Neuropsychological adverse drug reactions of Remdesivir: analysis using VigiBase, the WHO global database of individual case safety reports.

OBJECTIVE: Although remdesivir (GS-5734) has recently demonstrated clinical benefits against the pandemic outbreak of coronavirus disease 2019 (COVID-19), neuropsychological adverse reactions (ADRs) remain to be examined in real-world settings. Therefore, we aimed to identify and characterize the neuropsychological ADRs associated with remdesivir use. MATERIALS AND METHODS: We obtained data for this international pharmacovigilance cohort study from individual case safety reports (ICSRs) in a World Health Organization database (VigiBase) from the first report on remdesivir on February 17, 2020, until August 30, 2020 (n=1,403,532). ADRs reported to be relevant to remdesivir were compared with the full database by using a Bayesian neural network method to calculate the information component (IC). RESULTS: A total of 2,107 reported cases of neuropsychological ADRs suspected to be associated with remdesivir were identified from among all ICSRs in the database during the observation period. Although 108 neuropsychological ADRs (64 neurologic events and 44 psychologic events) were reported in association with the medication, no statistically significant pharmacovigilance signal could be detected; the IC025 value was negative for all of the neuropsychological dysfunctions (anxiety [n=13, 0.62%], seizures [n=12, 0.57%], lethargy [n=6, 0.28%], agitation [n=5, 0.25%], cerebral infarction [n=3, 0.14%], ischemic stroke [n=3, 0.14%], and hemiparesis [n=3, 0.14%]). CONCLUSIONS: Our study demonstrates that remdesivir, a novel drug applied to the treatment of COVID-19, does not have a significant association with adverse neurologic or psychiatric reactions in the real-world setting.

Tipping the immunostimulatory and inhibitory DAMP balance to harness immunogenic cell death.

Induction of tumor cell death is the therapeutic goal for most anticancer drugs. Yet, a mode of drug-induced cell death, known as immunogenic cell death (ICD), can propagate antitumoral immunity to augment therapeutic efficacy. Currently, the molecular hallmark of ICD features the release of damage-associated molecular patterns (DAMPs) by dying cancer cells. Here, we show that gemcitabine, a standard chemotherapy for various solid tumors, triggers hallmark immunostimualtory DAMP release (e.g., calreticulin, HSP70, and HMGB1); however, is unable to induce ICD. Mechanistic studies reveal gemcitabine concurrently triggers prostaglandin E2 release as an inhibitory DAMP to counterpoise the adjuvanticity of immunostimulatory DAMPs. Pharmacological blockade of prostaglandin E2 biosythesis favors CD103+ dendritic cell activation that primes a Tc1-polarized CD8+ T cell response to bolster tumor rejection. Herein, we postulate that an intricate balance between immunostimulatory and inhibitory DAMPs could determine the outcome of drug-induced ICD and pose COX-2/prostaglandin E2 blockade as a strategy to harness ICD.

Anatomical analysis to establish the optimal positioning of an osteotomy for genioglossal advancement: a trial in cadavers.

Genioglossal advancement, which is one of the treatments for obstructive sleep apnoea, can be effective only if it contains enough genial tubercle for an osteotomy. The aim of this study was to establish the position of the genial tubercle and of the optimal osteotomy during genioglossal advancement. Twenty-four adult cadavers with intact bony mandibular structures were included. Five variables were measured: the width and height of the genial tubercle (GTW); the distance from its inferior border to the inferior border of the mandible (IGT-IBM); the distance from the superior border of the genial tubercle to the inferior border of the mandible (SGT-IBM); and the width of the intermental foramen (IMFW). The following mean (SD) (range) measurements were obtained: GTW 7.38 (1.43) (4.5-10.0); GTH 7.94 (1.45) (5.0-10.0); IGT-IBM 7.96 (2.29) (4.0-12.0); SGT-IBM 15.90 (2.29) (12.0-20.0); and IMFW 56.65 (6.44) (43.0-67.0) mm. Of the 24 cadavers, 22 showed evidence of optimal positioning when the osteotomy was placed 2mm higher than the SGT-IBM measured on the inner table. This suggests that an optimal osteotomy, which includes the genial tubercle, may be possible in most patients when the osteotomy is positioned 2mm higher at the SGT-IBM.

Identifying the potential long-term survivors among breast cancer patients with distant metastasis.

