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Y Ko

Publications and source records attributed to Y Ko.

At least 19 recordsLinked to original sources
PubMed1999

Cytokine-inducible growth factor gene expression in human umbilical endothelial cells.

Endothelial cells are known to be involved in different growth promoting processes like angioneogenesis, atherosclerosis or haematopoiesis. A great number of polypeptide growth factors crucial in this context have been isolated and they may be expressed in endothelial cells in either a constitutional or an inducible manner. The aim of the study was to examine the cytokine-inducibility of growth factor gene expression in endothelial cells. As uniform stimulators interleukin 1-alpha (IL-1alpha) and tumour necrosis factor (TNF)-alpha were chosen. Human umbilical arterial endothelial cells (HUAEC) were treated with either IL-1alpha or TNF-alpha and the gene expression of various growth factors was detected by reverse transcription-polymerase chain reaction (RT-PCR). We could demonstrate in HUAEC that stimulation with IL-1alpha- and TNF-alpha led to the mRNA expression of basic fibroblast growth factor (bFGF) and vascular endothelial growth factor (VEGF) which are crucial in the process of angioneogenesis and atherosclerosis as well as of the granulocyte-colony stimulating factor (G-CSF), granulocyte macrophage-colony stimulating factor (GM-CSF) and stem cell factor (SCF) which are main growth factors in haematopoiesis. The demonstration of the inducibility of a wide range of various growth factor genes in endothelial cells is of major interest regarding the growth regulatory role of the endothelium.

Cells, Cultured↗
PubMed1999

Lysophosphatidic acid stimulates protein kinase C isoforms alpha, beta, epsilon, and zeta in a pertussis toxin sensitive pathway in vascular smooth muscle cells.

The natural phospholipid lysophosphatidic acid (LPA) has been characterized as an important vascular smooth muscle cell (VSMC) mitogen whose effects are mainly mediated by pertussis toxin (PTX)-sensitive guanosine triphosphate (GTP)-binding protein (Gi-protein). Protein kinase C (PKC) isoforms play an important role in intracellular signaling cascades and in growth of VSMC. In the present study we investigated the effect of LPA on activation of PKC isoforms alpha, beta, epsilon, and zeta in VSMC by Western blot of cytosolic and membrane fractions. Furthermore, we examined the role of PKC activation on LPA-induced growth of VSMC using PKC inhibitor 19-27. Stimulation of VSMC by 5 microg/mL LPA for 10 min increased the amount of PKC alpha, beta, epsilon, and zeta in the particulate fraction by 689%, 285%, 424%, and 510%, respectively, and returned to control level after 30 min. Correspondingly, the amount of PKC alpha, beta, epsilon, and zeta in the cytosolic fraction decreased by 32%, 94%, 44%, and 95%, respectively, compared to control. Furthermore, we could show that LPA-induced activation of PKC alpha, beta, epsilon, and zeta isoforms was PTX sensitive. Incubation of VSMC with nonspecific PKC inhibitor 19-27 (10 micromol/L) for 24 h resulted in a 30% inhibition of LPA-induced DNA synthesis as measured by [3H]thymidine incorporation. In conclusion, in VSMC LPA stimulated translocation of PKC isoforms alpha, beta, epsilon, and zeta in a PTX-sensitive manner. Furthermore stimulation of PKC might be critically involved in LPA-induced mitogenesis in VSMC.

Animals↗
PubMed1999

Occurrence of urinary tract tumors in miners highly exposed to dinitrotoluene.

Between 1984 and 1997, six cases of urothelial cancer and 14 cases of renal cell cancer occurred in a group of 500 underground mining workers in the copper-mining industry of the former German Democratic Republic, with high exposures to explosives containing technical dinitrotoluene. Exposure durations ranged from 7 to 37 years, and latency periods ranged from 21 to 46 years. The incidences of both urothelial and renal cell tumors in this group were much higher than anticipated on the basis of the cancer registers of the German Democratic Republic by factors of 4.5 and 14.3, respectively. The cancer cases and a representative group of 183 formerly dinitrotoluene-exposed miners of this local industry were interviewed for their working history and grouped into four exposure categories. This categorization of the 14 renal cell tumor cases revealed no dose-dependency concerning explosives in any of the four exposure categories and was similar to that of the representative group of employees, whereas the urothelial tumor cases were predominantly confined to the high-exposure categories. Furthermore, all identified tumor patients were genotyped by polymerase chain reaction, using lymphocyte DNA, regarding their genetic status of the polymorphic xenobiotic metabolizing enzymes, including the N-acetyltransferase 2 and the glutathione-S-transferases M1 and T1. This genotyping revealed remarkable distributions only for the urothelial tumor cases, who were exclusively identified as "slow acetylators." This points to the possibility of human carcinogenicity of dinitrotoluene, with regard to the urothelium as the target tissue.

