Background/Aims: Tight control of inflammation and adjustment of treatment if activity persists is the current strategy for the management of Crohn’s disease (CD). The usefulness of fecal calprotectin (FC) in isolated involvement of the small intestine in CD is controversial. To assess the usefulness of FC to determine the inflammatory activity detected by intestinal ultrasonography (IUS) in ileal CD. Methods: Patients with exclusively ileal involvement CD who underwent IUS and an FC were prospectively included. Simple ultrasound index was used to determine inflammatory activity. The usual statistical tests for comparison of diagnostic techniques were used. Results: One hundred and five patients were included, IUS showed inflammatory activity in 59% of patients and complications in 18.1%. FC showed a significant correlation with IUS in the weak range (Spearman coefficient r=0.502; P<0.001); the area under the receiver operating characteristic curve was 0.79 (95% confidence interval, 0.70–0.88; P<0.001). The FC value that best reflected the activity in IUS was 100 μg/g with sensitivity, specificity, and positive and negative predictive values of 73.0%, 71.4%, 79.3% and 63.8%, respectively. There were no differences in FC concentration between patients with or without transmural complications. The addition of serum C-reactive protein to FC did not improve the ability to assess IUS activity. Conclusions FC has a significant correlation with IUS to monitor ileal CD activity. This correlation is weak and it does not allow assessing the presence of CD complications. Both tests should be used in conjunction for tight control of ileal CD. More studies on noninvasive tests in this location are needed.

Objective: In this video, we present our technique for ureter assessment during pelvic ultrasound examination. Methods: We used a general electric Voluson E10 (General electric, Wauwatosa, WI, USA) to perform transvaginal ultrasonography. These images were shared after thorough counselling, and obtaining informed consent from the patient. This video was edited using FinalCut ProX® (Apple Inc, Cupertino, CA, USA). Results: We systematized this routine after assessing the cervix, uterus, and adnexa. The vaginal probe was slightly removed to focus on the urethra. Next, we approached the hand on the contralateral thigh to the ureter. At this point, the probe was directed to the lateral pelvic wall where the ureteric orifice was found. Then, we raised our hands and perform an internal rotation movement to ascend the ureteral segments until it is related to the iliac vessels. Conclusion The urinary tract may be involved in gynecological pathologies. Transvaginal ultrasound is an easy, reproducible, and well-tolerated examination that can be used to evaluate the ureters below the pelvic brim.

The immune response against Trichinella spiralis at the intestinal level depends on the CD4⁺ T cells, which can both suppress or promote the inflammatory response through the synthesis of diverse cytokines. During the intestinal phase, the immune response is mixed (Th1/Th2) with the initial predominance of the Th1 response and the subsequent domination of Th2 response, which favor the development of intestinal pathology. In this context, the glucocorticoids (GC) are the pharmacotherapy for the intestinal inflammatory response in trichinellosis. However, its therapeutic use is limited, since studies have shown that treatment with GC suppresses the host immune system, favoring T. spiralis infection. In the search for novel pharmacological strategies that inhibit the Th1 immune response (proinflammatory) and assist the host against T. spiralis infection, recent studies showed that resiniferatoxin (RTX) had anti-inflammatory activity, which decreased the serum levels of IL-12, INF-γ, IL-1β, TNF-α, NO, and PGE₂, as well the number of eosinophils in the blood, associated with decreased intestinal pathology and muscle parasite burden. These researches demonstrate that RTX is capable to inhibit the production of Th1 cytokines, contributing to the defense against T. spiralis infection, which places it as a new potential drug modulator of the immune response.
Cytokines ; Drug Therapy ; Eosinophils ; Glucocorticoids ; Immune System ; Inflammation* ; Interleukin-12 ; Parasites ; Pathology ; T-Lymphocytes ; Therapeutic Uses* ; Trichinella spiralis ; Trichinellosis*

