Background: The inflammasome, a multiprotein complex, is crucial in the pathogenesis of various autoinflammatory disorders. In particular, the NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome has recently been associated with diseases such as psoriasis, vitiligo, lupus, and alopecia areata (AA). Objective: The objective of this study is to investigate the potential involvement of the inflammasome in the pathogenesis of AA and to determine its correlation with clinical manifestations. Methods: A total of 144 patients with AA and 22 healthy controls were included. Scalp skin and serum samples were collected to assess the levels of NLRP3-related molecules in lesional tissue and blood, respectively. Additionally, we performed immunostaining to measure the expression of NLRP3 and caspase-1 in the outer root sheath (ORS). Results: Lesional interleukin-1β expression was significantly elevated in patients with AA at all stages compared with controls. In the progressive stage, lesional C-X-C motif chemokine ligand 10 levels were markedly higher than those in controls and other stages. Serum interferon-γ levels were also significantly increased during the progressive stage of AA compared with controls. Immunostaining revealed strong NLRP3 and caspase-1 positivity in the ORS during the initial and progressive stages of AA, in contrast to the recovery stage. Conclusion These results highlight the functional role of the inflammasomes in the pathogenesis of AA.

Recurrent scalp compromise following deep brain stimulation (DBS) implantation remains a challenging reconstructive problem, particularly in patients with chronic infection and repeated revision procedures. We present an acellular dermal matrix (ADM)-assisted salvage strategy using rotational scalp flap coverage with adjunctive calvarial recession for preservation of exposed DBS hardware. After debridement and subperiosteal flap elevation, ADM was applied over the exposed hardware as a biologic reinforcement layer prior to tension-free closure. Adjunctive calvarial recession was performed to reduce hardware prominence. Postoperative computed tomography demonstrated decreased hardware projection, and stable wound healing without recurrent dehiscence or infection was maintained during follow-up. This combined approach may represent an effective salvage option for recurrent DBS scalp compromise while preserving functional neuromodulation hardware.

Background: The prevalence of diabetes mellitus and early-onset dementia (EOD), defined as dementia diagnosed at an age <65 years, is increasing worldwide, with significant socioeconomic implications. We investigated the association between diabetes, prediabetes, and EOD, focusing on the influence of diabetes duration on EOD risk. Methods: Using the Korean National Health Insurance Service database, we analyzed data from 1,979,509 patients aged 40–60 years who underwent health checkups in 2009. Patients were categorized into five groups: normal, impaired fasting glucose (IFG), newly diagnosed diabetes, diabetes duration <5 years, and diabetes duration ≥5 years. Cox proportional hazard models were used to estimate the adjusted hazard ratios (aHRs) for EOD after adjusting for demographic and clinical covariates. Results: During the observation period (mean 7.75 years), 8,921 patients with EOD were identified. The diabetes group demonstrated a significantly higher incidence of EOD compared to the normal group (aHR, 1.334; 95% confidence interval [CI], 1.226 to 1.451). EOD risk increased with longer diabetes duration, with the highest risk observed in patients with diabetes ≥5 years (aHR, 1.543; 95% CI, 1.368 to 1.741). No significant difference was observed between the IFG and normal groups (aHR, 0.989; 95% CI, 0.938 to 1.043). Additionally, the hypertension group exhibited a significantly higher incidence of EOD compared to the non-hypertension group (aHR, 1.364; 95% CI, 1.291 to 1.442). Conclusion Diabetes is independently associated with increased risk of EOD, and this risk increases with longer diabetes duration. This association remained significant regardless of the presence and duration of hypertension.

Background: To investigate the impact of alcohol consumption on all-cause and cancer mortalities in patients with type 2 diabetes (T2D). Methods: This nationwide cohort study included Korean patients with T2D aged >20 years from a national health exams cohort (2009 to 2012). Participants were categorized based on alcohol consumption: non, mild (<30 g/day), and heavy drinkers (≥30 g/day). Primary outcomes were all-cause and cancer mortality rates. Cox proportional hazard regression analyses were used to calculate adjusted hazard ratios (aHRs) with a 95% confidence interval (CI) with adjustments for age, sex, body mass index, smoking, exercise, comorbidities, diabetes duration, and medications. Results: Among 2,642,359 participants (median follow-up, 7.8 years), 57.2%, 32.7%, and 10.1% were non, mild, and heavy drinkers, respectively. Compared to non-drinkers, mild alcohol consumption was associated with reduced all-cause mortality (aHR, 0.81; 95% CI, 0.80 to 0.82) and cancer mortality (aHR, 0.88; 95% CI, 0.86 to 0.89), while heavy drinking increased both all-cause (aHR, 1.06; 95% CI, 1.04 to 1.07) and cancer mortalities (aHR, 1.09; 95% CI, 1.06 to 1.11). Subgroup analyses revealed variations: in chronic kidney disease and older age groups, heavy drinkers showed lower risk of all-cause mortality compared to non-drinkers. Regarding cancer mortality, younger and middle-aged groups showed protective effects of alcohol even for heavy drinkers, while females showed linear association between alcohol consumption and cancer mortality. Conclusion This study indicates a J-shaped relationship between alcohol consumption and all-cause and cancer mortality risk in patients with T2D, with variations across subgroups. These findings suggest the need for personalized recommendations considering individual risk factors.

