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D K Kim

Publications and source records attributed to D K Kim.

At least 289 records · Page 16Linked to original sources
PubMed1989

[Study on the shape and depth of the occlusal central fissure in permanent molar teeth].

The purpose of this study was to operation the efficient pit and fissure sealing among the caries preventive methods. The authors examined the shape and depth of occlusal fissure in 48 extracted molar teeth and the following conclusions were obtained. 1. The percentages on the occlusal fissure type were 58.0% in I type, 21.0% in U type, 15.0% in K type, 6.0% in V type. 2. In each type, the average mean depth of the occlusal fissure were 1.15mm in I type, 0.53mm in U type. 1.11mm in K type, 0.56mm in V type.

Dental Fissures↗
PubMed1988

Cholera toxin discriminates between murine T lymphocyte proliferation stimulated by activators of protein kinase C and proliferation stimulated by IL-2. Possible role for intracellular cAMP.

The regulation of the activation of T lymphocyte proliferation is not well understood. It is known that the tumor promoter, PMA, which activates protein kinase C (PKC), can induce the proliferation of several murine CTL clones; in combination with calcium ionophores, which raise the level of intracellular Ca2+, PMA can also stimulate the proliferation of several HTL clones. Activation of the TCR is believed to result in the liberation of diacylglycerol, which is an activator of PKC, and inositol 1,4,5-trisphosphate, which stimulates an increase in intracellular levels of calcium. We now report that pretreatment with cholera toxin (CT) inhibits the proliferation of murine T cell clones stimulated through the TCR/CD3 complex. In addition, CT-pretreatment blocks the proliferation of CTL clones activated with PMA or of HTL clones activated with PMA + calcium ionophore. In contrast, CT-pre-treatment inhibits much less effectively (100- to 1000-fold) the proliferation of these T cell clones stimulated with IL-2. Furthermore, activators of PKC, but not IL-2, potentiate the CT-induced cAMP elevation in T cell clones. The ability of CT to inhibit much more effectively the proliferation triggered by putative activators of PKC than that induced by IL-2 may be mediated by cAMP-dependent mechanisms.

Adenosine Monophosphate↗
PubMed1988

Agents that mimic antigen receptor signaling inhibit proliferation of cloned murine T lymphocytes induced by IL-2.

We have shown previously that stimulation of cloned murine T lymphocytes via the TCR inhibits their responsiveness to rIL-2. Signaling via the TCR is believed to result in a variety of biochemical events that include a rise in intracellular free calcium and activation (translocation) of protein kinase C. These two signals also can be generated by calcium ionophores, such as ionomycin, and by activators of protein kinase C, such as PMA. We report here that treatment of cloned murine T lymphocytes with PMA, ionomycin, or the combination led to a dose-dependent inhibition of IL-2-dependent proliferation but did not inhibit lymphokine secretion. Concentrations of PMA and ionomycin that maximally inhibited proliferation stimulated maximal lymphokine secretion and increased mitochondrial activity as assessed by measurement of cleavage of 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium-bromide. Furthermore, PMA, ionomycin, the combination, or immobilized anti-CD3 mAb added after 12 to 16 h of culture with IL-2 could inhibit proliferation. These results demonstrate that PMA and ionomycin mimic stimulation of the TCR by high concentrations of immobilized anti-TCR mAb in that proliferation is inhibited and lymphokine secretion is induced. In addition, PMA or ionomycin could independently inhibit proliferation of some cells. These findings suggest that alternative mechanisms exist to regulate proliferation. Either increased levels of intracellular calcium or the physiologic events corresponding to those induced by PMA can inhibit IL-2-dependent replication of T lymphocytes.

Animals↗
PubMed1988

Detection in human platelets of phospholipase A2 activity which preferentially hydrolyzes an arachidonoyl residue.

