pancrelipase (Ultrase MT20 / Ultrase MT / Ultresa)

Implementation of 7-1-7 for improving timeliness in outbreak detection and response in Thailand: A mixed-methods study on challenges in application and achievement of targets in 2024-25.

Watakulsin Peeriya P, Jitpeera Charuttaporn C, Promduangsi Pitiphon P, Yueayai Khanuengnij K et al.

Infectious disease outbreaks result in unfavourable outcomes when swift actions fail. The 7-1-7 target (detect within 7 days, notify within 1 day, respond within 7 days) was proposed to improve timeliness. Thailand piloted 7-1-7 in 2024 and scaled it up nationwide in 2025. This study aimed to quantify the 7-1-7 target achievement, identify bottlenecks and enablers, and describe challenges and solutions for applying the 7-1-7 metrics. A mixed-methods study was conducted with quantitative assessment of all events meeting the national health threat criteria during January 2024 and June 2025 for timeliness, bottlenecks and enablers for meeting the 7-1-7 target. A qualitative descriptive study with in-depth interviews of key stakeholders explored challenges and solutions for applying the 7-1-7 framework. Of the 1,435 events assessed, 15% were dangerous communicable diseases and 3% occurred in hotels. Among all the events, 50% achieved the 7-1-7 target; 85%, 73%, and 83% were detected, notified and responded to in a timely manner, respectively. The median (interquartile range) duration for detection, notification and response were 0 (0-5) days, 0 (0-2) days and 2 (0-5) days, respectively. Among events that occurred in hotels, none met the 7-1-7 target. Dangerous communicable diseases had the highest notification (95%) and response performance (99%), despite lower timely detection (71%). Key bottlenecks included delayed care-seeking and weak coordination. Key stakeholders felt that the 7-1-7 metrics was useful, but the lack of standardised data sources, disease-specific guidelines and centralised data extraction made implementation difficult. Proposed solutions focused on streamlining and decentralizing the application of 7-1-7. It is appreciable that Thailand was able to apply the 7-1-7 framework and half of the events met the 7-1-7 target. However, to better the application of 7-1-7, future work should focus on strengthening data integration and formulating disease specific guidelines.

"They Call Us Cheaters": Exploring Stigma Management Communication Strategies During GLP-1 Medication Use.

Lazenby Braidyn B, Guidry Ashley A, Price Sarah S, Shuvo Md Sazzad Mahmud MSM et al.

As GLP-1 receptor agonist medications become more popular, conversations surrounding the medication's use are becoming increasingly more complicated. Emerging research suggests that individuals taking these medications often feel stigmatized. However, understanding how individuals manage stigma through communication is less explored. Using stigma management communication theory, the current study seeks to better understand how individuals communicatively manage stigma surrounding GLP-1 medication use. A reflexive thematic analysis of interviews with GLP-1 users (n = 34) suggests that individuals evaluate their interpretations of both their own self-stigma and the public's understanding of GLP-1 and engage in various different stigma management communication strategies in response. These strategies, while effective for stigma management, may inadvertently contribute to ongoing stigmatizing discourse surrounding GLP-1 use.

Herpes simplex virus 1 subverts the mitochondrial network to support the infection: A lesson on mitochondrial versatility.

Saud Rabina R, Foster-Lemieur Kimberly K, Duguay Brett B, Swerdlow Russell R et al.

Herpes simplex virus 1 (HSV-1) infects approximately 67% of the population worldwide. It establishes lifelong reservoirs in sensory neurons and has been linked to several diseases including neuronal dysfunction. Disruption of mitochondrial homeostasis is a hallmark of HSV-1 infection, however a molecular understanding of these changes and their significance is not yet well defined. HSV-1 infection causes a UL12.5-dependent inhibition of mitochondrial biogenesis through the loss of mitochondrial DNA and mitochondrial transcription factors, PGC-1α (peroxisome proliferator-activated receptor-gamma co-activator) and TFAM (mitochondrial transcription factor). Conversely, UL12.5-independent mechanisms inhibit mitochondrial fusion by activating the OMA1 metallopeptidase that cleaves the inner mitochondrial membrane fusion protein OPA1 (optic atrophy protein 1) and by down-modulating the outer mitochondrial membrane fusion protein MFN2 (mitofusin 2). This inhibition of fusion results in a smaller mitochondrial network that clusters to perinuclear regions, likely supplying energy for viral replication and envelopment. The inner mitochondrial membrane protein TIM23 is also down-modulated during infection in a UL12.5-independent mechanism. Failure of the virus to promote these changes negatively impacts the infection. Despite these changes, mitochondria are protected from mitophagy due to the viral-induced degradation of several mitophagy adaptor proteins, whereby damaged mitochondrial components, including mitochondrial DNA, are extruded via extracellular vesicles. These mitochondrial changes still support functions necessary for HSV-1 infection. Basal cell respiration is preserved, while spare respiratory capacity and extracellular acidification rates increase, indicating glycolytic activity. Mitochondrial membrane potential is also preserved. Overall, our studies provide mechanistic insight into how HSV-1 impacts mitochondria, which could contribute to viral pathogenesis. Mitochondria are often referred to as the "powerhouse" of the cell because they are the main energy producers. Disruption of mitochondrial homeostasis is associated with multiple diseases and occurs after infection with pathogens such as HSV-1. By investigating the mechanism(s) by which HSV-1 disrupts mitochondrial homeostasis, we can better understand how HSV-1 causes pathogenesis. HSV-1 infection impacts mitochondrial homeostasis through disruption of four key processes, including: 1) inhibition of mitochondrial biogenesis and the generation of new mitochondria; 2) inhibition of mitochondrial fusion, which rescues reversibly damaged mitochondria; 3) sustaining mitochondrial fission, which removes damaged content; and 4) preventing mitophagy, which clears damaged mitochondria. UL12.5-dependent and UL12.5- independent events during HSV-1 infection disrupt mitochondrial homeostasis, redirecting mitochondrial resources towards progeny virus production. These changes cause irreversible damage to host cells, ultimately driving pathogenesis.

Retraction Note: Prevalence and pathologic effects of colibactin and cytotoxic necrotizing factor‑1 (Cnf 1) in Escherichia coli: experimental and bioinformatics analyses.

Morgan Radwa N RN, Saleh Sarra E SE, Farrag Hala A HA, Aboulwafa Mohammad M MM