Lindgaardwilson0904

th outcomes including new ADL and IADL dependency and mortality 1 year after discharge among older hospitalized patients.Emerging evidence indicates that A1 reactive astrocytes play crucial roles in the pathogenesis of Parkinson's disease (PD). Thus, development of agents that could inhibit the formation of A1 reactive astrocytes could be used to treat PD. Simvastatin has been touted as a potential neuroprotective agent for neurologic disorders such as PD, but the specific underlying mechanism remains unclear. The 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of PD and primary astrocytes/neurons were prepared to investigate the effects of simvastatin on PD and its underlying mechanisms in vitro and in vivo. We show that simvastatin protects against the loss of dopamine neurons and behavioral deficits in the MPTP mouse model of PD. We also found that simvastatin suppressed the expression of A1 astrocytic specific markers in vivo and in vitro. In addition, simvastatin alleviated neuron death induced by A1 astrocytes. Our findings reveal that simvastatin is neuroprotective via the prevention of conversion of astrocytes to an A1 neurotoxic phenotype. In light of simvastatin favorable properties, it should be evaluated in the treatment of PD and related neurologic disorders characterized by A1 reactive astrocytes.Background Dysregulation of metabolic regulatory hormones often occurs during the progress of obesity. Key regulatory hormone Insulin-GH balance has recently been proposed to maintain metabolism profiles. Time-restricted feeding (TRF) is an effective strategy against obesity without detailed research on pulsatile GH releasing patterns. Methods TRF was performed in an over-eating MC4RKO obese mouse model using normal food. Body weight and food intake were measured. Series of blood samples were collected for 6 h pulsatile GH profile, glucose tolerance test and insulin tolerance test at 5, 8, and 9 weeks of TRF, respectively. Indirect calorimetric recordings were performed by Phenomaster system at 6 weeks for 1 week and body composition was measured by Nuclear magnetic resonance spectroscopy (NMR). Substrate and energy metabolism related gene expression were measured in terminal liver and subcutaneous white adipose tissues. Results TRF increased pulsatile GH secretion in dark phase and suppressed hyperinsulinemia in MC4RKO obese mice to reach a reduced insulin/GH ratio. This was accompanied by the improvement in insulin sensitivity, metabolic flexibility, glucose tolerance and decreased glucose fluctuation, together with appropriate modification of gene expression involved in substrate metabolism and adipose tissue browning. NMR measurement showed that TRF decreased fat mass but increased lean mass. Indirect calorimeter recording indicated that TRF decreased the respiratory exchange ratio (RER) reflecting consumption of more fatty acid in energy production in light phase and increased the oxygen consumption during activities in dark phase. Conclusions TRF effectively decreases hyperinsulinemia and restores pulsatile GH secretion in the overeating obese mice with significant improvement in substrate and energy metabolism and body composition without reducing total caloric intake.

Juvenile xanthogranuloma (JXG) is a disorder of histiocytic proliferation that affects young children and usually presents as spontaneously regressing cutaneous lesions. CF-102 agonist molecular weight JXG with systemic involvement is a rare entity associated with significant morbidity and mortality. Intracranial solitary lesions are uncommon, and when comorbid with multiple lesions of the central nervous system in young children, it has an extremely worse prognosis.

We have reported here an unusual case of a 6-year-old boy who initially presented with the complaints of headache, vomiting, seizure, and speech disorder without cutaneous and other organ involvement and a neurological tendency to sleep. Acute hydrocephalus was detected in his brain CT. As an emergency intervention, ventriculo-peritoneal shunt operation was performed on the patient. His postoperative MRI revealed a disseminated intracranial disease involving the extensive dural, sellar-suprasellar region, the orbit, and the brain parenchyma. The patient accordingly underwenture.

Neonatal thrombosis is a frequently encountered complication in a neonatal intensive care unit. Dalteparin can be used to treat thrombosis in newborn infants.

In this study, we evaluate the current recommended starting dose of 129 ± 43 U/kg/24 h, hypothesizing that this dose is too low to reach therapeutic anti-Xa levels.

From 2008 until 2017, all infants treated with dalteparin in the University Medical Centre Utrecht were included in this study. In this retrospective cohort study, the correlation between dose and anti-Xa level was observed.

Sixty-six infants were included. The most common thrombus types were catheter-related (29 patients, 44%) and venous sinus thrombosis (28 patients, 43%). The mean dalteparin dose needed for the first adequate anti-Xa level (0.5-1.0 IU/mL) was 297.6 U/kg/12 h. Two infants developed a first bleeding episode under dalteparin therapy; they both had anti-Xa levels in the therapeutic range.

The increase of the starting dose of dalteparin will lead to earlier therapeutic levels of anti-Xa in the studied population and appears to be safe. However, this needs to be evaluated in further study.

The increase of the starting dose of dalteparin will lead to earlier therapeutic levels of anti-Xa in the studied population and appears to be safe. However, this needs to be evaluated in further study.

Since cognitive impairment (CI) occurs on average in 45% of multiple sclerosis (MS) patients, the early detection of patients "at risk" of CI is important in order to promptly apply preventive strategies. The aim of the present study was to investigate the prevalence and risk factors for CI in MS patients using the Brief International Cognitive Assessment for Multiple Sclerosis (BICAMS) as a screening test.

During the 1-year period, CI was evaluated in 82 consecutives mild relapsing-remitting MS (EDSS ≤ 3.5) patients. Patients with 1 altered BICAMS test were defined "at risk." Both "at risk" and CI patients underwent an extensive neuropsychological battery.

We found that (i) 23% had CI, (ii), 25% were "at risk" of CI, and (iii) 76% of the "at risk" patients were already impaired at the NP assessment. In particular, the Symbol Digit Modalities Test was the most compromised (70% of "at risk" and 79% of CI patients). Patients with CI had more frequently an EDSS ≥ 2.5 (p = 0.05), lower education (p = 0.05), and relapses in the last 12 months (p = 0.