx) MXenes has made them an area of research in the electrochemical field. However, their properties are subjected to their correct synthesis. Various synthesis methods have been reported; however, those methods employ high energy consumption. To reduce the cost, researchers have tried to synthesize using inexpensive precursors; however, fewer have resorted to the use of an alternative technique. This study employed the use of the tungsten inert gas welding process to synthesize the Ti3AlC2 MAX phase, which was later etched using the in situ hydrogen fluoride acid technique. Alternatively, another MAX phase was prepared using an atmosphere furnace under the purging of argon gas. However, impurities were detected in the MAX phase and later detected in titanium powder. [ABSTRACT FROM AUTHOR]

Objective: To determine the frequency of protein energy wasting among end stage renal disease patients on maintenance hemodialysis. Study Design: Cross-sectional analytical study. Place and Duration of Study: Department of Nephrology, Pak Emirates Military Hospital, Rawalpindi Pakistan, from May 2019 to Mar 2020. Methodology: Two hundered patients diagnosed with end-stage renal disease on maintenance hemodialysis were included in the study. Protein-energy wasting was assessed using the Malnutrition inflammatory score comprising four x components: medical history, physical examination, laboratory parameters and body mass index. Malnutrition inflammatory score was used to categorize protein-energy wasting. Results: Out of 200 patients with ESRD on maintenance hemodialysis, 73(36.5%) patients had mild, 120(60.0 %) patients had moderate, and 7(3.5%) patients had severe protein-energy wasting. The advanced age group, multiple comorbid (diabetes mellitus, hypertension, ischemic heart disease), and duration of hemodialysis (> 2 years) had a statistically significant association with the protein energy wasting (p-value < 0.05). Protein-energy wasting was also more prevalent in patients with low monthly income (p-value 0.04). Conclusion: Protein-energy wasting is common among patients with end stage renal disease on maintenance hemodialysis. Old age group, multiple comorbid, and duration of hemodialysis are important risk factors. [ABSTRACT FROM AUTHOR]

Objective: To determine the frequency of protein energy wasting among end stage renal disease patients on maintenance hemodialysis. Study Design: Cross-sectional analytical study. Place and Duration of Study: Department of Nephrology, Pak Emirates Military Hospital, Rawalpindi Pakistan, from May 2019 to Mar 2020. Methodology: Two hundered patients diagnosed with end-stage renal disease on maintenance hemodialysis were included in the study. Protein-energy wasting was assessed using the Malnutrition inflammatory score comprising four x components: medical history, physical examination, laboratory parameters and body mass index. Malnutrition inflammatory score was used to categorize protein-energy wasting. Results: Out of 200 patients with ESRD on maintenance hemodialysis, 73(36.5%) patients had mild, 120(60.0%) patients had moderate, and 7(3.5%) patients had severe protein-energy wasting. The advanced age group, multiple comorbid (diabetes mellitus, hypertension, ischemic heart disease), and duration of hemodialysis (> 2 years) had a statistically significant association with the protein energy wasting (p-value < 0.05). Protein-energy wasting was also more prevalent in patients with low monthly income (p-value 0.04). Conclusion: Protein-energy wasting is common among patients with end stage renal disease on maintenance hemodialysis. Old age group, multiple comorbid, and duration of hemodialysis are important risk factors. [ABSTRACT FROM AUTHOR]

The cell cycle has the capacity to safeguard the cell's DNA from damage. Thus, cell cycle arrest can allow tumor cells to investigate their own DNA repair processes. Cancer cells become extremely reliant on G1-phase cyclin-dependent kinases due to mutated oncogenes and deactivated tumor suppressors, producing replication stress and DNA damage during the S phase and destroying checkpoints that facilitate progression through the S/G2/M phase. DNA damage checkpoints activate DNA repair pathways to prevent cell proliferation, which occurs when the genome is damaged. However, research on how cells recommence division after a DNA lesion-induced arrest is insufficient which is merely the result of cancer cells' susceptibility to cell cycle arrest. For example, defects in the G1 arrest checkpoint may cause a cancer cell to proliferate more aggressively, and attempts to fix these complications may cause the cell to grow more slowly and eventually die. Defects in the G2-M arrest checkpoint may enable a damaged cell to enter mitosis and suffer apoptosis, and attempts to boost the effectiveness of chemotherapy may increase its cytotoxicity. Alternatively, attempts to promote G2-M arrest have also been linked to increased apoptosis in the laboratory. Furthermore, variables, such as hyperthermia, contact inhibition, nucleotide shortage, mitotic spindle damage, and resting phase effects, and DNA replication inhibitors add together to halt the cell cycle. In this review, we look at how nucleotide excision repair, MMR, and other variables, such as DNA replication inhibitors, hyperthermia, and contact inhibition, contribute to the outlined processes and functional capacities that cause cell cycle arrest., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)