Biomedical subjects

Kei Hayashi

Publications and source records attributed to Kei Hayashi.

10 recordsLinked to original sources

PubMed2005

Inelastic photoemission due to scattering by surface adsorbate vibrations.

By measuring the very low energy photoemission spectra of the CO/Cu(001) surface with a high resolution, we have found the energy loss components due to inelastic scattering of electrons near the Fermi level by the CO vibrational modes. The main energy loss structure appears as a step at 254 meV below the Fermi edge for 12C16O. An isotope shift of the step to 240 meV was observed when 13C18O was adsorbed. This observation confirms that this step arises from the energy loss of photoelectrons near the Fermi level through the excitation of the C-O stretching mode.

Journal Article↗

PubMed2005

[Results of local ablation therapy for liver metastases from colorectal cancer using radiofrequency ablation and microwave coagulation therapy (RFA/MCT)].

UNLABELLED: In addition to hepatectomy and chemotherapy with intra-arterial infusion, local ablation therapy using RFA and MCT has been used for treatment of liver metastases derived from colorectal cancer. We investigated the results of local ablation therapy in such cases conducted at our department. SUBJECTS AND METHODS: This study was conducted in 9 out of 21 patients with liver metastases derived from colorectal cancer, who underwent local ablation therapy with RFA from September 2001. As adjuvant therapy, the divided administration of low-doses CDDP/FU was conducted in all cases. RESULTS: RFA and MCT were used in 9 cases (25 lesions) and in 15 cases (82 lesions), respectively. The three cases of RFA were combined with MCT. The severity of liver metastasis was H1 and H2 in one case each and H3 in seven cases. The tumor diameter was 1.0-4.7 cm (mean, 2.7 cm) and patients underwent cauterization from 1-6 times (mean, 2.4 times). Although there were no critical complications, pyrexia and increased AST/ALT were found. The three-year survival rate was 50%, and thus favorable prognoses were obtained. CONCLUSION: There were no notable complications associated with local ablation therapy for liver metastases derived from colorectal cancer, and this method was thus indicated to be effective for local control in cases in which hepatectomy is impossible.

Aged↗

PubMed2004

Energy loss of photoelectrons by interaction with image charge.

By measuring the photoelectron spectra of the Cu(001) and Cu(110) surfaces excited by tunable-laser photons of very low energy (4.50-4.95 eV), we have found that the photoelectron can lose energy through interaction with its image charge. This energy loss occurs just outside the solid surface and appears as a spike structure at the vacuum edge in the photoemission spectra. The requirement for observing this energy loss structure is the absence of unoccupied states at the vacuum level at the Gamma point to which zero kinetic energy electrons can return.

Journal Article↗

PubMed2003

Evaluation of ligament fibroblast viability in ruptured cranial cruciate ligament of dogs.

OBJECTIVE: To determine fibroblast viability, assess development of apoptosis, and evaluate tissue hypoxia via histochemical, in-situ hybridization, or immunohistochemical staining in ruptured and intact cranial cruciate ligaments (CCLs) of dogs. ANIMALS: 32 dogs with ruptured CCLs, and 8 aged and 19 young dogs with intact CCLs. PROCEDURE: Markers of cell viability (lactate dehydrogenase [LDH]), apoptosis (terminal deoxynucleatidyl transferase-mediated deoxyuridine triphosphate-nick end labeling [TUNEL] method), and hypoxia (hypoxia-inducible factor-1alpha [HIF-1alpha] monoclonal antibody) were applied to CCL specimens; positive cells were assessed objectively (LDH) and subjectively (TUNEL and HIF-1alpha) in the main axial tissue component (core) and synovial intima and subintima (epiligamentous tissue). RESULTS: Viable fibroblasts were seen in all intact and ruptured CCLs. More nonviable cells were found in the core regions of ruptured CCLs and intact CCLs of young dogs than in the epiligamentous regions. Number of nonviable cells in the core region of ruptured CCLs was greater than that in intact CCLs of young and aged dogs, whereas the number in the epiligamentous region was similar in all specimens. The TUNEL and HIF-1alpha staining was only found in the epiligamentous region of ruptured CCLs. CONCLUSIONS AND CLINICAL RELEVANCE: Ruptured CCLs contained a high number of nonviable cells but not a great number of apoptotic cells. Repair processes in the epiligamentous region of the CCL include a metabolic response to hypoxia, suggesting that necrosis of ligament fibroblasts and transformation of surviving cells to a spheroid phenotype may be a response to hypoxia cause by microinjury or inadequate blood flow.

