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The pandemic caused by SARS-CoV-2 virus, also known as COVID-19, has generated shockwaves in medical and surgical practice. It has necessitated re-deployment of staff and resources to cater for the unpredictable increase in footfall and demand on healthcare systems. This study aimed to investigate how the restructuring of our service altered the triage and management of non-melanoma skin cancer (NMSC) during the pandemic's first wave rise and peak. We retrospectively analysed all patients who underwent a skin excision under local anaesthetic which revealed the presence of a basal cell carcinoma (BCC) or squamous cell carcinoma (SCC) on histopathological analysis between 1st February 2020 - 31st May 2020 compared with the same period in 2019. There was a 158% increase in patients with excision of lesions confirmed on histopathological analysis as a NMSC during the COVID-19 period (168 vs. 65). In 2020, more excisions were performed by consultants (42.9% v 21.5%, p = 0.002) with a lower proportion of excisions with a close margin (27.7% v 17.8%, p = 0.096) and an involved margin (3.1% v 1.8%, p = 0.62). Five of these patients had their further management altered due to service constraints at this time The resource constraints secondary to the pandemic have yielded beneficial service adaptations with the incorporation of a more efficient model for the NMSC service. The sustainability of this model and its impact on training will require further examination when non-urgent and benign elective workload is slowly reinstated and plastic surgery trainees return to their original posts.

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An inquiry concerning the prevalence of urinary incontinence for the moroccan women has been archived about 1000 women aged more than 18 years to study prevalence, epidemiology and risk factors of urinary incontinence. 271 women among the 1000 women said that they had suffered from the mictional disorder at least one time during the last month, let 27.1%; 48.7% of the incontinent women are from 30 to 60 years; 22.5% are less than 30 years old, and 8.85% are more than 75 years old. Among these 271 women, 49.44% suffered from leakage after making an effort; 42.80% an imperiosity, and 7.76% spontaneous leakage. Seventy per cent among these women had level of study at least medium; 85.97% among these women suffered the discomfort; but 8.48% of them had been consulted for this disorder, 78.96% are able to consult a medical and to have a clinical or paraclinical exams. The elements who are responsible of this disorder are: menopause, parity, the use of forceps, the weight of first child birth over 3.5 kg, the perineal tearing. Among the medical antecedents we find: chronic bronchitis, urinary infections, chronic constipation, diabetes, and in the other way among surgical antecedents are: hysterectomy and prolapsus cure.

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OBJECTIVE: Evaluate the effect of the addition of clonidine to lidocaine on postoperative pain after intravenous regional anaesthesia. STUDY DESIGN: Double blind prospective study. PATIENTS AND METHODS: Forty-five patients were randomly allocated to two groups: group 1 (n = 25) receiving 3 mg.kg-1 of lidocaine 0.5% added to saline and group 2 (n = 20) receiving 3 mg.kg-1 of lidocaine 0.5% added to clonidine (150 micrograms). Postoperative analgesia was assessed using a visual analogue pain score (VAPS) and the time to first analgesic request. The incidence of side effects after tourniquet release was noted. Analysis of variance, Kruskall Wallis and chi 2 tests were used for statistical analysis. A p-value of < 0.05 was considered significant. RESULTS: Age, ASA class, duration and type of surgery, tourniquet time and sensory block duration were comparable for the two groups. The time to first antalgic request after deflation of tourniquet was similar in the two groups (38 +/- 15 min versus 44 +/- 19 min), while VAPS score was lower (p < 0.05) in the clonidine group (5.2 versus 6.8). The incidence of side effects was comparable in the two groups. CONCLUSION: The addition of clonidine (150 micrograms) to lidocaine for intravenous regional anaesthesia improved postoperative analgesia but in a limited and short-lasting manner.

