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The “Luigi Cattaneo” Anatomical Wax Collection belongs to the network of Museums and Collections of the University of Bologna. It is closely related to the Anatomy Centre of the Department of Biomedical and Neuromotor Sciences of the University of Bologna, and holds a significant place in the history of medicine, art, and scientific innovation. This review explores the museum’s rich historical background, its cultural importance, and its role in promoting the encounter between the past and the present. Preserving the legacy of anatomical wax modelling, the museum adapts to modern education and to research needs. It bridges artistic expression and scientific knowledge, emphasizing the importance of art as a tool of medical education. In this context, augmented reality, 3D models, CT scan and new methods of communication, integrate tradition and progress, expanding anatomical exploration. As part of the University of Bologna, the Collection catalyzes interdisciplinary collaboration, unlocking new scientific avenues. It works as a bridge through time, uniting craftsmanship, exploration, and knowledge-seeking in the study of the human body. [ABSTRACT FROM AUTHOR]

Anomalies of the brachial plexus including the distribution of the nerves as well as its terminal branches in the upper limb have been largely described in the literature. In this case report we describe a further variant of brachial plexus formation identified during routine anatomical dissection of the right upper limb of a 62-year-old Caucasian female cadaver. On the right side no musculocutaneous nerve was identified, the median nerve was formed as expected but a short extra branch communicating between the lateral cord and the medial head of the median nerve appeared. Coracobrachialis muscle was innervated by a direct branch from the lateral cord, while biceps brachialis and brachialis muscles were reached by collaterals of the median nerve. Moreover, in the distal half of the upper limb, the median nerve contributed to the innervation of the lateral aspect of the forearm skin via the lateral cutaneous nerve of the forearm. In order to analyze this specific variant relevance we compared it with all the similar previous reported cases, trying to explain the embryological bases of the variant. The knowledge of anatomical variations of peripheral nerves is pivotal not only for surgeons, radiologists and anesthesiologists that may operate on the axilla, but also for every medical doctor to understand inexplicable clinical signs. [ABSTRACT FROM AUTHOR]

The article focuses on the discovery of left vertebral artery hypoplasia (VAH) in a 78-year-old cadaver, with the abnormal artery having a significantly smaller diameter than the right one, potentially raising questions about the clinical significance of such variations and their relation.

The article focuses on a potential pharmacological strategy to enhance the sensitivity of glioblastoma cells to oxidative stress by exploiting the accumulation of prelamin A, a precursor of lamin A, which results in morphological changes, reduced cell aggressiveness, and impaired survival.

The article focuses on a project called Pro.dono, which uses Graphic Medicine as a means to raise awareness about whole-body donation for medical research and education, particularly in the field of cadaver dissection, addressing factors like age, education, and culture.

The article focuses on the progression of micro-anatomical, molecular, and metabolic changes affecting the liver of patients with TYMP derived mitochondrial disease (MNGIE), revealing that the liver is a target organ in MNGIE with significant morphological and metabolic alterations.

The article focuses on anatomical measurements related to the placement of zygomatic implants in the orbital floor to prevent complications and ensure safe implant insertion, based on a study conducted on human cadaver heads.

The article focuses on studying the influence of the pterygomandibular raphe tendinous (PMR) in Mandibular Advancement of Obstructive Sleep Apnea Syndrome (OSAS) treatment, specifically its presence or absence and its impact on the efficacy of oral mandibular advancement devices (MAD).

The article focuses on the regulation of nuclear inositide signaling pathways in Myelodysplastic Syndromes (MDS), particularly their role in hematopoietic stem cell proliferation and differentiation, which is crucial for understanding MDS pathogenesis and developing targeted therapies.

The article focuses on investigating how mutations in collagen VI (COL6) genes, which lead to COL6-related myopathies, affect the regenerative potential of pericytes, highlighting the importance of pericytes in muscle repair in response to injury in these conditions.

The article focuses on the role of Nuclear Phospholipase C (PLC) β1 in Myelodysplastic Syndromes (MDS) and Acute Myeloid Leukemia (AML) progression, studying how PLCβ1 modulation affects leukemic cells and their interactions with mesenchymal stromal cells (MSCs) in the bone marrow microenvironment.

