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Biomedical subjects

G Ernst

Publications and source records attributed to G Ernst.

At least 37 records · Page 2Linked to original sources
PubMed1999

[Drug-induced headache--pathomechanisms of addiction].

The pathogenesis of drug abuse in patients suffering from drug-induced headache is not known in detail. It is unclear whether drug abuse in chronic daily headache should be classified as a form of drug dependence. Current findings concerning the neurobiological correlates of addictive behavior and affective disorders point to the importance of monoaminergic dysregulation, especially a dysfunction of central serotonergic neurotransmission. We reviewed the literature on drug-induced headache and examined hypothetical pathomechanisms of addiction. Drugs causing drug-induced headache such as paracetamol, coffein and ergotamine interfere with behavior patterns or neurotransmitter systems that are also affected by drugs of abuse. Several drugs that ameliorate acute headache interact with central serotonergic neurotransmission and may affect anxiety and depression in patients with chronic daily headache. Non human primate and human studies revealed mechanisms of serotonergic dysfunction in drug dependence, which may also be relevant for drug-abuse in medication-induced headache. Medication-induced dysfunction of monoaminergic, especially serotonergic neurotransmission, may affect drug dependence by exacerbating mood disorders. Further studies are necessary to assess serotonergic neurotransmission in patients with drug-induced headache and abuse of medication.

English Abstract↗
PubMed1999

[The prognostic value of dobutamine stress echocardiography. A long-term follow-up study].

BACKGROUND AND OBJECTIVE: The prognostic value of dobutamine stress echocardiography in patients with suspected or known coronary heart disease has not exactly been assessed. Purpose of the study was the assessment of the prognostic value of DSE regarding cardiac events, especially in patients with a normal DSE finding. PATIENTS AND METHODS: 316 patients (168 men, 148 women, mean age 61 +/- 10 years), included in this follow-up study, underwent DSE between January 1994 and December 1996 to evaluate clinically suspected or known coronary heart disease. DSE was classified according to resting and stress echocardiography as either "normal-normal (NN)", "normal-ischemic (NI)", "abnormal-normal (AN)", "abnormal-ischemic (AI)" or "inconclusive (C)". Follow-up by telephone took place between June 1997 and April 1998. "Events" were survived myocardial infarction and death. "Interventions" were revascularisation procedures, either percutaneous transluminal coronary angioplasty (PTCA) with or without stenting or aortocoronary bypass surgery. RESULTS: In 161 patients, DSE was NN, NI in 27 patients, AN in 55 patients, AI in 54 patients and C in 19 patients. Mean follow-up duration was 28 months. Events occurred in 23 patients: survived myocardial infarction in 10, death in 13 persons. Interventions were carried out in 50 patients: PTCA with or without stenting in 19, aortocoronary bypass surgery in 31 persons. The event rate was significantly lower in patients with DSE classified as NN (P = 0.03 by log-rank) than in other groups. The intervention rate was significantly lower in the NN-group (P = 0.0001 by log-rank) than in the other groups, too. CONCLUSION: Patients with a normal rest echocardiography and DSE had a good prognosis in a long-term follow-up study.

Adult↗
PubMed1999

Determination of telomerase activity for differential analysis of multifocal renal cell carcinomas.

Secondary tumors are found in approximately 12 to 22% of all renal cell carcinoma, and their origin is currently unknown. To determine their potential for malignancy, we examined the telomerase activity of primary tumors and secondary lesions, and found that 86% of the lesions had an identical telomerase status as the related primary tumors, and thus probably share their malignancy potential.

Adenocarcinoma, Clear Cell↗
PubMed1999

Tumor suppressor gene p16 (CDKN2A) mutation status and promoter inactivation in head and neck cancer.

