Biomedical subjects
Publications and source records attributed to Y W Li.
Thoracic actinomycosis is rare in the pediatric age group. We report the unusual case of a 10-year-old girl who presented with prolonged fever and weight loss with a neck mass and multiple pulmonary nodules resembling lymphoma. Open lung biopsy confirmed the diagnosis of actinomycosis and the symptoms and signs improved after treatment with cephalosporin. The pathogenesis and radiographic manifestations are briefly discussed.
A case of vaginal and cervical endodermal sinus (yolk sac) tumor in a 6-month-old female infant is reported. The patient presented with an intermittent bloody discharge on her diapers. Pelvic CT showed an irregular soft tissue density mass with heterogeneous enhancement within the vagina and extending to the cervix. The histopathologic features were identical to those of endodermal sinus tumors.
We mapped the distribution of virus-labelled neurons in the brain after injection of Herpes simplex virus type 1 (HSV1) into the rabbit renal nerve. Seven days after injection, labelled neurons were observed in four brain regions, the rostral ventrolateral medulla (47 +/- 3% of neurons), the A5 area of the lower pons (38 +/- 4%), the caudal raphe nuclei and the parapyramidal area of the medulla (13 +/- 2%), and the paraventricular nucleus of the hypothalamus (1 +/- 1%). In the rostral ventrolateral medulla approximately one half of the HSV1-labelled neurons also contained tyrosine hydroxylase, characterizing them as C1 neurons. In the A5 area virtually all HSV1-labelled neurons also contained tyrosine hydroxylase. In the raphe nuclei and the parapyramidal area 47% of HSV1-positive neurons contained serotonin. The distribution of labelled neurons was similar to that observed after injection of HSV1 into the adrenal gland.
Renal sympathetic preganglionic neurons in the spinal cord of rabbits were transneuronally retrogradely labelled by injection of Herpes simplex virus type 1 into the renal nerve and immunohistochemical demonstration of viral antigen. The morphology of the labelled neurons was examined, particularly with respect to the shape and extent of their dendritic trees. Double-labelling immunohistochemical studies were performed to determine the relationship of neuropeptide Y-immunoreactive axons to virus-labelled perikarya and dendrites. The shape of the renal sympathetic preganglionic neurons differed according to whether the neurons were located in the intermediolateral cell column or in other sympathetic areas. The neurons in the intermediolateral cell column had very long dendrites, extending in the rostrocaudal and mediolateral directions. The medially oriented processes extended towards and beyond the central canal. The laterally oriented dendritic processes projected within the dorsolateral funiculus, towards the edge of the spinal cord. Neuropeptide Y-immunoreactive fibres were concentrated in regions containing renal sympathetic preganglionic neurons of the spinal segments examined (T7-L2). Immunoreactive varicose terminals were closely opposed to individual preganglionic neurons, especially to the dendritic processes of these neurons. Our findings indicate that neurotransmitter candidates such as neuropeptide Y are likely to influence renal preganglionic neurons by an input to dendritic processes at some distance from the perikarya. Electrophysiological and other functional studies utilizing applications of neurotransmitter candidates onto these neurons should take this into account.
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Polymerase chain reaction [PCR, reverse transcriptase-PCR (RT-PCR)] has been used to amplify the mRNA subspecies of the plasma membrane calcium pump isoform 1 (PMCA1) in total RNA extracted from hamster tissues. Two primers were synthesized that encompass the site at which a 154-bp exon is included totally (PMCA1a), partially (PMCA1c and d), or completely excluded (PMCA1b) in the carboxy-terminal regulatory region. PCR amplification revealed two bands (PMCA1b and 1c) that are more abundant in various tissues, while Southern hybridization of the samples after PCR amplification has detected two additional mRNA variants corresponding to PMCA1a and 1d. The distribution of these mRNA variants are tissue specific and correlate well with the pump protein distribution patterns on immunoblot. Since these multiple bands on the immunoblot are not derived from proteolysis, it is suggested that they represent the PMCA1 isozymes encoded by these alternatively spliced mRNAs. To our knowledge, this is the first report to show all four alternatively spliced mRNAs that are simultaneously detected in one single RNA sample using PCR technique. Since these isozymes are different in their regulatory domain, their tissue-specific expression may be physiologically important.