It has been generally considered that highly specific liberation of arachidonic acid is induced upon the stimulation of the platelets, although the molecular mechanism of the regulation of its action has not been well understood. An aim of the present study is to clarify the role of phospholipase A2 in the arachidonic acid metabolism within human platelets. Phosphatidylcholine or phosphatidylethanolamine with arachidonate at the sn-2 position of glycerol was cleaved efficiently by phospholipase A2 activity in homogenates as well as in the cytoplasmic fraction of human platelets, leading to the selective liberation of free arachidonate, whereas phospholipids with linoleate were hardly hydrolyzed under the same conditions. Double-reciprocal plots of kinetic data further strengthened the conclusion that human platelet phospholipase A2 showed high selectivity for arachidonoyl residue. This enzyme may play a crucial role in the intracellular metabolism of the arachidonate of phospholipids.

Arachidonic Acid↗
PubMed1987

Antibodies to the L3T4 and Lyt-2 molecules interfere with antigen receptor-driven activation of cloned murine T cells.

When L3T4+ cloned murine helper T lymphocytes (HTL) are stimulated with antigen or immobilized anti-T cell receptor (TCR) monoclonal antibodies (mAb) at concentrations which are optimal for proliferation, anti-L3T4 mAb inhibits activation as measured by proliferation and lymphokine production. Under similar conditions, IL 2-independent proliferation of Lyt-2+ cloned murine cytolytic T lymphocytes (CTL) stimulated by anti-TCR mAb is inhibited by anti-Lyt-2 antibodies. Proliferation of cloned HTL and CTL cells stimulated by IL 2 is not affected by the anti-L3T4 and anti-Lyt-2 mAb. The inhibition of TCR-induced activation of the T cell clones is not due to interference with the binding of the anti-TCR mAb. Stimulation of the TCR has been proposed to induce lymphokine secretion and proliferation by T cells through a pathway involving the activation of protein kinase C and the stimulation of an increase in the concentration of intracellular free calcium. However, proliferation of T cells stimulated by PMA (which activates protein kinase C) plus the calcium ionophore A23187 (which increases the concentration of intracellular free calcium) is not affected by mAb reactive with the Lyt-2 or L3T4 structures. If TCR stimulation does indeed activate T cells by activating protein kinase and increasing intracellular free calcium, then our data suggest that anti-L3T4 and anti-Lyt-2 mAb inhibit TCR-driven proliferation at some step before the activation of protein kinase C and the stimulation of a rise in intracellular free calcium concentration. Our results suggest that anti-L3T4 and anti-Lyt-2 mAb interfere with early biochemical processes induced by stimulation of the TCR. In HTL, which proliferate via an autocrine pathway, anti-L3T4 mAb appears to inhibit proliferation by interfering with signaling events involved in lymphokine production. Inhibition of IL 2-independent proliferation of Lyt-2+ cells by anti-Lyt-2 mAb appears to occur by a different mechanism. The precise molecular basis for the interference of each cell type has not yet been characterized.

Animals↗
PubMed1987

Inhibition of IL 2-driven proliferation of murine T lymphocyte clones by supraoptimal levels of immobilized anti-T cell receptor monoclonal antibody.

Both cloned murine helper T lymphocytes (HTL) and cytolytic T lymphocytes (CTL) proliferated and secreted lymphokines when stimulated with immobilized anti-T cell receptor monoclonal antibody (anti-TCR mAb). However, although proliferation of CTL increased and reached plateau levels as concentrations of anti-TCR mAb were increased, the proliferation of HTL decreased with high concentrations of anti-TCR mAb. A reduction of IL 2-dependent proliferation by CTL was observed when IL 2 was added to cultures of CTL in the presence of high concentrations of anti-TCR mAb, whereas IL 2-independent proliferation appeared to be unaffected by these concentrations of anti-TCR mAb. Inhibition of IL 2-driven proliferation caused by high concentrations of immobilized anti-TCR mAb did not seem to be mediated by soluble factors. Cells continued to express cell surface receptors for IL 2 and transferrin after treatment with immobilized anti-TCR mAb. Inhibition of IL 2-driven proliferation by high concentrations of immobilized anti-TCR mAb may represent a mechanism for regulating the proliferation of T lymphocytes. This inhibitory mechanism is initiated by stimulation of the T cell receptor, in this case by immobilized anti-TCR mAb, and is independent of other cells and factors.

