AbstractAim of the work We attempt here to describe 2 cases of Behçet’s disease (BD) with pulmonary vascular complications. Case presentation Two cases of Behçet’s disease with major vessel involvement are presented. The first case presented with hemoptysis and investigations revealed the presence of pulmonary artery aneurysm (PAA). The patient received pulsed methylprednisolone 1 gm/day for 3 successive days and pulse cyclophosphamide 600 mg monthly for 6 months, and oral maintenance therapy 1 mg/kg prednisolone daily. The patient’s symptoms improved within 2 weeks and a follow up \{CT\} angiography after 1 year revealed normal pulmonary arteries. The second case presented with dilated tortuous veins over the chest wall and was diagnosed to have superior vena cava (SVC) obstruction. The patient was prescribed pulsed methylprednisolone 1 gm/day for 3 successive days and pulse cyclophosphamide 600 mg/month for 6 months and oral prednisolone 1 mg/kg/day maintenance therapy, in addition to, oral warfarin therapy 5 mg/day to maintain his İNR\} at 2.5. The patient was discharged after stabilization of his condition. Conclusion Since a significant proportion of patients develops complications in arterial and venous vessels, vascular lesions should be included in the diagnostic criteria of BD. Challenges remain to identify those patients at risk, to understand the cause and best treatment of thrombosis in these patients, and to develop well tolerated and effective therapies to arrest or reverse the course of vasculitis in BD.

Background: The Air-Q intubating laryngeal airway is a new supraglottic airway device which overcomes some of the limitations inherent to the intubating laryngeal mask airway (ILMA Fastrach™) for tracheal intubation. Previous studies showed lower success rate of the Air-Q™ versus ILMA Fastrach™. This study was conducted to illustrate new maneuvers for increasing the success rate of Air-Q™ versus ILMA Fastrach™ and compare between both devices.Methods: One-hundred and seventy adult patients, ASA I or II, aged >16 years old undergoing elective surgery under general anesthesia were divided randomly into 2 equal groups (85 each). Group A: using Air-Q ILA size 3.5 or size 4.5 Group B: using ILMA size 4 or size 5 according to the manufacturer’s recommendations for body weight in both groups. The time and the total success rate of blind intubation through them in 2 attempts only were recorded. In Group A, extension of the head with cricoid pressure was applied. The hemodynamic response to devices insertion and the complications related to both devices were compared.
Results: In Group A, the total success rate in 2 attempts was 94.12%, while in Group B, it was 96.47%. However, this difference was not statistically significant. The first attempt success rate was 81.18% in Group A, while it was 82.35% in Group B. The total time to intubate the hemodynamic response to device insertion and the incidence of complications (sore throat, trauma and hoarseness of voice) showed no statistically significant difference between both groups.
Conclusion: This study showed that extension of the head with cricoid pressure greatly increases the success rate of blind intubation through the Air-Q to 94.12% versus the ILMA Fastrach 96.47% with no statistically significant difference between both devices.

OBJECTIVES: This study aimed to investigate the effect of bee venom, a form of alternative therapy, on rotenone-induced Parkinson's disease (PD) in mice. Moreover, the possible modulation by bee venom of the effect of L-dopa/carbidopa or rasagiline was examined.

MATERIALS AND METHODS: Rotenone (1.5 mg/kg, subcutaneously; SC) was administered every other day for two weeks and at the same time mice received the vehicle (DMSO, SC), bee venom (0.065, 0.13, and 0.26 mg/kg; intradermal; ID), L-dopa/carbidopa (25 mg/kg, intraperitoneal; IP), L-dopa/carbidopa+bee venom (0.13 mg/kg, ID), rasagiline (1 mg/kg, IP) or rasagiline+bee venom (0.13 mg/kg, ID). Then, wire hanging and staircase tests were performed and mice were euthanized and brains' striata separated. Oxidative stress biomarkers namely, malondialdehyde (MDA), nitric oxide (NO), reduced glutathione (GSH), paraoxonase-1 (PON-1), and total antioxidant capacity (TAC) were measured. Additionally, butyrylcholinesterase (BuChE), monocyte chemoattractant protein-1 (MCP-1), tumor necrosis factor-alpha (TNF-α), and dopamine (DA) were evaluated. Brain histopathological changes and caspase-3- expression were done.

RESULTS: Bee venom significantly enhanced motor performance and inhibited rotenone-induced oxidative/nitrosative stress, observed as a reduction in both MDA and NO along with increasing GSH, PON-1, and TAC. Besides, bee venom decreased MCP-1, TNF-α, and caspase-3 expression together with an increase in BuChE activity and DA content.

CONCLUSION: Bee venom alone or in combination with L-dopa/carbidopa or rasagiline alleviated neuronal degeneration compared with L-dopa/carbidopa or rasagiline treatment only. Bee venom via its antioxidant and cytokine reducing potentials might be of value either alone or as adjunctive therapy in the management of PD.