Aged↗
PubMed1998

Expression of transforming growth factor-beta receptor type II and tumorigenicity in human breast adenocarcinoma MCF-7 cells.

To analyze transforming growth factor-beta (TGF-beta) response during MCF-7 cell progression, early passage (MCF-7E, < 200 passage) and late passage (MCF-7L, > 500 passage) cells were compared. MCF-7E cells showed an IC50 of approximately 10 ng/ml of TGF-beta1, whereas MCF-7L cells were insensitive. MCF-7E cells contained approximately threefold higher levels of TGF-beta receptor type II (TbetaRII) mRNA than MCF-7L, but their TbetaRI levels were similar. MCF-7E parental cells showed higher TbetaRII promoter activity than MCF-7L cells, which could be attributed to changes in Sp1 nuclear protein levels. Receptor cross-linking studies indicated that the cell surface receptor levels parallel mRNA levels in both cell lines. Limiting dilution clones of MCF-7E cells were established to determine the heterogeneity of TbetaRII expression in this cell line, and they showed varying degrees of TbetaRII expression. Fibronectin was induced at higher levels in cells expressing higher TbetaRII levels. All three TGF-beta isoforms were detected in limiting dilution clones and parental cells, but TGF-beta1 was more abundant relative to TGF-beta2 or 3, and no correlation between TGF-beta isoform profile with TGF-beta sensitivity was found. MCF-7L cells were tumorigenic and formed xenografts rapidly and progressively, whereas MCF-7E parental and limiting dilution clonal cells showed transient tumor formation followed by regression. These results indicate that decreased TbetaRII transcription in breast cancer cells leads to a loss of TbetaRII expression, resulting in cellular resistance to TGF-beta which contributes to escape from negative growth regulation and tumor progression.

Adenocarcinoma↗
PubMed1998

Inhibition of glycosphingolipid synthesis by threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol (PDMP) and the modulation of IL-1beta-stimulated expression of inducible nitric oxide synthase in rat aortic smooth muscle cells.

1. The composition of glycosphingolipids is altered in atherosclerotic tissue. In order to study the possible modulation of interleukin-1beta (IL-1beta)-induced expression of inducible nitric oxide synthase (iNOS) by endogenously synthesized glycosphingolipids, we investigated rat aortic vascular smooth muscle cells (VSMC) grown in the presence of the inhibitor of glycosphingolipid synthesis, threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol (PDMP). 2. Depletion of glycosphingolipids by PDMP (20-30 microM) was demonstrated by thin-layer chromatography of D-[1-(14)C]-galactose- or L-[-U14C]-serine-labelled glycosphingolipids. Nitrite generation was measured by the diaminonaphthalene assay, nitric oxide was determined by the oxyhaemoglobin technique and iNOS protein was detected by immunocytochemistry. 3. In VSMC grown in the presence of PDMP, the glycosphingolipid content was reduced by 30-50%. In PDMP-treated VSMC, IL-1beta (3 micro ml[-1])-stimulated release of nitrite (135 +/- 4 nmol mg(-1) protein 48 h[-1]) was significantly increased as compared to IL-1beta-stimulated control cells (40 +/- 3 nmol mg(-1) protein 48 h(-1); n = 6, P < 0.001). Similarly, IL-1beta (3 micro ml(-1), 36 h)-stimulated release of nitric oxide was higher in PDMP-treated VSMC (6.1 +/- 0.5 nmol mg(-1) protein h[-1]) as compared to untreated cells (2.0 +/- 0.6 nmol mg(-1) protein h(-1); n = 3, P < 0.01). These findings were confirmed by the demonstration of increased expression of iNOS protein (14.9 +/- 1.2% vs 6.4 +/- 0.2%; n = 4, P < 0.001), as shown by immunocytochemistry. 4. Evidence is presented that endogenous glycosphingolipids are important modulators of cytokine-induced iNOS expression. In view of an altered glycosphingolipid profile in atherosclerotic arteries, these mechanisms might be of relevance for the pathogenesis of atherosclerosis and restenosis subsequent to vessel injury.

