Acanthamoeba is an opportunistic pathogen that causes Acanthamoeba keratitis, granulomatous amoebic encephalitis, and other cutaneous diseases. The life cycle of Acanthamoeba consists of 2 stages of trophozoites and cysts. Under adverse environmental conditions, Acanthamoeba encysts, while the conditions become favorable for growth, it reverts to the trophozoite form. Acanthamoeba excystation is crucial for its proliferation and can lead to recurrent infections after incomplete treatment. To identify the factors involved in excystation, A. castellanii was subjected to either encystation- or excystation-inducing conditions, and gene expression profiles were compared using mRNA sequencing. A. castellanii samples were collected at 8 h intervals for analysis under both conditions. Differentially expressed gene analysis revealed that 1,214 and 1,163 genes were upregulated and downregulated, respectively, by more than 2-fold during early excystation. Five genes markedly upregulated in early excystation (ACA1_031140, ACA1_032330, ACA1_374400, ACA1_275740, and ACA1_112650) were selected, and their expression levels were confirmed via real-time PCR. Small interfering RNA (siRNA) targeting these 5 genes was transfected into Acanthamoeba and gene knockdown was validated through real-time PCR. The silencing of ACA1_031140, ACA1_032330, ACA1_374400, and ACA1_112650 inhibited excystation and suggested that these genes might be essential for excystation. Our findings provide valuable insights for suppressing Acanthamoeba proliferation and recurrence.

Acanthamoeba is an opportunistic pathogen that causes Acanthamoeba keratitis, granulomatous amoebic encephalitis, and other cutaneous diseases. The life cycle of Acanthamoeba consists of 2 stages of trophozoites and cysts. Under adverse environmental conditions, Acanthamoeba encysts, while the conditions become favorable for growth, it reverts to the trophozoite form. Acanthamoeba excystation is crucial for its proliferation and can lead to recurrent infections after incomplete treatment. To identify the factors involved in excystation, A. castellanii was subjected to either encystation- or excystation-inducing conditions, and gene expression profiles were compared using mRNA sequencing. A. castellanii samples were collected at 8 h intervals for analysis under both conditions. Differentially expressed gene analysis revealed that 1,214 and 1,163 genes were upregulated and downregulated, respectively, by more than 2-fold during early excystation. Five genes markedly upregulated in early excystation (ACA1_031140, ACA1_032330, ACA1_374400, ACA1_275740, and ACA1_112650) were selected, and their expression levels were confirmed via real-time PCR. Small interfering RNA (siRNA) targeting these 5 genes was transfected into Acanthamoeba and gene knockdown was validated through real-time PCR. The silencing of ACA1_031140, ACA1_032330, ACA1_374400, and ACA1_112650 inhibited excystation and suggested that these genes might be essential for excystation. Our findings provide valuable insights for suppressing Acanthamoeba proliferation and recurrence.

Acanthamoeba is an opportunistic pathogen that causes Acanthamoeba keratitis, granulomatous amoebic encephalitis, and other cutaneous diseases. The life cycle of Acanthamoeba consists of 2 stages of trophozoites and cysts. Under adverse environmental conditions, Acanthamoeba encysts, while the conditions become favorable for growth, it reverts to the trophozoite form. Acanthamoeba excystation is crucial for its proliferation and can lead to recurrent infections after incomplete treatment. To identify the factors involved in excystation, A. castellanii was subjected to either encystation- or excystation-inducing conditions, and gene expression profiles were compared using mRNA sequencing. A. castellanii samples were collected at 8 h intervals for analysis under both conditions. Differentially expressed gene analysis revealed that 1,214 and 1,163 genes were upregulated and downregulated, respectively, by more than 2-fold during early excystation. Five genes markedly upregulated in early excystation (ACA1_031140, ACA1_032330, ACA1_374400, ACA1_275740, and ACA1_112650) were selected, and their expression levels were confirmed via real-time PCR. Small interfering RNA (siRNA) targeting these 5 genes was transfected into Acanthamoeba and gene knockdown was validated through real-time PCR. The silencing of ACA1_031140, ACA1_032330, ACA1_374400, and ACA1_112650 inhibited excystation and suggested that these genes might be essential for excystation. Our findings provide valuable insights for suppressing Acanthamoeba proliferation and recurrence.