Aging↗

PubMed2002

Healing of subfailure ligament injury: comparison between immature and mature ligaments in a rat model.

This study evaluated biomechanical properties of healing ligament following subfailure (grade II) injury by comparing young and mature animals in a rat lateral collateral ligament (LCL) model. One randomly selected LCL was stretched in situ using a custom designed device in eighteen young (21 days) and eighteen skeletally mature (8 months) male rats. Animals were euthanized at 0, 7, and 14 days post-surgery, and ligament ultimate stress, strain at failure and laxity were determined (n = 6 pairs per group). At time 0 after introduction of stretch injury, ligament laxity was present in both groups. The mature rats had 54 +/- 9% strength of the control while the immature rats had 58 +/- 11% of the strength of the control, representing a consistent and significant injury. The immature and mature ligaments showed similar patterns of cellular damage post-injury and had similar modes of mechanical failure. Ligament laxity decreased in each group as healing time increased, however ligament laxity did not completely recover in either group after 2 weeks of healing. After 7 and 14 days of healing, the mature rats, respectively, had only 63 +/- 14%% and 80 +/- 8% strengths of the controls while the immature rats had 94 +/- 6% and 94 +/- 10%. Hence, mechanical data showed that immature animals recovered their strength after a grade II sprain at a faster rate than mature animals. However, ligament laxity was still present in both groups two weeks after the injury and was not completely removed by growth in the immature group. These findings are clinically relevant since joint laxity after injury is common, and these results may explain the presence of continued instability in a joint injured at a young age. Hence, this study, with a new injury model, showed differences in ligament healing associated with maturity and quantified the clinically observed persistance of ligament laxity.

Age Factors↗

PubMed2002

Subfailure damage in ligament: a structural and cellular evaluation.

Subfailure damage in ligaments was evaluated macroscopically from a structural perspective (referring to the entire ligament as a structure) and microscopically from a cellular perspective. Freshly harvested rat medial collateral ligaments (MCLs) were used as a model in ex vivo experiments. Ligaments were preloaded with 0.1 N to establish a consistent point of reference for length (and strain) measurements. Ligament structural damage was characterized by nonrecoverable difference in tissue length after a subfailure stretch. The tissue's mechanical properties (via stress vs. strain curves measured from a preloaded state) after a single subfailure stretch were also evaluated (n = 6 pairs with a different stretch magnitude applied to each stretched ligament). Regions containing necrotic cells were used to characterize cellular damage after a single stretch. It should be noted that the number of damaged cells was not quantified and the difference between cellular area and area of fluorescence is not known. Structural and cellular damage were represented and compared as functions of subfailure MCL strains. Statistical analysis indicated that the onset of structural damage occurs at 5.14% strain (referenced from a preloaded length). Subfailure strains above the damage threshold changed the shape of the MCL stress-strain curve by elongating the toe region (i.e., increasing laxity) as well as decreasing the tangential modulus and ultimate stress. Cellular damage was induced at ligament strains significantly below the structural damage threshold. This cellular damage is likely to be part of the natural healing process in mildly sprained ligaments.

Algorithms↗

PubMed2002

Evaluation of tartrate-resistant acid phosphatase and cathepsin K in ruptured cranial cruciate ligaments in dogs.

OBJECTIVE: To determine localization of tartrate-resistant acid phosphatase (TRAP) and cathepsin K in ruptured and healthy cranial cruciate ligaments (CCL) in dogs. ANIMALS: 30 dogs with ruptured CCL, 8 aged dogs without ruptured CCL, and 9 young dogs without ruptured CCL. PROCEDURE: The CCL was examined histologically and cells containing TRAP and cathepsin K were identified histochemically and immunohistochemically, respectively. RESULTS: Cathepsin K and TRAP were detected within the same cells, principally within the epiligamentous region and to a lesser extent in the core region of ruptured CCL. Numbers of cells containing TRAP and cathepsin K were significantly greater in ruptured CCL, compared with CCL from young or aged dogs, and numbers of such cells were greater in CCL from aged dogs, compared with those of young dogs. In aged dogs, small numbers of cells containing TRAP and cathepsin K were seen in intact CCL associated with ligament fascicles in which there was chondroid transformation of ligament fibroblasts and disruption of the extracellular matrix. CONCLUSIONS AND CLINICAL RELEVANCE: Ruptured CCL contain greater numbers of cells with the proteinases TRAP and cathepsin K than CCL from healthy, young, or aged dogs. Results suggest that cell-signaling pathways that regulate expression of these proteinases may form part of the mechanism that leads to upregulation of collagenolytic ligament remodeling and progressive structural failure of the CCL over time.

