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To evaluate the effect of the COVID-19 pandemic on anxiety and depression of women during pregnancy and perinatal period.We systematically searched online databases to identify any report on maternal depression during pregnancy or postpartum using the Edinburgh Postnatal Depression Survey (EPDS) and maternal anxiety using the State-Trait Anxiety Inventory (STAI) until 5th July 2020. The random-effects model was used to pool the effect sizes and standardized mean differences (SMDs) and the corresponding 95% confidence intervals (CIs).Eight studies reported depressive and anxiety states of 7750 women, either pregnant or postpartum were included. The overall pooled EPDS score was higher among women during pandemic (SMD= 0.40, 95% CI: -0.05 - 0.86,The present meta-analysis provides evidence that the COVID-19 pandemic significantly increases the risk of anxiety among women during pregnancy and perinatal period. Support measures should be considered for women during pregnancy or perinatal period to guarantee mental health for this susceptible population.

Background: The appearance of symptoms that may be related to the worsening of the disease, as well as the toxicity of chemotherapy treatment or an acute complication, are the most frequent reasons for access to the emergency room (ER) for patients with cancer. To date, the Italian territorial health services, as well as local preventive medicine, are unable to provide adequate management of patients with cancer and, for this reason, diagnostic delays and inappropriate hospitalization in the oncology departments have occurred; moreover, it has been observed that many patients receive the first diagnosis of cancer directly in the ER, where the experience in the oncology field is often inadequate. Objectives: Cardarelli Hospital, in Naples, started twenty-two month Experimental Oncological Emergency Service, under the supervision of its own Oncology Department, with the double main objectives of encouraging de-hospitalization and improving diagnostic and therapeutic performance. Methods: We have developed a methodological protocol for patients’ admission to the ER, assuming that the host physician transfers patients with suspected cancer to a new hospital figure, the ER oncologist, who acts as supervisor and coordinator. The first consultation was carried out together with one or more specialists, identified by the supervisor. Based on their characteristics, the patients were divided into 4 categories: (1) Patients with a known diagnosis of cancer and already undergoing anticancer treatments; (2) patients who show complications due to ongoing cancer treatments; (3) patients who no longer respond to anticancer treatments due to the worsening of the disease; (4) patients who are first diagnosed with cancer in the ER. Each individual cohort of patients was directed towards what we have called diagnostic-therapeutic assistance paths (PDTA), specific protocols for each type of patient, which allowed us to reduce the time to diagnosis. Results: According to the data, the average hospitalization time for patients with lung cancer who followed the study was 10 days, compared to 16 days for patients who did not undergo cancer screening in the ER. Another relevant result demonstrated the improvement in the quality and efficiency of medical services by including first aid in the management of cancer patients regards de-hospitalization. In fact, thanks to the experimental protocol we applied, we were able to de-hospitalize 484 patients directly from the ER, which are over 34% of the total. Conclusions: Close integration between hospital medical fields and territorial medicine could improve the quality of cancer treatment and the efficiency of health services management. All of this without affecting the costs of public healthcare because of the considerable improvement in performance which allowed important savings.

Antiphospholipid antibodies (aPL) are a cluster of autoantibodies directed against plasma proteins with affinity for membrane phospholipids. The most frequently tested aPL are lupus anticoagulant (LA), anti-cardiolipin antibodies (aCL), and anti-β2-glycoprotein I antibodies (anti-β2GPI). aPL play a key pathogenic role in the development of the antiphospholipid syndrome (APS), a systemic autoimmune disease characterized by recurrent thrombotic and/or pregnancy complications in patients with persistent aPL. However, aPL positivity is occasionally documented in patients with no previous history of thrombotic or pregnancy morbidity. LA activity, multiple aPL positivity, high-titer aPL, and a concomitant systemic autoimmune disease are recognized risk factors for future thrombotic events in asymptomatic carriers. Moreover, an accelerated atherosclerosis with increased cardiovascular (CV) risk has also been associated with aPL positivity, thus exposing aPL carriers to fatal complications and chronic disability requiring cardiac rehabilitation. Overall, an accurate risk stratification is recommended for aPL-positive subjects in order to prevent both venous and arterial thrombotic complications. In this review, we provide an overview of the main antithrombotic and risk assessment strategies in aPL carriers.

Rare genetic obesity disorders are characterized by mutations of genes strongly involved in the central or peripheral regulation of energy balance. These mutations are effective in causing the early onset of severe obesity and insatiable hunger (hyperphagia), suggesting that the genetic component can contribute to 40–70% of obesity. However, genes’ roles in the processes leading to obesity are still unclear. This review is aimed to summarize the current knowledge of the genetic causes of obesity, especially monogenic obesity, describing the role of epigenetic mechanisms in obesity and metabolic diseases. A comprehensive understanding of the underlying genetic and epigenetic mechanisms, with the metabolic processes they control, will permit adequate management and prevention of obesity.

