ABSTRACT
Objective@#To summarize the characteristics of cuffed-tunneled catheters insertion and investigate the values of cuffed-tunneled catheters in pediatric patients.@*Methods@#Between March 2015 and July 2017, all the pediatric patients who received maintenance hemodialysis at least 3 consecutive months in our center were included. Sixteen cuffed-tunneled hemodialysis catheters were inserted in patients for long-term hemodialysis access. The clinical manifestations and complications were retrospectively reviewed.@*Results@#Fifteen pediatric patients with end stage ranal disease (ESRD) were included in this study and they received 16 cuffed-tunneled catheters for long-term vascular access, including 10 males and 5 females; median age at start of catheter insertion was 11.5 (4.2-14.5) years. Body weight was (27.8±8.0)kg (16.0-39.4 kg) . The size and the length of the catheters were based on the height of patients as follows: 28 cm for (115.6±10.6) cm (102.0-130.0 cm) ,36 cm for (148.6±9.9)cm (140.0-167.0 cm) . Cuffed-tunneled catheters outcome: 10 cuffed-tunneled catheters were still functional at the end of the study; 5 catheters were removed after successful kidney transplantation. Catheter failure occurred in 1 out of 16 cuffed-tunneled catheters due to catheter-related infections. The median catheter survival time was 11.9 months (range 3.5-21.3 months). Complications of cuffed-tunneled catheters: Catheter placements operation was successful in 15 cases using ultrasound guidance. No serious complications were observed in any patients receiving catheter inserting operation. The overall rate of catheter-related infections and thrombosis/malposition was 6.3% and 18.7%, respectively.@*Conclusions@#Ultrasound guidance is suggested in pediatric patients during the catheters insertion. The size and the length of the catheters should be based on the height of patients. Cuffed-tunneled hemodialysis catheters could be effectively used for maintenance of hemodialysis vascular access for pediatric patients with ESRD.
ABSTRACT
The pathological presentation of Alzheimer disease (AD), the leading cause of senile dementia, involves regionalized neuronal death and an accumulation of intraneuronal and extracellular filaments termed neurofibrillary tangles and senile plaques, respectively. One of the ?-amyloid peptides (A?), the A?1-42 form, is primarily responsible for neuronal damage and cell death that is the main component in the senile plaques. Over the past twenty years, the amyloid hypothesis has been strongly supported by a wealth of evidence, including data from genetic studies of Alzheimer disease. Amyloid cascade hypothesis states that the accumulation and deposition of fibrillar A? is the primary driver of neurodegeneration and cognitive decline leading to dementia. AD is a clinicopathological syndrome in which different gene defects can lead--directly or indirectly--to alter APP expression or proteolytic processing as such to change A? stability or aggregation. These result in a chronic imbalance between A? production and clearance. Gradual accumulation of aggregated A? initiates a complex, multistep cascade that includes gliosis, inflammatory changes, neuritic/synaptic change, tangles and transmitter loss. The evidence that links A? to the pathogenesis of AD is substantial, but the means by which these peptides exert their toxic effects, and where in neuronal cells they act, is far from clear. The up-to-date proceeding in the molecular mechanism of ?-amyloid peptides is overviewed.
ABSTRACT
AIM To study the pharmacokinetics of SJ SPM. METHOD The pharmacokinetics of SJ SPM was studied after oral doses in dog and in rat, compared with the pharmacokinetics of ASPM. Rat orally administed 40 mg?kg -1 SJ SPM, 72 h urine and bile recoveries were studied. Blood,urine and bile concentrations were tested with agar diffusion method. Pharmacokinetic parameters were calculated by 3p87 program in computer. RESULTS The plasma drug concentration time data for each subject were analyzed and fitted with a linear two compartment model. Following oral doses of 30,20,10 mg?kg -1 SJ SPM in dog, drug is rapidly and widely distributed throughout the body and lag time are 18～30 min; T max 1 43～2 44 h; C max 1 02～2 94 ?g?ml -1 ; T 1/2? 0 48～1 81 h; T 1/2? 8 40～10 52 h; Oral doses of 30,20,10 mg?kg -1 SJ SPM in dog and 120,80,40 mg?kg -1 in rat resulted in linear increase in the peak serum levels and areas under the serum concentration time curve. The MRT of SJ SPM,ASPM in rat and dog did not change significantly with an increase in oral dosage. Under the same conditions, the pharmacokinetics of ASPM was studied in dog, Oral doses of 30,20,10 mg?kg -1 ASPM in dog, lag time are 0 37～0 44 h; C max 0 87～3 34 ?g?ml -1 ; T max 1 49～2 26 h; T 1/2? 0 59～1 17 h; T 1/2? 7 42～12 04 h; MRT 7 56 h; AUC 7 65, 17 44, 26 25 ?g?ml -1 ?h -1 respectively. Following oral doses of 120,80,40 mg?kg -1 SJ SPM in rat, T max 1 57～2 45 h; C max 0 39～3 14 ?g?ml -1 ; T 1/2? 1 36～1 77 h; T 1/2? 15 63～20 64 h;MRT 13 0 h; AUC 8 44,16 54,37 58 ?g?ml -1 ?h -1 .Rat orally administered 40 mg?kg -1 SJ SPM, 72 h urine and bile recoveries are 2 18% and 4 70% respectively. CONCLUSION There are no significantal difference between SJ SPM and ASPM statistic.