The academic career of Max Clara in Padova.

The aim of the following investigation was to explore Max Clara's (1899-1966) early academic activity in Italy at the University of Padua. While Clara's career during the National-Socialist Party dictatorship was extensively studied in literature, little to no information is available regarding Clara's early academic years, with particular regard to his role at the University of Padua during his time in Italy. The scientific and didactic activities held by Clara during this timespan could sheld a light on his appointment as Professor of Anatomy at the University of Leipzig, clarifying the academic motives and political pretences behind it. To this end, systematic research has been conducted at the Historical Archives of the University of Padua, where our findings have revealed detailed records of Clara's teaching and research activity from 1929 to 1935. Our findings confirm that Clara held a paid position as free lecturer at the University of Padua, and was likely under the tutelage of Prof. Tullio Terni, who directed the Institute of Histology and General Embryology until 1933. Max Clara's didactic activity focused mainly on the teaching of microscopical anatomy, which was distinct from histology and considered within the field of anatomy. Even though Clara had a minimal amount of lectures assigned, our records suggest that he conducted part of his research in the laboratories of the University of Padua whilst also working independently in his private medical practice in Blumau (South Tyrol). It is therefore possible to speculate that the teaching of Microscopical Anatomy, rather than Histology, could have represented the pretext for appointing Clara as Professor of Anatomy, justifying his new, politically-driven role at Leipzig

Neurotransmitter and receptor systems in the subthalamic nucleus

The Subthalamic Nucleus (STh) is a lens-shaped subcortical structure located ventrally to the thalamus, that despite being embryologically derived from the diencephalon, is functionally implicated in the basal ganglia circuits. Because of this strict structural and functional relationship with the circuits of the basal ganglia, the STh is a current target for deep brain stimulation, a neurosurgical procedure employed to alleviate symptoms in movement disorders, such as Parkinson's disease and dystonia. However, despite the great relevance of this structure for both basal ganglia physiology and pathology, the neurochemical and molecular anatomy of the STh remains largely unknown. Few studies have specifically addressed the detection of neurotransmitter systems and their receptors within the structure, and even fewer have investigated their topographical distribution. Here, we have reviewed the scientific literature on neurotransmitters relevant in the STh function of rodents, non-human primates and humans including glutamate, GABA, dopamine, serotonin, noradrenaline with particular focus on their subcellular, cellular and topographical distribution. Inter-species differences were highlighted to provide a framework for further research priorities, particularly in humans

New loci for body fat percentage reveal link between adiposity and cardiometabolic disease risk

To increase our understanding of the genetic basis of adiposity and its links to cardiometabolic disease risk, we conducted a genome-wide association meta-analysis of body fat percentage (BF%) in up to 100,716 individuals. Twelve loci reached genome-wide significance (P<5 × 10−8), of which eight were previously associated with increased overall adiposity (BMI, BF%) and four (in or near COBLL1/GRB14, IGF2BP1, PLA2G6, CRTC1) were novel associations with BF%. Seven loci showed a larger effect on BF% than on BMI, suggestive of a primary association with adiposity, while five loci showed larger effects on BMI than on BF%, suggesting association with both fat and lean mass. In particular, the loci more strongly associated with BF% showed distinct cross-phenotype association signatures with a range of cardiometabolic traits revealing new insights in the link between adiposity and disease risk

Large meta-analysis of genome-wide association studies identifies five loci for lean body mass

Lean body mass, consisting mostly of skeletal muscle, is important for healthy aging. We performed a genome-wide association study for whole body (20 cohorts of European ancestry with n = 38,292) and appendicular (arms and legs) lean body mass (n = 28,330) measured using dual energy X-ray absorptiometry or bioelectrical impedance analysis, adjusted for sex, age, height, and fat mass. Twenty-one single-nucleotide polymorphisms were significantly associated with lean body mass either genome wide (p < 5 x 10(-8)) or suggestively genome wide (p < 2.3 x 10(-6)). Replication in 63,475 (47,227 of European ancestry) individuals from 33 cohorts for whole body lean body mass and in 45,090 (42,360 of European ancestry) subjects from 25 cohorts for appendicular lean body mass was successful for five single-nucleotide polymorphisms in/ near HSD17B11, VCAN, ADAMTSL3, IRS1, and FTO for total lean body mass and for three single-nucleotide polymorphisms in/ near VCAN, ADAMTSL3, and IRS1 for appendicular lean body mass. Our findings provide new insight into the genetics of lean body mass

New loci for body fat percentage reveal link between adiposity and cardiometabolic disease risk

To increase our understanding of the genetic basis of adiposity and its links to cardiometabolic disease risk, we conducted a genome-wide association meta-analysis of body fat percentage (BF%) in up to 100,716 individuals. Twelve loci reached genome-wide significance (P <5 x 10(-8)), of which eight were previously associated with increased overall adiposity (BMI, BF%) and four (in or near COBLL1/GRB14, IGF2BP1, PLA2G6, CRTC1) were novel associations with BF%. Seven loci showed a larger effect on BF% than on BMI, suggestive of a primary association with adiposity, while five loci showed larger effects on BMI than on BF%, suggesting association with both fat and lean mass. In particular, the loci more strongly associated with BF% showed distinct cross-phenotype association signatures with a range of cardiometabolic traits revealing new insights in the link between adiposity and disease risk.Peer reviewe

