Both direct and indirect environmental stress to brain were increase the expression of transcription factor c-fos in various populations of neurons. In this study, we examined whether the intraperitoneal injections of lidocaine at doses inducing convulsion within 10 min increased the level of c-fos mRNA and protein in forebrain areas. In situ hybridization using (35S)UTP-labeled antisense c-fos, cRNA increased c-fos mRNA levels though hippocampal formation, piriform cortex, septum, caudate-putamen, neostriatum, and amygdala within 2 hr. In parallel with the mRNA expression, c-FOS protein immunoreactivity was also observed in the same forebrain areas. In contrast to the seizure activity and widespread neuronal degeneration following a kainate treatment, injections of lidocaine did not produce neuronal death within 3 days. The present study indicates that lidocaine induces convulsion and c-fos expression without causing neuro-toxicity.
Adult* ; Amygdala ; Animals ; Brain* ; Hippocampus ; Humans ; In Situ Hybridization ; Injections, Intraperitoneal ; Kainic Acid ; Lidocaine* ; Neostriatum ; Neurons ; Prosencephalon ; Rats* ; RNA, Complementary ; RNA, Messenger* ; Seizures ; Transcription Factors

Adult ; Anesthesia ; Colloids ; Dizziness ; Equidae ; Fluid Therapy ; Headache ; Humans ; Orthognathic Surgery ; Postoperative Period ; Pulmonary Edema ; Surveys and Questionnaires ; Sleep Stages ; Surgery, Oral ; Thirst

BACKGROUND: The nasal mucosa is degenerated by inflammations, physical stimulations such as cessation of air flow, and other chemical stimulations. And it is regenerated regularly by newly differentiated cells. OBJECTIVES: In order to investigate the morphologic changes of the nasal mucosa and regenerating activities in sinusitis. MATERIALS AND METHODS: The authors made animal models of acute maxillary sinusitis by obstructing the natural ostium of maxillary sinus of rabbit and inoculating Staphylococcus aureus colonies. Each contralateral side was used as control. The rabbits were sacrificed after 1, 2, and 3 weeks. Morphologic changes of the nasal mucosa and regenerating activities of the olfactory mucosa were observed with Hematoxylin-eosin staining and immunohistochemistry using BrdU. RESULTS: Purulent sinusitis was developed in all rabbits. Light microscopy showed that nasal mucosa revealed inflammatory changes such as edema, inflammatory cell infiltration, goblet cell metaplasia, polypoid change, epithelial ulceration, and submucosal connective tissue proliferation. BrdU-labelled cells were observed mainly in the basal cell layer of the olfactory mucosa, and their numbers in the control sides were significantly higher than in the experimental sides. CONCLUSION: These results indicate that acute infection of the maxillary sinus induces inflammatory changes of both respiratory and olfactory mucosa of the nose and decreases the regenerating activity of olfactory mucosa.
Bromodeoxyuridine ; Connective Tissue ; Edema ; Goblet Cells ; Immunohistochemistry ; Inflammation ; Maxillary Sinus* ; Maxillary Sinusitis* ; Metaplasia ; Microscopy ; Models, Animal ; Nasal Mucosa* ; Nose ; Olfactory Mucosa ; Physical Stimulation ; Rabbits* ; Sinusitis ; Staphylococcus aureus ; Stimulation, Chemical ; Ulcer

