The Greater Omentum: Multifaceted Interactions in Neurological Recovery and Disease Progression.

The greater omentum, a unique anatomical structure composed of adipocytes, loose connective tissue, and a dense vascular network. Plays a pivotal role beyond its traditional understanding. It houses specialized immunological units known as 'Milky spots,' making it a key player in immune response. Moreover, the omentum's capacity to enhance tissue perfusion, absorb edema fluid, boost acetylcholine synthesis, and foster neuron repair have rendered it a topic of interest in the context of various diseases, especially neurological disorders. This review provides a comprehensive overview of the intricate anatomy and histology of the greater omentum, casting light on its multifaceted functions and its associations with a spectrum of diseases. With a specific focus on neurological ailments, we delineate the intricate relationship that the omentum shares with other pathologies like stroke and we underly its contribution to serving as a therapeutic agent in neurological disorders. By deciphering the underlying mechanisms and emphasizing areas that demand further investigation. This review aims to spark renewed interest and pave the way for comprehensive studies exploring the greater omentum's potential in neurology and broader medicine overall. Given these diverse interactions that yet remain elusive, we must investigate and understand the nuanced relationship between the greater omentum and pathologies, especially its role in stroke's pathophysiology and therapeutic interventions so as to enhance patient care.

Geographic landscape of foreign medical graduates in US neurosurgery training programs from 2007 to 2017.

OBJECTIVE: Although foreign medical graduates (FMGs) have been essential to the US physician workforce, the increasing competitiveness has made it progressively challenging for FMGs to match in US neurosurgery programs. We describe geographic origins and characteristics associated with successful match into US neurosurgery training programs. METHODS: Retrospective review of AANS membership data (2007-2017). Scopus was used to collect bibliometrics. RESULTS: From 2009 neurosurgical residents, 165 (8.2%) were FMGs. Most were male (n = 148; 89.6%) with a median age of 34.0 years. Top six feeder countries (TFC) included India (13.9%; n = 23), Lebanon and Pakistan (9.1%; n = 15), Caribbean Region (7.2%; n = 12), Mexico (6.67%; n = 11), and Greece (3.6%; n = 6). Compared to FMGs from non-top feeder countries (NTFC), TFC FMGs had higher H-indices (2 vs 4, p = 0.049), greater number of publications (2 vs 5, p = 0.04), were more likely to have an MBBS/MBBCh (n = 38 vs n = 17, p = 0.03), and had twice as many candidates from major feeder medical schools that successfully matched into a US neurosurgery program (n = 43 vs NTFC = 20, p < 0.001). NTFC FMGs were almost 3-times more likely to match at an affiliated neurosurgery program (8 vs TFC = 3, p = 0.03), while TFC FMGs were 1.5-times more likely to match at an NIH Top-40 program (33 vs NTFC = 21, p = 0.03). CONCLUSIONS: TFC graduates have higher bibliometrics, frequently come from major feeder schools, and have greater match success at a broader selection of programs and NIH top-40 programs. Future studies characterizing FMG country and medical school origins may enable foreign students to geographically target institutions of interest and could allow US programs to better evaluate foreign training environments.

Expandable Cage Technology-Transforaminal, Anterior, and Lateral Lumbar Interbody Fusion.

This review of the literature will focus on the indications, surgical techniques, and outcomes for expandable transforaminal lumbar interbody fusion (TLIF), anterior lumbar interbody fusion (ALIF), and lateral lumbar interbody fusion (LLIF) operations. The expandable TLIF cage has become a workhorse for common degenerative pathology, whereas expandable ALIF cages carry the promise of greater lordotic correction while evading the diseased posterior elements. Expandable LLIF cages call upon minimally invasive techniques for a retroperitoneal, transpsoas approach to the disc space, obviating the need for an access surgeon and decreasing risk of injury to the critical neurovascular structures. Nuances between expandable and static cages for all 3 TLIF, ALIF, and LLIF operations are discussed in this review.

Muscle BDNF improves synaptic and contractile muscle strength in Kennedy's disease mice in a muscle-type specific manner.

KEY POINTS: Muscle-derived neurotrophic factors may offer therapeutic promise for treating neuromuscular diseases. We report that a muscle-derived neurotrophic factor, BDNF, rescues synaptic and muscle function in a muscle-type specific manner in mice modelling Kennedy's disease (KD). We also find that BDNF rescues select molecular mechanisms in slow and fast muscle that may underlie the improved cellular function. We also report for the first time that expression of BDNF, but not other members of the neurotrophin family, is perturbed in muscle from patients with KD. Given that muscle BDNF had divergent therapeutic effects that depended on muscle type, a combination of neurotrophic factors may optimally rescue neuromuscular function via effects on both pre- and postsynaptic function, in the face of disease. ABSTRACT: Deficits in muscle brain-derived neurotrophic factor (BDNF) correlate with neuromuscular deficits in mouse models of Kennedy's disease (KD), suggesting that restoring muscle BDNF might restore function. To test this possibility, transgenic mice expressing human BDNF in skeletal muscle were crossed with '97Q' KD mice. We found that muscle BDNF slowed disease, doubling the time between symptom onset and endstage. BDNF also improved expression of genes in muscle known to play key roles in neuromuscular function, including counteracting the expression of neonatal isoforms induced by disease. Intriguingly, BDNF's ameliorative effects differed between muscle types: synaptic strength was rescued only in slow-twitch muscle, while contractile strength was improved only in fast-twitch muscle. In sum, muscle BDNF slows disease progression, rescuing select cellular and molecular mechanisms that depend on fibre type. Muscle BDNF expression was also affected in KD patients, reinforcing its translational and therapeutic potential for treating this disorder.