The p16INK4A (CDKN2A/MTS1) putative tumor suppressor gene encodes a cyclin dependent kinase inhibitor which plays an important role in the regulation of the G1/S phase cell cycle checkpoint. A high frequency of various p16 gene alterations were consequently observed in many primary tumors. P16 can be inactivated by different mechanisms: i) homozygous deletion, ii) methylation of the promoter region or iii) point mutation. In order to investigate p16 alterations in head and neck cancer (HNC) we analyzed 70 primary tumors of the larynx, pharynx and oral cavity including their corresponding normal mucosa for mutation inactivation by direct sequencing exon 2. We detected only one so far undescribed transversion G to T at position 322 (Asp108Tyr) and a known polymorphism (Ala148Thr) in five cases. The methylation status of the p16 promoter region was analyzed by an improved highly sensitive methylation-specific PCR protocol. P16 methylation inactivation was found in 16 of 55 cases (29%). Our data indicate that p16 point mutations in HNC are less frequent, but inactivation by methylation of the promoter region could be involved in genesis and progression of HNC.

Base Sequence↗
PubMed1999

P53 genotyping - an effective concept for molecular testing of head and neck cancer?

P53 mutations are currently recognized as the most common genetic alteration in human tumors. The purpose of our study was to evaluate the significance and reliability of p53 genotyping in head and neck cancer as a possible marker permitting the prediction of tumor behavior and clinical outcome. P53 genotyping in our study refers to highly sensitive molecular screening in order to detect structural alterations in the nucleic acid sequence of the gene. Exons 2-11 and adjacent intronic regions were screened for mutations by direct genomic sequencing or by bi-directional dideoxyfingerprinting in 66 primary tumors of the larynx, pharynx and oral cavity. Alterations in the of the p53 gene were detected in 36% (24 of 66) of the analyzed tumors, no mutation was found in our cohort outside exons 5-8. The frequency of p53 mutation had no correlation to the tumor stage or tumor site. The recurrence rate in patients with a p53 alteration was not significantly higher compared to patients without a p53 mutation in their primary tumors. Summarizing the results of our study only limited reliability of p53 genotyping as an effective concept for molecular testing of head and neck cancer was found.

Biomarkers, Tumor↗
PubMed1998

[Effect on morphine and other opioids on immune function].

PROBLEM: Already 1898 first clinical observations of a possible immune suppression after morphine intake were published. Today there are many reports describing opioid effects on nearly all parameters of the immune system. The question arises, whether there exists any evidence for clinical (harming) effects on patients. METHOD: Recent experimental and clinical publications are reviewed. Results are summarized, pathophysiological mechanisms and clinical conclusions discussed. RESULTS: Morphine and other opioids have immunomodulating effects on nearly all measurable parts of the immune system (macrophages, granulocytes, nk-cells; mediators like Interleukin 1, 2 and 6, TNF). However, most studies did not include pain models, and in addition, high morphine doses were used. First studies using a combined pain/morphine-approach report immune stimulating effects. There are three pathophysiological mechanisms under discussion, including opioid receptors on immune competent cells, central opioid receptors activating the adrenergic system and opioid-induced steroid release with consecutive immunosuppression. It is completely unclear, if there is any relevance of these findings for clinical settings. CONCLUSIONS: The question whether use of opioids can harm chronic pain patients is unsolved. There is an urgent need for studies in clinical settings with clinical relevant parameters.

English Abstract↗
PubMed1998

Phantom-limb pain.

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Amputation, Surgical↗
PubMed1998

Chest pain in cardiac syndrome X--caused by neuromuscular disorders?

We wanted to find out if chest pain in cardiac syndrome X can be a manifestation of neuromuscular disorders. Five patients with cardiac syndrome X (3 women, 2 men), aged 34 to 70 years, consented with a clinical neurological examination, muscle enzyme testing, electroneurography of the right median and peroneal nerves and electromyography of the right brachial biceps and anterior tibial muscles. A neuromuscular disorder was found in 1 of the 5 investigated patients. The 60-year-old man presented with a monoparesis of the left leg and sensory dysfunction of the left upper and lower limb. He was diagnosed as having either posttraumatic myelopathy or radiculopathy. Since chest pain in cardiac syndrome X can be caused by neuromuscular disorders, a comprehensive neurological examination is recommended in patients with this disorder.

Adult↗
PubMed1998

Gain of DNA copy number on chromosomes 3q26-qter and 5p14-pter is a frequent finding in head and neck squamous cell carcinomas.

