Pain relief and good functional outcomes after hip endoscopy via posterior approach in patients with ischiofemoral impingement.

PURPOSE: Ischiofemoral impingement is considered to be an uncommon and difficult pathology to diagnose with respect to hip pain etiology. The objective was to describe the clinical results of endoscopic lesser trochanter resection via a posterior approach in patients with Ischiofemoral impingement. METHODS: This was a retrospective observational study of consecutive patients with Ischiofemoral impingement, who underwent endoscopic resection of the lesser trochanter via a posterior approach, between 2015 and 2018. Clinical results were evaluated using the ischiofemoral impingement test, long-stride walking test, modified Harris Hip Score (mHHS) and the Oxford scale to assess the strength of the iliopsoas muscle as well as the presence of complications. Preoperative and postoperative ischiofemoral space was measured to assess whether the resection of the lesser trochanter was adequate. RESULTS: 16 hips in 13 patients (mean age: 34.4 ± 12.1 years, 11 women) with a follow-up period between 24 and 59 months were included. Preoperative ischiofemoral space ranged from 6.4 to 22.4 mm, a measure > 17.0 mm was achieved in 15 hips without the presence of pain in IFI test and long-strides walking test. Function improved postoperatively, as reflected by a higher mean mHHS (preoperative: 44.6 ± 21.5, postoperative: 81.2 ± 15.1, p < 0.05). After surgery, the strength of the iliopsoas muscle was not decreased compared to the preoperative measure. Three complications were reported, including two cases that required revision surgery. CONCLUSIONS: Endoscopic resection of the lesser trochanter via posterior approach provides satisfactory outcomes with symptom relief and good functional results in patients with Ischiofemoral impingement. It is important to discuss the benefits and risks when offering this treatment choice. LEVEL OF EVIDENCE: Level IV.

The autophagy protein Def8 is altered in Alzheimer's disease and Aß42-expressing Drosophila brains.

Alzheimer's disease (AD) is the most common neurodegenerative disorder, characterized by protein accumulation in the brain as a main neuropathological hallmark. Among them, Aß42 peptides tend to aggregate and create oligomers and plaques. Macroautophagy, a form of autophagy characterized by a double-membrane vesicle, plays a crucial role in maintaining neuronal homeostasis by degrading protein aggregates and dysfunctional organelles as a quality control process. Recently, DEF8, a relatively uncharacterized protein, has been proposed as a participant in vesicular traffic and autophagy pathways. We have reported increased DEF8 levels in lymphocytes from mild cognitive impairment (MCI) and early-stage AD patients and a neuronal profile in a murine transgenic AD model. Here, we analyzed DEF8 localization and levels in the postmortem frontal cortex of AD patients, finding increased levels compared to healthy controls. To evaluate the potential function of DEF8 in the nervous system, we performed an in silico assessment of its expression and network profiles, followed by an in vivo evaluation of a neuronal Def8 deficient model using a Drosophila melanogaster model of AD based on Aß42 expression. Our findings show that DEF8 is an essential protein for maintaining cellular homeostasis in the nervous system, and it is upregulated under stress conditions generated by Aß42 aggregation. This study suggests DEF8 as a novel actor in the physiopathology of AD, and its exploration may lead to new treatment avenues.

Benznidazole prevents endothelial damage in an experimental model of Chagas disease.

OBJECTIVES: To evaluate the effect of benznidazole on endothelial activation in a murine model of Chagas disease. METHODS: A low (30mg/kg/day) and a high (100mg/kg/day) dose of benznidazole were administered to mice infected with Trypanosoma cruzi during the early phases of the infection. The effects of the treatments were assessed at 24 and 90 days postinfection by evaluating the parasitaemia, mortality, histopathological changes and expression of ICAM in the cardiac tissue. The blood levels of thromboxane A2, soluble ICAM and E-selectin were also measured. T. cruzi clearance was assessed by the detection of parasite DNA in the heart tissue of infected mice. RESULTS: Benznidazole decreased the cardiac damage induced by the parasite, and amastigote nests disappeared at 90 days postinfection. Both doses cleared the parasite from the cardiac tissue at 24 and 90 days postinfection. In addition, benznidazole decreased the thromboxane levels and normalized the plasma sICAM and sE-selectin levels by 90 days postinfection. CONCLUSIONS: Early administration of benznidazole at a dose as low as 30mg/kg eradicates T. cruzi from cardiac tissue. Additionally, benznidazole prevents cardiac damage and modulates endothelial activation as part of its antichagasic activity.