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H K Wolf

Publications and source records attributed to H K Wolf.

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

[Bilateral elastofibroma dorsi].

A 75-year-old man had painless, slowly enlarging tumors in the right and left infrascapular regions. Clinically, the tumors were nontender and semimobile. MR imaging and the operative exploration revealed tumors infiltrating the lateral thoracic muscles and periost of the scapula and underlying ribs. At surgery, the tumors were thought to be malignant, most likely liposarcomas. The histological examination showed the characteristic appearance of elastofibromas with spindle-shaped fibroblasts, which were separated by thick eosinophilic collagenous and elastic fibers. Elastofibromas are benign mesenchymal soft-tissue lesions that mainly affect elderly women. In 10 % of the patients bilateral, often asynchronous tumors are seen. Ninety-nine percent of the lesions are located in the subscapular region. Occasional elastofibromas have been described in the extremities, head, and in the abdominal and thoracic cavities.

Aged↗
PubMed1999

An increase of hippocampal calretinin-immunoreactive neurons correlates with early febrile seizures in temporal lobe epilepsy.

Numerous studies indicate that initial precipitating injuries (IPI) such as febrile seizures during early childhood may play a pivotal role in the pathogenesis of temporal lobe epilepsy (TLE) and Ammon's horn sclerosis (AHS). Previous data demonstrate an increase of horizontally oriented neurons in molecular layers of hippocampal subfields, which are immunoreactive for calretinin (CR-ir) and resemble Cajal-Retzius-like cells. Cajal-Retzius cells are transiently expressed in the murine developing hippocampus and are critically involved in neuronal pattern formation. Here we investigated a potential relationship between the distribution of horizontally oriented calretinin-immunoreactive neurons and the clinical history of TLE patients with AHS. Horizontally oriented neurons in the molecular layer of the hippocampal formation have been visualized by antibodies against the calcium-binding proteins calretinin and calbindin D-28k. Cell counts derived from 27 epilepsy patients with AHS were compared with autopsy specimens from developing and adult normal human hippocampus (n = 26). During ontogeny, CR-ir cells showed a marked perinatal peak in the CA1 and dentate gyrus molecular layer (CA1-ML, DG-ML) followed by a gradual postnatal decline. In hippocampal specimens from TLE patients with AHS and seizure onset before the age of 4 years, significantly higher levels of CR-ir neurons in CA1-ML (P = 0.05) and DG-ML (P < 0.05) were encountered than in AHS patients without precipitating seizures or with an uneventful early medical history. However, all three groups had higher levels of CR-ir neurons compared to adult controls obtained at autopsy (P < 0.01). In addition, AHS specimens showed increased CR-ir neuropil staining throughout the DG-ML compared with the restricted distribution of CR-ir fibers within the superficial granule cell layer visible in controls. These findings suggest that a considerable number of TLE patients with AHS display signs of impaired hippocampal maturation and circuitry formation as indicated by increased numbers of Cajal-Retzius like cells. It remains to be elucidated, how these changes contribute to the pathogenesis of TLE.

Adolescent↗
PubMed1999

The CD34 epitope is expressed in neoplastic and malformative lesions associated with chronic, focal epilepsies.

The etiology and pathogenesis of complex focal lesions associated with chronic, intractable epilepsy are largely unknown. Some data indicate that malformative changes of the central nervous system may precede the development of gangliogliomas and other epilepsy-associated neoplasms. In the present immunhistochemical study, we have examined epilepsy-associated lesions for CD34, a stem cell marker transiently expressed during early neurulation. Surprisingly, most tissue samples from patients with chronic epilepsy (n = 262) revealed neural cells immunoreactive for CD34. Prominent immunoreactivity was detected in gangliogliomas (74%), low-grade astrocytomas (62%) and oligodendrogliomas (59%). Only 52% of non-neoplastic, malformative pathologies, such as glio-neuronal hamartias or hamartomas showed solitary or small clusters of CD34-immunoreactive cells. None of the adult control tissues (n = 22), none of the specimens obtained from the developing human brain (n = 44) and none of those tumor samples from patients without epilepsy (n = 63) contained CD34-immunoreactive neural cells. However, a malignant teratoma with microscopic features of early neural differentiation displayed a focal CD34-immunoreactive staining pattern. The majority of CD34-immunoreactive cells co-localized with S-100 protein and a small subpopulation was also immunoreactive for neuronal antigens. CD34 may, thus, represent a valuable marker for the diagnostic evaluation of neoplastic and/or malformative pathological changes in epilepsy patients. The CD34 immunoreactivity of these lesions indicates an origin from dysplastic or atypically differentiated neural precursors. Further studies may elucidate the functional significance of CD34 expression during the pathogenesis of epilepsy-related focal lesions as well as during neurogenesis.