Objective: : Spontaneous intracranial hemorrhage is a life-threatening disease, and non-lesional spontaneous intraparenchymal hemorrhage (nIPH) and aneurysmal subarachnoid hemorrhage (aSAH) are the leading causes of spontaneous intracranial hemorrhage. Only a few studies have assessed the association between prior physical activity or triggering events and the occurrence of nIPH or aSAH. The purpose of this study is to investigate the role of specific physical activities and triggering events in the occurrence of nIPH and aSAH. Methods: : We retrospectively reviewed 824 consecutive patients with spontaneous intracranial hemorrhage between January 2010 and December 2018. Among the 824 patients, 132 patients were excluded due to insufficient clinical data and other etiologies of spontaneous intracranial hemorrhage. The medical records of 692 patients were reviewed, and the following parameters were assessed : age, sex, history of hypertension, smoking, history of stroke, use of antiplatelet or anticoagulation agents, season and time of onset, physical activities performed according to the metabolic equivalents, and triggering event at onset. Events that suddenly raised the blood pressure such as sudden postural changes, defecation or urination, sexual intercourse, unexpected emotional stress, sauna bath, and medical examination were defined as triggering events. These clinical data were compared between the nIPH and aSAH groups. Results: : Both nIPH and aSAH most commonly occurred during non-strenuous physical activity, and there was no significant difference between the two groups (p=0.524). Thirty-two patients (6.6%) in the nIPH group and 39 patients (8.1%) in the aSAH group experienced triggering events at onset, and there was a significant difference between the two groups (p=0.034). The most common triggering events were defecation or urination in both groups. Conclusion : Specific physical activity dose no affect the incidence of nIPH and aSAH. The relationship between the occurrence of intracranial hemorrhage and triggering events is higher in aSAH than nIPH.

The enamel matrix derivative (EMD) has been recently used in the periodontal regenerative techniques. The present study was established to investigate the influence of EMD on human periodontal ligament cells using expression of mRNA of periodontal ligament specific gene (PDLs)17, PDLs22, type I collagen when EMD applied to periodontal ligament cells. Periodontal ligament cells were obtained from a healthy periodontium and cultured in Dulbecco's modified Eagle's medium (DMEM) plus 10% fetal bovine serum and beta-glycerophosphate with ascorbic acid. Test groups were two; One adds EMD in culture media and another added EMD and Dexamethasone (DEX) in culture media. Positive control group added DEX in culture media, and negative control group adds niether of EMD nor DEX. Emdogain(R) (Biora, Sweden, 30 mg/ml) was diluted by 75 microgram/ml concentration to culture media. For reverse transcription-polymerase chain reaction (RT-PCR), total RNA isolated on days 0, 7, 14 and 21. mRNA of PDLs17 was expressed on days 14 and 21 in EMD or DEX group, and expressed on days 7, 14 and 21 in EMD plus DEX group, the other side, expressed on days 21 in negative control group. mRNA of PDLs22 expressed on days 7, 14 and 21 in EMD group, and expressed on days 14 and 21 in DEX group, and expressed on days 7, 14 and 21 in EMD plus DEX group. Negative control group expressed on days 14 and 21. Type I collagen was expressed on all days and all groups. These results indicate that EMD promotes differentiation of periodontal ligament cells, and this is considered to offer basis that can apply EMD to periodontal tissue regeneration technique.
Ascorbic Acid ; Collagen Type I ; Culture Media ; Dental Enamel* ; Dexamethasone ; Humans* ; Periodontal Ligament* ; Periodontium ; Regeneration ; RNA ; RNA, Messenger ; Sweden

Leptomeningeal carcinomatosis (LMC) is rare metastatic form of gastric cancer. Most cases are diagnosed in the final stage after multiple distant metastasis. An 84-year-old woman was admitted with melena, headache and vomiting. Esophagogastro-duodenoscopy showed an ulceroinfiltrating lesion at the stomach (Borrmann class III), and biopsy revealed a signet ring cell carcinoma. The abdominal-pelvic CT showed no evidence of metastasis. A sudden decrease of consciousness was noted, but the brain CT showed no active lesion while the brain MRI revealed enhancement of leptomeninges. A lumbar puncture was performed and the cerebrospinal fluid study revealed malignant neoplastic cells. With family consent, no further evaluation and treatment were administered and she died six weeks after the diagnosis of gastric cancer. We report an extremely rare case of a patient who initially presented with neurologic symptoms, and was diagnosed LMC from advanced gastric cancer without any evidence of metastasis in abdomen and pelvis.
Abdomen ; Aged, 80 and over ; Biopsy ; Brain ; Carcinoma, Signet Ring Cell ; Cerebrospinal Fluid ; Consciousness ; Diagnosis ; Female ; Headache ; Humans ; Magnetic Resonance Imaging ; Melena ; Meningeal Carcinomatosis* ; Neoplasm Metastasis ; Neurologic Manifestations ; Pelvis ; Spinal Puncture ; Stomach ; Stomach Neoplasms* ; Vomiting

