Biomedical subjects

J Schwalb

Publications and source records attributed to J Schwalb.

7 recordsLinked to original sources

PubMed2003

[Submental transcutaneous electrical stimulation for obstructive sleep apnea].

BACKGROUND: Transcutaneous electrical stimulation while asleep has been used to treat obstructive sleep apnea (OSA), although without convincing results. Modern strategies consist of electrical muscle training for a number of weeks during wakefulness rather than stimulation during sleep. OBJECTIVE: The purpose of this study was to assess the practicability, safety, and efficacy of a new device, SilentOne (Imperpuls, Chemnitz, Germany). PATIENTS AND METHODS: Fifteen patients with various degrees of OSA used transcutaneous submental electrical stimulation therapy for 4-5 weeks every day, day and night. A patient's diary recorded practicability and potential adverse events. Respiratory parameters were recorded by fully attended polysomnography in the sleep lab. Daytime sleepiness and snoring were assessed by questionnaires. RESULTS: The apnea-hypopnea-index decreased from 29.2 before to 21.2 after therapy (P<0.05). Daytime sleepiness improved significantly (P<0.01) as did snoring (P<0.005). CONCLUSIONS. Transcutaneous electrical stimulation therapy using SilentOne proved to be safe, easy to use, and potent. However, therapy showed a limited cure rate.

Adult↗

PubMed2000

Serum levels of vascular endothelial growth factor in patients with head and neck cancer.

Angiogenesis is now considered to be crucial for tumor growth and metastasis. In several tumors, microvascular density has been shown to be correlated with metastasis and aggressiveness. Vascular endothelial growth factor (VEGF) is a secreted endothelial cell-specific mitogen, which is induced by hypoxia and is angiogenic in vivo. VEGF has been identified in a wide variety of malignancies including head and neck squamous cell carcinomas (HNSCC). We investigated the circulating level of VEGF in sera from patients with various head and neck squamous cell carcinomas (n = 71) as well as from healthy normal controls (n = 47). Serum VEGF concentrations were determined as serum immunoreactivity by using a quantitative sandwich enzyme immunoassay technique. For statistical analysis, the Wilcoxon 2-sample test and Kruskal-Wallis test were performed. The majority of the patients with HNSCC were found to have high concentrations of serum VEGE The levels of VEGF in the sera of patients with cancer ranged from below the detection limit to 937.1 pg/ml (mean, 144.5 pg/ml). In contrast, the VEGF serum levels in 47 healthy individuals ranged from below the detection limit to 168.1 pg/ml (mean, 32.7 pg/ml), VEGF serum concentration being significantly higher in HNSCC patients (P = < 0.001). These findings indicate that a positive angiogenesis regulator such as VEGF might function as an endocrine growth factor, particularly for solid HNSCC tumors and may be a useful marker for clinical monitoring.

Adult↗

PubMed2000

[Coexpression of VEGF and bFGF is associated with increased vascular density in head and neck carcinomas].

BACKGROUND: Angiogenesis is crucial for tumor growth and metastasis. In several tumors, microvascular density has been shown to correlate with metastasis and aggressiveness. Vascular endothelial growth factor (VEGF) and basic Fibroblast Growth Factor (bFGF) are known to have potent angiogenic activity. Their expression has been identified in a wide variety of malignancies including head and neck squamous cell carcinoma (HNSCC). Aim of our study was to investigate the role of co-expression of VEGF and bFGF for angiogenesis in HNSCC. MATERIAL AND METHODS: Cryostat sections of 51 primary HNSCC were immunostained for VEGF and bFGF using a standard streptavidin-biotin complex procedure. To evaluate angiogenesis, endothelial cells were stained immunohistochemically using anti-vWF polyclonal antibody. Microvessels were quantified by counting vessels in a x200 field in the most vascular area of the tumor. RESULTS: 25/51 (49%) of the investigated carcinomas showed co-expression of both factors (VEGF+/bFGF+), while 6/51 (11.7%) carcinomas only expressed VEGF and 13/51 (25.5%) carcinomas expressed bFGF. 7/51 (13.7%) tumors showed no expression of these factors (VEGF-/bFGF-). Carcinomas with a co-expression of VEGF and bFGF showed a significantly increased mean microvessel density (88.3 +/- 24.4) compared to tumors expressing only VEGF (77 +/- 16.8) or bFGF (71.1 +/- 15.8) (p = 0.022) or tumors with no expression of both factors (51.1 +/- 13.4) (p < 0.001). The association of VEGF and bFGF expression level was not significant (p = 0.178). CONCLUSIONS: The positive correlation of the co-expression of angiogenic VEGF and bFGF with increased microvessel density underlines the importance of both factors for tumor angiogenesis in HNSCC. VEGF and bFGF might act cooperatively in the process of neovascularization in human head and neck cancer.

Adult↗

PubMed2000

Vascular endothelial growth factor expression correlates with p53 mutation and angiogenesis in squamous cell carcinoma of the head and neck.

Vascular endothelial growth factor (VEGF) has potent angiogenic activity and has been identified in a wide variety of malignancies, including head and neck squamous cell carcinoma (HNSCC). The tumour-suppressor gene p53 has been thought to regulate VEGF. Cryostat sections of 33 head and neck squamous cell carcinomas (HNSCC) were immunostained for VEGF using a standard streptavidin-biotin complex procedure. To evaluate angiogenesis, microvascular density was counted by staining endothelial cells immunohistochemically using anti-vWF monoclonal antibody. The p53 gene status was analysed using a PCR-SSCP analysis and direct sequencing. VEGF positive staining was detected in 18 (55%) out of 33 tumours. VEGF immunoreactivity did not correlate with the main clinicopathological characteristics of the patients (localization, T-stage, N-status, histological grading). Statistical analysis gave a clear correlation between the tumour vascularity and the VEGF protein expression (p = 0.0036). VEGF negative tumours showed a lower mean number of microvessels per microscopic field (60.3 +/- 15.5) than VEGF positive tumours (79.6 +/- 22.9). P53 mutations were identified in 12 (36.4%) of 33 tumours. The association of p53 mutations and VEGF expression level was significant (0.027). The higher microvessel density in VEGF positive tumours supports the importance of VEGF for tumour angiogenesis in HNSCC. Our results support the hypothesis of a p53 regulation on the angiogenic process through a VEGF up-regulation.