Animals↗
PubMed1987

Susceptibility of astrocytes to class I MHC antigen-specific cytotoxicity.

Cell-mediated immune mechanisms contribute to tissue injury within the central nervous system (CNS) in a number of experimental diseases, including experimental allergic encephalomyelitis and some viral infections, and may mediate lesion formation in multiple sclerosis. We investigated the conditions under which murine astrocytes can become susceptible targets of cytotoxic T cells. We demonstrate that mouse astrocytes in vitro can be susceptible targets of class I major histocompatibility complex (MHC)-specific cytotoxicity mediated by L3 cytotoxic T lymphocytes (CTL). Expression of appropriate class I MHC antigen on the astrocytes is a requirement, because only cells bearing the H-2d phenotype are susceptible to lysis by L3 cells. BALB/c-H-2dm2 astrocytes lacking the specific determinant recognized by L3 cells are not susceptible to lysis. Astrocyte lysis can, however, occur under culture conditions in which MHC antigen expression is immunocytochemically low or undetectable. Cytolysis can be inhibited by pretreatment of the effector L3 cells with either anti-Lyt-2 monoclonal antibody (mAb) or anti-clonotypic mAb and by preincubation of the glial target cells with an appropriate anti-H-2 antibody (anti-H-2Ld). mAb to lymphocyte function-associated antigen does not inhibit cytotoxicity of the L3 clone against glial cells. Knowledge regarding the role of CTL within the CNS, including the surface molecules involved in glial cell lysis, could further the development of immunotherapies designed to effect immune reactivity within the CNS.

Animals↗
PubMed1987

Trends in death and consultation rates of ischemic heart disease in Japan and the risk factors in a rural community.

In Japan, the age-adjusted death rate from ischemic heart disease has decreased for both male and female since 1970, although the rate appears to be slightly affected by mortality from senility without mention of psychosis, "cardiac insufficiency", and sudden death in elderly persons. On the other hand, consultation rate has shown an increase, suggesting an increase in the number of recovered patients and a lengthening in the duration of ischemic heart disease from onset to termination by CCU treatment. A 7.5-year prospective study of ischemic heart disease (myocardial infarction + angina pectoris on effort + sudden death) among residents 40 years and older was conducted at a rural community, Akadani-Ijimino district in Niigata Prefecture. Statistically significant risk factors appeared to be age, hypertension, ECG abnormalities and fuduscopic changes. Even in 1977-1984 when Japanese dietary habits were westernized, neither hyperlipidemia nor obesity was related to the development of ischemic heart disease in this agricultural district. Statistically significant risk ratios were not observed for any nutrient or food, although the ratio for animal fat, calcium, salted vegetables and caloric percent of animal protein was more than one respectively.

Adult↗
PubMed1986

PMA alone induces proliferation of some murine T cell clones but not others.

The responses of cloned murine T cell lines to the phorbol ester, phorbol myristate acetate (PMA), were investigated. PMA alone was able to stimulate proliferation of some clones but not others. Two Lyt-2+, cloned cytolytic T lymphocyte (CTL) lines proliferated in response to stimulation by PMA alone, but several L3T4+, cloned helper T lymphocyte (HTL) lines did not. In contrast, all clones tested released lymphokines in response to stimulation by the combination of PMA and the calcium ionophore A23187. Moreover, all clones proliferated in response to stimulation by the combination of PMA and A23187. The proliferation of HTL in response to PMA + A23187 could be completely inhibited either by cyclosporine A (CsA) or by PC61.5, a monoclonal antibody directed against the murine IL 2 receptor; however, the proliferation of CTL in response to PMA alone was not affected either by CsA or by PC61.5. These results suggest that of the murine T cell clones tested, HTL proliferate in response to stimulation via an IL 2-dependent, autocrine pathway; in contrast, CTL, in addition to an IL 2-dependent pathway, may possess an additional IL 2-independent pathway of proliferation. CTL that proliferate in response to stimulation by PMA alone may be useful models in the study of T cell proliferation.

Animals↗
PubMed1986

Interleukin-2 differentially regulates IL-2 receptors on murine cloned cytolytic and helper T cells.

