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Biomedical subjects

S Kusaka

Publications and source records attributed to S Kusaka.

At least 55 records · Page 3Linked to original sources
PubMed1996

Condensation of silicone oil on the posterior surface of a silicone intraocular lens during vitrectomy.

PURPOSE: We experienced a complication caused by the condensation of silicone oil on the surface of a silicone intraocular lens during pars plana vitrectomy. METHODS: A 74-year-old woman with proliferative vitreoretinopathy underwent a pars plana vitrectomy in her left eye, which contained silicone oil and a silicone intraocular lens. RESULTS: Intraoperatively, condensation of silicone oil on the posterior surface of a silicone intraocular lens caused a loss of visibility during fluid/gas exchange. The silicone oil droplets could not be removed. CONCLUSION: Surgeons should avoid direct contact of silicone oil with silicone intraocular lens.

Aged↗
PubMed1996

Retinal detachments with crescent-shaped retinal breaks in patients with atopic dermatitis.

BACKGROUND: There has been increasing number of reports of retinal detachments associated with atopic dermatitis. However, little is known about the etiology of these rhegmatogenous detachments. The authors encountered two patients with retinal detachments associated with a crescent-shaped retinal break combined with another break located at or anterior to the ora. METHODS: Preoperative and intraoperative findings in these cases were evaluated. RESULTS: In both cases, vitreoretinal adhesions were observed on the anterior and posterior edges of a crescent-shaped retinal break. Vitreous traction between the crescent-shaped retinal break and the break located at or anterior to the ora was also observed. No abnormalities were detected in the choroid in either case. A possible causative factor for the retinal detachments in these patients was the habit of rubbing and slapping their faces, apparently to alleviate extreme itching. CONCLUSION: Crescent-shaped retinal breaks, which were different from conventional horseshoe tears or atrophic retinal holes, were an interesting and unusual feature of two patients with atopic dermatitis and rhegmatogenous retinal detachments. These crescent-shaped retinal breaks may have been caused by ocular contusion.

Adolescent↗
PubMed1995

Microchimerism linked to cytotoxic T lymphocyte functional unresponsiveness (clonal anergy) in a tolerant renal transplant recipient.

A patient was found to be functionally tolerant of a maternal kidney allograft as evidenced by good graft function 5 years after cessation of all immunosuppressive drug therapy. Despite normal in vitro proliferative and IL-2 responses, patient anti-donor 1 degree MLR cultures yielded little donor-specific CTL activity in either bulk or limiting dilution analysis (LDA) cultures. Using polymerase chain reaction, the patient's PBL and skin were found to contain donor-derived Bw6+ cells. Removal of Bw6+ donor cells from the patient PBL with mAb and immunomagnetic beads before stimulation with donor PBL on day 0 failed to restore donor-specific CTL in either bulk 1 degree MLR or LDA cultures. Restimulation of 1 degree cultures with donor stimulator cells plus exogenous IL-2, however, completely restored anti-donor HLA class I-specific CTL, indicating class I-specific CTL precursors were not clonally deleted. Fresh patient PBL, as well as donor cell-enriched fractions, when added at the initiation of 3 degrees MLR cultures, inhibited the generation of anti-donor CTL, whereas donor cell-depleted fractions did not. The inhibition was cell dose-dependent, was specific for the anti-donor response, and was radioresistant (1200 rad). Thus, the clinical tolerance observed in patients with microchimerism may be due to the presence of veto cells within the circulating donor cell pool.

Base Sequence↗
PubMed1995

Prediction of relapses after interferon-alpha therapy by hepatitis C virus RNA in peripheral blood mononuclear cells.

To investigate the predictive value of hepatitis C virus (HCV)-RNA in peripheral blood mononuclear cells in the response to interferon therapy in patients with chronic hepatitis C, 15 patients with histologically proven chronic active hepatitis and who were positive for serum HCV-RNA were treated with interferon-alpha (6 million units; i.m.) every day for two weeks and then three times a week for 22 weeks. Ten of the 15 patients were responders whose alanine aminotransferase levels decreased to the normal range at the end of interferon therapy. In four of the 10 responders, HCV-RNA was not detected by reverse transcription-polymerase chain reaction in peripheral blood mononuclear cells nor in serum at the end of treatment. These four patients were complete responders, with alanine aminotransferase levels remaining normal for the next 24 weeks. In five of the 10 responders, HCV-RNA was detected in peripheral blood mononuclear cells but not in serum at the end of treatment. All of these relapsed within the next 24 weeks. In the remaining responder, HCV-RNA was detected both in peripheral blood mononuclear cells and in serum at the end of treatment. This responder also had a relapse within the next 24 weeks. Five of the 15 patients were non-responders, in whom HCV-RNA was detected both in peripheral blood mononuclear cells and in serum. Thus, detection of HCV-RNA in peripheral blood mononuclear cells may be a good clinical marker to predict relapse after interferon treatment.

