HolsboerMaschmeyer NeuroChemie (Germany)

The aim of this study was to compare the intraoperative and postoperative outcomes between a robot-assisted versus a navigated transpedicular fusion technique. This retrospective analysis included patients who underwent transpedicular posterior fusion of the spine due to trauma, pyogenic spondylodiscitis and osteoporosis. Surgery was done either with a robot-assisted or a percutaneous navigated transpedicular fusion technique. The outcome analysis included the duration of surgery, the radiation exposure, the postoperative screw position and complications. A total of 60 patients were operated and 491 screws were analysed. No statistical difference was seen in the applied cumulative effective radiation dose per patient. The radiological assessment revealed a more accurate screw placement with robot assistance. A learning curve could be observed in robot-assisted fusion. Robot-assisted and navigated transpedicular fusion techniques are both effective and safe. Robot-assisted transpedicular spine fusion goes along with higher placement accuracy but its implementation needs an adequate learning curve.

AimsThe aim of this study was to determine whether there is a correlation between the grade of humeral osteoarthritis (OA) and the severity of glenoid morphology according to Walch. We hypothesized that there would be a correlation.MethodsOveral, 143 shoulders in 135 patients (73 females, 62 males) undergoing shoulder arthroplasty surgery for primary glenohumeral OA were included consecutively. Mean age was 69.3 years (47 to 85). Humeral head (HH), osteophyte length (OL), and morphology (transverse decentering of the apex, transverse, or coronal asphericity) on radiographs were correlated to the glenoid morphology according to Walch (A1, A2, B1, B2, B3), glenoid retroversion, and humeral subluxation on CT images.ResultsIncreased humeral OL correlated with a higher grade of glenoid morphology (A1-A2-B1-B2-B3) according to Walch (r = 0.672; p < 0.0001). It also correlated with glenoid retroversion (r = 0.707; p < 0.0001), and posterior humeral subluxation (r = 0.452; p < 0.0001). A higher humeral OL (odds ratio (OR) 1.17; 95% confidence interval (CI) 1.03 to 1.32; p = 0.013), posterior humeral subluxation (OR 1.11; 95% CI 1.01 to 1.22; p = 0.031), and glenoid retroversion (OR 1.48; 95% CI 1.30 to 1.68; p < 0.001) were independent factors for a higher glenoid morphology. More specifically, a humeral OL of ≥ 13 mm was indicative of eccentric glenoid types B2 and B3 (OR 14.20; 95% CI 5.96 to 33.85). Presence of an aspherical HH in the coronal plane was suggestive of glenoid types B2 and B3 (OR 3.34; 95% CI 1.67 to 6.68).ConclusionThe criteria of humeral OL and HH morphology are associated with increasing glenoid retroversion, posterior humeral subluxation, and eccentric glenoid wear. Therefore, humeral radiological parameters might hint at the morphology on the glenoid side.Cite this article: Bone Jt Open 2022;3(6):463–469.

ObjectiveThe aim of the present paper is to analyze mid‐term and long‐term alterations of human anterior cruciate ligament (ACL) grafts during the remodeling process with special regards to cellularity, α‐smooth muscle protein (αSMP) expression, and crimp length in comparison to the native ACL.MethodsA total of 34 patients were included (23 male and 11 female). Biopsies of 13 semitendinosus tendon and 14 patellar tendon autografts were obtained during surgical revision secondary to an ACL reconstruction. According to the interval between the index procedure and sample collection, the patients were divided into four groups: 4–12 months, 13–60 months, 61–108 months, and >108 months. Seven samples of native ruptured ACL tissue obtained during surgical intervention served as control. All biopsies were taken from the intraligamentous part of the ACL or the graft. Histomorphological and immunohistochemical analyses were conducted after samples were stained using hematoxylin–eosin, Giemsa, and αSMP enzyme‐labeled antibodies. The total cell density, the numbers of fibroblasts and fibrocytes, the fibroblast/fibrocyte ratio, the number of αSMP+ cell nuclei, and the percentage of αSMP+ cells per fibroblast as well as the crimp lengths were determined using light microscopy.ResultsIn the early phase of remodeling, the grafts featured extensively high total cell counts (1021.2 ± 327.8, P = 0.001), with high numbers of fibroblasts (841.4 ± 245.2, P = 0.002), fibrocytes (174.5 ± 113.0, P = 0.04), and αSMP+ cells (78.3 ± 95.0, P = 0.02) compared to controls (390.1 ± 141.7, 304.5 ± 160.8, 65.6 ± 31.4 and 2.3 ± 2.6, respectively). Thereafter, the numbers of all cell entities decreased. After more than 108 months, the percentage of αSMP+ cells per fibroblast reached physiological values (ratio 1.3 ± 1.0, P = 0.41; control 0.8 ± 0.8), while the total cell count (834.3 ± 183.7, P = 0.001) as well as the numbers of fibroblasts (663.5 ± 192.6, P = 0.006) and fibrocytes (134.1 ± 73.0, P = 0.049) remained significantly high. The fibroblast/fibrocyte ratio showed no significant alterations over the course of time compared to the controls. The collagen crimp lengths were elongated by tendency in the early phase (28.8 ± 12.9 mm, P = 0.15; control 20.7 ± 2.2 mm) and significantly shortened over time, with the lowest values in the long term (14.8 ± 2.0 mm, P = 0.001). The comparison of biopsies from semitendinosus tendon and patellar tendon autografts revealed no significant differences for any of the histomorphological parameters investigated.ConclusionThis study reveals distinctive mid‐term and long‐term immunomorphological alterations during human ACL graft remodeling. These data clearly indicate that the remodeling is a process that continues for 9 years or more. Furthermore, it seems to be a process of adaptation rather than full restoration. Even in the long run, several biological properties of the native ACL are not completely reestablished.

