Effects of metformin on recognition memory and hippocampal neuroplasticity in rats with metabolic syndrome

Metabolic syndrome (MS) is a health problem that is characterized by body fat accumulation, hypertension, dyslipidemia, and hyperglycemia; recently, it has been demonstrated that MS also damages memory processes. The first-line drug in the treatment of MS and type 2 diabetes mellitus is metformin, which is an antihyperglycemic agent. This drug has been shown to produce neuroprotection and to improve memory processes. However, the mechanism involved in this neuroprotection is unknown. A 90-day administration of metformin improved the cognitive processes of rats with MS as evaluated by the novel object recognition test, and this finding could be explained by an increase in the neuronal spine density and spine length. We also found that metformin increased the immunoreactivity of synaptophysin, sirtuin-1, AMP-activated protein kinase, and brain-derived neuronal factor, which are important plasticity markers. We conclude that metformin is an important therapeutic agent that increases neural plasticity and protects cognitive processes. The use of this drug is important in the minimization of the damage caused by MS.     

Maternal personality traits,antenatal depressive symptoms and the postpartum mother–infant relationship: a prospective observational study

Social Psychiatry and Psychiatric Epidemiology - Maternal depression has been associated with bonding difficulties and lower maternal sensitivity in observed mother–infant interactions....     

Natural compulsive‐like behaviour in the deer mouse (Peromyscus maniculatus bairdii) is associated with altered gut microbiota composition

Obsessive–compulsive disorder (OCD) is a psychiatric illness that significantly impacts affected patients and available treatments yield suboptimal therapeutic response. Recently, the role of the gut–brain axis (GBA) in psychiatric illness has emerged as a potential target for therapeutic exploration. However, studies concerning the role of the GBA in OCD are limited. To investigate whether a naturally occurring obsessive–compulsive‐like phenotype in a rodent model, that is large nest building in deer mice, is associated with perturbations in the gut microbiome, we investigated and characterised the gut microbiota in specific‐pathogen‐free bred and housed large (LNB) and normal (NNB) nest‐building deer mice of both sexes (n = 11 per group, including three males and eight females). Following baseline characterisation of nest‐building behaviour, a single faecal sample was collected from each animal and the gut microbiota analysed. Our results reveal the overall microbial composition of LNB animals to be distinctly different compared to controls (PERMANOVA p < .05). While no genera were found to be significantly differentially abundant after correcting for multiple comparisons, the normal phenotype showed a higher loading of Prevotella and Anaeroplasma, while the OC phenotype demonstrated a higher loading of Desulfovermiculus, Aestuariispira, Peptococcus and Holdemanella (cut‐off threshold for loading at 0.2 in either the first or second component of the PCA). These findings not only provide proof‐of‐concept for continued investigation of the GBA in OCD, but also highlight a potential underlying aetiological association between alterations in the gut microbiota and the natural development of obsessive–compulsive‐like behaviours.     

Tankyrase represses autoinflammation through the attenuation of TLR2 signaling

Dysregulation of Toll-like receptor (TLR) signaling contributes to the pathogenesis of autoimmune diseases. Here, we provide genetic evidence that tankyrase, a member of the poly(ADP-ribose) polymerase (PARP) family, negatively regulates TLR2 signaling. We show that mice lacking tankyrase in myeloid cells developed severe systemic inflammation with high serum inflammatory cytokine levels. We provide mechanistic evidence that tankyrase deficiency resulted in tyrosine phosphorylation and activation of TLR2 and show that phosphorylation of tyrosine 647 within the TIR domain by SRC and SYK kinases was critical for TLR2 stabilization and signaling. Last, we show that the elevated cytokine production and inflammation observed in mice lacking tankyrase in myeloid cells were dependent on the adaptor protein 3BP2, which is required for SRC and SYK activation. These data demonstrate that tankyrase provides a checkpoint on the TLR-mediated innate immune response.     

