Levator scapulae and rhomboid minor are united.

Pain over the superior angle of the scapula is a common musculoskeletal symptom. It is often accompanied by radiating pain to the neck, head, and shoulder. The aetiologies can be varied but may also be idiopathic in nature. To explore the fascial connections of this region, we studied 26 unembalmed, -two Thiel and one alcohol body-donors of science, by dissection, histological probes, and plastinations. When removing the descending and transverse fibres of the trapezius, a large prominent triangular area of white connectives is revealed, varying in mass. A subdivision of these connectives can be further dissected to prove that the rhomboid minor and levator scapulae muscles are interconnected and enclosed by connectives. Between these two muscles a bridge of connective tissue, containing fat, is observed. These connectives end cranially at the surface of the splenius capitis, and at the midline, containing vessels and nerves, as supported by histology and plastinations. This unification is separate from the rhomboid major muscle but overlaps with the latter dorsally. It connects to the superior angle of scapula and its upper medial borders, respectively, and cranially to the root of the spine of the scapula. Beneath the united levator scapulae and rhomboid minor, described here, the serratus posterior superior and possibly serratus anterior form a hypomochlion or fulcrum at the superior angle of the scapula. Any tension on this unified entity can unbalance this fulcrum. Investigating the connections between these two unified muscles may help explain the often idiopathic nature of superior scapular pain, and the success or failure of surgery, and other treatments.

The comparative analyses of decalcification procedures and methyl benzoate pre-treatment on tissue preservation and antigenicity in human acetabular labra.

The histological processing of musculoskeletal tissue might be challenging. The alteration of tissue composition e.g. by calcification of soft tissue in the elderly, after trauma or surgical interventions makes the histological processing of fixed tissue difficult. Additional steps of decalcification are then needed that probably affect the staining quality. In the present work, the effects of different decalcification agents and the intermedium methyl benzoate on histological staining methods and immunohistochemistry have been compared. Acetabular labra were fixed with 4% paraformaldehyde, left untreated or decalcified using 30% ethylenediaminetetraacetic acid (EDTA; Chelaplex®) or 6% trichloroacetic acid (TCA) for 1-4 days to investigate the effects of decalcification duration. Moreover, samples were pretreated with methyl benzoate or conventionally paraffin embedded independent of decalcification procedure and duration. The specimens were evaluated using hemalaun-eosin, Azur II- methylene blue staining or immunohistochemistry against ankyrin B to visualize nerve fibers. Decalcification with Chelaplex® or TCA reduced cutting artifacts without affecting the tissue morphology and proteoglycan staining but decreased antigenicity in immunohistochemistry. Interestingly, methyl benzoate further reduced cutting artifacts without altering tissue morphology and elevated antigenicity for Chelaplex® decalcified tissue samples in immunohistochemistry. The decalcification with Chelaplex® or 6% TCA preserves tissue morphology and proteoglycan staining similar to non- decalcified tissue but facilitates section processing. In immunohistochemistry both decalcification agents decreased antigenicity. Chelaplex® decalcified, methyl benzoate treated samples yielded an improved antigenicity.

Comparative Examination of Temporal Glyoxalase 1 Variations Following Perforant Pathway Transection, Excitotoxicity, and Controlled Cortical Impact Injury.

Following acute neuronal lesions, metabolic imbalance occurs, the rate of glycolysis increases, and methylglyoxal (MGO) forms, finally leading to metabolic dysfunction and inflammation. The glyoxalase system is the main detoxification system for MGO and is impaired following excitotoxicity and stroke. However, it is not known yet whether alterations of the glyoxalase system are also characteristic for other neuronal damage models. Neuronal damage was induced in organotypic hippocampal slice cultures by transection of perforant pathway (PPT; 5 min to 72 h) and N-methyl-D-aspartate (NMDA; 50 µM for 4 h) or in vivo after controlled cortical impact (CCI) injury (2 h to 14 days). Temporal and spatial changes of glyoxalase I (GLO1) were investigated by Western blot analyses and immunohistochemistry. In immunoblot, the GLO1 protein content was not significantly affected by PPT at all investigated time points. As described previously, NMDA treatment led to a GLO1 increase 24 and 48 h after the lesion, whereas PPT increased GLO1 immunoreactivity within neurons only at 48 h postinjury. Immunohistochemistry of brain tissue subjected to CCI unveiled positive GLO1 immunoreactivity in neurons and astrocytes at 1 and 3 days after injury. Two hours and 14 days after CCI, no GLO1 immunoreactivity was observed. GLO1 protein content changes are associated with excitotoxicity but seemingly not to fiber transection. Cell-specific changes in GLO1 immunoreactivity after different in vitro and in vivo lesion types might be a common phenomenon in the aftermath of neuronal lesions.

