Objective: This study examined the efficacy of artificial intelligence (AI) algorithm-based diagnostic assistant solutions in the interpretation of brain computed tomography (CT) by emergency medicine (EM) residents. Methods: This study included 350 patients who visited a local emergency medical center over 5 months and underwent brain CT scans. EM residents initially interpreted the patients’ scans. A second interpretation was performed using an AI algorithm-based solution. The initial and second interpretations were compared with that of a radiology physician. Results: The first interpretation by EM residents showed agreement in 318 cases (90.9%), while the second, assisted by an AI algorithm-based solution, showed agreement in 308 cases (88.0%). The first interpretation had an accuracy, sensitivity, and specificity of 93.1%, 43.9%, and 99.7%, respectively, and the second had an accuracy, sensitivity, and specificity of 92.0%, 39.0%, and 99.0%, respectively (P<0.001). Most of the discrepancies observed in the first and second interpretations were classified as Grade 1. Conclusion The interpretations assisted by the AI algorithm-based solution resulted in lower accuracy and higher discrepancy rates than independent interpretations by EM residents. The AI algorithm-based solution provided efficacy in accurate interpretation depending on the cases. Further study will be needed to address the weaknesses of the function and utility of AI.

Purpose: To compare long-term disease-free survival (DFS) between patients receiving tegafur/gimeracil/oteracil (S-1) or capecitabine plus oxaliplatin (CAPOX) adjuvant chemotherapy (AC) for gastric cancer (GC). Materials and Methods: This retrospective multicenter observational study enrolled 983 patients who underwent curative gastrectomy with consecutive AC with S-1 or CAPOX for stage II or III GC at 27 hospitals in Korea between February 2012 and December 2013. We conducted propensity score matching to reduce selection bias. Long-term oncologic outcomes, including DFS rate over 5 years (over-5yr DFS), were analyzed postoperatively. Results: The median and longest follow-up period were 59.0 and 87.6 months, respectively. DFS rate did not differ between patients who received S-1 and CAPOX for pathologic stage II (P=0.677) and stage III (P=0.899) GC. Moreover, hazard ratio (HR) for recurrence did not differ significantly between S-1 and CAPOX (reference) in stage II (HR, 1.846; 95% confidence interval [CI], 0.693–4.919; P=0.220) and stage III (HR, 0.942; 95% CI, 0.664–1.337; P=0.738) GC. After adjustment for significance in multivariate analysis, pT (4 vs. 1) (HR, 11.667; 95% CI, 1.595–85.351; P=0.016), pN stage (0 vs. 3) (HR, 2.788; 95% CI, 1.502–5.174; P=0.001), and completion of planned chemotherapy (HR, 2.213; 95% CI, 1.618–3.028; P<0.001) were determined as independent prognostic factors for DFS. Conclusions S-1 and CAPOX AC regimens did not show significant difference in over-5yr DFS after curative gastrectomy in patients with stage II or III GC. The pT, pN stage, and completion of planned chemotherapy were prognostic factors for GC recurrence.

PURPOSE: Laparoscopy-assisted distal gastrectomy for early gastric cancer has gained acceptance and popularity worldwide. However, laparoscopy-assisted distal gastrectomy for advanced gastric cancer is still controversial. Therefore, we propose this prospective randomized controlled multi-center trial in order to evaluate the safety and feasibility of laparoscopy assisted D2-gastrectomy for advanced stage gastric cancer. MATERIALS AND METHODS: Patients undergoing distal gastrectomy for advanced gastric cancer staged cT2/3/4 cN0/1/2/3a cM0 by endoscopy and computed tomography are eligible for enrollment after giving their informed consent. Patients will be randomized either to laparoscopy-assisted distal gastrectomy or open distal gastrectomy. Sample size calculation revealed that 102 patients are to be included per treatment arm. The primary endpoint is the non-compliance rate of D2 dissection; relevant secondary endpoints are three-year disease free survival, surgical and postoperative complications, hospital stay and unanimity rate of D2 dissection evaluated by reviewing the intraoperative video documentation. DISCUSSION: Oncologic safety is the major concern regarding laparoscopy-assisted distal gastrectomy for advanced gastric cancer. Therefore, the non-compliance rate of clearing the N2 area was chosen as the most important parameter for the technical feasibility of the laparoscopic procedure. Furthermore, surgical quality will be carefully reviewed, that is, three independent experts will review the video records and score with a check list. For a long-term result, disease free survival is considered a secondary endpoint for this trial. This study will offer promising evidence of the feasibility and safety of Laparoscopy-assisted distal gastrectomy for advanced gastric cancer.Trial Registration: NCT01088204 (international), NCCCTS-09-448 (Korea).
Arm ; Disease-Free Survival ; Endoscopy ; Gastrectomy ; Humans ; Informed Consent ; Laparoscopy ; Length of Stay ; Lymph Node Excision ; Lymph Nodes ; Postoperative Complications ; Prospective Studies ; Sample Size ; Stomach Neoplasms

