There are sufficient diagnostic and prospective validation studies to fulfill the US Food and Drug Administration criteria for a biomarker to support the inclusion of corneal confocal microscopy as a primary end point in clinical trials of disease-modifying therapies in diabetic neuropathy.There are sufficient diagnostic and prospective validation studies to fulfill the US Food and Drug Administration criteria for a biomarker to support the inclusion of corneal confocal microscopy as a primary end point in clinical trials of disease-modifying therapies in diabetic neuropathy. In RCT of adults with decompensated cirrhosis, GCSF mobilizes hematopoietic stem cells HSC and improves short-term outcome. An FDA-IND for sequential Kasai-GCSF treatment in biliary atresia BA was approved. This phase 1 study examines GCSF safety in Kasai subjects. Preliminary short-term outcome was evaluated. GCSF (Neupogen) at 5 or 10 μg/kg (n=3/group) was given in 3 daily doses starting on day 3 of Kasai surgery (NCT03395028). Serum CD34+ HSC cell counts, and 1-month of GCSF-related adverse events were monitored. The 6-months Phase 1 clinical outcome was compared against 10 subsequent post Phase 1 Kasai patients who did not receive GCSF. With GCSF, WBC and platelet count transiently increased, LFT and serum creatinine remained stable. Reversible splenic enlargement (by 8.5-20%) occurred in 5/6 subjects. HSC count increased 12-fold and 17.5-fold for the 5μg/kg and10 ug/kg dose respectively; with respective median total bilirubin levels for GCSF vs no-GCSF groups of 55vs 91μM at 1 month, p=0.05; 15vs 37μM at 3 months, p=0.24); and the 6-months cholangitis frequency of 40% vs 90%, p=0.077. GCSF safely mobilizes HSC in Kasai infants and may improve short-term biliary drainage and cholangitis. Phase 2 efficacy outcome of GCSF adjunct therapy for sequential Kasai and GCSF is pending.GCSF safely mobilizes HSC in Kasai infants and may improve short-term biliary drainage and cholangitis. Phase 2 efficacy outcome of GCSF adjunct therapy for sequential Kasai and GCSF is pending. Portoenterostomy is the standard treatment for biliary atresia (BA) that reduces jaundice in two thirds of cases. However, progressive liver fibrosis is common, leading to cirrhosis in most patients. Autotaxin is a new marker for the progression of hepatic fibrosis. We examined the relationship between serum autotaxin levels and liver histological findings in patients with BA. BA patients with native livers were identified in our hospital. Patients underwent protocol liver biopsies every 1 to 5 years, and liver fibrosis was evaluated based on the METAVIR score. Serum autotaxin levels were compared with the last available pathological findings. Thirty-five patients were included and the median age was 10.6 years. Serum autotaxin levels was median 1.6mg/L. The mean autotaxin level was 1.08mg/L in F0, 1.07mg/L in F1, 0.95mg/L in F2, 2.17mg/L in F3, and 2.50mg/L in F4; it was significantly higher in F4 than in F0-F2 (P<0.0024). For predicting cirrhosis (F4) and advanced liver fibrosis (≥F3), autotaxin had the almost same areas under the curve (AUCs 0.78 and 0.90, respectively) as well as M2BPGi. Autotaxin levels could be used to evaluate the status of native liver fibrosis.Autotaxin levels could be used to evaluate the status of native liver fibrosis.According to previous reports, diabetes seems to be associated with serious clinical events due to COVID-19. But is diabetes per se a risk factor of being infected by the virus? We discuss these points. Data about the antidiabetic drugs are scarce. Dipeptidylpeptidase-4 (DPP-4) is found as both a cell surface protein ubiquitously expressed in many tissues and as a soluble molecule found in serum/plasma, fluids. DPP-4 is involved in infection of cells by some viruses. We relate data about the use of DPP-4 inhibitors in diabetic patients. We conclude relating French and international recommendations in people with diabetes.A 10-year national program to improve prevention and management of allergic diseases and asthma was implemented in Finland (population 5.5. million) in 2008-2018. The main aim was to reduce the long-term burden of these conditions. The strategy was changed from traditional avoidance to tolerance and resilience of the population. Health was endorsed instead of medicalization of mild symptoms. selleck Disease severity was reevaluated, and disabling clinical manifestations were given high priority. For health care, 5 quantitative goals and 1 qualitative goal were set. For each of the goals, specific tasks, tools, and outcome evaluation were stipulated. During the program, 376 educational sessions gathered 24,000 health care participants. An information campaign targeted the lay public, and social media was used to contact people. In the 10 years of the program, the prevalence of allergic diseases and asthma leveled off. Asthma caused fewer symptoms and less disability, and 50% fewer hospital days. Food allergy diets in day care and schools decreased by half. Occupational allergies were reduced by 45%. In 2018, the direct and indirect costs of allergic diseases and asthma ranged from €1.5 million to €1.8 million, with the 2018 figures being 30% less than in the respective figures in 2007. The Finnish proactive and real-world intervention markedly reduced the public health burden of allergic disorders. The allergy paradigm was revisited to improve management with systematic education.The development and plasticity of the endocrine pancreas responds to both the intrauterine and postnatal exposome in a constant attempt to predict and respond to alterations in nutritional availability and metabolic requirements. Both under- and over-nutrition in utero, or exposure to adverse environmental pollutants or maternal behaviors, can each lead to altered β-cell or function at birth, and a subsequent mismatch in pancreatic hormonal demands and secretory capacity postnatally. This can be further exacerbated by metabolic stress postnatally such as from obesity or pregnancy, resulting in an increased risk of gestational diabetes, type 2 diabetes, and even type 1 diabetes. This review will discuss evidence identifying the cellular pathways in early life whereby the plasticity of the endocrine pancreatic can become pathologically limited. By necessity, much of this evidence has been gained from animal models, although extrapolation to human fetal development is possible from the fetal growth trajectory and study of the newborn.