Temporal dynamics of glyoxalase 1 in secondary neuronal injury.

BACKGROUND: Enhanced glycolysis leads to elevated levels of the toxic metabolite methylglyoxal which contributes to loss of protein-function, metabolic imbalance and cell death. Neurons were shown being highly susceptible to methylglyoxal toxicity. Glyoxalase 1 as an ubiquitous enzyme reflects the main detoxifying enzyme of methylglyoxal and underlies changes during aging and neurodegeneration. However, little is known about dynamics of Glyoxalase 1 following neuronal lesions so far. METHODS: To determine a possible involvement of Glyoxalase 1 in acute brain injury, we analysed the temporal dynamics of Glyoxalase 1 distribution and expression by immunohistochemistry and Western Blot analysis. Organotypic hippocampal slice cultures were excitotoxically (N-methyl-D-aspartate, 50 µM for 4 hours) lesioned in vitro (5 minutes to 72 hours). Additionally, permanent middle cerebral artery occlusion was performed (75 minutes to 60 days). RESULTS: We found (i) a predominant localisation of Glyoxalase 1 in endothelial cells in non-lesioned brains (ii) a time-dependent up-regulation and re-distribution of Glyoxalase 1 in neurons and astrocytes and (iii) a strong increase in Glyoxalase 1 dimers after neuronal injury (24 hours to 72 hours) when compared to monomers of the protein. CONCLUSIONS: The high dynamics of Glyoxalase 1 expression and distribution following neuronal injury may indicate a novel role of Glyoxalase 1.

The ductal origin of structural and functional heterogeneity between pancreatic islets.

Islets form in the pancreas after the first endocrine cells have arisen as either single cells or small cell clusters in the epithelial cords. These cords constitute the developing pancreas in one of its earliest recognizable stages. Islet formation begins at the time the cords transform into a branching ductal system, continues while the ductal system expands, and finally stops before the exocrine tissue of ducts and acini reaches its final expansion. Thus, islets continuously arise from founder cells located in the branching and ramifying ducts. Islets arising from proximal duct cells locate between the exocrine lobules, develop strong autonomic and sensory innervations, and pass their blood to efferent veins (insulo-venous efferent system). Islets arising from cells of more distal ducts locate within the exocrine lobules, respond to nerve impulses ending at neighbouring blood vessels, and pass their blood to the surrounding acini (insulo-acinar portal system). Consequently, the section of the ductal system from which an islet arises determines to a large extent its future neighbouring tissue, architecture, properties, and functions. We note that islets interlobular in position are frequently found in rodents (rats and mice), whereas intralobularly-located, peripheral duct islets prevail in humans and cattle. Also, we expound on bovine foetal Laguesse islets as a prominent foetal type of type 1 interlobular neuro-insular complexes, similar to neuro-insular associations frequently found in rodents. Finally, we consider the probable physiological and pathophysiological implications of the different islet positions within and between species.

Site-specific and time-dependent activation of the endocannabinoid system after transection of long-range projections.

BACKGROUND: After focal neuronal injury the endocannabinioid system becomes activated and protects or harms neurons depending on cannabinoid derivates and receptor subtypes. Endocannabinoids (eCBs) play a central role in controlling local responses and influencing neural plasticity and survival. However, little is known about the functional relevance of eCBs in long-range projection damage as observed in stroke or spinal cord injury (SCI). METHODS: In rat organotypic entorhino-hippocampal slice cultures (OHSC) as a relevant and suitable model for investigating projection fibers in the CNS we performed perforant pathway transection (PPT) and subsequently analyzed the spatial and temporal dynamics of eCB levels. This approach allows proper distinction of responses in originating neurons (entorhinal cortex), areas of deafferentiation/anterograde axonal degeneration (dentate gyrus) and putative changes in more distant but synaptically connected subfields (cornu ammonis (CA) 1 region). RESULTS: Using LC-MS/MS, we measured a strong increase in arachidonoylethanolamide (AEA), oleoylethanolamide (OEA) and palmitoylethanolamide (PEA) levels in the denervation zone (dentate gyrus) 24 hours post lesion (hpl), whereas entorhinal cortex and CA1 region exhibited little if any changes. NAPE-PLD, responsible for biosynthesis of eCBs, was increased early, whereas FAAH, a catabolizing enzyme, was up-regulated 48hpl. CONCLUSION: Neuronal damage as assessed by transection of long-range projections apparently provides a strong time-dependent and area-confined signal for de novo synthesis of eCB, presumably to restrict neuronal damage. The present data underlines the importance of activation of the eCB system in CNS pathologies and identifies a novel site-specific intrinsic regulation of eCBs after long-range projection damage.

