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Biomedical subjects

J Weise

Publications and source records attributed to J Weise.

18 recordsLinked to original sources
PubMed2003

Detection of acute thalamo-mesencephalic infarction: diffusion abnormality precedes T2 hyperintensity.

OBJECTIVE: To examine the time course of signal changes in diffusion-weighted magnetic resonance imaging (DW-MRI) and T2-weighted MRI in a case of cerebral infarction in the posterior circulation territory. MATERIALS AND METHODS: Diffusion- and T2-weighted MRI and comparison of signal changes in these sequences at 4 h, 1 day and 4 days after the onset of clinical symptoms caused by acute thalamo-mesencephalic infarction. RESULTS: Four hours after the onset of symptoms, signal changes in DW-MRI revealed an infarction in the territory of the posterior perforating thalamic artery, whereas no signal changes were detected in T2-weighted MRI. In follow-up MRI 1 and 4 days after infarction, however, a marked hyperintensity matching the location of the diffusion deficit could be identified in T2 images. CONCLUSION: Signal changes in DW-MRI precede T2 hyperintensity after infarction in the posterior circulation territory after hemispheric infarction.

Acute Disease↗
PubMed2002

The mutual information: detecting and evaluating dependencies between variables.

MOTIVATION: Clustering co-expressed genes usually requires the definition of 'distance' or 'similarity' between measured datasets, the most common choices being Pearson correlation or Euclidean distance. With the size of available datasets steadily increasing, it has become feasible to consider other, more general, definitions as well. One alternative, based on information theory, is the mutual information, providing a general measure of dependencies between variables. While the use of mutual information in cluster analysis and visualization of large-scale gene expression data has been suggested previously, the earlier studies did not focus on comparing different algorithms to estimate the mutual information from finite data. RESULTS: Here we describe and review several approaches to estimate the mutual information from finite datasets. Our findings show that the algorithms used so far may be quite substantially improved upon. In particular when dealing with small datasets, finite sample effects and other sources of potentially misleading results have to be taken into account.

Algorithms↗
PubMed2001

Double-blind placebo-controlled administration of fluoxetine in restricting- and restricting-purging-type anorexia nervosa.

BACKGROUND: Anorexia nervosa is an often chronic disorder with high morbidity and mortality. Many people relapse after weight restoration. This study was designed to determine whether a selective serotonin reuptake inhibitor would improve outcome and reduce relapse after weight restoration by contributing to maintenance of a healthy normal weight and a reduction of symptoms. METHODS: We administered a double-blind placebo-controlled trial of fluoxetine to 35 patients with restricting-type anorexia nervosa. Anorexics were randomly assigned to fluoxetine (n = 16) or a placebo (n = 19) after inpatient weight gain and then were observed as outpatients for 1 year. RESULTS: Ten of 16 (63%) subjects remained on fluoxetine for a year, whereas only three of 19 (16%) remained on the placebo for a year (p =.006). Those subjects remaining on fluoxetine for a year had reduced relapse as determined by a significant increase in weight and reduction in symptoms. CONCLUSIONS: This study offers preliminary evidence that fluoxetine may be useful in improving outcome and preventing relapse of patients with anorexia nervosa after weight restoration.

Adolescent↗
PubMed2001

[Bithalamic infarcts as the etiology of acute stupor. Early diagnosis with diffusion-weighted MRI].

Fast diagnostic evaluation of somnolent or unconscious patients is a demanding task for neurologists. Apart from postictal, metabolic, and toxic causes, vascular syndromes must be rapidly identified in order to initiate a specific fibrinolytic therapy. Given its high mortality if not treated in time, this dictum holds especially true for basilar artery occlusion. However, certain ischemic lesions in the vascular territory of the basilar artery without occlusion of the basilar artery itself can also result in somnolence, sopor, or even unconsciousness. Here we report early imaging signs of bithalamic infarctions as the cause of acute sopor using diffusion-weighted (DW)-MRI, which reliably identifies acute bithalamic infarctions as a possible cause of acute consciousness disturbance, even with noncooperative patients.

Acute Disease↗
PubMed2001

Increased expression and activation of poly(ADP-ribose) polymerase (PARP) contribute to retinal ganglion cell death following rat optic nerve transection.

