Search

Purpose: This study was performed to propose a strategy for repeat laparoscopic liver resection (RLLR) and investigate the preoperative predictive factors for RLLR difficulty., Methods: Data from 43 patients who underwent RLLR using various techniques at 2 participating hospitals from April 2020 to March 2022 were retrospectively reviewed. Surgical outcomes, short-term outcomes, and feasibility and safety of the proposed techniques were evaluated. The relationship between potential predictive factors for difficult RLLR and perioperative outcomes was evaluated. Difficulties associated with RLLR were analyzed separately in two surgical phases: the Pringle maneuver phase and the liver parenchymal transection phase., Results: The open conversion rate was 7%. The median surgical time and intraoperative blood loss were 235 min and 200 mL, respectively. The Pringle maneuver was successfully performed in 81% of patients using the laparoscopic Satinsky vascular clamp (LSVC). Clavien-Dindo class ≥III postoperative complications were observed in 12% of patients without mortality. An analysis of the risk factors for predicting difficult RLLR showed that a history of open liver resection was an independent risk factor for difficulty in the Pringle maneuver phase., Conclusion: We present a feasible and safe approach to address RLLR difficulty, especially difficulty with the Pringle maneuver using an LSVC, which is extremely useful in RLLR. The Pringle maneuver is more challenging in patients with a history of open liver resection., (© 2023. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)

Among the various causes of intraoperative neurosurgical complications, a major arterial injury is one of the most devastating. Herein, the authors present a case of a 76-year-old patient who underwent removal of a craniopharyngioma via the pterional approach and experienced severe damage of her sclerotic left internal carotid artery because it was retracted excessively by a brain spatula, which resulted in complete sacrifice of the vessel. Despite stable parameters on intraoperative monitoring of motor evoked potentials and sufficient collateral blood flow, confirmed by Doppler flowmetry, a large infarct in the left cerebral hemisphere was noted after surgery. Although retraction of movable arteries, veins, and cranial nerves can often be done safely during neurosurgical procedures for effective exposure of the operative field, forced displacement of a sclerotic internal carotid artery in its paraclinoid portion anchored to the fixed distal dural ring should definitely be avoided because it poses a significant risk of major vessel damage., (© 2023. Springer Nature Switzerland AG.)

Introduction: Although pancreatectomy with lymph node (LN) and nerve plexus dissection has usually been performed for pancreatic cancer, recent randomized controlled trials have questioned its survival benefits. However, superior mesenteric artery (SMA) LN dissection has still been included in standard treatment guidelines., Methods: A total of 94 patients who underwent pancreaticoduodenectomy for resectable pancreatic cancer without LN enlargement around the SMA on imaging were identified between 2008 and 2017. Disease-free survival (DFS), overall survival (OS), and complications were compared between those with LN and hemicircumferential nerve plexus dissection around the SMA (SMA ly+) and those without thorough LN and nerve plexus dissection around the SMA (SMA ly-) after adjusting for major prognostic factors., Results: A total of 78 and 16 patients with SMA ly+ and SMA ly- were identified, respectively. Our data demonstrated no difference in DFS and OS rates between both groups (P = 0.18 and 0.83, respectively). Patients with SMA ly+ had significantly more complications, particularly severe diarrhea, compared to those with SMA ly- (P = 0.001)., Conclusion: LN and nerve plexus dissection around the SMA did not prolong survival and significantly increased the frequency of severe diarrhea, suggesting that performing in all cases carries less practical significance.