BACKGROUND: We aimed to develop a prediction model to identify long-term survivors after developing distant metastasis from breast cancer. PATIENTS AND METHODS: From the institution's database, we collected data of 547 patients who developed distant metastasis during their follow-ups. We developed a model that predicts the post-metastasis overall survival (PMOS) based on the clinicopathologic factors of the primary tumors and the characteristics of the distant metastasis. For validation, the survival data of 254 patients from four independent institutions were used. RESULTS: The median duration of the PMOS was 31.0 months. The characteristics of the initial primary tumor, such as tumor stage, hormone receptor status, and Ki-67 expression level, and the characteristics of the distant metastasis presentation including the duration of disease-free interval, the site of metastasis, and the presence of metastasis-related symptoms were independent prognostic factors determining the PMOS. The association between tumor stage and the PMOS was only seen in tumors with early relapses. The PMOS score, which was developed based on the above six factors, successfully identified patients with superior survival after metastasis. The median PMOS for patients with a PMOS score of <2 and for patients with a PMOS score of >5 were 71.0 and 12 months, respectively. The clinical significance of the PMOS score was further validated using independent multicenter datasets. CONCLUSIONS: We have developed a novel prediction model that can classify breast cancer patients with distant metastasis according to their survival after metastasis. Our model can be a valuable tool to identify long-term survivors who can be potential candidates for more intensive multidisciplinary approaches. Furthermore, our model can provide a more reliable survival information for both physicians and patients during their informed decision-making process.

Effects of Palonosetron on Perioperative Cardiovascular Complications in Patients Undergoing Noncardiac Surgery With General Anesthesia: A Retrospective Cohort Study.

We retrospectively investigated whether palonosetron administered during the induction of general anesthesia is associated with an increased risk of perioperative cardiovascular complications in a single tertiary center cohort consisting of 4,517 palonosetron-exposed patients and 4,517 propensity score-matched patients without palonosetron exposure. The primary endpoint was a composite of perioperative cardiovascular complications, including intraoperative cardiac arrhythmia, intraoperative cardiac death, and myocardial injury within the first postoperative week, and there was no significant difference between the groups (odds ratio [OR] = 1.04; 95% confidence interval [CI] = 0.92-1.19). As secondary endpoints, intraoperative cardioversion, cardiac compression, use of cardiovascular drugs, postoperative hospital stay, and in-hospital mortality showed no differences between the groups. However, the palonosetron group showed decreased intraoperative hypotension (OR = 0.88; 95% CI = 0.79-0.97) and length of postoperative intensive care unit (ICU) stay (4.26 ± 9.86 vs. 6.14 ± 16.75; P = 0.026). Palonosetron did not increase the rate of perioperative cardiovascular complications, and can therefore be used safely during anesthetic induction.

Comparison of steroid administration methods in patients with idiopathic sudden sensorineural hearing loss: a retrospective observational study.

OBJECTIVES: To compare the recovery rates of patients with idiopathic sudden sensorineural hearing loss (ISSHL) treated with oral systemic steroids (PO) or intratympanic steroid injection (IT) or both. DESIGN: A retrospective observational study. SETTING: Tertiary referral centre. PARTICIPANTS: Eight hundred and forty-four patients diagnosed with ISSHL within 14 days of the onset of symptoms. The patients were divided into three groups by treatment modality. MAIN OUTCOME MEASURES: Threshold of pure-tone tests, age, accompanying symptoms and underlying diseases were compared. The level of final hearing recovery was evaluated by the application of the results of the pure-tone test that was performed at least 3 months after the completion of each treatment. RESULTS: Final hearing recovery rate differed significantly by the type of treatment (P = 0.031). Recovery rates in the PO and combined groups were significantly higher in patients with mild (85.1% and 88.6%, respectively) than with profound (52.8% and 69.0%, respectively) hearing loss (P < 0.05). In contrast, severity and recovery rate were not significantly correlated in the IT group (P > 0.05). Combined treatment yielded significantly higher recovery rates than other treatment modalities in patients without hypertension (HTN) and diabetes mellitus (DM) (P = 0.021). CONCLUSION: In the group treated with combined therapy, better hearing improvement was obtained than in the groups treated with systemic steroid only or with intratympanic steroid injection only without complications. These findings suggest that the combination of systemic administration and intratympanic injection may improve patient prognosis.