Correlations between First 72 h Hypophosphatemia,Energy Deficit,Length of Ventilation,and Mortality—A Retrospective Cohort Study

Introduction. Hypophosphatemia may prolong ventilation and induce weaning failure. Some studies have associated hypophosphatemia with increased mortality. Starting or restarting nutrition in a critically ill patient may be associated with refeeding syndrome and hypophosphatemia. The correlation between nutrition, mechanical ventilation, and hypophosphatemia has not yet been fully elucidated. Methods. A retrospective cohort study of 825 admissions during two consecutive years was conducted. Using the electronic medical chart, demographic and clinical data were obtained. Hypophosphatemia was defined as a phosphate level below 2.5 mg/dL (0.81 mmol/L) in the first 72 h of ICU admission. Comparisons between baseline characteristics and outcomes and multivariate analysis were performed. Results. A total of 324 (39.27%) patients had hypophosphatemia during the first 72 h of ICU admission. Patients with hypophosphatemia tended to be younger, with lower APACHE-II, SOFA24, and ΔSOFA scores. They had a longer length of stay and length of ventilation, more prevalent prolonged ventilation, and decreased mortality. Their energy deficit was lower. There was no effect of hypophosphatemia severity on these results. In multivariate analysis, hypophosphatemia was not found to be statistically significant either with respect to mortality or survivor’s length of ventilation, but lower average daily energy deficit and SOFA24 were found to be statistically significant with respect to survivor’s length of ventilation. Conclusion. Hypophosphatemia had no effect on mortality or length of ventilation. Lower average daily energy deficit is associated with a longer survivor’s length of ventilation.     

Hyperthermia catheter implantation and therapy in the brain. Technical note

For the treatment of malignant gliomas, a technique for implanting hyperthermia catheters was developed that utilized a stereotactic template and head-stabilization frame mounted on a computerized tomography (CT) scanner. Computerized tomography scans were used to measure tumor dimensions and to determine the number, implantation depths, and active heating lengths of the catheters, which were implanted through twist-drill holes while the patient was in the CT room. Heat was subsequently delivered via implanted catheters using a computer-controlled hyperthermia system, which partially compensates for heterogeneous and time-varying tumor blood flow.     

Diagnostic value of blood D-dimer level in acute mesenteric ischaemia in the rat: an experimental study

OBJECTIVE: The high mortality rate of mesenteric ischaemia is mainly due to delay in diagnosis. For this reason, it is of great importance to find a specific and rapidly elevating marker. The present study investigated the diagnostic value of blood D-dimer level as a potential marker for acute mesenteric ischaemia in a rat model. METHODS: Thirty male Wistar albino rats were divided into three groups. Basal D-dimer and L-lactate levels were determined in the non-operative control group (I). In the operated control group (II), the superior mesenteric artery was simply manipulated, while the artery was ligated in Group III. Blood samples were drawn in all groups for D-dimer and L-lactate assays. RESULTS: Both Group II (p=0.016) and Group III (p=0.001) had significantly higher mean D-dimer levels in the first postoperative hour compared with the basal level in Group I. However, there was no difference between the levels in Groups II and III. The mean level in Group II in the sixth hour had dropped to a statistically insignificant level compared with the basal value, while the mean value in Group III kept rising during this period (p=0.001). Nevertheless, there was no significant difference between Groups II and III. On the other hand, the mean L-lactate level in the first postoperative hour in Group III was significantly higher than the basal level in Group I (p=0.003). No significant rises were recorded in Group II in the first and sixth postoperative hours. The difference between Groups II and III in the first hour was significant (p=0.005). Group III also had significantly higher mean serum L-lactate value in the sixth hour compared with both the basal value in Group I (p=0.001) and the sixth-hour value in Group II (p=0.003). CONCLUSION: These results do not adequately support the use of blood D-dimer level as an independent parameter in the diagnosis of mesenteric ischaemia due to arterial thrombosis. However, this parameter can be used together with other tests in eliminating the possibility of a thromboembolic event.