OBJECTIVES: When a patient who attempts suicide visits the emergency room, it is important that the departments of emergency medicine, internal medicine, and psychiatry communicate with each other and prioritize treatment. This study was conducted to verify the effectiveness of the multidisciplinary emergency consultation system (ECS) for drug intoxicated patients. METHODS: We retrospectively analyzed the data from medical records prior to the ECS, from July 2017 to May 2018, and after the ECS, from July 2018 to May 2019, to verify the effectiveness of the system. RESULTS: After the ECS, admission to open wards was significantly higher than to the intensive care units (χ²=8.567, p=0.014). In addition, the proportion of consultations to the department of psychiatry among patients admitted to other departments tended to increase (χ²=4.202, p=0.053), and the time required for consultation response decreased (Z=−2.031, p=0.042). As a result of the consultation, the proportion of the patients who had been transferred to the department of psychiatry was increased (χ²=4.692, p=0.043), and the time spent to transfer tended to decrease (Z=−1.941, p=0.052). CONCLUSIONS After implementing the ECS for drug intoxicated patients, unnecessary intensive care unit admissions, consultation response time, and the time spent to transfer were reduced, and the rate of consultation referrals and transfer rates increased. This means that the multidisciplinary consultation system rapidly provided essential medical services to patients at lower medical costs.

PURPOSE: It is known that carriage rates of Staphylococcus aureus (S. aureus) are highest in newborns and that the asymptomatic carriage of methicillin-resistant Staphylococcus aureus (MRSA) is associated with invasive MRSA infection with the colonizing strain. This study was carried out to investigate the carriage rates of MRSA in neonates with neonatal jaundice. METHODS: We reviewed the medical records of 545 neonates admitted with neonatal jaundice to neonatal intensive care units between January 2006 and December 2010. Nasal and inguinal swab specimens had been taken from them and cultured for the isolation of S. aureus. Antimicrobial susceptibility tests had been done for such isolates to determine methicillin-resistance. RESULTS: Out of 545 neonates, 318 (58.3%) were colonized with S. aureus and 214 (39.3%) were colonized with MRSA. Results of the antibiogram analysis showed that 65.7% of MRSA isolates were likely to be community-associated (CA) MRSA. CONCLUSION: Based on the MRSA carriage rate of 39.3%, a surveillance program for MRSA colonization is considered necessary in neonates transferred from other clinics or hospitals. Out of MRSA isolates, 65.7% were likely to be CA-MRSA. This suggests that CA-MRSA strains were already present in obstetric clinic environments where the neonates were born. It is thought that MRSA surveillance programs in these environments are also necessary.
Colon ; Humans ; Infant, Newborn ; Intensive Care Units, Neonatal ; Jaundice, Neonatal ; Medical Records ; Methicillin Resistance ; Methicillin-Resistant Staphylococcus aureus ; Microbial Sensitivity Tests ; Sprains and Strains ; Staphylococcus aureus

The HELLP syndrome, which is characterized by hemolysis, elevated liver enzymes and low platelets, complicates 4 to 14% of preeclamptic or eclamptic pregnancy. Its course is usually benign except when spontaneous hepatic rupture, a rare catastrophic event, threatens life. The authors have experienced one case of spontaneous hepatic rupture in HELLP syndrome during immediate postpartum period, which was treated with surgical intervention on the first postpartum day. We report this case with a brief review of the literatures.
Female ; HELLP Syndrome* ; Hemolysis ; Hemorrhage* ; Liver ; Postpartum Period* ; Pregnancy ; Rupture*

