OBJECTIVE: The prefabrication of customized cranioplastic implants has been introduced to overcome the difficulties of intra-operative implant molding. The authors present a new technique, which consists of the prefabrication of implant molds using three-dimensional (3D) printers and polymethyl-methacrylate (PMMA) casting. METHODS: A total of 16 patients with large skull defects (>100 cm2) underwent cranioplasty between November 2009 and April 2011. For unilateral cranial defects, 3D images of the skull were obtained from preoperative axial 1-mm spiral computed tomography (CT) scans. The image of the implant was generated by a digital subtraction mirror-imaging process using the normal side of the cranium as a model. For bilateral cranial defects, precraniectomy routine spiral CT scan data were merged with postcraniectomy 3D CT images following a smoothing process. Prefabrication of the mold was performed by the 3D printer. Intraoperatively, the PMMA implant was created with the prefabricated mold, and fit into the cranial defect. RESULTS: The median operation time was 184.36+/-26.07 minutes. Postoperative CT scans showed excellent restoration of the symmetrical contours and curvature of the cranium in all cases. The median follow-up period was 23 months (range, 14-28 months). Postoperative infection was developed in one case (6.2%) who had an open wound defect previously. CONCLUSION: Customized cranioplasty PMMA implants using 3D printer may be a useful technique for the reconstruction of various cranial defects.
Computer-Aided Design ; Decompressive Craniectomy ; Follow-Up Studies ; Fungi ; Humans ; Methylmethacrylate ; Polymethyl Methacrylate ; Reconstructive Surgical Procedures ; Skull ; Tomography, Spiral Computed

BACKGROUND: To reduce surgical stress, fentanyl is frequently used for neurosurgical procedure where focal and/or global ischemia may occur. However, the effect of fentanyl on the cytokine level during ischemia/reperfusion is still uncertain. The goal of this study was to evaluate the effect of fentanyl infusion on the proinflammatory cytokine, TNF-alpha and IL-1beta, levels during global cerebral ischemia/reperfusion (I/R) in rats using the intracerebral microdialysis technique. METHODS: Forty male S-D rats weighing 280 320 g were randomly assigned to four groups. Group 1: no fentanyl infusion and only I/R, Group 2: 1.5 ng/ml of fentanyl infusion during I/R, Group 3: 3.0 ng/ml of fentanyl infusion during I/R (n = 10 in each group). Rats were anesthetized with a intraperitoneal injection of pentobarbital (50 mg/kg), intubated and ventilated with room air using an animal ventilator. Two femoral arteries and one femoral vein were cannulated with PE-50 tubing for hemorrhagic hypotension, drug infusion and hydration. Both carotid arteries were dissected and a sling was placed for brain ischemia. The head was fixed on a stereotaxic device and a small burrhole was made for probe insertion. A CMA-12 probe was inserted into the left hippocampal CA-1 region according to the guidelines. Artificial CSF was run from the inserted microdialysis probe and infused with or without fentanyl at 3 microliter/min using a microinjection syringe pump during I/R. Ischemia was induced by clamping the carotid arteries while hemorrhagic hypotension for 17 min via the femoral artery and reperfusion were accomplished by the unclamping of the sling and reinfusing the blood via the femoral artery. Nasopharyngeal and rectal temperatures were maintained within the normal range during the whole procedure. After 2 hours of stabilization, the microdialysate was collected every 17 min just before (control) and during I/R and stored at 80oC until analysis using HPLC. RESULTS: During global I/R, TNF-alpha and IL-1 beta significantly increased at reperfusion (R5) compared to the control value (P < 0.05). However, in both cases of fentanyl infusion, TNF-alpha and IL-1 beta did not increase compared to the control value. CONCLUSIONS: Fentanyl inhibited the increase of proinflammatory cytokine TNF-alpha and IL-1 beta levels during global cerebral ischemia/reperfusion in rats.
Animals ; Brain Ischemia ; Carotid Arteries ; Chromatography, High Pressure Liquid ; Constriction ; Femoral Artery ; Femoral Vein ; Fentanyl* ; Head ; Humans ; Hypotension ; Injections, Intraperitoneal ; Interleukin-1beta ; Ischemia ; Male ; Microdialysis ; Microinjections ; Neurosurgical Procedures ; Pentobarbital ; Rats* ; Reference Values ; Reperfusion ; Syringes ; Tumor Necrosis Factor-alpha* ; Ventilators, Mechanical