Mesenchymal stem cells (MSCs) have desirable characteristics for use in therapy in animal models and veterinary medicine, due to their capacity of inducing tissue regeneration and immunomodulation. The objective of this study was to evaluate the differences between canine adipose tissue-derived MSCs (AD-MSCs) extracted from subcutaneous (Sc) and visceral (Vs) sites. Surface antigenic markers, in vitro differentiation, and mineralized matrix quantification of AD-MSCs at different passages (P₄, P₆, and P₈) were studied. Immunophenotypic analysis showed that AD-MSCs from both sites were CD44+, CD90+, and CD45−. Moreover, they were able, in vitro, to differentiate into fat, cartilage, and bone. Sc-AD-MSCs preserve in vitro multipotentiality up to P₈, but Vs-AD-MSCs only tri-differentiated up to P₄. In addition, compared to Vs-AD-MSCs, Sc-AD-MSCs had greater capacity for in vitro mineralized matrix synthesis. In conclusion, Sc-AD-MSCs have advantages over Vs-AD-MSCs, as Sc AD-MSCs preserve multipotentiality during a greater number of passages, have more osteogenic potential, and require less invasive extraction.
Antigens, Surface ; Cartilage ; Immunomodulation ; Immunophenotyping ; In Vitro Techniques ; Mesenchymal Stromal Cells ; Miners ; Models, Animal ; Regeneration ; Veterinary Medicine

Purpose: Patients with autism spectrum disorder (ASD) often present with sleep disturbances. We evaluated the effectiveness of pediatric prolonged-release melatonin (PedPRM) in real clinical practice, focusing on a population of complex neuropediatric patients with highly refractory insomnia in Spain. Methods: The patients were aged 2 to 18 years, diagnosed with ASD, had sleep maintenance insomnia and/or early morning awakening insomnia, and were refractory to prior therapy. The starting dose of PedPRM was 2 or 5 mg (increased to 10 mg, if necessary). Evaluation at 6 months consisted of a sleep diary, the Sleep Disturbance Scale for Children (SDSC), the Pediatric Daytime Sleepiness Scale (PDSS), and the Clinical Global Impression Scale of Improvement (CGI-I) and Severity (CGI-S). Results: The median age of the 23 patients was 11.0 years, 56.5% were male, 73.9% had epilepsy, and 78.3% had intellectual disability. One patient discontinued treatment. The mean total sleep time did not change significantly. PedPRM improved sleep latency (median 30.0 to 15.0 minutes; P=0.001) and reduced the number of nocturnal awakenings (median 3.00 to 1.0; P<0.001). PedPRM significantly improved PDSS scores (14.6±4.5 to 10.4±3.5; P<0.001) and SDSC total scores (75.1±12.9 to 61.6±10.9; P<0.001). The CGI-I scale improved in 73.3% of patients; 46.7% of patients were normal, borderline, or mildly ill per CGI-S scale at the end of treatment. Conclusion In real clinical practice, PedPRM significantly improved sleep parameters in patients with ASD who were heavily medicated for comorbidities and were highly refractory to other insomnia treatments.

Purpose: Patients with autism spectrum disorder (ASD) often present with sleep disturbances. We evaluated the effectiveness of pediatric prolonged-release melatonin (PedPRM) in real clinical practice, focusing on a population of complex neuropediatric patients with highly refractory insomnia in Spain. Methods: The patients were aged 2 to 18 years, diagnosed with ASD, had sleep maintenance insomnia and/or early morning awakening insomnia, and were refractory to prior therapy. The starting dose of PedPRM was 2 or 5 mg (increased to 10 mg, if necessary). Evaluation at 6 months consisted of a sleep diary, the Sleep Disturbance Scale for Children (SDSC), the Pediatric Daytime Sleepiness Scale (PDSS), and the Clinical Global Impression Scale of Improvement (CGI-I) and Severity (CGI-S). Results: The median age of the 23 patients was 11.0 years, 56.5% were male, 73.9% had epilepsy, and 78.3% had intellectual disability. One patient discontinued treatment. The mean total sleep time did not change significantly. PedPRM improved sleep latency (median 30.0 to 15.0 minutes; P=0.001) and reduced the number of nocturnal awakenings (median 3.00 to 1.0; P<0.001). PedPRM significantly improved PDSS scores (14.6±4.5 to 10.4±3.5; P<0.001) and SDSC total scores (75.1±12.9 to 61.6±10.9; P<0.001). The CGI-I scale improved in 73.3% of patients; 46.7% of patients were normal, borderline, or mildly ill per CGI-S scale at the end of treatment. Conclusion In real clinical practice, PedPRM significantly improved sleep parameters in patients with ASD who were heavily medicated for comorbidities and were highly refractory to other insomnia treatments.

