Biology subjects

Broz, K.

Publications and source records attributed to Broz, K..

3 recordsLinked to original sources

bioRxiv2024

The progression of infiltrating neurovascular features and chemokine production of the caudal intervertebral disc following injury

Inflammatory cytokine production and de novo neurovascularization have been identified in painful, degenerated intervertebral discs (IVDs). However, the temporal trajectories of these key pathoanatomical features, including the cascade of inflammatory chemokines and neo-vessel and neurite infiltration, and their associations with IVD degeneration, remain relatively unknown. Investigating this process in the caudal mouse IVD enables the opportunity to study the tissue-specific response without confounding inflammatory signaling from neighboring structures. Thus this study aims to define the progression of chemokine production and neurovascular invasion during the IVD degeneration initiated by injury in the caudal spine 3-month-old C57BL6/J mice. Forty-nine IVD-secreted chemokines and matrix metalloproteinases (MMPs) was measured using multiplex ELISA, and the intradiscal infiltrating vessels (endomucin) and nerves (protein-gene-product 9.5) was quantified in the tissue volume using immunohistochemistry. Injury provoked the increase secretion of IL6, CCL2, CCL12, CCL17, CCL20, CCL21, CCL22, CXCL2 and MMP2 proteins. The centrality and structure of inflammatory networks in IVDs evolved over the 12 post-injury weeks, highlighting distinct responses between the acute and chronic phases. Neurites propagated rapidly within 2-weeks post-injury and remained relatively constant until 12-weeks. Vascular vessel length was observed to peak at 4-weeks post-injury and it regressed by 12-weeks. These findings identified the temporal flux of inflammatory chemokines and pain-associated pathoanatomy in a model of IVD degeneration using the mouse caudal spine.

bioengineering↗

bioRxiv2023

Assessment of bovine cortical bone fracture behavior using impact microindentation as a surrogate of fracture toughness

The fracture behavior of bone is critically important for assessing its mechanical competence and ability to resist fractures. Fracture toughness, which quantifies a materials resistance to crack propagation under controlled geometry, is regarded as the gold standard for evaluating a materials resistance to fracture. However properly conducting this test requires access to calibrated mechanical load frames the destruction of the bone samples, making it impractical for obtaining clinical measurement of bone fracture. Impact microindentation offers a potential alternative by mimicking certain aspects of fracture toughness measurements, but its relationship with mechanistic fracture toughness remains unknown. In this study, we aimed to compare measurements of notched fracture toughness and impact microindentation in fresh and boiled bovine bone. Skeletally mature bovine bone specimens (n=48) were prepared, and half of them were boiled to denature the organic matrix, while the other half remained preserved in frozen conditions. Notched fracture toughness tests were conducted on all samples to determine Initiation toughness (KIC), and an impact microindentation test using the OsteoProbe was performed to obtain the Bone Material Strength index. Boiling the bone samples resulted increased the denatured collagen without affecting mineral density or porosity. The boiled bones also showed significant reduction in both KIC (p < 0.0001) and the average Bone Material Strength index (p < 0.0001), leading to impaired resistance of bone to crack propagation. Remarkably, the average Bone Material Strength index exhibited a high correlation with KIC (r = 0.86; p < 0.001). The ranked order difference analysis confirmed excellent agreement between the two measures. This study provides the first evidence that impact microindentation could serve as a surrogate measure for bone fracture behavior. The potential of impact microindentation to non-destructively assess bone fracture resistance could offer valuable insights into bone health without the need for elaborate testing equipment and sample destruction.

bioengineering↗

bioRxiv2021

The Fusarium graminearum transporters Abc1 and Abc6 are important for xenobiotic resistance, trichothecene accumulation, and virulence to wheat.

The plant pathogenic fungus Fusarium graminearum is the causal agent of Fusarium Head Blight (FHB) disease on small grain cereals. F. graminearum produces trichothecene mycotoxins such as deoxynivalenol (DON) that are required for full virulence. DON must be exported outside the cell to cause FHB disease, a process that may require the involvement of membrane-bound transporters. In this study we how the deletion of membrane-bound transporters results in reduced DON accumulation as well as reduced FHB symptoms on wheat. Deletion of the ATP-Binding Cassette (ABC) transporter Abc1 results in the most severe reduction in DON accumulation and virulence. Deletion of another ABC transporter, Abc6, also reduces FHB symptoms to a lesser degree. Combining deletions fails to reduce DON accumulation or virulence in an additive fashion, even when including an{Delta} abc1 deletion. Heterologous expression of F. graminearum transporters in a DON-sensitive strain of yeast confirms Abc1 as a major DON resistance mechanism. Yeast expression further indicates that multiple transporters, including Abc1 play an important role in resistance to the wheat phytoalexin 2-benzoxazolinone (BOA) and other xenobiotics. Thus, Abc1 may contribute to wheat virulence both by allowing export of DON and by providing resistance to the wheat phytoalexin BOA. This research provides useful information which may aid in designing novel management techniques of FHB or other destructive plant diseases.

molecular biology↗