Adult↗

PubMed2000

Expression of 92-kDa type IV collagenase correlates with angiogenic markers and poor survival in head and neck squamous cell carcinoma.

MMP-9, which degrades extracellular matrix, is believed to play a crucial role in tumor invasion and metastasis. Angiogenesis is also perceived as an important step in tumor growth and metastasis. The aim of this study was to investigate the expression of MMP-9 in tumor samples of HNSCC patients and to study a possible correlation to angiogenic markers. Cryostat sections of 52 HNSCC tumors were immunostained for MMP-9, bFGF and VEGF using a standard streptavidin-biotin complex procedure for light microscopic investigation. Microvessel density (MVD) was determined by staining of endothelial cells immunohistochemically using anti-vWF monoclonal antibody. MMP-9 positive staining was detected in 27/52 (52%) of the tumors. MMP-9 immunoreactivity did not correlate with the main clinicopathological characteristics of the patients (localisation, T-stage, N-stage, histological grading), but correlated with worse survival of the patients. MMP-9 negative tumors showed a significant lower mean MVD per microscopic field than MMP-9 positive tumors (p<0. 001). There was a significant association of MMP-9 and VEGF expression (p<0.05). The presence of MMP-9 in HNSCC cancer and the positive correlation with MVD and VEGF expression supports the theory that MMP-9 functions as a regulator of tumor angiogenesis supporting endothelial cell invasion. MMP-9 and VEGF might act co-operatively in the process of neovascularization in human head and neck cancer.

Adult↗

PubMed1994

Retinoic acid inhibition of IL-1-induced IL-6 production by human lung fibroblasts.

IL-6 is a multi-functional cytokine that plays an important role in normal biologic homeostasis and disease pathogenesis. Retinoids are vitamin A analogs that regulate the function of a wide variety of inflammatory and structural cells. To further understand the biology of retinoids and IL-6 we determined whether all-trans-retinoic acid (RA) and other retinoids regulate lung fibroblast IL-6 production. RA did not stimulate fibroblast IL-6 production. Instead, it inhibited the production of IL-6 by IL-1-stimulated cells. This effect was dose-dependent with an IC50 of 10(-7) M RA and significant inhibition being noted with doses of RA as low as 10(-8) M. These inhibitory effects could not be explained by cytotoxicity or a shift in the kinetics of IL-6 production. They also did not appear to involve alterations in the early events in IL-1-induced IL-6 production, because RA inhibited IL-6 production even when added 6 h after IL-1 and RA did not inhibit IL-1 binding to cell surface IL-1 receptors. RA inhibition of IL-6 protein production was associated with a comparable decrease in IL-6 mRNA accumulation and gene transcription. 13-cis-retinoic acid, retinol, retinaldehyde, all-trans etretin, Ro 13-6298, and 9-cis retinoic acid also inhibited IL-1-induced IL-6 production. However, 4-hydroxyphenyl retinamide and etretinate did not share this property. The inhibitory effects of these analogues may be mediated by nuclear retinoic acid receptors as mRNA encoding RAR-alpha, RAR-gamma, and RXR-alpha were present, and RAR-beta was induced by RA in human lung fibroblasts. These studies demonstrate that RA and other retinoid analogs inhibit IL-1-induced IL-6 production and that this effect is analog-specific and, at least partially, transcriptionally mediated.

Cell Line↗

PubMedDate not supplied

Serum levels of matrix metalloproteinase-2 and -9 in patients with head and neck squamous cell carcinoma.

BACKGROUND: Matrix Metalloproteinases (MMPs) have been implicated as playing an important role in cancer invasion and metastasis. MMPs have been identified in a wide variety of malignancies including head and neck squamous cell carcinomas (HNSCC). MATERIAL AND METHODS: We investigated the circulating level of MMP-2 (gelatinase A or 72-kD type IV collagenase) and MMP-9 (gelatinase B or 92-kD type IV collagenase) in sera from patients with various head and neck squamous cell carcinomas (n = 86) as well as from healthy normal controls (n = 47). Serum MMP concentrations were determined as serum immunoreactivity by using a quantitative sandwich enzyme immunoassay technique. For statistical analysis, the t-test and Kruskal-Wallis test were performed. RESULTS: The majority of the patients with HNSCC were found to have high concentrations of serum MMP-9. The levels of MMP-9 in the sera of patients with cancer ranged from 39 to 1547 ng/ml (mean, 417 ng/ml). In contrast, the MMP-9 serum levels in 47 healthy individuals ranged from 30 to 537 ng/ml (mean, 189 ng/ml), MMP-9 serum concentration being significantly higher in HNSCC patients (p = 0.001). MMP-9 serum concentrations of patients with advanced stage HNSCC were significantly higher (p = 0.0449) compared to patients with early stage cancer. No significant difference of MMP-2 serum levels was seen when comparing HNSCC patients and normal controls. CONCLUSION: The present data indicate that the elevation of serum levels of MMP-9, but not MMP-2, may be a useful marker for clinical monitoring of HNSCC patients.

Adult↗