Centenario della nascita di Pietro Parenzan

EnThe 100th anniversary of the birth of Pietro Parenzan, the founder of the Marine Biology Station of Porto Cesareo, and of the journal Thalassia Salentina, has been commemorated at the Museum of the cited Marine Biology Station on 21 December 2002. Program of the commemotation consisted in an exhibition opening and a meeting.The exhibition, based on bibliographic investigation in his publications, illustrated the numerous fields of interest in which Pietro Parenzan worked: Speleology, Parasitology, Teratology, Malacology, Marine Biology and many others. Meeting was subdivided in two sections: life, to commemorate the personage, and studies, to remember his naturalistic activity. In the first section Paolo Parenzan, Pietro’s son, remembered his father; Raffaele Sambati, first major of Porto Cesareo, and Livio Ruggiero, first responsible of the collaboration with University, talked about relations among Pietro Parenzan, Porto Cesareo town and University of Lecce; Michele Camassa, the last Parenzan’s pupil, remembered the other Museum founded by Pietro Parenzan: the Subsoil Biology Museum of Latiano. Some of the numerous scientific activity were remembered in the second section from Marco Oliverio (University of Rome I) about malacology and Genuario Belmonte (University of Lecce) about naturalistic expeditions

The role of subsidence in a weakly unstable marine boundary layer: a case study

The diurnal evolution of a cloud free, marine boundary layer is studied by means of experimental measurements and numerical simulations. Experimental data belong to an investigation of the mixing height over inner Danish waters. The mixed-layer height measured over the sea is generally nearly constant, and does not exhibit the diurnal cycle characteristic of boundary layers over land. A case study, during summer, showing an anomalous development of the mixed layer under unstable and nearly neutral atmospheric conditions, is selected in the campaign. Subsidence is identified as the main physical mechanism causing the sudden decrease in the mixing layer height. This is quantified by comparing radiosounding profiles with data from numerical simulations of a mesoscale model, and a large-eddy simulation model. Subsidence not only affects the mixing layer height, but also the turbulent fluctuations within it. By analyzing wind and scalar spectra, the role of subsidence is further investigated and a more complete interpretation of the experimental results emerges

Riordino e aggiornamento tassonomico della "Collezione di Malacologia Ecologica" di Pietro Parenzan - Prima parte

Collection was realized dredging sea bottoms along the coasts of Apulia and through specimens exchange activities with other famous malacologists. The present work represents a first contribution to the restitution of the historical and documentary heritage named "Ecological Malacology Collection" by the Prof. P. Parenzan to the scientific community. Such a purpose has been pursued through photographic documentation, ordering and conservation renewal activities, but also through the realization of a digital catalogue and by a modernization of the taxonomical positioning of specimens which, by now, is limited to 1241 mono specific shell groups (on a total of 6794)

Respiratory Complex I dysfunction in cancer: from a maze of cellular adaptive responses to potential therapeutic strategies

Mitochondria act as key organelles in cellular bioenergetics and biosynthetic processes producing signals that regulate different molecular networks for proliferation and cell death. This ability is also preserved in pathologic contexts such as tumorigenesis, during which bioenergetic changes and metabolic reprogramming confer flexibility favoring cancer cells survival in a hostile microenvironment. Although different studies epitomize mitochondrial dysfunction as a pro-tumorigenic hit, genetic ablation or pharmacological inhibition of respiratory Complex I causing a severe impairment are associated with a low proliferative phenotype. In this scenario, it must be considered that despite the initial delay in growth, cancer cells may become able to resume proliferation exploiting molecular mechanisms to overcome growth arrest. Here we highlight the current knowledge on molecular responses activated by Complex I-defective cancer cells to bypass physiological control systems and to re-adapt their fitness during microenvironment changes. Such adaptive mechanisms could reveal possible novel molecular players in synthetic lethality with Complex I impairment, thus providing new synergistic strategies for mitochondria-based anti-cancer therapy

Electrochemotherapy in Vulvar Cancer and Cisplatin Combined with Electroporation. Systematic Review and In Vitro Studies

Electrochemotherapy (ECT) is an emerging treatment for solid tumors and an attractive research field due to its clinical results. This therapy represents an alternative local treatment to the standard ones and is based on the tumor-directed delivery of non-ablative electrical pulses to maximize the action of specific cytotoxic drugs such as cisplatin (CSP) and bleomycin (BLM) and to promote cancer cell death. Nowadays, ECT is mainly recommended as palliative treatment. However, it can be applied to a wide range of superficial cancers, having an impact in preventing or delaying tumor progression and therefore in improving quality of life. In addition, during the natural history of the tumor, early ECT may improve patient outcomes. Our group has extensive clinical and research experience on ECT in vulvar tumors in the palliative setting, with 70% overall response rate. So far, in most studies, ECT was based on BLM. However, the potential of CSP in this setting seems interesting due to some theoretical advantages. The purpose of this report is to: (i) compare the efficacy of CSP and BLM-based ECT through a systematic literature review; (ii) report the results of our studies on CSP-resistant squamous cell tumors cell lines and the possibility to overcome chemoresistance using ECT; (iii) discuss the future ECT role in gynecological tumors and in particular in vulvar carcinoma

Infected pancreatic necrosis: outcomes and clinical predictors of mortality. A post hoc analysis of the MANCTRA-1 international study

: The identification of high-risk patients in the early stages of infected pancreatic necrosis (IPN) is critical, because it could help the clinicians to adopt more effective management strategies. We conducted a post hoc analysis of the MANCTRA-1 international study to assess the association between clinical risk factors and mortality among adult patients with IPN. Univariable and multivariable logistic regression models were used to identify prognostic factors of mortality. We identified 247 consecutive patients with IPN hospitalised between January 2019 and December 2020. History of uncontrolled arterial hypertension (p = 0.032; 95% CI 1.135-15.882; aOR 4.245), qSOFA (p = 0.005; 95% CI 1.359-5.879; aOR 2.828), renal failure (p = 0.022; 95% CI 1.138-5.442; aOR 2.489), and haemodynamic failure (p = 0.018; 95% CI 1.184-5.978; aOR 2.661), were identified as independent predictors of mortality in IPN patients. Cholangitis (p = 0.003; 95% CI 1.598-9.930; aOR 3.983), abdominal compartment syndrome (p = 0.032; 95% CI 1.090-6.967; aOR 2.735), and gastrointestinal/intra-abdominal bleeding (p = 0.009; 95% CI 1.286-5.712; aOR 2.710) were independently associated with the risk of mortality. Upfront open surgical necrosectomy was strongly associated with the risk of mortality (p < 0.001; 95% CI 1.912-7.442; aOR 3.772), whereas endoscopic drainage of pancreatic necrosis (p = 0.018; 95% CI 0.138-0.834; aOR 0.339) and enteral nutrition (p = 0.003; 95% CI 0.143-0.716; aOR 0.320) were found as protective factors. Organ failure, acute cholangitis, and upfront open surgical necrosectomy were the most significant predictors of mortality. Our study confirmed that, even in a subgroup of particularly ill patients such as those with IPN, upfront open surgery should be avoided as much as possible. Study protocol registered in ClinicalTrials.Gov (I.D. Number NCT04747990)