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The aim of this study was to optimize extracion of flaxseed oil process by ultrasonic treatment and determination of its effect on ω-3 fatty acid. The extraction of flaxseed oil was optimized by using different solvents like methanol, acetone, petroleum ether, ethanol, hexane and dichloromethane. The ultrasonication treatment was optimized with respect to amplitude (20–80 kHz), temperature (25–40 °C), sonication time (20–80 min) and solid to solvent ratio (1:5, 1:10 and 1:15) for extraction of flaxseed oil. The extracted oil was subjected to GC analysis to determine ω-3 fatty acid. The recovery of flaxseed oil was higher with hexane followed by dichloromethane. The ultrasonic treatment at frequency of 40 kHz, temperature of 30 °C, extraction time of 40 min and solid to solvent ratio: 1:10 gave best results for extraction. The ultrasonic assisted extraction improves the extraction yield by 11.5% with similar amount of solvent. The chromatograph showed that there were no significant effects on α-Linolenic acid (ω-3) by the ultrasonic assisted extraction. This will beneficial to the oil extractor to recover higher amount of oil from same amount of the raw materials.

Introduction: Male breast cancer (MBC) is an uncommon malignancy. In spite of conventional Allopathic treatment, long-term disease-free survival (DFS) of more than 10 years in MBC is rare, due to its aggressive nature., Case Presentation: We report a case of 56 years old, stage IIB and grade III invasive ductal cell carcinoma MBC (Lt) patient, operated for left modified radical mastectomy with axillary clearance followed by six cycles of chemotherapy during October 2010-January 2011. Patient was on hormonal treatment from March 2011 till May 2021. He opted for adjunct Ayurvedic treatment throughout the conventional treatments for the period of 10 years. Ayurvedic treatment in the form of treatment for pacifying imbalanced humors (Doshas) and disease (Shamana chikitsa) and treatment for immunomodulation (Rasayana Chikitsa); and periodic detoxifying treatment (Panchakarma Chikitsa) was given in this patient. He was also advised healthy diet and lifestyle at our center. The treatment chosen was mainly to reduce side effects of chemotherapy like anorexia, nausea, vomiting, constipation, diarrhoea, taste disturbance, mucositis, fatigue and fever. It also helped in improving quality of life and increasing DFS., Conclusion: The long DFS of 10 years and 3 months with good Quality of Life and minimal side effects of conventional cancer therapy could be ascribed to the adjunct Ayurvedic treatment given to this patient. We have to observe the benefits in more number of patients in future to define usefulness of this treatment modality., Competing Interests: Declaration of competing interest The authors declare no conflict of interest., (Copyright © 2024 The Authors. Published by Elsevier B.V. All rights reserved.)

Rationale: CD40L figures prominently in chronic inflammatory diseases such as atherosclerosis. However, since CD40L potently regulates immune function and hemostasis by interaction with CD40 receptor and the platelet integrin GPIIb/IIIa, its global inhibition compromises host defense and generated thromboembolic complications in clinical trials. We recently reported that CD40L mediates atherogenesis independently of CD40 and proposed Mac-1 as an alternate receptor., Objective: Here, we molecularly characterized the CD40L-Mac-1 interaction and tested whether its selective inhibition by a small peptide modulates inflammation and atherogenesis in vivo., Methods and Results: CD40L concentration-dependently bound to Mac-1 I-domain in solid phase binding assays, and a high-affinity interaction was revealed by surface-plasmon-resonance analysis. We identified the motif EQLKKSKTL, an exposed loop between the α1 helix and the β-sheet B, on Mac-1 as binding site for CD40L. A linear peptide mimicking this sequence, M7, specifically inhibited the interaction of CD40L and Mac-1. A cyclisized version optimized for in vivo use, cM7, decreased peritoneal inflammation and inflammatory cell recruitment in vivo. Finally, LDLr(-/-) mice treated with intraperitoneal injections of cM7 developed smaller, less inflamed atherosclerotic lesions featuring characteristics of stability. However, cM7 did not interfere with CD40L-CD40 binding in vitro and CD40L-GPIIb/IIIa-mediated thrombus formation in vivo., Conclusions: We present the novel finding that CD40L binds to the EQLKKSKTL motif on Mac-1 mediating leukocyte recruitment and atherogenesis. Specific inhibition of CD40L-Mac-1 binding may represent an attractive anti-inflammatory treatment strategy for atherosclerosis and other inflammatory conditions, potentially avoiding the unwanted immunologic and thrombotic effects of global inhibition of CD40L.