Since 1993, vivax malaria has been recognized as a public health burden in Korea. Despite of pan-governmental malaria-control efforts and the dramatic reduction in the burden of this disease over the last 10 years, vivax malaria has not been well controlled and has remained continuously endemic. We focused interviewed and examined the charts of 28 confirmed vivax malaria patients given malarial therapy for whom daily records were kept from Gimpo-si, Gyeonggido of Korea. Various epidemiological characteristics of vivax malaria, including the incubation period, medication used, and recurrence, and an evaluation of the parasitic characteristics from the focused interviews of patients from this region are described here. Most of the participants indicated the 3 most common symptoms of malaria (headache, chills and fever). Of the 28 cases, 2 experienced a second attack and there were 17 and 11 cases with short- and long-term incubation periods, respectively, yielding a short-term to long-term ratio of 1.5. Based on the parasitemia stages, most of the participants were tested at 5 to 7 days (11 cases) and 7 to 15 days (11 cases) after initial wave of asexual parasites. In conclusion, public health authorities should consider developing management measures to decrease the time lag for diagnosis and drafting unified and robust guidelines for drug use for malaria and drawing up unified and robust guidelines on the use of medication for malaria. It also suggests that routine monitoring, surveillance, and precise medical surveys in high-risk vivax malaria endemic areas are pivotal to controlling this persistent public disease and finally eliminating it from Korea.

In contrast to ventricular myocytes, the structural and functional importance of atrial transverse tubules (T-tubules) is not fully understood. Therefore, we investigated the ultrastructure of T-tubules of living rat atrial myocytes in comparison with ventricular myocytes. Nanoscale cell surface imaging by scanning ion conductance microscopy (SICM) was accompanied by confocal imaging of intracellular T-tubule network, and the effect of removal of T-tubules on atrial excitation-contraction coupling (EC-coupling) was observed. By SICM imaging, we classified atrial cell surface into 4 subtypes. About 38% of atrial myocytes had smooth cell surface with no clear T-tubule openings and intracellular T-tubules (smooth-type). In 33% of cells, we found a novel membrane nanostructure running in the direction of cell length and named it 'longitudinal fissures' (LFs-type). Interestingly, T-tubule openings were often found inside the LFs. About 17% of atrial cells resembled ventricular myocytes, but they had smaller T-tubule openings and a lower Z-groove ratio than the ventricle (ventricular-type). The remaining 12% of cells showed a mixed structure of each subtype (mixed-type). The LFs-, ventricular-, and mixed-type had an appreciable amount of reticular form of intracellular T-tubules. Formamide-induced detubulation effectively removed atrial T-tubules, which was confirmed by both confocal images and decreased cell capacitance. However, the LFs remained intact after detubulation. Detubulation reduced action potential duration and L-type Ca2+ channel (LTCC) density, and prolonged relaxation time of the myocytes. Taken together, we observed heterogeneity of rat atrial T-tubules and membranous ultrastructure, and the alteration of atrial EC-coupling by disruption of T-tubules.

In contrast to ventricular myocytes, the structural and functional importance of atrial transverse tubules (T-tubules) is not fully understood. Therefore, we investigated the ultrastructure of T-tubules of living rat atrial myocytes in comparison with ventricular myocytes. Nanoscale cell surface imaging by scanning ion conductance microscopy (SICM) was accompanied by confocal imaging of intracellular T-tubule network, and the effect of removal of T-tubules on atrial excitation-contraction coupling (EC-coupling) was observed. By SICM imaging, we classified atrial cell surface into 4 subtypes. About 38% of atrial myocytes had smooth cell surface with no clear T-tubule openings and intracellular T-tubules (smooth-type). In 33% of cells, we found a novel membrane nanostructure running in the direction of cell length and named it 'longitudinal fissures' (LFs-type). Interestingly, T-tubule openings were often found inside the LFs. About 17% of atrial cells resembled ventricular myocytes, but they had smaller T-tubule openings and a lower Z-groove ratio than the ventricle (ventricular-type). The remaining 12% of cells showed a mixed structure of each subtype (mixed-type). The LFs-, ventricular-, and mixed-type had an appreciable amount of reticular form of intracellular T-tubules. Formamide-induced detubulation effectively removed atrial T-tubules, which was confirmed by both confocal images and decreased cell capacitance. However, the LFs remained intact after detubulation. Detubulation reduced action potential duration and L-type Ca2+ channel (LTCC) density, and prolonged relaxation time of the myocytes. Taken together, we observed heterogeneity of rat atrial T-tubules and membranous ultrastructure, and the alteration of atrial EC-coupling by disruption of T-tubules.