Background: The number of elderly patients with aneurysmal subarachnoid hemorrhage (SAH) is increasing. Although advanced age is one of the recognized risk factors for poor outcome, conservative treatment for aneurysmal subarachnoid hemorrhage cannot provide satisfactory outcome in elderly patients. The aim of this study is to assess the outcome in patients aged 90 or older, for whom ruptured aneurysms were treated by clipping., Methods: We retrospectively reviewed the medical records of non-traumatic SAH patients who were hospitalized at the Chiba Neurosurgical Clinic between 2004 and 2013. Of the 702 patients, 8 patients (1.1 %) were aged 90 or older. Of them, four underwent clipping surgery and the other four died or were managed conservatively. Their preoperative conditions were evaluated with the World Federation of Neurosurgical Societies Grading Scale of SAH, and the Fisher classification was used to assess the bleeding severity. The location of the ruptured aneurysm was determined by three-dimensional computed tomographic angiography or cerebral angiography. The Glasgow Outcome Scale evaluation was assigned at discharge., Results: Four patients (four female, all WFNS grade 1), aged 90 or older, underwent clipping surgery. Fisher classification was three in two patients and four in the other two. Location of the ruptured aneurysm was internal carotid artery in two, anterior communicating artery in one, and posterior inferior cerebellar artery in one patient. Two of these four patients had a favorable outcome., Conclusions: We propose that advanced age alone does not exclude suitable surgical clipping in patients with aneurysmal rupture in the tenth decade of life.

Background: Paraclinoid carotid aneurysm is widely treated with coil embolization. However, all paraclinoid carotid aneurysms cannot be obliterated by the endovascular approach., Methods: Our direct surgical procedure was presented. The clinical data of surgically treated paraclinoid carotid aneurysms were retrospectively reviewed., Results: One hundred ninety paraclinoid carotid aneurysms in 181 patients were directly obliterated at the Shinshu University Hospital and its affiliated hospitals between 1991 and 2013., Conclusions: Direct surgical repair of the paraclinoid carotid aneurysm is still useful, even in the era of endovascular treatment.

Background: A child's body size is not accurately reflected by volume CT dose index (CTDIvol) and dose-length product (DLP). Size-specific dose estimation (SSDE) was introduced recently as a new index of radiation dose. However, it has not yet been established as a diagnostic reference level (DRL)., Objective: To calculate the SSDE of abdominal/pelvic CT and compare the SSDE with CTDIvol. To calculate the DRLs of CTDIvol and SSDE. Our hypotheses are: SSDE values will be greater than CTDIvol, and our DRL will be smaller than the known DRLs of other countries., Materials and Methods: The CTDIvol and DLP of 117 children who underwent abdominal/pelvic CT were collected retrospectively. The SSDE was calculated from the sum of the lateral and anteroposterior diameters. The relationships between body weight and effective diameter and between effective diameter and CTDIvol/SSDE were compared. Further, the local DRL was compared with the DRLs of other countries., Results: Body weight and effective diameter and effective diameter and SSDE were positively correlated. In children ages 1, 5 and 10 years, the SSDE is closer to the exposure dose of CTDIvol for the 16-cm phantom, while in children ages 15 years, the SSDE falls between CTDIvol for the 16-cm phantom and that for the 32-cm phantom. The local DRL was lower than those of other countries., Conclusion: With SSDE, the radiation dose increased with increasing body weight. Since SSDE takes body size into account, it proved to be a useful indicator for estimating the exposure dose.

Background: Recently, computed tomography (CT) has been used to diagnose fetal skeletal dysplasia. However, no surveys have been conducted to determine the radiation exposure dose and the diagnostic reference level (DRL)., Objective: To collect CT dose index volume (CTDIvol) and dose length product (DLP) data from domestic hospitals implementing fetal skeletal 3-D CT and to establish DRLs for Japan., Materials and Methods: Scan data of 125 cases of 20 protocols from 16 hospitals were analyzed. The minimum, first-quartile, median, third-quartile and maximum values of CTDIvol and DLP were determined. The time-dependent change in radiation dose setting in hospitals with three or more cases with scans was also examined., Results: The minimum, first-quartile, median, third-quartile and maximum CTDIvol values were 2.1, 3.7, 7.7, 11.3 and 23.1 mGy, respectively, and these values for DLP were 69.0, 122.3, 276.8, 382.6 and 1025.6 mGy·cm, respectively. Six of the 12 institutions reduced the dose setting during the implementation period., Conclusions: The DRLs of CTDIvol and DLP for fetal CT were 11.3 mGy and 382.6 mGy·cm, respectively. Institutions implementing fetal CT should use these established DRLs as the standard and make an effort to reduce radiation exposure by voluntarily decreasing the dose.

