A severely infected diabetic foot treated successfully without using systemic antibiotics.

About 50% to 70% of all lower extremity amputations are related to diabetes infection. And antibiotic therapy is routinely used for all infected wounds to reduce the mortality of diabetic foot. Here, we report a case of diabetic foot with acute and deep severe infection.

[Effects of advanced glycation end products and its receptor on oxidative stress in diabetic wounds].

Objective: To investigate the accumulation of advanced glycation end products (AGE) and the inflammatory response of skin and wound in diabetic patients, and to analyze their relationship in vitro.

Methods: Histological staining and immunohistochemical staining was respectively performed on skin and wound tissue specimens collected from 10 patients with Type II diabetes mellitus (diabetes group) and 12 non-diabetic patients with skin injury (control group) to observe the arrangement of collagen and the distribution of inflammatory cells, and to determine the expression levels of AGE and its receptor (RAGE). Malondialdehyde (MDA) levels in skin and wound tissue homogenates were assayed by enzyme-linked immunosorbent assay.

[Relationship between cutaneous glycometabolic disorders and cutaneous neuropathy in diabetic rats].

Objective: To analyze the relationship between cutaneous glycometabolic disorders and cutaneous neuropathy in diabetic rats, and to look for the mechanism of neuropathy and impaired wound healing.

Methods: Eighty male SD rats were randomly divided into the normal control group (NC, n = 20), diabetic group (D, n = 20), aminoguanidine-interfered group (AI, n = 20), and insulin-interfered group (II, n = 20) by drawing lots. Diabetes was reproduced in rats of D, AI, and II groups with intraperitoneal injection of streptozotocin (STZ).

[Effect of topical application of aminoguanidine cream on skin tissue of rats with diabetes].

Objective: To investigate the effects of aminoguanidine cream on the proliferation of keratinocytes (KC), content of advanced glycosylation end products (AGE) and oxidative stress in skin tissue of rats with diabetes.

Methods: Stearic acid, liquid paraffin, vaseline, lanolin, isopropyl myristate fat, glycerol, 50 g/L alcohol paraben, aminoguanidine hydrochloride etc. were mixed in certain proportion to make aminoguanidine cream, and cream without aminoguanidine was used as matrix.

Clinical application of split skin graft from scar tissue for plastic reconstruction in post-extensive burn patients.

We evaluated the use of autologous split-thickness skin taken from scars on the backs of patients with extensive burns, without sufficient normal donor skin. Between 1998 and 2008, a total of 15 patients underwent 47 operations using split-thickness skin grafts from scar tissue. Split-thickness skin was harvested from scars on the patient's back.

[Effect of advanced glycosylation end products on cell cycle of epidermal keratinocyte and the role of signal pathway].

Objective: To investigate the effect of advanced glycosylation end products (AGE) on cell cycle of epidermal keratinocyte and its possible signal pathway.

Methods: 150 mg/L AGE-human serum albumin (AGE-HSA) was prepared in vitro. Primary cultured keratinocytes in logarithmic growth phase were harvested and divided randomly into: A group [with treatment of defined keratinocyte-SFM (DK-SFM) serum-free medium], B group (with treatment of DK-SFM medium including 150 mg/L AGE-HSA), C group (with DK-SFM medium after treatment of U0126) and group D (with D K-SFM medium including 150 mg/L AGE-HSA after treatment of U0126).

[A potential mechanism for impaired wound healing--cutaneous environmental disorders in diabetes mellitus].

Impaired wound healing in diabetes is a significant clinical problem which is thought to be associated with neuropathy and angiopathy previously . The present study indicates that accumulation of glucose and glycometabolic products in skin tissue, as the result of glycometabolic disorders, which contributes to cutaneous environmental alterations in diabetes mellitus, and subsequently induces the abnormal cell behaviors, cytokine alteration and matrix modification. Thus, diabetic neuropathy and angiopathy might be regarded as the pathological outcome of cutaneous environmental alterations.

[Study on the biological function of dermal fibroblasts in the wounds of diabetic and non-diabetic rats with deep burns].

Objective: To explore the changes of the biological function of dermal fibroblasts (FBs) in the wounds of diabetic and non-diabetic burned rats and the pathogenesis of impaired wound healing in diabetes.

Methods: 80 Sprague-Dawley (SD) rats weighing 220 g were randomly divided into control and STZ-induced diabetic groups, and then deep partial thickness scald involving 10% TBSA was reproduced in the two groups. The diabetic groups were randomized into pre-scalding, post-scalding day (PSD 3), PSD 7, PSD 14 and PSD 21 groups, with 6 rats in each group.

[Study on the proliferation of epidermal cells of wound edge in deep partial thickness scald injury in rat].

Objective: To investigate the rule and possible mechanism of epidermal proliferation in wound edge of deep partial thickness scald injury in rat.

Methods: Twenty-four Sprague-Dawley rats inflicted with deep partial thickness scald were randomized into pre-scalding, 3 post-scalding day (PSD), 7PSD and 14PSD groups, with 6 rats in each group. Skin specimens from the wound edge were harvested for the observation of the histological characteristics of the epidermis.

[The influence of L-arginine on the angiogenesis in burn wounds in diabetic rats].

Objective: To investigate the possible mechanism of L-arginine supplementation on the angiogenesis of burn wounds in diabetic rats.

Methods: One hundred male Sprague-Dawley (SD) rats were used in the study and were randomly divided into A (scalding control, n = 25), B (scalding of the rats with diabetes, n = 25), C (L-glycine control, n = 25) and D (L-arginine supplementation, n = 25) groups. Diabetes was produced by intra-peritoneal injection of streptozotocin (STZ) in B, C and D groups.