Modulation of dendritic cell function by the radiation-mediated secretory protein γ-synuclein.

Recently, γ-synuclein (SNCG), which is also known as breast cancer-specific gene-1, has been demonstrated to be an adverse and aggressive marker in breast cancer. In our previous study, SNCG was significantly upregulated in irradiated human breast cancer cells. The aim of this study was to investigate whether radiation-induced, tumor-derived SNCG can influence dendritic cell (DC) function in immune systems. The phenotypical and functional changes of DCs in the presence or absence of SNCG were investigated by FACS analysis, ELISA, and real-time PCR. The ability of SNCG-treated DCs to influence T cells was also examined by coculturing with T cells. The treatment of DCs with SNCG protein inhibited the surface expression of the co-stimulatory molecules CD40 and CD86, and decreased the mRNA levels of pro-inflammatory cytokines. The SNCG-treated DCs inhibited T-cell proliferation slightly, but distinctively increased the population of regulatory T cells. In addition, the production of TGF-ß from T cells was significantly increased when they were cocultured with SNCG-treated DCs. Taken together, these results demonstrate that tumor-derived SNCG contributes to immunosuppressive effects via the inhibition of DC differentiation and activation, thus making it a potential target for cancer treatment.

CHK2 kinase promotes pre-mRNA splicing via phosphorylating CDK11(p110).

Checkpoint kinase 2 (CHK2) kinase is a key mediator in many cellular responses to genotoxic stresses, including ionizing radiation (IR) and topoisomerase inhibitors. Upon IR, CHK2 is activated by ataxia telangiectasia mutated kinase and regulates the S-phase and G1-S checkpoints, apoptosis and DNA repair by phosphorylating downstream target proteins, such as p53 and Brca1. In addition, CHK2 is thought to be a multi-organ cancer susceptibility gene. In this study, we used a tandem affinity purification strategy to identify proteins that interact with CHK2 kinase. Cyclin-dependent kinase 11 (CDK11)(p110) kinase, implicated in pre-mRNA splicing and transcription, was identified as a CHK2-interacting protein. CHK2 kinase phosphorylated CDK11(p110) on serine 737 in vitro. Unexpectedly, CHK2 kinase constitutively phosphorylated CDK11(p110) in a DNA damage-independent manner. At a molecular level, CDK11(p110) phosphorylation was required for homodimerization without affecting its kinase activity. Overexpression of CHK2 promoted pre-mRNA splicing. Conversely, CHK2 depletion decreased endogenous splicing activity. Mutation of the phosphorylation site in CDK11(p110) to alanine abrogated its splicing-activating activity. These results provide the first evidence that CHK2 kinase promotes pre-mRNA splicing via phosphorylating CDK11(p110).

Establishment of isolation and expansion protocols for human cardiac C-kit-positive progenitor cells for stem cell therapy.

Although cardiac stem cells (CSCs) have emerged in regeneration research, the number of isolated CSCs is low, making a sufficient supply of functional elements an important consideration in cardiovascular research. In this study, we established an efficient method for CSC isolation. We directly compared cultures of single cells to human cardiac-derived c-kit-positive progenitor cells (hCPCs(c-kit+)). The two protocols employed enzymatically digested hCPCs(c-kit+) (ED-hCPCs) with tissue-expanded hCPC(c-kit+) (TE-hCPCs). Using fluorescence-activated cell sorting, we showed the concentration of c-kit in TE-hCPCs to be higher than in ED-hCPCs, although the total number of c-kit positive cells resulting from ED-hCPCs was similar to that resulting from TE-hCPCs. The cardiomyocyte-associated proteins, GATA4 and Nkx2-5, which were expressed during hCPCs expansion, did not differ between the isolation methods. Importantly, the expression of the CSC stem cell marker, c-kit, was more efficiently preserved using the ED-hCPCs versus the TE-hCPCs method. In a cell proliferation assay, the ED-hCPCs method produced a significantly greater number of cells. Finally, hCPCs derived using both protocols differentiated into endothelial, smooth muscle, and cardiomyocyte lineages. In conclusion, the single-cell culture protocol using an enzymatic digestion method may be more useful to isolate human cardiac-derived c-kit-positive elements compared with the tissue expansion method.

Polyethylene glycol bowel preparation does not eliminate the risk of acute renal failure: a population-based case-crossover study.