Adolescent↗
PubMed1999

Clinical relevance of amygdala sclerosis in temporal lobe epilepsy.

OBJECT: The goal of this study was to define the incidence and clinical significance of amygdala sclerosis (AS) in patients with temporal lobe epilepsy (TLE). METHODS: Surgical specimens of the lateral amygdaloid nucleus and the hippocampus excised from 71 patients who were treated for medically intractable TLE were quantitatively evaluated using a computer-assisted image-analysis system and compared with 10 normal autopsy specimens. Densities of neurons and reactive astrocytes in the patients with TLE were correlated with clinical, neuropsychological, and depth-electroencephalography data. The neuron counts of the lateral amygdaloid nucleus did not correlate with various presumed etiological factors of TLE including hereditary seizures, birth complications, febrile convulsions, traumatic brain injury, infections, seizure semiology, and epileptological outcome. However, patient age at surgery was significantly higher (mean difference 10 years) when AS was present, as compared with patients without AS (p < 0.01). Seizure origin, as determined by using amygdalohippocampal depth electrodes, did not correlate with the presence or absence of AS. Neuropsychologically, there was a significant correlation between the neuronal densities of the lateral amygdaloid nucleus and both preoperative visual recognition and postoperative deterioration of short-term verbal memory performance (p < 0.05). CONCLUSIONS: Except for the relatively long history of epilepsy, the presence of AS is not associated with specific clinical or electrocorticographic features of mesial TLE. However, patients without AS are particularly at risk for deterioration of short-term verbal memory following amygdalohippocampectomy.

Adolescent↗
PubMed1999

[Histopathologic examination of rectal carcinoma].

In patients with rectal carcinoma, the histopathological evaluation of the surgical specimen provides pivotal prognostic and therapeutic information. Important parameters are tumor site, depth of invasion, histological type and grade, pattern of invasion (diffusely infiltrating versus expanding margin), degree of peritumoral lymphocytic infiltration, and tumor involvement of surgical margins and lymph nodes. Evaluation of the circumferential (deep, lateral) margin is of utmost importance. It should be labeled with ink in the gross specimen and should be examined histologically using several tissue blocks. The number of lymph node metastases and the total number of lymph nodes examined should be reported. A histological evaluation of the distal mesorectum in its entirety is recommended to detect discontinuous distal mesorectal tumor spread. The histopathological findings should be summarized using the TNM-classification.

Adenocarcinoma↗
PubMed1998

Expression of the c-Kit receptor and its ligand SCF in non-small-cell lung carcinomas.

Increasing experimental evidence indicates that stem-cell factor (SCF) and its cognate receptor c-Kit may participate in the growth control of various solid human malignancies. In the present study, we have extended this analysis to non-small-cell lung carcinomas (NSCLC). The results of an immunohistochemical analysis demonstrated that c-Kit/SCF are expressed by 30%/58% of adenocarcinomas, 15%/37% of squamous-cell carcinomas and by 40%/30% of undifferentiated carcinomas respectively. In 15% of primary and 18% of metastatic tumors, co-expression of the receptor and its ligand was documented. Western-blot assays of tumor extracts demonstrated that both molecules exhibit features of the normal receptor and ligand. Since biologically active SCF is physiologically present in the bloodstream, our data indicate that SCF is available to c-kit-expressing NSCLC cells via autocrine, paracrine or endocrine mechanisms. Thus activation of c-Kit in these tumors may contribute critically to their progression.

Carcinoma, Non-Small-Cell Lung↗
PubMed1998

MRI in sporadic Creutzfeldt-Jakob disease: correlation with clinical and neuropathological data.