Excessive activation of the nuclear enzyme poly(ADP-ribose) polymerase (PARP) by free-radical damaged DNA mediates necrotic cell death in injury models of cerebral ischemia-reperfusion and excitotoxicity. We recently reported that secondary retinal ganglion cell (RGC) death following rat optic nerve (ON) transection is mainly apoptotic and can significantly but not entirely be blocked by caspase inhibition. In the present study, we demonstrate transient, RGC-specific PARP activation and increased retinal PARP expression early after ON axotomy. In addition, intravitreal injections of 3-aminobenzamide blocked PARP activation in RGCs and resulted in an increased number of surviving RGCs when compared to control animals 14 days after ON transection. These data indicate that secondary degeneration of a subset of axotomized RGCs results from a necrotic-type cell death mediated by PARP activation and increased PARP expression. Furthermore, PARP inhibition may constitute a relevant strategy for clinical treatment of traumatic brain injury.

Animals↗
PubMed2000

Degeneration and regeneration of ganglion cell axons.

The retino-tectal system has been used to study developmental aspects of axon growth, synapse formation and the establishment of a precise topographic order as well as degeneration and regeneration of adult retinal ganglion cell (RGC) axons after axonal lesion. This paper reviews some novel findings that provide new insights into the mechanisms of developmental RGC axon growth, pathfinding, and target formation. It also focuses on the cellular and molecular cascades that underlie RGC degeneration following an axonal lesion and on some therapeutic strategies to enhance survival of axotomized RGCs in vivo. In addition, this review deals with problems related to the induction of regeneration after axonal lesion in the adult CNS using the retino-tectal system as model. Different therapeutic approaches to promote RGC regeneration and requirements for specific target formation of regenerating RGCs in vitro and in vivo are discussed.

Animals↗
PubMed2000

Adenovirus-mediated expression of ciliary neurotrophic factor (CNTF) rescues axotomized rat retinal ganglion cells but does not support axonal regeneration in vivo.

Rat optic nerve (ON) transection leads to mainly apoptotic cell death of about 85% of the retinal ganglion cell (RGC) population within 14 days after lesion. In the present study, we tested the effect of adenovirally delivered CNTF (Ad-CNTF) on survival and regeneration of axotomized adult RGCs in vivo. Single intravitreal Ad-CNTF injection led to stable CNTF mRNA and protein expression for at least 18 days and significantly enhanced RGC survival by 155% when compared to control animals 14 days after ON transection. ON stump application of Ad-CNTF also resulted in an increased number of surviving RGCs. Ad-CNTF injection led to better preservation of intraretinal RGC axons but did not support regeneration of axotomized RGCs into a peripheral nerve graft. Thus, adenovirus-mediated neurotrophic factor supply is a suitable approach for reducing axotomy-induced RGC death in vivo and may constitute a relevant strategy for clinical treatment of traumatic brain injury.

Adenoviridae↗
PubMed1998

Axonal injury alters alternative splicing of the retinal NR1 receptor: the preferential expression of the NR1b isoforms is crucial for retinal ganglion cell survival.

Cellular-specific splicing of the retinal NMDAR1 receptor (NR1) and expression of NMDAR2 receptor (NR2) subunits in response to optic nerve injury was investigated by in situ hybridization in adult rats. A controlled optic nerve crush led to a clear alteration in the expression of alternatively spliced NR1 variants in the retinal ganglion cell layer (GCL). The NR1-2b and NR1-4b isoforms were preferentially expressed between 2 d and 1 week after injury, whereas expression for all other isoforms remained either unchanged or decreased to barely detectable levels within 4 weeks. Cellular silver grain density for NR2 subunits also declined in the GCL after trauma. To directly test the hypothesis that NR1b expression is crucial for cell survival after axonal trauma, we administered intraocularly an antisense oligonucleotide against the NR1b isoform 2 and 3 d after injury. This led to a drastic loss of retrogradely labeled retinal ganglion cells (RGCs). Antisense targeting clearly reduced retinal NR1 protein levels, as judged by Western blot analysis, but had no effect on the cell number in control retinas. These findings point toward injury-specific changes in alternative splicing of the NR1 receptor, which are crucial for the survival of RGCs after partial axonal trauma. We therefore propose that this reflects an adaptive, rather than a pathogenic, cellular response to neurotrauma.