The article focuses on Autosomal Dominant Leukodystrophy (ADLD), an ultra-rare neurodegenerative disorder, and reveals that LMNB1 overexpression in astrocytes triggers inflammation and inhibits myelination, shedding light on a new role for astrocytes in ADLD demyelination.

The article focuses on developing and validating a method for extracting the secretome directly from glioma patients' tissue, which can provide valuable insights into glioma pathogenesis, identify therapeutic targets, and enable personalized treatment approaches by comprehensively.

The article presents a study on Mir-192-5p expression in MDS progenitor cells during response to azacitidine and lenalidomide therapy. Topics include information on how BCL2 expression is deregulated in hematopoietic stem cells; how small non-coding RNAs that act on the epigenetic machinery; and how expression of mRNAs is linked to cancer development and could give a proliferative clonal advantage to Myelodysplastic Syndromes (MDS) cells.

Objective: Mitochondrial neurogastrointestinal encephalomyopathy (MNGIE) is an extremely rare disease caused by a genetically-driven thymidine phosphorylase (TP) defect. TP converts the nucleosides thymidine and deoxyuridine into respective nucleotides. In MNGIE, these nucleosides accumulate promoting tissue damage and mtDNA abnormalities responsible for neurological impairment and severe gastrointestinal dysmotility. The resulting clinical phenotype has a tremendous impact on patients' poor quality of life and fatal outcome.1;2 One possible treatment strategy to MNGIE patients is the stable reduction of circulating toxic nucleosides via liver transplantation. This approach has been successfully achieved in MNGIE patients in Italy and in many Western Countries.3 Although the liver has never been described as a target organ of the disease, explanted livers of MNGIE patients show clear macroscopic changes. Aim: The objective of our study was to provide an accurate morphologic and metabolic analysis of MNGIE liver tissue vs. controls (CTR). Methods: Liver tissue biopsies (1x1 cm each sample) were collected from n=7 MNGIE (2F; 20-38 yrs) and n=7 CTR (2F; 22-67 yrs) subjects. Formalin fixed-paraffin embedded tissue sections were processed for: 1) Hematoxylin and Eosin staining to evaluate architectural changes; 2) Sirius Red/Fast Green collagen assay to localize and quantify fibrosis; 3) Orcein, vascular endothelial cells growth factor and CD31 immunostaining to assess vascular changes; 4) hypoxia-inducible-factor-1a (HIF-1a) immunostaining to test hypoxia. Part of the liver tissue biopsies (0.5x0.5 cm each sample) were collected and snap frozen from n=3 MNGIE and n=3 CTR for metabolomic NMR assay. Results: MNGIE liver was characterized by intense steatosis. Fibrosis increases (P=0.0025) with patient age leading to the formation of porto-portal and porto-central collagen septa. The vascular and biliary branches were altered and these findings correlated with the increased hypoxia in hepatocytes, as indicated by HIF-1a positive staining. Preliminary analysis performed with NMR indicated a rearrangement characterized by triglyceride production and a significant decline in aerobic metabolism. Conclusions: Our data, showing marked morphological and metabolic changes, indicate that the liver is a target organ of MNGIE. Liver alterations should be carefully taken into account as a compromised liver may interfere with the clinical response to targeted treatments. [ABSTRACT FROM AUTHOR]