Anoctamin 5 (ANO5)/TMEM16E belongs to a member of the ANO/TMEM16 family member of anion channels. However, it is a matter of debate whether ANO5 functions as a genuine plasma membrane chloride channel. It has been recognized that mutations in the ANO5 gene cause many skeletal muscle diseases such as limb girdle muscular dystrophy type 2L (LGMD2L) and Miyoshi muscular dystrophy type 3 (MMD3) in human. However, the molecular mechanisms of the skeletal myopathies caused by ANO5 defects are poorly understood. To understand the role of ANO5 in skeletal muscle development and function, we silenced the ANO5 gene in C2C12 myoblasts and evaluated whether it impairs myogenesis and myotube function. ANO5 knockdown (ANO5-KD) by shRNA resulted in clustered or aggregated nuclei at the body of myotubes without affecting differentiation or myotube formation. Nuclear positioning defect of ANO5-KD myotubes was accompanied with reduced expression of Kif5b protein, a kinesin-related motor protein that controls nuclear transport during myogenesis. ANO5-KD impaired depolarization-induced [Ca²⁺]i transient and reduced sarcoplasmic reticulum (SR) Ca²⁺ storage. ANO5-KD resulted in reduced protein expression of the dihydropyridine receptor (DHPR) and SR Ca²⁺-ATPase subtype 1. In addition, ANO5-KD compromised co-localization between DHPR and ryanodine receptor subtype 1. It is concluded that ANO5-KD causes nuclear positioning defect by reduction of Kif5b expression, and compromises Ca²⁺ signaling by downregulating the expression of DHPR and SERCA proteins.
Active Transport, Cell Nucleus ; Calcium Channels, L-Type ; Cell Membrane ; Chloride Channels ; Humans ; Muscle Development ; Muscle Fibers, Skeletal ; Muscle, Skeletal ; Muscular Diseases ; Muscular Dystrophies ; Muscular Dystrophies, Limb-Girdle ; Myoblasts ; RNA, Small Interfering ; Ryanodine Receptor Calcium Release Channel ; Sarcoplasmic Reticulum

BACKGROUND: Current dilemma working with surgically-induced OA (osteoarthritis) model include inconsistent pathological state due to various influence from surrounding tissues. On the contrary, biochemical induction of OA using collagenase II has several advantageous points in a sense that it does not involve surgery to induce model and the extent of induced cartilage degeneration is almost uniform. However, concerns still exists because biochemical OA model induce abrupt destruction of cartilage tissues through enzymatic digestion in a short period of time, and this might accompany systemic inflammatory response, which is rather a trait of RA (rheumatoid arthritis) than being a trait of OA. METHODS: To clear the concern about the systemic inflammatory response that might be caused by abrupt destruction of cartilage tissue, OA was induced to only one leg of an animal and the other leg was examined to confirm the presence of systemic degenerative effect. RESULTS: Although the cartilage tissues were rapidly degenerated during short period of time upon biochemical induction of OA, they did not accompanied with RA-like process based on the histology data showing degeneration of articular cartilage occurred only in the collagenase-injected knee joint. Scoring evaluation data indicated that the cartilage tissues in non-induced joint remained intact. Neutrophil count transiently increase between day 8 and day 16, and there were no significant change in other complete blood count profile showing a characteristics of OA disease. CONCLUSION: These study shows that biochemically induced cartilage degeneration truly represented uniform and reliable OA state.
Animals* ; Blood Cell Count ; Cartilage ; Cartilage, Articular ; Clothing ; Collagenases* ; Digestion ; Inflammation ; Joints ; Knee Joint ; Leg ; Models, Animal* ; Neutrophils ; Osteoarthritis* ; Regeneration