Purpose: Sex hormones are known to affect the gut microbiota. Previously, we reported that endogenous and exogenous testosterone are associated with colorectal cancer (CRC) development and submucosal invasion. In the present study, we investigated whether the gut microbiota is affected by orchiectomy (ORX) and testosterone propionate (TP) administration using an azoxymethane/dextran sulfate sodium (AOM/DSS)-induced CRC mouse model. Materials and Methods: Gut microbiota was evaluated by means of 16S rRNA gene sequencing of stool DNA extracted from feces that were obtained at 13 weeks after AOM injection (from 22-week-old animals) and stored in a gas-generating pouch. Results: The increase in microbial diversity (Chao1 and Phylogenetic Diversity index) and Firmicutes/Bacteroidetes (F/B) ratio upon AOM/DSS treatment in ORX mice was significantly decreased by TP supplementation. The ratio of commensal bacteria to opportunistic pathogens was lower in the TP-administered females and ORX mice than in the AOM/DSS group. Opportunistic pathogens (Mucispirillum schaedleri or Akkermansia muciniphila) were identified only in the TP group. In addition, microbial diversity and F/B ratio were higher in male controls than in female and ORX controls. Flintibacter butyricus, Ruminococcus bromii, and Romboutsia timonensis showed similar changes in the male control group as those in the female and ORX controls. Conclusion In conclusion, testosterone determines the dysbiosis of gut microbiota, which suggests that it plays a role in the sex-related differences in colorectal carcinogenesis.

Purpose: 17β-Estradiol (E2) supplementation suppresses MC38 tumor growth by downregulating the expression of programmed death-ligand 1 (PD-L1). This study aims to figure out the gut microbiota that respond to anti–PD-L1 and/or estrogen treatment in MC38 colon cancer model. Materials and Methods: A syngeneic colon tumor model was developed by injection of MC38 cells into C57BL/6 background male and female mice. Three days before MC38 cells injection, E2 was supplemented to male mice daily for 1 week. Male and female mice with MC38 tumors (50-100 mm3) were injected with anti–PD-L1 antibody. Fresh feces were collected 26 days after injection of MC38 cells and 16S rRNA metagenomics sequencing of DNA extracted from feces was used to assess gut microbial composition. Results: At the taxonomic family level, Muribaculaceae was enriched only in the MC38 male control group. In male mice, linear discriminant analysis effect size analysis at the species level revealed that the four microorganisms were commonly regulated in single and combination treatment with anti–PD-L1 and/or E2; a decrease in PAC001068_g_uc and PAC001070_s (family Muribaculaceae) and increase in PAC001716_s and PAC001785_s (family Ruminococcaceae). Interestingly, in the anti–PD-L1 plus E2 group, a decrease in opportunistic pathogens (Enterobacteriaceae group) and an increase in commensal bacteria (Lactobacillus murinus group and Parabacteroides goldsteinii) were observed. Furthermore, the abundance of Parabacteroides goldsteinii was increased in both males and females in the anti–PD-L1 group. Conclusion Our results suggest that gut microbial changes induced by the pretreatment of estrogen before anti–PD-L1 might contribute to treatment of MC38 colon cancer.

BACKGROUND: This study investigates the effect of alendronate-treated osteoblasts, as well as the effect of low-level laser therapy (LLLT) on the alendronate-treated osteoblasts. Bisphosphonate decreases the osteoblastic activity. Various treatment modalities are used to enhance the bisphosphonate-treated osteoblasts; however, there were no cell culture studies conducted using a low-level laser. METHODS: Human fetal osteoblastic (hFOB 1.19) cells were treated with 50 μM alendronate. Then, they were irradiated with a 1.2 J/cm² low-level Ga-Al-As laser (λ = 808 ± 3 nm, 80 mW, and 80 mA; spot size, 1 cm²; NDLux, Seoul, Korea). The cell survivability was measured with the MTT assay. The three cytokines of osteoblasts, receptor activator of nuclear factor κB ligand (RANKL), osteoprotegerin (OPG), and macrophage colony-stimulating factor (M-CSF) were analyzed. RESULTS: In the cells treated with alendronate at concentrations of 50 μM and higher, cell survivability significantly decreased after 48 h (p < 0.05). After the applications of low-level laser on alendronate-treated cells, cell survivability significantly increased at 72 h (p < 0.05). The expressions of OPG, RANKL, and M-CSF have decreased via the alendronate. The RANKL and M-CSF expressions have increased, but the OPG was not significantly affected by the LLLT. CONCLUSIONS: The LLLT does not affect the OPG expression in the hFOB cell line, but it may increase the RANKL and M-CSF expressions, thereby resulting in positive effects on osteoclastogenesis and bone remodeling.
Alendronate ; Bone Remodeling ; Cell Culture Techniques ; Cell Line ; Cytokines ; Humans ; Low-Level Light Therapy* ; Macrophage Colony-Stimulating Factor ; Osteoblasts* ; Osteoprotegerin ; Seoul