PURPOSE: Transforming growth factor (TGF)-beta1 reportedly increases neuronal survival by inhibiting the induction of inducible nitric oxide synthase (NOS) in astrocytes and protecting neurons after excitotoxic injury. However, the neuroprotective mechanism of TGF-beta1 on hypoxic-ischemic (HI) brain injury in neonatal rats is not clear. The aim of this study was to determine whether TGF-beta1 has neuroprotective effects via a NO-mediated mechanism and N-methyl-D-aspartate (NMDA) receptor modulation on perinatal HI brain injury. METHODS: Cortical cells were cultured using 19-day-pregnant Sprague-Dawley (SD) rats treated with TGF-beta1 (1, 5, or 10 ng/mL) and incubated in a 1% O2 incubator for hypoxia. Seven-day-old SD rat pups were subjected to left carotid occlusion followed by 2 h of hypoxic exposure (7.5% O2). TGF-beta1 (0.5 ng/kg) was administered intracerebrally to the rats 30 min before HI brain injury. The expressions of NOS and NMDA receptors were measured. RESULTS: In the in vitro model, the expressions of endothelial NOS (eNOS) and neuronal NOS (nNOS) increased in the hypoxic group and decreased in the 1 ng/mL TGF-beta1-treated group. In the in vivo model, the expression of inducible NOS (iNOS) decreased in the hypoxia group and increased in the TGF-beta1-treated group. The expressions of eNOS and nNOS were reversed compared with the expression of iNOS. The expressions of all NMDA receptor subunits decreased in hypoxia group and increased in the TGF-beta1-treated group except NR2C. CONCLUSION: The administration of TGF-beta1 could significantly protect against perinatal HI brain injury via some parts of the NO-mediated or excitotoxic mechanism.
Animals ; Anoxia ; Astrocytes ; Brain ; Brain Injuries ; Incubators ; Ischemia ; N-Methylaspartate ; Neurons ; Neuroprotective Agents ; Nitric Oxide ; Nitric Oxide Synthase ; Nitric Oxide Synthase Type II ; Rats ; Receptors, N-Methyl-D-Aspartate ; Transforming Growth Factor beta1 ; Transforming Growth Factors

PURPOSE: Transforming growth factor (TGF)-beta1 reportedly increases neuronal survival by inhibiting the induction of inducible nitric oxide synthase (NOS) in astrocytes and protecting neurons after excitotoxic injury. However, the neuroprotective mechanism of TGF-beta1 on hypoxic-ischemic (HI) brain injury in neonatal rats is not clear. The aim of this study was to determine whether TGF-beta1 has neuroprotective effects via a NO-mediated mechanism and N-methyl-D-aspartate (NMDA) receptor modulation on perinatal HI brain injury. METHODS: Cortical cells were cultured using 19-day-pregnant Sprague-Dawley (SD) rats treated with TGF-beta1 (1, 5, or 10 ng/mL) and incubated in a 1% O2 incubator for hypoxia. Seven-day-old SD rat pups were subjected to left carotid occlusion followed by 2 h of hypoxic exposure (7.5% O2). TGF-beta1 (0.5 ng/kg) was administered intracerebrally to the rats 30 min before HI brain injury. The expressions of NOS and NMDA receptors were measured. RESULTS: In the in vitro model, the expressions of endothelial NOS (eNOS) and neuronal NOS (nNOS) increased in the hypoxic group and decreased in the 1 ng/mL TGF-beta1-treated group. In the in vivo model, the expression of inducible NOS (iNOS) decreased in the hypoxia group and increased in the TGF-beta1-treated group. The expressions of eNOS and nNOS were reversed compared with the expression of iNOS. The expressions of all NMDA receptor subunits decreased in hypoxia group and increased in the TGF-beta1-treated group except NR2C. CONCLUSION: The administration of TGF-beta1 could significantly protect against perinatal HI brain injury via some parts of the NO-mediated or excitotoxic mechanism.
Animals ; Anoxia ; Astrocytes ; Brain ; Brain Injuries ; Incubators ; Ischemia ; N-Methylaspartate ; Neurons ; Neuroprotective Agents ; Nitric Oxide ; Nitric Oxide Synthase ; Nitric Oxide Synthase Type II ; Rats ; Receptors, N-Methyl-D-Aspartate ; Transforming Growth Factor beta1 ; Transforming Growth Factors