Alterations of inositide signalling regulated by PI-PLCbeta1/Cyclin D3/PKCalpha or Akt/mTOR pathways are associated with MDS1. Most MDS patients may need transfusions of RBCs to correct anemia, but iron overload and increased oxidative stress are common collateral effects of this approach2, that is why they are treated with Deferasirox (DFX) as iron chelator3. Here, we further analyzed the molecular effect of iron stress and DFX therapy on inositide signalling, using hematopoietic cell lines and MDS samples, with the aim to identify new molecular markers of DFX response. The study included BM samples obtained from 6 transfusion-dependent MDS patients treated with DFX from 2006 to 2019, and 6 BM samples from healthy subjects who had given informed consent according to the Declaration of Helsinki. 3 patients were responders, and 3 were non responders. All samples came from the Institute of Hematology "L e A Seràgnoli", Bologna, Italy, where also the clinical data were collected. Gene/protein expression were evaluated on mononuclear cells at diagnosis and during the therapy, by Real-Time PCR and immunocytochemistry. Cell lines were treated with 150 µM FeCl for 48h and DFX 50 µM for 6h, used alone or in combination to imitate in vitro the patients' dose. Cell cycle and apoptosis were examined by flow cytometry, along with the analysis of ROS production. We also studied the expression of enzymes related to inositide signalling, cytokine secretion and Akt/mTOR activation. Responder patients showed higher baseline levels of PI-PLCbeta1/Cyclin D3/PKCalpha expression, as compared both with non-responders and healthy subjects. During DFX therapy, ROS production and inositide signalling increased only in non responder patients, while in responder patients, as well as in K562 cells treated with FeCl +DFX, gene and protein expression remained almost constant. On the contrary, THP-1 cells were not affected. All in all, our results show for the first time that the expression of PI-PLCbeta1/Cyclin D3/PKCalpha pathway is directly associated with iron-induced oxidative stress and ROS production in MDS and hematopoietic cells. The apparent nuclear localization of inositides during treatment could hint at a specific involvement of this signalling pathway during oxidative stress, that could be linked to a specific regulation of hematopoietic differentiation and needs further investigation, first in a larger number of patients' cells, then in other in vitro experimental models. [ABSTRACT FROM AUTHOR]

Palmaris longus (PL) muscle is a superficial flexor of the forearm with restricted functions (its harvest or absence does not result in any functional disorder) but great clinical importance. It is used as landmark to identify median nerve, it is the first choice as tendon graft in reconstructive plastic, orthopedic, ophthalmologic and oto-laryngologic surgery and its variation can lead to some compression syndromes. It is phylogenetically classified as a retrogressive muscle and one of the most variable muscles of the human body. Agenesis is the most common anatomical variation while anomalies in insertion are quite rare, having an overall incidence of less than 1% [1]. During routine dissections of 32 forearms (from 16 embalmed cadavers) in the dissecting room of the University of Bologna, a female Caucasian cadaver aged 78 years was found to present a variation of insertion of the right PL tendon. The flattened tendon, measuring 10 cm in length and 0.6 cm in width, presented a cleft about 3.5 cm from the palmar aponeurosis. The lateral division was slender, located more superficially and fanned out distally into the palmar aponeurosis. The medial division, sharing a common sheet with the lateral one, run deeper and inserted at the ipothenar eminence. Median nerve crossed the lateral division. Such a V-shaped distal insertion is known as the PL bicaudatus of Gruber [2]. We conducted a detailed review of the literature and surprisingly we discovered that Luigi Cattaneo Anatomical Wax Collection of Alma Mater Studiorum, which displays a rich collection of anatomical preparations dating back to the 19th century, hosted a dry specimen of a left forearm. This preparation, displayed on a wooden platform, exhibited a case of bicaudatus PL tendon, described by professor Calori in 1868 [3] and likely prepared in the Anatomical Cabinet to faithfully display and reproduce the variation observed during autopsies/dissections. Even more fascinatingly, a hint to PL variability was already found in Vesalius' masterpiece De Humani Corporis Fabrica [4]. The iconic second book tables in fact seemed to depict a bicaudatus insertion of PL at the right wrist. Though it is a vestigial muscle, the PL continues to arouse interest because of its great variability. Understanding anatomical variants is certainly a fundamental skill of anatomists as well as of clinicians involved in diagnostic and surgical techniques. Acknowledgements. Authors wish to sincerely thank people who donated their body to science with the purpose of performing medical education and anatomical research. Results can potentially improve patient care and increase mankind's overall knowledge. Therefore, these donors and their families deserve our highest gratitude. [ABSTRACT FROM AUTHOR]