Objective: To evaluate the effects of Capsosiphon fulvescens (C. fulvescens) ethanolic extract on inflammation in lipopolysaccharide (LPS)-induced RAW296.7 macrophages. Methods: The protective effects of C. fulvescens ethanolic extract on LPS-induced inflammation in RAW264.7 macrophages were assessed using biochemical analysis, including enzyme-linked immunosorbent assay, quantitative reverse transcription-polymerase chain reaction, and Western blot analysis. To examine reactive oxygen species (ROS) production, flow cytometry analysis, and immunofluorescence staining were used. Furthermore, the modulatory effect of C. fulvescens ethanolic extract on NF-κB activation was investigated. Results: C. fulvescens ethanolic extract significantly attenuated LPS-induced levels of pro-inflammatory cytokines and notably reduced the secretion and mRNA levels of LPS-mediated matrix metalloproteinases. In addition, C. fulvescens ethanolic extract decreased ROS production and suppressed the TLR4/NF-κB signaling pathway. Conclusions: C. fulvescens ethanolic extract alleviates inflammation as well as oxidative stress by modulating the TLR4/NF-κB signaling in LPS-induced RAW264.7 macrophages. C. fulvescens can be used as a potential therapeutic agent to suppress inflammation and oxidative stress-associated diseases.

Background: Carbapenem resistance in Pseudomonas aeruginosa is a serious global health problem. We investigated the clonal distribution and its association with the carbapenem resistance mechanisms of carbapenem-non-susceptible P. aeruginosa isolates from three Korean hospitals. Methods: A total of 155 carbapenem-non-susceptible P. aeruginosa isolates collected between 2011 and 2019 were analyzed for sequence types (STs), antimicrobial susceptibility, and carbapenem resistance mechanisms, including carbapenemase production, the presence of resistance genes, OprD mutations, and the hyperproduction of AmpC β-lactamase. Results: Sixty STs were identified in carbapenem-non-susceptible P. aeruginosa isolates.Two high-risk clones, ST235 (N = 41) and ST111 (N = 20), were predominant; however, sporadic STs were more prevalent than high-risk clones. The resistance rate to amikacin was the lowest (49.7%), whereas that to piperacillin was the highest (92.3%). Of the 155 carbapenem-non-susceptible isolates, 43 (27.7%) produced carbapenemases. Three metalloβ-lactamase (MBL) genes, blaIMP-6 (N = 38), blaVIM-2 (N = 3), and blaNDM-1 (N = 2), were detected. blaIMP-6 was detected in clonal complex 235 isolates. Two ST773 isolates carried blaNDM-1 and rmtB. Frameshift mutations in oprD were identified in all isolates tested, regardless of the presence of MBL genes. Hyperproduction of AmpC was detected in MBL gene–negative isolates. Conclusions Frameshift mutations in oprD combined with MBL production or hyperproduction of AmpC are responsible for carbapenem resistance in P. aeruginosa. Further attention is required to curb the emergence and spread of new carbapenem-resistant P. aeruginosa clones.

Background: Carbapenem resistance in Pseudomonas aeruginosa is a serious global health problem. We investigated the clonal distribution and its association with the carbapenem resistance mechanisms of carbapenem-non-susceptible P. aeruginosa isolates from three Korean hospitals. Methods: A total of 155 carbapenem-non-susceptible P. aeruginosa isolates collected between 2011 and 2019 were analyzed for sequence types (STs), antimicrobial susceptibility, and carbapenem resistance mechanisms, including carbapenemase production, the presence of resistance genes, OprD mutations, and the hyperproduction of AmpC β-lactamase. Results: Sixty STs were identified in carbapenem-non-susceptible P. aeruginosa isolates.Two high-risk clones, ST235 (N = 41) and ST111 (N = 20), were predominant; however, sporadic STs were more prevalent than high-risk clones. The resistance rate to amikacin was the lowest (49.7%), whereas that to piperacillin was the highest (92.3%). Of the 155 carbapenem-non-susceptible isolates, 43 (27.7%) produced carbapenemases. Three metalloβ-lactamase (MBL) genes, blaIMP-6 (N = 38), blaVIM-2 (N = 3), and blaNDM-1 (N = 2), were detected. blaIMP-6 was detected in clonal complex 235 isolates. Two ST773 isolates carried blaNDM-1 and rmtB. Frameshift mutations in oprD were identified in all isolates tested, regardless of the presence of MBL genes. Hyperproduction of AmpC was detected in MBL gene–negative isolates. Conclusions Frameshift mutations in oprD combined with MBL production or hyperproduction of AmpC are responsible for carbapenem resistance in P. aeruginosa. Further attention is required to curb the emergence and spread of new carbapenem-resistant P. aeruginosa clones.

