Background: Several studies have reported short and medium-term outcomes of laparoscopic sleeve gastrectomy (LSG) in patients with class I obesity and type 2 diabetes mellitus (T2DM). However, literature on outcomes beyond three years is scarce. The present study discusses the 5-year results of a previously reported cohort of 20 patients with class I obesity and T2DM, who had undergone LSG between March 2012 and March 2015.
Materials And Methods: Patients were followed up in the bariatric clinic at yearly intervals as per institute protocol. Primary outcome was proportion of patients with a glycated haemoglobin (HbA1c) level of 6.5% or less, 5 years after LSG. Secondary outcomes were percentage total weight loss (%TWL), excess weight loss (EWL), weight regain and complications.
Results: Out of 20 patients, 9 (45%) were male and 11 (55%) were female. Mean age was 41.6 ± 9.5 years. Mean pre-operative weight and BMI were 94.8 ± 14.4 kg and 33.4 ± 1.2 kg/m, respectively. Median duration of diabetes was 42 months. Mean pre-operative fasting plasma glucose (FPG) and HbA1c were 171.1 ± 56.8 mg/dL and 8.7 ± 1.6%, respectively. Of the 17 patients available for follow-up at 5 years, 9 (52.9%) achieved HbA1c < 6.5% without medication, while 7 (41.2%) patients had improvement of their glycaemic status. One patient had recurrence of diabetes after initial remission. Mean %TWL and %EWL were 18% and 65.1%, respectively.
Conclusion: Laparoscopic sleeve gastrectomy is a reasonable option as a metabolic procedure for patients with T2DM and class I obesity.
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Background: The armamentarium of medical therapies to treat inflammatory bowel disease (IBD) continues to grow, which has expanded treatment options, particularly after first biologic failure. Currently, there are limited studies investigating the predictive value of first biologic primary non-response (PNR) on subsequent biologic success. Our objective was to determine if PNR to the first biologic for IBD is predictive of response to subsequent biologic therapy.
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Postgraduate Program in Biochemistry, Federal University of Espírito Santo (UFES), Vitória, Espírito Santo, Brazil.
Asthma is a complex disease with varied clinical manifestations resulting from the interaction between environmental and genetic factors. While chronic airway inflammation and hyperresponsiveness are central features, the etiology of asthma is multifaceted, leading to a diversity of phenotypes and endotypes. Although most research into the genetics of asthma focused on the analysis of single nucleotide polymorphisms (SNPs), studies highlight the importance of structural variations, such as copy number variations (CNVs), in the inheritance of complex characteristics, but their role has not yet been fully elucidated in asthma.
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Zentalis Pharmaceuticals, Inc., San Diego, CA, USA.
Upregulation of Cyclin E1 and subsequent activation of CDK2 accelerates cell cycle progression from G1 to S phase and is a common oncogenic driver in gynecological malignancies. WEE1 kinase counteracts the effects of Cyclin E1/CDK2 activation by regulating multiple cell cycle checkpoints. Here we characterized the relationship between Cyclin E1/CDK2 activation and sensitivity to the selective WEE1 inhibitor azenosertib.
View Article and Find Full Text PDFSci Rep
January 2025
Chaum Life Center, CHA University School of Medicine, Seoul, 06062, Korea.
No biomarker can effectively screen for early gastric cancer (EGC). Players in the A disintegrin and metalloproteinase (ADAM)-natural killer group 2 member D (NKG2D) receptor axis may have a role for that. As a proof-of-concept pilot study, the expression of ADAM8, ADAM9, ADAM10, ADAM12, ADAM17, and major histocompatibility complex (MHC) class I chain-related sequence A (MICA), a ligand for NKG2D, in gastric cancer was investigated in silico using The Cancer Genome Atlas (TCGA) database.
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January 2025
Department of Cardiology, Xijing Hospital, Fourth Military Medical University, Xi'an, Shaanxi, China.
Doxorubicin, a representative drug of the anthracycline class, is widely used in cancer treatment. However, Doxorubicin-induced cardiotoxicity (DIC) presents a significant challenge in its clinical application. Mitochondrial dysfunction plays a central role in DIC, primarily through disrupting mitochondrial dynamics.
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