Animals↗
PubMed1998

Role of mitogen-activated protein kinase in the angiotensin II-induced DNA synthesis in vascular smooth muscle cells.

The activation of mitogen-activated protein (MAP) kinase and increase in intracellular free calcium concentration ([Ca2+]i) are discussed in reference to activation of different protein kinases and growth of vascular smooth muscle cells (VSMCs). The aim of the present study was to investigate the role of angiotensin (Ang) II-induced increase in [Ca2+]i for activation of 44-kD/42-kD MAP kinase (p44mapk/p42mapk) and DNA synthesis in VSMCs. Experiments were performed by chelation of [Ca2+]i by the intracellular chelator 1,2-bis-(o-amino-5-methylphenoxy)ethane-N,N,N',N'-tetraacetic acid tetraacetoxymethyl ester (MAPTAM). Ca2+ was measured by the fura 2 method. MAP kinase activation was determined by the Western blotting method. DNA synthesis was determined by measurement of [3H]thymidine incorporation into the cell DNA. Treatment of VSMCs with 20 micromol/L MAPTAM for 30 minutes resulted in a complete abolishment of the maximal Ang II-induced increase at 10 seconds. Ang II phosphorylated the p44mapk/p42mapk in a time-dependent manner, showing a maximum at 3 minutes. In MAPTAM-treated cells, the maximal phosphorylation of MAP kinase isoforms was shifted to 5 minutes, and dephosphorylation was delayed compared with untreated cells. In concordance with this finding, the induction of the MAP kinase phosphatase-1 was markedly impaired in MAPTAM-treated cells. Ang II induced a 2.3-fold increase in [3H]thymidine incorporation into DNA synthesis in untreated cells. This effect was not reduced in MAPTAM-treated cells. Treatment of the cells with PD 98059 (10 micromol/L), a MAP kinase kinase inhibitor, caused 85% inhibition of the Ang II-induced activation of MAP kinases but did not inhibit the Ang II-induced DNA synthesis. In conclusion, the Ang II-induced stimulation of the MAP kinase is a Ca2+-dependent process. Furthermore, blockade of the Ang II-induced stimulation of the early intracellular events, such as increase in [Ca2+]i or phosphorylation of the MAP kinase, is not accompanied by an inhibition of the Ang II-induced DNA synthesis.

Angiotensin II↗
PubMed1998

A kinase-defective transforming growth factor-beta receptor type II is a dominant-negative regulator for human breast carcinoma MCF-7 cells.

The role of transforming growth factor (TGF)-beta type II receptor (T beta RII) in TGF-beta resistance and tumor progression is now well recognized. To test the effects of T beta RII loss in determining malignancy, we transfected a T beta RII-expressing, TGF-beta-sensitive, MCF-7 cell strain (ME24) with a tetracycline-repressible truncated T beta RII (kdT beta RII) construct lacking the cytoplasmic domain of the receptor. Transfection of kdT beta RII into parental ME24 cells (designated ME24t6 after transfection) resulted in high expression levels of kdT beta RII mRNA and cell surface protein which were reversible by tetracycline treatment. ME24t6 cells did not respond to exogenous TGF-beta 1 as measured by inhibition of proliferation or fibronectin (FN) induction, indicating that the truncated T beta RII acted as a dominant-negative inhibitor of both the growth inhibitory and extracellular matrix (ECM) stimulatory TGF-beta effects. Furthermore, inhibition of kdT beta RII expression by tetracycline treatment led to TGF-beta 1-mediated cell growth arrest in the G1 phase of cell cycle and to the accumulation of the hypophosphorylated form of retinoblastoma (Rb) protein. However, compared to parental ME24 cells, transfectants failed to show increased tumorigenicity, indicating that loss of T beta RII itself is not sufficient to account for differences in the malignant properties of T beta RII-expressing and non-expressing MCF-7 cell strains.

Adenocarcinoma↗
PubMed1998

Limitations of the reverse transcription-polymerase chain reaction method for the detection of carcinoembryonic antigen-positive tumor cells in peripheral blood.