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Within the pediatric population, the rare aortic aneurysm is most often brought on by congenital cardiovascular malformation or connective tissue disorder, trauma, inflammatory disease, or infection. Thus our 8-year-old patient who had multiple aortic aneurysms and evidence of mucopolysaccharidosis presented a doubly unique case. Three and one-half months after the patient underwent emergency aortic valve replacement, we performed resection and graft replacement of both her descending thoracic aorta and thoracoabdominal aorta. Histologic analysis of the aneurysm wall displayed severe medial degeneration with large deposits of acid mucopolysaccharides. Subsequent evaluation, although negative for connective tissue disorders, showed glycosaminoglycans, chondroitin sulfate, and heparan sulfate in the patient's urine. These findings are diagnostic for a heterogeneous group of storage diseases termed mucopolysaccharidoses, although testing of the patient's cultured fibroblasts failed to reveal any specific previously described enzymatic defect. After reviewing the literature, we believe that this is the first known successfully treated pediatric aortic aneurysm associated with mucopolysaccharidosis.

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AT III is a physiologic inhibitor of blood clot formation: its deficiency is manifested by venous thrombosis. The authors reported case of mesenteric venous infarction in a 42-years-old woman. AT III deficiency was transient and caused by an oral contraceptive. In patients with AT III acquired deficiency it is necessary to suppress any risk factors of venous thrombosis.

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E-selectin was evaluated for its ability to support neutrophil adhesion under conditions of flow. At a wall shear stress of 1.85 dyn/cm2, neutrophils were found to attach to E-selectin expressed on the apical surface of L cell monolayers. The initial intercellular contact was most often evidenced by neutrophils rolling on the monolayer at a mean rate of congruent to 10 microns/s. Anti-E-selectin monoclonal antibody, CL2/6, inhibited this interaction by > 90%. Rolling neutrophils often transiently stopped, but in contrast to the behavior on stimulated endothelial cells, they remained spherical in shape and did not migrate on or beneath the monolayer. A possible contribution of neutrophil L-selectin to this interaction was indicated by the findings that anti-L-selectin monoclonal antibody, DREG-56, inhibited E-selectin-dependent adhesion under flow by > 65%, and there was a highly significant correlation between surface levels of L-selectin and E-selectin-dependent adhesion under flow. E-selectin also appeared to support neutrophil adhesion to IL-1 beta-stimulated endothelial cells under conditions of flow, but it accounted for only congruent to 30% of the level of adherence, in contrast to L-selectin which accounted for > 65%. Thus, both L-selectin and E-selectin can support neutrophil adhesion at wall shear stresses that preclude intercellular adhesion molecule-1-dependent adhesion, and they participate in neutrophil adherence to stimulated endothelial cells under conditions of flow.

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In postcapillary venules, marginating neutrophils (PMNs) are often seen rolling along the vessel wall prior to stopping and emigrating. There is substantial evidence in vitro and in vivo that the adhesion receptors E- and L-selectin participate in this phenomenon on cytokine-stimulated endothelium, and recent evidence has shown that a closely related adhesion receptor, P-selectin, is capable of mediating neutrophil rolling on an artificial membrane. Here we demonstrate and characterize PMN rolling on monolayers of human umbilical vein endothelial cells (HUVECs) stimulated with histamine to induce surface expression of P-selectin. Peak association of PMNs with the HUVECs occurs 10 min after histamine stimulation, and at a postcapillary venular wall shear stress of 2.0 dyn/cm2 the rolling velocity is 14 microns/s. Approximately 95% of the PMNs roll on the endothelial cells, 5% adhere firmly, and none migrate beneath the endothelial monolayer. Monoclonal antibody (MAb) G1, which binds P-selectin and blocks its adhesive function, completely prevents association of the PMNs with histamine-stimulated HUVEC, whereas the nonblocking anti-P-selectin MAb S12 does not. Treatment of PMNs with the anti-L-selectin MAb DREG56 reduces PMN adherence by approximately 50%. Anti-CD54 MAb R6.5 and anti-CD18 MAb R15.7 have little effect on the number of PMNs rolling on the HUVECs but completely prevent PMNs from stopping and significantly increase rolling velocity. Nonblocking control MAbs for R6.5 (CL203) and R15.7 (CL18/1D1) lack these effects. Rolling adhesion of PMNs on histamine-stimulated HUVECs therefore appears to be completely dependent on endothelial cell P-selectin, with a minor adhesion-stabilizing contribution from intercellular adhesion molecule 1 and beta 2 integrins. The partial inhibition of rolling with DREG56 suggests that L-selectin may also play a role in neutrophil interactions with histamine-stimulated endothelium. We further characterize these interactions by determining the effects of the various MAbs and wall shear stresses on adhesion patterns, rolling velocities, and distributions of rolling velocities.