Comparative genomic hybridization (CGH) was used to study genomic imbalances in 77 squamous cell carcinomas of the head and neck (HNSCC) and in four cell lines derived from oral carcinomas. Particular attention was paid to all tumors characterized by a gain of two specific chromosomal segments, i.e. 3q26-qter and 5p14-p15. The 57 tumors containing both or one of the two imbalances were compared with 20 tumors lacking both with regard to genomic complexity, as well as to associated genomic, histopathologic and clinical peculiarities. 60% of the oral, and 66% of the non-oral cancers exhibited a gain of 3q26-qter, while a gain of 5p14-p15 was found in 66% of the oral, but only in 48% of the non-oral tumors. 48% of all tumors were characterized by both gains together, 26% exhibited only one of the two alterations. It could be shown that presence of both, gain of 3q26-qter and 5p14-p15, was clearly associated with a significantly higher complexity of genomic changes which was not only expressed as a high frequency of DNA copy number alterations (CNAs) but was also connected with a considerable number of additional amplifications of various chromosomal segments and a high conformity of the patterns of genomic imbalances in these tumors. Clear differences of the extent and of the patterns of genomic imbalance could be observed between oral and non-oral tumors. With respect to histopathological parameters, no clear association could be found for specific imbalances to the grade of differentiation, nor the invasiveness or metastatic status of the tumors. However, a higher number of patients with tumors characterized by gain of 3q26-qter plus 5p14-p15 died within a short period (i.e. less than 15 months) after excision of the tumor compared to the group without these imbalances. The implications of these findings are discussed from the oncogenetic and clinical aspects and in comparison with other reports.

Journal Article↗
PubMed1998

Open and closed kinetic chain exercises improve shoulder joint reposition sense equally in healthy subjects.

OBJECTIVE: To compare the effects of open and closed kinetic chain exercise on shoulder joint reposition sense. DESIGN AND SETTING: Subjects with no previous upper extremity injury participated in a 6-week exercise program consisting of 3 sessions per week. SUBJECTS: Thirty-nine healthy male military cadets: 13 each in the open, closed, and control groups. MEASUREMENTS: Each subject was pretested and posttested for both active and passive joint reposition sense at 30 degrees external rotation, 30 degrees internal rotation, and 10 degrees from full external rotation. RESULTS: The open and closed kinetic chain groups de- creased in reposition sense error scores in comparison with the control group, but no difference was found between the 2 training groups. CONCLUSION: Our findings suggest that shoulder joint reposition sense can be enhanced with training in healthy subjects. Also, open and closed kinetic chain exercises appear to be equally effective in improving shoulder joint reposition sense.

Journal Article↗
PubMed1997

[Adverse reactions to acupuncture].

Acupuncture is frequently used as an alternative therapy to drugs in the treatment of pain patients. In this review we discuss adverse reactions to acupuncture by means of case reports and our own clinical experience. Frequent side effects of acupuncture are local pain, autonomic nervous system reactions (including fainting) and small local bleeding or hematomas. There are, however, some case reports of serious adverse reactions. Since 1980, there have been 18 pneumothoraces post acupuncture therapy reported in the literature. Hepatitis due to inadequate hygiene standards has also been reported. Some patients with valvular heart disease have developed endocarditis after acupuncture. Ear acupuncture with permanent needles can cause chondritis or perichondritis. For any acupuncture treatment, a careful case history and exact diagnosis are necessary. In particular, it should be determined whether wound-healing disorders, immunosuppression, coagulation defects, valvular heart disease or pregnancy are present, as all of these constitute relative contraindications to acupuncture. Hygiene standards have to be observed. Bearing these points in mind, acupuncture is a reliable method with few side effects.

English Abstract↗
PubMed1997

[Telomeres and telomerase].