Background: Carbapenem resistance in Pseudomonas aeruginosa is a serious global health problem. We investigated the clonal distribution and its association with the carbapenem resistance mechanisms of carbapenem-non-susceptible P. aeruginosa isolates from three Korean hospitals. Methods: A total of 155 carbapenem-non-susceptible P. aeruginosa isolates collected between 2011 and 2019 were analyzed for sequence types (STs), antimicrobial susceptibility, and carbapenem resistance mechanisms, including carbapenemase production, the presence of resistance genes, OprD mutations, and the hyperproduction of AmpC β-lactamase. Results: Sixty STs were identified in carbapenem-non-susceptible P. aeruginosa isolates.Two high-risk clones, ST235 (N = 41) and ST111 (N = 20), were predominant; however, sporadic STs were more prevalent than high-risk clones. The resistance rate to amikacin was the lowest (49.7%), whereas that to piperacillin was the highest (92.3%). Of the 155 carbapenem-non-susceptible isolates, 43 (27.7%) produced carbapenemases. Three metalloβ-lactamase (MBL) genes, blaIMP-6 (N = 38), blaVIM-2 (N = 3), and blaNDM-1 (N = 2), were detected. blaIMP-6 was detected in clonal complex 235 isolates. Two ST773 isolates carried blaNDM-1 and rmtB. Frameshift mutations in oprD were identified in all isolates tested, regardless of the presence of MBL genes. Hyperproduction of AmpC was detected in MBL gene–negative isolates. Conclusions Frameshift mutations in oprD combined with MBL production or hyperproduction of AmpC are responsible for carbapenem resistance in P. aeruginosa. Further attention is required to curb the emergence and spread of new carbapenem-resistant P. aeruginosa clones.

Background: Carbapenem resistance in Pseudomonas aeruginosa is a serious global health problem. We investigated the clonal distribution and its association with the carbapenem resistance mechanisms of carbapenem-non-susceptible P. aeruginosa isolates from three Korean hospitals. Methods: A total of 155 carbapenem-non-susceptible P. aeruginosa isolates collected between 2011 and 2019 were analyzed for sequence types (STs), antimicrobial susceptibility, and carbapenem resistance mechanisms, including carbapenemase production, the presence of resistance genes, OprD mutations, and the hyperproduction of AmpC β-lactamase. Results: Sixty STs were identified in carbapenem-non-susceptible P. aeruginosa isolates.Two high-risk clones, ST235 (N = 41) and ST111 (N = 20), were predominant; however, sporadic STs were more prevalent than high-risk clones. The resistance rate to amikacin was the lowest (49.7%), whereas that to piperacillin was the highest (92.3%). Of the 155 carbapenem-non-susceptible isolates, 43 (27.7%) produced carbapenemases. Three metalloβ-lactamase (MBL) genes, blaIMP-6 (N = 38), blaVIM-2 (N = 3), and blaNDM-1 (N = 2), were detected. blaIMP-6 was detected in clonal complex 235 isolates. Two ST773 isolates carried blaNDM-1 and rmtB. Frameshift mutations in oprD were identified in all isolates tested, regardless of the presence of MBL genes. Hyperproduction of AmpC was detected in MBL gene–negative isolates. Conclusions Frameshift mutations in oprD combined with MBL production or hyperproduction of AmpC are responsible for carbapenem resistance in P. aeruginosa. Further attention is required to curb the emergence and spread of new carbapenem-resistant P. aeruginosa clones.

Alopecia areata (AA) is common causes of non-scarring hair loss. Recently, a relationship with inflammatory bowel disease (IBD) was observed. Herein, we introduced cases of AA in patients with IBD. Six patients were diagnosed with AA and IBD. Three presented with alopecia totalis (AT), two presented with patchy-type AA, and one demonstrated acute diffuse and total alopecia. The most frequent type of IBD was ulcerative colitis (UC), except for one Crohn’s disease. The onset of AA relative to that of IBD was mixed; AA developed previously in all adolescents. Only one was receiving anti-tumor necrosis factor-alpha agents for IBD treatment and the hair loss worsened. Patients with patchy-type AA demonstrated favorable outcomes rather than patients with AT. This study confirmed that the ratio of AT and UC was high, suggesting that alopecia is more strongly associated with UC.Also, we emphasize the importance of careful observation of IBD symptoms in patients with AA, especially in adolescents.