Hyang-Ah Lee

Transvaginal ultrasound-guided radiofrequency myolysis for uterine myomas

BACKGROUND Myolysis is one of the procedures that is claimed to provide significant improvement in myoma status without hysterectomy. Myolysis procedures have been generally performed via laparoscopy, and there are limited data on transvaginal radiofrequency (RF) myolysis. This study investigated the feasibility, efficacy and safety of transvaginal ultrasound-guided RF myolysis. METHODS Transvaginal ultrasound-guided RF myolysis was performed on 69 premenopausal women with symptomatic uterine myomas as an outpatient procedure. Outcomes were assessed 1, 3, 6 and 12 months after RF myolysis. Myoma volumes were measured by ulrasonography. Menorrhagia was evaluated by the number of soaked normal-sized sanitary products used per menstrual period and overall symptoms were evaluated using the symptom severity subscale of the uterine fibroids symptom questionnaire. RESULTS Mean (± SD) age of patients was 39.8 ± 6.5 years. Mean baseline volume of the dominant myomas was 304.6 ± 229.1 cm(3) and its volume at 3 months following RF myolysis decreased compared with the previous examination (P = 0.002). An improvement of menorrhagia occurred 1, 3, 6 and 12 months after operation (all P < 0.001 versus baseline). Overall symptoms at 1, 3, 6 and 12 months after RF myolysis also improved (all P < 0.001 versus baseline). No major complications were observed or reported. After 12 months, three patients had successfully conceived and delivered and there were no complications during labor or delivery. CONCLUSIONS Transvaginal ultrasound-guided RF myolysis might be a safe, effective and minimally invasive outpatient procedure for uterine myoma in terms of size reduction, symptom improvement and safety.

Correlation between preoperative serum levels of five biomarkers and relationships between these biomarkers and cancer stage in epithelial overian cancer

OBJECTIVE To examine the correlation among the preoperative serum levels of five biomarkers presumed to be useful for early detection of epithelial ovarian cancer and evaluate the relationships between serum levels of these five biomarkers and epithelial ovarian cancer stage. METHODS We analyzed 56 newly diagnosed epithelial ovarian cancer patients. Preoperative serum levels of leptin, prolactin, osteopontin (OPN), insulin-like growth factor-II, and CA-125 were determined by ELISA. We also examined the correlation between the serum levels of the biomarkers and ovarian cancer stage. Significant differences in the mean serum levels of two proteins, leptin and CA-125, were observed between stage subsets. RESULTS There was a significant negative correlation between prolactin and leptin and a significant positive correlation between prolactin and OPN. Of the five biomarkers, only the mean serum CA-125 level showed a significant positive correlation with cancer stage (Spearman rho=0.24, p<0.01). OPN showed a marginally significant positive correlation with stage (Spearman rho=0.14, p=0.07). CONCLUSION We demonstrated the relationship between five biomarkers in epithelial ovarian cancer. These tumor markers may be useful in screening for ovarian cancer, in characterizing disease states, and in developing therapeutic interventions targeting these marker proteins. Large-scale studies that include potential confounding factors and modifiers are necessary to more accurately define the value of these novel biomarkers in ovarian cancer.

Histochemical Study on Neurodegeneration in the Olfactory Bulb after Transient Forebrain Ischaemia in the Mongolian Gerbil

In the present study, we investigated the ischaemia‐related neurodegeneration in the main and accessory olfactory bulb (AOB) after 5 min transient forebrain ischaemia in the Mongolian gerbil using the acid fuchsin staining method. Between 5 and 15 days after ischaemia, acid fuchsin positive cells markedly increased in the external plexiform layer (EPL), mitral cell layer (ML) and glomerular layer (GL) of the main olfactory bulb (MOB), and in the mixed cell layer (MCL) and GL of the AOB. By 30 days after ischaemia reperfusion, acid fuchsin positive neurons were shrunken and showed low acidophilia in somata. Many necrotic vacuoles were found in the EPL and GL of the MOB 30 days after ischaemia. At this time, necrotic vacuoles were very few in the AOB. Therefore, our results suggest that the GL and EPL of the MOB are vulnerable to ischaemic damage at a later time after ischaemic insult, and that the AOB is more resistant to ischaemic damage as compared with the MOB.