Introduction: Chronic intestinal pseudo-obstruction (CIPO) is a rare syndrome characterized by severe gastrointestinal (GI) dysmotility that mimics a GI obstruction in the absence of any mechanical cause CIPO is due to muscular-neuronal-glial-interstitial cells of Cajal abnormalities ¹ and can be idiopathic or secondary to a genetic cause Recently we documented that changes in the microvasculature supplying the gut contribute to GI abnormalities in a genetically driven form of CIPO2 Aim: The object of this study was to investigate if jejunal microvasculature alterations may occur and contribute to the disease also in idiopathic forms of CIPO. Methods: Full thickness jejunal biopsies were collected from n=23 CIPO and n=10 controls. Formalin fixed-paraffin embedded tissue sections were 1) stained with orcein to identify, meas- ure and count blood vessels, that were subdivided in >300μm (large), 300-101μm (medium), 100-51μm (small) and <50μm (very small), 2) stained with Sirius Red/Fast Green- collagen- assay to measure longitudinal muscle layer thickness and to spectrophotometrically determine fibrosis. Frozen tissue was used to assess by western blot Thymidine Phosphorylase (TP) protein expression, as this enzyme is involved in physio-pathological angiogenesis and was found absent in the previously documented form of CIPO secondary to a genetic disorder ² ; and the expression of HIF-1α as marker of hypoxia. Results: CIPO patients showed a lower vascular area with more vessels/mm² submucosa vs. controls. Vessels <50 μm increased at the expense of medium and large vessels. As com- pared to controls, CIPO showed, a higher fi brosis index, hypoxia, a decreased thickness of the longitudinal muscle layer and a decreased number of myenteric neurons. Finally, TP enzyme expression was found decreased in the jejunum of CIPO patients. Conclusion: Our results indicate that the jejunum of CIPO patients is characterized by quantitative and qualitative vascular changes, muscular and neuronal atrophy, fibrosis and hypoxia. Thus, this study allows us to hypothesize that abnormal GI vascularization might be a possible mechanism underlying gut dysfunction in CIPO. [ABSTRACT FROM AUTHOR]

The article presents a study which explores the potential role of phospholipase C beta 2 (PLCβ2) in Doxorubicin (DOX)-induced cardiotoxicity. It mentions that Anthracycline therapy, a cornerstone in the treatment of several cancers. It discusses that anthracycline therapy as limited by cumulative dose-dependent cardiotoxicity which imply a decrease of long-term survival of patients.

The article offers information about the role of astrocytes in Autosomal-dominant leukodystrophy (ADLD), characterized by Lamin B1 (LMNB1) gene alterations. It demonstrate that LMNB1 accumulation leads to cell sufferance, probably related to the induction of astrocytes reactivity that could be associated to ADLD pathology.

The article presents a study on key regulators of Glioblastoma aggressiveness and progression. Topics include information on the importance of lipid signaling and phospholipases (PLCs) in the regulation of different mechanisms in the central nervous system; information on pathogenesis of human glioblastoma; and how Glioblastoma is the most aggressive and lethal brain tumor in adults.

The article presents a study on the mechanosignaling network under mechanical strain. Topics include information on muscle-tendon unit (MTU) which regulates motor function; information on environmental chemical and mechanical signals induced by MTU; and musculoskeletal system with high degree of heterogeneity in terms of cell population, cell density, and physical and mechanical properties.

Objectives: Mandibular defect is one of the common defects of facial region, which can seriously affect the appearance, chew and speech. Functional reconstruction of mandibular defect is due to restore denture, occlusal function and mandibular bone. Vascularized bone grafting on mandibular defect is an effective method for reconstruction especially in larger defects treatment. To promote the reconstruction of mandibular defect treatment and improve the quality of reconstruction, in this study was evaluated the possibility of the use of a galeo-pericranial flap, pedicled and free, evaluating the vascular caliber and course of superficial temporal vessels comparing with facial and superior thyroid vessels and its osteogenic potential. Materials and methods: Ten cadaveric anatomical bilaterally head and neck specimens, obtained by donors, were used to simulate the surgical procedure evaluating the vascular calibers of the temporal and cervical arteries. For the clinical study was used Augmented Reality (AR) navigation in order to obtain three-dimensional image of the vascular pedicle supplying the flap. Mandibular defects were realized and then replaced using the pedicled flaps. The Ethics Committee for application of the galeo-pericranial free flap to mandibular reconstruction was obtained. Results and conclusion: The facial arteries seem to have a slightly larger diameter, while there is no clear anatomical evaluation concerning the caliber of cadaveric superior thyroid vessels in literature. Clinical results not demonstrated to have a functional issue at either the recipient or donor site. All patients showed good healing during recovery and follow-up visits with an average follow-up of nine months. Microsurgical free flap is shown to be a valuable and reliable method in head and neck surgery. In particular, galeo-pericranial flaps for mandibular reconstruction demonstrated improved functional and morphological outcomes, with higher success rates. [ABSTRACT FROM AUTHOR]

The article presents a study on 36 fresh frozen cadavers related to the placement of zygomatic implants. Topics include information on source of anchorage for zygomatic implants; malar and zygomatic arch bone and distances with the relevant anatomical structures; and how malar bone can offer adequate spaces to arbour two zygomatic implants for a fixed prosthetic rehabilitation.