To examine the limitations of reverse transcription (RT)-PCR for the detection of circulating tumor cells in blood, we established a RT-PCR for carcinoembryonic antigen (CEA). Whole blood (10(7) nucleated cells) was mixed with cells from the colon cancer cell line LS174T (concentrations ranging from 0 to 10(6) cells). RT-PCR was performed to detect CEA mRNA in blood under various conditions. Healthy blood donors (n = 24) were examined by the established method for detecting CEA mRNA in blood. We were able to show that there is a detection limit for RT-PCR of 10 tumor cells in total and of 1 tumor cell in 10(5) nucleated cells. To obtain these results, a high number of PCR cycles (first PCR, 30 cycles; nested PCR, 45 cycles) was required. Under these PCR conditions, we found a positive PCR signal in 33% of healthy blood donors (n = 8). To overcome this problem, we reduced the nested PCR to 35 cycles. At that point, none of the controls showed a positive signal for CEA, and there was a subsequent decrease of the detection limit to 1 tumor cell in 10(2)-10(3) nucleated cells, lower than the detection limit of an immunocytological examination (1 tumor cell in 10(4) nucleated cells). When the amplification was performed with the tumor cells only and with no nucleated blood cells present, under exactly the same conditions, there was still a detection limit of 1 tumor cell in 106 nucleated cells. Our data clearly show that there is a severe loss of expected sensitivity of RT-PCR if it is performed in blood or nucleated blood cells. We conclude that PCR for CEA mRNA expression is not more sensitive than immunocytology and is, furthermore, plagued by the problem of a high percentage of false positive results.

Carcinoembryonic Antigen↗
PubMed1997

Elevated serum concentrations of soluble adhesion molecules in coronary artery disease and acute myocardial infarction.

OBJECTIVES: Adhesion molecules are involved in a number of chronic conditions and diseases like rheumatoid arthritis, tumor growth and wound repair. Soluble adhesion molecules (SAM) play an important role in angiogenesis which is a common aspect of the conditions mentioned above and atherosclerosis. The aim of the present study was to assess the prevalence and the impact of elevated soluble adhesive molecule plasma concentrations in patients with atherosclerosis. DESIGN AND SUBJECTS: In this study, we measured the soluble forms of intercellular adhesive molecule (sICAM), endothelial adhesive molecule (sELAM) and vascular adhesive molecule (sVCAM) using a sandwich ELISA technique in plasma of patients with acute myocardial infarction (AMI), coronary heart disease (CHD) and in healthy subjects (HS). RESULTS: Patients suffering from CHD and AMI showed significant higher plasma concentrations of sICAM (p <0. 05 and p <0.005), sELAM (p <0.01 and p <0.001) and sVCAM (p <0.001 and p <0.005) than HS. In patients with fatal outcome of myocardial infarction the plasma concentrations of sICAM, sELAM and sVCAM were significantly elevated compared to surviving patients (p <0.005; p <0.005; p <0.05). In patients undergoing thrombolytic therapy there were no significant differences of plasma adhesive molecule concentrations. The levels of SAM were not related to other risk factors like diabetes, nicotin abuse, hyperlipidemia, hypertension and a familiary history of cardiovascular disease. CONCLUSIONS: Elevated levels of SAMs are found in patients with coronary heart disease. High SAM levels in plasma seem to be a prognostic factor in acute myocardial infarction. This effect is independent from other concomitant risk factors. Our results suggest that SAMs are involved both in acute phase of myocardial infarction and chronic process of atherosclerosis. It seems that similiar to other chronic inflammatory diseases, atherosclerosis seems to be modulated by soluble forms of adhesive molecules.

Adult↗
PubMed1997

Blockade of transforming growth factor-beta signaling does not abrogate antiestrogen-induced growth inhibition of human breast carcinoma cells.

We have studied the role of autocrine transforming growth factor-beta (TGF-beta) signaling on antiestrogen-mediated growth inhibition of hormone-dependent T47D and MCF-7 human breast carcinoma cells. Tamoxifen treatment increased the secretion of TGF-beta activity into serum-free cell medium and the cellular content of affinity cross-linked type I and III TGF-beta receptors in both cell lines. Anti-pan-TGF-beta antibodies did not block anti-estrogen-induced recruitment in G1 and inhibition of anchorage-dependent and -independent growth of both cell lines. Early passage MCF-7 cells, which exhibit detectable type II TGF-beta receptors at the cell surface and exquisite sensitivity to exogenous TGF-beta1, were transfected with a tetracycline-controllable dominant-negative TGF-betaRII (DeltaRII) construct. Although the TGF-beta1 response was blocked by removal of tetracycline in MCF-7/DeltaRII cells, tamoxifen-mediated suppression of Rb phosphorylation, recruitment in G1, and inhibition of cell proliferation were identical in the presence and absence of tetracycline. TGF-beta1 treatment up-regulated the Cdk inhibitor p21 and induced its association with Cdk2 in MCF-7 cells; these responses were blocked by the DeltaRII transgene product. In MCF-7 cells with a functional TGF-beta signaling pathway, tamoxifen did not up-regulate p21 nor did it induce association of p21 with Cdk2, suggesting alternative mechanisms for antiestrogen-mediated cytostasis. Finally, transfection of late-passage, TGF-beta1 unresponsive MCF-7 cells with high levels of TGF-betaRII restored TGF-beta1-induced growth inhibition but did not enhance tamoxifen response in culture. Taken together these data strongly argue against any role for TGF-beta signaling on tamoxifen-mediated growth inhibition of hormone-dependent breast cancer cells.

