Purpose Aim of our study was to investigate the homing and differentiation of human amniotic stem cell (hAFC) and rat vascular stromal adipocite GFP positive cells (rGFP) in a rat model of heart failure. Methods and Materials Male Sprague‐Dowley rats were injected with monocrotaline to develop right heart failure. hAFC or rat GFP cells were injected via tail vein three weeks after MCT injection. Stem cells differentiation were studied by double immunofluorescence technique. Results Plasma brain natriuretic peptide (BNP), was elevated in HF compared to controls (2.01±0.12 HF rats;0.56±0.37 ng/ml controls, p< 0.0001),while was similar to controls in HF animals injected with stem cells (0.75±0.06 ng/ml,p<0.001). HF stem cells animals showed a RVM/Vol value lower than HF and similar to controls (0.34±0.02 treated animals;0.49±0.29 in controls, p<0.001). Both rGFP and hAFC were detected in the lung (1.01±0.6% hAFC and 0.44±0.4% rGFP) and few of them (0.11±0.1% of hAFC) were differentiated into vascular cells. In the heart stem cells were 0.36±0.3% for hAFC and 0.55±0.2 for rGFP positive cells and hAFC showed a 0.01±0.01 % and rGFP 0.16±0.1% of SMA differentiation. In skeletal muscle stem cells were hAFC 0,31±0,09% and rGFP 0,36±0,2%. Conclusions These results suggest that hAFC and rGFP cells are both engrafted with a topographical recruitment gradient in the lung, heart and skeletal muscle and seems to reduce heart remodelling and failure.
Human papilloma virus (HPV) is known as the main cause of cervical cancer. Data also indicate its role in head–neck cancer, especially oropharyngeal cancer. The correlation between high-risk HPV and oral cancer is still controversial. HPV-related lesions of the oral cavity are frequent and, in most cases, benign. The primary aim of this study was to establish if there is a different follow-up necessity between HPV-positive compared to HPV-negative oral lesions. The secondary aim was to evaluate the recurrence of HPV-related lesions. All patients who underwent a surgical procedure of oral biopsy between 2018 and 2022, with ulterior histopathological examination and HPV typing, were examined. A total of 230 patients were included: 75 received traumatic fibroma as diagnosis, 131 HPV-related lesions, 9 proliferative verrucous leukoplakia, and 15 leukoplakia. The frequency and period of follow-up varied in relation to HPV positivity and diagnosis. This study confirms what has already been reported by other authors regarding the absence of recommendations of follow-up necessity in patients with oral mucosal lesions. However, the data demonstrate that there was a statistically significant difference in the sample analyzed regarding the follow-up of HPV-positive vs. HPV-negative patients. It also confirms the low recurrence frequency of HPV-related oral lesions.
Cardiorenal syndrome type 1 (CRS1) pathophysiology is complex, and immune-mediated damage, including alterations in the immune response with monocyte apoptosis and cytokine release, has been reported as a potential mechanism. In this study, we examined the putative role of renal tubular epithelial cell (RTC) apoptosis as a pathogenic mechanism in CRS1. In particular, we investigated the caspase pathways involved in induced apoptosis. We enrolled 29 patients with acute heart failure (AHF), 11 patients with CRS1, and 15 controls (CTR) without AHF or acute kidney injury (AKI). Patients who had AKI prior to the episode of AHF or who had any other potential causes of AKI were excluded. Plasma from different groups was incubated with RTCs for 24 h. Subsequently, cell apoptosis, DNA fragmentation, and caspase-3, -8, and -9 activities were investigated in RTCs incubated with AHF, CRS1, and CTR plasma. A p value <0.5 was considered statistically significant. A quantitative analysis of apoptosis showed significantly higher apoptosis rates in CRS1 patients compared to AHF patients and CTR (p < 0.01). This increase in apoptosis was strongly confirmed by caspase-3 levels (ρ = 0.73). Caspase-8 and -9 were significantly higher in CRS1 patients compared to AHF patients and CTR (p < 0.01). Furthermore, caspase-3 levels showed a significantly positive correlation with caspase-8 (ρ = 0.57) and -9 (ρ = 0.47; p < 0.001). This study demonstrated the significantly heightened presence of dual apoptotic disequilibrium in CRS1. Our findings indicated that apoptosis may have a central role in the mechanism of CRS1, and it could be a potential therapeutic target in this syndrome.
