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H Schmoll

Publications and source records attributed to H Schmoll.

15 recordsLinked to original sources
PubMed2004

Observations on experimental marginal periodontitis in rats.

OBJECTIVE: The purpose of this study was to assess periodontal destruction following experimentally induced marginal periodontitis in rats by ligatures over a 60-day observation period. The extent to which the physiological movement of teeth influenced the effect of the ligatures was also examined. In addition, two methods for measuring bone loss in the defleshed jaw were compared. METHODS: Thirty-five male Sprague-Dawley rats (SD) were divided into five groups. Marginal periodontitis was induced by ligatures on the second maxillary molars. Rats were killed after 15, 30, and 60 days. Rats in the control group were killed on day 1 and day 60. Bone loss was determined with two different methods on the buccal and palatinal surfaces of the defleshed jaw. In the first method, the distance of the cementoenamel junction (CEJ) from the alveolar bone crest (ABC) was measured at different sites; in the second method, the area of the exposed root surface of the molars was measured. RESULTS: Comparison of the control groups from day 1 and day 60 using both measuring methods showed significant differences in bone loss. In the area where the ligature was located, test rats exhibited significantly greater bone loss than control rats. Comparison of control rats from day 1 with test rats from day 15 showed that the increase in bone loss between the groups within the area of the ligature was significantly greater than outside it. The age-dependent bone loss increases over the entire observation period of 60 days. The ligature-induced bone loss increased most from day 1 to day 15; on days 30 and 60, slighter increases in bone loss were observed. CONCLUSIONS: The application of this model can only be recommended for short (</=15 days) observation periods. The distance method should be preferred to the area method.

Age Factors↗
PubMed2001

Dynamics of gene expression for immediate early- and late genes after seizure activity in aged rats.

The ability of the rodent brain to support plasticity-related phenomena declines with increasing age. A decreased coordination of genes implicated in brain plasticity may be one factor contributing to this decline. Synaptic rearrangement that occurs after seizure activity is regarded as a model of brain plasticity. In a rat model of seizure-related brain plasticity, we found that the induction of immediate-early genes, as exemplified by c-fos and tissue plasminogen activator ( tPA), is not impaired in the aged rat brain. However, the aged rat brain responded more slowly to chemically induced seizure, and the levels of c-fos and tPA mRNAs induction are decreased in the cortex and in the hippocampus of 30 month old rats, as compared to the levels expressed by 3 month old rats. In addition, at the peak induction, the TPA transcripts were restricted to certain cortical layers of the older rats. Surprisingly, in applying the same experimental paradigm to late genes, we found that there was a shift toward earlier times in the maximum expression of growth-related molecules, the microtubule-associated protein 1B (MAP1B) mRNA, which was very evident in 18 month old rats. Aberrant immunolabeling of MAP1B occurred in cortical layer VI of the aged rats where, unlike in young rats, there was heavy staining of neuronal somata. These results suggest that (1) one consequence of aging, besides decreases in the levels of mRNA, is a progressive loss of coordination in gene activity following the administration of a stimulus; (2) since c-fos, TPA and MAP1B have been implicated in neuronal plasticity, these findings could explain, in part, the limited plasticity of the aging brain.

Journal Article↗
PubMed2000

Brain plasticity: to what extent do aged animals retain the capacity to coordinate gene activity in response to acute challenges.

The ability of the rodent brain to support plasticity-related phenomena declines with increasing age. A decreased coordination of genes implicated in brain plasticity may be one factor contributing to this decline. Synaptic rearrangement that occurs after seizure activity is regarded as a model of brain plasticity. In a rat model of seizure-related brain plasticity, we found that the induction of immediate-early genes, as exemplified by c-fos and tissue plasminogen activator (TPA) is not impaired in the aged rat brain. However, the aged rat brain responded more slowly to chemically induced seizure and the levels of c-fos and TPA mRNAs induction are decreased in the cortex and in the hippocampus of 30-month-old rats, as compared to the levels expressed by 3-month-old rats. In addition, at the peak induction the TPA transcripts were restricted to certain cortical layers of the older rats. Surprisingly, in applying the same experimental paradigm to late genes we found that there was a shift toward earlier times in the maximum expression of growth-related molecule, the microtubule-associated protein 1B (MAP1B) mRNA, which was very evident in 18-month-old rats. Aberrant immunolabeling of MAP1B occurred in cortical layer VI of the aged rats where, unlike in young rats, there was heavy staining of neuronal somata. These results suggest that (i) one consequence of aging, besides decreases in the levels of mRNA, is a progressive loss of coordination in gene activity following the administration of a stimulus; (ii) since c-fos, TPA and MAP1B have been implicated in neuronal plasticity, these findings could explain, in part, the limited plasticity of the aging brain.