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The emigration of neutrophils at sites of inflammation apparently requires intercellular adhesion. Initially, leukocyte adherence is observed in postcapillary venules where neutrophils roll along the luminal surface of the endothelial cells before stopping, changing shape, and migrating into the perivascular tissue. Recent evidence indicates that the adhesion molecules supporting the rolling phenomenon are distinct from those required for stopping and transmigration. The contribution of E-selectin (ELAM-1) to neutrophil adhesion and rolling was investigated using anti-E-selectin monoclonal antibody in an in vitro adhesion assay of isolated human neutrophils to murine L-cell monolayers stably transfected with human E-selectin cDNA. Isolated human neutrophils adhered to E-selectin expressing L-cell monolayers under physiological wall shear stress of 1.85 dynes/cm2 but not to untransfected L-cells or ICAM-1 expressing L-cells. 47.8 +/- 6.0% of these adherent cells were rolling at an average rolling velocity of 10.6 +/- 1.7 microns/second. This adhesion and rolling was almost completely blocked by anti-E-selectin monoclonal antibody. Monoclonal antibody to L-selectin also reduced adhesion to E-selectin expressing cells by 70%. Chemotactic stimulation of neutrophils reduced both the number of adherent and rolling cells and the average velocity of the rolling cells without influencing the percentage of attached cells that were rolling. Pretreatment with anti-CD18 monoclonal antibody did not reduce the adhesion of the activated neutrophils but reversed the reduction in velocity caused by activation of these cells. The inhibitory potential of the anti-E-selectin monoclonal antibody was much less pronounced in adhesion of isolated neutrophils to human umbilical vein endothelial cell monolayers under conditions of flow and was limited to one third of the total adhesion. The proportion of the adherent neutrophils which transmigrated to the subluminal space of the endothelial cell monolayers was independent of pretreatment with anti-E-selectin monoclonal antibody.

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The contributions of the canine neutrophil lectin adhesion molecule-1 (LECAM-1) (canine homologue of the murine MEL-14 Ag) in neutrophil-endothelial cell adhesion and transendothelial migration were studied using anti-LECAM-1 mAb, CL2/6, and SL1 under static conditions and at wall shear stresses of up to 1.85 dynes/cm2 (dpc). Both mAb were found to inhibit attachment of neutrophils to cytokine-stimulated canine jugular vein endothelium. The inhibitory effects of the anti-LECAM-1 mAb were more evident at a wall shear stress of 1.85 dpc (greater than 50%) than at 0.23 dpc or under static conditions (approximately 30%). In contrast the anti-CD18 mAb, R15.7, exhibited higher inhibitory ability at the lower shear stress and under static conditions with marginal inhibition of adhesion at 1.85 dpc. Anti-LECAM-1 and anti-CD18 mAb showed additive inhibitory effects at the lower wall shear stress and under static conditions. Chemotactic stimulation of the neutrophils caused rapid down-regulation of LECAM-1 from the neutrophil surface and reduced adhesion by 60% at a wall shear stress of 1.85 dpc. This inhibition was not additive to anti-LECAM-1 mAb. Pretreatment with CL2/6 or SL1 did not affect trans-endothelial migration of adherent neutrophils under any experimental conditions tested. Anti-CD18 mAb, however, blocked transendothelial migration by 98% and 56% under static condition and at a wall shear stress of 0.23 dpc, respectively. The results in this report indicate that canine LECAM-1 is involved in the initial adhesion of unstimulated neutrophils to cytokine-stimulated endothelial cells under flow, but in contrast to CD18-integrins, plays no role in the transendothelial migration.

