Clinical Analysis of Dizziness Patients Who Visited Emergency Room / 대한이비인후과학회지

Background and Objectives@#Dizziness has diverse underlying causes, so the diagnosis is challenging especially in the emergency room. The aim of this study is to identify clinical characteristics of patients’ complaints of dizziness in the emergency room.Subjects and Method We retrospectively reviewed the medical records of 10367 patients who visited the emergency room with the chief complaint of dizziness from January 2016 to December 2020. Patients’ clinical information including age, sex, final diagnoses, consulting departments, treatment results and seasonal incidences were thoroughly assessed. @*Results@#Of the total patients who visited the emergency room, 4.64% complained of dizziness. The mean age of patients was 57.6 years old. The most common age group was over 70’s (28.1%). There were 6322 (61.1%) female patients, while 4035 (38.9%) were male patients. Nearly half 4932 (47.6%) of the patients were managed by the emergency department, followed by 3204, who were managed by the department of otolaryngorhinology (30.9%), and 1166 (11.2%) managed by the neurology department. The dizziness was classified as peripheral vertigo (33.8%), nonspecific dizziness (27.4%), medical conditions (13.9%), central dizziness (11.0%), cardiac dizziness (6.2%), and other miscellaneous causes of trauma, neoplasm and psychogenic causes (7.7%). In peripheral vertigo, the incidence of BPPV, vestibular neuritis and Meniere’s disease were 23.5%, 8.8% and 0.6%, respectively. @*Conclusion@#Peripheral vertigo accounted for the majority for the patients with chief complaints of dizziness in the emergency room. As diverse medical conditions may cause dizziness, specialized departments have to be involved in the diagnostic process of dizziness.

A Case of Brain Herniation and Cerebrospinal Fluid Leakage during Endoscopic Marsupialization of Ethmoid Sinus Mucocele / 대한이비인후과학회지

Paranasal sinus mucocele is a slowly growing benign cystic lesion. It usually involves the frontal and ethmoid sinuses and can extend to adjacent structures, especially to the orbit, skull base and brain parenchyma. Prompt surgical intervention is needed when symptoms occur. Complete resection of mucocele is approached via endoscopic sinus surgery, while marsupialization is also widely considered. Recently, we encountered a case of spontaneous brain herniation and cerebrospinal fluid leakage during endoscopic marsupialization of ethmoid sinus mucocele. Herein, we report the case with a review of the literature.

A Case of Rotational Vertebral Artery Syndrome after Vertebral Artery Dissection / 대한이비인후과학회지

Rotational vertebral artery syndrome (RVAS), also called Bow-Hunter syndrome, is characterized by position-aggravated reversible vertebra-basillarischemia. By rotating the head to one side, the mechanical compression of a dominant vertebral artery (VA) in the setting of a hypoplastic contralateral VA might cause tinnitus, vertigo and syncope. A 60-year-old male experienced recurrent tinnitus and vertigo while rotating the head to the right side. Neck CT images showed no abnormal structures near the course of both VAs. In 3-phase dynamic neck CT angiography, a focal vertebral artery dissection was identified at the right C6 transverse foramen. Close observation and anticoagulation therapy were started to prevent thrombo-embolic complications. Herein, we report a case of RVAS with vertebral artery dissection with a review of the literatures.

Clinical Characteristics of Infectious Mononucleosis: A Retrospective Study / 대한이비인후과학회지

BACKGROUND AND OBJECTIVES@#Infectious mononucleosis is mainly caused by Epstein-Barr virus infection and it presents sore throat, fever, tonsillar enlargement with exudate, cervical lymphadenopathy, hepatosplenomegaly, and etc. Therefore, it is often misdiagnosed with acute tonsillitis. The aim of this study was to evaluate the clinical characteristics of patients with infectious mononucleosis and recent changes.SUBJECTS AND METHOD: From January 2008 to December 2017, we retrospectively studied 83 patients who were diagnosed with infectious mononucleosis. We evaluated the patients' clinical characteristics such as sex, age, onset of disease, the department first visited, period of hospital stay, symptoms, signs, the results of serologic test, and complications.@*RESULTS@#Among 83 patients, 41 were male and 42 were female. The mean age was 16.1±7.28, with the oldest patient being 38 years old and the youngest patient being 2 years old. The proportion of patients older than 25 years was 10.8%. The most common symptom was sore throat (77%), followed by fever (67%), upper respiratory infection symptoms such as cough, sputum, rhinorrhea (37%), abdominal pain (16%), neck mass or neck pain (13%), and headache (4%). The most common sign was tonsillar enlargement (85%), followed by tonsillar white patch (68%), hepatosplenomegaly (67%), and cervical lymphadenopathy (60%). Complication occurred in 2 patients with mild jaundice, and there was no critical complication. The department patients first visited was mostly otolaryngology (61%), followed by pediatrics (21%), gastroenterology (9%), and others (6%).@*CONCLUSION@#Patients with infectious mononucleosis mostly appeared to have fever, pharyngitis or cervical lymphadenitis, and the complication rate was low. The primary infection age of infectious mononucleosis tended to increase in recent years. In adult patients, cervical lymphadenitis was less, and white blood cell count and the proportion of lymphocyte was lower compared to pediatric patients.