Abstract The wealth of information captured by multiparameter flow cytometry (MFC) can be analyzed by recent methods of computer vision when represented as a single image file. We therefore transformed MFC raw data into a multicolor 2D image by a self-organizing map (SOM) and classified this representation using a convolutional neural network (CNN). By this means, we built an artificial intelligence that is not only able to distinguish diseased from healthy samples, but that can also differentiate seven subtypes of mature B-cell neoplasm (B-NHL). We trained our model with 18,274 cases including chronic lymphocytic leukemia (CLL) and its precursor monoclonal B-cell lymphocytosis (MBL), marginal zone lymphoma (MZL), mantle cell lymphoma (MCL), prolymphocytic leukemia (PL), follicular lymphoma (FL), hairy cell leukemia (HCL), lymphoplasmacytic lymphoma (LPL) and achieved a weighted F1 score of 0.94 on a separate test set of 2,348 cases. Furthermore, we estimated the trustworthiness of a classification and could classify 70% of all cases with a confidence of 0.95 and higher. Our performance analyses indicate that particularly for rare subtypes further improvement can be expected when even more samples are available for training.

Objectives Hypercoagulability is one mechanism to explain the increased risk of incident atherothrombotic disease in patients with major depressive disorder (MDD). We examined whether patients with remitted MDD show an enhanced procoagulant state. Methods 63 individuals (median age 35 years, 59% women), 40 with a DSM-IV diagnosis of remitted MDD, made by a clinical interview, and 23 healthy controls provided blood samples for the measurement of fibrinogen, D-dimer, von Willebrand factor, and plasminogen activator inhibitor-1. Standardised z-scores of plasma levels of these haemostatic factors were added to form a procoagulant index (PCI) as the primary outcome variable. Self-ratings of residual depressive symptoms and trait anxiety were also obtained. Results Compared with controls, remitted MDD patients had higher PCI (p = 0.013, Cohen’s d = 0.69) and fibrinogen (p = 0.001, d = 0.91), controlling for age, sex, body mass index, smoking and C-reactive protein. There were no significant associations of the PCI and individual haemostatic molecules with age of MDD onset, time since the last MDD episode, the number of previous MDD episodes and residual depressive symptoms. Additional adjustment for anxiety symptoms did not change these results. Conclusions Remitted MDD is associated with an enhanced procoagulant state. Hypercoagulability seems more a trait than a state characteristic of depression.

The hippocampal formation is a brain structure integrally involved in episodic memory, spatial navigation, cognition and stress responsiveness. Structural abnormalities in hippocampal volume and shape are found in several common neuropsychiatric disorders. To identify the genetic underpinnings of hippocampal structure here we perform a genome-wide association study (GWAS) of 33,536 individuals and discover six independent loci significantly associated with hippocampal volume, four of them novel. Of the novel loci, three lie within genes (ASTN2, DPP4 and MAST4) and one is found 200 kb upstream of SHH. A hippocampal subfield analysis shows that a locus within the MSRB3 gene shows evidence of a localized effect along the dentate gyrus, subiculum, CA1 and fissure. Further, we show that genetic variants associated with decreased hippocampal volume are also associated with increased risk for Alzheimer’s disease (rg=−0.155). Our findings suggest novel biological pathways through which human genetic variation influences hippocampal volume and risk for neuropsychiatric illness.

Zusammenfassung. Die Diagnostik depressiver Erkrankungen beruht auf kategorialen Klassifikationssystemen, die eine Vielzahl heterogener und teils konträrer Symptome zusammenfassen, deren komplexe biologische Grundlagen noch weitgehend ungeklärt sind. Die Diagnosestellung in der Psychiatrie und die damit verbundene Wahl der Behandlung erfolgen primär nur durch Sprache. Die biologische Charakterisierung der Pathophysiologie und Therapiemechanismen durch Biomarker und Gentests stellt eine der Sprache überlegene Organisation der Behandlung mit entsprechend höherer Erfolgsrate in Aussicht. Mithilfe von genetischen Untersuchungen, proteomischen und metabolomischen Profilen, neuroendokrinen und elektrophysiologischen Parametern und multimodaler zerebraler Bildgebung konnten bereits potentiell wichtige Biomarker für die biologische Charakterisierung depressiver Störungen und die Vorhersage des antidepressiven Behandlungserfolges identifiziert werden. Daraus wurden spezifische pathophysiologische Modelle entwickelt, so z. B. das Stress-Modell der Depression, das Serotoninmodell und das Modell der frontocingulären Dysfunktion. Dennoch konnte bislang kein Biomarker Eingang in die klinische Praxis der Depressionsbehandlung finden. Bis Ergebnisse aus der Labordiagnostik in die klinische Behandlungsroutine integriert werden, wird in der Depressionsbehandlung weiterhin die Sprache das letzte Wort haben.