PURPOSE: Resveratrol, extracted from red wine and grapes, has an anti-cancer effect, an antiinflammatory effect, and an antioxidative effect mainly in heart disease and also has neuroprotective effects in the adult animal model. No studies for neuroprotective effects during the neonatal periods have been reported. Therefore, we studied the neuroprotective effect of resveratrol on hypoxic-ischemic brain damage in neonatal rats via anti-apoptosis. METHODS: Embryonic cortical neuronal cell culture of rat brain was performed using pregnant Sprague-Dawley (SD) rats at 18 days of gestation (E1 8) for the in vitro approach. We injured the cells with hypoxia and administered resveratrol (1, 10, and 30 microg/mL) to the cells at 30 minutes before hypoxic insults. In addition, unilateral carotid artery ligation with hypoxia was induced in 7 -day-old neonatal rats for the in vivo approach. We injected resveratrol (30 mg/kg) intraperitoneally into animal models. Real-time PCR and Western blotting were performed to identify the neuroprotective effects of resveratrol through anti-apoptosis. RESULTS: In the in vitro approach of hypoxia, the expression of Bax, caspase-3, and the ratio of Bax/Bcl-2, indicators of the level of apoptosis, were significantly increased in the hypoxia group compared to the normoxia group. In the case of the resveratrol-treated group, expression was significantly decreased compared to the hypoxia group. And the results in the in vivo approach were the same as in the in vitro approach. CONCLUSION: The present study demonstrates that resveratrol plays neuroprotective role in hypoxic-ischemic brain damage during neonatal periods through the mechanism of anti-apoptosis.
Adult ; Animals ; Anoxia ; Apoptosis ; Blotting, Western ; Brain ; Brain Injuries ; Carotid Arteries ; Caspase 3 ; Cell Culture Techniques ; Heart Diseases ; Humans ; Infant, Newborn ; Ligation ; Models, Animal ; Neurons ; Neuroprotective Agents ; Pregnancy ; Rats ; Real-Time Polymerase Chain Reaction ; Stilbenes ; Vitis ; Wine

OBJECTIVE: Resveratrol, a polyphenolic phytoalexin, is extracted abundantly from the red wine and grapes and biosynthesized as a defense agent to infection, ultraviolet and ozon etc. Recently, The cancer-preventive, anti-inflammatory and anti-oxidative effects of resveratrol have been reported. The aim of this study was to investigate the effect of resveratrol on the expression of nitric oxide synthases in hypoxic-ischemic brain injury in the neonatal rat model. METHODS: Embryonic cortical neuronal cell culture of rat brain was performed with pregnant Sprague-Dawley (SD) rats at 18 days of gestation (E18) for in vitro approaches. In addition, unilateral carotid artery ligation was induced in seven-days old neonatal rats for in vivo approaches. The real-time PCR using iNOS, eNOS and nNOS primer, and the western blotting using the same antibodies were done to identify the effects of resveratrol. RESULTS: The expression of iNOS, eNOS and nNOS in both cell culture and animal model of neonatal HI brain injury revealed that, as indicated by western blotting and real-time PCR, the expression of iNOS was decreased in the hypoxia group while those of eNOS and nNOS were increased in the hypoxia group compared with the normoxia group. The expression of iNOS was increased in the resveratrol-treated group while those of eNOS and nNOS decreased in the resveratrol-treated group compared with a hypoxic group. CONCLUSION: The present study demonstrates resveratrol might affect nitric oxide synthases expression in HI injury of the perinatal period
Animals ; Anoxia ; Antibodies ; Blotting, Western ; Brain ; Brain Injuries ; Carotid Arteries ; Cell Culture Techniques ; Ligation ; Models, Animal ; Neurons ; Nitric Oxide ; Pregnancy ; Rats ; Real-Time Polymerase Chain Reaction ; Sesquiterpenes ; Stilbenes ; Vitis ; Wine

Duplication of chromosome 12p has been rarely reported and are thought to be associated with congenital malformations and impaired development. We report a baby boy born with multiple dysmorphic features and congenital malformations. His karyotype was 46,XY, add(12)(p13.3). He has suffered from intrauterine growth restriction at birth. He showed abnormal cranio-facial findings such as microcephaly, hypognathia, clepft palate and low set ear. He presented with absence of uvula, micropenis and rocker bottom features of both feet, congenital heart disease, poor corticomedullary differentiation of kidney, and sensorineuronal hearing loss. We have been follow up him for seizure disorder and delayed development at out patient department.
Chromosomes, Human, Pair 12 ; Ear ; Epilepsy ; Follow-Up Studies ; Foot ; Genital Diseases, Male ; Hearing Loss ; Heart Diseases ; Humans ; Karyotype ; Kidney ; Microcephaly ; Palate ; Parturition ; Penis ; Uvula