To ascertain whether increased grey matter signal intensity on T2-weighted images in patients with sporadic Creutzfeldt-Jakob disease (CJD) corresponds to the stage and severity of this disease, we correlated MRI findings in four of our own and previously reported patients with sporadic CJD with the clinical variants, neuropathological changes at autopsy, duration of the disease and survival time after MRI examination. Of 15 patients with the extrapyramidal type of CJD, 10 showed increased signal in the basal ganglia on T2-weighted images. One of seven patients with the Heidenhain variant had increased signal in the occipital cortex. Patients without increased grey matter signal intensity had a longer overall duration of CJD (P = 0.035). Although the interval between onset of neurological symptoms and MRI was not different, patients without increased grey matter signal also survived longer after MRI examination (P = 0.022).

Aged↗
PubMed1998

Ten-year trends of heart disease risk factors in the Halifax County MONICA population. MONItoring of trends and determinants in CArdiovascular disease.

OBJECTIVE: To investigate trends in heart disease risk factors (RFs) in the general population of Halifax County, Nova Scotia during a 10-year period. DESIGN: Two independent random samples of the population of Halifax County were surveyed in 1985 and 1995; age ranges were 25-64 years and 25-74 years. Blood pressure, cholesterol and body weight were measured. Smoking and health history were obtained by questionnaire. MAIN RESULTS: Participation rate was 66.3% in 1985 and 1995. All RFs were negatively correlated with education attainment. RF changes from 1985 to 1995 were related to education level. Among survey participants, mean body mass index increased from 26.7 kg/m2 to 27.6 kg/m2 (P + 0.005) for men, and from 25.5 kg/m2 to 27.3 kg/m2 (P < 0.00001) for women. Average smoking rate increased from 32.0% to 34.6% (not significant) in men and from 27.7% to 29.1% (not significant) in women. Age-specific smoking rate increased by 13% (P = 0.14) in younger women and decreased by 10% in older women. (P = 0.00). Mean levels of blood cholesterol decreased by 0.2 mmol/L (P = 0.002) in men and 0.1 mmol/L (P = 0.20) in women. Systolic blood pressure increased by 6.3 mmHg (P < 0.0001) in men and by 7.9 mmHg (P < 0.0001) in women, being steepest in the lower education group. Mortality predicted from RFs declined between the survey years, but less than the observed mortality. This discrepancy may result from the effect of medical care or the delayed effect of RF changes. CONCLUSIONS: Some risk factors show a disturbing trend, indicating that an increased effort or a change in strategy is needed to combat the risk of ischemic heart disease.

Adult↗
PubMed1997

Medulloblastomas of the desmoplastic variant carry mutations of the human homologue of Drosophila patched.

Inactivating mutations in the PTCH gene, a human homologue of the Drosophila segment polarity gene patched, have been identified recently in patients with nevoid basal cell carcinoma syndrome. These patients are predisposed to various neoplasias including basal cell carcinomas and medulloblastomas (MBs). To determine the involvement of PTCH in sporadic MBs, which represent the most frequent malignant brain tumors in children, we screened for PTCH alterations in an unselected panel of 64 biopsy samples from 62 patients and four continuous MB cell lines, all derived from patients with sporadic MBs. Using single-strand conformational polymorphism analysis, we screened exons 2-22 and detected nonconservative PTCH mutations in 3 of 11 samples from sporadic cases of the desmoplastic variant of MB but none in 57 MBs with classical (nondesmoplastic) histology. In two of the tumors with mutations and in two additional desmoplastic cases, loss of heterozygosity was found at 9q22. These findings suggest that PTCH represents a tumor suppressor gene involved in the development of the desmoplastic variant of MB.

Adolescent↗
PubMed1997

The apolipoprotein E epsilon 4 allele is not associated with early onset temporal lobe epilepsy.

A polymorphism of the apolipoprotein E gene, in particular the epsilon 4 allele (ApoE4), has been associated with impaired neuronal phospholipid metabolism and synapse reorganization and has been implicated in several neurodegenerative disorders. Since selective neuronal cell lose and aberrant axonal reorganization represent hall-marks of Ammon's horn sclerosis (AHS) in patients with chronic temporal lobe epilepsy (TLE), the ApoE polymorphism was studied in 125 patients with TLE. The genotype analysis revealed a frequency of 15.5% for epsilon 4, and 74.8% and 9.8% for epsilon 3 and epsilon 2, respectively. These figures were not significantly different from those reported in the normal European population. In addition, no correlation was found between the ApoE4 allelotype and the age of epilepsy onset, seizure type, febrile seizures, family history of epilepsy, surgical outcome and neuropathological findings in patients with TLE. These data virtually exclude ApoE as a susceptibility gene involved in the pathogenesis of early onset TLE or AHS.