Adult↗
PubMed1995

Products of neutrophil metabolism increase ammonia-induced gastric mucosal damage.

Recent studies have indicated that ammonia is involved in the pathophysiology of Helicobacter pylori-associated gastric mucosal damage. Helicobacter pylori-associated chronic active gastritis is characterized by an invasion of neutrophils. We investigated the interrelationship among hypochlorous acid (oxidant produced by neutrophil), ammonia (product of Helicobacter pylori urease), and monochloramine (product of ammonia and hypochlorous acid) in the development of gastric mucosal damage in rats. Gastric mucosal lesions were produced by exposure of the gastric mucosa to ammonia, urea with urease, or urea with Helicobacter pylori in rats subjected to ischemia. Pretreatment with taurine (scavenger of hypochlorous acid) or antineutrophil serum significantly attenuated gastric mucosal lesions induced by the above test agents. Ammonia-induced gastric mucosal lesions were exacerbated in the presence of hypochlorous acid with concomitant generation of monochloramine. These results suggest that the ammonia, hypochlorous acid, and monochloramine triad may be important in Helicobacter pylori-mediated gastric mucosal damage.

Ammonia↗
PubMed1995

Therapeutic effects of lansoprazole on peptic ulcers in elderly patients.

We studied the effects of lansoprazole on ulcer healing and Helicobacter pylori infection in elderly patients with peptic ulcers. In a group of 24 patients with gastric ulcers, the H. pylori infection rate was 100%. In the course of gastric ulcer healing with famotidine or lansoprazole alone, the H. pylori infection showed no signs of decline. The ulcer healing rates after 8 weeks were similar between the H2-receptor antagonist famotidine (73%), and the proton pump inhibitor lansoprazole (82%). When eradication of H. pylori infection was attempted by concomitant administration of lansoprazole and amoxicillin 500 mg b.i.d. for 2 weeks, the eradication rate was 33% in the group given lansoprazole 30 mg q.d. plus ampicillin 500 mg b.i.d., whereas it was 77% in the group given lansoprazole 30 mg b.i.d. plus ampicillin 500 mg b.i.d. Lansoprazole is considered to be a useful agent for the treatment of patients with peptic ulcers and H. pylori infection and its effectiveness in H. pylori eradication is improved by b.i.d. administration along with ampicillin.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed1994

Effect of gastric mucosal blood flow on the pathogenesis of ammonia in Helicobacter pylori-induced gastric mucosal injury.

PURPOSE: We investigated the effects of the gastric mucosal blood flow on the pathophysiology of ammonia-induced gastric mucosal damage. DESIGN: The study was designed to show whether the damaging effect of ammonia, a product of Helicobacter pylori urease, on the gastric mucosa is increased by the decrease in gastric mucosal blood flow in rats subjected to ischemia. RESULTS: Although ammonium chloride at concentrations of 15-60 mmol/l produced no significant macroscopical lesion in normotensive rats, it caused severe macroscopic hemorrhagic gastric lesions in the stomachs of rats subjected to ischemia. Exposure of the stomach to the combination of ischemia and ammonium chloride (60-600 mmol/l, pH adjusted to 7-9 with sodium hydroxide) produced macroscopic hemorrhagic lesions. However, exposure of the mucosa to the combination of ischemia and sodium hydroxide (60-600 mmol/l, pH was reduced to 7-9 with hydrochloric acid) produced no significant lesions. CONCLUSIONS: These results indicate that the mucosal lesions observed in patients infected with H. pylori are not caused by the alkalinity of H. pylori-produced ammonia and suggest that concomitant infection with H. pylori in the ischemic stomach may lead to the development of ulceration in these patients.

Ammonium Hydroxide↗
PubMed1994

[Rapid growth of eyelid squamous cell carcinoma in elderly patients with multiple cancers].

