Background: Histone deacetylase 6 (HDAC6), belonging to class IIb of histone deacetylases, regulates theacetylation of the cytoplasmic protein α-tubulin. The overexpression of HDAC6 is linked to the development oftumors, and inhibiting HDAC6 is known to trigger apoptosis in multiple myeloma cells. In addition to its application in cancer treatment, bortezomib, a proteasome inhibitor, is widely used in managing multiple myeloma and has shown effectiveness in patients with both newly diagnosed and relapsed disease. However, the treatment regimen may be delayed or discontinued due to the risk of peripheral neuropathy, a significant non-hematologic side effect. Methods: Animal models of peripheral neuropathy induced by various anti-cancer drugs were established, confirming the potential of HDAC6 inhibitors as a treatment for this condition. Six- to eight-week-old male Sprague Dawley rats were utilized to create these models. Mechanical allodynia and electron microscopy served as indicators of peripheral neuropathy. The HDAC6 inhibitor CKD-011 was administered at doses of 5, 10, 20, and 40 mg/kg. Results: In an animal model of bortezomib-induced peripheral neuropathy, CKD-011, an HDAC6 inhibitor, effectively ameliorated peripheral neuropathy. Similarly, CKD-011 administration demonstrated recovery from peripheral neuropathy in models induced with oxaliplatin, paclitaxel, and cisplatin. Conclusions These findings suggest that HDAC6 inhibitors have the potential to mitigate peripheral neuropathy induced by chemotherapeutic agents.

Background: Histone deacetylase 6 (HDAC6), belonging to class IIb of histone deacetylases, regulates theacetylation of the cytoplasmic protein α-tubulin. The overexpression of HDAC6 is linked to the development oftumors, and inhibiting HDAC6 is known to trigger apoptosis in multiple myeloma cells. In addition to its application in cancer treatment, bortezomib, a proteasome inhibitor, is widely used in managing multiple myeloma and has shown effectiveness in patients with both newly diagnosed and relapsed disease. However, the treatment regimen may be delayed or discontinued due to the risk of peripheral neuropathy, a significant non-hematologic side effect. Methods: Animal models of peripheral neuropathy induced by various anti-cancer drugs were established, confirming the potential of HDAC6 inhibitors as a treatment for this condition. Six- to eight-week-old male Sprague Dawley rats were utilized to create these models. Mechanical allodynia and electron microscopy served as indicators of peripheral neuropathy. The HDAC6 inhibitor CKD-011 was administered at doses of 5, 10, 20, and 40 mg/kg. Results: In an animal model of bortezomib-induced peripheral neuropathy, CKD-011, an HDAC6 inhibitor, effectively ameliorated peripheral neuropathy. Similarly, CKD-011 administration demonstrated recovery from peripheral neuropathy in models induced with oxaliplatin, paclitaxel, and cisplatin. Conclusions These findings suggest that HDAC6 inhibitors have the potential to mitigate peripheral neuropathy induced by chemotherapeutic agents.

Background: Histone deacetylase 6 (HDAC6), belonging to class IIb of histone deacetylases, regulates theacetylation of the cytoplasmic protein α-tubulin. The overexpression of HDAC6 is linked to the development oftumors, and inhibiting HDAC6 is known to trigger apoptosis in multiple myeloma cells. In addition to its application in cancer treatment, bortezomib, a proteasome inhibitor, is widely used in managing multiple myeloma and has shown effectiveness in patients with both newly diagnosed and relapsed disease. However, the treatment regimen may be delayed or discontinued due to the risk of peripheral neuropathy, a significant non-hematologic side effect. Methods: Animal models of peripheral neuropathy induced by various anti-cancer drugs were established, confirming the potential of HDAC6 inhibitors as a treatment for this condition. Six- to eight-week-old male Sprague Dawley rats were utilized to create these models. Mechanical allodynia and electron microscopy served as indicators of peripheral neuropathy. The HDAC6 inhibitor CKD-011 was administered at doses of 5, 10, 20, and 40 mg/kg. Results: In an animal model of bortezomib-induced peripheral neuropathy, CKD-011, an HDAC6 inhibitor, effectively ameliorated peripheral neuropathy. Similarly, CKD-011 administration demonstrated recovery from peripheral neuropathy in models induced with oxaliplatin, paclitaxel, and cisplatin. Conclusions These findings suggest that HDAC6 inhibitors have the potential to mitigate peripheral neuropathy induced by chemotherapeutic agents.

