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1.
Cureus ; 16(3): e56889, 2024 Mar.
Artículo en Inglés | MEDLINE | ID: mdl-38659564

RESUMEN

Bilateral acetabular fractures, though rare, pose significant challenges in both diagnosis and management due to their association with high-energy trauma and the potential for long-term disability. This case report presents the clinical course of a 27-year-old female who presented to our department after a motorcycle accident with bilateral acetabular fractures. Initial assessment revealed nondisplaced bilateral acetabular fractures, along with associated injuries including a right ulnar styloid fracture. Further evaluation via 3D CT scan delineated associated column fractures on the right and posterior + anterior wall fractures on the left, classified according to the Letournel and Judet system. Notably, this specific combination of acetabular fractures has not been documented in existing literature as per our investigation. The surgical intervention involved an anterior intrapelvic approach for open reduction and internal fixation (ORIF) of the right acetabulum, while the left acetabulum was managed conservatively. Postoperatively, the patient is scheduled for non-weightbearing activity until radiographic evidence of fracture healing is observed. This case underscores the importance of tailored surgical approaches and comprehensive management strategies in optimizing outcomes for patients with bilateral acetabular fractures.

2.
Am J Physiol Gastrointest Liver Physiol ; 320(4): G658-G674, 2021 04 01.
Artículo en Inglés | MEDLINE | ID: mdl-33566727

RESUMEN

Necrotizing enterocolitis (NEC), a life-threatening intestinal disease, is becoming a larger proportionate cause of morbidity and mortality in premature infants. To date, therapeutic options remain elusive. Based on recent cell therapy studies, we investigated the effect of a human placental-derived stem cell (hPSC) therapy on intestinal damage in an experimental NEC rat pup model. NEC was induced in newborn Sprague-Dawley rat pups for 4 days via formula feeding, hypoxia, and LPS. NEC pups received intraperitoneal (ip) injections of either saline or hPSC (NEC-hPSC) at 32 and 56 h into NEC induction. At 4 days, intestinal macroscopic and histological damage, epithelial cell composition, and inflammatory marker expression of the ileum were assessed. Breastfed (BF) littermates were used as controls. NEC pups developed significant bowel dilation and fragility in the ileum. Further, NEC induced loss of normal villi-crypt morphology, disruption of epithelial proliferation and apoptosis, and loss of critical progenitor/stem cell and Paneth cell populations in the crypt. hPSC treatment improved macroscopic intestinal health with reduced ileal dilation and fragility. Histologically, hPSC administration had a significant reparative effect on the villi-crypt morphology and epithelium. In addition to a trend of decreased inflammatory marker expression, hPSC-NEC pups had increased epithelial proliferation and decreased apoptosis when compared with NEC littermates. Further, the intestinal stem cell and crypt niche that include Paneth cells, SOX9+ cells, and LGR5+ stem cells were restored with hPSC therapy. Together, these data demonstrate hPSC can promote epithelial healing of NEC intestinal damage.NEW & NOTEWORTHY These studies demonstrate a human placental-derived stem cell (hPSC) therapeutic strategy for necrotizing enterocolitis (NEC). In an experimental model of NEC, hPSC administration improved macroscopic intestinal health, ameliorated epithelial morphology, and supported the intestinal stem cell niche. Our data suggest that hPSC are a potential therapeutic approach to attenuate established intestinal NEC damage. Further, we show hPSC are a novel research tool that can be utilized to elucidate critical neonatal repair mechanisms to overcome NEC.


Asunto(s)
Apoptosis , Proliferación Celular , Enterocolitis Necrotizante/cirugía , Íleon/patología , Mucosa Intestinal/patología , Células de Paneth/patología , Placenta/trasplante , Trasplante de Células Madre , Animales , Animales Recién Nacidos , Células Cultivadas , Citocinas/genética , Citocinas/metabolismo , Modelos Animales de Enfermedad , Enterocolitis Necrotizante/genética , Enterocolitis Necrotizante/metabolismo , Enterocolitis Necrotizante/patología , Femenino , Humanos , Íleon/metabolismo , Mediadores de Inflamación/metabolismo , Mucosa Intestinal/metabolismo , Células de Paneth/metabolismo , Placenta/citología , Embarazo , Ratas Sprague-Dawley , Receptores Acoplados a Proteínas G/metabolismo , Factor de Transcripción SOX9 , Nicho de Células Madre , Cicatrización de Heridas
3.
Sci Rep ; 9(1): 13107, 2019 09 11.
Artículo en Inglés | MEDLINE | ID: mdl-31511562

RESUMEN

The rapid and accurate diagnosis of Plasmodium falciparum malaria infection is an essential factor in malaria control. Currently, malaria diagnosis in the field depends heavily on using rapid diagnostic tests (RDTs) many of which detect circulating parasite-derived histidine-rich protein 2 antigen (PfHRP2) in capillary blood. P. falciparum strains lacking PfHRP2, due to pfhrp2 gene deletions, are an emerging threat to malaria control programs. The novel assay described here, named qHRP2/3-del, is well suited for high-throughput screening of P. falciparum isolates to identify these gene deletions. The qHRP2/3-del assay identified pfhrp2 and pfhrp3 deletion status correctly in 93.4% of samples with parasitemia levels higher than 5 parasites/µL when compared to nested PCR. The qHRP2/3-del assay can correctly identify pfhrp2 and pfhrp3 gene deletions in multiple strain co-infections, particularly prevalent in Sub-Saharan countries. Deployment of this qHRP2/3-del assay will provide rapid insight into the prevalence and potential spread of P. falciparum isolates that escape surveillance by RDTs.


Asunto(s)
Antígenos de Protozoos/genética , Antígenos de Protozoos/metabolismo , Eliminación de Gen , Plasmodium falciparum/genética , Reacción en Cadena de la Polimerasa/métodos , Proteínas Protozoarias/genética , Proteínas Protozoarias/metabolismo , Plasmodium falciparum/fisiología
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