Complex mechanisms have evolved in mammalian cells for regulating cellular lifespan. Normal cells demonstrate a strictly limited growth potential and senescence after a defined number of cell divisions. In contrast, tumor cells often exhibit an apparently unlimited proliferation potential and are termed immortalized. It has been proposed that the progressive shortening of the tips of the eukaryotic chromosomes--the telomeres--is an important component of senescence and is involved in the control of cell cycle. The enzyme telomerase adds TTAGGG repeats onto mammalian telomeres, preventing their shortening. Telomerase is normally inactive in most somatic cells, but detectable in tumor cells. The activation of telomerase in malignant cancers seems to be an important step in tumorigenesis in order to gain the ability of indefinite proliferation and to become immortal. This review describes the present knowledge of telomeres and telomerase and their role in cellular senescence and human aging. It summarizes aspects of telomerase in cancer and its function as a diagnostic and prognostic tumor marker.

Animals↗
PubMed1997

Telomeres and telomerase: biological and clinical importance.

We review the present knowledge of telomeres and telomerase with special attention to their role in cell proliferation, cellular senescence, and human aging. We summarize the functional aspects of telomerase in cancer, as well as its role as a useful diagnostic and prognostic tumor marker, and discuss possible approaches to telomerase inhibition as a target for cancer therapy.

Aging↗
PubMed1996

Changes in telomere lengths in renal cell carcinomas.

Telomeres, the extreme ends of chromosomes, play an important role in chromosome structure and function. The shortening of telomeres is one of the supposed mechanisms of cellular aging and death. Because of end replication problems the length of telomeres decreases with every cell cycle. This may lead to chromosome instability and additional genetic alterations possibly responsible of significant tumor development. In many cancer cells the length of telomeres depends on a balance between the loss of telomeric repeats, at each replication cycle, and the telomere lengthening, by the enzyme telomerase, which is repressed in most normal somatic cells. Many tumor cells demonstrate shortened telomeres in comparison to the corresponding normal tissue. In some types of human cancers the reduction of telomeric repeats was correlated with increasing disease severity. We analyzed Southern blots of HINF1-digested DNA of a large number of renal cell carcinomas (RCC) including different tumor areas, secondary tumors and metastases (76 cases with 142 tumor samples) for changes in the length of telomeric repeats using the oligonucleotide probe (TTAGGG)3 and found telomere shortening in 54%, suggesting that a reduction of the telomeric repeat length is not a general characteristic in RCC. Intratumor heterogeneity was demonstrated in seven cases. But also two RCC, with elongated telomeres in the tumor tissue, were observed. Shortened telomeres do not seem to be associated with advanced stages of tumor development or specific histopathological subtypes of RCC.

Adult↗
PubMed1995

Morphology of the left atrial appendage.

BACKGROUND: When examining the left atrial appendage by transesophageal echocardiography, differences in size and shape of the left atrial appendage are to be observed. The study was carried out with the aim of investigating the morphology of the left atrial appendage and to find associations with pathologic cardiac findings. METHODS AND RESULTS: In 220 cases (106 female, 114 male, mean age 72 +/- 13 years) a cast of the left atrial appendage was made after the post mortem examination by using synthetic resin. In 198 cases an ECG was available (sinus rhythm n = 143, atrial fibrillation n = 55). The casts were described in respect to course and ramifications of the principal axis. The casts were measured concerning orifice diameters, outline, and volume. Most frequently (42%) the course of the principal axis was angulated below 100 degrees. More than five ramifications of the principal axis were found in 56% of the casts. The volume ranged from 770-19,270 mm3 (mean 5,220 +/- 3,041). When comparing the clinical and autopsy-data of the patients with the morphology of the casts, associations could be found between the volume of the casts and atrial fibrillation (7,060 mm3 as compared to 4,645 mm3 in sinus rhythm, P < 0.01), left ventricular hypertrophy (5,740 mm3 as compared to 4,639 mm3 without hypertrophy, P < 0.01), myocardial scars (5,923 mm3 as compared to 4,891 mm3 without scars, P < 0.05), closed foramen ovale (5,515 mm3 as compared to 4,037 mm3 with patent foramen ovale, P < 0.01), and left atrial appendage thrombi (8,566 mm3 as compared to 5,027 mm3 without thrombi, P < 0.01). CONCLUSION: Left atrial appendages are formations greatly varying in volume and shape. This variability should be considered when interpreting images of the left atrial appendage, and in particular when diagnosing thrombi.

Adult↗