OBJECTIVE: Infection and bone resorption are major complications of cranioplasty and have been well recognized. However, there are few clinical series describing the epidural fluid collection (EFC) as complication of cranioplasty. This study was planned to identify the predictive factors and fate of EFC after cranioplasty. METHODS: We reviewed retrospectively the demographic, clinical, and radiographic data in 59 patients who underwent a first cranioplsty following decompressive craniectomy during a period of 6 years, from January 2004 to December 2009. We compared demographic, clinical, and radiographic factors between EFC group and no EFC group. The predictive factors associated with the development of EFC were assessed by logistic regression analysis. RESULTS: Overall, 22 of 59 patients (37.3%) suffered from EFC following cranioplasty. EFC had disappeared (n=6, 31.8%) or regressed (n=6, 31.8%) over time on follow up brain computed tomographic (CT) scans. However, 5 patients (22.7%) required reoperation due to symptomatic and persistent EFC. Predictive factors for EFC were male [odds ratio (OR), 5.48; 95% CI, 1.26-23.79], air bubbles in the epidural space (OR, 12.52; 95% CI, 2.26-69.28), and dural calcification on postoperative brain CT scan (OR, 4.21; 95% CI, 1.12-15.84). CONCLUSION: The most of EFCs could be treated by conservative therapy. Air bubble in the epidural space and dural calcification are proposed to be the predictive factors in the formation of EFC after cranioplasty.
Bone Resorption ; Brain ; Decompressive Craniectomy ; Epidural Space ; Follow-Up Studies ; Humans ; Logistic Models ; Male ; Reoperation ; Retrospective Studies ; Tomography, X-Ray Computed

BACKGROUND AND OBJECTIVES: G protein-coupled receptors were considered to be the only natural substrates of G protein-coupled receptor kinases (GRKs). However, it was recently demonstrated that GRKs can also bind to other signal molecules. The purpose of this study was to investigate new molecules that might interact with the GRK5 using a yeast two-hybrid system to screen the cDNA library. MATERIALS AND MEDTHODS: For the yeast two-hybrid system, the "bait" was constructed to generate a LexA-GRK5 fusion protein in the EGY48 yeast strain. Rat library cDNA was inserted into the "prey". The first step in the library screening was performed by a galactose dependent leucine orthotrophism. For the second step screening, a beta-galactosidase dependent discoloration of colonies was used. Sequencing and searching of the gene bank was undertaken to characterize the clones. RESULTS: We screened a total of 1.3X10 6 clones from the cDNA library. On the first screening, 162 clones were identified by leucine orhotrophism. Another 54 clones were identified on the second screening by beta-galactosidase activation. Seven clones were selected by PCR and restriction patterns. Sequencing of seven molecules revealed that four of the clones were emerin fragments, with 2 of the remaining 3 clones being: an ID2 protein and a mitochondrial cytochrome c oxidase subunit II, with the last one remaining an unknown molecule. For the emerin fragments, their interactions with the GRK5 were confirmed by immunoprecipitation. CONCLUSION: We describe the novel protein-protein interactions of the GRK5, specifically, with three molecules. At first, these proteins may modulate the activation of the GRK5 through this specific protein-protein interaction desensitizing the beta-adrenergic receptors. Conversely, the localization of these molecules inside the cell indicates a potential new physiological role for the GRK5.
Animals ; beta-Galactosidase ; Clone Cells ; DNA, Complementary ; Electron Transport Complex IV ; Galactose ; Gene Library ; GTP-Binding Proteins ; Heart ; Immunoprecipitation ; Leucine ; Mass Screening ; Phosphotransferases* ; Polymerase Chain Reaction ; Rats ; Receptors, Adrenergic, beta ; Two-Hybrid System Techniques* ; Yeasts*