Background: Clinical use of 3D CT for fetal skeletal malformations is controversial., Objective: The purpose of this study was to evaluate the efficacy of fetal 3D CT using three protocols with different radiation doses and through comparing findings between fetal CT and conventional postnatal radiographic skeletal survey., Materials and Methods: Seventeen fetuses underwent CT for suspected skeletal dysplasia. A relay of three CT protocols with stepwise dose-reduction were used over the study period. The concordance between the CT diagnosis and the final diagnosis was assessed. Ninety-three radiological findings identifiable on radiographs were compared with CT., Results: Fetal CT provided the correct diagnosis in all 17 fetuses, the detectability rate of cardinal findings was 93.5 %. In 59 % of the fetuses an US-based diagnosis was changed prenatally due to CT findings. The estimated fetal radiation dose in the final protocol was 3.4 mSv (50 %) of the initial protocol, and this dose reduction did not result in degraded image quality., Conclusion: The capability of fetal CT to delineate the skeleton was almost the same as that of postnatal skeletal survey. The perinatal management was altered due to these more specific CT findings, which aided in counseling and in the management of the pregnancy.

Purpose: We previously demonstrated that hepatic ischemia and reperfusion (I/R) injury increased liver metastasis and cancer growth of RCN-H4 cells. Using a rat model of hepatic I/R-induced liver metastasis, we investigated the metastasis-suppressing effect of polysaccharide-K (PSK), a biological response modifier composed of protein-bound polysaccharide., Methods: Fischer rats underwent 60 min of 70% partial hepatic ischemia. After 60 min of reperfusion, rat colon adenocarcinoma cells (RCN-H4) were inoculated intrasplenically. PSK was administered orally before I/R, after I/R, or before and after I/R. The weights of metastatic lesions of the liver or the numbers of liver metastatic nodules were determined on day 21. The effect of PSK on angiogenesis was studied by a rat cornea model using RCN-H4 cells or a vascular endothelial growth factor (VEGF)-containing pellet and an in vitro VEGF-induced endothelial cell migration assay., Results: PSK administration significantly (p < 0.05) suppressed the I/R-induced increase in hepatic metastasis of RCN-H4 cells. The suppression of I/R-promoted metastasis was observed irrespective of the timing of administration. Furthermore, PSK significantly suppressed angiogenesis induced by RCN-H4 cells (p < 0.05) and the VEGF pellet (p < 0.01). PSK significantly suppressed the VEGF-induced migration of vascular endothelial cells (p < 0.05)., Conclusion: PSK may suppress metastasis induced by hepatic I/R. The suppression of angiogenesis by PSK may be one of the mechanisms of the inhibition of hepatic metastasis.

In vivo imaging of reactive small molecule metabolites with high spatial resolution and specificity could give clues to understanding pathophysiology of various diseases. We herein applied time of flight-secondary ion mass spectrometry (TOF-SIMS) to newly developed silver-deposited plates that were stamped on mouse tissues, and succeeded in visualization of halide (Cl(-), Br(-), and I(-)) and pseudohalide thiocyanate (SCN(-)) anions, a class of substrates for neutrophils/eosinophil peroxidases to produce hypohalous acids (HOX/OX(-) mixture; X: (pseudo)halides), as well as hydrogen sulfide (H(2)S). Forty-micrometer frozen mouse kidney sections on cover glasses were attached to 37 °C preheated silver-deposited plates and incubated at -10 °C for 1 h. After sputter cleaning to remove surface contaminants, the plates were analyzed by TOF-SIMS to identify distribution of Br(-), AgBr(2)(-), I(-), AgI(2)(-), SCN(-), as well as S(2-) and AgS(-) as products of tissue-derived H(2)S. Br(-), AgBr(2)(-), I(-), and SCN(-) anions were mainly distributed in core regions including the inner medulla and inner stripe of the outer medulla (except for I(-)), rather than outer regions such as the cortex and outer stripe of the outer medulla. AgI(2)(-) anion was spread over the whole kidney, although its levels were relatively low. In contrast, S(2-) and AgS(-) anions were mainly present in the outer regions. To our knowledge, this is the first imaging study to reveal the distribution of (pseudo)halides and H(2)S in animal tissue sections.