Two cases of squamous cell carcinoma of the eyelid are reported. Both patients had multiple cancers. Case 1 was an 81-year-old man who had a squamous cell carcinoma on his right upper eyelid and on his right palm, and Bowen's disease in his left thumb. Case 2 was an 87-year-old woman who had a squamous cell carcinoma on her right lower eyelid, an adenocarcinoma in her colon, and a uterus cancer of unknown histology. In spite of their advanced age, the eyelid tumors showed rapid growth in both cases. The reason for this rapid growth was unclear. However, the presence of cancers in other organs may provide clues, because the immunological ability in patients with multiple cancers is considered to be weakened.

Adenocarcinoma↗
PubMed1993

Gastric ammonia has a potent ulcerogenic action on the rat stomach.

BACKGROUND: The pathophysiological mechanism by which Helicobacter pylori induces mucosal injury has not been clarified. The aim of this study was to investigate the role of urea, urease, and ammonia in rat gastric mucosal lesions using an ex vivo chamber model. METHODS: Two groups of rats, normotensive rats and those subjected to ischemia, were studied. The gastric mucosa was examined histologically and macroscopically, and the transmucosal potential difference was measured. RESULTS: Instillation of urea into the stomach generated ammonia in the presence of urease. The amount of ammonia was increased depending on the concentration of urea and was closely associated with the severity of the histological lesions. The exposure of the stomach to 15-60 mmol/L ammonium hydroxide induced both a reduction in transmucosal potential difference and microscopic damage to the gastric mucosa in normotensive rats. Moreover, 15-60 mmol/L ammonium hydroxide produced severe macroscopic gastric lesions in the rats subjected to ischemia. CONCLUSIONS: These results show that ammonia is deleterious to the gastric mucosa and suggest the importance of urea, urease, and ammonia in the pathophysiology of gastric diseases in H. pylori-infected patients.

Action Potentials↗
PubMed1992

Analysis of suppressor T cells induced by donor-specific transfusion (DST): establishment of a human T cell hybridoma producing an antigen-nonspecific suppressor factor.

Formation of suppressor T cells (Ts) induced by donor-specific transfusion (DST) is one of the most commonly suggested mechanisms for the beneficial effect of DST. In this study, we established a human T cell hybridoma derived from the peripheral blood lymphocytes (PBL) of a DST-treated patient, which produced an antigen-nonspecific suppressor factor. Post-DST PBL were fused with an azaguanine-resistant mutant of a human T cell leukemia cell line, CCRF-CEM(AG). After selection and cloning, we established one clone producing the mixed lymphocyte reaction (MLR) inhibitory factor (C524: 18%-43% suppression). Suppressive activity of the supernatant obtained from C524 after activation by PHA was highly augmented (64%-88% MLR suppression). This factor inhibited MLR dose-dependently in an antigen-nonspecific and HLA non-restricted manner. These results indicated that Ts clones could be generated in patients receiving DST and that the immunoregulatory factors produced by activated clones may play a role in the prolongation of renal allograft survival.

Antibody Specificity↗
PubMed1992

Effects of interleukin 2 receptor b chain (P75)-specific monoclonal antibody on the generation of cytotoxic T lymphocytes and suppressor T cells in mixed lymphocyte culture.

The interaction of interleukin 2 (IL-2) with its receptor (IL-2R) plays an essential role in the proliferation and differentiation of T cells. The IL-2R beta-chain is considered to function directly in the intracellular signal transduction. In this study, we investigated using a newly established IL-2R beta-chain-specific monoclonal antibody (MAb) (TU-25) and an IL-2R alpha-chain-specific MAb (H-31). The IL-2-induced proliferation of concanavalin blasts and the mixed lymphocyte reaction (MLR) were suppressed by TU-25 in combination with H-31. This combination had a greater suppressive effect than each of them alone. The generation of cytotoxic T lymphocytes (CTL) using a cell-mediated lympholysis (CML) assay, was not inhibited by TU-25 alone. TU-25 in combination with H-31 suppressed the generation of CTL completely in this assay even if recombinant IL-2 (rIL-2) was added. Although the CTL generation was inhibited, cells that suppressed a fresh MLR were preserved. Our study suggests that the combination of TU-25 with H-31 completely blocks the functional high-affinity binding site of IL-2 but does not inhibit the generation of suppressor cells. This may lead to immunosuppressive therapy using an IL-2R beta-chain-specific MAb in combination with an IL-2R alpha-chain-specific MAb in clinical organ transplantation.

Antibodies, Monoclonal↗