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Biomedical subjects

K M Rosen

Publications and source records attributed to K M Rosen.

At least 19 recordsLinked to original sources
PubMed1992

Brief visual experience induces immediate early gene expression in the cat visual cortex.

Brief visual experience causes rapid physiological changes in the visual cortex during early postnatal development. A possible mediator of these effects is the immediate early genes whose protein products are involved in the rapid response of neurons to transsynaptic stimulation. Here we report evidence that the levels of immediate early gene mRNAs in the visual cortex can be altered by manipulating the visual environment. Specifically, we find that brief (1 h) visual experience in dark-reared cats causes dramatic transient inductions of egr1, c-fos, and junB mRNAs in the visual cortex but not in the frontal cortex. Levels of c-jun and c-myc mRNAs are unaffected. These results suggest that select combinatorial interactions of immediate early gene proteins are an important step in the cascade of events through which visually elicited activity controls visual cortical development.

Animals↗
PubMed1992

Changes in immediate early gene expression during postnatal development of cat cortex and cerebellum.

Postnatal brain development involves interactions between extracellular signals and preprogrammed genetic events. Immediate early genes (IEGs) are a group of genes that are induced by extracellular signals and their protein products alter transcription by binding regulatory elements in other genes. Using Northern and slot blot analysis of total RNA isolated from visual cortex, frontal cortex, and cerebellum of cats, we have determined the postnatal development patterns of mRNA expression for 5 of these genes, c-fos, erg-1, c-jun, jun-B, and c-myc. Each gene had a distinct developmental pattern of mRNA expression, and for a given gene, these patterns were often different in different brain structures. These results suggest that temporal changes in the combinatorial interaction of different IEGs during early postnatal life are important for normal brain development.

Aging↗
PubMed1992

Messenger ribonucleic acid for transforming growth factor-alpha, but not for epidermal growth factor, is expressed in fetal and neonatal mouse brain.

OBJECTIVE: Little is known concerning the presence of transforming growth factor-alpha in fetal and neonatal tissues. Our objective was to analyze messenger ribonucleic acid expression for transforming growth factor-alpha and epidermal growth factor, the structural and biochemical analog of transforming growth factor-alpha in fetal and neonatal murine brain. STUDY DESIGN: Messenger ribonucleic acid was prepared from whole brains of mice from these developmental stages: embryonic days 14, 15, and 17, postnatal days 0, 4, 10, and adult. Polymerase chain reaction was performed on the complementary deoxyribonucleic acid obtained from reverse transcription of messenger ribonucleic acid with transforming growth factor-alpha and epidermal growth factor primers. In addition, ribonuclease protection assay was used to identify transforming growth factor-alpha transcripts. RESULTS: We found messenger ribonucleic acid encoding transforming growth factor-alpha in all stages of development used. Epidermal growth factor messenger ribonucleic acid was not found in any stage. Ribonuclease protection assay confirmed transforming growth factor-alpha transcripts in these tissues. CONCLUSION: Transforming growth factor-alpha may play an autocrine or paracrine role in the differentiation or maintenance of murine fetal and neonatal brains.

Aging↗
PubMed1992

Insulin-like growth factor II expression in the developing human brain.

Insulin-like growth factor II (IGF-II) is a polypeptide hormone with insulin-like metabolic activity and neurotrophic activity in vitro that has been implicated in human brain development. In this study, we used northern blot analysis to examine the patterns of IGF-II mRNA expression in selected regions of 18 human brains from cases ranging in age from 20 gestational weeks to 2.5 years (median age 31 gestational weeks). The expression of IGF-II mRNA was widespread throughout the brain from midgestation through the perinatal period. Each region showed a distinct developmental pattern of expression and IGF-II mRNA levels varied considerably between regions. The highest levels of expression at all ages were in leptomeninges and choroid plexus. After two postnatal months, IGF-II mRNA virtually disappeared from parenchymal regions. Beyond the perinatal period, IGF-II expression persisted primarily in choroid plexus. Transcripts of both 6.0 and 4.8 kb were detected in most brain regions. A developmental change in the relative amounts of the two transcripts occurred in choroid plexus, leptomeninges and medulla. The expression of IGF-II mRNA in the brain parenchyma during the last half of gestation correlates with a period of major brain growth and supports the hypothesis that high levels of IGF-II stimulate the proliferation and differentiation of neural cells early in development.

Blotting, Northern↗
PubMed1991

Enhanced insulin-like growth factor I gene expression in regenerating rat pancreas.

