Shift Volume Directly Impacts Neuroradiology Error Rate at a Large Academic Medical Center: The Case for Volume Limits.

BACKGROUND AND PURPOSE: Unlike in Europe and Japan, guidelines or recommendations from specialized radiological societies on workflow management and adaptive intervention to reduce error rates are currently lacking in the United States. This study of neuroradiologic reads at a large US academic medical center, which may hopefully contribute to this discussion, found a direct relationship between error rate and shift volume. MATERIALS AND METHODS: CT and MR imaging reports from our institution's Neuroradiology Quality Assurance database (years 2014-2020) were searched for attending physician errors. Data were collected on shift volume specific error rates per 1000 interpreted studies and RADPEER scores. Optimal cutoff points for 2, 3 and 4 groups of shift volumes were computed along with subgroups' error rates. RESULTS: A total of 643 errors were found, 91.7% of which were clinically significant (RADPEER 2b, 3b). The overall error rate (errors/1000 examinations) was 2.36. The best single shift volume cutoff point generated 2 groups: ≤ 26 studies (error rate 1.59) and > 26 studies (2.58; OR: 1.63, P < .001). The best 2 shift volume cutoff points generated 3 shift volume groups: ≤ 19 (1.34), 20-28 (1.88; OR: 1.4, P = .1) and ≥ 29 (2.6; OR: 1.94, P < .001). The best 3 shift volume cutoff points generated 4 groups: ≤ 24 (1.59), 25-66 (2.44; OR: 1.54, P < .001), 67-90 (3.03; OR: 1.91, P < .001), and ≥ 91 (2.07; OR: 1.30, P = .25). The group with shift volume ≥ 91 had a limited sample size. CONCLUSIONS: Lower shift volumes yielded significantly lower error rates. The lowest error rates were observed with shift volumes that were limited to 19-26 studies. Error rates at shift volumes between 67-90 studies were 226% higher, compared with the error rate at shift volumes of ≤ 19 studies.

Autoimmune diseases of the spine and spinal cord.

Magnetic resonance imaging (MRI) and clinicopathological tools have led to the identification of a wide spectrum of autoimmune entities that involve the spine. A clearer understanding of the unique imaging features of these disorders, along with their clinical presentations, will prove invaluable to clinicians and potentially limit the need for more invasive procedures such as tissue biopsies. Here, we review various autoimmune diseases affecting the spine and highlight salient imaging features that distinguish them radiologically from other disease entities.

Retrospective cohort study demonstrates that modified CT Severity Index directly correlates with lipase values at or above 600.

BACKGROUND: Elevated lipase is considered an important biomarker for pancreatitis. The aim of this study was to assess a potential correlation between elevated lipase and characteristic imaging findings, as per the well-established Modified CT Severity index (MCTSI). MATERIALS AND METHODS: This retrospective, single centre cohort study reviewed the radiologic findings and medical records of 200 consecutive patients with elevated lipase values. Subgroups were then created categorizing patients into low lipase elevation, medium lipase elevation, and high lipase elevation groups. CT exams evaluated by a single fellowship trained radiologist was used to establish MCTSI criteria. RESULTS: Statistical significance was calculated by an independent statistician using a linear regression model which demonstrated a statistically significant correlation between the high lipase group, (≥600 U/L) and MCTSI with p-value of <0.05. No significant correlation existed between MCTSI and lipase values below 600 U/L. CONCLUSIONS: The previously held notion that lipase values do not correlate with severity of pancreatitis does not hold true for lipase values ≥ 600 U/L. This suggests a likelihood of higher morbidity and may justify earlier use of contrast enhanced CT imaging in patients with pancreatitis whose lipase values are >600 U/L. This needs to be further validated with a multisite blinded prospective study.

Response of cervicogenic headaches and occipital neuralgia to radiofrequency ablation of the C2 dorsal root ganglion and/or third occipital nerve.

OBJECTIVE: This article investigates the degree and duration of pain relief from cervicogenic headaches or occipital neuralgia following treatment with radiofrequency ablation of the C2 dorsal root ganglion and/or third occipital nerves. It also addresses the procedure's complication rate and patient's willingness to repeat the procedure if severe symptoms recur. METHODS: This is a single-center retrospective observational study of 40 patients with refractory cervicogenic headaches and or occipital neuralgia. Patients were all referred by a headache specialty clinic for evaluation for radiofrequency ablation of the C2 dorsal root ganglion and/or third occipital nerves. After treatment, patients were followed for a minimum of 6 months to a year. Patient demographics and the results of radiofrequency ablation were recorded on the same day, after 3-4 days, and at 6 months to 1 year following treatment. RESULTS: Thirty-five percent of patients reported 100% pain relief and 70% reported 80% or greater pain relief. The mean duration of improvement is 22.35 weeks. Complication rate was 12-13%. 92.5% of patients reported they would undergo the procedure again if severe symptoms returned. CONCLUSIONS: Radiofrequency ablation of the C2 dorsal root ganglion and/or third occipital nerve can provide many months of greater than 50% pain relief in the vast majority of recipients with an expected length of symptom improvement of 5-6 months.

C5 inhibitor rEV576 protects against neural injury in an in vitro mouse model of Miller Fisher syndrome.

