This work explores in depth the simultaneous self-assembly and mineralization of type I collagen by a base-acid neutralization technique to prepare biomimetic collagen-apatite fibrils with varying mineralization extent and doped with luminescent bactericidal Tb3+ ions. Two variants of the method are tested base-acid titration, a solution of Ca(OH)2 is added dropwise to a stirred solution containing type I collagen dispersed in H3 PO4 ; and direct mixing, the Ca(OH)2 solution is added by fast dripping onto the acidic solution. Only the direct mixing variant yielded an effective control of calcium phosphate polymorphism. Luminescence spectroscopy reveals the long luminescence lifetime and high relative luminescence intensity of the Tb3+ -doped materials, while two-photon confocal fluorescence microscopy shows the characteristic green fluorescence light when using excitation wavelength of 458 nm, which is not harmful to bone tissue. Cytotoxicity/viability tests reveal that direct mixing samples show higher cell proliferation than titration samples. Additionally, osteogenic differentiation essays show that all mineralized fibrils promote the osteogenic differentiation, but the effect is more pronounced when using samples prepared by direct mixing, and more notably when using the Tb3+ -doped mineralized fibrils. Based on these findings it is concluded that the new nanocomposite is an ideal candidate for bone regenerative therapy.There are few studies on how patients with psoriasis who are on biologic therapy are affected by the COVID-19 pandemic. We analyzed the impact of the COVID-19 pandemic on patients with psoriasis receiving biologic therapy, patients' current status at a single center in Turkey. A total of 133 patients (mean age; 44.6 ± 13.5 years) were on maintenance biological treatment for moderate-to-severe psoriasis during the pandemic. A standardized questionnaire was administered by phone interviews to determine patients' perceptions, attitudes, and adherence to therapy and identify the frequency of COVID-19 infection, psoriasis status, and new comorbidities during the pandemic. All patients had been receiving a biological agent including ustekinumab, etanercept, adalimumab, secukinumab, infliximab, ixekizumab, or certolizumab pegol. Ninety-one patients (68.4%) had at least one comorbid condition, including psoriatic arthritis (35.3%), hypertension (19.5%), diabetes mellitus (16.5%), obesity, coronary artery disease, and dyslipidemia. During the first 3 months of the pandemic, 52 patients (39%) suspended their biological therapies for short (n = 33) or long (n = 19) periods without medical advice for reasons of fear, worry, and anxiety. All but one patient restarted their medications as a result of therapeutic counseling. Five patients reported suspicious symptoms, but only one had PCR-confirmed COVID-19. Our findings suggest that biologic treatment for moderate-to-severe psoriasis would not pose an additional risk for COVID-19 infection and its life-threatening complications, even in the presence of a high frequency of cardiometabolic comorbidities, provided that all patients are informed and necessary pandemic-directed precautions are well adopted by the patients.
  Psychotic-like experiences (PLEs) index an increased risk for subsequent psychotic disorders. A risky family environment is a well-established risk factor for PLEs; however, different contextual and personal resiliency factors may differentially mediate its effect on PLEs.
 
  In this study, we propose a two-dimensional model of resilience. Our aim is to address separately the mediational role of personal and contextual resiliency factors between a risky family environment and PLEs in a community sample.
 
  Five-hundred University students completed an on-line questionnaire, including the Resilience Scale for Adults (RSA), the 16-item version of the Prodromal Questionnaire (iPQ-16) and the Risky Family Questionnaire (RFQ).  https://www.selleckchem.com/Androgen-Receptor.html  Mediation was assessed using Structural Equation Modelling with bootstrapping estimation of indirect effect.
 
  The direct effects of personal and contextual resilience on PLEs were respectively -0.69 [-0.97, -0.41] (P < .001) and - 0.19 [-0.58, 0.20] (ns); the indirect effect through personal resilience was 0.03[0.01, 0.04] (P < .001). Personal resilience mediated 27.4% of the total effect of risky family environment on PLEs.
 
  Personal resilience, as opposite to contextual resilience, mediates the effect of a risky family environment on PLEs. Low personal resilience may represent an individual risk factor that transmits the effect of risky family environment on PLEs and could represent a central aspect of individualized prevention and treatment strategies.
 Personal resilience, as opposite to contextual resilience, mediates the effect of a risky family environment on PLEs. Low personal resilience may represent an individual risk factor that transmits the effect of risky family environment on PLEs and could represent a central aspect of individualized prevention and treatment strategies.The semaphorin protein family is a diverse set of extracellular signaling proteins that perform fundamental roles in the development and operation of numerous biological systems, notably the nervous, musculoskeletal, cardiovascular, endocrine, and reproductive systems. Recently, recessive loss-of-function (LoF) variants in SEMA3A (semaphorin 3A) have been shown to result in a recognizable syndrome characterized by short stature, skeletal abnormalities, congenital heart defects, and variable additional anomalies. Here, we describe the clinical and molecular characterization of a female patient presenting with skeletal dysplasia, hypogonadotropic hypogonadism (HH), and anosmia who harbors a nonsense variant c.1633C>T (p.Arg555*) and a deletion of exons 15, 16, and 17 in SEMA3A in the compound heterozygous state. These variants were identified through next-generation sequencing analysis of a panel of 26 genes known to be associated with HH/Kallmann syndrome. Our findings further substantiate the notion that biallelic LoF SEMA3A variants cause a syndromic form of short stature and expand the phenotypic spectrum associated with this condition to include features of Kallmann syndrome.