Background: Histone deacetylase 6 (HDAC6), belonging to class IIb of histone deacetylases, regulates theacetylation of the cytoplasmic protein α-tubulin. The overexpression of HDAC6 is linked to the development oftumors, and inhibiting HDAC6 is known to trigger apoptosis in multiple myeloma cells. In addition to its application in cancer treatment, bortezomib, a proteasome inhibitor, is widely used in managing multiple myeloma and has shown effectiveness in patients with both newly diagnosed and relapsed disease. However, the treatment regimen may be delayed or discontinued due to the risk of peripheral neuropathy, a significant non-hematologic side effect. Methods: Animal models of peripheral neuropathy induced by various anti-cancer drugs were established, confirming the potential of HDAC6 inhibitors as a treatment for this condition. Six- to eight-week-old male Sprague Dawley rats were utilized to create these models. Mechanical allodynia and electron microscopy served as indicators of peripheral neuropathy. The HDAC6 inhibitor CKD-011 was administered at doses of 5, 10, 20, and 40 mg/kg. Results: In an animal model of bortezomib-induced peripheral neuropathy, CKD-011, an HDAC6 inhibitor, effectively ameliorated peripheral neuropathy. Similarly, CKD-011 administration demonstrated recovery from peripheral neuropathy in models induced with oxaliplatin, paclitaxel, and cisplatin. Conclusions These findings suggest that HDAC6 inhibitors have the potential to mitigate peripheral neuropathy induced by chemotherapeutic agents.

Background: Histone deacetylase 6 (HDAC6), belonging to class IIb of histone deacetylases, regulates theacetylation of the cytoplasmic protein α-tubulin. The overexpression of HDAC6 is linked to the development oftumors, and inhibiting HDAC6 is known to trigger apoptosis in multiple myeloma cells. In addition to its application in cancer treatment, bortezomib, a proteasome inhibitor, is widely used in managing multiple myeloma and has shown effectiveness in patients with both newly diagnosed and relapsed disease. However, the treatment regimen may be delayed or discontinued due to the risk of peripheral neuropathy, a significant non-hematologic side effect. Methods: Animal models of peripheral neuropathy induced by various anti-cancer drugs were established, confirming the potential of HDAC6 inhibitors as a treatment for this condition. Six- to eight-week-old male Sprague Dawley rats were utilized to create these models. Mechanical allodynia and electron microscopy served as indicators of peripheral neuropathy. The HDAC6 inhibitor CKD-011 was administered at doses of 5, 10, 20, and 40 mg/kg. Results: In an animal model of bortezomib-induced peripheral neuropathy, CKD-011, an HDAC6 inhibitor, effectively ameliorated peripheral neuropathy. Similarly, CKD-011 administration demonstrated recovery from peripheral neuropathy in models induced with oxaliplatin, paclitaxel, and cisplatin. Conclusions These findings suggest that HDAC6 inhibitors have the potential to mitigate peripheral neuropathy induced by chemotherapeutic agents.

Progressive cognitive declines are the main clinical symptoms of Alzheimer’s disease (AD). Cognitive impairment in AD is directly correlated with amyloid beta (Aβ)-mediated synaptic deficits. It is known that upregulation of neurogranin (Ng), a postsynaptic protein, contributes to the enhancement of synaptic plasticity and cognitive function. By contrast, downregulation of Ng expression results in learning and memory impairments. Interestingly, Ng expression is significantly reduced in the parenchyma of brains with AD. However, the pathological role that downregulated Ng plays in the cognitive dysfunctions observed in AD remains unclear. Therefore, the present study examined whether enhancing Ng expression affected cognitive functions in 5XFAD mice, an animal model of AD. We found that the Ng reductions and cognitive decline observed in 5XFAD mice were restored in mice that were intrahippocampally injected with an Ng-expressing lentiviral vector. Furthermore, overexpression of Ng upregulated expression of postsynaptic density protein-95 in the hippocampus of 5XFAD mice. These results suggest that the cause of cognitive decline in AD may be at least partially associated with reduced Ng levels, and thus, supplementation of Ng may be an appropriate therapeutic strategy for individuals with AD.

PURPOSE: This study was to evaluate the effects of bacterial cellulose (BC) membranes as a barrier membrane on guided bone regeneration (GBR) in comparison with those of the resorbable collagen membranes. MATERIALS AND METHODS: BC membranes were fabricated using biomimetic technology. Surface properties were analyzed, Mechanical properties were measured, in vitro cell proliferation test were performed with NIH3T3 cells and in vivo study were performed with rat calvarial defect and histomorphometric analysis was done. The Mann-Whitney U test and the Wilcoxon signed rank test was used (alpha<.05). RESULTS: BC membrane showed significantly higher mechanical properties such as wet tensile strength than collagen membrane and represented a three-dimensional multilayered structure cross-linked by nano-fibers with 60 % porosity. In vitro study, cell adhesion and proliferation were observed on BC membrane. However, morphology of the cells was found to be less differentiated, and the cell proliferation rate was lower than those of the cells on collagen membrane. In vivo study, the grafted BC membrane did not induce inflammatory response, and maintained adequate space for bone regeneration. An amount of new bone formation in defect region loaded with BC membrane was significantly similar to that of collagen membrane application. CONCLUSION: BC membrane has potential to be used as a barrier membrane, and efficacy of the membrane on GBR is comparable to that of collagen membrane.
Animals ; Biomimetics ; Bone Regeneration* ; Cell Adhesion ; Cell Proliferation ; Cellulose* ; Collagen* ; Membranes* ; Osteogenesis ; Porosity ; Rats ; Surface Properties ; Tensile Strength ; Transplants