BACKGROUND AND STUDY AIMS: Polyethylene glycol (PEG) bowel preparations are regarded as effective and safe for colonoscopy; however, recent reports have indicated a risk of acute renal failure (ARF). This population-based case-crossover study evaluated the association between PEG and ARF in screening colonoscopy patients aged ≥ 50 years. PATIENTS AND METHODS: Korean Health Insurance Review and Assessment Service (HIRA) claims data from 1 January 2005 to 31 December 2009 were used in the study. The study population consisted of patients aged ≥ 50 years who were first hospitalized for ARF following colonoscopy involving PEG bowel preparation. For each patient, PEG use in a 1-, 2-, or 4-week period prior to the first hospital admission date for ARF (hazard period) was compared with PEG use in four earlier 1-, 2-, or 4-week control periods. Conditional logistic regression analysis was used to estimate odds ratios (ORs) and 95 % confidence intervals (CIs), adjusting for concomitant medications that could induce ARF. RESULTS: The total number of study patients was 1064 (59 % were male). A greater proportion of patients used PEG during the hazard period than during the control periods (for 4-week time window: 8.8 % vs. 3.2 %). The adjusted ORs for ARF incidence when applying the 1-, 2-, and 4-week periods were 3.1 (95 %CI 2.06 - 4.73), 2.5 (95 %CI 1.76 - 3.53), and 2.1 (95 %CI 1.61 - 4.85), respectively. CONCLUSIONS: The use of PEG was associated with the risk of ARF. Adequate hydration and renal function monitoring should be assured before and after colonoscopy, regardless of the bowel preparation regimen used.

Long-term clinical outcomes and risk factors for the occurrence of post-operative complications after cardiovascular surgery in patients with Behçet's disease.

OBJECTIVES: Cardiovascular surgery in patients with Behçet's disease (BD) frequently leads to postoperative complications such as anastomotic leakage, occlusion or pseudoaneurysm. We evaluated the clinical outcomes and related risk factors of postoperative complications in BD patients undergoing cardiovascular surgeries, as well as the long-term efficiency of postoperative immunosuppressive treatment. METHODS: Forty-one patients with BD who had undergone cardiovascular surgery between 1990 and 2009 were studied. We evaluated the patients' clinical data, postoperative complications, and survival rate. Risk factors related to the occurrence of postoperative complications were identified by univariate analysis using the Kaplan-Meier method with the log-rank test and multivariate analysis using the Cox proportional hazards regression model. RESULTS: Fifty-nine operations were performed in 41 patients. During the mean follow-up period of 65.3±48.1 months, complications such as paravalvular leakage, dehiscence, fistula, graft occlusion, or pseudoaneurysm occurred in 29 operations (49.2%). The cumulative occurrence rate of postoperative complication was 10.2% at three months, 32.8% at 12 months, and 43.8% at 24 months. Upon univariate analysis, young age, high Creactive protein levels, lack of postoperative immunosuppression, and short disease duration were identified as significant factors responsible for the occurrence of postoperative complications. In multivariate analysis, postoperative immunosuppression was found to independently lower the risk of complications. The 5-year survival rate was significantly higher in patients with postoperative immunosup immunosuppression than in those without (84.5% vs. 45.0%, p=0.011). CONCLUSIONS: The present study suggests that postoperative immunosuppressive therapy after cardiovascular surgeries in BD patients is important for reducing the development of serious postoperative complications.

Short-acting nifedipine and risk of stroke in elderly hypertensive patients.

OBJECTIVES: Short-acting nifedipine is frequently prescribed in elderly hypertensive patients, despite warnings of possible harmful cardiovascular effects. We conducted a case-crossover study to estimate the risk of stroke episodes associated with use of short-acting nifedipine in elderly hypertensive patients. METHODS: We used the Korea Health Insurance Review & Assessment Service database. Cases included elderly hypertensive patients with hospitalization or emergency department visits for first stroke (International Classification of Diseases-10, I60-I64) between July 1, 2005, and June 30, 2006. Patients with prior stroke-related hospital admission or any visit related to TIA were excluded. Exposure to a short-acting nifedipine formulation was assessed within 7 days before the incident stroke episode (case period) and within a 7-day period preceding 60 days before the episode (control period). Odds ratios (ORs) with 95% confidence intervals (CIs) were calculated by conditional logistic regression, with adjusting for antihypertensives, anticoagulants, antiplatelet agents, and pneumonia. RESULTS: A total of 16,069 stroke patients with a mean (±SD) age of 68.3 (±2.1) years were studied, of whom 8,573 (53.3%) were female. Short-acting nifedipine was prescribed at least once to 301 (1.9%) patients during the case period. An increased risk of stroke associated with use of short-acting nifedipine within 7 days (adjusted OR 2.56; 95% CI 1.96-3.37) was observed. Patients who were newly prescribed nifedipine within the recent 7 days showed an OR of 4.17 (95% CI 2.93-5.93) compared with nonusers. CONCLUSION: Use of short-acting nifedipine was associated with increased risk of stroke occurrence in elderly hypertensive patients.