OBJECTIVE: Necrotizing pneumonia (NP) is a severe complication of lobar pneumonia caused by various pathogens. The immunopathogenesis and clinical characteristics of NP in children are not clearly understood. We wanted to evaluate the clinical characteristics and suggest in part the immunopathogenesis of NP. METHODS: We reviewed retrospectively the medical charts and radiographic materials of eight patients with NP, who were diagnosed by chest radiography and chest computed tomography at the Department of Pediatrics, Soonchunhyang University Hospitals at Cheonan and Bucheon from January 2002 to December 2011. RESULTS: They were previously healthy, 2.1 to 4.6 years of ages (mean, 2.8+/-1.0 years) and three boys and five girls. All of them had pleural effusion. Five patients had pneumonic consolidations in right upper lung field. Three patients had pneumatocele. They developed leukocytosis (mean, 19,400+/-6,400/mm3), higher C-reactive protein level (mean, 25.1+/-8.0 mg/dL). The etiologic agents were revealed in two patients; Streptococcus pneumonia (S. pneumonia) was revealed in one patient and S. pneumonia and Mycoplasma pneumonia in the other patient. Three patients were treated with additional intravenous immunoglobulin. Clinical improvement was prolonged: fever lasted 10 to 23 days, and length of hospitalization was 15 to 36 days. NP or pneumatocele were completely resolved on the follow-up radiographic studies in all of the patients. CONCLUSION: Although the previously healthy young children with NP had protracted clinical course, they recovered without any problematic sequelae. Our results suggest that the immunopathogenesis of NP in children may be associated with the exaggerated immune reaction of the host to insults from initial bacterial infections, rather than the pathogen-induced cytopathies.
Bacterial Infections ; C-Reactive Protein ; Child* ; Chungcheongnam-do ; Female ; Fever ; Follow-Up Studies ; Gyeonggi-do ; Hospitalization ; Hospitals, University ; Humans ; Immunoglobulins ; Leukocytosis ; Lung ; Pediatrics ; Pleural Effusion ; Pneumonia* ; Pneumonia, Mycoplasma ; Radiography ; Retrospective Studies ; Streptococcus ; Thorax

We report a case of 42-day-old girl with multiple abscesses in soft tissue sites and osteomyelitis caused by Staphylococcus aureus after an intradermal Bacillus Calmette-Guerin (BCG) vaccination. This may be an unusual complication of intradermal BCG vaccination.
Abscess* ; Bacillus ; Bacteremia* ; BCG Vaccine ; Female ; Humans ; Injections, Intradermal ; Mycobacterium bovis* ; Osteomyelitis ; Staphylococcus aureus* ; Staphylococcus* ; Vaccination*