Intrinsic up-regulation of 2-AG favors an area specific neuronal survival in different in vitro models of neuronal damage.

BACKGROUND: The endocannabinoid 2-arachidonoyl glycerol (2-AG) acts as a retrograde messenger and modulates synaptic signaling e. g. in the hippocampus. 2-AG also exerts neuroprotective effects under pathological situations. To better understand the mechanism beyond physiological signaling we used Organotypic Entorhino-Hippocampal Slice Cultures (OHSC) and investigated the temporal regulation of 2-AG in different cell subsets during excitotoxic lesion and dendritic lesion of long range projections in the enthorhinal cortex (EC), dentate gyrus (DG) and the cornu ammonis region 1 (CA1). RESULTS: 2-AG levels were elevated 24 h after excitotoxic lesion in CA1 and DG (but not EC) and 24 h after perforant pathway transection (PPT) in the DG only. After PPT diacylglycerol lipase alpha (DAGL) protein, the synthesizing enzyme of 2-AG was decreased when Dagl mRNA expression and 2-AG levels were enhanced. In contrast to DAGL, the 2-AG hydrolyzing enzyme monoacylglycerol lipase (MAGL) showed no alterations in total protein and mRNA expression after PPT in OHSC. MAGL immunoreaction underwent a redistribution after PPT and excitotoxic lesion since MAGL IR disappeared in astrocytes of lesioned OHSC. DAGL and MAGL immunoreactions were not detectable in microglia at all investigated time points. Thus, induction of the neuroprotective endocannabinoid 2-AG might be generally accomplished by down-regulation of MAGL in astrocytes after neuronal lesions. CONCLUSION: Increase in 2-AG levels during secondary neuronal damage reflects a general neuroprotective mechanism since it occurred independently in both different lesion models. This intrinsic up-regulation of 2-AG is synergistically controlled by DAGL and MAGL in neurons and astrocytes and thus represents a protective system for neurons that is involved in dendritic reorganisation.

Clinical review: behavioral interventions to prevent childhood obesity: a systematic review and metaanalyses of randomized trials.

CONTEXT: The efficacy of lifestyle interventions to encourage healthy lifestyle behaviors to prevent pediatric obesity remains unclear. OBJECTIVE: Our objective was to summarize evidence on the efficacy of interventions aimed at changing lifestyle behaviors (increased physical activity, decreased sedentary activity, increased healthy dietary habits, and decreased unhealthy dietary habits) to prevent obesity. DATA SOURCES: Data sources included librarian-designed searches of nine electronic databases, references from included studies and reviews (from inception until February 2006), and content expert recommendations. STUDY SELECTION: Eligible studies were randomized trials enrolling children and adolescents assessing the impact of interventions on both lifestyle behaviors and body mass index (BMI). DATA EXTRACTION: Two reviewers independently abstracted data on methodological quality, study characteristics, intervention components, and treatment effects. DATA ANALYSIS: We conducted random-effects metaanalyses, quantified inconsistency using I(2), and conducted planned subgroup analyses for each examined outcome. DATA SYNTHESIS: Regarding target behaviors, the pooled effect size for physical activity (22 comparisons; n = 9891 participants) was 0.12 [95% confidence interval (CI) = 0.04-0.20; I(2) = 63%], for sedentary activity (14 comparisons; n = 3003) was -0.29, (CI = -0.35 to -0.22; I(2) = 0%), for healthy dietary habits (14 comparisons, n = 5468) was 0.00 (CI = -0.20; 0.20; I(2) = 83%), and for unhealthy dietary habits (23 comparisons, n = 9578) was -0.20 (CI = -0.31 to -0.09; I(2) = 34%). The effect of these interventions on BMI (43 comparisons, n = 32,003) was trivial (-0.02; CI = -0.06-0.02; I(2) = 17%) compared with control. Trials with interventions lasting more than 6 months (vs. shorter trials) and trials with postintervention outcomes (vs. in-treatment outcomes) yielded marginally larger effects. CONCLUSION: Pediatric obesity prevention programs caused small changes in target behaviors and no significant effect on BMI compared with control. Trials evaluating promising interventions applied over a long period, using responsive outcomes, with longer measurement timeframes are urgently needed.