Evaluation of the radioactive Cs concentration in brown rice based on the K nutritional status of shoots.

The radioactive cesium ((134,137)Cs) concentration in brown rice is correlated with that in the straw/husk. The distribution of (134,137)Cs, resembles that of potassium (K), a homologous element of Cs, in the rice plant body. The relative isotopic abundance of (40)K is 0.0117 %; thus, 1 g K contains 30.4 Bq 4°K, and the mass of 4,000 Bq (40)K is 0.0154 g, indicating that the K concentration can be calculated from (40)K concentration. We examined if the radioactive Cs concentration in brown rice can be estimated from (40)K concentrations in straw, and especially might be predicted from the (40)K:(134,137)Cs ratio in straw. We determined the concentrations of (40)K and radioactive Cs in straw and brown rice, and found a strong correlated-equation (y = 72.922 x(-0.759); r = 0.907) between the radioactive Cs concentration in brown rice and the 4°K:(134,137)Cs ratio in straw. The estimated-radioactive Cs concentration in brown rice can be as much as double, depending on the K nutritional status changing the 4°K:(134,137)Cs ratio in straw. We herein propose a nutritional diagnosis that radioactive Cs concentrations in brown rice can be predicted from the 4°K:(134,137)Cs ratio in shoots.

US3 protein kinase of herpes simplex virus type 2 is required for the stability of the UL46-encoded tegument protein and its association with virus particles.

The herpes simplex virus (HSV) US3 gene encodes a serine/threonine protein kinase (PK). Although US3 PK is not essential for virus replication in cell culture, it plays an important role in the regulation of apoptosis in infected cells. However, the role of US3 PK in virus replication and pathogenicity is not well understood. The UL46 gene encodes virion tegument phosphoproteins, the properties and functions of which are poorly understood. In this study, it is shown that the UL46 protein of HSV type 2 (HSV-2) is affected strikingly by the presence of US3 PK. In the absence of US3 PK, UL46 protein was quite unstable, being much more susceptible to degradation. UL46 protein was undetectable in the extracellular virions of US3-deficient virus. Moreover, in vitro kinase assays using recombinant US3 PK show that UL46 protein is phosphorylated by the US3 PK, suggesting that UL46 can be a direct substrate for US3 PK in infected cells. Together, these findings shed new light on the physiological functions of US3 PK.

Conehead wedging screw for distal radius fractures in elderly patients.

A retrospective study was done of the treatment of 76 distal radius fractures in patients older than 55 years, using intrafocal fixation with a conehead wedging screw or a threaded Kirschner wire. The average age of the 57 women and 19 men was 65.9 years. The fracture types classified according to Frykman were: 10 Type I, four Type II, two Type III, 11 Type IV, eight Type V, 10 Type VI, eight Type VII, and 23 Type VIII. The fixation materials used were a threaded Kirschner wire in 37 patients, and a conehead wedging screw in 39 patients. Followups for the two groups were 28 and 26 months, respectively. The conehead wedging screws were superior to the threaded Kirschner wires in maintaining postoperative reduction in displaced, moderately comminuted intraarticular fractures in elderly patients and had a lower complication rate. Intrafocal fixation using a conehead wedging screw may be indicated for treatment of intraarticular fractures with moderate comminution in elderly patients.

Losses in chromosomes 17, 19, and 22q in neurofibromatosis type 1 and sporadic neurofibromas: a comparative genomic hybridization analysis.

Neurofibromatosis type 1 (von Recklinghausen's NF1) is an autosomal dominant disease associated with an increased risk of benign and malignant neoplasia including malignant peripheral nerve sheath tumors (MPNSTs). In this study, we employed comparative genomic hybridization (CGH) to determine changes in the relative chromosome copy number in 24 patients with neurofibromas, including 12 NF1-associated and 12 sporadic cases. Differences in the frequency and distribution of chromosomal imbalances were observed in both NF1-asociated and sporadic neurofibromas. Chromosomal imbalances were more common in NF1-associated tumors than in sporadic neurofibromas. In both groups, the number of losses was higher than the number of gains, suggesting a predominant role of tumor suppressor gene in tumorigenesis. A number of new chromosomal imbalances were noted including chromosomes 17, 19, and chromosome arm 22q, which may be related to oncogenes or tumor suppressor genes in neurofibromas. In NF1-associated neurofibromas, the most frequent losses were found in chromosome 17 (the minimal common regions were 17p11.2-->p13 in nine cases and 17q24-->q25 in six cases) and 19p (19p13.2 in nine cases). In addition, both NF1-associated and sporadic neurofibromas often exhibited losses at chromosome arms 19q and 22q (in NF1 tumors, the minimal common regions were 19q13.2-->qter in seven cases).

Frequent genomic imbalances in chromosomes 17, 19, and 22q in peripheral nerve sheath tumours detected by comparative genomic hybridization analysis.

Comparative genomic hybridization (CGH) was used to detect changes in relative chromosome copy number in 50 cases of peripheral nerve sheath tumour (PNSTs), including nine malignant peripheral nerve sheath tumours (MPNSTs), 27 neurofibromas (with three plexiform neurofibromas) and 14 schwannomas. Chromosome imbalances were frequently detected in benign as well as malignant PNSTs. In both NF1-associated and sporadic MPNSTs, the number of gains was higher than the number of losses, suggesting proto-oncogene activation during MPNST progression. NF1-asociated MPNSTs exhibited gains of chromosomes 17q and X (2/4 cases each), whereas sporadic MPNSTs showed gains of chromosome 4q (3/5 cases). On the other hand, in benign neurofibromas and schwannomas, the number of losses was higher than the number of gains, suggesting a predominant role of tumour suppressor genes in tumourigenesis. Both sporadic and NF1-associated neurofibromas exhibited losses at chromosome 22q in more than 50% of cases. These chromosomal regions may contain common chromosomal abnormalities characteristic of both types of neurofibromas. In NF1-associated neurofibromas, most frequent losses were found in chromosomes 17 [17p11.2-p13 in nine cases (60%); 17q24-25 in 6 cases (40%)] and 19 [19p13.2 in eight cases (53%); 19q13.2-qter in eight cases (53%)], whereas in sporadic neurofibromas and schwannomas losses of chromosomes 17 and 19 were detected in less than 50% of cases. Since this 17p11.2-p13 region is known to contain the tumour suppressor gene TP53, patients with NF1 may be at high risk of malignant neoplasms including MPNSTs. Gains were more frequently detected in plexiform neurofibromas (2/3 cases) than other benign tumours, suggesting proto-oncogene activation in tumourigenesis of plexiform neurofibroma. The significance of the losses of chromosome 19 in these cases is not clear at present, but in NF1-associated neurofibromas, the presence of some as yet unknown tumour suppressor genes on chromosome 19 cannot be ruled out.