The article presents a study on recovery of mtDNA depletion in the ileum of a Mitochondrial Nero-Gastrointestinal Encephalomyopathy (MNGIE) patient receiving liver transplant. Topics include information on mitochondrial neurogastrointestinal encephalomyopathy (MNGIE); gene encoding for thymidine phosphorylase (TP); and imbalance of mitochondrial nucleotide pool impaired mtDNA replication and depletion.

Autosomal Dominant Leukodystrophy (ADLD) is a rare and fatal adult-onset neurodegenerative disorder that affects the central nervous system. It is characterized by Lamin B1 (LMNB1) gene duplication or deletion upstream the gene1, but the molecular mechanisms responsible for driving its onset and development are not clear yet. Considering the pivotal role that glial cells as oligodendrocytes and astrocytes and Leukemia Inhibitory Factor (LIF)-activated pathways have in the myelination process, this work aims to analyze the specific alterations in different cell populations. Specific morpho-functional aspects of primary cells deriving from ADLD patients and engineered cellular models overexpressing Lamin B1 have been analyzed. Result demonstrated that cells from ADLD patients and astrocytes overexpressing LMNB1 show nuclear alterations, not present in oligodendrocytes. Moreover, Lamin B1 accumulation in astrocytes induces a reduction in LIF and LIF-R levels with a consequential decrease in LIF secretion, leading to Jak/Stat3 and PI3K/Akt axes downregulation. Administrating exogenous LIF, the toxic effects, induced by LMNB1 accumulation, may be partially reverted with differences between astrocytes and oligodendrocytes2. In addition, Lamin B1 overexpression induces alterations in cell survival pathways with GSK3ß inactivation, but not the upregulation of ß-catenin targets resulting in a reduction of astrocyte survival. Moreover, Lamin B1 build up affects proliferation and cell cycle progression with PPARγ and p27 increase and Cyclin D1 decrease. These events are associated to cell viability reduction and apoptosis, suggesting a great sufferance of this specific cell population. Interestingly, astrocytes overexpressing Lamin B1 show increased immunoreactivity for both GFAP and vimentin together with NF-kB nuclear translocation and c-Fos increase, suggesting astrocytes reactivity and substantial cellular activation. Moreover, it has been shown the activation of proinflammatory mechanisms and the increase of reactive oxygen species (ROS) in ADLD patients' cells. These data demonstrate that Lamin B1 accumulation is correlated to cell sufferance, probably related to the induction of reactive astrocytes phenotype that could be associated to ADLD pathological mechanisms. Our studies, for the first time, hint at a pivotal role of astrocytes in the development of the disease. [ABSTRACT FROM AUTHOR]

Gliomas are primary brain tumors originated from the supporting neuroglial cells of the Central Nervous System (CNS). Gliomas can be classified into different histopathologic grades according to World Health Organization (WHO) grading system and the grade of gliomas is highly correlated with the type of prognosis. Gliomas can, therefore, be classified into highgrade gliomas (HGG), including Glioblastoma Multiforme (GBM) as the most common malignant brain tumor in adults, and low-grade gliomas (LGG). Today the main therapies for this type of cancers are based on neurosurgical, chemotherapeutical and radiotherapeutical procedures that are highly invasive for all gliomas and cannot cure definitively the tumor in highgrade patients. For this reason, the management of gliomas represents today a great challenge and the understanding of the molecular mechanisms related to tumor transformation could help to find a successful targeted therapeutic strategy. Several studies have shown the key role of phosphoinositides (PIs), and in particular of phospholipase C β1 (PLCβ1) in the regulation of many mechanisms within the CNS1 such as cell adhesion, migration and cell cycle that, interestingly, are altered in GBM2. In silico studies have already evidenced that PLCβ1 gene expression is inversely correlated with the gliomas' pathological grade, suggesting PLCβ1 as a potential prognostic factor and novel signature gene in the molecular classification of high-grade gliomas3. This study aims to determine the pathological impact of PLCβ1 in GBM patients' samples, in engineered cell lines and primary astrocytes. PLCβ1 gene expression was analyzed through qPCR. Mesenchymal markers and survival pathway targets were evaluated by Western Blot and Immunofluorescence. Migration and invasion were carried out through transwell and wound healing assays. This study confirmed that PLCβ1 gene expression is lower in 50 GBM samples compared to 20 healthy controls. Moreover, PLCβ1 silencing in U87-MG, U-251 MG cell lines and HA primary astrocytes, leads to a more aggressive cellular phenotype by increasing cell migration, invasion, proliferation and by the activation of the main survival pathways, such as β-catenin, Stat3 and ERK1/2 pathways. These data confirm that PLCβ1 is involved in GBM pathogenesis and a complete understanding of its role may be strategical from both pathological and clinical point of view. [ABSTRACT FROM AUTHOR]