Aging↗
PubMed2000

Delayed and blunted induction of mRNA for tissue plasminogen activator in the brain of old rats following pentylenetetrazole-induced seizure activity.

The ability of the rodent brain to support plasticity-related phenomena declines with increasing age. Here we investigated the extent to which old rats retain the capacity to initiate transcription for immediate early genes, particularly as it relates to brain plasticity, in response to a strong stimulus. The intraperitoneal administration of pentylenetetrazole (PTZ) to rats of various ages evoked tonic-clonic seizures. Using an RNA gel-blot and in situ hybridization analysis, we found that 1 hour after the onset of seizure, messenger RNA (mRNA) for tissue plasminogen activator (TPA) was increased approximately 3.7-fold in the hippocampi of 3-month-old rats. The levels of TPA mRNA in the hippocampi and cortices of 3-month-old rats returned to control levels by 3 hours after PTZ administration. The levels of TPA mRNA increased 2.5-fold in the hippocampi of 18-month-old rats and 1.8-fold in the brains of the 28-month-old-rats at 3 hours and returned to basal levels by 15 hours following PTZ treatment. Quantitatively similar increases were calculated for the cortex. At peak induction the transcripts were localized throughout the cortical layers of the 3-month-old rats, whereas the TPA mRNA expression was restricted to cortical layer V of the older rats. Our results suggest that although the aging brain retains the capacity to respond to chemically induced seizures, the induction of TPA mRNA is temporarily delayed and the levels are diminished with increasing age. Because TPA has been implicated in neuronal plasticity, this finding suggests that immediate early genes are important factors in the limited plasticity of the aging brain.

Aging↗
PubMed1999

Anomalous expression of microtubule-associated protein 1B in the hippocampus and cortex of aged rats treated with pentylenetetrazole.

The aim of the present study was to assess the age-dependent response of microtubule-associated protein 1B, a plasticity-associated protein deriving from a late gene, following administration of an epileptogenic stimulus. The effect of a single administration of the convulsant pentylenetetrazole on microtubule-associated protein 1B expression in the hippocampal formation and cortex of three-, 18- and 28-month-old rats was assessed using northern blot analysis, in situ hybridization and immunohistochemistry. In three-month-old rats, we detected initial increases in microtubule-associated protein 1B messenger RNA at 15 h following pentylenetetrazole administration in the granule cells of the dentate gyrus, in the CA3 region of the hippocampus and in layers II/III of the entorhinal cortex, and these reached a maximum at 44 h. However, in the hippocampus and cortex of 18-month-old rats, the peak occurred at 15 h, and in the brains of 28-month-old rats a blunted peak was reached at 3 h. Pentylenetetrazole treatment in young rats resulted in a robust induction of microtubule-associated protein 1B immunoreactivity in the granule cells of the dentate gyrus and in layers II/III of the entorhinal cortex, but also produced a large decrease in the retrosplenial cortex. However, following pentylenetetrazole treatment in older rats, the granule cells of the dentate gyrus were nearly devoid of microtubule-associated protein 1B immunoreactivity, whereas the retrosplenial cortex showed no changes at all, and the entorhinal cortex had an expression pattern similar to that of young rats. Aberrant immunolabeling of microtubule-associated protein 1B occurred in cortical layer VI of the aged rats where, unlike in young rats, there was heavy staining of neuronal somata. These results suggest that the regulation of the plasticity-associated protein microtubule-associated protein 1B is altered in the ageing rat brain, with the peak of expression shifted to earlier times in 18-month-old rats and blunted, variable increases at even earlier times in 28-month-old rats.

Aging↗
PubMed1999

Upregulation of MAP1B and MAP2 in the rat brain after middle cerebral artery occlusion: effect of age.