PURPOSE: Mycophenolic acid (MPA), a potent inhibitor of inosine-monophosphate dehydrogenase (IMPDH), was used as a new immunosuppressive drug since 1990s. It was reported that MPA increased neuronal survival after excitotoxic injury, induced apoptosis in microglial cells, inhibited the induction of inducible nitric oxide synthase (iNOS) in astrocytes. and inhibited microglial cell proliferation in N-methyl-D-aspartate (NMDA) induced hippocampal cells. However, the effects of MPA on the perinatal hypoxic-ischemic (HI) brain injury had not been yet evaluated. Therefore, we examined whether MPA could be neuroprotective in the HI brain injury. METHODS: Cortical cells were cultured using a 18-day-pregnant Sprague-Dawley (SD) rats and incubated in 1% O2 incubator for hypoxia. MPA (10 ug/mL) before or after a HI insult were treated. Seven-day-old SD rat pups were subjected to left carotid occlusion followed by 2.5 hours of hypoxic exposure (8% O2). MPA (10 mg/kg) were administrated intraperitoneally before or after a HI insult. Nitric oxide (NO) activity and expression of N-methyl-D-aspartate (NMDA) receptors also measured using Real-time PCR with primer pairs of isoforms of NOS; iNOS, endothelial NOS (eNOS), neuronal NOS (nNOS), and subunits of NMDA receptors; NR1, NR2A, NR2B, NR2C, NR2D. RESULTS: The expression of iNOS was decreased in the hypoxia group but increased in the MPA-treated group. However express or that eNOS and nNOS were inversed. The expression of all NMDA receptor subunits except NR2B was decreased in the hypoxia group but increased in the MPA-treated group. CONCLUSION: This study indicates that the administration of MPA before a HI insult could significantly protect against perinatal HI brain injury via some parts of NO-mediated or excitotoxic mechanisms.
Animals ; Anoxia ; Apoptosis ; Astrocytes ; Brain Injuries* ; Brain* ; Cell Proliferation ; Incubators ; Mycophenolic Acid* ; N-Methylaspartate* ; Neurons ; Nitric Oxide Synthase Type II ; Nitric Oxide Synthase* ; Nitric Oxide* ; Oxidoreductases ; Protein Isoforms* ; Rats ; Rats, Sprague-Dawley ; Real-Time Polymerase Chain Reaction ; Receptors, N-Methyl-D-Aspartate

PURPOSE: Mycophenolic acid (MPA), the active metabolite of mycophenolate mofetil (MMF), is a potent inhibitor of inosine-monophosphate dehydrogenase (IMPDH), a new immunosuppressive drug used. It was reported that MPA protected neurons after excitotoxic injury, induced apoptosis in microglial cells. However, the effects of MPA on hypoxic-ischemic (HI) brain injury has not been yet evaluated. Therefore, we examined whether MPA could be neuroprotective in perinatal HI brain injury using Rice-Vannucci model (in vivo) and in rat brain cortical cell culture induced by hypoxia (in vitro). METHODS: Cortical cells were cultured using a 18-day-pregnant Sprague-Dawley (SD) rats and incubated in 1% O2 incubator for hypoxia. MPA (10 microgram/mL) before or after a HI insult was treated. Seven-day-old SD rat pups were subjected to left carotid occlusion followed by 2 hours of hypoxic exposure (8% O2). MPA (10 mg/kg) before or after a HI insult were administrated intraperitoneally. Apoptosis was measured using western blot and real-time PCR for Bcl-2, Bax, caspase-3. RESULTS: H&E stain revealed increased brain volume in the MPA-treated group in vivo animal model of neonatal HI brain injury. Western blot and real-time PCR showed the expression of caspase-3 and Bax/Bcl-2 were decreased in the MPA-treated group In in vitro and in vivo model of perinatal HI brain injury, CONCLUSION: These results may suggest that the administration of MPA before HI insult could significantly protect against perinatal HI brain injury via anti-apoptotic mechanisms, which offers the possibility of MPA application for the treatment of neonatal HI encephalopathy.
Animals ; Anoxia ; Apoptosis ; Blotting, Western ; Brain Injuries* ; Brain* ; Caspase 3 ; Cell Culture Techniques ; Incubators ; Models, Animal ; Mycophenolic Acid* ; Neurons ; Neuroprotective Agents* ; Oxidoreductases ; Rats ; Rats, Sprague-Dawley ; Real-Time Polymerase Chain Reaction