Acid Phosphatase↗

PubMedDate not supplied

Histologic changes in ruptured canine cranial cruciate ligament.

OBJECTIVES: To determine changes to the cells and collagenous and amorphous extracellular matrix (ECM) structure in ruptured canine cranial cruciate ligaments (CCL). STUDY DESIGN: Prospective clinical study. ANIMALS: CCL specimens obtained from 29 dogs with ruptured CCL and 6 young dogs with intact CCL. METHODS: Ligament fibroblast number density and phenotype were determined in the core and epiligamentous regions. ECM birefringence and crimp structure in the core region were also studied. RESULTS: Loss of fibroblasts from the core region of ruptured CCL was seen (P <.001), whereas, in the epiligamentous region, cell number densities were similar in ruptured and intact CCL (P =.7). In ruptured CCL, numbers of typical ligament fibroblasts (fusiform and ovoid cells) were decreased, and numbers of cells exhibiting chondroid transformation (spheroid cells) were increased in the core region (P <.001). Expansion of the volume of the epiligamentous region was also seen, although bridging scar tissue was not seen between the ends of ruptured CCL. The structure of the ECM collagen in the core region was extensively disrupted in ruptured CCL. This was, in part, because of decreased birefringence and elongation of the crimp in the remaining collagen fibers when compared with intact CCL (P <.01). CONCLUSIONS: Extensive alterations to the cell populations and collagenous ECM structure were seen in ruptured CCL. Although a proliferative epiligamentous repair response was seen in ruptured CCL, there was a lack of any bridging scar between the ruptured ends of the CCL. CLINICAL RELEVANCE: The cellular and ECM changes in ruptured CCL that we have described appear to result from the cumulative effects of remodeling and adaptation to mechanical loading and microinjury. Treatment of early cruciate disease in dogs will need to inhibit or reverse these progressive changes to CCL tissue, which are directly associated with partial or complete structural failure of the CCL under conditions of normal activity.

Animals↗

PubMedDate not supplied

Cisterna chyli ablation with thoracic duct ligation for chylothorax: results in eight dogs.

OBJECTIVE: To report use of combined cisterna chyli ablation (CCA) and thoracic duct ligation (TDL) for treatment of spontaneously occurring chylothorax in dogs. STUDY DESIGN: Retrospective study. ANIMALS: Eight dogs with chylothorax. METHODS: TDL was performed through a right caudal intercostal thoracotomy and CCA through a left flank paracostal approach or ventral median celiotomy. Long-term outcome (range, 2-48 months; median, 11.5 months) was evaluated by telephone communication with owners. RESULTS: Seven dogs were free of clinical signs related to chylothorax at last follow-up (range, 4-48 months; median, 15.5 months). One dog was euthanatized 2 months after surgery because of lack of improvement. No major complications occurred from CCA. CONCLUSION: CCA and TDL resolved chylothorax in most dogs (88%). CLINICAL RELEVANCE: CCA combined with TDL may improve the outcome of chylothorax in dogs.

Animals↗

PubMedDate not supplied

Cranial cruciate ligament pathophysiology in dogs with cruciate disease: a review.

Cruciate disease is a common cause of chronic lameness in dogs. Midsubstance rupture of the cranial cruciate ligament (CCL) arises from progressive pathological failure, often under conditions of normal loading in adult dogs with CCL instability. A high risk of rupture is associated with inflammation of the synovium and adaptive or degenerative changes in the cells and matrix of the CCL. In contrast, CCL rupture in puppies is usually associated with traumatic injury and avulsion of the CCL from its sites of attachment.

Age Factors↗