Biomedical subjects
B Bloch
Publications and source records attributed to B Bloch.
The influence of hormonal status on excision margins after large loop excision of the transformation zone (LLETZ).
To evaluate the influence of the type of contraception used and post-menopausal status on the involvement of excision margins with CIN after Large Loop Excision of the Transformation Zone (LLETZ), the authors reviewed a computerised database and the clinical files of 451 sequential women treated by LLETZ, for CIN diagnosed on cytology and colposcopy. There was a statistically significant association between both the use of Long Acting Injectable Progesterone (LAIP) and post menopausal status with histological report of incomplete excision of CIN on the endocervical excision margin. Therefore, the authors conclude that both progesterone-only containing contraception and menopause induced atrophy of the endocervical epithelium significantly increase the risk of involvement of the endocervical excision margin with CIN in the treatment by LLETZ. This parameter is of particular importance, as it is one of the known factors for recurrence.
Patient sedation for routine genital examination.
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Down syndrome-critical region contains a gene homologous to Drosophila sim expressed during rat and human central nervous system development.
Many features of Down syndrome might result from the overdosage of only a few genes located in a critical region of chromosome 21. To search for these genes, cosmids mapping in this region were isolated and used for trapping exons. One of the trapped exons obtained has a sequence very similar to part of the Drosophila single-minded (sim) gene, a master regulator of the early development of the fly central nervous system midline. Mapping data indicated that this exonic sequence is only present in the Down syndrome-critical region in the human genome. Hybridization of this exonic sequence with human fetal kidney poly(A)+ RNA revealed two transcripts of 6 and 4.3 kb. In situ hybridization of a probe derived from this exon with human and rat fetuses showed that the corresponding gene is expressed during early fetal life in the central nervous system and in other tissues, including the facial, skull, palate, and vertebra primordia. The expression pattern of this gene suggests that it might be involved in the pathogenesis of some of the morphological features and brain anomalies observed in Down syndrome.
Ontogeny of the striatal neurons expressing neuropeptide genes in the human fetus and neonate.
The distribution patterns of neurons expressing mRNAs for four neuropeptides in the human striatum were studied during ontogeny by the use of in situ hybridization. The results of our study demonstrate that somatostatin, enkephalin, dynorphin, and substance P mRNAs are present in striatal neuronal populations from week 12 of fetal life. Each neuronal population undergoes a specific differentiation. Neurons containing somatostatin mRNA are scattered throughout the caudate-putamen up until birth. Neurons containing enkephalin, dynorphin, or substance P mRNAs evolve throughout fetal life in relation to caudate-putamen and patch-matrix compartmentalization. Neurons containing enkephalin mRNA (distinct from those containing substance P or dynorphin mRNAs) are present in the matrix from week 12 of fetal life. These neurons are preferentially distributed in the matrix and, at birth, display higher enkephalin mRNA content in the matrix than in the patches. Dynorphin mRNA is found in the caudate and putamen, preferentially in the patch neurons; nevertheless, a low level of dynorphin mRNA is also present in neurons of the caudate matrix. Substance P mRNA is initially restricted to caudate neurons. At birth, both substance P and dynorphin mRNAs are expressed at high levels in the patches. These results demonstrate that each neuropeptide gene is expressed during human fetal life in neurons with a specific topology and pace of development in relation to caudate-putamen and patch-matrix differentiation. These results also contribute evidence that neurochemical evolution of the striatal neuronal populations is not complete at birth in humans.
kappa-Opioid receptor in humans: cDNA and genomic cloning, chromosomal assignment, functional expression, pharmacology, and expression pattern in the central nervous system.
Using the mouse delta-opioid receptor cDNA as a probe, we have isolated genomic clones encoding the human mu- and kappa-opioid receptor genes. Their organization appears similar to that of the human delta receptor gene, with exon-intron boundaries located after putative transmembrane domains 1 and 4. The kappa gene was mapped at position q11-12 in human chromosome 8. A full-length cDNA encoding the human kappa-opioid receptor has been isolated. The cloned receptor expressed in COS cells presents a typical kappa 1 pharmacological profile and is negatively coupled to adenylate cyclase. The expression of kappa-opioid receptor mRNA in human brain, as estimated by reverse transcription-polymerase chain reaction, is consistent with the involvement of kappa-opioid receptors in pain perception, neuroendocrine physiology, affective behavior, and cognition. In situ hybridization studies performed on human fetal spinal cord demonstrate the presence of the transcript specifically in lamina II of the dorsal horn. Some divergences in structural, pharmacological, and anatomical properties are noted between the cloned human and rodent receptors.
[Scientific raisins from 125 years SMW (Swiss Medical Weekly). Clinical demonstrations from the Zurich dermatology clinic. 1926].