Acanthamoeba is an opportunistic pathogen that causes Acanthamoeba keratitis, granulomatous amoebic encephalitis, and other cutaneous diseases. The life cycle of Acanthamoeba consists of 2 stages of trophozoites and cysts. Under adverse environmental conditions, Acanthamoeba encysts, while the conditions become favorable for growth, it reverts to the trophozoite form. Acanthamoeba excystation is crucial for its proliferation and can lead to recurrent infections after incomplete treatment. To identify the factors involved in excystation, A. castellanii was subjected to either encystation- or excystation-inducing conditions, and gene expression profiles were compared using mRNA sequencing. A. castellanii samples were collected at 8 h intervals for analysis under both conditions. Differentially expressed gene analysis revealed that 1,214 and 1,163 genes were upregulated and downregulated, respectively, by more than 2-fold during early excystation. Five genes markedly upregulated in early excystation (ACA1_031140, ACA1_032330, ACA1_374400, ACA1_275740, and ACA1_112650) were selected, and their expression levels were confirmed via real-time PCR. Small interfering RNA (siRNA) targeting these 5 genes was transfected into Acanthamoeba and gene knockdown was validated through real-time PCR. The silencing of ACA1_031140, ACA1_032330, ACA1_374400, and ACA1_112650 inhibited excystation and suggested that these genes might be essential for excystation. Our findings provide valuable insights for suppressing Acanthamoeba proliferation and recurrence.

Acanthamoeba is an opportunistic pathogen that causes Acanthamoeba keratitis, granulomatous amoebic encephalitis, and other cutaneous diseases. The life cycle of Acanthamoeba consists of 2 stages of trophozoites and cysts. Under adverse environmental conditions, Acanthamoeba encysts, while the conditions become favorable for growth, it reverts to the trophozoite form. Acanthamoeba excystation is crucial for its proliferation and can lead to recurrent infections after incomplete treatment. To identify the factors involved in excystation, A. castellanii was subjected to either encystation- or excystation-inducing conditions, and gene expression profiles were compared using mRNA sequencing. A. castellanii samples were collected at 8 h intervals for analysis under both conditions. Differentially expressed gene analysis revealed that 1,214 and 1,163 genes were upregulated and downregulated, respectively, by more than 2-fold during early excystation. Five genes markedly upregulated in early excystation (ACA1_031140, ACA1_032330, ACA1_374400, ACA1_275740, and ACA1_112650) were selected, and their expression levels were confirmed via real-time PCR. Small interfering RNA (siRNA) targeting these 5 genes was transfected into Acanthamoeba and gene knockdown was validated through real-time PCR. The silencing of ACA1_031140, ACA1_032330, ACA1_374400, and ACA1_112650 inhibited excystation and suggested that these genes might be essential for excystation. Our findings provide valuable insights for suppressing Acanthamoeba proliferation and recurrence.

Objective: Microsurgical treatment could be a good alternative for the treatment of recurrent cerebral aneurysm after coil embolization. The purpose of this study was to present our experience of microsurgical treatment for recurrent cerebral aneurysm previously treated using coil embolization. Methods: From June 2012 to May 2019, 34 patients consecutively received microsurgical treatment for a recurrent cerebral aneurysm previously treated using coil embolization after it ruptured. Results: Of the 34 patients with aneurysm, 33 had the aneurysm located in the anterior circulation. The most common location was the anterior communicating artery (13 cases). Immediate radiologic outcome at coil embolization was completed (n=6), residual neck (n=26), and residual sac (n=2). The reason for microsurgical treatment included rebleeding (n=12), persistent residual sac (n=1), and recurrence on follow-up study (n=21). Rebleeding occurred within 10 days after coil embolization in 10 cases, and the other 2 were due to regrowth. In the 20 recurred and saccular aneurysms, coil compaction was present in 11 aneurysms and regrowth in 9 aneurysms. Simple neck clipping (n=29) and clipping with coil mass extraction (n=3) was possible in the saccular aneurysms. The blood blister like aneurysm (n=2) were treated using bypass and endovascular internal carotid artery trapping. In the follow-up study group after microsurgical treatment there were no severe complications due to the treatment. Age, cause of retreatment, and modified Rankin Scale before microsurgery were associated with good outcome (p<0.001). Conclusions Microsurgical treatment may be a viable and effective option for treating recurrent aneurysms previously treated by endovascular techniques.

BACKGROUND: Metabolic syndrome is associated with type 2 diabetes and cardiovascular disease in patients with prediabetes. The aim of this study was to investigate and compare WHtR (Waist-to-Height Ratio) as a predictor of metabolic syndrome with other anthropometric indices as in Body Mass Index (BMI), Waist Circumference (WC) and Waist to Hip Ratio (WHR) in prediabetes. METHODS: A total of 816 subjects with prediabetes were recruited from a community based Cohort Study. Receiver operating characteristic (ROC) curve was performed to find the optimal cutoff value of WHtR. Area under the curve (AUC) was calculated for each anthropometric index and correlation coefficient between WHtR and various dermographic and clinical factors was calculated. RESULTS: WHtR had a significant correlation with metabolic parameters except for fasting glucose and increased with increasing number of risk factors for metabolic syndrome. AUC of WHtR was significantly higher than that of other anthropometric indices. The optimal cutoff value of WHtR was 0.53 for metabolic syndrome in prediabetes. CONCLUSION: WHtR may be the simple and effective anthropometric index for predicting metabolic syndrome in prediabetic patients.
Area Under Curve ; Body Mass Index ; Cardiovascular Diseases ; Cohort Studies ; Fasting ; Glucose ; Humans ; Prediabetic State ; Risk Factors ; ROC Curve ; Waist Circumference ; Waist-Hip Ratio