The effects of interleukin-2 (IL-2) on the expression of IL-2 receptors by cloned cytolytic and helper T lymphocytes were studied using three anti-IL-2 receptor antibodies. IL-2 enhanced the expression of IL-2 receptors on all clones tested. A steep dose-response curve was observed with no measurable effect seen below 2 units/ml and maximal IL-2 receptor expression with greater than 5 units/ml. IL-2 receptor expression peaked 24-48 hr after the addition of IL-2. The subsequent decrease in IL-2 receptor expression correlated with a decrease in the levels of IL-2 remaining in the culture supernatants of cytolytic T lymphocyte cells. Removing residual IL-2 from cultures resulted in the rapid return of IL-2 receptor expression to unstimulated levels. The daily addition of low levels of IL-2 to cultures resulted in the prolonged expression of high levels of IL-2 receptors by non-IL-2-producing cloned cytolytic T cells. Cloned helper T cells which make IL-2 showed the initial increase in IL-2 receptor levels, but the daily addition of IL-2 did not prolong IL-2 receptor expression in these cells. These data suggest that IL-2 receptors on those cells which do not make IL-2 are regulated differently from receptors on cells which themselves make IL-2.

Animals↗
PubMed1981

The seventies evolution in liver surgery for cancer.

During the past decade, one of the major changes in the field of oncology has been in the surgical approach to primary and secondary cancer of the liver. As a result of data and experience gained in liver transplantation programs and with the application of vascular surgical principles, resectability rates have been increased. The present rate of 32% has been achieved with an overall 30-day operative mortality rate of 9%. More sophisticated intraoperative and postoperative supports have been essential in achieving these results. The median operating time is now 4 3/4 hours in length. Complications are minimal. The median postoperative hospital stay is now 13 days. During the past decade, 436 patients with liver tumors were treated by the authors. It has become apparent in this experience and in that reported by others that an increasing number of patients with primary liver cancer or metastatic cancer in the liver can be cured by surgery with minimal operative risk. Adjuvant chemotherapy may increase the salvage rate. Current therapeutic results are best evaluated after staging of the liver disease: Stage I (no involvement of margins of resection, hepatic vascular structures or bile ducts; all gross disease removed): 85% three-year survival estimate, using the Kaplan-Meier method, for individuals with primary liver cancer; 71% for those with metastatic colorectal cancer. Stages II and III (regional or extrahepatic spread): 22% three-year survival for individuals with primary liver cancer but no survivors at two years with metastatic colorectal cancer. These data permit better selection of patients who are most likely to benefit from surgery.

Adolescent↗
PubMed1980

Immunologic function in patients with carcinoma of the pancreas.

The immune fuction of 41 patients with duct cell adenocarcinoma of the pancreas or carcinoma of the periampullary region was studied by skin testing with 2,4-dinitrocholorobenzene and common microbial antigens, in vitro lymphocyte reactivity to mitogens, T-lymphocyte and B-lymphocyte cell counts and measurements of complement levels. Results show that a great proportion of patients had depressed immune function. Depression is particularly severe in lymphocyte reactivity. Positive response to skin tests with a microbial antigen carries a slightly better prognosis. The complement level is usually normal or elevated. Correlation between immune function, prognosis and tumor resectability in individual patients is generally poor.

Adenocarcinoma↗
PubMed1980

The two stage provocative test for pancreatic disease by serum enzyme measurements.

The pancreas can be studied for obstructive disease by measuring serum lipase levels in the two stage provocative test. The test is nonspecific but noninvasive and applicable to all stages of pancreatic diseases. In this test, the pancreas is stimulated twice in two hour intervals before measuring the serum enzyme levels: first, with pancreozyin and secretin--the stage 1 test and, second, with pancreozymin, secretin, betazole hydrochloride and morphine sulfate--the stage 2 test. Among the pancreatic enzymes measured, lipase was most reliable. Serum lipase level elevation in the stage 1 test indicates a pancreatic abnormality and it completes the test. Patients who fail to respond to the stage 1 test have either a normal pancreas or pancreatic insufficiency and need the stage 2 test for differential diagnosis. In the stage 2 test, the serum lipase level is elevated in patients with a normal pancreas but not in those with pancreatic insufficiency. As a preliminary study, ten patients with carcinoma of the pancreas, two with pancreatitis and ten in the control group were studied. All patients with a known pancreatic disease demonstrated an abnormality in the test. Two of ten in the control group also had abnormal results. The two stage provocative test may be used prior to undertaking more invasive examinations, such as an arteriogram, in patients who are suspected of having pancreatic disease, yet other tests have failed to indicate it.