Few studies have evaluated the apoptosis-inducing efficacy of NaF on cancer cells in vitro but there has been no previous investigation of the apoptotic effects of NaF on human oral squamous cell carcinoma cells. In this study, we have investigated the mechanisms underlying the apoptotic response to NaF treatment in the YD9 human squamous cell carcinoma cell line. The viability of YD9 cells and their growth inhibition were assessed by MTT and clonogenic assays, respectively. Hoechst staining, DNA electrophoresis and TUNEL staining were conducted to detect apoptosis. YD9 cells were treated with NaF, and western blotting, immunocytochemistry, confocal microscopy, FACScan flow cytometry, and MMP and proteasome activity assays were performed sequentially. The NaF treatment resulted in a time- and dose-dependent decrease in YD9 cell viability, a dose-dependent inhibition of cell growth, and the induction of apoptotic cell death. The apoptotic response of these cells was manifested by nuclear condensation, DNA fragmentation, the reduction of MMP and proteasome activity, a decreased DNA content, the release of cytochrome c into the cytosol, the translocation of AIF and DFF40 (CAD) into the nucleus, a significant shift of the Bax/Bcl-2 ratio, and the activation of caspase-9, caspase-3, PARP, Lamin A/C and DFF45 (ICAD). Furthermore, NaF treatment resulted in the downregulation of G1 cell cyclerelated proteins, and upregulation of p53 and the Cdk inhibitor p27KIP1. Taken collectively, our present findings demonstrate that NaF strongly inhibits YD9 cell proliferation by modulating the expression of G1 cell cycle-related proteins and inducing apoptosis via mitochondrial and caspase pathways.
Apoptosis ; Blotting, Western ; Carcinoma, Squamous Cell ; Caspase 3 ; Caspase 9 ; Cell Death ; Cell Line ; Cell Proliferation ; Cell Survival ; Cytochromes c ; Cytosol ; DNA ; DNA Fragmentation ; Down-Regulation ; Electrophoresis ; Flow Cytometry ; Humans ; Immunohistochemistry ; In Situ Nick-End Labeling ; Microscopy, Confocal ; Proteasome Endopeptidase Complex ; Proteins ; Up-Regulation

Few studies have evaluated the apoptosis-inducing efficacy of NaF on cancer cells in vitro but there has been no previous investigation of the apoptotic effects of NaF on human oral squamous cell carcinoma cells. In this study, we have investigated the mechanisms underlying the apoptotic response to NaF treatment in the YD9 human squamous cell carcinoma cell line. The viability of YD9 cells and their growth inhibition were assessed by MTT and clonogenic assays, respectively. Hoechst staining, DNA electrophoresis and TUNEL staining were conducted to detect apoptosis. YD9 cells were treated with NaF, and western blotting, immunocytochemistry, confocal microscopy, FACScan flow cytometry, and MMP and proteasome activity assays were performed sequentially. The NaF treatment resulted in a time- and dose-dependent decrease in YD9 cell viability, a dose-dependent inhibition of cell growth, and the induction of apoptotic cell death. The apoptotic response of these cells was manifested by nuclear condensation, DNA fragmentation, the reduction of MMP and proteasome activity, a decreased DNA content, the release of cytochrome c into the cytosol, the translocation of AIF and DFF40 (CAD) into the nucleus, a significant shift of the Bax/Bcl-2 ratio, and the activation of caspase-9, caspase-3, PARP, Lamin A/C and DFF45 (ICAD). Furthermore, NaF treatment resulted in the downregulation of G1 cell cyclerelated proteins, and upregulation of p53 and the Cdk inhibitor p27KIP1. Taken collectively, our present findings demonstrate that NaF strongly inhibits YD9 cell proliferation by modulating the expression of G1 cell cycle-related proteins and inducing apoptosis via mitochondrial and caspase pathways.
Apoptosis ; Blotting, Western ; Carcinoma, Squamous Cell ; Caspase 3 ; Caspase 9 ; Cell Death ; Cell Line ; Cell Proliferation ; Cell Survival ; Cytochromes c ; Cytosol ; DNA ; DNA Fragmentation ; Down-Regulation ; Electrophoresis ; Flow Cytometry ; Humans ; Immunohistochemistry ; In Situ Nick-End Labeling ; Microscopy, Confocal ; Proteasome Endopeptidase Complex ; Proteins ; Up-Regulation

