A nerve block is an effective tool for diagnostic and therapeutic methods. If a diagnostic nerve block is successful for pain relief and the subsequent therapeutic nerve block is effective for only a limited duration, the next step that should be considered is a nerve ablation or modulation. The nerve ablation causes iatrogenic neural degeneration aiming only for sensory or sympathetic denervation without motor deficits. Nerve ablation produces the interruption of axonal continuity, degeneration of nerve fibers distal to the lesion (Wallerian degeneration), and the eventual death of axotomized neurons. The nerve ablation methods currently available for resection/removal of innervation are performed by either chemical or thermal ablation. Meanwhile, the nerve modulation method for interruption of innervation is performed using an electromagnetic field of pulsed radiofrequency. According to Sunderland's classification, it is first and foremost suggested that current neural ablations produce third degree peripheral nerve injury (PNI) to the myelin, axon, and endoneurium without any disruption of the fascicular arrangement, perineurium, and epineurium. The merit of Sunderland's third degree PNI is to produce a reversible injury. However, its shortcoming is the recurrence of pain and the necessity of repeated ablative procedures. The molecular mechanisms related to axonal regeneration after injury include cross-talk between axons and glial cells, neurotrophic factors, extracellular matrix molecules, and their receptors. It is essential to establish a safe, long-standing denervation method without any complications in future practices based on the mechanisms of nerve degeneration as well as following regeneration.

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ObjectiveAdenomyosis and endometriosis are relatively common gynecological diseases that exhibit many common features. This study identified gynecological and non-gynecological diseases that exhibited comorbidity with adenomyosis and endometriosis in Korean women.MethodsWe used Health Insurance Review and Assessment data from 2009 to 2011 and searched for adenomyosis and endometriosis (coded as N80.1 and D25 in International Classification of Disease, 10th revision [ICD-10], respectively). We selected records from patients who had independent disease occurrences in each year, and comorbidities were estimated using Fisher's exact test. We computed each year's similarities and combined 3 years' results using Fisher's P-value summation method.ResultsA total of 61,516 patients' data were collected during the study period. The prevalence of adenomyosis and endometriosis were similar each year: 12.4% and 9.3% in 2009, 12.5% and 9.4% in 2010 and 13.3% and 9.1% in 2011, respectively. Meta-analysis revealed that 31 ICD-10 codes were significantly related with adenomyosis, and 44 ICD-10 codes were related with endometriosis. Gynecological diseases, such as leiomyoma and benign ovarian tumor, were significantly related to adenomyosis and endometriosis. Non-gynecological diseases, such as anemia and hypercholesterolemia, were also related to adenomyosis and endometriosis.ConclusionWe must monitor for the presence of gynecological and non-gynecological diseases with co-morbidities during evaluations and follow-up of patients with adenomyosis or endometriosis.

Background: The endothelial glycocalyx layer (EGL) coats the alveolar capillary endothelium and plays important roles in pulmonary vascular protection, modulation, and hemostasis. Ischemia-reperfusion, which occurs during lung resection surgery with one lung ventilation (OLV), can damage the EGL. Sevoflurane is known for its protective effect against ischemia-reperfusion injury. Therefore, we hypothesized that lung resection surgery produces EGL damage and sevoflurane protects the EGL better than the intravenous anesthetic propofol. Methods: Seventy-eight patients undergoing pulmonary resection were randomly allocated into the sevoflurane (n=38) and propofol (n=40) groups. All patients received OLV and protective ventilation under sevoflurane-or propofol-based anesthesia. The concentrations of EGL injury markers (heparan sulfate and human syndecan-1) and an inflammatory marker (vascular cell adhesion molecule-1) were measured from blood samples drawn at five time points (after induction, 60 min after OLV, 120 min after OLV, end of OLV, and end of surgery). Results: OLV increased the concentrations of EGL injury markers; heparan sulfate concentrations increased from 120 minutes after OLV (120 minutes after OLV: sevoflurane, 13.3±6.8 ng/mL, P<0.05; propofol, 14.8±6.9 ng/mL, P<0.05). Human syndecan-1 concentrations also increased from 120 minutes after OLV (120 minutes after OLV: sevoflurane, 20.4±8.9 ng/mL, P<0.05; propofol, 20.5±11.8 ng/mL, P>0.05). However, no difference in EGL injury markers was observed between the sevoflurane and propofol groups at any time point. Vascular cell adhesion molecule-1 concentrations did not show any temporal changes in either group. Conclusions: Lung resection surgery with OLV produced EGL damage without any increase in inflammation. Although shedding of heparan sulfate induced by EGL injury during lung resection surgery with OLV, was less than propofol, it was not statistically significant.

Diminished ANK3 contributes to cell survival by inhibiting detachment-induced apoptosis. TP53BP1 that interacts with p53 and MFN1 that encodes a mitochondrial membrane protein are considered to have tumor suppressor gene (TSG) functions. HACD4 involving fatty acid synthesis and TCPL10 with transcription regulation functions are considered TSGs. Many genes involved in DNA methylations such as LCMT2, RNMT, TRMT6, METTL8 and METTL16 are often perturbed in cancer. The aim of our study was to find whether these genes were mutated in colorectal cancer (CRC). In a genome database, we observed that each of these genes harbored mononucleotide repeats in the coding sequences, which could be mutated in cancers with high microsatellite instability (MSI-H). For this, we studied 124 CRCs for the frameshift mutations of these genes and their intratumoral heterogeneity (ITH). ANK3, HACD4, TCP10L, TP53BP1, MFN1, LCMT2, RNMT, TRMT6, METTL8 and METTL16 harbored 11 (13.9%), 3 (3.8%), 0 (0%), 5 (6.3%), 1 (1.3%), 2 (2.5%), 4 (5.1%), 3 (3.8%), 2 (2.5%) and 2 (2.5%) of 79 CRCs with MSI-H, respectively. However, we found no such mutations in microsatellite stable (MSS) cancers in the nucleotide repeats. There were ITH of the frameshift mutations of ANK3, MFN1 and TP53BP1 in 1 (6.3%), 1 (6.3%) and 1 (6.3%) cases, respectively. Our data exhibit that cancer-related genes ANK3, HACD4, TP53BP1, MFN1, LCMT2, RNMT, TRMT6, METTL8 and METTL16 harbor mutational ITH as well as the frameshift mutations in CRC with MSI-H. Also, the results suggest that frameshift mutations of these genes might play a role in tumorigenesis through their inactivation in CRC.