The synergistic effect of Mig-6 and Pten ablation on endometrial cancer development and progression.

Ablation of Mig-6 in the murine uterus leads to the development of endometrial hyperplasia and estrogen-induced endometrial cancer. An additional endometrial cancer mouse model is generated by the ablation of phosphatase and tensin homolog deleted from chromosome 10 (Pten) (either as heterozygotes or by conditional uterine ablation). To determine the interplay between Mig-6 and the PTEN/phosphoinositide 3-kinase signaling pathway during endometrial tumorigenesis, we generated mice with Mig-6 and Pten conditionally ablated in progesterone receptor-positive cells (PR(cre/+)Mig-6(f/f)Pten(f/f); Mig-6(d/d)Pten(d/d)). The ablation of both Mig-6 and Pten dramatically accelerated the development of endometrial cancer compared with the single ablation of either gene. The epithelium of Mig-6(d/d)Pten(d/d) mice showed a significant decrease in the number of apoptotic cells compared with Pten(d/d) mice. The expression of the estrogen-induced apoptotic inhibitors Birc1 was significantly increased in Mig-6(d/d)Pten(d/d) mice. We identified extracellular signal-regulated kinase 2 (ERK2) as an MIG-6 interacting protein by coimmunoprecipitation and demonstrated that the level of ERK2 phosphorylation was increased upon Mig-6 ablation either singly or in combination with Pten ablation. These results suggest that Mig-6 exerts a tumor-suppressor function in endometrial cancer by promoting epithelial cell apoptosis through the downregulation of the estrogen-induced apoptosis inhibitors Birc1 and the inhibition of ERK2 phosphorylation.

TRIM72 negatively regulates myogenesis via targeting insulin receptor substrate-1.

Lipid rafts have been known to be platforms to initiate cellular signal transduction of insulin-like growth factor (IGF) inducing skeletal muscle differentiation and hypertrophy. Here, tripartite motif 72 (TRIM72), with a really interesting new gene (RING)-finger domain, a B-box, two coiled-coil domains, and a SPRY (SPla and RYanodine receptor) domain, was revealed to be predominantly expressed in the sarcolemma lipid rafts of skeletal and cardiac muscles. Adenoviral TRIM72 overexpression prevented but RNAi-mediated TRIM72 silencing enhanced C2C12 myogenesis by modulating the IGF-induced insulin receptor substrate-1 (IRS-1) activation through the molecular association of TRIM72 with IRS-1. Furthermore, myogenic activity was highly enhanced with increased IGF-induced Akt activation in the satellite cells of TRIM72(-/-) mice, compared to those of TRIM72+/+ mice. Because TRIM72 promoter analysis shows that two proximal E-boxes in TRIM72 promoter were essential for MyoD- and Akt-dependent TRIM72 transcription, we can conclude that TRIM72 is a novel antagonist of IRS-1, and is essential as a negative regulator of IGF-induced muscle differentiation.

Epidermolysis bullosa simplex in Japanese and Korean patients: genetic studies in 19 cases.

