Equivalent squares for small field dosimetry

The use of equivalent squares is of value when determining output and depth dose data for rectangular fields. We have looked at the variation with field shape of head scatter factors (S(c)), phantom scatter factors (S(p)) and tissue phantom ratios (TPRs) using measurements on a 6 MV linac with a Moduleaf mini-multileaf collimator. Measurements were made for fields with dimensions down to 1 cm. A different approach to calculating equivalent squares needs to be made depending on the quantity of interest. For TPRs, good agreement for rectangular fields can be obtained using the well established E = 2XY/(X+Y) formula where E is the equivalent square field size and X and Y are the field dimensions. For S(c) measurements, where a collimator exchange effect is observed, better agreement is obtained using E = (1+A)XY/(AX+Y), where A is an empirically determined constant. For S(p) measurements, E = 2XY/(X+Y) only gives agreement with measurements when the minimum field dimension is at least 2.5 cm. For smaller fields, the equivalent square overestimates S(p), with the difference being strongly related to the value of the smaller dimension. We propose an empirical formula, based on the size of the smaller dimension.     

Intestinal ischemia-reperfusion injury does not lead to acute central nervous system damage

BACKGROUND: The detrimental effects of intestinal ischemia reperfusion (IIR) injury on secondary organs including the liver, lungs, heart, and kidney have been widely investigated in animal models. However, the effect of IIR on the central nervous system (CNS) is largely unknown. We investigated the effect of IIR on the CNS as it may be of clinical relevance to patients at high risk of neurological injury. MATERIALS AND METHODS: Adult male rats underwent IIR (60 min superior mesenteric artery occlusion followed by 120 min reperfusion, n = 7) or sham operation (n = 6) under anesthesia. Following the procedure, the cerebral hemispheres were removed for histological assessment and measurement of N-acetyl-aspartate (NAA), a marker of neuronal damage, by HPLC. Blood was taken for determination of plasma S100B concentration, a measure of glial cell damage by ELISA. Data are median (range). RESULTS: Cerebral tissue from all animals from both groups was macroscopically and microscopically normal with no evidence of inflammation. NAA in brain homogenate was similar in the IIR group (0.2 [0.1-0.32] nmol/mg protein) and sham-operated group (0.19 [0.12-0.34], P = 0.83). Plasma S100B levels were higher in the IIR group compared to sham-operated animals but this difference was not statistically significant (1.13 [0.24-7.26] versus 0.55 [0.23-2.84] mug/l, P = 0.18). CONCLUSIONS: In this model, IIR injury did not produce histological CNS changes nor biochemical changes suggestive of neuronal damage. Further work is required to elucidate any functional effect of IIR injury on the CNS.     

Can cost utility evaluations inform decision making about interventions for low back pain?

Background contextLow back pain (LBP) is associated with high health-care utilization and lost productivity. Numerous interventions are routinely used, although few are supported by strong evidence. Cost utility analyses (CUAs) may be helpful to inform decision makers.PurposeTo conduct a systematic review of CUAs of interventions for LBP.Study designSystematic review.MethodsA search strategy combining medical subject headings and free text related to LBP and health economic evaluations was executed in MEDLINE. Cost utility analyses combined with randomized controlled trials for LBP were included. Studies that were published before 1998, non-English, decision analyses, and duplicate reports were excluded. Search results were evaluated by two reviewers, who extracted data independently related to clinical study design, economic study design, direct cost components, utility results, cost results, and CUA results.ResultsThe search produced 319 citations, and of these 15 met eligibility criteria. Most were from the United Kingdom (n=8), published in the past 3 years (n=12), studied chronic LBP or radiculopathy (n=13), and had a follow-up >12 months (n=13). Combined, there were 33 study groups who received a mean 2.1 interventions, most commonly education (n=17), exercise therapy (n=13), spinal manipulation therapy (n=7), surgery (n=7), and usual care from a general practitioner (n=7). Mean baseline utility was 0.57, improving to 0.67 at follow-up; the mean difference in utility improvement between study groups was 0.04. Based on available data and converted to US dollars, the cost per quality-adjusted life year ranged from $304 to $579,527, with a median of $13,015.ConclusionsFew CUAs were identified for LBP, and there was heterogeneity in the interventions compared, direct cost components measured, indirect costs, other methods, and results. Reporting quality was mixed. Currently published CUAs do not provide sufficient information to assist decision makers. Future CUAs should attempt to measure all known direct cost components relevant to LBP, estimate indirect costs such as lost productivity, have a follow-up period sufficient to capture meaningful changes, and clearly report methods and results to facilitate interpretation and comparison.     