Although stroke in humans usually afflicts the elderly, most experimental studies on the nature of cerebral ischemia have used young animals. This is especially important when studying restorative processes that are age dependent. To explore the potential of older animals to initiate regenerative processes after cerebral ischemia, the authors studied the expression of the juvenile-specific cytoskeletal protein, microtubule-associated protein (MAP) 1B, and the adult-specific protein, MAP2, in male Sprague-Dawley rats at 3 months and 20 months of age. The levels of MAP1B and MAP2 transcripts and the corresponding proteins declined with increasing age in the hippocampus. In the cortex, the levels of the transcripts did not change significantly with age, but the morphologic features of immunostained fibers were clearly affected by age; that is, cortical MAP1B fibers became thicker, and MAP2 fibers, more diffuse, in aged rats. Focal cerebral ischemia, produced by reversible occlusion of the right middle cerebral artery, resulted in a large decrease in the expression of both MAP1B and MAP2 in the infarct core at the messenger ribonucleic acid and protein levels. However, at 1 week after the stroke, there was vigorous expression of MAP1B and its messenger ribonucleic acid, as well as MAP2 protein, in the border zone adjacent to the infarct of 3-month-old and 20 month-old male Sprague-Dawley rats. The upregulation of these key cytologic elements generally was diminished in aged rats compared with young animals, although the morphologic features of fibers in the infarct border zone were similar in both age groups. These results suggest that the regenerative potential of the aged rat brain appears to be competent, although attenuated, at least with respect to MAP1B and MAP2 expression up to 20 months of age.

Aging↗
PubMed1998

Altered expression of microtubule-associated protein 1B in cerebral cortical structures of pentylenetetrazole-treated rats.

Using Northern blot, immunoblotting, immunocytochemistry, and in situ hybridization, we show that a single administration of the convulsant pentylenetetrazole leads to robust, long-term changes in microtubule-associated protein 1B and its mRNA, in the adult rat brain. The first increases in MAP1B mRNA were detected at 15 hr following pentylenetetrazole administration in the temporal (Te2) and perirhinal cortex followed by increases in microtubule-associated protein 1B immunoreactivity at 72 hr postseizure. In contrast, the levels of microtubule-associated protein 1B mRNA and protein in layers I-II of the retrosplenial and parietal cortex (Par2) declined visibly by 24 hr and 72 h, respectively, post-seizure. The changes included loss of staining in layers I-II and development of structures resembling "strings-of-beads" along the fibers of projection neurons of layer V. The levels of microtubule-associated protein 1B mRNA in the entorhinal cortex peaked at later times (72 h), especially in layers II-III, and returned to control levels by 10 days. Whereas the levels of microtubule-associated protein 1B immunoreactivity in the retrosplenial and parietal cortex recovered by 5-10 days, it persisted at high levels through day 35 in layer V of the temporal cortex (Te2), layers II-III of the perirhinal cortex and layers I-II of the lateral entorhinal cortex. These results indicate that seizure activity leads to long-term upregulation of genes coding for structural elements that are characteristic of the immature brain such as microtubule-associated protein 1B.

Animals↗
PubMed1997

Increased expression of microtubule-associated protein 1B in the hippocampus, subiculum, and perforant path of rats treated with a high dose of pentylenetetrazole.

A single administration of the convulsant pentylenetetrazole (PTZ) initiates a complex pattern of long-term changes in microtubule-associated protein 1B (MAP1B) expression across the hippocampal formation. Using Northern blot and in situ hybridization we show that the first increases in MAP1B mRNA were detected at 15 h following PTZ administration in the granule cells of the dentate gyrus and CA3 region of the hippocampus and reached a maximum at 44 h. The levels of MAP1B mRNA in the subiculum peaked at later times (5 days). At 72 h MAP1B immunoreactivity was mainly localized in the granule-cell bodies and dentate inner and midmolecular layer as well as in neuronal cell bodies and the stratum lucidum, including the mossy fiber pathway of the CA3 region. By 5-10 days the levels of MAP1B in the pyramidal cells in the CA3 region decreased to very low levels; rather, heavy staining of interneuron-like cells and "strings-of-bead" structures all over the hippocampus and at the stratum oriens/alveus border were seen. The levels of MAP1B in the hippocampus returned to control levels by 20 days after PTZ administration. MAP1B immunoreactivity in the alvear path was also evident at 5 days postinjection at the CA1/alveus border. The intensity of MAP1B staining increased gradually in the perforant path starting at 72 h and persisted at high levels until day 35. Our studies show that (i) MAP1B is a temporal and regional marker for rapid and acute epileptic seizures and (ii) long-term increases in MAP1B in the perforant path might play a role in PTZ-induced seizures.