Age‐related Change of Somatostatin‐immunoreactive Neurones in the Main Olfactory Bulb of the Rat

Somatostatin is found in the olfactory system, including the main olfactory bulb (MOB), and is thought to be one of the neuroactive substances for olfaction. However, somatostatin immunoreactivity in the olfactory system has not been determined during ageing. Hence, we examined the age‐related changes of somatostatin‐immunoreactive (IR) neurones in the rat MOB over a period of 2 years, at the following various ageing stages: post‐natal month 1 (PM 1), PM 3, PM 6, PM 12 and PM 24. In PM 1 group, a few somatostatin‐IR neurones were detected in the granule cell layer (GCL), and had slender or oval somata and short processes. At PM 3, somatostatin‐IR neurones were observed in the glomerular, external plexiform and GCL. The size of somatostatin‐IR somata was larger than that at PM 1. In PM 6 group, the number and size of somatostatin‐IR neurones increased, and their processes became longer while running in various directions. At PM 12, somatostatin‐IR neurones increased in number, and their processes became markedly longer than those at PM 6. At this stage, somatostatin‐IR neurones had multipolar somata, and were the largest in size. In PM 24 group, somatostatin‐IR neurones were most numerous. However, the processes of somatostatin‐IR neurones were shorter than those at PM 12. This study suggests that the increased number of somatostatin‐IR neurones in the MOB of aged rats may play a role to compensate for any decrease of olfactory function.

Cilostazol Improves Developmental Competence of Pig Oocytes by Increasing Intraoocyte Cyclic Adenosine Monophosphate Level and Delaying Meiotic Resumption

Cilostazol (CLZ) is a cyclic adenosine monophosphate (cAMP) modulator that influences the steady state of the meiotic stage. This study was conducted to determine the effects of CLZ treatment during in vitro maturation (IVM) on developmental competence of pig oocytes. Immature oocytes were exposed to 0 (control), 0.5, 2 and 4 μm CLZ during the first 22 h of IVM. Nuclear maturation, intraoocyte glutathione content and embryo cleavage after parthenogenesis (PA) and somatic cell nuclear transfer (SCNT) were not influenced by CLZ at any concentrations. However, 4 μm CLZ significantly (p < 0.05) improved blastocyst formation after PA (52.1% vs 38.7-46.0%) and SCNT relative to other concentrations (40.8% vs 25.0-30.7%). The mean cell numbers of SCNT blastocysts were significantly increased by 4 μm CLZ compared to the control (42.6 cells vs 35.3 cells/blastocyst). CLZ treatment significantly increased the intraoocyte cAMP level and effectively arrested oocytes at the germinal vesicle (GV) and GV break down stages compared to the control (74.5% vs 45.4%). Our results demonstrated that improved developmental competence of PA and SCNT pig embryos occurred via better synchronization of nuclear and cytoplasmic maturation induced by increased cAMP and delayed meiotic resumption after CLZ treatment.

Chronological alterations of P2X3 receptor expression in the trigeminal ganglion after ischaemic insult in the Mongolian gerbil.

P2X receptors play a role in the transduction of sensory signals like pain. Few studies have been undertaken on altered P2X3 receptor (P2X3) expression in sensory neurones after peripheral nerve injury. In the present study, we investigated chronological alterations in P2X3 immunoreactivity and its protein content in the trigeminal ganglion after ischaemic insult in the Mongolian gerbil. In the sham‐operated group, P2X3‐immunoreactive neurones were found abundantly in small‐ and medium‐sized neurones. From 1 day after ischaemic insult, the number of P2X3‐immunoreactive neurones decreased significantly. At 5 days after ischaemic insult, P2X3 immunoreactivity was observed in few neurones, but its immunoreactivity was weak. However, the number of cresyl violet‐positive neurones was unchanged throughout this period in all groups. These results suggest that transient trigeminal ganglion ischaemia may provoke a decrease of P2X3 expression and its protein content, and that this down‐regulation of P2X3 may be related to the altered pain and thermal sensation without being associated with a transient ischaemic insult.

Changes of Calbindin D-28k Immunoreactivity in the Hippocampus after Adrenalectomy in the Seizure Sensitive Gerbil

Calbindin D‐28k (CB), a calcium‐binding protein, containing neurons in the hippocampus plays an important role in hippocampal excitability in epilepsy. In the present study, we investigated changes of CB immunoreactivity after adrenalectomy (ADX) in the hippocampus and dentate gyrus of the seizure sensitive gerbil, which is susceptible to seizure to identify roles of CB in epileptogenesis. The changes of the CB immunoreactivity after ADX were significant in the hippocampal CA1 region. By 24 h after ADX, CB‐immunoreactive CA1 pyramidal cells and CB immunoreactivity increased. At this time, well‐stained dendrites projected to the stratum radiatum. Thereafter, the CB immunoreactivity decreased time dependently by 96 h after ADX. In the dentate gyrus, the changes of CB‐immunoreactive neurons were mainly observed in the granule cell layer. The number and immunoreactivity of CB‐immunoreactive neurons was high at 24 h after ADX, thereafter, those decreased by 96 h after ADX. These results suggest that glucocorticoid has an important role in modulating the seizure activity and CB serves an inhibitory function, which regulates the seizure activity and output signals from the hippocampus.