OBJECTIVES: Apathy Evaluation Scale (AES) is one of the most frequently used scales to evaluate apathy. The purpose of this study was to evaluate the reliability and validity of the Korean version of the AES (K-AES) and to apply the K-AES in examining the characteristics of apathy in the Korean patients with schizophrenia. METHODS: 129 healthy people and 29 patients with schizophrenia have been evaluated using the K-AES, Physical Anhedonia Scale (PAS), Social Anhedonia Scale (SAS), and the Beck's Depression Inventory (BDI). Split-half reliability and internal consistency were evaluated and factor analysis and correlation analysis was conducted. Between-group comparison was conducted using independent sample t-tests. RESULTS: K-AES showed good reliability and validity. Factor analysis confirmed 3 factors, which represented interest and drive, initiative, self-awareness and self-assessment. Patients with schizophrenia showed significantly higher K-AES and BDI scores than the healthy group. K-AES scores in patients with schizophrenia were significantly correlated with the PAS score, but did not correlate with SAS and BDI scores. CONCLUSION: This study demonstrates the reliability and validity of the K-AES. Our findings also suggest that the K-AES may be a reliable instrument in assessing apathy as a negative symptom in patients with schizophrenia.
Anhedonia ; Apathy* ; Depression ; Factor Analysis, Statistical ; Humans ; Reproducibility of Results* ; Schizophrenia* ; Self-Assessment ; Weights and Measures

BACKGROUND/AIMS: Little information is available on whether the speed of eating differs between individuals with and without dyspepsia, mainly because controlled studies are usually not feasible. METHODS: A survey was applied to 89 individuals with relatively controlled eating patterns, using questionnaires that assessed eating time and functional dyspepsia (FD) based on the Rome III criteria. RESULTS: The prevalence of FD was 12% (11 of 89 participants), and 7% (6 of 89) were diagnosed with gastroesophageal reflux disease (GERD). The proportion of individuals reporting that they ate their meals rapidly was higher for those with FD than for those without FD or GERD (control) (46% vs 17%, p=0.043), as was the reported eating speed (7.1+/-1.5 vs 5.8+/-2.0 [mean+/-SD], p=0.045; visual analog scale on which a higher score indicated faster eating). However, the measured eating time did not differ significantly between FD and controls (11.0+/-2.8 vs 12.8+/-3.3 minutes, p=0.098). The proportion of individuals who ate their meals within 13 minutes was significantly higher for those with FD than for controls (91% vs 51%, p=0.020). CONCLUSIONS: The results of this study suggest that eating speed affects dyspepsia. Further studies are warranted.
Dyspepsia ; Eating ; Female ; Food Habits ; Gastroesophageal Reflux ; Humans ; Meals ; Prevalence ; Rome ; Surveys and Questionnaires

BACKGROUND/AIMS: The aims of this study were to estimate the frequency of symptoms of gastroesophageal reflux disease and reflux esophagitis, to evaluate the difference in characteristics among groups subdivided by symptoms, and to compare clinical features between a reflux esophagitis group and a non reflux esophagitis group in Chuncheon City. METHODS: A total of 1,011 persons who underwent endoscopy for health check up were enrolled between July 1, 2005, and June 30, 2006. All persons were given a validated, self reported questionnaire, which inquired about the presence, frequency, and severity of typical symptoms (heartburn and acid regurgitation) and atypical symptoms. The questionnaire also inquired about smoking, alcohol intake, and Helicobacter pyroli eradication. The subjects were subdivided into typical symptomatic, atypical symptomatic, no discomfort, and asymptomatic groups. RESULTS: The prevalence of heartburn and acid regurgitation occurring at least weekly was 7.5%. Reflux esophagitis, hiatal hernia, smoking, and alcohol intake were more common in males (p<0.05). Ninety eight cases (9.7%) were endoscopically diagnosed as reflux esophagitis, and sixty nine cases (6.8%) were endoscopically suspected esophageal metaplasia (ESEM). Subjects in the symptomatic group more frequently manifested reflux esophagitis than subjects in the asymptomatic group (p<0.05). CONCLUSIONS: The presence of reflux induced symptoms is related to reflux esophagitis, but the intensity and frequency of symptoms are poor predictors of the presence or severity of endoscopic mucosal breaks.
Barrett Esophagus ; Endoscopy ; Esophagitis ; Esophagitis, Peptic ; Gastroesophageal Reflux ; Heartburn ; Helicobacter ; Hernia, Hiatal ; Humans ; Male ; Metaplasia ; Prevalence ; Self Report ; Smoke ; Smoking ; Surveys and Questionnaires