PURPOSE: To evaluate the impact of location of a silicone tube tip in the anterior chamber on corneal endothelium after Ahmed glaucoma valve implantation. METHODS: We measured the distance from the tip of a silicone tube in the anterior chamber to the posterior surface of the cornea by anterior segment optical coherence tomography (OCT) in 24 eyes of 21 patients who underwent Ahmed glaucoma valve implantation. All surgeries were performed by a single surgeon. The corneal endothelial cells of central, superior, superotemporal, and superonasal area of the cornea were examined by specular microscope before and after surgery. RESULTS: The distance from the tip of the silicone tube in the anterior chamber to the posterior surface of the cornea and the corneal endothelium were measured at 19.2 +/- 11.8 months (2.8-41.2 months) after surgery. At the central corneal area, a statistically significant decrease in the number of corneal endothelial cells (2278 +/- 565/mm2 vs. 2177 +/- 529/mm2, p = 0.043) after surgery was observed, but no relationship was found between the amount of decrease and distance from the tip to the posterior surface of the cornea. At the superotemporal corneal area where the tip of the silicone tube was located in the anterior chamber, there was more significant loss of corneal endothelial cells than in the other areas after surgery (p = 0.006). Moreover, the amount of endothelial cell loss at the superotemporal area was negatively correlated to the distance from the tip to the posterior surface of the cornea (partial correlation coefficient by time -0.558, p = 0.031). CONCLUSIONS: To minimize the loss of corneal endothelial cells after Ahmed glaucoma valve implantation, ensuring a sufficient distance from the tip of the silicone tube to the posterior surface of the cornea is important.
Anterior Chamber ; Cornea ; Endothelial Cells ; Endothelium, Corneal ; Eye ; Glaucoma ; Humans ; Silicones ; Tomography, Optical Coherence

No abstract available.
Infarction

No abstract available.
Humans ; Inpatients*

No abstract available.

No abstract available.

No abstract available.
Muscle, Skeletal* ; Tibial Nerve*

Rhizome of Alisma orientale has been used as a traditional medicine for treating kidney diseases in East Asian countries. Its inhibitory effects on hypersensitivity responses have been reported for methanol extracts, with alisol B 23-acetate (AB23Ac) being the most active constituent among six terpenes in inhibiting the direct passive Arthus reaction. However, whether AB23Ac has efficacy against allergic asthma has not been tested to date. The in vivo efficacy of AB23Ac in an ovalbumin (OVA)-induced allergic asthma mouse model was evaluated by administrating AB23Ac before OVA sensitization or OVA challenge in BALB/c mice. AB23Ac suppressed antigen-induced degranulation of RBL-2H3 mast cells in a concentration-dependent manner. The administration of AB23Ac both before OVA sensitization and OVA challenge greatly lowered pulmonary resistance and the increase in immune cell counts and inflammatory responses around the peribronchial and perivascular regions. In addition, the inflammatory cytokine levels of Th1/Th2/Th17 cells in the bronchoalveolar lavage fluid decreased in the AB23Ac-treated groups. AB23Ac reduced the number of PAS-stained cells in the lungs. Furthermore, a computer modeling study indicated that AB23Ac can bind tightly to spleen tyrosine kinase (Syk). These results suggest that AB23Ac may ameliorate allergic asthma by suppressing immune responses in dendritic cells during sensitization and in mast cells during challenge periods.

OBJECTIVE: To determine of the regulation of cyclooxygenase-2 (COX-2) expression by Interleukin-1beta in WISH cells. METHODS: Amnion WISH cells were incubated in media containing increasing concentrations of IL-1beta or with various inhibitors. Increased COX-2 expression was determined by Western blot analysis with anti-COX-2 antibody. Concomitant measurements of culture media PGE2 were made by an enzyme immunoassay. RESULTS: The COX-2 and prostaglandin E2 production induced by IL-1beta increased in a dose- and time-dependent manner. One of the regulating factors that induced COX-2 by IL-1beta was protein kinase C (PKC). PKC inhibitor, Ro 31-8220 was pretreated and continued treating by IL-1beta. Then, PKC inhibitor completely blocked COX-2 protein induction by IL-1beta. In contrast, COX-2 induction by IL-1beta after pretreating PKC stimulator, phobol 12-myristate 13-acetate was potentiated with synergism. Another factor in controlling COX-2 protein induction was identified as phosphatidylinositol 3-kinase (PI 3K). COX-2 protein induction by IL-1beta after pretreating PI 3K inhibitors, wortmannin and LY294002 strongly increased. This kind of result reflected that PI 3K act as negative regulator. COX-2 induction by IL-1beta was known to be regulated in not only transcription step, but also translation step after performing experiment of actinomycin and cycloheximide treatment. CONCLUSION: COX-2 protein and prostaglandin E2 production induced by IL-1beta were controlled by many factors in amnion cell. Among those factors, PKC and PI 3K have an important role, but their control mechanism act as positive and negative, respectively.
Amnion ; Blotting, Western ; Culture Media ; Cycloheximide ; Cyclooxygenase 2* ; Dactinomycin ; Dinoprostone ; Immunoenzyme Techniques ; Interleukin-1beta* ; Phosphatidylinositol 3-Kinase ; Protein Kinase C