Osmidrosis develops in many young people due to the apocrine gland becoming active after the adolescent period and can cause difficulty in social activities and personal relationships. We compared 2 surgical treatment methods for osmidrosis, superficial suction and subdermal excision, to determine how many of apocrine glands could be removed and examine if a significant difference was present in treatment outcome. The subjects used for the present study included 62 patients of whom 46 patients underwent subdermal excision and 16, superficial suction. We counted the total number of apocrine glands in tissue samples obtained using those 2 methods, fixed in formalin and treated with usual histologic treatment. We calculated the number of apocrine glands per unit area by measuring the axillary area of the surgery site determined before surgery. The patients who underwent surgery using those 2 methods were divided into satisfactory group and unsatisfactory group by evaluating the results subjectively and objectively after surgery. The satisfactory rate was 95.7% in 46 patients who underwent subdermal excision and 81.25% in 16 patients who underwent superficial suction. An average of 127.82 apocrine glands/ cm2 were removed through subdermal excision and 72.71 apocrine glands/cm2, through superficial suction. We determined that more apocrine glands were removed with a statistical significance using subdermal excision. However, considering the result that 81.25% satisfactory rate was seen despite 57% of apocrine glands being removed with superficial suction compared with subdermal excision, superficial suction would be also effective in reducing the number of apocrine glands to below a threshold.
Adolescent ; Apocrine Glands ; Formaldehyde ; Humans ; Suction* ; Treatment Outcome

Chios gum mastic (CGM) is a resinous exudate obtained from the stem and the main leaves of Pistacia lenticulus tree native to Mediterranean areas. Recently, it was reported that CGM induced apoptosis in a few cancer cells in vitro. Since recent studies indicated the synergistic interactions between the apoptotic stimulus and a proteasome inhibitor, the ubiquintin-proteasome pathway has become an attractive target in cancer therapy. And to date, there has been no report of the synergistic apoptotic effect between CGM and a proteasome inhibitor to become an attractive target in cancer therapy. Therefore, this study was undertaken to investigate the synergistic apoptotic effect of co-treatment with a natural product, CGM, and a proteasome inhibitor, lactacystin, on human osteosarcoma (HOS) cells. To investigate whether the co-treatment of CGM and lactacystin compared with each single treatment efficiently induced apoptosis on HOS cells, MTT assay, DNA electrophoresis, Hoechst staining, DNA hypoploidy assay, Westen blot analysis, immunofluorescent staining, proteasome activity and mitochondrial membrane potential (MMP) change were performed. In this study, HOS cells co-treated with CGM and lactacystin showed several lines of apoptotic manifestation such as nuclear condensation, DNA fragmentation, the reduction of MMP and proteasome activity, the decrease of DNA content, the release of cytochrome c into cytosol, the translocation of AIF and DFF40 (CAD) onto nuclei, and activation of caspase-7, caspase-3, PARP and DFF45 (ICAD) whereas each single treated HOS cells hardly showed. We presented data indicating that the co-treatment of CGM and lactacystin induced potentially apoptosis whereas each single treatment did slightly. Moreover, the co-treatment of CGM and lactacystin potentiated the inhibition of proteasome activity. Therefore, our data provide the possibility that combination therapy of CGM and lactacystin could be considered as a novel therapeutic strategy for human osteosarcoma.
Acetylcysteine ; Apoptosis ; Caspase 3 ; Caspase 7 ; Cytochromes c ; Cytosol ; DNA ; DNA Fragmentation ; Electrophoresis ; Exudates and Transudates ; Gingiva ; Humans ; Membrane Potential, Mitochondrial ; Osteosarcoma ; Pistacia ; Proteasome Endopeptidase Complex ; Proteasome Inhibitors ; Resins, Plant ; Trees