Abstract Introduction No data are available on the values and role of lung clearance index (LCI) in cystic fibrosis (CF) Screen Positive Inconclusive Diagnosis (CFSPID) progressed to CF diagnosis (CFSPID > CF). This study aimed to assess the value of the LCI in correctly predicting the progression of CFSPID to CF. Methods This is a prospective study carried out at the CF Regional Center of Florence, Italy from September 1, 2019. We compared LCI values in children with CF diagnosed for positive newborn screening (NBS), CFSPID or CFSPID > CF for pathological sweat chloride (SC). The Exhalyzer‐D (EcoMedics AG, Duernten, Switzerland, software version 3.3.1) was used to conduct the LCI tests, every 6 months on stable children. Results Forty‐two cooperating children were enrolled (mean age at LCI tests: 5.4 years, range: 2.7−8.7): 26 (62%) had CF, 8 (19%) were CFSPID > CF for positive SC, while 8 (19%) kept the CFSPID label at last LCI test. The mean LCI value for patients with CF (7.39; 5.98−10.24) was statistically higher compared to both the mean LCI in the CFSPID > CF (6.62; 5.69−7.58) and in CFSPID (6.56; 5.64−7.21). Conclusions Most of asymptomatic CFSPID or progressed to CF have normal LCI. Further data on the longitudinal course of LCI during follow up of CFSPID and on larger cohorts is needed.
Objective: The aim of this study is to evaluate the cause of CFR impairment in DCM patients by correlating functional CFR assessed and microvascular structural abnormalities measured on endomyocardial biopsy (EMB). Materials and methods: We evaluated EMBs from 26 consecutive DCM patients and EMBs from 11 consecutive Heart Transplant patients. We performed morphometric analysis on EMBs. We measured myocyte mean diameter, capillary density, microvascular remodeling (vessel media area/total vessel area ratio (%)). Coronary flow velocity in the left anterior descending coronary artery was detected by Transthoracic Doppler Echocardiography (TDE) at rest and during adenosine infusion. CFR was the ratio of hyperemic diastolic flow velocity (DFV) to resting DFV. A CFR≤2.5 was considered abnormal. The results were compared to a control group, consisted of 11 heart-transplant (HTx) patients with impaired CFR due to microvascular remodeling. Results: Despite CFR in DCM patients is comparable to the HTx pts (2,25±0,61 vs. 2,0±0,5, p=0.4), microvascular remodeling is significantly lower in DCM pts compared to HTx group (43,93±7,12% vs. 72,3±8,0%, p<0,0001). In DCM patients capillary density (194,83±22,63 vs. 157,2±42,4, p=0,03), fibrosis (19,44±7,55% vs. 6,8±5,0%, p<0,02) and myocyte mean diameter (23,79±3,01μm vs. 20,5±3,7μm, p=0,5) are significantly higher than in HTx group. In DCM patients CFR shows a significant inverse correlation with central venous pressure (r= -0,692, p=0,02), with right heart pressure (r= -0,609, p=0,05) and with NTproBNP (r= -0,754, p=0,01) and a positive correlation with cardiac output (r=0,737, p=0,01) and oxygen consumption (r=0,412, p=0,02). Conclusion: CFR impairment in DCM patients is not related to microvascular remodeling. It is closely related to cardiac performance and the patient's clinical status. Patients with pathological CFR (CFR<2,5) have a poorer prognosis, since they have worsen clinical and hemodynamic conditions.