This report documents the cloning and sequencing of a previously unknown intron of the Her-2/neu gene and compares three different cloning strategies for efficient PCR cloning. Although successful results have previously been documented using blunt-end ligation strategies, the TA cloning system (Invitrogen, CA) offered the best result in our hands using a PCR-amplified DNA fragment of Her-2/neu (ERBB2) gene containing an unreported intron. The TA cloning system is easy to manipulate and the cloned DNA can be easily sequenced without further subcloning into the M13 vector. Additionally, this cloning strategy does not require (i) any prior selection of restriction sites during primer design, (ii) post PCR restriction digestion, and/or (iii) gel purification of PCR-amplified DNA. The newly identified and sequenced DNA of the Her-2/neu neu intron (GenBank Accession No. M95667) may help in designing primers for the analysis of the Her-2/neu gene in biological specimens. Therefore, we recommend the TA cloning system as the preferred choice for cloning any DNA fragments generated by PCR.
McCune-Albright syndrome is one of the causes of isosexual precocity in girls. Recurrent ovarian cysts are not uncommon in McCune-Albright syndrome; however, treatment for these cysts is still controversial. We report on a six-year-old girl with sexual precocity due to recurrent ovarian cysts. Initially, she received a left salpingo-ophorectomy for an ovarian cyst at the age of two years and one month; the postoperative course was uneventful. Unfortunately, sexual precocity and a cyst on the remaining ovary were noted four years later. A series of studies revealed a hyperpigmented area with an irregular margin on the back and probable fibrous dysplasia of the orbital bone. A luteinizing hormone-releasing hormone test showed a prepubertal response. Cyproterone acetate was tried under the diagnosis of McCune-Albright syndrome, and her secondary sexual characteristics disappeared after treatment.
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Neuronal expression of c-fos protein (Fos) in the medulla in response to baroreceptor activation was studied in conscious rabbits. Raising arterial pressure resulted in a marked increase, compared to control animals, in Fos immunoreactivity in the nucleus tractus solitarius, area postrema and ventrolateral medulla (VLM). Fos-immunoreactive neurons in the VLM extended from the level just rostral to the obex to 3 mm more caudal. Only a small proportion of these neurons showed tyrosine hydroxylase immunoreactivity. The results indicate that baroreceptor activation induces Fos expression in circumscribed medullary regions which have previously been shown to receive excitatory baroreceptor inputs.
We made extracellular recordings from 107 spontaneously active neurons in the caudal ventrolateral medulla, after identifying the cells by antidromically activating them from the rostral ventrolateral medulla, in urethane-anesthetized rabbits. We tested the response of these neurons to inputs from baroreceptors and chemoreceptors. The median conduction velocity for antidromically activated neurons was 0.84 m/s. Raising blood pressure with intravenous noradrenaline excited 22% of 96 neurons tested, inhibited 61%, and had no effect on the remaining 17%. The spontaneous discharge rate of neurons excited by an increase in blood pressure was 1.6 +/- 0.3 spikes/s, lower than the discharge rate of neurons inhibited by this procedure (4.9 +/- 0.5 spikes/s). Excitation of chemoreceptors by hypoxia increased the discharge rate of 14/16 neurons tested in the group excited by baroreceptor inputs. In the group inhibited by baroreceptor inputs 21/35 neurons tested were excited and 12/35 neurons were inhibited by chemoreceptor inputs. Neurons excited by an increase in blood pressure were located in the previously defined caudal vasodepressor region and in a region just rostral to the obex, intermediate between the vasodepressor region and the rostral sympathoexcitatory region. These neurons may form part of the central inhibitory link in the baroreceptor-vasomotor pathway. Other antidromically activated neurons in the vasodepressor region may be inhibitory vasomotor cells with a function relatively independent of baroreceptor inputs, or they may be A1 catecholamine neurons, with axons passing through the rostral medulla en route to the forebrain.
We examined the vasomotor and respiratory effects of angiotensin II microinjection into the rabbit ventrolateral medulla (VLM). Angiotensin II in the rostral and caudal VLM increased and decreased arterial pressure, respectively, but had no effect on phrenic nerve activity. In contrast, L-glutamate injections in the same areas altered both arterial pressure and phrenic nerve activity. The results suggest that angiotensin II may activate specifically vasomotor neurons but not respiratory neurons in the VLM.
