Stillinghudson4291

We are investigating a new class of therapeutics, virus-derived immune modulators; One that targets coagulation pathway serine proteases and a second that inhibits chemokines. We have demonstrated that local infusion of these biologics after SCI reduces inflammation providing early improved motor function. Serp-1 is a Myxomavirus-derived serine protease inhibitor, a serpin, that inhibits both thrombotic and thrombolytic proteases. M-T7 is a virus-derived chemokine modulator. Here we review the roles of thrombotic and thrombolytic serine proteases and chemoattractant proteins, chemokines, as potential therapeutic targets for SCI. We discuss virus-derived immune modulators as treatments to reduce progressive inflammation and ongoing nerve damage after SCI.As one of the most important elements in our body, zinc plays a part in both the pathophysiology of depression and the antidepressant response. Patients suffering from major depression show significantly reduced zinc levels, which are normalized following successful antidepressant treatment. Recent studies have shown the interaction between zinc, GPR39 and neuropeptides, including galanin and neuropeptide Y (NPY). The zinc-sensing receptor GPR39 forms heterotrimers with 5-HT1A and the galanin receptor GalR1 upon their co-expression in mammalian cells. The oligomerization of these heterotrimers is regulated by the zinc concentration, and this may have an influence on depressive-like behavior. The antidepressant-like effect of zinc is linked to elevated levels of brain-derived neurotrophic factor (BDNF) in brain structures associated with emotion, such as the hippocampus and the amygdala. BDNF regulates neuropeptides, including NPY, cholecystokinin (CCK), and substance P or galanin, which are also implicated in mood disorders. This review focuses for the first time on the interaction between zinc, the GPR39 zinc receptor, BDNF and selected neuropeptides in terms of depression in order to determine its possible role in the neuropharmacology of that illness.Great progress has been made in specifically identifying the central neural circuits (CNCs) of the core body temperature (Tcore), sleep-wakefulness states (SWs), and general anesthesia states (GAs), mainly utilizing optogenetic or chemogenetic manipulations. We summarize the neuronal populations and neural pathways of these three CNCs, which gives evidence for the orchestration within these three CNCs, and the integrative regulation of these three CNCs by different environmental light signals. We also outline some transient receptor potential (TRP) channels that function in the CNCs-Tcore and are modulated by some general anesthetics, which makes TRP channels possible targets for addressing the general-anestheticsinduced- hypothermia (GAIH). We suggest this review will provide new orientations for further consummating these CNCs and elucidating the central mechanisms of GAIH.Traumatic brain injury (TBI) is a major cause of disability and death worldwide. The initial mechanical insult results in tissue and vascular disruption with hemorrhages and cellular necrosis that is followed by dynamic secondary brain damage that presumably results in additional destruction of the brain. In order to minimize deleterious consequences of the secondary brain damage- such as inflammation, bleeding or reduced oxygen supply. The old concept of the -staircase approach- has been updated in recent years by most guidelines and should be followed as it is considered the only validated approach for the treatment of TBI. Besides, a variety of novel therapies have been proposed as neuroprotectants. The molecular mechanisms of each drug involved in the inhibition of secondary brain injury can result as a potential target for the early and late treatment of TBI. However, no specific recommendation is available on their use in the clinical setting. The administration of both synthetic and natural compounds, which act on specific pathways involved in the destructive processes after TBI, even if usually employed for the treatment of other diseases, can show potential benefits. This review represents a massive effort towards current and novel therapies for TBI that have been investigated in both pre-clinical and clinical settings. This review aims to summarize the advancement in therapeutic strategies based on specific and distinct -target of therapies- brain edema, ICP control, neuronal activity and plasticity, anti-inflammatory and immunomodulatory effects, cerebral autoregulation, antioxidant properties, and future perspectives with the adoption of mesenchymal stromal cells.

Our study investigated the association between the level of HbA1c (glycated hemoglobin) at admission and the prognosis of aneurysmal subarachnoid hemorrhage (SAH).

A total of 510 patients treated with neuro-intervention for aneurysmal SAH and with data for admission HbA1c (glycated hemoglobin) were included. Favorable clinical outcome was defined as modified Rankin Scale (mRS) score of 0-2 at 3 months. Receiver operating characteristic (ROC) curve analysis was used to identify the optimal cutoff value of HbA1C for unfavorable clinical outcomes. Logistic regression was used to evaluate the association between HbA1C level and outcomes.

The optimal cutoff value of HbA1C was identified as 6.0% (P < 0.001), and patients with a high HbA1C (≥ 6.0%) had a lower prevalence of favorable clinical outcomes than patients with low HbA1C (< 6.0%) (P < 0.001). click here High HbA1C (≥ 6.0%) was independently associated with unfavorable clinical outcome (OR 2.84; 95% CI 1.52-5.44; P = 0.004). The risk of unfavorable clinical outcome was significantly increased in patients with HbA1C (≥ 7.0%, < 8%) and HbA1C (≥ 8.0%) compared with lower baseline HbA1C (≥ 6.0%, < 7%) values (OR 2.17; 95% CI 1.87-5.13; P = 0.011 and OR 4.25; 95% CI 3.17-8.41; P = 0.005).

Our study showed that HbA1C could be an independent predictor of worse outcomes following neuro-intervention for aneurysmal SAH. High HbA1C (≥ 6.0%) was associated with unfavorable clinical outcomes, and gradual elevation of HbA1C contributed to an increase in the risk of worse clinical outcomes after SAH.

Our study showed that HbA1C could be an independent predictor of worse outcomes following neuro-intervention for aneurysmal SAH. High HbA1C (≥ 6.0%) was associated with unfavorable clinical outcomes, and gradual elevation of HbA1C contributed to an increase in the risk of worse clinical outcomes after SAH.