Cellular senescence, a type of cytostasis, is the irreversible inhibition of the natural cell division in proliferating cells, resulting from various cellular stresses, including telomere shortening, DNA damage, mitochondrial dysfunctions, and pro-inflammatory responses. While cellular senescence can facilitate beneficial physiological processes such as tissue repair and wound healing, senescent cells also contribute to pathophysiological processes of agerelated diseases, including fibrotic lung diseases. The cellular senescence model and co-culture system were established to explore the underlying mechanisms associated with cellular senescence and fibrosis. Rutaecarpine is a bioactive alkaloid isolated from Evodia rutaecarpa (Rutaceae), a traditional herbal medicine. Rutaecarpine enhanced the promotor activity of E-cadherin, reduced TGF-β-induced reorganization of the actin cytoskeleton, and finally inhibited epithelialmesenchymal transition. Rutaecarpine also attenuated fibrotic and senescence features in bleomycin-induced lung fibrosis model. Here, we suggest the relevance between senescence and fibrosis, and a potential therapeutic approach of targeting senescence to attenuate lung fibrosis development.

Cellular senescence, a type of cytostasis, is the irreversible inhibition of the natural cell division in proliferating cells, resulting from various cellular stresses, including telomere shortening, DNA damage, mitochondrial dysfunctions, and pro-inflammatory responses. While cellular senescence can facilitate beneficial physiological processes such as tissue repair and wound healing, senescent cells also contribute to pathophysiological processes of agerelated diseases, including fibrotic lung diseases. The cellular senescence model and co-culture system were established to explore the underlying mechanisms associated with cellular senescence and fibrosis. Rutaecarpine is a bioactive alkaloid isolated from Evodia rutaecarpa (Rutaceae), a traditional herbal medicine. Rutaecarpine enhanced the promotor activity of E-cadherin, reduced TGF-β-induced reorganization of the actin cytoskeleton, and finally inhibited epithelialmesenchymal transition. Rutaecarpine also attenuated fibrotic and senescence features in bleomycin-induced lung fibrosis model. Here, we suggest the relevance between senescence and fibrosis, and a potential therapeutic approach of targeting senescence to attenuate lung fibrosis development.

Cellular senescence, a type of cytostasis, is the irreversible inhibition of the natural cell division in proliferating cells, resulting from various cellular stresses, including telomere shortening, DNA damage, mitochondrial dysfunctions, and pro-inflammatory responses. While cellular senescence can facilitate beneficial physiological processes such as tissue repair and wound healing, senescent cells also contribute to pathophysiological processes of agerelated diseases, including fibrotic lung diseases. The cellular senescence model and co-culture system were established to explore the underlying mechanisms associated with cellular senescence and fibrosis. Rutaecarpine is a bioactive alkaloid isolated from Evodia rutaecarpa (Rutaceae), a traditional herbal medicine. Rutaecarpine enhanced the promotor activity of E-cadherin, reduced TGF-β-induced reorganization of the actin cytoskeleton, and finally inhibited epithelialmesenchymal transition. Rutaecarpine also attenuated fibrotic and senescence features in bleomycin-induced lung fibrosis model. Here, we suggest the relevance between senescence and fibrosis, and a potential therapeutic approach of targeting senescence to attenuate lung fibrosis development.

Cellular senescence, a type of cytostasis, is the irreversible inhibition of the natural cell division in proliferating cells, resulting from various cellular stresses, including telomere shortening, DNA damage, mitochondrial dysfunctions, and pro-inflammatory responses. While cellular senescence can facilitate beneficial physiological processes such as tissue repair and wound healing, senescent cells also contribute to pathophysiological processes of agerelated diseases, including fibrotic lung diseases. The cellular senescence model and co-culture system were established to explore the underlying mechanisms associated with cellular senescence and fibrosis. Rutaecarpine is a bioactive alkaloid isolated from Evodia rutaecarpa (Rutaceae), a traditional herbal medicine. Rutaecarpine enhanced the promotor activity of E-cadherin, reduced TGF-β-induced reorganization of the actin cytoskeleton, and finally inhibited epithelialmesenchymal transition. Rutaecarpine also attenuated fibrotic and senescence features in bleomycin-induced lung fibrosis model. Here, we suggest the relevance between senescence and fibrosis, and a potential therapeutic approach of targeting senescence to attenuate lung fibrosis development.

BACKGROUND: To determine if exogenously injected bone marrow derived platelet-rich plasma (PRP) plus bone morphogenetic protein (BMP)-2 could accelerate the healing of bone-tendon junction injuries and increase the junction holding strength during the early regeneration period. METHODS: A direct injury model of the bone-tendon junction was made using an Achilles tendon-calcaneus bone junction in a rabbit. In the PRP/BMP-2/fibrin group, 0.05 mL of bone marrow derived PRP and 100 ng/mL of BMP-2 both incorporated into 0.1 mL of fibrin glue were injected into Achilles tendon-calcaneus bone junctions. The effect of the intervention was tested by comparing the results of an intervention group to a control group. The results of biomechanical testing, and histological and gross analyses were compared between the 2 groups at the following time points after surgery: 2 weeks, 4 weeks, and 8 weeks. RESULTS: Histologic examinations showed that woven bone developed in tendon-bone junctions at 2 weeks after surgery in the PRP/BMP-2/fibrin group. Mechanical test results showed no significant difference between the PRP/BMP-2/fibrin and control groups at 2 and 4 weeks after surgery, but the mean maximal load in the PRP/BMP-2/fibrin group was significantly higher than in the control group (p < 0.05) at 8 weeks after surgery. CONCLUSIONS: Bone marrow derived PRP and BMP-2 in fibrin glue accelerated healing in a rabbit model of tendon-bone junction injury.
Achilles Tendon/*injuries ; Animals ; Bone Marrow ; Bone Morphogenetic Protein 2/*therapeutic use ; Calcaneus/*injuries ; Male ; *Platelet-Rich Plasma ; Rabbits

A macroinvasive pituitary adenoma with plurihormonality usually causes acromegaly and hyperprolactinemia, and also accompanies with neurologic symptoms such as visual disturbances. However, its concurrent presentation with a rectal carcinoid tumor is rarely observed. This study reports the history, biochemical, colonoscopic and immunohistochemical results of a 48-year-old female with acromegaly and hyperprolactinemia. Despite the large size and invasive nature of the pituitary adenoma to adjacent anatomical structures, she did not complain of any neurologic symptoms such as visual disturbance or headache. Immunohistochemical staining of the surgical specimen from the pituitary adenoma revealed that the tumor cells were positive for growth hormone (GH), prolactin (PRL), and thyroid stimulating hormone (TSH). Staining for pituitary-specific transcription factor-1 (Pit-1) was shown to be strongly positive, which could have been possibly contributing to the plurihormonality of this adenoma. Colonoscopy found a rectal polyp that was identified to be a carcinoid tumor using immunohistochemical staining. A macroinvasive pituitary adenoma with concomitant rectal carcinoid tumor was secreting GH, PRL, and TSH, which were believed to be in association with over-expression of Pit-1. This is the first case report of double primary tumors comprising a plurihormonal pituitary macroadenoma and rectal carcinoid tumor.
Acromegaly* ; Adenoma ; Carcinoid Tumor* ; Colonoscopy ; Female ; Growth Hormone ; Headache ; Humans ; Hyperprolactinemia ; Middle Aged ; Neurologic Manifestations ; Pituitary Neoplasms* ; Polyps ; Prolactin ; Thyrotropin