Preclinical development of a humanized neutralizing antibody targeting HGF

Hepatocyte growth factor (HGF) and its receptor, cMET, play critical roles in cell proliferation, angiogenesis and invasion in a wide variety of cancers. We therefore examined the anti-tumor activity of the humanized monoclonal anti-HGF antibody, YYB-101, in nude mice bearing human glioblastoma xenografts as a single agent or in combination with temozolomide. HGF neutralization, The extracellular signal-related kinases 1 and 2 (ERK1/2) phosphorylation, and HGF-induced scattering were assessed in HGF-expressing cell lines treated with YYB-101. To support clinical development, we also evaluated the preclinical pharmacokinetics and toxicokinetics in cynomolgus monkeys, and human and cynomolgus monkey tissue was stained with YYB-101 to test tissue cross-reactivity. We found that YYB-101 inhibited cMET activation in vitro and suppressed tumor growth in the orthotopic mouse model of human glioblastoma. Combination treatment with YYB-101 and temozolomide decreased tumor growth and increased overall survival compared with the effects of either agent alone. Five cancer-related genes (TMEM119, FST, RSPO3, ROS1 and NBL1) were overexpressed in YYB-101-treated mice that showed tumor regrowth. In the tissue cross-reactivity assay, critical cross-reactivity was not observed. The terminal elimination half-life was 21.7 days. Taken together, the in vitro and in vivo data demonstrated the anti-tumor efficacy of YYB-101, which appeared to be mediated by blocking the HGF/cMET interaction. The preclinical pharmacokinetics, toxicokinetics and tissue cross-reactivity data support the clinical development of YYB-101 for advanced cancer.

Purification and Identification of Ubiquitin Binding Proteins from Erythrocytes of Patients with Dementia

OBJECTIVE: The continuous synthesis and degradation of proteins in the cell are essential for the maintenance of cellular homeostasis. Intracellular protein degradation largely occurs in the lysosome and cytoplasm. The protein degradation in the cytoplasm (ubiquitin mediated protein degradation) is distinct from the well studied lysosomal protein degradation (nonselective protein degradation) and require energy (ATP), ubiquitin and ubiquitin conjugating enzymes such as E1, E2 and E3. Dementia caused by the deposition of abnormal proteins in brain cells followed by brain cells damage are not fully understood. To better understand the possible mechanism of dementia, we attempted to purify ubiquitin conjugating enzymes (such as E1 and E2 proteins) from the blood of normal persons and patients with dementia and tested their electrophoretic mob)ility on SDS-polyacrylamide gel electrophoresis. METHOD: The E1 and E2 enzymes of the red blood cell lysate fraction from the normal person and the patients with dementia were purified from ammonium sulfate precipitatant of DEAE-cellulose eluate fraction. Following ubiquitin-sepharose column chromatography, the E1 enzyme of the normal and the patients with dementia group showed homogeneous form and various kinds of E2 isoforms were identified by the SDS-polyacrylamide gel electrophoresis. RESULTS: The E1 and E2 enzymes showed no difference on electrophoretic mobility, but the E2 isozyme containing fraction was observed to great difference between the two groups. The 44 kDa protein of E2 isozyme containing fraction was significantly increased in alcoholic dementia and clearly increased in patients with Alzheimer's disease. In addition, another 11 kDa protein was significantly increased in the patients with Alzheimer's disease, but 11 kDa protein of alcoholic dementia was similar to that of the normal person. The 44 kDa and 11 kDa proteins showed a reverse relationship between alcoholic dementia and the patients with Alzheimer's disease. These proteins seems to be different molecules from the well known studied beta-amyloid, presenilin, tau protein and apolipoprotein E (Apo E). CONCLUSIONS: These results might be useful for the elucidation of dementia and the identification of these proteins are now in progress.

