Seemingly complete removal of histologically benign intracranial meningioma: late recurrence rate and factors predicting recurrence in 657 patients. A multivariate analysis.

Twenty-six consecutive cadet athletes sustained an acute, initial anterior shoulder dislocation. All dislocations required a manual reduction for initial treatment. Arthroscopy was performed within 10 days in all patients. The Beach chair position and interscalene anesthesia were used in each case. At arthroscopy, 25 patients had an avulsion of the anterior-inferior capsulolabral complex (Bankart lesion) from the glenoid rim. One patient had a lateral detachment of the inferior glenohumeral ligament from the humeral neck. Twenty-three patients had a Hill-Sachs lesion and 3 SLAP tears were noted. All Bankart lesions were repaired with a cannulated bioabsorbable fixation device. Nineteen patients, over 1 year postoperative, are the subject of this preliminary report. The average age was 19.5 years (range, 17 to 23 years). Follow-up averaged 19 months (range, 12 to 24 months). The average loss of external rotation was 3°. There have been no recurrent dislocations and 1 patient has had a single episode of resubluxation. Using the Rowe point score, 16 patients were rated excellent, 2 good, and 1 fair. All of the athletes in this study have returned to preinjury performance status. Acute stabilization of initial anterior shoulder dislocations appears to be an effective treatment option in young athletes known to have high recurrence rates with nonoperative treatment. This particular technique has been safe with little morbidity.

Arthroscopic bioabsorbable tack stabilization of initial anterior shoulder dislocations: a preliminary report

Pneumonia treated with imipenem/cilastatin.

Minimal Change Disease (MCD) is a clinical condition characterized by acute nephrotic syndrome, no evident renal lesions at histology and good response to steroids. However, frequent recurrence of the disease requires additional therapies associated with steroids. Such multi-drug dependence and frequent relapses may cause disease evolution to focal and segmental glomerulosclerosis (FSGS) over time. The differences between the two conditions are not well defined, since molecular mechanisms may be shared by the two diseases. In some cases, genetic analysis can make it possible to distinguish MCD from FSGS; however, there are cases of overlap. Several hypotheses on mechanisms underlying MCD and potential molecular triggers have been proposed. Most studies were conducted on animal models of proteinuria that partially mimic MCD and may be useful to study glomerulosclerosis evolution; however, they do not demonstrate a clear-cut separation between MCD and FSGS. Puromycin Aminonucleoside and Adriamycin nephrosis are models of glomerular oxidative damage, characterized by loss of glomerular basement membrane polyanions resembling MCD at the onset and, at more advanced stages, by glomerulosclerosis resembling FSGS. Also Buffalo/Mna rats present initial lesions of MCD, subsequently evolving to FSGS; this mechanism of renal damage is clearer since this rat strain inherits the unique characteristic of overexpressing Th2 cytokines. In Lipopolysaccharide nephropathy, an immunological condition of renal toxicity linked to B7-1(CD80), mice develop transient proteinuria that lasts a few days. Overall, animal models are useful and necessary considering that they reproduce the evolution from MCD to FSGS that is, in part, due to persistence of proteinuria. The role of T/Treg/Bcells on human MCD has been discussed. Many cytokines, immunomodulatory mechanisms, and several molecules have been defined as a specific cause of proteinuria. However, the hypothesis of a single cell subset or molecule as cause of MCD is not supported by research and an interactive process seems more logical. The implication or interactive role of oxidants, Th2 cytokines, Th17, Tregs, B7-1(CD80), CD40/CD40L, c-Mip, TNF, uPA/suPAR, Angiopoietin-like 4 still awaits a definitive confirmation. Whole genome sequencing studies could help to define specific genetic features that justify a definition of MCD as a "clinical-pathology-genetic entity."

Molecular and Cellular Mechanisms for Proteinuria in Minimal Change Disease.

The therapeutic efficacy of B-cell depletion by anti-CD20 treatment in pediatric and, more recently, in adult idiopathic nephrotic syndrome patients suggests a key role of B cells in the pathogenesis of the disease. However, their exact role is still unclear. B cells are able to secrete a large variety of antibodies that can protect against infections. However, B-cell dysregulation is well-established in a variety of autoimmune diseases. In parallel with their ability to produce antibodies, pathogenic B cells display altered effector functions by expressing activating surface molecules, which can strongly modify the immune homeostasis, or by producing specific cytokines, which can directly affect either podocyte structure and functions or modulate T-cell homeostasis. Herein, we report the most relevant clinical and experimental evidences of a pathogenic role of B cells in idiopathic nephrotic syndrome. We further highlight similarities and differences between children and adults affected by non-genetic forms of the disease and discuss what needs to be investigated in order to define the exact mechanisms underlying the pathogenic role of B cells and to identify more tailored therapeutic approaches.

/pdf/b-cell-dysregulation-in-idiopathic-nephrotic-syndrome-what-hes04go6.pdf

B-Cell Dysregulation in Idiopathic Nephrotic Syndrome: What We Know and What We Need to Discover

A Retrospective Study in 18 Cases

Steroid Responsive Tremor Syndrome in a Maltese Dog

https://www.koreascience.or.kr:443/article/JAKO200633242260442.pdf

A Successful Therapy of Mite Infection with Topical and Spray Application of Ivermectin in Four Pruritic Pigeons

Acquired Myasthenia Gravis in a Dog

Primary Dilated Cardiomyopathy in a Miniature Pinscher Dog

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