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D1 and D2 dopamine receptor gene expression in the rat striatum: sensitive cRNA probes demonstrate prominent segregation of D1 and D2 mRNAs in distinct neuronal populations of the dorsal and ventral striatum.
The postsynaptic effects of dopamine in the striatum are mediated mainly by receptors encoded by D1, D2, and D3 dopamine receptor genes. The D1 and D2 genes are the most widely expressed in the caudate-putamen, the accumbens nucleus, and the olfactory tubercle. Several anatomical studies, including studies using in situ hybridization with oligonucleotide and cDNA probes, have suggested that D1 and D2 receptors are segregated into distinct efferent neuronal populations of the striatum: D1 in substance P striatonigral neurons and D2 in enkephalin striatopallidal neurons. In contrast, on the basis of several in vivo and in vitro studies, other authors have suggested the existence of an extensive colocalization of D1 and D2 in the same striatal neurons. Our study was undertaken in order to analyze in detail the expression of the D1 and D2 receptor genes in the efferent striatal populations, with special reference to the various striatal areas, and to yield insights into the question about D1 and D2 mRNA localization in the striatum. We have, therefore, used highly sensitive digoxigenin- and 35S-labeled cRNA probes to address this question. The present results demonstrate that the D1 and D2 receptor mRNAs are segregated, respectively, in substance P and enkephalin neurons in the caudate-putamen and accumbens nucleus (shell and core) and in the olfactory tubercle (for their largest part). A very small percentage of neurons may coexpress both genes. These results confirm that the D1 and D2 receptor genes are expressed in distinct populations of striatal efferent neurons in the normal adult rat.
D1 and D2 receptor gene expression in the rat frontal cortex: cellular localization in different classes of efferent neurons.
The dopaminergic input to the frontal cortex has an important role in motor and cognitive functions. These effects are mediated by dopamine receptors both of type D1 and of type D2, although the neural circuits involved are not completely understood. We used in situ hybridization to determine the cellular localization of D1 and D2 receptor mRNAs in the rat frontal cortex. Retrograde tracing was used in the same animals to identify the main cortical efferent populations. Fluorogold was injected into the different cortical targets of the frontal cortex and sections were hybridized with D1 and D2 35S-labelled cRNA probes. D1 and D2 mRNA-containing neurons were present in all the cortical areas investigated, with greater expression in the medial prefrontal, insular and cingulate cortexes and lower expression in the motor and parietal cortexes. Neurons containing D1 mRNA were most abundant in layer VIb; they were also present in layers VIa and V of all cortical layers and in layer II of the medial prefrontal, cingulate and insular areas. Double labelling with fluorogold demonstrated that D1 mRNA was present in corticocortical, corticothalamic and corticostriatal neurons. Neurons containing D2 mRNA were essentially restricted to layer V, but only in corticostriatal and corticocortical neurons. Neither D1 nor D2 mRNA was found in corticospinal or corticopontine neurons. The present results demonstrate that D1 and D2 receptor genes are expressed in efferent cortical populations, with higher expression for D1. In spite of an overlap in some cortical layers, the expression of D1 and D2 receptor genes is specific for different categories of pyramidal neurons.
Ontogeny of the D1 dopamine receptor in the rat striatonigral system: an immunohistochemical study.
Antibodies were raised against a recombinant protein to analyse the pre- and postnatal ontogeny of the neurons expressing the D1 dopamine receptor in the striatum by immunohistochemistry. We report that D1 immunoreactivity is detectable from gestational day (G) 15 and is distributed homogeneously throughout the striatum from G15 to G18. From G19-20 to postnatal day (P) 3, D1 immunoreactivity becomes heterogeneous and predominates in cell bodies of the patch compartment while very limited immunoreactivity is detectable in the matricial compartment. The differential intensity between patches and matrix reaches its peak around P0. From P2, the pattern of D1 immunoreactivity progressively assumes the homogeneous distribution characteristic of the adult striatum. The expression of D1 mRNA in striatal neurons, as investigated by in situ hybridization, displays a similar pattern during this period. Substance P mRNA is also preferentially expressed in the patch compartment during the same period. D1 immunoreactivity appears at G17 in the substantia nigra as clusters of fibres and increases subsequently until reaching its adult form during the first postnatal week. These results demonstrate that the two compartments of the developing striatum display differential transcriptional and translational activity for the D1 gene and consequently two different and successive patterns of expression of D1 protein: patch neurons first express D1 receptor intensely while matrix neurons express it later and in smaller amounts so that D1 receptor appears transiently during the perinatal period as a marker of the patch compartment.
Placental site trophoblastic tumor: three case reports and literature review.
