Search PubMed⌕ Search

Biomedical subjects

A Berger

Publications and source records attributed to A Berger.

At least 73 records · Page 4Linked to original sources
PubMed2001

The role of viral load determination for the management of human immunodeficiency virus, hepatitis B virus and hepatitis C virus infection.

During the last 5 years, considerable scientific and financial efforts have been made in the development of quantitative nucleic acid detection technology. For detection of human immunodeficiency virus (HIV), quantitative culture is time consuming, cumbersome and requires appropriate laboratory safety equipment. Quantitative determination of p24 antigen by enzyme immunoassay is of limited value due to its relatively poor sensitivity. Therefore, quantitative determination of viral load using nucleic acid amplification techniques is the most accurate, prognostic marker for HIV type 1 infection, independently of the CD4+ cell count. Hepatitis B virus (HBV) is not cultivable in vitro. Serological assays allow an accurate diagnosis and follow-up of acute or chronic infection. Quantification of HBV DNA is used for the monitoring of antiviral therapy, determination of infectivity and for resolution of unclear serological profiles, e.g. isolated anti-HBc reactivity, as well as for patients in which HBV mutants are suspected. Hepatitis C virus (HCV) can only be detected by molecular based assays because no cell culture system, which permits a reliable isolation of clinical specimens, is currently available. Furthermore, early diagnosis and follow-up of infection cannot be achieved with antibody serology. The prognostic relevance of quantitative HCV RNA determination is of limited value for the long-term prognosis of chronic hepatitis C. However, viral load may predict the outcome of antiviral therapy. Genetic diversity is another challenge for HCV RNA quantification.

HIV Infections↗
PubMed2001

Sealing of postoperative axillary leakage after axillary lymphadenectomy using a fibrin glue coated collagen patch: a prospective randomised study.

Seroma formation after axillary lymphadenectomy in women with breast cancer remains a problem despite many efforts to reduce surgery-related morbidity. In a prospective, randomised, open, parallel-group, controlled clinical trial we evaluated the effect of a fibrin-glue coated collagen patch (TachoComb H, Nycomed Pharma AS, Denmark) on volume and duration of postoperative axillary drainage, duration of hospital stay, and procedural safety. Sixty patients were included in the study. Patients did not differ with respect to general characteristics, such as age, body mass index, treatment modality, and tumor stage distribution. In 29 patients, a fibrin-glue coated collagen patch was applied from the apex axillae to the thoracic longus nerve and half a patch was applied to the lateral border of the axillary nerve-vessel bundle. Thirty-one patients were randomised to standard closure of the axillary lymphadenectomy area. The mean duration of axillary drainage was 3.8 +/- 1.9 days in the fibrin-glue treatment group and 3.9 +/- 1.8 days in the control group (p = NS). The mean total drainage volume was 338.5 +/- 251.8 ml in the fibrin-glue treatment group and 370.8 +/- 314.6 ml in the standard closure group (p = NS). The mean length of post-operative hospital stay was 9.1 +/- 2.7 days in the fibrin-glue treatment group and 9.3 +/- 3.6 days in the standard closure group (p = NS). Seven patients (25%) and eight patients (25%) were diagnosed with local inflammation in the fibrin-glue treatment group and the standard closure group, respectively (p = NS). Seroma formation after drain removal was found in 11 patients (39%) in the fibrin-glue treatment group and in 13 patients (42%) in the standard closure group (p = NS). In summary, we observed no statistically significant differences with respect to axillary drainage time, drainage volume, length of hospital stay, local inflammation, and seroma formation after drainage removal.

Axilla↗
PubMed2001

Transcription of SST2 somatostatin receptor gene in human pancreatic cancer cells is altered by single nucleotide promoter polymorphism.

BACKGROUND & AIMS: The somatostatin receptor SST2 mediates the antiproliferative effect of stable somatostatin analogues. SST2 gene expression is lost in most human pancreatic carcinomas. We investigated the mechanisms that could be involved in this defect. METHODS: SST2 gene structure was investigated by sequencing and restriction fragment length polymorphism. Characterization of the polymorphism was performed by electrophoretic mobility shift, cross-linking, and transcription assays. RESULTS: No major deletion of the SST2 coding sequence was found in pancreatic carcinoma specimens, but 2 point mutations were frequently detected in the promoter sequence at positions -83 (A-->G) and -57 (C-->G) from the major transcription initiation site. These mutations were present in pancreatic cancer but also in normal pancreatic tissues or leukocytes and thus correspond to a genetic polymorphism. In the 2 human pancreatic cancer cell lines MiaPaCa-2 and AsPC-1, the naturally occurring mutation -57G had no effect on transcription of SST2 gene, whereas -83G mutation reduced it by 60%-70%. We showed that the -83G mutation creates a specific binding site for the nuclear factor I. Cotransfection experiments showed that the nuclear factor I-A1.1 isoform was responsible for SST2 promoter repression. CONCLUSIONS: The -83G polymorphism identified on human SST2 gene promoter is responsible for the specific fixation of nuclear factor I and repression of SST2 transcription in human pancreatic cancer cells. However, its contribution to pancreatic tumorigenesis remains unknown.

5' Untranslated Regions↗
PubMed2001

[Value of EEG monitoring in intensive care patients in plastic surgery--indications and experiences].

EEG monitoring can be performed at the patients' bedside and it is a valuable support in therapeutic decision making providing unique information about the functional state of the brain. Due to newer technical developments, EEG monitoring can be conducted rather easily. In this article, indications for EEG monitoring in plastic surgical patients are presented: controlling the level of sedation, use in states of increased intracranial pressure, screening the cerebral state in comatose patients, diagnosis and therapy of epileptic seizures, and the search for circumscribed cerebral abnormalities. Furthermore, practical experience with the use of the new EEG monitor Narcotrend, which is provided with an automatic EEG classification, is described.