Uveal melanoma (UM) results from the transformation of melanocytes in the uveal tract of the eye and is the most common intraocular malignancy in adults, with >50% chance of forming highly aggressive metastases for which no effective treatment exists. Unlike cutaneous melanoma, UM harbors somatic, mutually exclusive mutations in Guanine nucleotide-binding protein G(q) subunit a (GNAQ) and its paralogue GNA11, which encode closely related members of the Gaq/11 family of G proteins that operate downstream of G protein-coupled receptors (GPCRs) to activate Phospholipase Cb4 (PLCb4), leading to an increase in intracellular Ca2+. Approximately 95% of GNAQ and GNA11 mutations in UM encode the Q209L mutation that results in constitutive activity of the GTP-ase and melanocyte transformation. Recent data revealed additional mutations in PLCb4 and Cysteinyl leukotriene receptor 2 (CYSLTR2) mutually exclusive with Gaq/11 mutations, suggesting that UM is defined by activating mutations in the Gaq/11 pathway1. Uncovering the mechanisms involved in UM requires a thorough investigation of Gaq/11 signaling in uveal melanocytes and understanding whether the activating mutations are necessary and sufficient for UM development. The Oancea lab has recently discovered in human epidermal melanocytes a Gaq/11-mediated pathway activated by physiological doses of UVA2a protective response mediated by epidermal melanocytes, chronic exposure can lead to skin cancer and photoaging. However, the molecular mechanisms that allow human skin to detect and respond to UVR remain incompletely understood. UVR stimulates a retinaldependent signaling cascade in human melanocytes that requires GTP hydrolysis and phospholipase C \u03b2 (PLC\u03b2. Our preliminary results show that this pathway is conserved in 4 different UM cell lines and reveal significant differences between the UM cells that harbor the Q209L mutation compared to the ones that express the wild type Gaq/11. To understand the function of Gaq/11 in non-transformed cells, we extracted and cultured primary uveal melanocytes from the choroid, ciliary body and iris of cow eyes. In addition, the RNAseq data analysis performed on 80 UM patients highlighted that several G-proteins and GPCRs are highly expressed suggesting a possible correlation with the tumor genesis. Our goal is to develop a functional uveal melanocyte culture based on cow eyes and to compare UVA and other signaling pathways mediated by Gaq/11 in primary cells and UM lines. As a first step, we will determine the baseline and UVA-evoked levels of Ca2+ and ROS, two important second messengers that control many signaling pathways downstream of Gaq/11. The results of these studies will significantly advance our understanding of how signal transduction pathways are altered in UM and will reveal novel potential targets for UM treatment. [ABSTRACT FROM AUTHOR]