The clinical features of three patients with placental site trophoblastic tumour (PSTT) are presented. Two patients had probable nephrotic syndrome, which was unrecognized at the time. The nephrotic syndrome disappeared after hysterectomy in one patient and the other demised after one cycle of chemotherapy. The use of hysteroscopy in one patient and the management of a pulmonary metastasis in another are described.
Concurrent herpes simplex type 1 necrotizing encephalitis, cytomegalovirus ventriculoencephalitis and cerebral lymphoma in an AIDS patient.
Unlike cytomegalovirus (CMV) ventriculoencephalitis, herpes simplex virus type 1 necrotizing encephalitis has only rarely been observed in AIDS patients. A 40-year-old bisexual man was followed for an HIV1 infection from 1987 onwards. In June 1993 he was referred for sudden confusion, left hemiparesia and fever. The blood contained less than 10 CD4 lymphocytes/mm3. The patient remained comatose and febrile, and died 4 weeks later. In coronal sections of the brain there was necrosis of the internal parts of the left temporal lobe, necrosis of certain areas of the ventricular walls and a small tumor at the top of the right frontal lobe, which proved to be a polymorphic high-grade lymphoma. CMV ventriculoencephalitis lesions were prominent in the ventricular walls of the occipital lobes and there was a strong nuclear signal for CMV using in situ hybridization. Herpes simplex virus type 1 was shown in the nuclei and cytoplasm of certain neurons and astrocytes in the borders of the necrotized temporal lobe areas by immunohistochemistry, in situ hybridization and electron microscopy, whereas in situ hybridization and immunohistochemistry for CMV were negative in such areas. Necrotizing type 1 encephalitis must not be overlooked in immunodeficient patients.
Localization of dopamine D2 receptor mRNA in glomus cells of the rabbit carotid body by in situ hybridization.
The localization of mRNA coding for the dopamine D2 receptor was studied in the rabbit carotid body using in situ hybridization with synthetic 35S-labelled oligodeoxynucleotides. Using autoradiography on cryostat or semi-thin sections, labelling was observed over the cytoplasm of glomus cells, but not over sustentacular cells. A quantitative study showed that labelling intensity (silver grain density) was increased by haloperidol treatment. These results suggest that glomus cells express the dopamine D2 receptor gene and that this expression is regulated.
Effect of reserpine treatment on enkephalin mRNA level in the rat striatum: an in situ hybridization study.
We investigated the molecular mechanisms responsible for the preproenkephalin A mRNA increase following catecholamine depletion by reserpine using quantitative in situ hybridization at the cellular level. Macroscopic analysis showed that short term reserpine treatment increases the preproenkephalin A mRNA level in the rat striatum to +40.2 +/- 9%. Microautoradiography analysis demonstrated different increases in the preproenkephalin A mRNA level in different parts of the striatum: +124 +/- 22% in the dorso-median striatum, +131 +/- 19% in the dorso-lateral striatum, +119 +/- 8% in the ventro-lateral striatum and +75 +/- 6% in the ventro-median striatum. We found no difference in the number of cells expressing PPA mRNA in reserpine treated rats suggesting that these increases are only due to an increase in the number of mRNA expressed by cell.
Anatomical analysis of the neurons expressing the acetylcholinesterase gene in the rat brain, with special reference to the striatum.
The localization of the neurons expressing the acetylcholinesterase gene in the rat central nervous system was studied by in situ hybridization. The striatal and nigral neurons containing acetylcholinesterase messenger RNA were especially identified. Acetylcholinesterase messenger RNA was detected in numerous areas of the central nervous system, including cholinergic areas, like striatum, nucleus basalis of Meynert, septum and diagonal band of Broca, but also non-cholinergic areas, like the cerebral cortex, the hippocampus, the cerebellum and the raphe dorsalis. In the striatum, 75% of the neurons expressing the acetylcholinesterase gene were identified as cholinergic neurons and 25% as somatostatin-producing neurons. All dopaminergic neurons of the substantia nigra pars compacta and ventral tegmental area were demonstrated to express the acetylcholinesterase gene. Our results suggest that several neuronal populations could contribute to the presence of acetylcholinesterase in the striatum: the striatal cholinergic and somatostatin-containing interneurons, the nigral dopaminergic neurons and other neurons that may be the corticostriatal, thalamostriatal and raphe-striatal neurons. This demonstrates that, especially in the striatum, acetylcholinesterase is not a specific marker of the cholinergic neurons. The diversity of the origins of striatal acetylcholinesterase suggests a multiplicity of functions for this enzyme: besides its cholinolytic actions, it may also possibly play a non-cholinolytic role in neuromodulation.
Chronic treatment with dizocilpine maleate increases the number of striatal neurons expressing the D2 receptor gene.
