Cerebral hyperperfusion syndrome (HPS) is a rare complication of carotid endarterectomy (CEA) and stenting. There are only a few case reports about HPS after intracranial stenting, and its clinical course remains unclear. We report an unusual case of HPS after intracranial internal carotid artery (ICA) stenting. An 87-year-old woman underwent uneventful balloon angioplasty for the right intracranial ICA one year ago; then she presented with restenosis at the same arterial location. She then underwent an ICA stent placement procedure. Preoperative cerebral blood flow (CBF) studies revealed hemodynamic ischemia. At the time of surgery, the stenotic lesion was near-occlusion. Twelve hours after the successful stenting procedure, the patient became restless, and near-infrared spectroscopy (NIRS) indicated a blood flow increase to the affected side. Arterial spin labeling (ASL) imaging performed on the same day showed high signal intensity only in the right hemisphere. She was treated with sedation, blood pressure control, and minocycline hydrochloride administration. Because of the strict management under continuous monitoring with NIRS, her symptoms gradually improved over the next 6 days. The right-to-left difference observed with ASL imaging resolved 6 days after surgery, and she was discharged with no neurological deficit. This case highlights the utility of NIRS monitoring in the management of HPS after intracranial stenting.
The AhR binds to contain ligands, such as 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin, 3-methylcholantrene, or β-naphthoflavone. The activation mechanism of AhRis not yet fully understood, but it is known that AhR associates with the molecular chaperone HSP90 in the cytoplasm. There are a few reports about the association or dissociation of AhR and HSP90, and which domain of HSP90 binds to AhR. We reported the association and activation mechanisms between HSP90 and AhR-PAS or AhR-bHLH. In the current study, we found that cisplatin inhibits the AhR activation. Although ATP and 17-DMAG have no effect on the dissociation of HSP90 from AhR, some contents of HSP90 were dissociated from AhR in the presence of cisplatin. We could detect the increase of CYP1A in the presence of 3-MC. On the contrary, the induction of CYP1A1 was inhibited in the presence of cisplatin. We couldn't detect AhR in the HeLa cell soluble fraction in the presence of 50 μM cisplatin. In the presence of MG-132, we could detect AhR. These results suggested that AhR was dissociated from the HSP90 chaperone complex and processed during the protein proteasome degradation system in the presence of cisplatin.
Colistin is an antimicrobial cationic peptide that belongs to the polymyxin family. Colistin was clinically used for the treatment of gram-negative infections but fell out of favour because of its significant side effects including neurotoxicity and nephrotoxicity. More recently, colistin has been regarded as one of the important options for nosocomial infections caused by multidrug resistant bacteria. Mechanisms of both the side effect onset of the drug and the side effect reduction are yet to be elucidated. In this study, we identified the specific binding protein of colistin using an affinity column chromatography. Colistin binds to the molecular chaperone HSP90. Although colistin slightly suppressed the chaperone activity of HSP90, there are no effects on the ATPase activity for a low concentration of colistin. Interestingly, colistin-induced aggregation of HSP90 via the N-domain. As for the cell viability of the SHSY5Y cell, the cell viability decreased to approximately 80% by the colistin 300 μM. However, the cell viability recovered to approximately 100% by adding ATP dosage. The same result was obtained by dot blot assay using anti-HSP90 antibody. Our results may help to understand the side effect mechanism of colistin.
Severe intrathoracic hemorrhage from pulmonary parenchyma is the most serious complication of pulmonary laceration after blunt trauma requiring immediate surgical hemostasis through open thoracotomy. The safety and efficacy of video-assisted thoracoscopic surgery (VATS) techniques for this life-threatening condition have not been fully evaluated yet. We report a case of pulmonary laceration with a massive hemothorax after blunt trauma successfully treated using a combination of muscle-sparing minithoracotomy with VATS techniques (video-assisted minithoracotomy). A 22-year-old man was transferred to our department after a falling accident. A diagnosis of right-sided pneumothorax was made on physical examination and urgent chest decompression was performed with a tube thoracostomy. Chest computed tomographic scan revealed pulmonary laceration with hematoma in the right lung. The pulmonary hematoma extending along segmental pulmonary artery in the helium of the middle lobe ruptured suddenly into the thoracic cavity, resulting in hemorrhagic shock on the fourth day after admission. Emergency right middle lobectomy was performed through video-assisted minithoracotomy. We used two cotton dissectors as a chopstick for achieving compression hemostasis during surgery. The patient recovered satisfactorily. Video-assisted minithoracotomy can be an alternative approach for the treatment of pulmonary lacerations with a massive hemothorax in hemodynamically unstable patients.
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