Objective: to investigate the effects of endostar, a recombined humanized endostatin, on the growth, lymphangiogenesis and lymphatic metastasis of Lewis lung carcinoma xenograft in mice.
Methods: lewis lung carcinoma (LLC) xenograft were established in C57 mice by intravenous transplantation of 1 × 10(6) cells. Then tumor-bearing mice were assigned into two groups: control group received caudal vein injections of 0.2 ml of 0.9% sodium chloride for 15 days, and treatment group received 500 µg endostar daily. Six weeks after LLC cell injection mice were sacrificed, and then tumor numbers and size were recorded. The expression of vascular endothelial growth factor-c (VEGF-C) and microlymphatic vessel density (MLVD) were observed by immunohistochemical staining.
Results: tumor number and size of control group were significantly higher than those of treatment group. The microlymphatic vessel density (MLVD) was 5.7 ± 1.6 in the treatment group, which was markedly lower than in the control mice (7.8 ± 1.6). Two lymph node metastases were observed in treatment group, and eight in control group. Lymphatic metastases were more frequent in control group than in treatment group. Expression of VEGF-C in control group was significantly higher than that in treatment group.
Conclusion: endostar significantly inhibits the growth, lymphangiogenesis and lymphatic metastasis of Lewis lung carcinoma xenografts, and the inhibitory effect is due to its ability to regulate the expression of VEGF-C of tumors in part.
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Physiother Res Int
January 2025
College of Rehabilitation Sciences, Shanghai University of Medicine and Health Sciences, Shanghai, China.
Background: Proprioceptive deficits are common among stroke survivors and can negatively impact their balance and postural control. However, there has been little evaluation of the change in proprioceptive deficits in the lower limbs over time after stroke. This study aimed to examine proprioceptive deficits over time after stroke in both the affected and "unaffected" lower limbs.
View Article and Find Full Text PDFAnn Intensive Care
January 2025
Service de Médecine Intensive-Réanimation, Hôpital de Bicêtre, DMU CORREVE, Inserm UMR S_999, FHU SEPSIS, Groupe de Recherche Clinique CARMAS, Université Paris-Saclay, AP-HP, Le Kremlin-Bicêtre, France.
Background: Excessive tachycardia is associated with impaired hemodynamics and worse outcome in critically ill patients. Previous studies suggested beneficial effect of β-blockers administration in ICU patients, including those with septic shock. However, comparisons in ICU settings are lacking.
View Article and Find Full Text PDFNaunyn Schmiedebergs Arch Pharmacol
January 2025
Graduate School of Dalian Medical University, Dalian, China.
Immune infiltration plays a significant role in the pathogenesis of rheumatoid arthritis (RA). Cuproptosis, a newly characterized form of programmed cell death, remains insufficiently investigated regarding its genetic regulation of immune infiltration in RA. Data from the GEO database were analyzed to determine the relationship between cuproptosis-related genes and immune infiltration.
View Article and Find Full Text PDFEur J Nucl Med Mol Imaging
January 2025
Department of Internal Medicine, Division of Cardiology, National Taiwan University Hospital and National Taiwan University College of Medicine, Taipei, Taiwan.
Objective: Tafamidis has shown potential in slowing disease progression in patients with transthyretin amyloid cardiomyopathy (ATTR-CM). This study aimed to evaluate serial changes on [Tc]Tc-pyrophosphate (PYP) scintigraphy during tafamidis treatment for hereditary ATTR-CM.
Methods: We retrospectively analyzed a prospectively collected cohort of Ala97Ser (A97S) hereditary ATTR-CM patients treated with tafamidis (61 mg/day) and a control group comprising A97S hereditary ATTR-CM patients who had not received disease-modifying medications.
Sci Rep
January 2025
Department of Psychiatry and Psychotherapy, Central Institute of Mental Health, Medical Faculty Mannheim, University of Heidelberg, J5, 68159, Mannheim, Germany.
Inflammatory processes have been implicated in the pathophysiology of depression. In human studies, inflammation has been shown to act as a critical disease modifier, promoting susceptibility to depression and modulating specific endophenotypes of depression. However, there is scant documentation of how inflammatory processes are associated with neural activity in patients with depression.
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