Outcomes of Intravascular Lithotripsy in the Treatment of Chronic Limb-Threatening Ischemia: A Single-Center Retrospective Study.

PURPOSE: Vascular calcification is an important risk factor for endovascular treatment failure and complications in patients with chronic limb-threatening ischemia (CLTI). Intravascular lithotripsy (IVL) is a pulsatile balloon-based device that has emerged as a tool in the treatment of calcified vessels. The purpose of this study is to evaluate the efficacy and safety of IVL in the treatment of peripheral calcified lesions in CLTI patients. MATERIALS AND METHODS: A retrospective study was performed within a single institution. Thirty-six CLTI patients treated with IVL for peripheral calcified lesions from 2018 to 2022 were identified. Data on pre- and post-IVL luminal stenosis measured by digital subtraction angiography, lesion location, adjunctive therapies, ankle-brachial index (ABI), and intra-procedural complications were obtained. A total of 41 target lesions in twenty-eight patients were included, with ABI data available in 20 treated lower extremities. RESULTS: Across all 41 target lesions, IVL produced clinically significant luminal gain of 75.5% ± 23.0. Luminal gain by vessel location was 87.3% ± 15.8, 57% ± 25.7, and 78.5% ± 20.6 in the aortoiliac (n = 8), common femoral (n = 9), and femoropopliteal (n = 24) segments, respectively. Lesions treated with IVL alone yielded a luminal gain of 71.4% ± 25.6 (n = 10), while IVL alongside adjunctive therapy produced a luminal gain of 76.8% ± 22.4. In 20 treated lower extremities, ABI improvement of 0.20 ± 0.26 (p = 0.002) was recorded. Intra-procedural complications occurred in 1/36 patients, which was one instance of thrombus occurring prior to IVL. CONCLUSION: IVL may be an effective option for creating safe luminal gain and vessel preparation in patients with CLTI. Level of Evidence 2: Retrospective Cohort Study.

A Role for Maternal Factors in Suppressing Cytoplasmic Incompatibility.

Wolbachia are maternally transmitted bacterial endosymbionts, carried by approximately half of all insect species. Wolbachia prevalence in nature stems from manipulation of host reproduction to favor the success of infected females. The best known reproductive modification induced by Wolbachia is referred to as sperm-egg Cytoplasmic Incompatibility (CI). In CI, the sperm of Wolbachia-infected males cause embryonic lethality, attributed to paternal chromatin segregation defects during early mitotic divisions. Remarkably, the embryos of Wolbachia-infected females "rescue" CI lethality, yielding egg hatch rates equivalent to uninfected female crosses. Several models have been discussed as the basis for Rescue, and functional evidence indicates a major contribution by Wolbachia CI factors. A role for host contributions to Rescue remains largely untested. In this study, we used a chemical feeding approach to test for CI suppression capabilities by Drosophila simulans. We found that uninfected females exhibited significantly higher CI egg hatch rates in response to seven chemical treatments that affect DNA integrity, cell cycle control, and protein turnover. Three of these treatments suppressed CI induced by endogenous wRi Wolbachia, as well as an ectopic wMel Wolbachia infection. The results implicate DNA integrity as a focal aspect of CI suppression for different Wolbachia strains. The framework presented here, applied to diverse CI models, will further enrich our understanding of host reproductive manipulation by insect endosymbionts.

Borrelia burgdorferi chemotaxis toward tick protein Salp12 contributes to acquisition.

Lyme disease is a common tick-borne infection caused by the spirochete Borrelia burgdorferi sensu stricto (s.s.). B. burgdorferi s.s. may utilize chemotaxis, the directional migration towards or away from a chemical stimulus, for transmission, acquisition, and infection. However, the specific signals recognized by the spirochete for these events have not been defined. In this study, we identify an Ixodes scapularis salivary gland protein, Salp12, that is a chemoattractant for the spirochete. We demonstrate that Salp12 is expressed in the I. scapularis salivary glands and midgut and expression is not impacted by B. burgdorferi s.s. infection. Knockdown of Salp12 in the salivary glands or passive immunization against Salp12 reduces acquisition of the spirochete by ticks but acquisition is not completely prevented. Knockdown does not impact transmission of B. burgdorferi s.s. This work suggests a new role for chemotaxis in acquisition of the spirochete and suggests that recognition of Salp12 contributes to this phenomenon.