Regulation of leptin gene expression by insulin and growth hormone in mouse adipocytes

The role of leptin in the control of obesity, insulin resistance and type II diabetes has been reported, however, the regulatory mechanism of leptin in animals affected by hormones is not clearly understood. In this study, the effects of insulin, epinephrine, growth hormone or dexamethasone on the expression of leptin was examined in mouse primary adipocytes. The leptin expression was also studied in the adipose tissue of the mouse treated with insulin or growth hormone (0.3 or 0.6 units/animal). Insulin (100 nM) or dexamethasone (100 nM) stimulated leptin mRNA transcription while epinephrine (100 nM) alleviated its transcription in mouse primary adipocytes. The level of leptin protein in cultured media of adipocytes treated with insulin or dexamethasone was higher than that of the control group but growth hormone or epinephrine treatment had no effect on them. Insulin administration (0.6 units/mouse) enhanced leptin mRNA as well as leptin protein in mouse adipose tissue but growth hormone administration (0.3 or 0.6 units/mouse) had no effect on them. Leptin protein level in sera of mice injected with insulin or growth hormone was not significantly different from that of control group. These results indicate that both insulin and dexamethasone stimulate leptin gene expression and secretion of its product, whereas, growth hormone has no effect on the expression of leptin gene in mouse adipocytes.

Regulation of leptin gene expression by insulin and growth hormone in mouse adipocytes

The role of leptin in the control of obesity, insulin resistance and type II diabetes has been reported, however, the regulatory mechanism of leptin in animals affected by hormones is not clearly understood. In this study, the effects of insulin, epinephrine, growth hormone or dexamethasone on the expression of leptin was examined in mouse primary adipocytes. The leptin expression was also studied in the adipose tissue of the mouse treated with insulin or growth hormone (0.3 or 0.6 units/animal). Insulin (100 nM) or dexamethasone (100 nM) stimulated leptin mRNA transcription while epinephrine (100 nM) alleviated its transcription in mouse primary adipocytes. The level of leptin protein in cultured media of adipocytes treated with insulin or dexamethasone was higher than that of the control group but growth hormone or epinephrine treatment had no effect on them. Insulin administration (0.6 units/mouse) enhanced leptin mRNA as well as leptin protein in mouse adipose tissue but growth hormone administration (0.3 or 0.6 units/mouse) had no effect on them. Leptin protein level in sera of mice injected with insulin or growth hormone was not significantly different from that of control group. These results indicate that both insulin and dexamethasone stimulate leptin gene expression and secretion of its product, whereas, growth hormone has no effect on the expression of leptin gene in mouse adipocytes.

Preliminary Study on von Hippel-Lindau Gene Mutations in Sporadic Clear Cell Renal Carcinomas / 대한비뇨기과학회지

No abstract available.

Endoplasmic reticulum retention and degradation of T cell antigen receptor beta chain

The T cell antigen receptor-CD3 (TCR/CD3) complex is assembled in the endoplasmic reticulum (ER) of T cells after synthesis of individual chains, and is transported to the cell surface for immune recognition and regulation. Partially assembled or unassembled TCR chains are retained and rapidly degraded in the ER. These processes are strictly regulated in the ER at post-translational level for the maintenance of cellular homeostasis. In order to identify the region responsible for the ER retention and rapid degradation of the TCR beta chain, number of mutants were engineered and their fates, after synthesis in the ER of the HeLa cells, were investigated. Extensive mutagenic analysis of TCR beta chain, including changing the charged amino acid residues and two tyrosine residues of the transmembrane region into hydrophobic amino acid residues, did not alter the ER retention and rapid degradation. Soluble TCR beta chain and cytoplasmic tail truncation mutant were also rapidly degraded in the ER. However, N-glycosylation rate of soluble TCR beta chain in the ER was significantly increased possibly due to the increased exposure of the N-glycosylation site. These results suggest that the ER retention of TCR beta chain is mediated through its extracellular and transmembrane-cytoplasmic regions and that the rapid ER degradation can be caused by an exposure of unassembled subregion of TCR beta chain, either extracellular domain or hydrophobic transmembrane region to the hydrophilic environment (lumen of the ER) rather than by presence of a specific degradation signal.