Purpose: Patients with autism spectrum disorder (ASD) often present with sleep disturbances. We evaluated the effectiveness of pediatric prolonged-release melatonin (PedPRM) in real clinical practice, focusing on a population of complex neuropediatric patients with highly refractory insomnia in Spain. Methods: The patients were aged 2 to 18 years, diagnosed with ASD, had sleep maintenance insomnia and/or early morning awakening insomnia, and were refractory to prior therapy. The starting dose of PedPRM was 2 or 5 mg (increased to 10 mg, if necessary). Evaluation at 6 months consisted of a sleep diary, the Sleep Disturbance Scale for Children (SDSC), the Pediatric Daytime Sleepiness Scale (PDSS), and the Clinical Global Impression Scale of Improvement (CGI-I) and Severity (CGI-S). Results: The median age of the 23 patients was 11.0 years, 56.5% were male, 73.9% had epilepsy, and 78.3% had intellectual disability. One patient discontinued treatment. The mean total sleep time did not change significantly. PedPRM improved sleep latency (median 30.0 to 15.0 minutes; P=0.001) and reduced the number of nocturnal awakenings (median 3.00 to 1.0; P<0.001). PedPRM significantly improved PDSS scores (14.6±4.5 to 10.4±3.5; P<0.001) and SDSC total scores (75.1±12.9 to 61.6±10.9; P<0.001). The CGI-I scale improved in 73.3% of patients; 46.7% of patients were normal, borderline, or mildly ill per CGI-S scale at the end of treatment. Conclusion In real clinical practice, PedPRM significantly improved sleep parameters in patients with ASD who were heavily medicated for comorbidities and were highly refractory to other insomnia treatments.

Purpose: Patients with autism spectrum disorder (ASD) often present with sleep disturbances. We evaluated the effectiveness of pediatric prolonged-release melatonin (PedPRM) in real clinical practice, focusing on a population of complex neuropediatric patients with highly refractory insomnia in Spain. Methods: The patients were aged 2 to 18 years, diagnosed with ASD, had sleep maintenance insomnia and/or early morning awakening insomnia, and were refractory to prior therapy. The starting dose of PedPRM was 2 or 5 mg (increased to 10 mg, if necessary). Evaluation at 6 months consisted of a sleep diary, the Sleep Disturbance Scale for Children (SDSC), the Pediatric Daytime Sleepiness Scale (PDSS), and the Clinical Global Impression Scale of Improvement (CGI-I) and Severity (CGI-S). Results: The median age of the 23 patients was 11.0 years, 56.5% were male, 73.9% had epilepsy, and 78.3% had intellectual disability. One patient discontinued treatment. The mean total sleep time did not change significantly. PedPRM improved sleep latency (median 30.0 to 15.0 minutes; P=0.001) and reduced the number of nocturnal awakenings (median 3.00 to 1.0; P<0.001). PedPRM significantly improved PDSS scores (14.6±4.5 to 10.4±3.5; P<0.001) and SDSC total scores (75.1±12.9 to 61.6±10.9; P<0.001). The CGI-I scale improved in 73.3% of patients; 46.7% of patients were normal, borderline, or mildly ill per CGI-S scale at the end of treatment. Conclusion In real clinical practice, PedPRM significantly improved sleep parameters in patients with ASD who were heavily medicated for comorbidities and were highly refractory to other insomnia treatments.

Purpose: Patients with autism spectrum disorder (ASD) often present with sleep disturbances. We evaluated the effectiveness of pediatric prolonged-release melatonin (PedPRM) in real clinical practice, focusing on a population of complex neuropediatric patients with highly refractory insomnia in Spain. Methods: The patients were aged 2 to 18 years, diagnosed with ASD, had sleep maintenance insomnia and/or early morning awakening insomnia, and were refractory to prior therapy. The starting dose of PedPRM was 2 or 5 mg (increased to 10 mg, if necessary). Evaluation at 6 months consisted of a sleep diary, the Sleep Disturbance Scale for Children (SDSC), the Pediatric Daytime Sleepiness Scale (PDSS), and the Clinical Global Impression Scale of Improvement (CGI-I) and Severity (CGI-S). Results: The median age of the 23 patients was 11.0 years, 56.5% were male, 73.9% had epilepsy, and 78.3% had intellectual disability. One patient discontinued treatment. The mean total sleep time did not change significantly. PedPRM improved sleep latency (median 30.0 to 15.0 minutes; P=0.001) and reduced the number of nocturnal awakenings (median 3.00 to 1.0; P<0.001). PedPRM significantly improved PDSS scores (14.6±4.5 to 10.4±3.5; P<0.001) and SDSC total scores (75.1±12.9 to 61.6±10.9; P<0.001). The CGI-I scale improved in 73.3% of patients; 46.7% of patients were normal, borderline, or mildly ill per CGI-S scale at the end of treatment. Conclusion In real clinical practice, PedPRM significantly improved sleep parameters in patients with ASD who were heavily medicated for comorbidities and were highly refractory to other insomnia treatments.