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To define further the molecular basis for abnormal interactions of cord blood or neonatal neutrophils with endothelial cells in vitro, we studied neutrophil adhesion and migration under experimental conditions specifically designed to evaluate CD18-independent mechanisms. Unstimulated cord blood neutrophils of healthy term neonates demonstrated significantly diminished adhesion to IL-1-stimulated endothelial cell monolayers under conditions of shear stress (congruent to 1.85 dynes/cm2); overall levels of migration by neonatal cells were also significantly diminished, although the adherent subpopulation of these cells migrated relatively normally. A mAb (DREG-56) against the human homologue of the murine MEL-14 antigen (termed lectin-, epidermal growth factor-, complement binding domain-cell adhesion molecule-1 (LECAM-1), a member of the LEC-CAM family of adhesion molecules) markedly inhibited adhesion of healthy adult but not cord blood neutrophils. In additional assessments of endothelial cell adhesion or migration in the absence of shear forces, cord blood neutrophils demonstrated significantly diminished values compared to adult controls. Moreover, mAb DREG-56 significantly diminished adhesion of healthy adult but not cord blood suspensions in the presence or absence of the anti-CD18 mAb R15.7. Immunofluorescence assessments of unstimulated cord blood neutrophils or neutrophils of neonates 12 to 48 h of age showed dramatically diminished levels of surface LECAM-1 compared to adult neutrophils. Chemotactic stimuli (FMLP, 10 nM, 15 min) consistently "down-regulated" surface LECAM-1 on adult neutrophils to levels approximately 10% of unstimulated suspensions and comparable to those of most unstimulated neonatal suspensions. Moreover, FMLP stimuli elicited little or no down-regulation of LECAM-1 on neonatal cells. In comparative studies, endothelial cell adhesion of unstimulated cord blood or adult control neutrophils (assessed under conditions of flow) was directly related to levels of neutrophil surface LECAM-1. Although FMLP stimulation significantly diminished both adhesion and LECAM-1 surface levels of adult control cells, the adhesion and LECAM-1 expression observed with cord blood cells were not significantly influenced by this stimulus. The mechanisms underlying diminished LECAM-1 expression and LECAM-1-dependent adhesion of neonatal neutrophils and the physiologic significance of these abnormalities deserve investigation.

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Monoclonal antibodies recognizing CD18, CD11a, CD11b, and neutrophil lectin adhesion molecule 1 (LECAM-1), i.e., the human homologue of the murine MEL-14 antigen, were used to assess the relative contribution of these glycoproteins to neutrophil-endothelial adhesion. Under static conditions, the adhesion of neutrophils to IL-1-stimulated human umbilical vein endothelial cell (HUVEC) monolayers was inhibited by antibodies to CD18, CD11a, and the neutrophil LECAM-1, and the effect of combining anti-LECAM-1 and anti-CD11a was almost additive. Under flow at a wall shear stress 1.85 dyn/cm2, a condition where CD18-dependent adhesion is minimal, anti-LECAM-1 inhibited adhesion by greater than 50%. Chemotactic stimulation of neutrophils induced a rapid loss of LECAM-1 from the neutrophil surface, and the level of neutrophil surface LECAM-1 was closely correlated with adhesion under flow. Neutrophils contacting the activated endothelial cells for 30 min lost much of their surface LECAM-1, a phenomenon induced by a soluble factor or factors released into the medium by the stimulated monolayers, and a high percentage migrated through the HUVEC monolayer. This migration was almost completely inhibited by anti-CD18, but was unaffected by antibodies to neutrophil LECAM-1. These results support the concept that LECAM-1 is a neutrophil adhesion molecule that participates in the adherence of unstimulated neutrophils to cytokine-stimulated endothelial cells under conditions of flow, and is then lost from the neutrophil surface coincident with the engagement of CD18-dependent mechanisms leading to transendothelial migration.

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