385 research outputs found
Diversity of cervical microbiota in asymptomatic chlamydia trachomatis genital infection: a pilot study
Chlamydia trachomatis genital infection continues to be an important public health problem worldwide due to its increasing incidence. C. trachomatis infection can lead to severe sequelae, such as pelvic inflammatory disease, obstructive infertility, and preterm birth. Recently, it has been suggested that the cervico-vaginal microbiota may be an important defense factor toward C. trachomatis infection as well as the development of chronic sequelae. Therefore, the investigation of microbial profiles associated to chlamydial infection is of the utmost importance. Here we present a pilot study aiming to characterize, through the metagenomic analysis of sequenced 16s rRNA gene amplicons, the cervical microbiota from reproductive age women positive to C. trachomatis infection. The main finding of our study showed a marked increase in bacterial diversity in asymptomatic C. trachomatis positive women as compared to healthy controls in terms of Shannon's diversity and Shannon's evenness (P = 0.031 and P = 0.026, respectively). More importantly, the cervical microbiota from C. trachomatis positive women and from healthy controls significantly separated into two clusters in the weighted UniFrac analysis (P = 0.0027), suggesting that differences between the two groups depended entirely on the relative abundance of bacterial taxa rather than on the types of bacterial taxa present. Furthermore, C. trachomatis positive women showed an overall decrease in Lactobacillus spp. and an increase in anaerobes. These findings are part of an ongoing larger epidemiological study that will evaluate the potential role of distinct bacterial communities of the cervical microbiota in C. trachomatis infection
Quality in the extra-analytical phases of urinalysis
The chemical, physical and morphologic urine examination has undergone radical changes over the last few years, so that the time has come for introducing further changes and modifications in various steps of this important test. The breakthroughs of new technologies have allowed making the laboratory report much more informative for the stakeholders. Nevertheless, important considerations for improving the quality throughout the testing process were also raised, especially in the preanalytical phase. Currently, it might be advisable to pursue consolidation and standardization of the analytical phase, as well as redefinition of clinical targets through construction of a complete, integrated and much more clinically meaningful report. This article aims to review the state of the art in urinalysis, as well as providing useful information for achieving more standardization and quality of this useful diagnostic test
173. Insulin B9-23 LV-Driven Expression in Hepatocytes Combined With Suboptimal Dose of Anti-CD3 mAb Cures Type 1 Diabetes in NOD Mice
Type 1 diabetes (T1D) is an autoimmune disease resulting in complete destruction of insulin-producing pancreatic β cells. In T1D in human and in the non-obese diabetic (NOD) mouse, the spontaneous murine model of T1D, auto-reactive T cells target islet-associated antigens. Induction of antigen (Ag)-specific tolerance could cure Type 1 Diabetes (T1D) but it has not been achieved yet. We previously showed that lentiviral vector (LV)-mediated gene expression in hepatocytes induces active tolerance toward the encoded-Ag. Systemic administration of a single dose of Integrase competent (IC) or integrase defective (ID) LV.ET.InsB9-23.142T, enabling stable and transient expression of InsB9-23 in hepatocytes, respectively, arrests β cell destruction in NOD mice at advanced pre-diabetic stage by generating InsB9-23-specific FoxP3+ T regulatory cells (Tregs). In the present study we tested the efficacy of hepatocytes-directed LV.ET. InsB9-23.142T gene transfer in protecting from disease progression at later stages and in reversing T1D.Treatment with LV.ET.InsB9-23.142T in NOD mice with glucose levels ranging from 200mg/mL to 250mg/mL blocked T1D progression in only 27% of the mice. Co-expression of the late auto-Ags-derived epitopes GAD206-220 and IGRP195-214 in hepatocytes did not improve the efficacy of LV.ET.InsB9-23.142T treatment. LV.ET.InsB9-23.142T treatment in diabetic NOD mice with blood glucose levels ranging from 250mg/mL to 300mg/mL did not result in reversion to normoglycemic levels in any of the treated mice.We next combined InsB9-23 gene transfer with anti-CD3 monoclonal antibody (mAb) treatment. Treatment with anti-CD3 mAb at optimal