Impairment in spinal inhibition caused by quantitative alteration of GABAergic elements following peripheral nerve injury has been postulated to mediate neuropathic pain. In the present study, we tested whether neuropathic pain could be induced or reversed by pharmacologically modulating spinal GABAergic activity, and whether quantitative alteration of spinal GABAergic elements after peripheral nerve injury was related to the impairment of GABAergic inhibition or neuropathic pain. To these aims, we first analyzed the pain behaviors following the spinal administration of GABA antagonists (1 microgram bicuculline/rat and 5 microgram phaclofen/rat), agonists (1 microgram muscimol/rat and 0.5 microgram baclofen/rat) or GABA transporter (GAT) inhibitors (20 microgram NNC-711/rat and 1 microgram SNAP-5114/rat) into naive or neuropathic animals. Then, using Western blotting, PCR or immunohistochemistry, we compared the quantities of spinal GABA, its synthesizing enzymes (GAD65, 67) and its receptors (GABAA and GABAB) and transporters (GAT-1, and -3) between two groups of rats with different severity of neuropathic pain following partial injury of tail-innervating nerves; the allodynic and non-allodynic groups. Intrathecal administration of GABA antagonists markedly lowered tail-withdrawal threshold in naive animals, and GABA agonists or GAT inhibitors significantly attenuated neuropathic pain in nerve-injured animals. However, any quantitative changes in spinal GABAergic elements were not observed in both the allodynic and non-allodynic groups. These results suggest that although the impairment in spinal GABAergic inhibition may play a role in mediation of neuropathic pain, it is not accomplished by the quantitative change in spinal elements for GABAergic inhibition and therefore these elements are not related to the generation of neuropathic pain following peripheral nerve injury.
Animals ; Blotting, Western ; GABA Agonists ; GABA Antagonists ; gamma-Aminobutyric Acid ; Immunohistochemistry ; Negotiating ; Neuralgia ; Peptides ; Peripheral Nerve Injuries ; Polymerase Chain Reaction ; Rats

PURPOSE : Since the year 2000, lung cancer has been the leading cause of cancer death in South Korea and also in many other parts of the world. MATERIALS AND METHODS : We developed a multidisciplinary (MD) care system for lung cancer patients in 1996. Here, we report the results obtained in the process of development of MD team (MDT). RESULTS : The MDT was launched with including medical doctors, chest surgeons, radiation oncologists, radiologists, nuclear medicine specialists and physician assistants. To facilitate co-operation between the MDT members, a specialized out-patient clinic was located within a sector of the hospital. A common ward was allocated for lung cancer patients regardless of the department of the attending physician. Shared electronic medical record forms that were specialized for lung cancer were developed. The MDT operates weekly lung cancer conferences and multidisciplinary out-patient clinics. To make diagnostic or therapeutic decisions early on, the electronic medical records of the patients were previewed or consulted by the specialists before they meet the individual patients. CONCLUSION : Despite every effort, we still need to shorten the waiting time from presentation to the first treatment and we need to improve the patients' satisfaction. We also have a mission to develop our own regulations and guidelines for our lung cancer MD care system. Clinical trials and basic research should also be encouraged along with improving the quality of life of the team members
Congresses as Topic ; Electronic Health Records ; Humans ; Lung ; Lung Neoplasms ; Missions and Missionaries ; Nuclear Medicine ; Outpatients ; Physician Assistants ; Quality of Life ; Republic of Korea ; Social Control, Formal ; Specialization ; Thorax

PURPOSE: We wished to compare the ability of ultrasonography and radiography performed on the same day to detect rib fractures in minor chest injuries. MATERIALS AND METHODS: Two hundred and fifteen patients with minor chest injuries were selected. Radiography and ultrasonography were performed on the same day with these patients. Chest wall pain was the only presenting symptom. Two radiologists performed ultrasonography. Fractures were identified by a disruption of the anterior margin of the rib and costal cartilage. The incidence and location of fractures and complications revealed by radiography and ultrasonography were compared. RESULTS: Radiographs revealed the presence of 70 rib fractures in 50 (23%) of 215 patients and ultrasonography revealed the presence of 203 rib fractures in 133 (62%) of 215 patients. Ultrasonography uniquely identified 133 rib fractures in 83 patients. Ultrasonography identified a 2.9 fold increase in the number of fractures in a 2.6 fold number of subjects as compared to radiography. Of the 203 sonographically detected fractures, 201 were located in the rib, one was located at the costochondral junction, and one in the costal cartilage. There were no complications seen by either radiography or ultrasonography. CONCLUSION: Ultrasonography reveals more fractures than those that may be overlooked on radiography for minor chest injuries.
Cartilage ; Humans ; Incidence ; Radiography* ; Rib Fractures* ; Ribs* ; Thoracic Injuries* ; Thoracic Wall ; Thorax* ; Ultrasonography*