Amylases↗
PubMed1978

Major hepatic resection for neoplasia: personal experience in 108 patients.

One hundred eight patients have undergone major hepatic resection by the senior author during the eight year period April 1970 to April 1978. Primary liver cancer was present in 36; metastatic colorectal cancer in 25, miscellaneous metastatic cancers in 15, hepatoblastoma in 5, gallbladder cancer in 4, and bile duct cancer in 3. Benign tumors, principally giant hemangioma, were resected in 20 additional patients. The 30 day operative mortality rate was 9% overall. Prior to 1975, 41 of the resections were done using the vascular isolation perfusion technique. The operative mortality rate of 17% for this technique is a reflection of early experience and the advanced stage of disease of many patients. The operative mortality for the standard resection has been only 4%. Subphrenic abscess has developed in only 13% of patients during the past three years. Postoperative hospitalization has been shortened, being a median of 13 days. The resectability rate for malignant disease was 33%. Forty-six percent of the resections were performed with curative intent. Fifty-four per cent were palliative, performed in individuals with regional spread or distant metastasis. After curative surgery, three year survival was 88% for individuals with primary liver cancer and 72% with metastatic colorectal cancer. After palliative resection, the rates were 31 and 0%, respectively. The three year survival rate is 46% overall, being 81% for the curative resection group and 18% for the palliative group. Tumor markers proved useful in monitoring patients after hepatic resection.

Bile Duct Neoplasms↗
PubMed1977

Limb-preserving vascular surgery for malignant tumors of the lower extremity.

Monobloc soft-part resections have been carried out with excision of segments of the illac and femoral vessels in seven patients with cancer in the lower extremity. Amputation would have been necessary otherwise. Ischemic loss of the extremity did not occur. In four of the earlier patients, vascular reconstruction was not performed, and postoperative lymphedema was a major complication. In the recently treated three patients, complete reconstitution of the circulation by simultaneous arterial and venous grafting permitted smooth postoperative recovery and absence of notable edema. Creation of a distal arteriovenous fistula appears essential to maintain venous patency. Six of the seven patients are alive at six months, 1, 3, 4, 7, and 18 years, respectively. One patient died of pulmonary metastases at three years after operation. Two patients developed local recurrences requiring limb disarticulation, both in the earlier group in which excision and grafting of both artery and vein was not done. It is concluded that excision and simultaneous reconstruction of major blood vessels can extend the scope of soft-part resections for cancer of the extremities, offering opportunities for preservation of limbs that would otherwise require amputation for control of disease.

Adult↗
PubMed1977

Surgical management of hepatic vein occlusion by tumor: Budd-Chiari syndrome.

We report new operative approaches to the treatment of hepatic vein occlusion due to malignant tumors in the liver and their results in four patients. Two patients had hepatoma, one had metastatic melanoma, and one had metastatic leiomyosarcoma. All of them had abdominal pain, abdominal distention secondary to ascites, and massive hepatomegaly. The right lobe and medial segment of the left lobe of the liver were involved in three patients, and the involvement was diffuse throughout the liver in one. Hepatic veins were occluded completely in one patient, and two of three veins were occluded in the others. Two patients were treated by hepatic resection and removal of tumor thrombus from the hepatic vein under isolation-perfusion technique. They lived 18 and six months, respectively, without recurrence of Budd-Chiari syndrome. Tumors in the other patients were diffuse and could not be resected. The hepatic artery was ligated and chemotherapy was given postoperatively. Ascites and abdominal pain disappeared completely in one, who survived 17 months. The other patient had significant palliation and lived nine months.

Antineoplastic Agents↗