New Surgical Approach To Overcome The Inability Of Injured Mammalian Axons To Grow Within Their Environment

We present a new method for creating conditions conducive to axonal growth in injured optic nerves of adult rabbits. The surgical approach consists of making a cavity in the adult rabbit optic nerve, into which a piece of nitrocellulose soaked with conditioned medium originating from regenerating fish optic nerves is implanted. In addition, daily irradiation (10 days, 5 min, 35 mW) with low energy He-Ne laser is carried out. Such a combined treatment may open a door to neurobiologists and clinicians, hoping to unravel the enigma of mammalian CNS regeneration

Inhibition of Sema-3A Promotes Cell Migration, Axonal Growth, and Retinal Ganglion Cell Survival

Semaphorin 3A (Sema-3A) is a secreted protein that deflects axons from inappropriate regions and induces neuronal cell death. Intravitreal application of polyclonal antibodies against Sema-3A prevents loss of retinal ganglion cells ensuing from axotomy of optic nerves. This suggested a therapeutic approach for neuroprotection via inhibition of the Sema-3A pathway.Funded by the EU seventh framework program, Grant Agreement #604884.Peer reviewe

Effects of PEG-SMLA treatment on food intake and adipose tissues mass.

<p>(A) Food consumption (g) is calculated reported to body weight of each mouse on first or second week of treatment. PEG-SMLA injections are represented within hatched bars. b, p<0.001 related to Control WT mice. (B) At the end of treatment, the intact abdominal fat depot (delimited lines) is shown on both genotypes. (C) Ratio of adipose depot mass per body weight. b, p<0.001 and c, p<0.01 related to Control WT mice. (n = 7–10/group).</p

Chronic renal comorbidities in pyoderma gangrenosum: a retrospective cohort study

The coexistence of pyoderma gangrenosum (PG) and chronic renal comorbidities has been reported anecdotally. We aimed to assess the bidirectional association between PG and the following chronic renal comorbidities: chronic renal failure (CRF), dialysis, kidney transplantation (KT), and other kidney diseases (OKD). That is to evaluate (i) the risk of the aforementioned diseases among patients with PG (ii) and the odds of PG after a diagnosis of renal comorbidities. A population-based retrospective cohort study was conducted comparing PG patients (n=302) with age-, sex-, and ethnicity-matched control subjects (n=1497) with regard to incident cases of renal comorbidities. A case-control design was additionally adopted to estimate the odds of PG in those with a preexisting history of renal comorbidities. Adjusted hazard ratios (HRs) and adjusted odds ratios (ORs) were estimated by Cox regression and logistic regression, respectively. Patients with PG demonstrated an increased risk of CRF (adjusted HR, 3.68; 95% CI, 2.72-5.97), dialysis (adjusted HR, 27.79; 95% CI, 3.24-238.14), and OKD (adjusted HR, 2.71; 95% CI, 1.55-4.74). In addition, the odds of PG were increased after the diagnosis of CRF (adjusted OR, 2.34; 95% CI, 1.33-4.11), KT (adjusted OR, 5.03; 95% CI, 1.01-25.12), and OKD (adjusted OR, 1.69; 95% CI, 1.04-2.74). Patients with a dual diagnosis of PG and renal diseases presented with PG at an older age and had a higher prevalence of comorbid conditions. In conclusion, a bidirectional association exists between PG and chronic renal conditions. Awareness of this comorbidity may be of benefit for physicians managing patients with PG

Effets du blocage de la leptine au cours de l'installation des circuits neuronaux de contrôle de la prise alimentaire

National audienc

Effets du blocage de la leptine au cours de l'installation des circuits neuronaux de contrôle de la prise alimentaire

National audienc

Expression of key adipose genes.

<p>(A–D) <i>Leptin, Zfp423, PPAR</i> and <i>aP2</i> gene expression was quantified by qPCR in each gonadal, peri-renal, inguinal adipose depot of WT and PRLR^−/− non-treated mice (Control) and treated animals (PEG-SMLA, hatched bars) respectively (n = 5–8/group) b, p<0.01. (E) Distribution of adipocyte surfaces in inguinal adipose tissue in untreated WT and PRLR^−/− (Control) and treated animals (PEG-SMLA, hatched bars). Statistical analysis was performed. b, p<0.01, c, p<0.001.</p

PEG-SMLA treatment induced glucose intolerance and insulin resistance on WT and PRLR−/− animals.

<p>(A) Fasting glycemia in saline treated and PEG-SMLA treated mice. b, *p<0.05. (B) Oral glucose tolerance test (2g/kg) was performed in WT and PRLR^−/− mice PEG-SMLA treated or not. (C) Fasting (left panel) and 30 minutes after glucose gavage (right panel) plasma insulin levels. (D) HOMA-IR index reflecting insulin resistance is calculated as follows: fasting plasma glucose (mg/dl) × fasting insulin (mU/L)/405.</p

Effect of PEG-SMLA treatment on weight gain of WT and PRLR^−/− mice.

<p>(A) Representative dorsal view of male mice after 20 days of saline (control) or PEG-SMLA injections. (B) Comparison of PEG-SMLA effects on weight gain of WT (open squares) or PRLR^−/− (black squares) male mice. PEG-SMLA was injected daily at 6 mg/kg. <i>***, p<0.005</i> between non-treated (Cont) and PEG-SMLA treated groups.</p

Effects of PEG-SMLA treatment on food intake and adipose tissues mass.

<p>(A) Food consumption (g) is calculated reported to body weight of each mouse on first or second week of treatment. PEG-SMLA injections are represented within hatched bars. b, p<0.001 related to Control WT mice. (B) At the end of treatment, the intact abdominal fat depot (delimited lines) is shown on both genotypes. (C) Ratio of adipose depot mass per body weight. b, p<0.001 and c, p<0.01 related to Control WT mice. (n = 7–10/group).</p