crush injury
Recently Published Documents


TOTAL DOCUMENTS

662
(FIVE YEARS 107)

H-INDEX

42
(FIVE YEARS 4)

2021 ◽  
Vol 36 (2) ◽  
pp. 144-147
Author(s):  
Chung-Min Yoon ◽  
Seung Cheol Lee ◽  
Ji-An Choi

We experienced a case of crush injury of the hand for which we performed a flap surgery and treated the necrotic parts placement using cultured allogeneic keratinocytes (Kaloderm<sup>®</sup> ) with good results. The patient was a 31-year-old woman whose left middle finger was caught in a door, causing a crush injury. Although primary repair was performed, a 2 × 2.5-cm-sized necrosis developed, and a V-Y advancement flap was performed after the removal of dead tissues. However, a 1 × 2-cm-sized partial necrosis occurred and was treated using Kaloderm <sup>®</sup> . After the use of Kaloderm<sup>®</sup> , the patient’s wound was healed, and no complications, except for mild pain, were observed for 1 year after the surgery. If a necrotic site appears after flap placement of fingertip, its treatment is difficult. If used well, Kaloderm<sup>®</sup> may be a good option for necrosis of the fingertips and other areas that are difficult to cure.


2021 ◽  
Vol 23 (1) ◽  
pp. 385
Author(s):  
Jie Chen ◽  
Hui Li ◽  
Changming Yang ◽  
Yinjia He ◽  
Tatsuo Arai ◽  
...  

Traumatic nerve injury activates cell stress pathways, resulting in neuronal death and loss of vital neural functions. To date, there are no available neuroprotectants for the treatment of traumatic neural injuries. Here, we studied three important flavanones of citrus components, in vitro and in vivo, to reveal their roles in inhibiting the JNK (c-Jun N-terminal kinase)-JUN pathway and their neuroprotective effects in the optic nerve crush injury model, a kind of traumatic nerve injury in the central nervous system. Results showed that both neural injury in vivo and cell stress in vitro activated the JNK-JUN pathway and increased JUN phosphorylation. We also demonstrated that naringenin treatment completely inhibited stress-induced JUN phosphorylation in cultured cells, whereas nobiletin and hesperidin only partially inhibited JUN phosphorylation. Neuroprotection studies in optic nerve crush injury mouse models revealed that naringenin treatment increased the survival of retinal ganglion cells after traumatic optic nerve injury, while the other two components had no neuroprotective effect. The neuroprotection effect of naringenin was due to the inhibition of JUN phosphorylation in crush-injured retinal ganglion cells. Therefore, the citrus component naringenin provides neuroprotection through the inhibition of the JNK-JUN pathway by inhibiting JUN phosphorylation, indicating the potential application of citrus chemical components in the clinical therapy of traumatic optic nerve injuries.


Neurosurgery ◽  
2021 ◽  
Vol 89 (Supplement_2) ◽  
pp. S139-S139
Author(s):  
Meei-Ling Sheu ◽  
Chiung-Chyi Shen ◽  
Hsi-Kai Tsou ◽  
Meng Yin Yang ◽  
Hong-Lin Su ◽  
...  

Author(s):  
Xue-Xin Wang ◽  
Hong-Shu Wang ◽  
Shi-Chu Xiao ◽  
Chun-Yang Wang ◽  
Shi-Zhao Ji ◽  
...  

Abstract Severe IV-degree thermal crush injury of limbs involved the subcutaneous fascia, muscle and bone, which may lead to amputation and has a great impact on the patient's quality of life. We can repair wounds with pedicle flaps or even free flaps, However, there are still huge challenges in bone defect of extremities and functional reconstruction. In recent years, with the development of functional prostheses, we have reconstructed limb functions in many patients helping them to complete their daily lives. We report a case where the right upper arm was injured by thermal crush, leading severe burns to the skin, fascia, muscle and bone. We applied a pedicled latissimus dorsi flap and a free anterolateral thigh flap to repair the wound, and realized the function of limb salvage and movement of the right upper arm by implanting 3D printed scapula, upper arm and elbow joint prostheses. This case illustrates that IV-degree burns involving bones have new technologies to repair and achieve mobility now.


Author(s):  
Fabio Castiglione ◽  
Maarten Albersen ◽  
Salvatore Fiorenzo ◽  
Petter Hedlund ◽  
Omer Onur Cakir ◽  
...  

2021 ◽  
Vol 22 (17) ◽  
pp. 9628
Author(s):  
Pao-Jen Kuo ◽  
Cheng-Shyuan Rau ◽  
Shao-Chun Wu ◽  
Chia-Wei Lin ◽  
Lien-Hung Huang ◽  
...  

Macrophages emerge in the milieu around innervated neurons after nerve injuries. Following nerve injury, autophagy is induced in macrophages and affects the regulation of inflammatory responses. It is closely linked to neuroinflammation, while the immunosuppressive drug tacrolimus (FK506) enhances nerve regeneration following nerve crush injury and nerve allotransplantation with additional neuroprotective and neurotrophic functions. The combined use of FK506 and adipose-derived stem cells (ADSCs) was employed in cell therapy for organ transplantation and vascularized composite allotransplantation. This study aimed to investigate the topical application of exosomes secreted by ADSCs following FK506 treatment (ADSC-F-exo) to the injured nerve in a mouse model of sciatic nerve crush injury. Furthermore, isobaric tags for relative and absolute quantitation (iTRAQ) were used to profile the potential exosomal proteins involved in autophagy. Immunohistochemical analysis revealed that nerve crush injuries significantly induced autophagy in the dorsal root ganglia and dorsal horn of the spinal segments. Locally applied ADSC-F-exo significantly reduced autophagy of macrophages in the spinal segments after nerve crush injury. Proteomic analysis showed that of the 22 abundant exosomal proteins detected in ADSC-F-exo, heat shock protein family A member 8 (HSPA8) and eukaryotic translation elongation factor 1 alpha 1 (EEF1A1) are involved in exosome-mediated autophagy reduction.


2021 ◽  
Vol 10 (9) ◽  
pp. 10108-10113
Author(s):  
Jie Zhang ◽  
Zaiwen Guo ◽  
Mingming Song ◽  
Jiandong Su ◽  
Bingwei Sun

Sign in / Sign up

Export Citation Format

Share Document