Engineering the substrate specificity of toluene degrading enzyme XylM using biosensor XylS and machine learning

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Impalement Injury of the Urinary Bladder: A Case Report

Impalement injury of the urinary bladder, especially secondary to rectal impalement, is extremely rare. In this case, a 31-year-old man sustained a steel pipe impalement injury through his perirectal region. He presented with gross hematuria, abdominal defense, and a penetrating wound. On the basis of the computed tomography findings and abdominal defense, we suspected a through-and-through bladder perforation from the rectal space to the intraperitoneum. Laparotomy revealed a through-and-through bladder perforation as well as damage to the right ureter, 3 distinct ileal injuries, and rectal anterior, anal, and right seminal vesicle injuries. Surgical repair of each damaged site was undertaken. The prompt diagnosis and surgical repair ensured good postoperative recovery

Preventive effects of metallothionein against DNA and lipid metabolic damages in dyslipidemic mice under repeated mild stress

The effects of repeated mild stress on DNA and lipid metabolic damages in multiple organs of dyslipidemic mice, and the preventive role of metallothionein (MT) were investigated. Female adult wild-type and MT-null mice fed high-fat diet (HFD) or standard diet (STD) were repeatedly subjected to fasting or restraint for three weeks. The liver, pancreas, spleen, bone marrow and serum samples were taken for evaluating DNA damage, MT, glutathione (GSH), corticosterone, carnitine and adiponectin. Body weights of restraint groups were reduced with the intensity of stress increased, even if the energy intakes were higher than those of STD group. Hepatic GSH levels were reduced in HFD control group and were further reduced in stress groups, especially in restraint groups, while the hepatic MT and serum corticosterone levels were increased in concert with the intensity of stress. Cellular DNA damages were generally increased by the restraint stress, especially in MT-null mice. Hepatic carnitine levels of MT-null mice were markedly lower than those of wild-type mice. The data suggest that MT plays a preventive role by acting as an antioxidant in corporation with GSH decreased by repeated stress and that MT may be an essential factor for inducing carnitine under the stress

Unleashing floret fertility in wheat through the mutation of a homeobox gene

Floret fertility is a key determinant of the number of grains per inflorescence in cereals. During the evolution of wheat (Triticum sp.), floret fertility has increased, such that current bread wheat (Triticum aestivum) cultivars set three to five grains per spikelet. However, little is known regarding the genetic basis of floret fertility. The locus Grain Number Increase 1 (GNI1) is shown here to be an important contributor to floret fertility. GNI1 evolved in the Triticeae through gene duplication. The gene, which encodes a homeodomain leucine zipper class I (HD-Zip I) transcription factor, was expressed most abundantly in the most apical floret primordia and in parts of the rachilla, suggesting that it acts to inhibit rachilla growth and development. The level of GNI1 expression has decreased over the course of wheat evolution under domestication, leading to the production of spikes bearing more fertile florets and setting more grains per spikelet. Genetic analysis has revealed that the reduced-function allele GNI-A1 contributes to the increased number of fertile florets per spikelet. The RNAi-based knockdown of GNI1 led to an increase in the number of both fertile florets and grains in hexaploid wheat. Mutants carrying an impaired GNI-A1 allele out-yielded WT allele carriers under field conditions. The data show that gene duplication generated evolutionary novelty affecting floret fertility while mutations favoring increased grain production have been under selection during wheat evolution under domestication

PLENTY, a hydroxyproline O-arabinosyltransferase, negatively regulates root nodule symbiosis in Lotus japonicus

Legumes can survive in nitrogen-deficient environments by forming root-nodule symbioses with rhizobial bacteria; however, forming nodules consumes energy, and nodule numbers must thus be strictly controlled. Previous studies identified major negative regulators of nodulation in Lotus japonicus, including the small peptides CLAVATA3/ESR (CLE)-RELATED-ROOT SIGNAL1 (CLE-RS1), CLE-RS2, and CLE-RS3, and their putative major receptor HYPERNODULATION AND ABERRANT ROOT FORMATION1 (HAR1). CLE-RS2 is known to be expressed in rhizobia-inoculated roots, and is predicted to be post-translationally arabinosylated, a modification essential for its activity. Moreover, all three CLE-RSs suppress nodulation in a HAR1-dependent manner. Here, we identified PLENTY as a gene responsible for the previously isolated hypernodulation mutant plenty. PLENTY encoded a hydroxyproline O-arabinosyltransferase orthologous to ROOT DETERMINED NODULATION1 in Medicago truncatula. PLENTY was localized to the Golgi, and an in vitro analysis of the recombinant protein demonstrated its arabinosylation activity, indicating that CLE-RS1/2/3 may be substrates for PLENTY. The constitutive expression experiments showed that CLE-RS3 was the major candidate substrate for PLENTY, suggesting the substrate preference of PLENTY for individual CLE-RS peptides. Furthermore, a genetic analysis of the plenty har1 double mutant indicated the existence of another PLENTY-dependent and HAR1-independent pathway negatively regulating nodulation

The Anti-Inflammatory Effects of Ulinastatin in Trauma Patients with Hemorrhagic Shock

We investigated the use of ulinastatin in association with the suppression of polymorphonuclear leukocyte elastase (PMNE), tumor necrosis factor alpha (TNF-α) and interleukin 6 (IL-6), and its effects on the prognosis of patients with traumatic hemorrhagic shock. Nineteen patients who visited the emergency department for traumatic hemorrhagic shock were enrolled. Eleven patients were randomly selected to receive a total of 300,000 IU of ulinastatin. Measurements of serum PMNE, TNF-α and IL-6 were taken before ulinastatin treatment at 24 hr, two days, three days, and seven days after admission. We compared the Systemic Inflammatory Response Syndrome scores, Multiple Organ Dysfunction Syndrome scores and Acute Physiology, age, Chronic Health Evaluation III scores of the control and ulinastatin groups. There were no significant differences in baseline values, laboratory data, treatment or mortality between the two groups. The serum PMNE levels in the ulinastatin group were lower than in the control group on the second hospitalized day. Serum TNF-α and IL-6 levels in the ulinastatin group decreased 24 hr after admission but had no significance. It is suggested that ulinastatin treatment could decrease the serum PMNE levels in trauma patients with hemorrhagic shock at 48 hr after treatment