To clone new replication origin(s) activated under RNase H-defective (rnh-) conditions in Escherichia coli cells, whole chromosomal DNA digested with EcoRI was to with a Kmr DNA fragment and transformed into an rnh- derivative host. From the Kmr transformants, we obtained eight kinds of plasmid-like DNA, each of which contained a specific DNA fragment, termed "Hot", derived from the E. coli genome. Seven of the Hot DNAs (HotA-G) mapped to various sites within a narrow DNA replication termination region (about 280 kb), without any particular selection. Because Hot DNA could not be transformed into a mutant strain in which the corresponding Hot region had been deleted from the chromosome, the Hot DNA, though obtained as covalently closed circular (ccc) DNA, must have arisen by excision from the host chromosome into which it had initially integrated, rather than by autonomous replication of the transformed species. While Hot DNA does not have a weak replication origin it does have a strong recombinational hotspot active in the absence of RNase H. This notion is supported by the finding that Chi activity was present on all Hot DNAs tested and no Hot-positive clone without Chi activity was obtained, with the exception of a DNA clone carrying the dif site.

The yeast genome has DNA replication fork blocking sites, that we have named sog sites, in the ribosomal RNA gene (rDNA) cluster. These are located at the 3' end of the 35S rRNA transcription unit and they block replication fork movement in a direction opposite to that of RNA polymerase I. We cloned this replication blocking site into a YEp-type plasmid and analyzed DNA replication intermediates, using two-dimensional (2D) agarose gel electrophoresis. The blocking activity remained even on a plasmid not involved in 35S rRNA transcription and inhibited fork movement in the same polar fashion as on the yeast chromosome. To define the site further, smaller fragments were subcloned into the YEp-type plasmid. A small 109 bp region exhibited sog activity and was located near the enhancer region for 35S rRNA transcription. It overlaps an essential element of the recombinational hot spot HOT1.

A double mutant of Escherichia coli K12 which carries a conditional lethal mutator mutation, dnaQ49 (Horiuchi et al. 1978), and a DNA polymerase III-deficient mutation, dnaE486 (Wechsler and Gross 1971), was found to be more thermolabile than was either of the dnaQ49 or dnaE486 single mutants. The double mutant is able to grow at 28 degrees C but not at 30 degrees C. Under the restrictive conditions DNA synthesis, but not protein synthesis, of the double mutant was suppressed. All the other combinations of dnaQ and dnaE mutation alleles tested so far rendered the cells thermolabile. A dnaZ mutation exerted a similar effect on the dnaQ strain. However, when non-specific temperature-sensitive growth mutations were combined with the dnaQ49 mutation, no such increase in thermosensitivity was observed. There is a possibility that the product of the dnaQ gene interacts directly with the DNA replicating enzyme complex.

A 4.32 kb DNA fragment, on which the DNA replication terminus (terR) site of plasmid R 6K was located, was inserted into the unique EcoRI site of plasmid pUC9. To detect replication intermediate molecules with a replication fork halted at the terR site, a cell DNA extract was digested with EcoRI, electrophoresed through an agarose gel and stained with ethidium bromide. In addition to two major bands, one derived from vector DNA and the other from the ter insert fragment, two extra minor bands were detected. Following DNA-DNA hybridization and electron microscopic observation we concluded that the two minor bands corresponded to the two Y-shaped molecules, produced from the theta-shaped intermediate molecules by EcoRI digestion.

