Seven years of preoperative BTA abdominal wall preparation and the Macquarie system for surgical management of complex ventral hernia.

PURPOSE: To assess 7-year outcomes after complex ventral hernia (CVH) repair using pre-operative Botulinum toxin A (BTA) injection and the Macquarie System of management. METHODS: Clinical examination and functional non-contrast abdominal CT scans were used to assess complications and recurrences encountered in a prospective series of 88 consecutive CVH repairs using pre-operative BTA injection (200 or 300 units) between November 2012 and December 2019. Pre-operative progressive pneumoperitoneum (PPP) and/or component separation (CS) were also used in some cases. RESULTS: All hernia defects (mean transverse width 12.9 ± 5.2 cm) were successfully closed using either laparoscopic or laparoscopic-assisted open techniques facilitated by pre-operative BTA injection. The mean pre-operative post-BTA lateral oblique length gain was 4.7 ± 2.2 cm/side (p < 0.001). In 43 patients with defects < 12 cm wide, closure was achieved using BTA-only in 33 (76.7%), BTA + PPP in 2 (4.7%), BTA + CS in 5 (11.6%) and BTA + PPP + CS in 3 (7.0%). In the remaining 45 patients with defects [Formula: see text] 12 cm wide, closure was achieved using BTA-only in 9 (20.0%), BTA + PPP in 11 (24.4%), BTA + CS in 5 (11.1%) and BTA + PPP + CS in 20 (44.4%). There was a significant correlation between increasing defect size and the need for 2 or more CVH closure procedures (χ2 = 25.28, p < 0.0005). There were no BTA complications. Two patients developed midline hernia recurrences. CONCLUSION: Pre-operative BTA injection of the abdominal wall is a safe procedure that facilitates hernia defect closure and reduces the need for CS, especially when defect size is less than 12 cm. BTA may also decrease the rate of hernia recurrence.

Brain Glucose-Sensing Mechanism and Energy Homeostasis.

The metabolic and energy state of the organism depends largely on the availability of substrates, such as glucose for ATP production, necessary for maintaining physiological functions. Deregulation in glucose levels leads to the appearance of pathological signs that result in failures in the cardiovascular system and various diseases, such as diabetes, obesity, nephropathy, and neuropathy. Particularly, the brain relies on glucose as fuel for the normal development of neuronal activity. Regions adjacent to the cerebral ventricles, such as the hypothalamus and brainstem, exercise central control in energy homeostasis. These centers house nuclei of neurons whose excitatory activity is sensitive to changes in glucose levels. Determining the different detection mechanisms, the phenotype of neurosecretion, and neural connections involving glucose-sensitive neurons is essential to understanding the response to hypoglycemia through modulation of food intake, thermogenesis, and activation of sympathetic and parasympathetic branches, inducing glucagon and epinephrine secretion and other hypothalamic-pituitary axis-dependent counterregulatory hormones, such as glucocorticoids and growth hormone. The aim of this review focuses on integrating the current understanding of various glucose-sensing mechanisms described in the brain, thereby establishing a relationship between neuroanatomy and control of physiological processes involved in both metabolic and energy balance. This will advance the understanding of increasingly prevalent diseases in the modern world, especially diabetes, and emphasize patterns that regulate and stimulate intake, thermogenesis, and the overall synergistic effect of the neuroendocrine system.

Expression of a Novel Ciliary Protein, IIIG9, During the Differentiation and Maturation of Ependymal Cells.