During several gynecological retroperitoneal pelvic surgeries, portions of the pelvic autonomic nervous system can be accidentally damaged, in particular hypogastric nerves, leading to significant visceral dysfunctions, dramatically affecting woman's quality of life. The aims of this study were to clarify the relationship of hypogastric nerve with definite anatomical landmarks and to assess any anatomical differences between the two sides of the pelvis. Detailed pelvic retroperitoneal dissection was performed in 5 nulliparous embalmed female cadavers and in 10 nulliparous women during in vivo laparoscopic surgery for rectosigmoid endometriosis without parametrial infiltration or radical hysterectomy (B1 according to Querleu-Morrow) for cervical cancer. On both hemipelvis, the closest distance between HNs and ureters, midsagittal plane, midcervical plane or uterosacral ligaments were documented. Comparison of anatomical data of the two hemipelvis were conducted. On cadavers and in vivo dissection, a right and left hypogastric nerves, covered by prehypogastric fascia, were identified in all specimens. Irrespective of the side, a wide anatomical variability was reported. Regarding differences between the two hemipelvis, we found that the right hypogastric nerve was further to the ureter and closer to the midsagittal plane than the left one. Mid-cervical plane was found 2.7 mm to the left of the midsagittal one. Right hypogastric nerve was found closer to mid-cervical plane and utero-sacral ligament than the left one. An accurate knowledge of the pelvic retroperitoneal anatomy and differences between the two sides of the pelvis are essential to preserve hypogastric nerve during surgical dissection. Because of the wide anatomical variability, the use of an interfascial approach between fascia propria recti and pre-hypogastric fascia could help to perform an efficient nerve-sparing surgery. [ABSTRACT FROM AUTHOR]

A central component of many non-infectious diseases is a chronic inflammatory state resulting in selected metabolic alterations affecting DNA repair, apoptosis and autophagy, metabolism and protein synthesis. The proto-oncogene AKT and the dsRNA-dependent kinase PKR are two of the best known kinases demonstrated to significantly influence these mechanisms. In order to identify signaling intermediates common to both kinases, we isolated potential AKT substrates from CCRF-CEM nuclear lysates, using a phospho-AKT substrate antibody and tandem mass spectrometry (MS/MS); then compared these to a list of proteins known to interact with PKR. Among the proteins of interest identified was ADAR1p110, the adenosine deaminase acting on dsRNA. It was determined that the ADAR1 identified corresponded to ADAR1p110, the constitutively expressed and most abundant form of ADAR1 in the nucleus. It was found that not only AKT1, but also AKT2 and AKT3 interact with ADAR1p110 as well as ADAR2 and phosphorylate these RNA editases. The ADARs and AKTs were found to reciprocally influence each other with AKT family members altering ADAR1 and 2 expression; and ADAR1 and ADAR2 suppressing AKT expression. Thus, AKT activation may have a direct and major impact on RNA processing. [ABSTRACT FROM AUTHOR]

During the last year we found a plethora of variants while performing anatomical dissection on human cadavers. In the present report we describe the previously quoted variation morphologies focusing on their clinical relevance. The first variant observed was a left vertebral artery (VA) arising from the aorticarch, it is present in the 5% to the 8 % of the individuals. The left VA of aortic origin showed a remarkably higher incidence of arterial dissection than left VA of a left subclavian artery origin. Also, the present pattern has to be taken into consideration before any intervention in the local region as to avoid unexpected events in relation to the aberrant vertebral artery. A second dissection study led to the finding of the right posterior communicating artery of the Circle of Willis absence. This morphology may be a relevant risk factor for ischemic cerebral infarction if the patient suffers of internal carotid artery occlusion or severe stenosis. The same cadaver presented another variant: anterior inferior cerebellar artery bilateral absence. While dissecting the vein of abdomen and thorax, we discover other two variants: bilateral iliolumbar veins draining into the testicular veins and three pulmonary veins entering into the right side of the left atrium. Cognition of the first variation it is critical during the anterior approach for spinal procedures, it will help surgeons to anticipate and to avoid potentially catastrophic complication such massive haemorrhages due to an avulsion of an unexpected extra vein; whether the knowledge of the pulmonary veins variant, compatible with R3a Marom's classification pattern, is essential for guidance during paroxysmal atrial fibrillation ablation procedures and preclude perioperative bleeding in video-assisted thoracoscopic surgery (VATS). Anatomical variant findings enlarge the current knowledge of anatomists, but also the cognition of surgeons and physicians that need to be aware and always up to date on the incidence level of the variable course of arteries, veins, and nerves especially while performing clinical tests and surgical operations. [ABSTRACT FROM AUTHOR]