Adolescent↗
PubMed1997

Sarcoidosis presenting as an intra- or extra-axial cranial mass: report of two cases.

Sarcoidosis may also present as an extra- or intra-axial mass involving the central nervous system. These lesions are sometimes operated upon, because a neoplasm is suspected. We report two cases of unusual tumour-like extra- and intra-axial sarcoidosis. The extra-axial mass was just medial to the jugular foramen. Its morphology and signal characteristics differed from the more common lesions in this area. The intra-axial mass was in the temporal lobe, with only minor leptomeningeal involvement. Extra-axial sarcoidosis can be confused with a meningioma because these lesions can give relatively low signal on T2-weighted images. Intra-axial masses are presumed to represent a propagation and fusion of multiple leptomeningeal granulomas through the Virchow-Robin spaces in the brain; this pattern can be sought on contrast-enhanced T1-weighted images.

Aged↗
PubMed1997

Tuberous sclerosis-like lesions in epileptogenic human neocortex lack allelic loss at the TSC1 and TSC2 regions.

Glioneuronal malformations with a striking histological resemblance to cortical tubers of tuberous sclerosis, but no extracerebral stigmata of this phacomatosis, are frequently encountered in patients with chronic pharmacoresistant epilepsies. It is controversial as to whether these lesion represent a forme fruste of tuberous sclerosis or a distinct entity. The recently reported loss of heterozygosity (LOH) at the regions of the TSC1 or TSC2 locus in hamartomas obtained from different organs of patients with established tuberous sclerosis, including cortical tubers, stimulated us to examine epilepsy-associated tuberous sclerosis-like glioneuronal malformations with respect to LOH at the TSC1 and TSC2 loci of chromosomes 9q34 and 16p 13.3, respectively. The analysis was carried out on DNA derived from paraffin-embedded brain tissues of 11 patients. For 5 patients, peripheral blood leukocytes were also available for DNA extraction. We performed microsatellite analysis with five markers on chromosome 9 and four markers on chromosome 16. In addition, polymerase chain reaction-restriction fragment length polymorphism (RFLP) analysis was performed using a polymorphic EcoRV restriction site in exon 40 of the TSC2 gene. No LOH was identified in any of the cases. These findings do not support a relationship between the epilepsy-associated glioneuronal lesions and tuberous sclerosis. However, tuberous sclerosis is genetically heterogeneous and microsatellite and RFLP analysis cannot exclude small deletions or point mutations. Thus, given the histopathological similarity of glioneuronal malformations in epilepsy patients to cortical tubers, further molecular genetic studies will be needed as our understanding of the molecular basis of tuberous sclerosis increases to completely clarify the relationship of these lesions to tuberous sclerosis.

Adolescent↗
PubMed1997

Expression and distribution of vascular endothelial growth factor protein in human brain tumors.

Marked neovascularization is a hallmark of many neoplasms in the nervous system. Recent reports indicate that the endothelial mitogen vascular endothelial growth factor (VEGF) may play a critical role in the regulation of vascular endothelial proliferation in malignant gliomas. Using novel monoclonal antibodies to the VEGF polypeptide we have determined the expression and cellular distribution of VEGF protein in a representative series of 171 human central nervous system (CNS) tumors by immunohistochemistry and immunoblotting. In agreement with previous in situ hybridization data, 19 out of 20 glioblastomas (95%) showed immunoreactivity for VEGF, whereas both the percentage of immunoreactive tumors and the extent of immunoreactivity for VEGF were significantly lower in astrocytomas. Of the pilocytic astrocytomas (WHO grade I) 44% were immunoreactive for VEGF, but we observed several cases with pronounced vascular proliferates in the absence of VEGF. In ependymomas, meningiomas, hemangioblastomas, and primitive neuroectodermal tumors, there was no correlation between VEGF expression, vascular endothelial proliferation and the grade of malignancy. Oligodendrogliomas and the oligodendroglial component of mixed gliomas lacked immunoreactive VEGF, indicating that endothelial growth factors other than VEGF may regulate tumor angiogenesis in these neoplasms. Western blot analysis showed a predominant VEGF protein species of 23 kDa and confirmed the immunohistochemical data in all cases. Our findings demonstrate that VEGF is expressed in a wide spectrum of brain tumors in which it may induce neovascularization. However, other angiogenic factors also appear to contribute to the vascularization of CNS neoplasms.