PURPOSE: In order to evaluate the effects of GAC, which is the combination of active hexose correlated compound (AHCC) and genistein combined polysaccharide (GCP), we investigated the changes in the biochemical profiles and the quality of life of prostate cancer patients with androgen suppression after the administration of GAC. MATERIALS AND METHODS: Thirty two eligible metastatic prostate cancer patients between the ages of 54 and 84 were enrolled in this study, and they were supplemented with 5g GAC per day (n=23) or placebo (n=9) for a 6 months period. Blood and urine sample analysis were taken and the quality of life (QoL) was assessed using the Visual Analogue Scale (VAS) and the Functional Assessment of Cancer Therapy Scale Questionnaire (FACT-G) at baseline and at post intervention (after 3 and 6 months). RESULTS: Twenty six patients (n=18 in the GAC group and n=8 in the placebo group) completed the 6 months intervention. No statistically significant adverse events were reported by the study participants. GAC had no significant effect on the serum biochemical parameters. However, all 7 GAC-treated hypercholesterolemic patients had their cholesterol level decreased after 3 months treatment (p<0.02). Results of Comet assay showed significant decreases in tail moment (p<0.009) and tail length (p<0.004) at 6 months compared to baseline for the GAC group. Although the results of the VAS were inconsistent, the score for physical well-being was increased in GAC group on the FACT-G analysis (p<0.05 between baseline and 3 months, respectively). CONCLUSIONS: Oral administration of GAC 5g per day for 6 months showed a decrease in DNA damage of blood lymphocytes and in the total serum cholesterol level in hypercholesterolemic patients without any significant influences on the serum biochemical parameters of the metastatic prostate cancer patients. Further studies on the role of GAC are necessary to clarify the advantage of GAC supplementation in prostate cancer patients with androgen suppression.
Administration, Oral ; Cholesterol ; Comet Assay ; DNA Damage ; Genistein ; Humans ; Lymphocytes ; Prostate* ; Prostatic Neoplasms* ; Quality of Life* ; Surveys and Questionnaires

BACKGROUND AND OBJECTIVES: The protective effect of angiotensin converting enzyme (ACE) inhibitor against ischemia/reperfusion injury has been demonstrated in animal models, however the effect of AT1 receptor antagonist is contradictory. The present study was designed to investigate the myocardial protective effects of the AT1 receptor antagonist irbesartan during myocardial ischemia/reperfusion in vivo. MATERIALS AND METHODS: Sprague-Dawley rats were subjected to a 45-minute left coronary artery ligation followed by a 2-hour re-perfusion. An inert vehicle (group I:n=14) or irbesartan (50 mg/kg/day:group II, n=12) was administered for 3 days before coronary occlusion. The ratio of the myocardial infarct area to the ischemic area at risk was assessed through triphenyltetrazolium chloride staining. Apoptosis was evaluated by analyzing DNA fragmentation and TdT-mediated dUDP nick end labeling staining. Western blot analysis was performed for MAP Kinases (ERK1/2 and p38) and Bcl-2 and Bax. RESULTS: The ratio of the infarct area to the ischemic area at risk of group II was smaller than that of group I (42.6+/-2.7% vs. 64.1+/-4.6%;p<0.005). Agarose gel electrophoresis revealed discrete DNA laddering in the ischemic zone of group I, however DNA ladder formation was attenuated in group II. The expressions of ERK1 MAPK and Bcl-2 were increased in the ischemic area of group II compared to that of group I. CONCLUSION: AT1 receptor antagonist was effective in reducing myocardial reperfusion injury in vivo. This effect can at least be partially attributed to the attenuation of cardiomyocyte apoptosis, and this anti-apoptotic effect appears to be related to the increased expression of Bcl-2 and alterations in MAP kinase signaling.
Angiotensin II* ; Angiotensins* ; Animals ; Apoptosis ; Blotting, Western ; Coronary Occlusion ; Coronary Vessels ; DNA ; DNA Fragmentation ; Electrophoresis, Agar Gel ; Ligation ; MAP Kinase Signaling System ; Models, Animal ; Myocardial Infarction ; Myocardial Ischemia* ; Myocardial Reperfusion Injury ; Myocytes, Cardiac ; Peptidyl-Dipeptidase A ; Phosphotransferases ; Rats* ; Rats, Sprague-Dawley ; Receptors, Angiotensin ; Reperfusion Injury* ; Reperfusion*