Cerebral Cortex↗
PubMed2001

Carbon dioxide concentration and nitrogen input affect the C and N storage pools in Amanita muscaria-Picea abies mycorrhizae.

We studied the influence of elevated atmospheric CO2 concentration ([CO2]) on the vacuolar storage pool of nitrogen-containing compounds and on the glycogen pool in the hyphal sheath of Amanita muscaria (L. ex Fr.) Hooker-Picea abies L. Karst. mycorrhizae grown with two concentrations of ammonium in the substrate. Mycorrhizal seedlings were grown in petri dishes on agar containing 5.3 or 53 mg N l(-1) and exposed to 350 or 700 microl CO2 l(-1) for 5 or 7 weeks, respectively. Numbers and area of nitrogen-containing bodies in the vacuoles of the mycorrhizal fungus were determined by light microscopy linked to an image analysis system. The relative concentration of nitrogen in the vacuolar bodies was measured by electron energy loss spectroscopy (EELS). Glycogen stored in the cytosol was determined at the ultrastructural level by image analysis after staining the sections (PATAg test). Shoot dry weight, net photosynthesis and relative amounts of N in vacuolar bodies were greater at the higher N and CO2 concentrations. The numbers and areas of vacuolar N-containing bodies were significantly greater at the higher N concentration only at ambient [CO2]. In the same treatment the percentage of hyphae containing glycogen declined to nearly zero. We conclude that, in the high N/low [CO2] treatment, the mycorrhizal fungus had an insufficient carbohydrate supply, partly because of increased amino acid synthesis by the non-mycorrhizal rootlets. When [CO2] was increased, the equilibrium between storage of glycogen and N-containing compounds was reestablished.

Amanita↗
PubMed2001

Poor storage and handling of tissue mimics mitochondrial DNA depletion.

Analysis of the mitochondrial DNA (mtDNA) is an important part in the diagnosis of mitochondrial disorders. Besides point mutations and deletions in the mitochondrial genome a reduction in the amount of mtDNA molecules (mtDNA depletion) can also be the reason for mitochondrial defects. The DNA stability in clinical samples is essential for proper performance and interpretation of DNA based diagnosis. The stability of mtDNA was compared with that of nuclear DNA under poor handling and storage conditions. Fresh and thawed muscle tissue specimens were kept at different temperatures for a certain period of time before DNA isolation. Quantitative Southern blot analysis revealed a time-dependent decrease in the amount of mtDNA compared with nuclear DNA in thawed tissue specimens. Therefore, the current study demonstrates that proper specimen storage is a critical issue in quantitative mtDNA analysis and that poor handling and storage of tissue may mimic a severe mtDNA depletion.

Blotting, Southern↗
PubMed2001

Local anesthetic inhibition of G protein-coupled receptor signaling by interference with Galpha(q) protein function.

Although local anesthetics are considered primarily Na(+) channel blockers, previous studies suggest a common intracellular site of action on different G protein-coupled receptors. In the present study, we characterized this site for the LPA, m1 muscarinic, and trypsin receptor. Xenopus laevis oocytes expressing endogenous LPA and trypsin or recombinant m1 receptors were two-electrode voltage clamped. We studied LPA inhibition in the presence of ropivacaine stereoisomers to determine whether LA act on a protein site. Ropivacaine inhibited LPA signaling in a stereoselective and noncompetitive manner, suggesting a protein interaction. Antisense injection was used to characterize G protein alpha-subunits involved in mediation of LPA, m1, trypsin, and angiotensin(1A) receptor signaling. Lidocaine and its analog QX314 were injected into oocytes expressing these receptors to examine a potential role for specific G protein alpha-subunits as targets for LA. Galpha(q) was shown to be among the primary G protein subunits mediating the LPA, m1, and trypsin receptor signaling, all of which were inhibited to a similar degree by intracellular injected QX314 (424 x 10(-6) M). Since the angiotensin(1A) receptor, previously shown not to be affected by LA, was found not to signal via Galpha(q), but via Galpha(o) and Galpha(14), the intracellular effect of LA most likely takes place at the Galpha(q)-subunit.

Amides↗
PubMed2001

Analysis of interleukin-18, interleukin-1 converting enzyme (ICE) and interleukin-18-related cytokines in Crohn's disease lesions.

A local increase of interleukin-18 (IL-18) expression has been recently demonstrated in Crohn's disease (CD), suggesting a role for mature IL-18 (cleaved by ICE protease) in the induction of proinflammatory cytokines and Th1 polarization observed in CD lesions. The aim of this study was to investigate IL-18 modulation and its potential immune consequences in CD lesions. We showed increased IL-18 production in chronic CD lesions and identified epithelial cells and macrophages as IL-18-producing cells. A twofold increase in ICE alpha, beta, and/or gamma mRNA that encodes for the complete mature peptide was required for ICE activity, and a marked increase in IL-18R-positive immune cells was observed in chronic lesions compared to uninvolved areas or normal control samples. Chronic lesions also displayed intense transcription of IL-18-induced cytokines, IFN-gamma, IL-1beta, TNF-alpha, and IL-8. By contrast, when neither IL-18 nor ICE mRNAs were enhanced (early asymptomatic CD lesions), IL-18-induced cytokines were not up-regulated. These results are in accordance with a putative role of mature IL-18 in the pathogenesis of CD.

Base Sequence↗