Obsessive Compulsive Tic Disorder: appropriate diagnosis and treatment as key elements to improve health and rationalize use of resources

Background: Obsessive Compulsive Tic Disorder (OCTD) has been described recently as an early onset and highly disabling endophenotype of Tic Disorder and Obsessive Compulsive Disorder. OCTD has a relevant but largely unknown clinical, social and economic burden for patients and their families. Our paper aimed to explore relevant aspects of the burden of OCTD. Methods: we conducted a literature review and a pilot study using retrospective demographic, clinical and economic data of patients with OCTD accessing the Galeazzi Hospital in Milan. Results: the literature review shows the absence of information on OCTD. From the pilot study we analysed data of 30 patients (80.0% male, 36.7% aged from 7 to 13 years, 63.3% aged from 15 to 48 years), 83.0% declared that obsessions and/or compulsions were the most important factors determining their social impairment. Adult patients refractory to drug treatment underwent Deep Brain Stimulation plus drugs. The mean clinical scores at the time of diagnosis indicated a severe condition for both tics and obsessive compulsive components. The mean time elapsed from symptoms onset to diagnosis of OCTD was 5.6 years, reaching up to 11 years in one case. Before reaching the correct diagnosis, different specialists visited the patients several times, 93.3% underwent diagnostic examinations and 86.7% took 2 or 3 different drugs. Ten patients were hospitalised and 8 had received psychotherapy. Discussion: Albeit preliminary, these results show that attention is mandatory for establishing correct diagnosis and treatment guidelines to improve health and rationally spend resources for OCTD

Cdk1 inactivation terminates mitotic checkpoint surveillance and stabilizes kinetochore attachments in anaphase

Two mechanisms safeguard the bipolar attachment of chromosomes in mitosis. A correction mechanism destabilizes erroneous attachments that do not generate tension across sister kinetochores [1]. In response to unattached kinetochores, the mitotic checkpoint delays anaphase onset by inhibiting the anaphase-promoting complex/cyclosome (APC/CCdc20) [2]. Upon satisfaction of both pathways, the APC/CCdc20 elicits the degradation of securin and cyclin B [3]. This liberates separase triggering sister chromatid disjunction and inactivates cyclin-dependent kinase 1 (Cdk1) causing mitotic exit. How eukaryotic cells avoid the engagement of attachment monitoring mechanisms when sister chromatids split and tension is lost at anaphase is poorly understood [4]. Here we show that Cdk1 inactivation disables mitotic checkpoint surveillance at anaphase onset in human cells. Preventing cyclin B1 proteolysis at the time of sister chromatid disjunction destabilizes kinetochore-microtubule attachments and triggers the engagement of the mitotic checkpoint. As a consequence, mitotic checkpoint proteins accumulate at anaphase kinetochores, the APC/CCdc20 is inhibited, and securin reaccumulates. Conversely, acute pharmacological inhibition of Cdk1 abrogates the engagement and maintenance of the mitotic checkpoint upon microtubule depolymerization. We propose that the simultaneous destruction of securin and cyclin B elicited by the APC/CCdc20 couples chromosome segregation to the dissolution of attachment monitoring mechanisms during mitotic exit

The Reptile Collection of the Museu de Zoologia, Universidade Federal da Bahia, Brazil

Brazilian scientific collections represent an important sample of the country’s biodiversity and are a testament to its history. The Reptile Collection of the Museu de Zoologia from Universidade Federal da Bahia (CRMZUFBA) has 5,206 specimens and 185 species (13 endemic to Brazil and 9 threatened) with one quarter of the known reptile species listed in Brazil, from over 175 municipalities. Although the CRMZUFBA houses species from all Brazilian biomes there is a strong regional presence. Knowledge of the species housed in smaller collections could avoid unrepresentative species descriptions and provide information concerning intraspecific variation, ecological features and geographic coverage

γ-Tubulin regulates the anaphase-promoting complex/cyclosome during interphase

Activation of the APC/C requires microtubule-nucleating independent aspects of γ-tubulin function

Why we shouldn’t blame women for gender disparity in academia : perspectives of women in zoology

The following letter, from a network of women zoologists, is a reply to the article of AlShebli et al. (2020), which suggests that female protégés reap more benefits when mentored by men and concludes that female mentors hinder the success of their female protégés and the quality of their impact. This contribution has two parts. First, we highlight the most relevant methodological flaws which, in our opinion, may have impacted the conclusions of AlShebli et al. (2020). Second, we discuss issues pertaining to women in science, bring a perspective of Women in Zoology and discuss how current diversity policies are positively changing our field

Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018.

Over the past decade, the Nomenclature Committee on Cell Death (NCCD) has formulated guidelines for the definition and interpretation of cell death from morphological, biochemical, and functional perspectives. Since the field continues to expand and novel mechanisms that orchestrate multiple cell death pathways are unveiled, we propose an updated classification of cell death subroutines focusing on mechanistic and essential (as opposed to correlative and dispensable) aspects of the process. As we provide molecularly oriented definitions of terms including intrinsic apoptosis, extrinsic apoptosis, mitochondrial permeability transition (MPT)-driven necrosis, necroptosis, ferroptosis, pyroptosis, parthanatos, entotic cell death, NETotic cell death, lysosome-dependent cell death, autophagy-dependent cell death, immunogenic cell death, cellular senescence, and mitotic catastrophe, we discuss the utility of neologisms that refer to highly specialized instances of these processes. The mission of the NCCD is to provide a widely accepted nomenclature on cell death in support of the continued development of the field

Insights into APC/C: from cellular function to diseases and therapeutics

Anaphase-promoting complex/cyclosome (APC/C) is a multifunctional ubiquitin-protein ligase that targets different substrates for ubiquitylation and therefore regulates a variety of cellular processes such as cell division, differentiation, genome stability, energy metabolism, cell death, autophagy as well as carcinogenesis. Activity of APC/C is principally governed by two WD-40 domain proteins, Cdc20 and Cdh1, in and beyond cell cycle. In the past decade, the results based on numerous biochemical, 3D structural, mouse genetic and small molecule inhibitor studies have largely attracted our attention into the emerging role of APC/C and its regulation in biological function, human diseases and potential therapeutics. This review will aim to summarize some recently reported insights into APC/C in regulating cellular function, connection of its dysfunction with human diseases and its implication of therapeutics