Guillain-Barré syndrome and its clinical variants, including the anti-GQ1b ganglioside-mediated Miller Fisher syndrome (MFS), comprise the world's leading cause of acute neuromuscular paralysis. Presently, no specific drug therapies exist. The complement cascade, which is activated in these patients, forms an attractive drug target. In this study, we tested whether the complement C5-inhibiting recombinant protein, rEV576, was able to prevent neural injury in a previously developed in vitro mouse model for MFS. Mouse hemidiaphragm preparations were treated with anti-GQ1b antibody and normal human serum as a source of complement with added rEV576 or control protein. Immunohistology in control tissue showed deposition of C3c and membrane attack complex at neuromuscular junctions (NMJs), along with terminal motor axonal neurofilament degradation as well as ethidium homodimer-2 staining showing perisynaptic Schwann cell (pSC) injury. Electrophysiological and functional analyses showed block of synaptic transmission at the NMJ after an initial period of a dramatically high level of asynchronous acetylcholine release. In tissue treated with rEV576, all these indicators of motor neuronal damage were absent, except for the presence of C3c, indicating effective inhibition of C5. These results demonstrate that rEV576 effectively prevents development of neuronal and pSC damage in experimental murine neuropathy.

In vivo characterization and therapeutic efficacy of a C5-specific inhibitor from the soft tick Ornithodoros moubata.

The involvement of complement (C) in inflammatory diseases has driven the search for agents capable of inhibiting dysregulated complement activation. Many of these reagents inhibit the C3 convertases during the early stages of the cascade. However, a drawback of total systemic C inhibition, particularly in longterm treatment of chronic disease, is potentiation of infection and immune complex disease due to an inability to opsonize complexes and foreign cells and to lyse pathogens. Recent identification of a C5-binding protein in the salivary gland of the soft tick Ornithodoros moubata has enabled development of a terminal pathway-specific reagent, OmCI, with potential to ameliorate disease while leaving key physiological processes unaffected. Here we demonstrated that OmCI has broad cross-species activity. When given intravenously to rodents, OmCI totally ablated complement hemolytic activity, which gradually restored as C5 was resynthesized. The circulating half-life of OmCI was 30 h, demonstrating a much slower clearance than other small, biological agents. Using C5-sufficient and C5-deficient mice we showed that prolonged half-life was due to binding to plasma C5. Surface plasmon resonance analysis of C5 binding to OmCI confirmed a high binding affinity with a slow dissociation rate. OmCI was effective in preventing experimental autoimmune myasthenia gravis induced by passive transfer in normal Lewis rats. OmCI ablated clinical disease, reduced C3 and C9 deposition at the neuro-muscular junction, and effected a marked reduction in cellular infiltration at this site. These data offer exciting prospects for targeted treatment of complement-mediated diseases without the detrimental inhibition of the opsonic roles of complement.

Cellular localization and role of kinase activity of PMK1 in Magnaporthe grisea.

A mitogen-activated protein (MAP) kinase gene, PMK1, is known to regulate appressorium formation and infectious hyphal growth in the rice blast fungus Magnaporthe grisea. In this study, we constructed a green fluorescent protein gene-PMK1 fusion (GFP-PMK1) to examine the expression and localization of PMK1 in M. grisea during infection-related morphogenesis. The GFP-PMK1 fusion encoded a functional protein that complemented the defect of the pmk1 deletion mutant in appressorium formation and plant infection. Although a weak GFP signal was detectable in vegetative hyphae, conidia, and germ tubes, the expression of GFP-Pmk1 was increased in appressoria and developing conidia. Nuclear localization of GFP-Pmk1 proteins was observed in a certain percentage of appressoria. A kinase-inactive allele and a nonphosphorylatable allele of PMK1 were constructed by site-directed mutagenesis. Expression of these mutant PMK1 alleles did not complement the pmk1 deletion mutant. These data confirm that kinase activity and activation of PMK1 by the upstream MAP kinase kinase are required for appressorium formation and plant infection in M. grisea. When overexpressed with the RP27 promoter in the wild-type strain, both the kinase-inactive and nonphosphorylatable PMK1 fusion proteins caused abnormal germ tube branching. Overexpression of these PMK1 mutant alleles may interfere with the function of native PMK1 during appressorium formation.

The bacterial transposon Tn7 causes premature polyadenylation of mRNA in eukaryotic organisms: TAGKO mutagenesis in filamentous fungi.

TAGKO is a Tn7-based transposition system for genome wide mutagenesis in filamentous fungi. The effects of transposon insertion on the expression of TAGKO alleles were examined in Magnaporthe grisea and Mycosphaerella graminicola. Northern analysis showed that stable, truncated transcripts were expressed in the TAGKO mutants. Mapping of the 3'-ends of TAGKO cDNAs revealed that they all contain Tn7 end sequences, regardless of the transposon orientation. Polyadenylation signals characteristic of eukaryotic genes, preceded by stop codons in all frames, are located in both ends of the bacterial transposon. Thus, TAGKO transcripts are prematurely polyadenylated, and truncated proteins are predicted to be translated in the fungal mutants. Depending on the extent of protein truncation, TAGKO mutations in HPD4 (encoding p-hydroxyphenylpyruvate dioxygenase) resulted in tyrosine sensitivity in the two fungi. Similarly, a particular M.grisea CBS1 (encoding cystathionine beta-synthase) TAGKO cDNA failed to complement cysteine auxotrophy in a yeast CBS mutant. TAGKO, therefore, represents a useful tool for in vivo study of truncated gene products in filamentous fungi.

Molecular characterization of a cystathionine beta-synthase gene, CBS1, in Magnaporthe grisea.

CBS1 from Magnaporthe grisea is a structural and functional homolog of the cystathionine beta-synthase (CBS) gene from Saccharomyces cerevisiae. Our studies indicated that M. grisea can utilize homocysteine and methionine through a CBS-independent pathway. The results also revealed responses of M. grisea to homocysteine that are reminiscent of human homocystinuria.