Neuronal injury and tumor necrosis factor-alpha immunoreactivity in the rat hippocampus in the early period of asphyxia-induced cardiac arrest under normothermia

Low survival rate occurs in patients who initially experience a spontaneous return of circulation after cardiac arrest (CA). In this study, we induced asphyxial CA in adult male Sprague-Daley rats, maintained their body temperature at 37 ± 0.5°C, and then observed the survival rate during the post-resuscitation phase. We examined neuronal damage in the hippocampus using cresyl violet (CV) and Fluore-Jade B (F-J B) staining, and pro-inflammatory response using ionized calcium-binding adapter molecule 1 (Iba-1), glial fibrillary acidic protein (GFAP), and tumor necrosis factor-alpha (TNF-α) immunohistochemistry in the hippocampus after asphyxial CA in rats under normothermia. Our results show that the survival rate decreased gradually post-CA (about 63% at 6 hours, 37% at 1 day, and 8% at 2 days post-CA). Rats were sacrificed at these points in time post-CA, and no neuronal damage was found in the hippocampus until 1 day post-CA. However, some neurons in the stratum pyramidale of the CA region in the hippocampus were dead 2 days post-CA. Iba-1 immunoreactive microglia in the CA1 region did not change until 1 day post-CA, and they were activated (enlarged cell bodies with short and thicken processes) in all layers 2 days post-CA. Meanwhile, GFAP-immunoreactive astrocytes did not change significantly until 2 days post-CA. TNF-α immunoreactivity decreased significantly in neurons of the stratum pyramidale in the CA1 region 6 hours post-CA, decreased gradually until 1 day post-CA, and increased significantly again 2 days post-CA. These findings suggest that low survival rate of normothermic rats in the early period of asphyxia-induced CA is related to increased TNF-α immunoreactivity, but not to neuronal damage in the hippocampal CA1 region.

Tumor necrosis factor receptor 2 is required for ischemic preconditioning-mediated neuroprotection in the hippocampus following a subsequent longer transient cerebral ischemia

ABSTRACT Tumor Necrosis Factor‐&agr; (TNF‐&agr;) is a proinflammatory cytokine implicated in neuronal damage in response to cerebral ischemia. Ischemic preconditioning (IPC) provides neuroprotection against a subsequent severer or longer transient ischemia by ischemic tolerance. Here, we focused on the role of TNF‐&agr; in IPC‐mediated neuroprotection against neuronal death following a subsequent longer transient cerebral ischemia (TCI). Gerbils used in this study were randomly assigned to eight groups; sham group, TCI operated group, IPC plus (+) sham group, IPC + TCI operated group, sham + etanercept (an inhibitor of TNF‐a) group, TCI + etanercept group, IPC + sham + etanercept group, and IPC + TCI + etanercept group. IPC was induced by a 2‐min sublethal transient ischemia, which was operated 1 day prior to a longer (5‐min) TCI. A significant death of neurons was found in the stratum pyramidale (SP) in the CA1 area (CA1) of the hippocampus 5 days after TCI; however, IPC protected SP neurons from TCI. We found that TNF‐&agr; immunoreactivity was significantly increased in CA1 pyramidal neurons in the TCI and IPC + TCI groups compared to the sham group. TNF‐R1 expression in CA1 pyramidal neurons of the TCI group was also increased 1 and 2 days after TCI; however, in the IPC + TCI group, TNF‐R1 expression was significantly lower than that in the TCI group. On the other hand, we did not detect TNF‐R2 immunoreactivity in CA1 pyramidal neurons 1 and 2 days after TCI; meanwhile, in the IPC + TCI group, TNF‐R2 expression was significantly increased compared to TNF‐R2 expression at 1 and 2 days after TCI. In addition, in this group, TNF‐R2 was newly expressed in pericytes, which are important cells in the blood brain barrier, from 1 day after TCI. When we treated etanercept to the IPC + TCI group, IPC‐induced neuroprotection was significantly weakened. In brief, this study indicates that IPC confers neuroprotection against TCI by TNF‐&agr; signaling through TNF‐R2 and suggests that the enhancement of TNF‐R2 expression by IPC may be a legitimate strategy for a therapeutic intervention of TCI. HighlightsIschemic preconditioning (IPC) protects CA1 pyramidal neurons from ischemic damage.IPC attenuates TNF‐&agr; and TNF‐R1 expressions in ischemic CA1 pyramidal neurons.IPC increases TNF‐R2 expressions in pericytes in CA1 area after ischemic insult.IPC‐mediated neuroprotective effect is reversed by etanercept (an inhibitor of TNF‐a) treatment.

Clinical characteristics and prognostic factors in patients with pulmonary tuberculosis as a primary cause of respiratory failure admitted to intensive care units

Tuberculosis (Tb) is currently the most frequent cause of death due to an infectious disease worldwide. The cases of Tb requiring intensive care present 1-3% of all patients with TB. Hospital mortality has been reported to be 60% for patients with respiratory failure due to pulmonary TB.