Astrocytoma↗
PubMed1997

Neuronal loss and gliosis of the amygdaloid nucleus in temporal lobe epilepsy. A quantitative analysis of 70 surgical specimens.

Although clinical and electrophysiological evidence indicates that the amygdaloid body plays an important role in the pathogenesis of temporal lobe epilepsy, there are very few detailed data on histopathological changes in this nucleus in epilepsy patients. In the present study we have examined the lateral nucleus of the amygdaloid body in 70 surgical specimens from patients with temporal lobe epilepsy and in 10 control specimens with respect to neuronal density and gliosis. The results were compared to the neuronal loss in the hippocampal formation. Our goal was to examine the pathological alterations of the amygdaloid body and their correlation with other morphological changes in temporal lobe epilepsy. In epilepsy patients with Ammon's horn sclerosis or focal lesions of the temporal lobe, the neuronal density of the lateral amygdaloid nucleus was significantly decreased as compared to normal controls (P < 0.001). Overall, the mean volumetric density in epilepsy patients was reduced to 59% of that in normal individuals. There was no correlation between the neuronal density in the lateral amygdaloid nucleus and that in the different segments of the hippocampal formation or to the age at onset or the duration of epilepsy. The neuronal loss of the amygdaloid nucleus correlated well with the presence of fibrillary gliosis. Our findings demonstrate that the amygdaloid body is severely altered in most patients with temporal lobe epilepsy and that these changes are independent of those in the hippocampus. The presence of neuronal loss and gliosis in the amygdaloid nucleus of patients with focal lesions but no Ammon's horn sclerosis is compatible with an involvement of the amygdala in secondary epileptogenesis.

Adolescent↗
PubMed1997

Neural antigens in oligodendrogliomas and dysembryoplastic neuroepithelial tumors.

Oligodendrogliomas and dysembryoplastic neuroepithelial tumors (DNT) are frequently associated with epilepsies and share the presence of oligodendroglia-like cells with small round nuclei and optically empty perinuclear halos. The two entities may be difficult to discriminate in small surgical specimens and the origin and differentiation of the oligodendroglia-like cells has been controversial. To better characterize and distinguish the two entities we examined 25 oligodendrogliomas and 16 DNT immunohistochemically for the presence of the proliferation-associated Ki-67 antigen and the following neural antigens: the alpha 1 subunit of the GABAA receptor (GABAR), N-methyl-D-aspartate receptor subunit 1 (NR1), glutamate decarboxylase, neuronal nuclei antigen (NeuN), the embryonal form of the neural cell adhesion molecule (E-NCAM), synaptophysin, neurofilament protein (NFP), and glial fibrillary acidic protein (GFAP). Labeling indices for the Ki-67 antigens were generally less than 1% in both entities. In oligodendrogliomas, more than 50% of the tumors contained NR1- or E-NCAM-positive oligodendroglia-like cells, whereas NeuN-positive tumor cells were never observed. In DNT, NeuN- and NR1-positive tumor cells were present in 44% of the cases each; E-NCAM positivity was less frequent (19%). In both entities, immunoreactivity of oligodendroglia-like cells for GABAR and glutamate decarboxylase was rare and positivity for synaptophysin and neurofilament protein was absent. Some GFAP-positive tumor cells were present in approximately 70% of the cases in both entities. Except for the striking difference in NeuN positivity, the immunohistochemical profiles of oligodendroglia-like cells in DNT and oligodendrogliomas largely overlap and the differential diagnosis continues to rest mainly on conventional histopathological features. The NR1 positivity and the recently reported generation of action potentials in oligodendroglioma cells are consistent with neuronal differentiation and may contribute to the high epileptogenic potential of oligodendrogliomas.

Adult↗