The nucleotide sequences of the recessive dnaQ49 and the dominant mutD5 mutator were determined. The dnaQ49 mutator has a single base substitution in the dnaQ gene, thus causing one amino acid change, 96Val (GTG)----Gly (GGG), in the DnaQ protein (epsilon subunit of DNA polymerase III holoenzyme). The mutD5 mutator possesses two base substitutions in the same gene, resulting in two amino acid changes, 73Leu (TTG)----Trp (TGG) and 164Ala (GCA)----Val (GTA), which were designated the mutD52 and mutD51 mutations, respectively. Construction of chimaeric genes carrying one or two of these mutations revealed: either mutD51 or mutD52 alone causes the dominant mutator phenotype when present in a multi-copy plasmid; mutator phenotype when present in a low-copy plasmid; the dominant mutD51 mutator activity is suppressed by the dnaQ49 mutation when both mutations are present in the same gene. Based on these findings, we devised a model for the action of these mutators.

The Escherichia coli mutator gene mutT, which causes A:T----C:G transversion, was cloned in pBR 322. mutT+ plasmids carry a 0.9 kb PvuII DNA fragment derived from the E. coli chromosome. Specific labelling of plasmid-encoded proteins by the maxicell method revealed that mutT codes for a polypeptide of about 15,000 daltons. The protein was overproduced when the mutT gene was placed under the control of the lac regulatory region on a multicopy runaway plasmid. The nucleotide sequence of the mutT gene was determined by the dideoxy method.

We report a new tRNA(1Asp) gene near the dnaQ gene, which is located at 5 min on the Escherichia coli linkage map. We named it aspV. The sequence corresponding to the mature tRNA is identical with that of the two previously identified tRNA(1Asp) genes (aspT and aspU), but there is no homology in the sequences of their 3'- and 5'-flanking regions.

Mutants of Escherichia coli completely deficient in RNase H activity were isolated by inserting transposon Tn3 into the structural gene for RNase H, rnh, and its promoter. These rnh- mutants exhibited the following phenotypes; (1) the mutants grew fairly normally, (2) rnh- cells could be transformed with ColE1 derivative plasmids, pBR322 and pML21, though the plasmids were relatively unstable, under non selective conditions, (3) rnh- mutations partially suppressed the temperature-sensitive phenotype of plasmid pSC301, a DNA replication initiation mutant derived from pSC101, (4) rnh- mutations suppressed the temperature-sensitive growth character of dnaAts mutant, (5) rnh- cells showed continued DNA synthesis in the presence of chloramphenicol (stable DNA replication). Based on these findings we propose a model for a role of RNase H in the initiation of chromosomal DNA replication. We suggest that two types of RNA primers for initiation of DNA replication are synthesized in a dnaA/oriC-dependent and -independent manner and that only the dnaA/oriC-dependent primer is involved in the normal DNA replication since the dnaA/oriC independent primer is selectively degraded by RNase H.

We have constructed a mini-F derivative (pKP1013) consisting of a 5.4 kilobase pairs (kb) segment (44.0 to 49.4 kb) of mini-F and fragments carrying the chloramphenicol and spectinomycin resistance genes that originated from the R plasmid NR1. The plasmid pKP1013 replicates autonomously in a manner indistinguishable from that of the parental mini-F. An amber mutant defective in replication has been isolated from pKP1013 by localized mutagenesis using N-methyl-N'-nitro-N-nitrosoguanidine. The virtual absence of incorporation of [3H]-thymidine into the plasmid DNA as well as the kinetics of appearance of plasmid-free segregants suggest that plasmid DNA synthesis is primarily affected under nonpermissive conditions. The amber mutation has been mapped within the 530 base pairs (bp) region that extends from 45.25 (XmaI) to 45.78 Kb (PstI) by extensive analysis of in vitro recombinants constructed from rep+ and rep- plasmids.

DNA sequencing shows that the mutational alteration resulting from an amber-suppressible replication-defective mutation of F plasmid is a single base pair change from C:G to T:A which yields an amber codon in the coding frame for a 29 kd polypeptide located in the minimal replication region. We thus identified the gene indispensable for F DNA replication as the coding frame which encodes a 29 kd polypeptide. We will designate this gene repA.