Alternative Splicing↗
PubMed1998

Cancer associated serum antigen (CASA) levels in patients with breast carcinoma and in 3 control groups without breast cancer.

We have examined the predictive value of measurements of CASA (Cancer Associated Serum Antigen) levels in patients with breast carcinoma. The measurement uses monoclonal antibodies that bind to an epitope on the polymorphic epithelial mucin. CASA levels were of less value compared with the levels of other tumor markers (CA 15-3, CA 549 and CEA) in the management of patients with early breast cancer.

Adult↗
PubMed1996

Increased expression of basic fibroblast growth factor (bFGF) following focal cerebral infarction in the rat.

Basic fibroblast growth factor (bFGF) is a polypeptide with potent trophic effects on brain neurons, glia, and endothelial cells. In the current study, we used Northern blotting, in situ hybridization, and immunohistochemical techniques to examine bFGF expression in brain following focal infarction due to permanent occlusion of the proximal middle cerebral artery in mature Sprague-Dawley rats. We found a four-fold increase in bFGF mRNA in tissue surrounding focal infarcts at 1 day after ischemia. In situ hybridization showed that this increase was found throughout several structures in the ipsilateral hemisphere, including frontoparietal, temporal, and cingulate cortex, as well as in caudoputamen, globus pallidus, septal nuclei, nucleus accumbens, and olfactory tubercle. Increased bFGF mRNA expression was associated with cells having the distinct morphological appearance of astroglia in these structures. Immunohistochemistry showed an increase in the size and number of bFGF-immunoreactive (IR) nuclei in these same structures, as well as a shift from nuclear to nuclear plus cytoplasmic localization of immunoreactivity, beginning at 1 day, and peaking at 3 days after ischemia. Double immunostaining identified bFGF-IR cells as astroglia in these structures. (An exception was the piriform cortex, in which both increased bFGF mRNA levels and increased bFGF-IR was found in neurons at 1 day after ischemia). Overall, the peak of increased bFGF expression preceded the peak in expression of the astroglial marker GFAP within the ipsilateral hemisphere. Increased bFGF expression may play an important role in the glial, neuronal, and vascular changes occurring after focal infarction.

Animals↗
PubMed1995

Delayed treatment with intravenous basic fibroblast growth factor reduces infarct size following permanent focal cerebral ischemia in rats.

Basic fibroblast growth factor (bFGF) is a polypeptide that supports the survival of brain cells (including neurons, glia, and endothelia) and protects neurons against a number of toxins and insults in vitro. This factor is also a potent dilator of cerebral pial arterioles in vivo. In previous studies, we found that intraventricularly administered bFGF reduced infarct volume in a model of focal cerebral ischemia in rats. In the current study, bFGF (45 micrograms/kg/h) in vehicle, or vehicle alone, was infused intravenously for 3 h, beginning at 30 min after permanent middle cerebral artery occlusion by intraluminal suture in mature Sprague-Dawley rats. After 24 h, neurological deficit (as assessed by a 0- to 5-point scale, with 5 = most severe) was 2.6 +/- 1.0 in vehicle-treated and 1.5 +/- 1.3 in bFGF-treated rats (mean +/- SD; N = 12 vs. 11; p = 0.009). Infarct volume was 297 +/- 65 mm3 in vehicle- and 143 +/- 135 mm3 in bFGF-treated animals (p = 0.002). During infusion, there was a modest decrease in mean arterial blood pressure but no changes in arterial blood gases or core or brain temperature in bFGF-treated rats. Autoradiography following intravenous administration of 111In-labeled bFGF showed that labeled bFGF crossed the damaged blood-brain barrier to enter the ischemic (but not the nonischemic) hemisphere. Whether the infarct-reducing effects of bFGF depend on intraparenchymal or intravascular mechanisms requires further study.

Animals↗
PubMed1995

Basic fibroblast growth factor protects against excitotoxicity and chemical hypoxia in both neonatal and adult rats.

