BML (Japan)

Carbapenemase-producing Enterobacter cloacae complex (CPEC) represents an emerging threat in healthcare settings; however, its spread across local and regional hospitals remains elusive. Between 2014 and 2022, 211 non-duplicate E. cloacae complex isolates (ECC) with reduced carbapenem susceptibility based on automated susceptibility testing were collected from 58 hospitals in 14 prefectures across Japan. PCR detected the blaIMP-1 group in 92.9% of isolates. Among these, 80 representative CPEC isolates underwent whole-genome sequencing. Two dominant high-risk clonal groups, ST78 and ST133 (including single-locus variants), accounted for 62.5% of sequenced isolates. Notably, ST133-rarely reported in Japan-was the second most common type and detected widely, suggesting gradual and inconspicuous dissemination. ST78 exhibited substantial genomic diversity, frequent co-carriage of extended-spectrum beta-lactamase genes, and multiple plasmid replicons, while ST133 formed a more uniform lineage with limited resistance determinants. Most isolates remained highly susceptible to amikacin and cefiderocol. Core-genome multi-locus sequence typing suggested possible intra-facility persistence and inter-facility transmission of closely related strains (≤10 allele differences) in some hospitals over time. Among the 46 facilities with blaIMP-1 group-positive isolates, 73.9% (34/46) were small hospitals (<200 beds). The proportion among screened ECC isolates was similarly high in small and large hospitals (90.5% vs 94.8%), with no significant difference, suggesting the need to extend molecular surveillance even in resource-limited settings. These findings highlight the utility of molecular confirmation and targeted genomic analysis, particularly in regions or settings where high-risk CPEC clones may circulate undetected, to support timely detection and containment efforts.

OPINION article Front. Microbiol., 21 February 2022 | https://doi.org/10.3389/fmicb.2022.808993

Objetivo: explorar una ruta teórico-conceptual que exhiba algunos momentos en la evolución de la Economía del Comportamiento (EC), también conocida como Behavioral Economics (BE). A través de la descripción de algunas aplicaciones y resultados obtenidos, generados a partir de los hallazgos dentro de esta disciplina; específicamente en el ámbito de política pública. Este método se ha convertido en una útil herramienta en el plano del diseño de política pública en otras regiones del mundo, pero para México es todavía un campo poco explorado, tanto en el ámbito académico como en la esfera gubernamental. Por lo que se convierte en un área de oportunidad para estas dos instancias. Metodología: Se recurrió a la revisión de bibliografía sobre el tema, guías específicas, conferencias en internet y artículos de revistas científicas. Resultados: Se constata que, con el BE se logra complementar los modelos del mainstream económico de la economía con elementos de la psicología, generando un patrón analítico que confronta a las anomalías de la teoría económica, con los hallazgos sobre el comportamiento económico del individuo. A partir de esto se amplía el conocimiento sobre el tema de toma de decisiones y, sobre esta plataforma conceptual y metodológica, eventualmente se pueden rediseñar las políticas de gobierno relacionadas a estos efectos. Limitaciones: no se encontró literatura que permita dar luz de la implementación del BE en la política pública de México, tampoco se detectó experimentación, ni formación de capital humano entrenado para estos fines. Conclusiones: Existe una deficiencia en la implementación de las aplicaciones y metodología del BE en nuestro País. Esto la convierte en un terreno fértil y de oportunidad, lo cual redunda en un refinamiento del entendimiento del comportamiento humano, tanto en el ámbito académico como para diseñadores de política pública.

BackgroundOncogenic human papillomavirus (HPV) infection, particularly multiple HPV types, is recognized as a necessary cause of anal cancer. However, a limited number of studies have reported the prevalence of anal HPV infection in Asia. We determined the prevalence, genotypes, and risk factors for anal HPV infection in Japanese HIV-positive men who have sex with men (MSM), heterosexual men, and women.MethodsThis cross-sectional study included 421 HIV-positive patients. At enrollment, we collected data on smoking, alcohol, co-morbidities, drugs, CD4 cell counts, HIV RNA levels, highly active anti-retroviral therapy (HAART) duration, sexually transmitted infections (STIs), and serological screening (syphilis, hepatitis B virus, Chlamydia trachomatis, Entamoeba histolytica). Anal swabs were collected for oncogenic HPV genotyping.ResultsOncogenic HPV rate was 75.9% in MSM, 20.6% in heterosexual men, and 19.2% in women. HPV 16/18 types were detected in 34.9% of MSM, 17.7% of heterosexual men, and 11.5% of women. Multiple oncogenic HPV (≥2 oncogenic types) rate was 54.6% in MSM, 8.8% in heterosexual men, and 0% in women. In univariate analysis, younger age, male sex, MSM, CD4 <100, HIV viral load >50,000, no administration of HAART, and having ≥2 sexually transmitted infections (STIs) were significantly associated with oncogenic HPV infection, whereas higher smoking index and corticosteroid use were marginally associated with oncogenic HPV infection. In multivariate analysis, younger age (OR, 0.98 [0.96–0.99]), MSM (OR, 5.85 [2.33–14.71]), CD4 <100 (OR, 2.24 [1.00–5.01]), and having ≥2 STIs (OR, 2.81 [1.72–4.61]) were independently associated with oncogenic HPV infection. These 4 variables were also significant risk factors for multiple oncogenic HPV infection.ConclusionsAmong Japanese HIV-infected patients, approximately two-thirds of MSM, one-fifth of heterosexual men, and one-fifth of women have anal oncogenic HPV infection. Younger age, MSM, ≥2 STIs, and immunosuppression confer a higher risk of infection with oncogenic HPV and multiple oncogenic types.