In order to study the mode of action of the tof gene product, which is an "autorepressor" of the bacteriophage lambda and plasmid lambdadv, we have purified a DNA-binding protein which is specifically produced in bacteria carrying lambdadv. This protein possesses characteristics expected for the product of the tof gene, since it is produced under conditions where cI-repressor is not made, and since it binds to oL and oR operators on the lambda phage genome. The molecular weight of the native protein is 16,000-17,000 daltons, and the monomeric molecular weight as measured by gel electrophoresis in the presence of sodium dodecyl sulfate is about 10,000 daltons. Denaturation and renaturation experiments demonstrated that the native protein is a dimer of 10,000-dalton monomers. The lambdaDNA-specific binding protein is not produced in cells carrying i21dv or ø80dv.

The presumptive tof gene product of Coli phage 434 has been purified from cells carrying lambdaimm434cIdv plasmid known to contain only some of the "early" genes of phage 434 and lambda. It was detected and tentatively identified as tof protein primarily by its ability to specifically bind to phage 434 DNA. The protein has a molecular weight of about 11,000 and requires Mg2+ for specific DNA binding, unlike 434 cI-repressor.

A conditional lethal mutator, dnaQ49, was found in Escherichia coli K12. The dnaQ49 mutation caused stimulation of rifampicin-, nalidixic acid- and streptomycin-resistant mutation frequencies 100 to 2000 fold at 30 degrees C and the frequencies were further increased 50 to 100 fold at 35 degrees C or higher temperatures. Cells carrying dnaQ49 were unable to grow in salt-free L-broth at 44.5 degrees C, and DNA synthesis but not protein synthesis of the cells was suppressed under the restrictive conditions. The dnaQ gene was located at about 5 min on the E. coli linkage map and the order of the genes residing in this region was determined to be ton A-dnaE-metD-dnaQ-pro A.

The uvrD gene of Escherichia coli that controls UV sensitivity and spontaneous mutation frequency has been cloned with phage lambda as vector. The increased sensitivity to ultraviolet light (UV) of uvrD3, uvrE502, recL152, and pdeB41 mutants, high mutability of uvrD3 and pdeB41 mutants, and conditional lethality of strain TS41 that carried pdeB41, polA1, and supl26 mutations were all suppressed by lysogenization of the mutant cells with lambda uvrD+. These results were consistent with the idea that the uvrD, uvrE, recL, and pdeB mutations are alleles of the uvrD gene. In addition to the uvrD gene, lambda uvrD+ carried the corA gene that controls transport of Mg++, Mn++, and Co++ through the cell membrane. Hybrid plasmids carrying both uvrD and corA genes were also constructed by using pKY2289 as a cloning vehicle. Orientational isomers that carried the same 12.0 kb fragment in the opposite direction were equally efficient in complementing the UvrD- as well as CorA- defects of the transformed host cells, suggesting that the DNA insert contains all the genetic signals needed to express the two gene products. Insertion of the gamma delta sequence into recombinant plasmids was performed to generate appropriate restriction endonuclease target sites in the cloned DNA fragments.

Coliphage 434 tof protein was purified to a substantially pure state from lambda imm434 cI dv carrier cells. The minimum molecular weight is 7,500 +/- 500 as estimated by polyacrylamide gel electrophoresis. The amino acid sequence of the nine NH2-terminal residues was determined, by manual Edman degradation of the intact protein, to be Met-Gln-Thr-Leu-Ser-Glu-Arg-Leu-(Lys)-. The purified protein at low concentrations binds specifically to lambda imm434 dv DNA and at high concentrations also binds to lambda imm21 dv and lambda dv DNA. The curve of the specific binding is of Michaelis type, while that of the nonspecific binding is sigmoidal. The specific binding does not show marked temperature dependency at 4 degrees - 37 degrees C. We have analyzed the equilibrium and kinetic data of specific binding. The equilibrium dissociation constant is 1.9 X 10(-11) M at O degree C. The association rate constant and the dissociation rate constant are 1.1-2.9 X 10(8) M-1s-1 and 2.7 X 10(-3)s-1, respectively, at 0 degrees C. The half life of the tof protein-operator DNA complex is 260 s. These results suggest that the tof protein-operator interaction is much weaker than the interaction between the cI repressor and the operator reported by other workers.