cover
Contact Name
Hamsu Kadriyan
Contact Email
lombokmedicaljournal@unram.ac.id
Phone
+62818366217
Journal Mail Official
lombokmedicaljournal@unram.ac.id
Editorial Address
Jalan Pendidikan No 37, Mataram, NTB
Location
Kota mataram,
Nusa tenggara barat
INDONESIA
Lombok Medical Journal
Published by Universitas Mataram
ISSN : -     EISSN : 28277686     DOI : -
Lombok Medical Journal (LMJ) is a peer-reviewed and open access journal that focuses on promoting medical sciences generated from basic sciences, clinical, community or public health research, and medical education to integrate researches in all aspects of human health. This journal publishes original articles, reviews, and case reports. Brief communications containing short features of medicine, latest developments in diagnostic procedures, treatment, or other health issues that is important for the development of health care system are also acceptable. Focus and Scope of Lombok Medical Journal (LMJ): Basic Science, Clinical Research, Community or public health research, Medical Education
Articles 182 Documents
Insulin Enhances the Viability of Doxorubicin-Exposed Luminal A Breast Cancer T-47D Cells Fadhilla Resendryana Esthya; Novrita Padauleng; Lale Maulin Prihatina
Lombok Medical Journal Vol. 5 No. 3 (2026): Lombok Medical Journal (InPress)
Publisher : Faculty of Medicine, Universitas Mataram

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.29303/tv98zw69

Abstract

Breast cancer is one of the most common cancers worldwide, with a high incidence rate. Doxorubicin is a chemotherapeutic agent used in breast cancer management. Nevertheless, chemoresistance remains a major challenge in breast cancer chemotherapy. Insulin contributes to chemoresistance through its mitogenic and prosurvival activities. To date, studies evaluating the effect of insulin on the viability of Luminal A breast cancer cells (T-47D) under doxorubicin exposure remain limited. This study aimed to analyse the effect of insulin supplementation on the viability of Luminal A breast cancer cells (T-47D) exposed to doxorubicin. An in vitro experimental study was conducted using T-47D cells treated with doxorubicin at various concentrations (3.13, 6.25, 12.5, 25, 50, and 100 μg/mL), with and without insulin supplementation. Cell viability was assessed using the 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and analysed using a paired-samples t-test. T-47D cells receiving insulin supplementation showed higher viability than those without insulin across all tested doxorubicin concentrations, with statistically significant differences (p < 0.05). The fold change in viability between the insulin and non-insulin groups increased with rising doxorubicin concentrations. In conclusion, insulin affects the viability of Luminal A breast cancer T-47D cells exposed to doxorubicin, indicating reduced cellular sensitivity to the cytotoxic effects of doxorubicin.  
Immunopathological Role Of Neutrophil Extracellular Traps (Nets) In Rare Autoimmune And Autoinflammatory Diseases: A Scoping Review Ratri Yasmin; Indra Prastiwi Jamaluddin
Lombok Medical Journal Vol. 5 No. 3 (2026): Lombok Medical Journal (InPress)
Publisher : Faculty of Medicine, Universitas Mataram

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.29303/2wpm0d37

Abstract

Neutrophil extracellular traps (NETs) are an important of the innate immune system that functions to protect the body from pathogens. However, when their formation and clearance processes are disrupted, NETs can contribute to the development of various autoimmune diseases, including rare conditions. Therefore, this study aims to describe the immunopathological role of NETs in rare autoimmune and autoinflammatory diseases through a scoping review approach. A literature search was conducted in the Scopus, PubMed, and Web of Science databases following the PRISMA-ScR guidelines. From a total of 525 identified articles, 10 studies met the inclusion criteria after the selection process and were analyzed further. The results show that the role of NETs can be classified into three main mechanisms. First, enhanced NET formation (enhanced NETosis), triggers the release of autoantigens and the formation of immune complexes. Second, impaired clearance, leads to the accumulation of NETs and prolongs the inflammatory process. Third, the interaction of NETs with other immune system components, including the complement system, which further amplifying the inflammatory response. These three mechanisms are interconnected and form a continuous inflammatory cycle, contributing to tissue damage in rare autoimmune diseases. These findings indicate that NETs represent a potential target for the development of more specific therapies in the future.