Bone mesh fixation for the treatment of suprailiac hernia. Report of two cases.

Hernias of the lateral abdominal wall are a rare entity. In most cases, they occur after surgery or trauma. We present two cases of lumbar hernia: the first one after iliac bone grafting and the second one after muscular tearing by the seatbelt during a car accident.

Biological and Technical Complications of Splinted or Nonsplinted Dental Implants: A Decision Tree for Selection.

Purpose: To present an in-depth review on splinting versus nonsplinting the restorations of adjacent dental implants, in addition to discussing biological and technical complications associated with either choice; and to provide the clinician with a decision tree that serves in everyday judgments when it comes to addressing this issue.

Materials And Methods: A comprehensive literature review was performed for articles comparing success of splinted versus nonsplinted dental implants.

Results: There is no evidence to suggest that implementing either prosthetic design results in higher implant survival.

Deregulation of autophagy in postmortem brains of Machado-Joseph disease patients.

Autophagy, the major pathway for protein turnover, is critical to maintain cellular homeostasis and has been implicated in neurodegenerative diseases. The aim of this research was to analyze the expression of autophagy markers in postmortem brains from Machado-Joseph disease (MJD) patients. The expression of autophagy markers in the cerebellum and the oculomotor nucleus from MJD patients and age-matched controls with no signs of neuropathology was inspected postmortem by immunohistochemistry (IHC) and Western blot.

Loss of spatacsin function alters lysosomal lipid clearance leading to upper and lower motor neuron degeneration.

Mutations in SPG11 account for the most common form of autosomal recessive hereditary spastic paraplegia (HSP), characterized by a gait disorder associated with various brain alterations. Mutations in the same gene are also responsible for rare forms of Charcot-Marie-Tooth (CMT) disease and progressive juvenile-onset amyotrophic lateral sclerosis (ALS). To elucidate the physiopathological mechanisms underlying these human pathologies, we disrupted the Spg11 gene in mice by inserting stop codons in exon 32, mimicking the most frequent mutations found in patients.

The endoplasmic reticulum-mitochondria interface is perturbed in PARK2 knockout mice and patients with PARK2 mutations.

Mutations in PARK2, encoding the E3 ubiquitin protein ligase Parkin, are a common cause of autosomal recessive Parkinson's disease (PD). Loss of PARK2 function compromises mitochondrial quality by affecting mitochondrial biogenesis, bioenergetics, dynamics, transport and turnover. We investigated the impact of PARK2 dysfunction on the endoplasmic reticulum (ER)-mitochondria interface, which mediates calcium (Ca) exchange between the two compartments and is essential for Parkin-dependent mitophagy.