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Introduction. The spontaneous rupture of the upper urinary tract’s cavity system, which includes the pelvicalyceal system and ureter, is sporadic. This phenomenon, where urine unexpectedly leaks out of the cavity system without any apparent cause of trauma or medical intervention, is a fascinating and puzzling aspect of urology. This condition is typically attributed to obstructive uropathy, which leads to increased pressure within the urinary tract. This article illustrates the sporadic occurrence of spontaneous ruptures within the pelvicalyceal system. It underscores the importance of prompt diagnosis and timely treatment to restore wall integrity without significant stenosis. Outlines of cases. We have recorded four cases of spontaneous rupture in urolithiasis, with a median patient age of 47.5 years. The clinical symptoms mimic those of renal colic. Ultrasound, computed tomography scans, and retrograde pyelography were used to diagnose the condition. Treatment consisted of inserting a JJ stent for an average duration of 2.5 months. In all cases, prompt diagnosis and treatment have led to a remarkable restoration of the pelvicalyceal system and the ureter’s wall, with spontaneous absorption of the extravasation and without significant ureteral strictures. Conclusion. The positive outcome underscores the importance of early diagnosis and treatment and offers hope for future cases.

The pathogenesis of peripheral neuropathies in adults is linked to maintenance mechanisms that are not well understood. Here, we elucidate a novel critical maintenance mechanism for Schwann cell (SC)-axon interaction. Using mouse genetics, ablation of the transcriptional regulators histone deacetylases 1 and 2 (HDAC1/2) in adult SCs severely affected paranodal and nodal integrity and led to demyelination/remyelination. Expression levels of the HDAC1/2 target gene myelin protein zero (P0) were reduced by half, accompanied by altered localization and stability of neurofascin (NFasc)155, NFasc186, and loss of Caspr and septate-like junctions. We identify P0 as a novel binding partner of NFasc155 and NFasc186, both in vivo and by in vitro adhesion assay. Furthermore, we demonstrate that HDAC1/2-dependent P0 expression is crucial for the maintenance of paranodal/nodal integrity and axonal function through interaction of P0 with neurofascins. In addition, we show that the latter mechanism is impaired by some P0 mutations that lead to late onset Charcot-Marie-Tooth disease.

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Introduction: The innervation pattern of the clavicular head of the deltoid muscle and its corresponding topography was investigated via cadaveric dissection in the present study, focusing on the lateral pectoral nerve., Materials and Methods: Fifty-eight upper extremities were dissected and the nerve supplies to the deltoid muscle and the variability of the lateral pectoral and axillary nerves, including their topographical patterns, were noted., Results: The clavicular portion of the deltoid muscle received a deltoid branch from the lateral pectoral nerve in 86.2% of cases. Two topographical patterns of the lateral pectoral nerve were observed, depending on the branching level from the brachial plexus: a proximal variant, where the nerve entered the pectoral region under the clavicle, and a distal variant, where the nerve entered the pectoral region from the axillary fossa around the caudal border of the pectoralis minor. These dissection findings were supported by histological confirmation of peripheral nerve tissue entering the clavicular part of the deltoid muscle., Conclusions: The topographical variations of the lateral pectoral nerve are relevant for orthopedic and trauma surgeons and neurologists. These new data could revise the interpretation of deltoid muscle atrophy and of thoracic outlet and pectoralis minor compression syndromes. They could also explain the residual anteversion function of the arm after axillary nerve injury and deficiency, which is often thought to be related to biceps brachii muscle function., (© 2020 The Authors. Clinical Anatomy published by Wiley Periodicals, Inc. on behalf of American Association of Clinical Anatomists.)

Microglia cells are the unique residential macrophages of the central nervous system (CNS). They have a special origin, as they derive from the embryonic yolk sac and enter the developing CNS at a very early stage. They play an important role during CNS development and adult homeostasis. They have a major contribution to adult neurogenesis and neuroinflammation. Thus, they participate in the pathogenesis of neurodegenerative diseases and contribute to aging. They play an important role in sustaining and breaking the blood-brain barrier. As innate immune cells, they contribute substantially to the immune response against infectious agents affecting the CNS. They play also a major role in the growth of tumours of the CNS. Microglia are consequently the key cell population linking the nervous and the immune system. This review covers all different aspects of microglia biology and pathology in a comprehensive way., Competing Interests: CONFLICTS OF INTEREST The authors declare no conflicts of interest.

The pathogenesis of peripheral neuropathies in adults is linked to maintenance mechanisms that are not well understood. Here, we elucidate a novel critical maintenance mechanism for Schwann cell (SC)-axon interaction. Using mouse genetics, ablation of the transcriptional regulators histone deacetylases 1 and 2 (HDAC1/2) in adult SCs severely affected paranodal and nodal integrity and led to demyelination/remyelination. Expression levels of the HDAC1/2 target gene myelin protein zero (P0) were reduced by half, accompanied by altered localization and stability of neurofascin (NFasc)155, NFasc186, and loss of Caspr and septate-like junctions. We identify P0 as a novel binding partner of NFasc155 and NFasc186, both in vivo and by in vitro adhesion assay. Furthermore, we demonstrate that HDAC1/2-dependent P0 expression is crucial for the maintenance of paranodal/nodal integrity and axonal function through interaction of P0 with neurofascins. In addition, we show that the latter mechanism is impaired by some P0 mutations that lead to late onset Charcot-Marie-Tooth disease.

The presence of the calcium-binding protein parvalbumin (PV) was studied in neuronal elements of the cat's inferior colliculus (IC) by means of light and electron microscopic immunocytochemistry. Immunostaining of PV was detected in all three main parts of the IC. Several subtypes of large neurons that differed in size and shape were immunostained, comprising approx. 15% of the total number of PV-containing neurons. Approx. half of the labeled neurons were medium sized. Two types of small neurons were found to be PV synthesizing, and comprised approx. 35% of the total PV-containing population. Ultrastructurally, many dendrites were heavily immunolabeled, and the reaction product was present in dendritic spines as well. Several types of synaptic boutons contained reaction product, and terminated on both labeled and unlabeled postsynaptic targets forming asymmetric and symmetric synapses. Approx. 70% of all PV-immunolabeled terminals contained round synaptic vesicles and formed asymmetric synapses. The majority of these boutons were of the "large round" type and corresponded to the terminals of cochlear nuclei. A lower number were of the "small round" type, and were probably corticotectal terminals. The remaining 30% of PV-containing terminals contained pleomorphic or elongated vesicles and formed symmetric synapses. These terminals corresponded with "P" and "F1" bouton types. Part of these boutons appeared to arise from nuclei of the lateral lemniscus and the superior olive, and a certain percentage likely represented endings of inhibitory interneurons.