Breast Neoplasms↗
PubMed1997

Angiotensin type-1 (AT1) receptor gene expression in primarily cultured human arterial umbilical endothelial cells.

The aim of this study was to investigate the interaction of angiotensin II (Ang II) and human umbilical arterial endothelial cells (HUAEC). Specific binding of 125I-ANG II to primarily cultured HUAEC showed a K(D) of 1.98 +/- 0.53 x 10(-9) M (n = 5) with a maximum binding site of 2.84 +/- 1.07 x 10(-13) mol/mg protein (n = 5). In later passages (third and fifth subculture), this binding site was no longer detectable. Gene expression analysis revealed a strong expression of the angiotensin type-I receptor (AT1-R) in the primarily cultured HUAEC, with a decrease in additional passages. In primarily cultured HUAEC, Ang II (10(-10)-10(-6) M) induced a concentration-dependent increase in intracellular free calcium ([Ca2+]i) that could be blocked by a preincubation with candesartan (TCV-112) but not by PD123319. These data show the expression of the AT1-R in primary cultures of HUAEC. The Ang II-induced increase in [Ca2+]i seems to be mediated by this receptor.

Angiotensin II↗
PubMed1997

Low density lipoprotein enhances the thrombin-induced growth of vascular smooth muscle cells.

OBJECTIVE: In the present study we investigated whether low density lipoprotein is able to enhance the growth promoting effects of thrombin in vascular smooth muscle cells. METHODS: DNA synthesis was examined by measurement of the [3H]thymidine incorporation into the cell DNA. Cell count was measured with a Neubauer cell box. Thrombin receptor mRNA was determined by Northern blotting. Ca2+ was measured by the fura 2-method. RESULTS: Thrombin (5 nmol/l), thrombin receptor activating protein (3 mumol/l) and low density lipoprotein (33 nmol/l) induce a 652 +/- 80%, 593 +/- 80% and a 316 +/- 60% increase in [3H]thymidine incorporation into DNA (mean +/- SD, n = 3), respectively. A coincubation of thrombin or thrombin receptor activating protein with low density lipoprotein led to a 1245 +/- 160% or 1200 +/- 40% increase of DNA synthesis (mean +/- SD, n = 3). Thus, coincubation of low density lipoprotein and thrombin causes a synergistic rather than an additive mitogenic effect on smooth muscle cells. Thrombin and low density lipoprotein induced a 22 +/- 8.4% and a 29% +/- 6% increase in cell number, respectively. Simultaneous treatment of vascular smooth muscle cells with thrombin and low density lipoprotein caused a 63 +/- 14% increase in cell number (mean +/- SD, n = 3). To further elucidate the underlying mechanism, we studied the effect of low density lipoprotein on the expression of thrombin receptor mRNA. Low density lipoprotein caused a 2.5-fold increase of thrombin receptor mRNA within 24 h, as assessed by Northern analysis. Preincubation of cells for 24 h with 33 nmol/l low density lipoprotein resulted in an elevation of the thrombin-induced increase in cytosolic free Ca2+ concentration from 538 +/- 54 to 923 +/- 75 nmol/l (mean +/- SD, n = 4). CONCLUSION: In summary, low density lipoprotein may enhance the mitogenic effect of thrombin probably by an up-regulation of thrombin receptor gene expression in vascular smooth muscle cells or by an elevation of the thrombin-induced increase in cytosolic free Ca2+ concentration.

Animals↗
PubMed1997

Lysophosphatidic acid and intracellular signalling in vascular smooth muscle cells.