IIIG9 is the regulatory subunit 32 of protein phosphatase 1 (PPP1R32), a key phosphatase in the regulation of ciliary movement. IIIG9 localization is restricted to cilia in the trachea, fallopian tube, and testicle, suggesting its involvement in the polarization of ciliary epithelium. In the adult brain, IIIG9 mRNA has only been detected in ciliated ependymal cells that cover the ventricular walls. In this work, we prepared a polyclonal antibody against rat IIIG9 and used this antibody to show for the first time the ciliary localization of this protein in adult ependymal cells. We demonstrated IIIG9 localization at the apical border of the ventricular wall of 17-day-old embryonic (E17) and 1-day-old postnatal (PN1) brains and at the level of ependymal cilia at 10- and 20-day-old postnatal (PN10-20) using temporospatial distribution analysis and comparing the localization with a ciliary marker. Spectral confocal and super-resolution Structured Illumination Microscopy (SIM) analysis allowed us to demonstrate that IIIG9 shows a punctate pattern that is preferentially located at the borders of ependymal cilia in situ and in cultures of ependymocytes obtained from adult rat brains. Finally, by immunogold ultrastructural analysis, we showed that IIIG9 is preferentially located between the axoneme and the ciliary membrane. Taken together, our data allow us to conclude that IIIG9 is localized in the cilia of adult ependymal cells and that its expression is correlated with the process of ependymal differentiation and with the maturation of radial glia. Similarly, its particular localization within ependymal cilia suggests a role of this protein in the regulation of ciliary movement.

Apical Polarization of SVCT2 in Apical Radial Glial Cells and Progenitors During Brain Development.

During brain development, radial glial (RG) cells and the different progenitor subtypes are characterized by their bipolar morphology that includes an ovoid cell body and one or two radial processes that span across the developing cerebral wall. Different cells transport the reduced form of vitamin C, ascorbic acid (AA), using sodium-dependent ascorbic acid cotransporters (SVCT1 or SVCT2). SVCT2 is mainly expressed in the nervous system (CNS); however, its localization in the central nervous system during embryonic development along with the mechanism by which RG take up vitamin C and its intracellular effects is unknown. Thus, we sought to determine the expression and localization of SVCT2 during CNS development. SVCT2 is preferentially localized in the RG body at the ventricular edge of the cortex during the neurogenic stage (E12 to E17). The localization of SVCT2 overexpressed by in utero electroporation of E14 embryos is consistent with ventricular polarization. A similar distribution pattern was observed in human brain tissue sections at 9 weeks of gestation; however, SVCT2 immunoreaction was also detected in the inner and outer subventricular zone (SVZ). Finally, we used C17.2 neural stem cell line, J1ES cells and primary cell cultures derived from the brain cortex to analyze functional SVCT2 activity, AA effects in progenitor cells bipolar morphology, and SVCT2 expression levels in different culture conditions. Our results indicate that basal RG cells and apical intermediate and subapical progenitors are the main cell types expressing SVCT2 in the lissencephalic brain. SVCT2 was mainly detected in the apical region of the ventricular zone cells, contacting the cerebrospinal fluid. In gyrencephalic brains, SVCT2 was also detected in progenitor cells located in the inner and outer SVZ. Finally, we defined that AA has a strong radializing (bipolar morphology) effect in progenitor cells in culture and the differentiation condition modulates SVCT2 expression.

Can customized implants correct enophthalmos and delayed diplopia in post-traumatic orbital deformities? A volumetric analysis.

The purpose of this study was to determine whether orbital reconstruction with customized implants can correct post-traumatic orbital deformities such as late enophthalmos and delayed diplopia. The hypothesis proposed was that an overcorrection of the orbital volume is needed to resolve enophthalmos. A retrospective observational descriptive study was conducted. Patients with a major trauma who required customized orbital implants for the delayed treatment of unilateral orbital fractures that had initially been operated on using titanium mesh and/or osteosynthesis plates were included. The orbital volumes of the unaffected contralateral side, of the affected orbit after initial reconstruction with mesh, and of the affected orbit subsequently reconstructed with the customized implant were calculated. All of the patients included in this study had diplopia in the gaze position prior to the installation of the implant. In addition, they all had severe enophthalmos. After surgery, no patient with a customized implant showed diplopia. The enophthalmos was corrected in all but one case. On average, orbits reconstructed with customized implants had lower volumes compared to the unaffected contralateral side. In cases where the enophthalmos was resolved, the volume was reduced by an average of 8.55%. Further studies using a larger number of cases and with controlled volumetric corrections using CAD/CAM are needed.