No abstract available.
Atherosclerosis ; Bacterial Infections ; Foot Ulcer ; Foot ; Tinea Pedis ; Tinea

No abstract available.
Hidrocystoma* ; Syringoma*

The nature of implant-related infections is complex. Currently, there is no definitive test for periprosthetic joint infection (PJI) and diagnosis remains challenging despite recent developments. Failure to diagnose and investigate pathologies of the hip appropriately results in delayed management and prolonged patient morbidity. A systematic approach to establishing clear diagnostic criteria for PJI is needed to improve our ability to avoid devastating outcomes associated with these infections. In the current review, we describe an algorithmic approach to the diagnosis of PJI and current controversies surrounding novel diagnostic methods.

Interscalene bracheal plexus block has became a popular method of anesthesia for surgical operation on the upper extremities. Possible complications are subarachnoid block, epidural block, phrenic nerve block, vagus or recurrent laryngeal nerve block, sympathetic nerve block, intravascular injection. But reported complications has been few and generally without prolonged effects. The following describes a patient who developed signs and symptoms suggestive of inadvertent phrenic nerve block and epidural anesthesia as complications of interscalene bracheal plexus block The complications were attributed to using of inferomedially directed 5 cm needle and then additional blind block of the brachial plexus with 5 or 6 times. We emphasize that if the appropriate length of needle and technique are not used, phrenic nerve paralysis and serious complications including total spinal or epidural block can occur as a result of a medially misdirected needle.
Anesthesia ; Anesthesia, Epidural ; Autonomic Nerve Block ; Brachial Plexus ; Humans ; Needles ; Paralysis* ; Phrenic Nerve* ; Recurrent Laryngeal Nerve ; Upper Extremity

No abstract available.
Myocardial Infarction*

No abstract available.
Liver Cirrhosis* ; Liver* ; Pregnancy*

BACKGROUND: The risk of bleeding during extracorporeal membrane oxygenation (ECMO) is a potential deterrent in performing tracheostomy at many centers. To evaluate the safety of surgical tracheostomy (ST) in critically ill patients supported by ECMO, we reviewed the clinical correlation between preoperative coagulation status and bleeding complication-related ST during ECMO. METHODS: From April 1, 2012 to March 31, 2016, ST was performed on 38 patients supported by ECMO. We retrospectively reviewed and analyzed the medical records including complications related to ST. RESULTS: Heparin was administered to 23 patients (60.5%) for anticoagulation during ECMO, but 15 patients (39.5%) underwent ECMO without anticoagulation. Of the 23 patients administered anticoagulation therapy, heparin infusion was briefly paused in 13 prior to ST. The median platelet count, international normalized ratio, and activated partial thromboplastin time before ST were 126 ×109/L (range, 46 to 434 ×109/L), 1.2 (range, 1 to 2.3) and 62 seconds (27 to 114.2 seconds), respectively. No peri-procedural clotting complications related to ECMO were observed. Two patients (5.3%) suffering from ST-related major bleeding required surgical hemostasis. Minor bleeding after ST occurred in two cases (5.3%). No significant difference was found according to anticoagulation management (P = 0.723). No fatality was attributable to ST. CONCLUSIONS: The complication rates of ST in the patients supported by ECMO were low. Therefore, ST performed by an experienced operator, and with careful optimization of coagulation status, is a relatively safe procedure; the use of ST with ECMO should thus not be dismissed on account of the potential for bleeding caused by the administration of anticoagulants.
Anticoagulants ; Critical Illness ; Extracorporeal Membrane Oxygenation* ; Hemorrhage ; Hemostasis, Surgical ; Heparin ; Humans ; International Normalized Ratio ; Medical Records ; Partial Thromboplastin Time ; Platelet Count ; Retrospective Studies ; Tracheostomy*

No abstract available.
Burns* ; Humans ; Spinal Cord Diseases*

Glutamate is a representative excitatory neurotransmitter. However, excessive glutamate exposure causes neuronal cell damage by generating neuronal excitotoxicity. Excitotoxicity in neonates caused by glutamate treatment induces neurological deficits in adults. The 14–3-3 family proteins are conserved proteins that are expressed ubiquitously in a variety of tissues. These proteins contribute to cellular processes, including signal transduction, protein synthesis, and cell cycle control. We proposed that glutamate induces neuronal cell damage by regulating 14–3-3 protein expression in newborn animals. In this study, we investigated the histopathological changes and 14–3-3 proteins expressions as a result of glutamate exposure in the neonatal cerebral cortex. Rat pups at post-natal day 7 were intraperitoneally administrated with vehicle or glutamate (10 mg/kg). Animals were sacrificed 4 h after treatment, and brain tissues were fixed for histological study. Cerebral cortices were isolated and frozen for proteomic study. We observed serious histopathological damages including shrunken dendrites and atypical neurons in glutamate-treated cerebral cortices. In addition, we identified that 14–3-3 family proteins decreased in glutamate-exposed cerebral cortices using a proteomic approach. Moreover, Western blot analysis provided results that glutamate treatment in neonates decreased 14–3-3 family proteins expressions, including the β/α, ζ/δ, γ, ε, τ, and η isoforms. 14–3-3 proteins are involved in signal transduction, metabolism, and anti-apoptotic functions. Thus, our findings suggest that glutamate induces neonatal neuronal cell damage by modulating 14–3-3 protein expression.

We evaluated the clinical effects of amlodipine in 10 patients(7 male and 3 female) with angina pectoris in terms of the effect on the anginal pain, hemodynamic changes and side effects. The results obtained were as follows; 1) The clinical improvement was obsebed in 8(80.8%) of 10 and 9(88.9%) of 9 patients at 2 and 10 weeks after oral amlodipine. 2) The systolic and diastolic blood pressure was decreased significantly(136.0+/-16.5mmHg vs 117.0+/-10.6mmHg, p<0.01 and 85.0+/-9.7mmHg vs 75.0+/-5.3mmHg, p<0.01 respectively) but the heart rate was indepentent of amlodipine administration. 3) The adverse effects of amlodipine were as headache in 3, facial flushing in 3, palpitation, dizziness, urinary difficulty in 1 respectively and one of them discontinued amlodipine due to severe palpitation and facial flushing.
Amlodipine* ; Angina Pectoris* ; Blood Pressure ; Dizziness ; Flushing ; Headache ; Heart Rate ; Hemodynamics ; Humans ; Male