Basal cell adenoma of parotid gland: two case reports and literature review.

Most of salivary tumors are benign in nature and are typically diagnosed and classified based on their histopathological presentation. Basal cell adenoma of the salivary glands is a rare, benign disease accounting for 1% to 3% of salivary gland tumors. Despite its low incidence, basal cell adenoma is the third most common benign tumor of the salivary gland after pleomorphic adenoma and Warthin's tumor. It usually appears as a firm and slow-growing mass. Due to the prognosis, differential diagnosis with basal cell adenocarcinoma, adenoid cystic carcinoma and basaloid squamous cell carcinoma is required. In this report, we present two cases; a 62-year-old woman who presented with an asymptomatic, and slow-growing mass and a 64-year-old woman with a static-sized mass in the parotid gland. In both cases, the mass was completely excised, postoperative pathology reports confirmed the diagnosis of basal cell adenoma. We also review the literature and discuss this rare entity.

The cover of an ear thermometer probe as a split-thickness skin graft mold in external auditory canal reconstruction.

Maintaining the patency of the external auditory canal (EAC) during reconstruction is important because of its physiological role in hearing and immunological protective functions. The curved shape of the EAC presents a challenge when performing a skin graft. One of the key points for a successful skin graft is to ensure compression on the wound bed, and many novel methods, including prefabricated ear molds, have been reported for this purpose. In this study, we present a case of a skin graft performed to reconstruct a skin defect following excision of actinic keratosis in the EAC, using the cover of an ear thermometer probe as a mold for the graft to match the curvature of the EAC. This is an economical and practical method for secure compression dressing of a skin graft in the EAC.

Safe and effective thrombolysis in free flap salvage: Intra-arterial urokinase infusion.

Despite the high success rate in reconstruction using free tissue transfer, flap failure is often caused by microvascular thrombosis. In a small percentage of cases with complete flap loss, a salvage procedure is performed. In the present study, the effectiveness of intra-arterial urokinase infusion through the free flap tissue was investigated to develop a protocol to prevent thrombotic failure. The retrospective study evaluated the medical records of patients who underwent salvage procedure with intra-arterial urokinase infusion after reconstruction with free flap transfer between January 2013 and July 2019. Thrombolysis with urokinase infusion was administered as salvage treatment for patients who experienced flap compromise more than 24 hours after free flap surgery. Because of an external venous drainage through the resected vein, 100,000 IU of urokinase was infused into the arterial pedicle only into the flap circulation. A total of 16 patients was included in the present study. The mean time to re-exploration was 45.4 hours (range: 24-88 hours), and the mean quantity of infused urokinase was 69,688 IU (range: 30,000-100,000 IU). 5 cases presented with both arterial and venous thrombosis, while 10 cases had only venous thrombosis and 1 case had only arterial thrombosis; in a study of 16 patients undergoing flap surgery, 11 flaps were found to have survived completely, while 2 flaps experienced transient partial necrosis and 3 were lost despite salvage efforts. In other word, 81.3% (13 of 16) of flaps survived. Systemic complications, including gastrointestinal bleeding, hematemesis, and hemorrhagic stroke, were not observed. The free flap can be effectively and safely salvaged without systemic hemorrhagic complications using high-dose intra-arterial urokinase infusion within a short period of time without systemic circulation, even in delayed salvage cases. Urokinase infusion results in successful salvage and low rate of fat necrosis.

Partial second-toe pulp free flap for fingertip reconstruction: Experience and surgical tips to minimize complications.

BACKGROUND: Traumatic fingertip injury is a common hand injury and various methods are available to address them. The partial second-toe pulp (PSTP) free flap is useful because of the similarity in shape, texture, and sensation to the fingertips. However, there may be many difficulties during surgery. The purpose of this report is to make the surgery easier and minimize complications by sharing the surgical tips of the authors obtained through many experiences. PATIENTS AND METHODS: Thirty patients who underwent PSTP free flap due to trauma were reviewed retrospectively from February 2015 to June 2018. The average age of the patients was 49.4 years. Seventeen were injured on the right side and 13 were on the left side. After removal of the injured tissue, a teardrop-shaped flap was harvested from the medial side of the second toe. When inset, skin graft or vein graft was performed if necessary. When primary closure of the donor site was difficult, skin graft was performed (n = 21). The factors noted during surgery were analyzed. RESULTS: The flap size was 2.39 (range: 1.5-5) x 1.29 (range: 1-1.8) cm2 . All flaps survived. Venous congestion was found in two patients, neuroma was found in one patient, and partial necrosis was found in two patients; all recovered with conservative care. The mean follow up periods was 5.79 (range: 2-18) months. None of the patients had functional impairment. CONCLUSION: Successful reconstruction and enhanced functional and cosmetic effects can be achieved using surgical tips.

A mutation in keratin 18 that causes caspase-digestion resistance protects homozygous transgenic mice from hepatic apoptosis and injury.

Cytoskeletal keratin 18 (K18) undergoes caspase-mediated digestion during apoptosis, which leads to dramatic disassembly of keratin filaments. We studied the significance of K18 caspase digestion in a mouse model and generated transgenic mice expressing the human K18 caspase digestion-resistant double-mutant K18-D238/397E in a mouse (m) K18-null background, and compared their response to injury mediated by administration of antibody against tumor necrosis factor receptor superfamily member 6 (Fas), anti-FasAb. Notably, K18-D238/397E;mK18-null mice were significantly more resistant to anti-FasAb-induced injury as compared with K18-WT;mK18-null mice (23% vs 57% lethality, respectively; P<0.001). The same applied when the toxin microcystin-LR (MLR) was used to induce liver injury, i.e. lethality of K18-D238/397E;mK18-null mice in response to MLR treatment was reduced compared with the control mouse strain. The lesser rate of apoptosis in K18-D238/397E;mK18-null livers is associated with delayed degradation and, thus, sustained activation of cell-survival-related protein kinases, including stress-activated protein kinases and the NF-κB transcription factor, up to 6-8 h after administration of anti-FasAb. However, activation of the kinases and NF-κB in K18-WT-reconstituted livers decreases dramatically 8 h after anti-FasAb administration. In addition, the D238/397E double-mutation results in prolonged stability of K18 protein in transfected cells and transgenic livers. Therefore, our results show that the caspase digestion-resistant K18 helps to maintain keratin filament organization and delays apoptosis, thereby resulting in protection from liver injury.