Although the cyclooxygenase metabolites PGs are known to be involved in the progression of arthritis, the role of PGD2 remains unclear. In this study, we evaluated the contribution of signaling mediated through a PGD2 receptor, chemoattractant receptor-homologous molecule expressed on Th2 cells (CRTH2), in the progression of adjuvant-induced joint inflammation. Injection of CFA into the ankle joint stimulated PGD2 production and induced paw swelling in both CRTH2-naive (WT) and CRTH2(-/-) mice. CRTH2(-/-) mice presented more severe arthritic manifestations than did WT mice. Through bone marrow transplantation experiments between WT and CRTH2(-/-) mice, we showed that CRTH2 deficiency in bone marrow-derived immune cells is involved in disease progression. Morphological studies showed that CRTH2 deficiency accelerated the infiltration of macrophages into the inflamed paw. Consistent with this finding, we observed that treatment with the macrophage inactivator GdCl3 or the macrophage-depleting agent liposomal clodronate improved arthritis symptoms in CRTH2(-/-) mice. Adoptive transfer of CRTH2(-/-) macrophages exacerbated joint inflammation in WT mice. In addition, CRTH2 deficiency accelerated, whereas CRTH2 agonism inhibited, the expression of a macrophage-activating cytokine (GM-CSF) and a chemokine receptor (CXCR2) in CFA-treated peritoneal macrophages. Together, these observations demonstrate that PGD2-CRTH2 signaling plays a protective role in joint inflammation by attenuating the infiltration of macrophages.

Urinary excretion of lipocalin-type PGD(2) synthase (L-PGDS), which converts PG H(2) to PGD(2), increases in early diabetic nephropathy. In addition, L-PGDS expression in the tubular epithelium increases in adriamycin-induced nephropathy, suggesting that locally produced L-PGDS may promote the development of CKD. In this study, we found that L-PGDS-derived PGD(2) contributes to the progression of renal fibrosis via CRTH2-mediated activation of Th2 lymphocytes. In a mouse model, the tubular epithelium synthesized L-PGDS de novo after unilateral ureteral obstruction (UUO). L-PGDS-knockout mice and CRTH2-knockout mice both exhibited less renal fibrosis, reduced infiltration of Th2 lymphocytes into the cortex, and decreased production of the Th2 cytokines IL-4 and IL-13. Furthermore, oral administration of a CRTH2 antagonist, beginning 3 days after UUO, suppressed the progression of renal fibrosis. Ablation of IL-4 and IL-13 also ameliorated renal fibrosis in the UUO kidney. Taken together, these data suggest that blocking the activation of CRTH2 by PGD(2) might be a strategy to slow the progression of renal fibrosis in CKD.

Influenza is a common respiratory virus infection. Although it causes significant morbidity, clinical courses of the infection are self-limited in most cases. However, the influenza viruses sometimes cause severe and lethal diseases such as acute respiratory distress syndrome, encephalopathy, and myocarditis. These severe infections usually occur in patients who had been apparently healthy and immunocompetent before infection, and underlying mechanisms for severity are often obscure. We describe a case of 9 year old boy with repeated severe influenza A infections in whom aberrant lymphocyte responses to influenza antigens in vitro were observed. He had been healthy except for egg allergy outgrown by age of 2 with no history of severe infections before the episodes of severe influenza. At age of 6, he was infected with influenza AH3N2 resulted in acute respiratory distress syndrome and brain edema within 24 hours of onset. With methylprednisolone pulse therapy he recovered without sequelae. He had second severe influenza A H1N1 infection leading to lobar pneumonia with severe hypoxemia at age of 9. Again, he could recover with an intensive care. At the time of discharge, eosinophilia (34%) was noted without symptoms.