Several randomized controlled trials (RCTs) have investigated the use of probiotic/synbiotic in PCOS patients, without clarifying the real use in clinical practice. The aim of this meta-analysis was to evaluate the effectiveness of probiotics and synbiotics on metabolic, hormonal and inflammatory parameters of PCOS. Electronic databases (MEDLINE, Scopus, EMBASE, ScienceDirect, The Cochrane Database of Systematic Reviews and ClinicalTrials.gov) were searched from their inception until May 2019. The study protocol was registered in PROSPERO with number CRD42018111534. Randomized controlled trials (RCTs) of PCOS’s women undergoing therapy at least 8 weeks with probiotics or synbiotics or without therapy were included. The primary outcomes were changes in anthropometric parameters, glucose/insulin metabolism, lipid profile, sex hormones profile, inflammation markers. 587 patients were included in nine RCT. The administration of probiotic/synbiotic were associated with a significant improvement in FPG, FBI, HOMA I-R, BMI. It also modified Ferriman-Gallway, serum triglycerides, serum testosterone, hs-CRP, NO, TAC, GSH, and MDA. Subgroup analysis of the type of intervention showed that probiotics were associated with greater testosterone and FPG reduction; synbiotics administration resulted in a more pronounced decrease of the FBI. Subgroup analyses on the duration of therapy showed that, probiotic/synbiotic administration had a significantly greater effect on QUICK-I in the case of women with 12-weeks of therapy than in the 8-weeks therapy group. Nevertheless, we did not observe any significant difference was observed in terms of FBI, HOMA-IR, and FPG. Probiotics and synbiotics seem to either an effect on/influence metabolic, hormonal and inflammatory parameters, or can influence them. Consequently, it could lead to an improvement of fertility in PCOS.

The reactive oxygen species (ROS) are known to play a major role in many pathophysiological conditions, such as ischemia and reperfusion injury. The present study was aimed to evaluate the in vivo cyanidin (anthocyanin) effects on damages induced by rat pial microvascular hypoperfusion-reperfusion injury by cerebral blood flow decrease (CBFD) and subsequent cerebral blood flow recovery (CBFR). In particular, the main purpose was to detect changes in ROS production after cyanidin administration. Rat pial microvasculature was investigated using fluorescence microscopy through a cranial window (closed); Strahler's method was utilized to define the geometric features of pial vessels. ROS production was investigated in vivo by 2′-7′-dichlorofluorescein-diacetate assay and neuronal damage was measured on isolated brain sections by 2,3,5-triphenyltetrazolium chloride staining. After 30 min of CBFD, induced by bilateral common carotid artery occlusion, and 60 min of CBFR, rats showed decrease of arteriolar diameter and capillary perfusion; furthermore, increase in microvascular leakage and leukocyte adhesion was observed. Conversely, cyanidin administration induced dose-related arteriolar dilation, reduction in microvascular permeability as well as leukocyte adhesion when compared to animals subjected to restriction of cerebral blood flow; moreover, capillary perfusion was protected. ROS generation increase and marked neuronal damage were detected in animals subjected to CBFD and CBFR. On the other hand, cyanidin was able to reduce ROS generation and neuronal damage. In conclusion, cyanidin treatment showed dose-related protective effects on rat pial microcirculation during CBFD and subsequent CBFR, inducing arteriolar dilation by nitric oxide release and inhibiting ROS formation, consequently preserving the blood brain barrier integrity.

The present study was aimed to evaluate the malvidin’s protective effects on damage induced by 30 min bilateral common carotid artery occlusion (BCCAO) and 60 min reperfusion in rat pial microcirculation. Rat pial microcirculation was observed using fluorescence microscopy through a closed cranial window. Western blotting analysis was performed to investigate the endothelial nitric oxide synthase (eNOS), phosphorylated eNOS (p-eNOS) and matrix metalloproteinase 9 (MMP-9) expression. Moreover, MMP-9 activity was evaluated by zymography. Finally, neuronal damage and radical oxygen species (ROS) formation were assessed. In all animals, pial arterioles were classified in five orders of branching according to Strahler’s method. In hypoperfused rats, 30 min BCCAO and 60 min reperfusion caused a decrease in arteriolar diameter, an increase in microvascular leakage and leukocyte adhesion, accompanied by decreased capillary perfusion and red blood cell velocity (VRBC). Moreover, marked neuronal damage and evident ROS generation were detected. Conversely, malvidin administration induced arteriolar dilation in dose-related manner, reducing microvascular leakage as well as leukocyte adhesion. Capillary perfusion and VRBC were protected. Nitric oxide synthase inhibition significantly attenuated malvidin’s effects on arteriolar diameter. Western blotting analysis revealed an increase in eNOS and p-eNOS expression, while zymography indicated a decrease in MMP-9 activity after malvidin’s administration. Furthermore, malvidin was able to prevent neuronal damage and to decrease ROS generation. In conclusion, malvidin protects rat pial microcirculation against BCCAO/reperfusion injury, preventing blood-brain impairment and neuronal loss. Malvidin’s effects appear to be mediated by eNOS activation and scavenger activity.