At the beginning of the ‘300, Mondino de' Liuzzi, a physician from Bologna, was the first anatomist who started again the dissection of human body neglected from the III century. He hinted at the existence of the conflict between book and body, between “auctoritas" and the direct observation of the human body . The Mondino'smasterwork “Anothomia" remained the key book up to the middle of the sixth century, when Andrea Vesalio wrote “De Umani Corporis Fabrica," in which the body (cadaver) eventually became the main player of the book . During the years, the technologic evolution led to the wrong convictionthat dissection could be dismissed, albeit, still in our day, doctors in training feel the need to associate the direct experience on the cadaver with the very valuable digital means and the modern imaging technologies even in 3D. Thinking to Anatomy as an already fully well known discipline is a mistake. The most advanced methodologies for surgical access, namely the minimally invasive surgery, require the evolution of the traditional anatomical knowledge. The Human Anatomy Institute of the University of Bologna, among the first in Italy, has recognized this need. Thanks to the generosity of the people enrolled in the Body donation programme for research and teaching, our Institute allows medical students to practice dissection on cadavers, beginning as Freshman, then Sophomore, Junior and Senior. The sharing of Bologna's experience could be the chance to think about the perspectives offered by the dissection of the corpse: a wide range of possibilities spanning from research projects to advanced training courses in collaboration with clinicians and surgeons belonging to different branches. Moreover the practice of corpsedissection is extremely important for the recruitment of young graduates in Medicine which, by means of the experience vested acting as “tutor of anatomy", acquire interest in the field of research of morphological sciences, spanning from macroscopic up to the cellular and molecular level. Hic mors gaudet succurrere vitae: the motto, reported in dissection room of most of the Italian anatomical institutes, represents the synthesis of the experience of an ancient discipline which, nowadays , has the chance to rewrite a new chapter dedicated to modern frontiers of scientific research and medical education. [ABSTRACT FROM AUTHOR]

Phospholipase C (PLC)-β1 catalytic activity plays an essential role in the initiation of myogenic differentiation but the effectors involved in its signaling pathway are not well defined[1,2]. Here, we show that the overexpression of the Inositol Polyphosphate Multikinase (IPMK) promotes myogenic differentiation, and that IPMK targets the same cyclin D3 promoter region activated by PLC-β1. Moreover, cyclin D3 promoter activation relies upon c-jun binding to the promoter, both in response to PLC-β1 and to IPMK overexpression. Furthermore, both IPMK and PLC-β1 overexpression determines an increase in β-catenin translocation and accumulation to the nuclei of differentiating myoblasts resulting in higher MyoD activation. Therefore, our data show that PLC-β1, IPMK and β-catenin are mediators of the same signaling pathway that regulates cyclin D3 and myosin heavy chain (MYH) induction during myogenic differentiation. [ABSTRACT FROM AUTHOR]

The estimation of the post-mortem interval (PMI) is a critical step in forensic medicine and remains one of the most challenging variables to determine. In general, the numerous methods currently used in estimating post-mortem interval yield to large post-mortem windows, are influenced by several factors and sometime contradict each other. With the aim to obtain a much more accurate determination of the post-mortem interval we combined morphological ultrastructural and immunoistochemical analyses to reach a more detailed knowledge on tissue organization and degradation after death. Samples of gingival tissues obtained from 20 cadavers at different post-mortem intervals were processed for transmission electron microscopy to evaluate ultrastructural modifications in the epithelium and connective tissue. Gingival cells and the extracellular matrix of gingival tissues have been observed by a transmission electron microscopy (TEM) in combination with the evaluation of potential post-mortem biochemical markers, with the final goal to find a tight correlation between the ultrastructural modifications, the biomarker expression and the time of death. All the samples were also immunostained with anti-hypoxia-induced factor 1-α (HIF1-α) antibody, a transcription factor expressed in response to hypoxia, in order to evaluate the expression of HIF1-α, and to establish a correlation between the protein presence and the time of death. Results showed nuclear chromatin changes and cytoplasmic vacuolization in both epithelial and connective tissues and a different pattern of expression of HIF1alpha protein that correlate to the time of death. In conclusion, our preliminary findings suggest that ultrastructural investigations in combination with immunohistochemistry techniques in gingival specimens may represent a new tool to accurately and systematically estimate post-mortem interval. [ABSTRACT FROM AUTHOR]