ABSTRACT
Objective To assess the protective effect of low melting point lead and field margin on the opposite testicular in testicular seminoma patients during postoperative radiation.Methods A patient with stage Ⅰ seminoma was selected and his phantom measurement was carried out.The PTW 0.6 cm3 type ionization chamber was used to measure the absorbed dose under the conditions of no lead and low melting point lead with thickness of 3,5,7,10 and 15 mm at different distances from the field edge,respectively.Results Under different lead thickness conditions,the measurement result and the distance between the measured points and the boundary of the field were exponentially attenuated.The relative target dose dropped from 8.41％ at 1 cm to 0.61％ at 25 cm without lead blocking,and dropped from 4.55％,3.98％ and 3.47％ at 1 cm to0.27％,0.21％ and0.17％ at 25 cm with 3,5,7 cmlead,respectively.With 10 mm lead,it dropped from 2.55％ at 1.5 cm to0.15％ at25 cm,and 1.86％ at2 cm to0.13％ at 25 cm with 15 mm lead.The lead shield of 3,7 and 15 mm thickness can be used to reduce the scatter dose of testis to below 0.5 Gy during radiotherapy for seminoma.Conclusions An appropriate thickness of low melting point lead might reduce the dose of testis conveniently and effectively,which would be beneficial to protect the fertility of the patients with testicular seminoma.
ABSTRACT
The aspartate kinase (AK) from Mycobacterium tuberculosis (Mtb) catalyzes the biosynthesis of aspartate family amino acids, including lysine, threonine, isoleucine and methionine. We determined the crystal structures of the regulatory subunit of aspartate kinase from Mtb alone (referred to as MtbAKβ) and in complex with threonine (referred to as MtbAKβ-Thr) at resolutions of 2.6 Å and 2.0 Å, respectively. MtbAKβ is composed of two perpendicular non-equivalent ACT domains [aspartate kinase, chorismate mutase, and TyrA (prephenate dehydrogenase)] per monomer. Each ACT domain contains two α helices and four antiparallel β strands. The structure of MtbAKβ shares high similarity with the regulatory subunit of the aspartate kinase from Corynebacterium glutamicum (referred to as CgAKβ), suggesting similar regulatory mechanisms. Biochemical assays in our study showed that MtbAK is inhibited by threonine. Based on crystal structure analysis, we discuss the regulatory mechanism of MtbAK.
Subject(s)
Amino Acid Sequence , Aspartate Kinase , Chemistry , Genetics , Metabolism , Binding Sites , Cloning, Molecular , Corynebacterium glutamicum , Crystallization , Methods , Crystallography, X-Ray , Enzyme Activation , Enzyme Assays , Escherichia coli , Genetics , Metabolism , Genetic Vectors , Genetics , Metabolism , Lysine , Pharmacology , Molecular Sequence Data , Mycobacterium tuberculosis , Plasmids , Genetics , Metabolism , Prephenate Dehydrogenase , Metabolism , Protein Structure, Secondary , Threonine , Metabolism , PharmacologyABSTRACT
Three hundred cerebrovascular disease (CVD) patients (disease onset <3 days) were evaluated for serum C-reactive protein (CRP) level at admission, and Scandinavian Stroke Scale (SSS) or Oxford Handicap Scale (OHS) at baseline and 3 months. Based on serum CRP levels, the participants were divided into group A [CRP(1.20 ±0.35)mg/L], group B[CRP(4.98 ± 1.08) mg/L] or group C[CRP (19.34±12.27)mg/L]. Our results showed that serum CRP level was positively correlated with SSS (r = 0.39 or0.43, both P<0.01) and OHS (r=0.40 or0.42, both P<0.01) at3 months. Thus, evaluating serum CRP level within 3 clays of disease onset might be helpful in predicting clinical outcomes of CVD patients.