Merkel Cell Carcinoma Arising from the Subcutaneous Fat of the Arm with Intact Skin

BACKGROUND: Merkel cell carcinoma is a rare malignant neuroendocrine neoplasm characteristically arising from the dermis of sunlight-exposed skin. It rarely arises outside the skin. OBJECTIVE: We present a patient with primary Merkel cell carcinoma arising from subcutaneous fat, with no involvement of the overlying skin. We describe the clinical manifestations and magnetic resonance imaging (MRI) findings. METHODS: We report a 63-year-old woman with a primary lesion of Merkel cell carcinoma that arose from the subcutaneous fat layer of the left arm. The lesion presented as a subcutaneous nodule with intact overlying skin. MRI showed that the nodular lesion was located entirely in the subcutaneous fat layer, with no involvement of the dermis. Peritumoral infiltration around the lesion and enlarged lymph nodes deep to the lesion were noted. The patient received wide excision of the lesion with dissection of the regional lymph nodes and adjuvant radiotherapy and chemotherapy. RESULTS: Histopathologic examination confirmed the diagnosis of Merkel cell carcinoma with local lymphatic metastasis, and the lesion was completely located in the subcutaneous fat, with no involvement of the dermis. These findings were well correlated with MRI findings. CONCLUSION: Primary Merkel cell carcinoma may arise from the subcutaneous fat and present as an entirely subcutaneous lesion with intact skin. MRI is helpful to evaluate the local extension of the lesion and regional lymphatic metastasis.     

The relationship between CR3 deficiency and neutrophil actin assembly

Polymorphonuclear leukocytes (PMN) with a deficiency of the complement receptor type 3 (CR3) membrane glycoprotein family have impairments in the ability to adhere to surfaces as well as chemotactic and phagocytic defects, processes that require a functional contractile apparatus. PMN from the patient with neutrophil actin dysfunction (NAD) displayed similar functional characteristics to those with CR3 deficiency suggesting the two disorders may be the same disease. In order to evaluate the relationship between CR3 deficiency and actin assembly, actin filament assembly was measured in PMN from six previously reported homozygotes (two severe and four moderate CR3-deficient patients) as well as five heterozygotes for CR3 deficiency. PMN from all patients had normal unstimulated concentrations of F-actin and after exposure to the chemotactic peptide FMLP (5 x 10(-7) mol/L for 5 to 40 seconds at 25 degrees C) assembled actin normally. Pretreatment of normal PMN with concentrations of monoclonal anti-alpha CR3 antibody, capable of blocking PMN adherence, also failed to impair FMLP- induced actin filament assembly. CR3 glycoprotein expression was measured in PMNs from the mother, father, and older sister of the NAD patient (N Engl J Med 291:1093, 1974). Actin filament assembly was recently shown to be defective in PMNs from all three family members. The total concentrations of the alpha and beta CR3 subunits were below normal in PMN detergent extracts from the mother (25% of simultaneous controls) and older sister (56% of control). PMN surface expression of these two subunits was also found to be depressed (mother, 50%; older sister, 63% of control). These findings suggest these two NAD family members are heterozygote carriers for CR3 deficiency as well as NAD. Simultaneous studies of the father, however, demonstrated normal total concentrations of both the alpha and beta CR3 subunits (126% of controls) as well as normal surface expression of both subunits after phorbol myristate acetate stimulation and incubation at 37 degrees C (mean, 112% of controls) but slightly lower than normal levels after FMLP stimulation (mean, 83%). These findings indicate that CR3 deficiency generally is not associated with defective actin filament assembly and support the conclusion that NAD represents a unique kindred in which PMN actin function differs from previously reported genotypes of CR3 deficiency.     

Complex and simple coronary artery stenoses: a new way to interpret coronary angiograms based on morphologic features of lesions

For many years, atherosclerotic coronary artery lesions have been described by angiographers only in terms of location and degree of narrowing. However, it has become apparent that coronary stenoses generally have distinct morphologic features that can be recognized at angiography and that allow them to be classified as either "simple" or "complex" plaques. Complex plaques are those characterized by ulcerated or ruptured surfaces, subintimal hemorrhage, superimposed partially occluding thrombi, recanalized thrombi, or some combination. Pathologic studies have shown a very high frequency of these lesions at sites of total thrombotic occlusion of coronary arteries. Clinical and angiographic studies have demonstrated a high frequency of such lesions in living patients with both unstable angina and acute myocardial infarction. The presence of complex stenoses has also been found to increase the risk of future myocardial infarction. Plaque morphology thus appears to significantly affect the prognosis of patients with coronary disease and should be carefully evaluated in interpretation of all coronary angiograms.