Growth of vascular smooth muscle cells (VSMC) plays an important role in the pathogenesis of atherosclerosis and hypertension. Lysophosphatidic acid (LPA), a natural phospholipid is thought to be an important VSMC mitogen and has recently been suggested to play an important role in the development of vascular disease. In the present study, we describe the effects of LPA on intracellular signalling pathways in VSMC. LPA (5 micrograms/ml) induced an increase of cytosolic free calcium concentration ([Ca2+]i) in the presence and absence of extracellular Ca2+ and markedly stimulated the Na+/H+ exchanger. LPA dose-dependently caused a stimulation of the 42-kDa mitogen-activated protein kinase (MAP kinase) isoform with a maximum at 5 min. Also, LPA induced a 5-fold increase in [3H]thymidine incorporation into cell DNA above the basal value, as well as a 42% increase in cell number. Pretreatment of VSMC with pertussis toxin (PTX) (100 ng/ml) for 24 h markedly blunted the LPA-dependent intracellular signalling transduction including the increase in [Ca2+]i, activation of the Na+/H+ exchanger, activation of MAP kinase and the increase in cell DNA synthesis. These findings demonstrate that the effects of LPA on intracellular signalling transduction pathway as well as on VSMC growth are mediated by PTX-sensitive guanosine triphosphate (GTP) binding protein (Gi protein).

Animals↗
PubMed1997

Endoscopic pituitary surgery: an early experience.

BACKGROUND: As an element of a minimally invasive management approach, we had developed an endonasal endoscopic transsphenoidal technique for the treatment of pituitary tumors. Initially, four patients were operated on via a sublabial, transseptal approach using a fiberoptic rigid endoscope in conjunction with the operating microscope. Encouraged by that experience, our subsequent 11 patients had undergone endonasal endoscopic transsphenoidal surgery without the use of a retractor or speculum. METHODS: Our group of patients included nine females and six males, with an age range of 17-88 years (median: 43 years). There were four microadenomas, four intrasellar macroadenomas, three macroadenomas with suprasellar extension, three invasive macroadenomas involving the cavernous sinus with suprasellar extension, and one metastatic adenocarcinoma. RESULTS: Thirteen patients with pituitary adenomas experienced resolution of their symptoms postoperatively. One patient with a recurrent prolactinoma responded partially following surgery and subsequently underwent gamma knife radiosurgery. Two patients were treated with postoperative fractionated radiation therapy, one for residual pituitary adenoma in the cavernous sinus, and the other for metastatic adenocarcinoma, respectively. The first patient, treated via an endonasal endoscopic approach for biopsy of the metastatic adenocarcinoma, developed postoperative cerebrospinal fluid (CSF) leak that was successfully managed with endoscopic packing of a fat graft. CONCLUSIONS: The endonasal endoscopic transsphenoidal approach facilitates faster postoperative recovery by the avoidance of traditional incision and postoperative nasal packing. It offers a panoramic view of the sphenoid sinus and excellent visualization of the sellar and suprasellar structures with increased illumination and magnification. Such visualization provides the potential for more complete tumor resection, as well as a better chance of preserving pituitary function and avoiding neurovascular injury.

Adenoma↗
PubMed1997

Glabellar approach: simplified midline anterior skull base approach.

As a simplified microsurgical technique for lesions at the midline anterior skull base, a glabellar approach through a small incision (5 cm) between the eyebrows crossing the nasion was developed in four cadaver dissections. To determine the ideal positioning of the patient, the angle of the surgical trajectory was measured in the sagittal plane. In an effort to make an operation simple and accurate through this limited exposure, measurements were made in distance from the midline nasion to various intradural structures. Average distance from the midline point of the nasion (MPNa) to the midline of the tuberculum sella was 6.37 +/- 0.29 cm, 6.98 +/- 0.26 cm to the midline of the optic chiasm, and 8.00 +/- 0.11 to the lamina terminalis. In addition, measurements to other various anatomical landmarks were made. The angle of the line drawn from the MPNa to the midline of the tuberculum sella was 5.2 +/- 1 degrees against a line drawn between the lateral canthus and the tragus (LC-T) in the sagittal plane. Based upon this study, the positioning of the patient's head would be better if the LC-T line is positioned at 25 degree extension when the operating microscope is set at 20 degree inclination. Within 6 to 8 cm in depth from the MPNa, important landmarks are exposed without brain retraction. If surgical instruments are marked with ruler calibration, the depth of the surgical instruments will suggest the anatomical location. This glabellar approach has been used in three patients successfully. A brain retractor was not necessary and not used during the operations. This technique provides key exposures to the midline anterior skull base.

Adult↗