Use of autologous iliac crest graft and free anterolateral femoral skin flap in diabetic foot ulcers: a case report.

BACKGROUND: Diabetic foot has a great impact on the life of patients. Its treatment involves a multi-disciplinary and multi-direction approach, which requires not only soft tissue repair, but also bone reconstruction and functional repair. CASE PRESENTATION: A 51-year-old Chinese man with a three-year history of diabetes was diagnosed with ulcers in his left foot. We performed a successful procedure, and the different strategies we adopted helped to avoid serious complications during treatment. The patient was treated with debridement, bone cement, iliac crest graft, and anterolateral femoral skin flap, and recovered well. CONCLUSION: There is a dearth of reports pertaining to treatment of diabetic foot in patients with midfoot bone and soft tissue loss. In this report, we present an effective method that we used to reconstruct the loss of midfoot in a patient with diabetic foot, illustrating a successful therapeutic strategy for saving limbs in this complex medical condition.

A successful process of treatment with necrotizing fasciitis of upper extremities in patients with diabetes mellitus: a case report.

Necrotizing fasciitis (NF) represents a rapidly progressive, life-threatening infection involving the fascia and subcutaneous tissue. Early diagnosis and intervention are crucial to treat, especially in diabetic patients. Case presentation: This case report presents on a patient with diabetes mellitus rapidly developed a NF of the upper extremities following a minor trauma in the palmar of greater thenar. In the initial stages of her hospital admission, severe hand soft tissue infection, and systemic toxicity is the most prominent clinical manifestation. During her hospitalization, efficacious multidisciplinary treatment was carried out to avoid severe consequences. Clinical discussion and conclusion: The objective of this case report is to present a successful individual strategy in a complex case to standardize the treatment process. Accurate and standardized management can improve the prognosis of patients affected from upper extremities NF of diabetic avoiding and severe complications and saving lives.

Maggot excretions/secretions promote diabetic wound angiogenesis via miR18a/19a - TSP-1 axis.

AIMS: The impaired angiogenesis is one of the main factors affecting the healing of diabetic foot ulcer (DFU) wounds. Maggot debridement therapy (MDT) promotes granulation tissue growth and angiogenesis during DFU wound healing. Non-coding microRNAs can also promote local angiogenesis in DFU wounds by regulating wound repairing related gene expression. The purpose of this study was to investigate the mechanism of microRNAs in MDT promoting DFU wound angiogenesis. METHODS: In this study, we applied MDT to treat DFU wound tissue and detect the expression of the miR-17-92 cluster. In vitro experiments, human umbilical vein endothelial cells (HUVECs) were treated with maggot excretions/secretions (ES), the miR-17-92 cluster and the predicted target gene expression were measured. Tube formation assay and cell scratch assay were performed when inhibition of miR-18a/19a or overexpression of thrombospondin-1 (TSP-1) were used in this study. RESULTS: miR-18a/19a transcription significantly up-regulated and TSP-1 expression down-regulated in patients wound tissue and in HUVECs. Inhibition of miR-18a/19a or overexpression of TSP-1 partially blocked the migration and tube formation ability stimulated by ES. CONCLUSION: Targeted activation of miR-18a/19a transcription levels and subsequent regulation of TSP-1 expression may be a novel therapeutic strategy for DFU.

Roles of autophagy in androgen-induced benign prostatic hyperplasia in castrated rats.

The present study investigated the role of androgen in the process of androgen-induced prostate hyperplasia in castrated rats and assessed the role of the phosphoinositide 3-kinase/protein kinase B/mechanistic target of rapamycin (PI3K/Akt/mTOR) pathway in this process. Furthermore, the extent to which autophagy may affect the level of androgen-induced benign prostatic hyperplasia was also explored. A total of 40 Sprague Dawley rats were randomly divided into four groups: Testosterone group, rapamycin group, 3-methyladenine (3-MA) group, and control group. The extent of hyperplasia in prostate tissue the apoptosis and autophagy were assayed. The prostate wet weight, volume and index in the testosterone group were significantly higher compared with the control group (P<0.05) and these factors were significantly lower in the rapamycin group compared with the testosterone group (P<0.05). HE staining demonstrated that prostate hyperplasia was obvious in the testosterone group. Western blotting revealed that caspase-3 levels were higher in the 3-MA group compared with the control group and Bcl-2 was higher in the testosterone group compared with the control group (P<0.05). Furthermore, in the rapamycin group, Bcl-2 protein expression levels were significantly lower than those in the testosterone group (P<0.05). The prostate tissue was analyzed using electron microscopy and autophagy bodies were identified in the rapamycin group. In the process of androgen-induced prostatic hyperplasia in castrated rats, the role of androgen may be related to the PI3K/Akt/mTOR signaling pathway. Rapamycin was able to inhibit the effect of testosterone and promoted prostate tissue hyperplasia by inhibiting the PI3K/Akt pathway. In addition to inhibiting apoptosis in prostate cells, androgen was able to induce rat prostate hyperplasia and may also be related to the promotion of the proliferation of prostate cells.