Basic fibroblast growth factor (bFGF) is a polypeptide growth factor that promotes neuronal survival. We recently found that systemic administration of bFGF protects against both excitotoxicity and hypoxia-ischemia in neonatal animals. In the present study, we examined whether systemically administered bFGF could prevent neuronal death induced by intrastriatal injection of N-methyl-D-aspartate (NMDA) or chemical hypoxia induced by intrastriatal injection of malonate in adult rats and 1-methyl-4-phenylpyridinium (MPP+) in neonatal rats. Systemic administration of bFGF (100 micrograms/kg) for three doses both before and after intrastriatal injection of either NMDA or malonate in adult rats produced a significant neuroprotective effect. In neonatal rats, bFGF produced dose-dependent significant neuroprotective effects against MPP+ neurotoxicity, with a maximal protection of approximately 50% seen with either a single dose of bFGF of 300 micrograms/kg or three doses of 100 micrograms/kg. These results show that systemic administration of bFGF is effective in preventing neuronal injury under circumstances in which the blood-brain barrier may be compromised, raising the possibility that this strategy could be effective in stroke.

1-Methyl-4-phenylpyridinium↗
PubMed1976

[Studies on the value of fecal tryptic and chymotryptic activity in the diagnosis and therapy of cystic fibrosis (author's transl)].

Under certain conditions the determination of the tryptic activity, especially of the chymotryptic activity in the feces mostly of infants in the first 4-6 weeks of life is considered to be an important step in the diagnosis of cystic fibrosis. The tryptic anc chymotryptic activity in the feces of children with cystic fibrosis declines when the substitution of pancreatic enzymes is stopped. On resubstitution, the activity rises in relation to the dose and attains the activity related to age as found in healthy children. A comparison of the proteolytic activity with the fat content of the feces during the study period without the enzyme substitution and during the period when the enzyme dosage varied showed no significant correlation. It is not possible to postulate a poor excretion of fats merely from the high proteolytic activity of the feces because the fecal proteolytic activity and the fat excretion are not inversely proportional to one another. For this reason, one cannot conclude that the grade of the proteolytic activity in the feces of patients with cystic fibrosis is a yardstick for the total digestive process when they are under pancreatic enzyme substitution.

Age Factors↗
PubMedDate not supplied

Cerebral perfusion alterations during the acute phase of experimental generalized status epilepticus: prediction of survival by using perfusion-weighted MR imaging and histopathology.

BACKGROUND AND PURPOSE: Persistent generalized status epilepticus (SE) is associated with alterations of cerebral perfusion (CP). Because perfusion-weighted MR imaging (PWI) allows noninvasive CP-determination, the aim of this study was to investigate CP alterations during acute experimental SE correlated with SE-induced neuronal cell loss. METHODS: The rat pilocarpine model was used to induce SE. Multilocal PWI was performed before (baseline) and 3, 15, 30, 60, and 120 minutes after onset of SE. Bolus-peak ratio (BPR) was calculated for the retrosplenial and piriform cortex, hippocampus, amygdala, and thalamus and compared with baseline. Neuronal cell loss was quantified at different time points after induction of SE by cresyle violet staining. RESULTS: Immediately after SE onset (3 minutes), BPR temporarily increased to 102%-130% in all regions, with a maximum in the amygdala (129 +/- 16%) and hippocampus (130 +/- 21%). At 15, 30, and 60 minutes, BPR decreased continuously to 57%-76%. BPR values <55% in the parietal and/or temporal cortex resulted in death. In surviving animals, BPR recovered to 66%-79% and there was a good correlation between neuronal cell loss in specific brain regions at 2 weeks after SE onset and maximal decrease in BPR (r > 0.73). CONCLUSION: PWI demonstrated a transient cerebral hyperperfusion immediately after SE onset, followed by a significant continuous decline to different perfusion levels. In our experimental setting, a decline of cortical BPR below 55% of baseline seems to be a prognostic threshold value associated with subsequent death. In surviving animals, there is good correlation between the maximal decrease in BPR in the acute phase of SE and late neuronal cell loss.

Acute Disease↗
PubMedDate not supplied

First experiences with the use of CASA in mammary carcinoma.

The expression of the tumor marker CASA (cancer associated serum antigen) was studied in patients with mammary carcinoma; increased values were almost exclusively seen in cases of manifest metastasis. No correlation existed between tumor stage, lymph node involvement and grading. Marker levels were tested by means of enzyme-immune-assay of the firm medac (Hamburg), with a cut-off value set at 4 U/ml.

Biomarkers, Tumor↗