Animals↗
PubMed1995

Complement C1q and C3 mRNA expression in the frontal cortex of Alzheimer's patients.

The levels and cellular localization of mRNA for complement C1q and C3 were examined by RNA gel blot and nonradioactive in situ hybridization in the frontal cortex of patients with Alzheimer's disease (AD) and age-matched controls. We found that the hybridization signal for C1q mRNA was markedly increased (approx. 3.5-fold) in the frontal cortex of AD patients compared to that in age-matched controls. In contrast to previous reports we also found that the levels of C3 mRNA, although well expressed, did not differ significantly between AD cases and age-matched controls. Nonradioactive in situ hybridization using digoxigenin-labeled ribo-probes revealed that transcripts coding for both C1q and C3 were closely associated with neurons. These results support the hypothesis that complement could play a role in neuronal degeneration which has been observed in the brain of AD patients.

Aged↗
PubMed1987

[Low-dose alpha-interferon treatment of hairy cell leukemia].

Fifteen patients (36-71 years old) with histologically proven hairy-cell leukemia were treated with a low dose of IFN-alpha. The treatment consisted of 1 million I.U. given daily subcutaneously. After 1 month the dose was reduced in all patients 1 million I.U. thrice weekly. Four of the 15 patients have been splenectomized, with two patients receiving chemotherapy prior to the IFN treatment. All patients exhibited at least one cytopenia. The IFN treatment was well tolerated. Only two of the 15 patients experienced mild fever after the first injection, one patient had apathia and mild somnolence after 2 months of therapy. At present 15 patients can be evaluated: 6-18 months after start of therapy two patients showed a complete response with normalization of both peripheral blood and bone marrow, 10 patients experienced a partial response, while one patient showed a slight response with improvement of the thrombocyte count only. Two patients showed no improvement after 3 months of therapy; these patients are presently being treated with 5 million I.U. IFN-alpha thrice weekly. In spite of the low number of patients these data strongly indicate that IFN-alpha-2 is effective in hairy-cell leukemia at this low dose.

Adult↗
PubMed1984

[Exposure technics for computed scintigrams].

The technique of making copies on radiographic films or on multiformat cameras from computer scintigrams, computer tomograms, digital radiographs or other similar digital images should be carefully studied in order to make the best use of the characteristics of the film. Contrast transfer was studied using a nuclear medicine camera computer system with registration on radiographic film. Possible difficulties in obtaining copies and a simple software arrangement are described, which would influence contrast transmission.

Absorptiometry, Photon↗
PubMedDate not supplied

Age influences the expression of GAP-43 in the rat hippocampus following seizure.

BACKGROUND: Normal aging is associated with impairments in learning and memory and motor function. One viable hypothesis is that these changes reflect an age-related decrease in brain plasticity. OBJECTIVE: The aim of the present study was to identify age-related changes in the time course of expression of the axonal growth associated protein 43 (GAP-43) in a rat model of brain plasticity. METHODS: We examined by Northern blotting, in situ hybridization, and immunohistochemistry the effects of age on the time course of the expression GAP-43 following pentylenetetrazole-induced seizure in the hippocampus of 3-, 18-, and 28-month-old rats. RESULTS: In this model of brain plasticity, young rats displayed a decrease in GAP-43 mRNA levels in CA1, CA3, and polymorphic regions, lasting from 10 h to 3 days after seizure. This was followed by recovery, with peak expression between days 10 and 20. The baseline levels of GAP-43 mRNA decreased with age, especially in the CA3 region. Despite lower baseline levels, middle-aged rats showed the same pattern of upregulation of GAP-43 mRNA expression as the young animals. Old rats showed only minimal upregulation, however, and this occurred only in the polymorphic layer. The level GAP-43 protein itself was higher in old control rats than in the other two control groups, a condition that was transiently reversed by seizure activity. CONCLUSIONS: Middle-aged rats are still capable of a sustained, though diminished, response to seizure activity, while old rats lose this ability. Disruption of the temporal and anatomical coordination of expression of GAP-43 may contribute to the general decline in brain plasticity with age.

Age Factors↗