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ABSTRACT This paper presents preliminary ecological data on the Cocco's lanternfish Lobianchia gemellarii (Cocco, 1838) (Osteichthyes: Myctophidae) in the Central Mediterranean and its first records from the northern Ionian Sea. A total of 28 specimens of lantern fish were collected using an experimental trawl net between August and September 2023 in a depth range of 500–701 m in the northern Ionian Sea (central Mediterranean), as part of the MEDITS project. Their morphological traits, the presence and arrangement of photophores together with the otolith characteristics allowed the identification of these specimens as L. gemellarii. In the study area, the standard length of individuals was up to a maximum of 109 mm, which is the largest size ever found for the species. A length‐age key was estimated through otoliths reading. The stomach content analysis for all individuals is also reported. Plastic fibers were found in the gut contents of two individuals. This study not only represents the first record of the species in the northern Ionian Sea but also provides information and a new contribution to the knowledge on the role of the species in the Mediterranean marine food web.

Abstract The integration of advanced materials and photonic nanostructures can lead to enhanced biodetection capabilities, crucial in clinical scenarios and point‐of‐care diagnostics, where simplified strategies are essential. Herein, a molecularly imprinted polymer (MIP) photonic nanostructure is demonstrated, which selectively binding to transforming growth factor‐beta (TGF‐β), in which the sensing transduction is enhanced by bound states in the continuum (BICs). The MIP operating as a synthetic antibody matrix and coupled with BIC resonance, enhances the optical response to TGF‐β at imprinted sites, leading to an augmented detection capability, thoroughly evaluated through spectral shift and optical lever analogue readout. The validation underscores the MIP‐BIC sensor capability to detect TGF‐β in spiked saliva, achieving a limit of detection of 10 fM and a resolution of 0.5 pM at physiological concentrations, with a precision of two orders of magnitude above discrimination threshold in patients. The MIP tailored selectivity is highlighted by an imprinting factor of 52, showcasing the sensor resistance to interference from other analytes. The MIP‐BIC sensor architecture streamlines the detection process eliminating the need for complex sandwich immunoassays and demonstrates the potential for high‐precision quantification. This positions the system as a robust tool for biomarker detection, especially in real‐world diagnostic scenarios.

Abstract Better understanding how fires respond to climate variability is an issue of current interest in light of ongoing climate change. However, evaluating the global‐scale temporal variability of fires in response to climate presents a challenge due to the intricate processes at play and the limitation of fire data. Here, we investigate the links between year‐to‐year variability of burned area (BA) and climate using BA data, the Fire Weather Index (FWI), and the Standardized Precipitation Evapotranspiration Index (SPEI) from 2001 to 2021 at ecoregion scales. Our results reveal complex spatial patterns in the dependence of BA variability on antecedent and concurrent weather conditions, highlighting where BA is mostly influenced by either FWI or SPEI and where the combined effect of both indicators must be considered. Our findings indicate that same‐season weather conditions have a more pronounced relationship with BA across various ecoregions, particularly in climatologically wetter areas. Additionally, we note that BA is also significantly associated with periods of antecedent wetness and coolness, with this association being especially evident in more arid ecoregions. About 60% of the interannual variations in BA can be explained by climatic variability in a large fraction (∼77%) of the world's burnable regions.

Abstract Solar and wind power are called to play a main role in the transition toward decarbonized electricity systems. However, their integration in the energy mix is highly compromised due to the intermittency of their production caused by weather and climate variability. To face the challenge, here we present research about actionable strategies for wind and solar photovoltaic facilities deployment that exploit their complementarity in order to minimize the volatility of their combined production while guaranteeing a certain supply. The developed methodology has been implemented in an open‐access step‐wise model called CLIMAX. It first identifies regions with homogeneous temporal variability of the resources, and then determines the optimal shares of each technology over such regions. In the simplistic application performed here, we customize the model to narrow the monthly deviations of the total wind‐plus‐solar electricity production from a given curve (here, the mean annual cycle of the total production) across five European domains. For the current shares of both technologies, the results show that an optimal siting of the power units would reduce the standard deviation of the monthly anomalies of the total wind‐plus‐solar power generation by up to 20% without loss in the mean capacity factor as compared to a baseline scenario with an evenly spatial distribution of the installations. This result further improves (up to 60% in specific regions) if the total shares of each technology are also optimized, thus encouraging the use of CLIMAX for practical guidance of next‐generation renewable energy scenarios.

