Concomitant midline ventral and inguinal hernia repair: can we create an algorithmic approach?

PURPOSE: International guidelines exist for surgical treatment of either ventral or inguinal hernias repair (VHR; IHR). However, approach for managing both of them remains unestablished and is further complicated by newly developed surgical techniques and modalities (namely, robotic). This highlights the need for a tailored, algorithmic strategy to streamline surgical management. METHODS: An algorithm was developed by the directors of the NYU Langone Abdominal Core Health program of which four treatment groups were described: Group 1: open VHR and either laparoscopic or robotic IHR; Group 2: robotic transabdominal pre-peritoneal (TAPP) approach for both VHR and IHR; Group 3: robotic retro-muscular VHR and IHR; and Group 4: open repair for both. Demographics, comorbidities, operative characteristics, and surgical outcomes from November 2021 to July 2023 were retrospectively compared. RESULTS: Ninety-two patients were included with a median age of 64 years, 90% (n = 83) were white, 85% (n = 78) were male, median BMI was 27 kg/m2, and 73% (n = 67) were ASA class II. Distribution of groups was: 48% (n = 44) in 1A, 8% (n = 7) in 1B, 8% (n = 7) in 2A, 3% (n = 3) in 2B, 23% (n = 21) in 3A, 8% (n = 7) in 3B, and 3% (n = 3) in 4. Ventral hernia size, OR time, and postoperative length of stay varied across groups. Postoperative outcomes at 30 days including emergency consults, readmissions, and complications, showed no differences across groups. CONCLUSION: Access without guidance to new minimally invasive surgical approaches can be a challenge for the general surgeon. We propose an algorithm for decision-making based on our experience of incorporating robotic surgery, when available, for repair of concomitant VHR and IHR with consistent favorable outcomes within a small sample of patients.

Hidden Magnetic States Emergent Under Electric Field, In A Room Temperature Composite Magnetoelectric Multiferroic.

The ability to control a magnetic phase with an electric field is of great current interest for a variety of low power electronics in which the magnetic state is used either for information storage or logic operations. Over the past several years, there has been a considerable amount of research on pathways to control the direction of magnetization with an electric field. More recently, an alternative pathway involving the change of the magnetic state (ferromagnet to antiferromagnet) has been proposed. In this paper, we demonstrate electric field control of the Anomalous Hall Transport in a metamagnetic FeRh thin film, accompanying an antiferromagnet (AFM) to ferromagnet (FM) phase transition. This approach provides us with a pathway to "hide" or "reveal" a given ferromagnetic region at zero magnetic field. By converting the AFM phase into the FM phase, the stray field, and hence sensitivity to external fields, is decreased or eliminated. Using detailed structural analyses of FeRh films of varying crystalline quality and chemical order, we relate the direct nanoscale origins of this memory effect to site disorder as well as variations of the net magnetic anisotropy of FM nuclei. Our work opens pathways toward a new generation of antiferromagnetic - ferromagnetic interactions for spintronics.

Metabolomics uncovers dietary omega-3 fatty acid-derived metabolites implicated in anti-nociceptive responses after experimental spinal cord injury.

Chronic neuropathic pain is a frequent comorbidity following spinal cord injury (SCI) and often fails to respond to conventional pain management strategies. Preventive administration of docosahexaenoic acid (DHA) or the consumption of a diet rich in omega-3 polyunsaturated fatty acids (O3PUFAs) confers potent prophylaxis against SCI and improves functional recovery. The present study examines whether this novel dietary strategy provides significant antinociceptive benefits in rats experiencing SCI-induced pain. Rats were fed control chow or chow enriched with O3PUFAs for 8weeks before being subjected to sham or cord contusion surgeries, continuing the same diets after surgery for another 8 more weeks. The paw sensitivity to noxious heat was quantified for at least 8weeks post-SCI using the Hargreaves test. We found that SCI rats consuming the preventive O3PUFA-enriched diet exhibited a significant reduction in thermal hyperalgesia compared to those consuming the normal diet. Functional neurometabolomic profiling revealed a distinctive deregulation in the metabolism of endocannabinoids (eCB) and related N-acyl ethanolamines (NAEs) at 8weeks post-SCI. We found that O3PUFAs consumption led to a robust accumulation of novel NAE precursors, including the glycerophospho-containing docosahexaenoyl ethanolamine (DHEA), docosapentaenoyl ethanolamine (DPEA), and eicosapentaenoyl ethanolamine (EPEA). The tissue levels of these metabolites were significantly correlated with the antihyperalgesic phenotype. In addition, rats consuming the O3PUFA-rich diet showed reduced sprouting of nociceptive fibers containing CGRP and dorsal horn neuron p38 mitogen-activated protein kinase (MAPK) expression, well-established biomarkers of pain. The spinal cord levels of inositols were positively correlated with thermal hyperalgesia, supporting their role as biomarkers of chronic neuropathic pain. Notably, the O3PUFA-rich dietary intervention reduced the levels of these metabolites. Collectively, these results demonstrate the prophylactic value of dietary O3PUFA against SCI-mediated chronic pain.

Phosphorylation sites in the integrin beta3 cytoplasmic domain in intact platelets.

Protein seryl/threonyl phosphatase inhibitors such as calyculin A block inside-out and outside-in platelet signaling. Our studies demonstrate that the addition of calyculin A blocks platelet adhesion and spreading on fibrinogen, responses that depend on integrin alphaIIb beta3 signaling. We hypothesized that this reflects a change in alphaIIb beta3 structure caused by a specific state of phosphorylation. We show that addition of calyculin A leads to increased phosphorylation of the beta3 subunit, and phosphoamino acid analysis reveals that only threonine residues become phosphorylated; sequence analysis by Edman degradation established that threonine 753 became stoichiometrically phosphorylated during inhibition of platelet phosphatases by calyculin A. This region of beta3 is linked to outside-in signaling such as platelet spreading responses. The effect of calyculin A on platelet adhesion and spreading and on the phosphorylation of T-753 in beta3 is reversed by the calcium ionophore A23187, demonstrating that these effects of calyculin A are not generally toxic ones. We propose that phosphorylation of beta3 on threonine 753, a region of beta3 linked to outside-in signaling, may be a mechanism by which integrin alphaIIb beta3 function is regulated.