N-methyl-D-aspartate antagonists have been proposed as potential therapeutic agents in different neurological diseases, including Parkinson's disease. The effects of gene expression of a chronic treatment with the non-competitive N-methyl-D-aspartate antagonist, dizocilpine maleate (0.8 mg/kg day, per os for 50 days) were analysed in rat striata. Using quantitative in situ hybridization, we measured the messenger RNA expression of the genes encoding D1, D2 dopamine receptors, N-methyl-D-aspartate receptor 1 subunit of N-methyl-D-aspartate receptor, preproenkephalin A and substance P. Chronic treatment with dizocilpine maleate induced a moderate but significant increase in messenger RNA of the N-methyl-D-aspartate receptor 1 subunit in the striatum and the adjacent cortex, suggesting an action of dizocilpine maleate in these two regions. This treatment did not induce any change in D1 receptor, preproenkephalin A or substance P messenger RNA content in the striatum, whereas D2 receptor messenger RNA was increased in the striatum of treated rats. Microscopic analysis revealed that it was the number of medium-sized neurons expressing D2 receptor messenger RNA that was significantly enhanced, while the mean amount of message per cell remained unchanged. These results demonstrate that glutamate via N-methyl-D-aspartate receptors, regulates the D2 receptor gene in striatal neurons. A chronic treatment with dizocilpine maleate increases the number of striatal neurons expressing the D2 receptor gene, suggesting a recruiting phenomenon.
Acute and chronic amphetamine treatments differently regulate neuropeptide messenger RNA levels and Fos immunoreactivity in rat striatal neurons.
Repeated administration of amphetamine results in the well known phenomenon of reverse tolerance or sensitization. However, little is known about cellular and molecular mechanisms underlying acute versus chronic response to amphetamine. In this paper, we investigated the effects of acute (1.5 or 5 mg/kg) and chronic (5 mg/kg/day for 14 days) amphetamine treatment on locomotor activity, stereotypy, Fos immunoreactivity and messenger RNA levels of molecules implicated in dopamine transmission in the rat striatum and substantia nigra. In agreement with other studies, acute amphetamine induced a dose dependent increase in locomotor activity and stereotypy. Also, a comparison between the behavior observed after the first injection and the last injection of amphetamine in chronically treated rats showed sensitization as demonstrated by a higher rating of stereotypy. We have found that acute and chronic amphetamine treatments differently modulate the activity of several output neurons. A double labeling procedure with Fos immunohistochemistry coupled with in situ hybridization demonstrated that acute amphetamine treatment induces Fos immunoreactivity predominantly in striatal neurons expressing substance P messenger RNA (77.07 +/- 1.42%). Only 32.6 +/- 2.07% of Fos immunoreactive neurons expressed preproenkephalin A messenger RNA. In chronic amphetamine treated rats, 56.21 +/- 1.32% of the Fos immunoreactive neurons expressed substance P messenger RNA while 52.12 +/- 1.84% expressed preproenkephalin A messenger RNA. Statistical analysis revealed that this difference is mainly due to a decrease in the density of substance P immunoreactive neurons in chronically treated rats in comparison to acute. Amphetamine treatments induced Fos immunoreactivity in the substantia nigra in non-dopamine neurons. As measured by quantitative in situ hybridization, acute amphetamine induced an increase in substance P, preproenkephalin A and dynorphin messenger RNA levels (+23 +/- 0.05%, +45 +/- 0.07% and +24 +/- 0.05%, respectively). No difference in these increases was observed in relation with the dose injected (1.5 or 5 mg/kg). Chronic amphetamine treatment enhanced only substance P and dynorphin messenger RNA levels (+23 +/- 0.04% and +42 +/- 0.04%, respectively). Neither acute nor chronic amphetamine treatment had any effects on D1 or D2 dopamine receptor messenger RNA levels. Our main conclusions are: (1) in acutely treated rats Fos is essentially expressed by substance P neurons; (2) in chronically treated rats, Fos immunoreactivity is expressed by the two efferent striatal populations (i.e. preproenkephalin A and substance P neurons) and the number of Fos immunoreactive neurons is reduced as compared with acute; (3) neuropeptide messenger RNA levels, but not dopamine receptor messenger RNAs, are affected in the response to acute or chronic treatment with amphetamine.
Pulmonary intravascular macrophages in the pathogenesis of bovine pulmonary lesions caused by Actinomyces pyogenes.
Rabbit antisera raised against somatic antigens from two strains of Actinomyces pyogenes reacted specifically in a peroxidase anti-peroxidase technique which was developed for the location of the bacteria in formalin-fixed tissues. The technique was applied on experimental murine and spontaneous bovine lesions caused by A. pyogenes. By electron microscopy and immunohistochemistry it was demonstrated that pulmonary intravascular macrophages play a role in the uptake of A. pyogenes from the blood, and in the production of pyaemic pulmonary lesions.