COVID-19 Neuropathology: disentangling the role of SARS-CoV-2 infection in neurological manifestations and neurodegenerative diseases

Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) is a novel strain of the Coronavirus Family (CoV) responsible for the disease known as Coronavirus Disease 2019 (COVID19). Although manifesting primarily as a respiratory disease, neurological manifestations are common in COVID-19, either presenting as new symptoms or disorders (e.g., stroke, encephalitis, Guillain-Barré syndrome) or as the exacerbation of pre-existing symptoms of known chronic neurological conditions, with particular regard to neurodegenerative diseases. These observations, along with the detection of the virus in post-mortem tissue and cerebrospinal fluid raise the question of whether SARS-CoV-2 possesses neurotropic properties, or observed neurological manifestations are rather to be ascribed to the effects of systemic infection, ongoing cytokine storm, inflammation and hypoxia. Furthermore, the burden of COVID-19 on the autonomic nervous system and on peripheral chemoceptors may represent a so far undervalued mechanism for a vicious circle between COVID-19 and the frequent comorbidities affecting patients susceptible to severe or even fatal manifestations of the disease. Our aim was to evaluate the pathological mechanisms underlying neurological manifestations in COVID-19, and assess the short- and (possible) long-term consequences of COVID-19 on the nervous system. For this purpose, we present a collection of seven peer-reviewed articles which aim to define the role of SARS-CoV-2 and COVID-19 on the peripheral nervous system, on peripheral chemoreceptorial structures, and on the central nervous system. While particular focus has been given to post-mortem investigations and neuropathology underlying COVID-19, we also evaluated the link between in-vivo neurological manifestations and viral genomic variants to further characterize the disease.Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) is a novel strain of the Coronavirus Family (CoV) responsible for the disease known as Coronavirus Disease 2019 (COVID19). Although manifesting primarily as a respiratory disease, neurological manifestations are common in COVID-19, either presenting as new symptoms or disorders (e.g., stroke, encephalitis, Guillain-Barré syndrome) or as the exacerbation of pre-existing symptoms of known chronic neurological conditions, with particular regard to neurodegenerative diseases. These observations, along with the detection of the virus in post-mortem tissue and cerebrospinal fluid raise the question of whether SARS-CoV-2 possesses neurotropic properties, or observed neurological manifestations are rather to be ascribed to the effects of systemic infection, ongoing cytokine storm, inflammation and hypoxia. Furthermore, the burden of COVID-19 on the autonomic nervous system and on peripheral chemoceptors may represent a so far undervalued mechanism for a vicious circle between COVID-19 and the frequent comorbidities affecting patients susceptible to severe or even fatal manifestations of the disease. Our aim was to evaluate the pathological mechanisms underlying neurological manifestations in COVID-19, and assess the short- and (possible) long-term consequences of COVID-19 on the nervous system. For this purpose, we present a collection of seven peer-reviewed articles which aim to define the role of SARS-CoV-2 and COVID-19 on the peripheral nervous system, on peripheral chemoreceptorial structures, and on the central nervous system. While particular focus has been given to post-mortem investigations and neuropathology underlying COVID-19, we also evaluated the link between in-vivo neurological manifestations and viral genomic variants to further characterize the disease

Sudden fatal haemorrhage in ulcerative Aspergillus laryngotracheitis – a paediatric Case report.

In this report, we describe an autopsy case of a child affected by acute lymphoblastic leukemia and opportunistic pulmonary aspergillosis. The patient died because of a full-thickness tracheal wall ulceration with right inferior thyroid artery lesion and sudden hemorrhage, likely ascribable to undiagnosed invasive Aspergillus laryngotracheitis. Aspergillus infection, particularly in immunocompromised patients, should be considered an urgent risk factor to manage as it may lead to sudden fatal events in absence of evident critical symptoms

Bridging Gaps in Peripheral Nerves: From Current Strategies to Future Perspectives in Conduit Design

In peripheral nerve injuries (PNI) with substance loss, where tensionless end-to-end suture is not achievable, the positioning of a graft is required. Available options include autografts (e.g., sural nerve, medial and lateral antebrachial cutaneous nerves, superficial branch of the radial nerve), allografts (Avance((R)); human origin), and hollow nerve conduits. There are eleven commercial hollow conduits approved for clinical, and they consist of devices made of a non-biodegradable synthetic polymer (polyvinyl alcohol), biodegradable synthetic polymers (poly(DL-lactide-e-caprolactone); polyglycolic acid), and biodegradable natural polymers (collagen type I with/without glycosaminoglycan; chitosan; porcine small intestinal submucosa); different resorption times are available for resorbable guides, ranging from three months to four years. Unfortunately, anatomical/functional nerve regeneration requirements are not satisfied by any of the possible alternatives; to date, focusing on wall and/or inner lumen organization/functionalization seems to be the most promising strategy for next-generation device fabrication. Porous or grooved walls as well as multichannel lumens and luminal fillers are the most intriguing options, eventually also including the addition of cells (Schwann cells, bone marrow-derived, and adipose tissue derived stem cells) to support nerve regeneration. This review aims to describe common alternatives for severe PNI recovery with a highlight of future conduits