We combined Phaseolus vulgaris leucoagglutinin anterograde tracing and Herpes simplex virus transneuronal retrograde tracing to determine whether neurons in the vasodepressor region of the rabbit caudal ventrolateral medulla project to brainstem neurons containing the virus after its transneuronal transport from the adrenal medulla. Five days after adrenal injection of virus, 764 +/- 159 virus-positive neurons were found bilaterally in the brainstem: 61% in the C1 sympathoexcitatory region of the rostral ventrolateral medulla, 30% in the A5 region, 5% in the parapyramidal region, and 3% in the paraventricular nucleus of the hypothalamus. Many of the virus-positive neurons in the C1 and A5 areas also contained tyrosine hydroxylase and, in the parapyramidal area, many contained 5-hydroxytryptamine. After iontophoretic deposit of leucoagglutinin into the vasodepressor region of the caudal ventrolateral medulla, brain regions containing varicose processes labeled with leucoagglutinin included the regions containing virus-positive neurons. We examined the C1 and A5 regions following injections of both tracers in the same rabbits, leucoagglutinin into the caudal ventrolateral medulla and virus into the adrenal gland. Varicosities containing leucoagglutinin were seen in contiguity with perikarya and dendritic branches of neurons containing HSV1, in both the C1 and A5 regions. Studies also revealed labeled varicosities in contiguity with TH-containing C1 and A5 neurons. The projection from the caudal medulla to presumed sympathetic premotor neurons in the C1 area, including some C1 cells, represents a potential pathway whereby activity of neurons in the caudal medulla could reduce blood pressure by inhibiting sympathoexcitatory neurons in the rostral medulla.
We mapped sympathetic renal preganglionic neurons in the rabbit spinal cord using Herpes simplex virus retrograde transneuronal tracing after application of the virus to the renal nerve. Virus-positive neurons were found in the spinal cord from T7 to L2, principally in the ipsilateral intermediolateral cell column. Renal and adrenal preganglionic neurons are largely separate populations. Extensive nonspecific spread of virus from infected cells to neighboring neurons does not appear to occur.
Vulnerability of specific brain regions and neuronal populations is a characteristic feature of Alzheimer disease and Down syndrome. Cholinergic neurons of the basal forebrain degenerate in both disorders. The basis for neuronal degeneration is unknown. Mouse trisomy 16 (Ts 16) is an animal model of Down syndrome. We sought an experimental system in which the survival and development of Ts 16 basal forebrain cholinergic neurons could be examined beyond the fetal period. As Ts 16 mice do not survive birth, we transplanted fetal Ts 16 and control basal forebrain into the hippocampus of young adult mice. Transplanted neurons survived and grew neurites in all grafts. Over time, we observed selective atrophy of cholinergic neurons in Ts 16 grafts. Denervation of the hippocampus produced a significant increase in the size of Ts 16 cholinergic neurons. This suggests that hippocampal-derived neurotrophic factors acted to prevent degeneration. beta/A4-amyloid-containing plaques were not seen. Ts 16 provides a model of spontaneous, genetically determined neurodegeneration that may be used to understand better the molecular pathogenesis of neuronal dysfunction in Alzheimer disease and Down syndrome.
In humans, trisomy 21 results in a specific phenotype known as Down syndrome (DS). The mechanism by which an extra copy of normal genes leads to the DS phenotype is unknown. Most studies in DS and other aneuploid organisms have shown that gene dose is proportional to gene expression. To date, most genes examined have encoded either metabolic enzymes or constitutively expressed products. In the trisomy 16 mouse, an animal model of DS, we found marked dysregulation of two developmentally regulated genes, App and Prn-p. Dysregulation varied from tissue to tissue and during development in the same tissue. We conclude that abnormal phenotypes seen in aneuploid conditions may result in part from disordered expression of developmentally regulated genes.
The retinoblastoma tumor suppressor gene (RB gene) has been reported to be deleted and/or modified in a number of human cancers, indicating that dysfunction of this tumor suppressor gene is perhaps critical in the development of many human tumors. In addition to deletion of one copy and/or mutational inactivation of the RB gene, this gene has also been reported to be altered by a small deletion in the promoter sequence in one case of small cell mixed adenocarcinoma of the prostate. A deletion of 105 nucleotides of the RB gene in exon 21, leading to an aberrant short-sized mRNA transcript, has also been reported in one cell line (DU 145) derived from brain metastasis of prostatic adenocarcinoma. We have analyzed tissues from 10 prostate specimens (3 hyperplastic and 7 neoplastic) and one prostate cancer cell line (DU 145) for the presence of short-sized mRNA transcript (exon 21 alterations) by polymerase chain reaction (PCR) using total RNA extracted from frozen tumors and the cell line. None of the prostate tissue showed any evidence of aberrant short-sized mRNA, although it was confirmed in the DU 145 cell line. Simultaneously, we have used DNA-PCR to investigate RB promoter deletion in 23 adenocarcinomas and one small cell carcinoma of the prostate. We also failed to demonstrate any indication of RB promoter deletion at the DNA level in adenocarcinomas. The single case of small cell carcinoma failed to show evidence of any aberration in RB promoter. We therefore conclude that neither RB promoter alterations nor the exon 21 deletion are associated with typical prostate adenocarcinoma.