Whether mutations in the BMPR2 gene may influence the response to PAH‐specific therapies has not yet been investigated. In this study, in 13 idiopathic, heritable or anorexigen‐associated PAH patients, in whom treatment escalation was performed by adding a prostanoid, a greater haemodynamic improvement was observed in BMPR2‐negative than in BMPR2‐positive patients.

Abstract Pulmonary veno‐occlusive disease (PVOD) is a rare disease. It may be idiopathic or associated, in particular, with connective tissue disease, or it may develop after radiation exposure; in heritable forms of PVOD, the inheritance is autosomal recessive due to the presence of homozygous or compound heterozygous pathogenic variants in the EIF2AK4 gene. We describe the case of a young man whose PVOD was initially misdiagnosed as chronic thromboembolic pulmonary hypertension despite worsening after riociguat, nonspecific computed tomography pulmonary angiogram findings, and parental consanguinity could suggest an autosomal recessive disease. The correct diagnosis and the correct treatment are crucial given the high mortality rate of this disease.

Abstract Background Unloading/disuse induces skeletal muscle atrophy in bedridden patients and aged people, who cannot prevent it by means of exercise. Because interventions against known atrophy initiators, such as oxidative stress and neuronal NO synthase (nNOS) redistribution, are only partially effective, we investigated the involvement of melusin, a muscle‐specific integrin‐associated protein and a recognized regulator of protein kinases and mechanotransduction in cardiomyocytes. Methods Muscle atrophy was induced in the rat soleus by tail suspension and in the human vastus lateralis by bed rest. Melusin expression was investigated at the protein and transcript level and after treatment of tail‐suspended rats with atrophy initiator inhibitors. Myofiber size, sarcolemmal nNOS activity, FoxO3 myonuclear localization, and myofiber carbonylation of the unloaded rat soleus were studied after in vivo melusin replacement by cDNA electroporation, and muscle force, myofiber size, and atrogene expression after adeno‐associated virus infection. In vivo interference of exogenous melusin with dominant‐negative kinases and other atrophy attenuators (Grp94 cDNA; 7‐nitroindazole) on size of unloaded rat myofibers was also explored. Results Unloading/disuse reduced muscle melusin protein levels to about 50%, already after 6 h in the tail‐suspended rat (P < 0.001), and to about 35% after 8 day bed rest in humans (P < 0.05). In the unloaded rat, melusin loss occurred despite of the maintenance of β1D integrin levels and was not abolished by treatments inhibiting mitochondrial oxidative stress, or nNOS activity and redistribution. Expression of exogenous melusin by cDNA transfection attenuated atrophy of 7 day unloaded rat myofibers (−31%), compared with controls (−48%, P = 0.001), without hampering the decrease in sarcolemmal nNOS activity and the increase in myonuclear FoxO3 and carbonylated myofibers. Infection with melusin‐expressing adeno‐associated virus ameliorated contractile properties of 7 day unloaded muscles (P ≤ 0.05) and relieved myofiber atrophy (−33%) by reducing Atrogin‐1 and MurF‐1 transcripts (P ≤ 0.002), despite of a two‐fold increase in FoxO3 protein levels (P = 0.03). Atrophy attenuation by exogenous melusin did not result from rescue of Akt, ERK, or focal adhesion kinase activity, because it persisted after co‐transfection with dominant‐negative kinase forms (P < 0.01). Conversely, melusin cDNA transfection, combined with 7‐nitroindazole treatment or with cDNA transfection of the nNOS‐interacting chaperone Grp94, abolished 7 day unloaded myofiber atrophy. Conclusions Disuse/unloading‐induced loss of melusin is an early event in muscle atrophy which occurs independently from mitochondrial oxidative stress, nNOS redistribution, and FoxO3 activation. Only preservation of melusin levels and sarcolemmal nNOS localization fully prevented muscle mass loss, demonstrating that both of them act as independent, but complementary, master switches of muscle disuse atrophy.

