Phantom calibration method for improved temporal characterization of hemodynamic response in event-related fMRI

In event-related functional MRI, there exist limits on the time length of the experiments on human subjects and the imaging speed. Due to these limitations, data truncation and undersampling have to be used in functional MRI signal acquisition. The effect of these factors on the hemodynamic deconvolution is investigated experimentally and a phantom calibration method to improve the hemodynamic response is developed. It is observed that the high frequency components generated due to data truncation can fold back into low frequencies when the sampling rate is not sufficiently high. This aliasing can introduce significant noise in hemodynamic deconvolution and can reduce the accuracy of the temporal characterization of hemodynamic response. A SMARTPHANTOM BOLD simulator is used to calibrate the aliasing effect in an event-related functional MRI experiment. With the calibration, an anti-aliasing method is used to suppress the aliasing and this resulted in an improved temporal characterization of hemodynamic response in event-related fMRI.     

Pseudoaneurysm of the profunda femoris artery: a rare complication of femoral intertrochanteric fracture fixation

Profunda femoris artery pseudo aneurysm is a rare occurrence following fractures of the proximal femur or their surgical fixation. They usually present late because of the deep position of the artery. Patients present with a painful expansile mass in the thigh with or without progressive anaemia. Modalities such as ultrasound scanning may aid in diagnosis but CT arteriography is used mostly for accurate diagnosis and intervention. We report a case of delayed presentation of profunda femoris pseudo aneurysm following dynamic hip screw fixation for intertrochanteric femur fracture.     

Stimulation of cAMP accumulation and superoxide production in human neutrophils and monocytes

The effect of sodium fluoride (NaF) on superoxide generation and cyclic adenosine monophosphate (cAMP) levels in human neutrophils and monocytes was investigated. NaF (greater than 10 mM) stimulated superoxide (O2-) production in both cell types in a time dependent manner. NaF (0.5 to 20 mM) increased cAMP levels by 1.5- to 3.-fold in both neutrophils and monocytes. Increases in cAMP levels were time-dependent; the maximal level was attained within 5 minutes after the addition of NaF, and cAMP levels remained elevated for up to 10 minutes. Only high concentrations of NaF (10 and 20 mM) increased both cAMP levels and O2- production. Therefore, a direct role of cAMP in O2- generation is not likely. It is speculated that since NaF (greater than 10 mM) can complex with extracellular Ca++, and thus reduce free Ca++ concentration required for O2- generation, a NaF-dependent increase in cAMP may restore cytosolic free Ca++ by mobilizing intracellular stores of Ca++. Further, in view of the proposed involvement of a phosphorylation-dephosphorylation mechanism in the regulation of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, we speculate that NaF, by inhibiting phosphoprotein phosphatase activity, may indirectly activate the NADPH oxidase system and thus superoxide generation.     

Mutation analysis of the parkin and PINK1 genes in American Caucasian early-onset Parkinson disease families

Mutations in the parkin gene and the PTEN-induced putative kinase 1 gene (PINK1) have been identified as the most common causes of autosomal recessive early-onset Parkinson disease (EOPD). To investigate the presence of the parkin and PINK1 gene mutation(s) and to explore genotype-phenotype correlations in American Caucasian families with EOPD from North American, we screened these two genes in probands of six families by direct sequencing, semi-quantitative PCR and RT-PCR. No PINK1 gene mutation was found in any of the probands, but compound heterozygous mutations (EX 3 del and EX 3_4 del) in the parkin gene were identified in one family. Extended analysis of the parkin-positive family showed the phenotype of patients was that of classic autosomal recessive EOPD, characterized by early age at onset, slow progression, beneficial response to levodopa, and levodopa-related motor complications. Three heterozygous mutation carriers (EX 3 del or EX 3_4 del) were free of any neurological symptoms. None of 62 healthy controls harbored EX 3 del or EX 3_4 del mutation. Our data suggest that compound heterozygous mutations (EX 3 and EX 3_4 del) in the parkin gene were the cause of EOPD in one of six Caucasian families; heterozygous EX 3 del and heterozygous EX 3_4 del forms were insufficient to cause this disorder, consistent with a loss-of-function mechanism of the parkin mutations. The results may provide new insights into the cause and diagnosis of PD and have implications for genetic counseling.     

Organ donation after cardiac death in amyotrophic lateral sclerosis

Patients with amyotrophic lateral sclerosis (ALS) are often told that solid organ donation is not possible following death, although the reasons for exclusion are not evidence based. Because ALS patients typically remain sentient until death, organs may be procured under donation after cardiac death protocols. Anticipating this need, our institution created a process for organ donation in ventilator-dependent ALS patients that was subsequently implemented. To our knowledge, this is the first report of organ donation in a patient with rapidly progressive ventilator-dependent ALS.