BACKGROUND: Oxidation plays an important role in acute lung injury. This study was conducted in order to elucidate the effect of repetitive post-treatment of N-acetylcysteine (NAC) in lipopolysaccaride (LPS)-induced acute lung injury (ALI) of rats. METHODS: Six-week-old male Sprague-Dawley rats were divided into 4 groups. LPS (Escherichia coli 5 mg/kg) was administered intravenously via the tail vein. NAC (20 mg/kg) was injected intraperitoneally 3, 6, and 12 hours after LPS injection. Broncho-alveolar lavage fluid (BALF) and lung tissues were obtained to evaluate the ALI at 24 hours after LPS injection. The concentration of tumor necrosis factor alpha (TNF-alpha) and interleukin 1beta (IL-1beta) were measured in BALF. Nuclear factor kappaB (NF-kappaB), lipid peroxidation (LPO), and myeloperoxidase (MPO) were measured using lung tissues. Micro-computed tomography (micro-CT) images were examined in each group at 72 hours apart from the main experiments in order to observe the delayed effects of NAC. RESULTS: TNF-alpha and IL-1beta concentration in BALF were not different between LPS and NAC treatment groups. The concentration of LPO in NAC treatment group was significantly lower than that of LPS group (5.5+/-2.8 nmol/mL vs. 16.5+/-1.6 nmol/mL) (p=0.001). The activity of MPO in NAC treatment group was significantly lower than that of LPS group (6.4+/-1.8 unit/g vs. 11.2+/-6.3 unit/g, tissue) (p<0.048). The concentration of NF-kappaB in NAC treatment group was significantly lower than that of LPS group (0.3+/-0.1 ng/microL vs. 0.4+/-0.2 ng/microL) (p=0.0001). Micro-CT showed less extent of lung injury in NAC treatment than LPS group. CONCLUSION: After induction of ALI with lipopolysaccharide, the therapeutic administration of NAC partially attenuated the extent of ALI through the inhibition of NF-kappaB activation.
Acetylcysteine ; Acute Lung Injury ; Animals ; Antioxidants ; Humans ; Interleukin-1beta ; Lipid Peroxidation ; Lung ; Lung Injury ; Male ; NF-kappa B ; Peroxidase ; Rats ; Rats, Sprague-Dawley ; Therapeutic Irrigation ; Tumor Necrosis Factor-alpha ; Veins

BACKGROUND: Oxidation plays an important role in acute lung injury. This study was conducted in order to elucidate the effect of repetitive post-treatment of N-acetylcysteine (NAC) in lipopolysaccaride (LPS)-induced acute lung injury (ALI) of rats. METHODS: Six-week-old male Sprague-Dawley rats were divided into 4 groups. LPS (Escherichia coli 5 mg/kg) was administered intravenously via the tail vein. NAC (20 mg/kg) was injected intraperitoneally 3, 6, and 12 hours after LPS injection. Broncho-alveolar lavage fluid (BALF) and lung tissues were obtained to evaluate the ALI at 24 hours after LPS injection. The concentration of tumor necrosis factor alpha (TNF-alpha) and interleukin 1beta (IL-1beta) were measured in BALF. Nuclear factor kappaB (NF-kappaB), lipid peroxidation (LPO), and myeloperoxidase (MPO) were measured using lung tissues. Micro-computed tomography (micro-CT) images were examined in each group at 72 hours apart from the main experiments in order to observe the delayed effects of NAC. RESULTS: TNF-alpha and IL-1beta concentration in BALF were not different between LPS and NAC treatment groups. The concentration of LPO in NAC treatment group was significantly lower than that of LPS group (5.5+/-2.8 nmol/mL vs. 16.5+/-1.6 nmol/mL) (p=0.001). The activity of MPO in NAC treatment group was significantly lower than that of LPS group (6.4+/-1.8 unit/g vs. 11.2+/-6.3 unit/g, tissue) (p<0.048). The concentration of NF-kappaB in NAC treatment group was significantly lower than that of LPS group (0.3+/-0.1 ng/microL vs. 0.4+/-0.2 ng/microL) (p=0.0001). Micro-CT showed less extent of lung injury in NAC treatment than LPS group. CONCLUSION: After induction of ALI with lipopolysaccharide, the therapeutic administration of NAC partially attenuated the extent of ALI through the inhibition of NF-kappaB activation.
Acetylcysteine ; Acute Lung Injury ; Animals ; Antioxidants ; Humans ; Interleukin-1beta ; Lipid Peroxidation ; Lung ; Lung Injury ; Male ; NF-kappa B ; Peroxidase ; Rats ; Rats, Sprague-Dawley ; Therapeutic Irrigation ; Tumor Necrosis Factor-alpha ; Veins