We have previously shown that secreted BAG3 is a potential target for the treatment of pancreatic ductal adenocarcinoma and that pancreatic tumor growth and metastatic dissemination can be reduced by treatment with an anti‐BAG3 murine antibody. Here, we used complementarity‐determining region (CDR) grafting to generate a humanized version of the anti‐BAG3 antibody that may be further developed for possible clinical use. We show that the humanized anti‐BAG3 antibody, named BAG3‐H2L4, abrogates BAG3 binding to macrophages and subsequent release of IL‐6. Furthermore, it specifically localizes into tumor tissues and significantly inhibits the growth of Mia PaCa‐2 pancreatic cancer cell xenografts. We propose BAG3‐H2L4 antibody as a potential clinical candidate for BAG3‐targeted therapy in pancreatic cancer.

Patients with end-stage heart failure (HF), pulmonary hypertension and elevated pulmonary vascular resistance (PVR) despite medical therapy are not eligible for heart transplantation (HTx). In this ‘proof of concept’ case series, we demonstrate the feasibility and efficacy of the MitraClip procedure as ‘bridge to list’ in end-stage HF patients not eligible for HTx. In fact, in the three patients reported, who were initially excluded from the HTx list because of elevated PVR, the MitraClip procedure was followed by a sustained improvement of PVR, allowing the patients’ risk to be reclassified, and they were then considered eligible for HTx.

Hereditary hemorrhagic telangiectasia (HTT) is an autosomal dominant disease, most frequently caused by a mutation in either ENG or ACVRL1 , which can be associated with pulmonary arterial hypertension (PAH). In this report, we describe a new unpublished ACVRL1 mutation segregating in three members of the same family, showing three different types of pulmonary hypertension (PH) in the absence of BMPR2 mutations. The first patient has a form of heritable PAH (HPAH) in the absence of hepatic arteriovenous malformations (AVMs); the second one has a severe form of portopulmonary hypertension (PoPAH) associated with multiple hepatic AVMs; the third one has hepatopulmonary syndrome (HPS) with numerous hepatic arteriovenous fistulas and a form of post-capillary PH due to high cardiac output. In summary, a single mutation in the ACVRL1 gene can be associated, in the same family, with an extreme phenotypic variability regarding not only the clinical presentation of HHT but also the type of PH in the absence of BMPR2 mutations. More studies are needed to evaluate if this variability can be explained by the presence of additional variants in other genes relevant for the pathogenesis of HHT.

Non-invasive tests to identify age and early disease-associated pathology within the kidney are needed. Specific populations of urinary extracellular vesicles (EVs) could potentially be used for such a diagnostic test. Random urine samples were obtained from age- and sex-stratified living kidney donors before kidney donation. A biopsy of the donor kidney was obtained at the time of transplantation to identify nephron hypertrophy (larger glomerular volume, cortex per glomerulus and mean profile tubular area) and nephrosclerosis (% fibrosis, % glomerulosclerosis and arteriosclerosis). Renal parenchymal-derived EVs in cell-free urine were quantified by digital flow cytometry. The relationship between these EV populations and structural pathology on the kidney biopsy was assessed. Clinical characteristics of the kidney donors (n=138, age range: 20–70 years, 50% women) were within the normative range. Overall, urine from women contained more EVs than that from men. The number of exosomes, juxtaglomerular cells and podocyte marker–positive EVs decreased (p

Purpose. To compare the capsule edges ultrastructure obtained by two femtosecond laser-assisted cataract surgery (FLACS) platforms and manual continuous curvilinear capsulorhexis (CCC) using scanning electron microscopy (SEM). Setting. Eye Clinic, University of Trieste, Italy. Design. Experimental comparative study. Methods. 150 anterior capsules were collected and divided into three groups as follows: Group 1 (50 capsules) obtained with manual CCC, Groups 2 and 3 (each with 50 capsules) obtained with the Catalys Laser and the LenSx Laser, respectively. All samples were imaged by means of SEM and regularity of the cut surface, and thickness of the capsule edge were evaluated and compared. Results. All femtosecond laser (FSL) capsules were perfectly circular, whereas some alteration of the circular shape was observed in the manual ones. Group 1 showed a smooth and regular capsule edge without any surface irregularity, conversely Groups 2 and 3 showed postage-stamp perforations on the capsule edge. The cut surface irregularity value in Group 2 was 1.4 ± 0.63, while it was 0.7 ± 0.49 in Group 3 (p