doses is able per se to reverse T1D in NOD mice. Therefore, we tested decreasing doses of anti-CD3 mAb in diabetic NOD mice with blood glucose levels ranging from 250mg/mL to 300mg/mL to identify the sub-optimal dose unable to revert T1D. We found that a single administration of anti-CD3 mAb at 5μg instead of 10μg results was not effective. This sub-optimal dose of anti-CD3 mAb (1X 5μg) was administered together with LV.ET.InsB9-23.142T to NOD mice with blood glucose levels ranging from 250mg/mL to 300mg/mL. Results showed T1D reversal in 75% of ICLV-treated and 40% of the IDLV-treated mice. These data indicate that the LV.ET. InsB9-23.142T treatment combined with sub-optimal anti-CD3 mAb treatment is able to reverse overt diabetes
intensive nutritional counselling and support and clinical outcomes in hemodialysis patients
Protein-energy wasting is frequently found in haemodialysis (HD) patients. Anorexia and hypophagia contribute to malnutrition, increased morbidity and mortality, but the clinical impact of correcting hypophagia remains uncertain. We evaluated whether correction of hypophagia influences morbidity and mortality in anorexic HD patients. Thirty-four HD patients were enrolled in a 2-year follow-up programme including regular nutritional assessment. Patients not meeting nutritional requirements during the follow-up, received nutritional counselling, consisting of advice, individually tailored diet and, in case of failure of dietary intervention, artificial nutrition. Biochemical, anthropometric, body composition parameters, morbidity and mortality were recorded in all patients at 12 and 24 months. At baseline, 14 patients (41%) were anorexic, and 20 patients (59%) non-anorexic. Anorexic patients were hypophagic and presented with reduced fat-free mass. After 12 and 24 months, cholesterol, albumin, lymphocyte count and BMI did not differ among groups, while FFM (%) in supplemented anorexic patients significantly improved, being not different any more vs non-anorexic (65.8±4.4 vs 65.4±8.9, respectively; p=n.s.; 65.8±4.4 vs 66.7±10.78, respectively; p=n.s.). Morbidity and mortality were not different among the two groups. In conclusion, in HD patients, nutritional counselling and nutritional support positively affect nutritional status in hypophagic patients and make the risk of morbidity and mortality in anorexic patients comparable to non-anorexic
Comparing inconsistency of pairwise comparison matrices depending on entries
Pairwise comparisons have been a long-standing technique for comparing alternatives/criteria and their role has been pivotal in the development of modern decision-making methods. Since several types of pairwise comparison matrices (e.g., multiplicative, additive, fuzzy) are proposed in literature, in this paper, we investigate, for which type of matrix, decision-makers are more coherent when they express their subjective preferences. By performing an experiment, we found that the additive approach provides the worst level of coherence
Fatigue in Patients on Chronic Hemodialysis: The Role of Indoleamine 2,3-Dioxygenase (IDO) Activity, Interleukin-6, and Muscularity
Fatigue is a frequent symptom in hemodialysis (HD), and the indolamine-2,3-dioxygenase (IDO) metabolic trap has been hypothesized in the pathogenesis of fatigue. The association between IDO activity according to fatigue and its relationship with muscle mass and function in HD patients was verified. Chronic HD patients were considered, and fatigue was assessed. The plasma kynurenines and tryptophan ratio (Kyn/Trp), as surrogate of IDO activity, and interleukin (IL)-6 were measured. Muscularity was assessed by BIA and muscle strength by hand-grip dynamometer. 50 HD patients were enrolled, and fatigue was present in 24% of the cohort. Patients with fatigue showed higher Kyn/Trp (p = 0.005), were older (p = 0.007), and IL-6 levels resulted higher than in non-fatigue patients (p < 0.001). HD patients with fatigue showed lower intracellular water (surrogate of muscle mass) (p < 0.001), as well as lower hand grip strength (p = 0.02). The Kyn/Trp ratio positively correlated with IL-6 and ECW/ICW (p = 0.004 and p = 0.014). By logistic regression analysis, higher ICW/h(2) was associated with lower odds of fatigue (OR, 0.10; 95% CI, 0.01 to 0.73). In conclusion, our cohort fatigue was associated with a higher Kyn/Trp ratio, indicating a modulation of IDO activity. The Kyn/Trp ratio correlated with IL-6, suggesting a potential role of IDO and inflammation in inducing fatigue and changes in muscularity
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