BACKGROUND: Epidermolysis bullosa simplex (EBS) comprises a group of hereditary bullous diseases characterized by intraepidermal blistering caused by mutations in either keratin gene, KRT5 or KRT14. Significant correlation between the position of mutations within these proteins and the clinical severity of EBS has been noted. A recent report showed EBS cases in Israel had unique genetic features compared with European or U.S.A. associated families, which suggests that the ethnic and geographical features of EBS patients may be different. OBJECTIVES: To assess the possibility that EBS may present with certain specific features in Japanese and Koreans and to identify additional EBS mutations for genotype/phenotype correlation. METHODS: EBS was clinically diagnosed and confirmed by transmission electron microscopic examination of a skin biopsy. Mutation analysis of KRT5 and KRT14 was performed by direct sequencing in 17 Japanese and two Korean EBS patients. RESULTS: We have identified six novel KRT5 missense mutations (V143D, D158V, V186M, Q191P, R352S, G517D). R352S is the first mutation in the 2A domain. Most of these novel mutations changed amino acids that were evolutionarily conserved. Eight including all five mutations in EBS-Dowling-Meara patients have been previously reported. We were unable to detect mutations in five sporadic EBS-Koebner patients. The proportion of mutations in KRT5 (11 of 14; 78%) is higher than that for KRT14 mutations (3 of 14; 21%) in these Japanese and Korean EBS patients. CONCLUSIONS: Japanese and Korean patients with EBS showed very similar phenotype and genotype correlations with patients from Western countries. Whether the higher proportion of KRT5 mutations is a definite characteristic of Japanese and Korean patients with EBS or not, requires further research into mutations in Japanese and Korean people.

Cytopathic changes in rat microglial cells induced by pathogenic Acanthamoeba culbertsoni: morphology and cytokine release.

To determine whether pathogenic Acanthamoeba culbertsoni trophozoites and lysate can induce cytopathic changes in primary-culture microglial cells, morphological changes were observed by transmission electron microscopy (TEM). In addition, the secretion of two kinds of cytokines, tumor necrosis factor alpha (TNF-alpha) and interleukin-1beta (IL-1beta), from microglial cells was observed. Trophozoites of pathogenic A. culbertsoni made contact with microglial cells and produced digipodia. TEM revealed that microglial cells cocultured with amoebic trophozoites underwent a necrotic process, accompanied by lysis of the cell membrane. TEM of microglial cells cocultured with amoebic lysate showed that the membranes of the small cytoplasmic vacuoles as well as the cell membrane were lysed. The amounts of TNF-alpha secreted from microglial cells cocultured with A. culbertsoni trophozoites or lysate increased at 6 h of incubation. The amounts of IL-1beta secreted from microglial cells cocultured with A. culbertsoni trophozoites at 6 h of incubation was similar to those secreted from the control group, but the amounts decreased during cultivation with A. culbertsoni lysate. These results suggest that pathogenic A. culbertsoni induces the cytopathic effects in primary-culture rat microglial cells, with the effects characterized by necrosis of microglial cells and changes in levels of secretion of TNF-alpha and IL-1beta from microglial cells.

Two distinct nuclear receptor-interaction domains and CREB-binding protein-dependent transactivation function of activating signal cointegrator-2.

ASC-2 is a recently isolated transcriptional cointegrator molecule, which is amplified in human cancers and stimulates transactivation by nuclear receptors, AP-1, nuclear factor kappaB (NFkappaB), serum response factor (SRF), and numerous other transcription factors. ASC-2 contained two nuclear receptor-interaction domains, both of which are dependent on the integrity of their core LXXLL sequences. Surprisingly, the C-terminal LXXLL motif specifically interacted with oxysterol receptor LXRss, whereas the N-terminal motif bound a broad range of nuclear receptors. These interactions appeared to be essential because a specific subregion of ASC-2 including the N- or C-terminal LXXLL motif acted as a potent dominant negative mutant with transactivation by appropriate nuclear receptors. In addition, the autonomous transactivation domain (AD) of ASC-2 was found to consist of three separable subregions; i.e. AD1, AD2, and AD3. In particular, AD2 and AD3 were binding sites for CREB binding protein (CBP), and CBP-neutralizing E1A repressed the autonomous transactivation function of ASC-2. Furthermore, the receptor transactivation was not enhanced by ASC-2 in the presence of E1A and significantly impaired by overexpressed AD2. From these results, we concluded that ASC-2 directly binds to nuclear receptors and recruits CBP to mediate the nuclear receptor transactivation in vivo.

Diphyllobothrium latum infection after eating domestic salmon flesh.

Diphyllobothrium latum infection in human is not common in Korea and only thirty seven cases have been reported since 1921. We report two cases of fish tapeworm infection after ingestion of raw cherry salmon (Oncorhynchus masou) caught in the domestic river. Among four family members who ate together raw salmon flesh six months ago, just two, mother and daughter, were infected. It is our expectation that the salmon associated tapeworm infections would be enlisted as one of the major parasitic problems with the growing consumption of salmon in Korea.