Insulin-like growth factor I (IGF-I) mRNA expression was studied after 90% partial pancreatectomy in the rat to determine whether IGF-I was associated with pancreatic regeneration. The level of IGF-I mRNA was maximally increased (4-fold above control value) 3 days after pancreatectomy, but thereafter gradually decreased, returning to control levels by 14 days after surgery. By in situ hybridization, IGF-I mRNA in both pancreatectomized and sham-operated rats was localized to capillary endothelial cells, indicating that this is the site of IGF-I expression in the normal rat pancreas. However, enhanced IGF-I mRNA expression was localized to focal areas of regeneration unique to pancreatectomized rats. In these areas, epithelial cells of proliferating ductules and individual connective tissue cells expressed IGF-I, suggesting that IGF-I may play an important role in the growth or differentiation of pancreatic tissue.

Animals↗
PubMed1991

Characterization of the gene and messages for vasoactive intestinal polypeptide (VIP) in rat and mouse.

We have studied the structure and expression of the gene for vasoactive intestinal polypeptide (VIP) in rodents. We used a human cDNA to identify and clone a fragment of the rat VIP gene. This genomic fragment contained two separate exons, one encoding VIP itself and the other encoding a closely related neuropeptide, peptide histidine-isoleucine (PHI-27). Probes containing either exon, or both, hybridized to two messages: a prominent 1700-base (b) mRNA and a rare 1000-b species. These messages are expressed together in a tissue-specific manner, with highest levels in polyadenylated RNA from cerebral cortex and from small intestine, paralleling the reported levels of the neuropeptides themselves in these tissues. Using the rat genomic fragment as a probe, we isolated the mouse VIP gene in its entirety. The mouse gene is similar in organization to its human counterpart, with a total of 7 exons spanning 8 kilobases (kb). The 7th and largest exon, which is transcribed into the bulk of the 3' untranslated region of the messages, bears two potential polyadenylation sites 700 basepairs (bp) apart. S-1 nuclease protection with a fragment of this exon indicated that the two identifiable VIP messages differ in the extent of their 3' untranslated regions. Conversely, we found no evidence for differential splicing to produce messages encoding only one of the neuropeptides. Instead, specific oligonucleotide-directed digestion with RNase H demonstrated that all of the detectable mRNA from this gene contains both VIP and PHI coding sequences.

Amino Acid Sequence↗
PubMed1990

Optimizing the northern blot procedure.

We describe methods for preparing formaldehyde-agarose gels for use in Northern blotting which yield consistent high quality results. Using these methods, we tested seven different commercially available membranes in Northern blots. Each membrane was handled as specified by the manufacturer in a course of hybridization, stripping and rehybridization. Filter background was low in all cases, but the intensity of the signal generated by specific hybridization varied markedly between filters after both the first and second hybridization.

Blotting, Northern↗
PubMed1989

Myosin light chain enhancer activates muscle-specific, developmentally regulated gene expression in transgenic mice.

The rat myosin light chain (MLC)1/3 gene locus contains a potent muscle-specific enhancer, located downstream of the coding region, greater than 24 kilobases away from the MLC1 transcription start site. To assess the role of this enhancer in the activation of MLC expression during development, transgenic mice were generated carrying multiple copies of a MLC1 promoter-chloramphenicol acetyltransferase (CAT) transcription unit linked to a genomic fragment including the enhancer. CAT expression was detected in four mouse lines, up to 1000-fold higher in skeletal muscles than in other tissues. Activation of endogenous MLC1 transcription in these animals 4 days before birth was reflected in the onset of CAT transgene expression. This study identifies the transcriptional control elements necessary to activate the 21-kilobase MLC1/3 locus at the appropriate fetal stage and indicates that the MLC enhancer is sufficient to induce developmentally regulated expression from the MLC1 promoter exclusively in skeletal muscle cells.

Aging↗
PubMed1979

Multiple reentrant tachycardias due to retrograde conduction of dual atrioventricular bundles with atrioventricular nodal-like properties.

A patient is presented who had two paroxysmal supraventricular tachycardias, one slow and incessant and the other fast. Both paroxysmal tachycardias appeared to be atrioventricular (A-V) reentrant, with anterograde conduction by way of a normal A-V pathway. Two pathways conducting in retrograde manner were demonstrated, characterized by different conduction times (fast and slow), identical abnormal atrial activation sequence and A-V nodal-like properties (retrograde Wenckebach periodicity with rapid ventricular pacing, and depression with ouabain and propranolol). Thus, there appeared to be two anomalous A-V bundles with nodal-like properties conducting in retrograde fashion. Whether the paroxysmal tachycardia was fast or slow depended on which of these pathways was utilized. Spontaneous cure of incessant paroxysmal tachycardia was observed and coincided with unexplained total loss of ability for ventriculoatrial conduction.

Atrioventricular Node↗
PubMed1979

Epicardial activation in human left anterior fascicular block.

Four patients with coronary artery disease and chronic marked left axis deviation, defined as a frontal QRS axis more negative than -45 degrees, were studied with epicardial mapping during coronary bypass surgery. All patients had normal right ventricular and inferior left ventricular epicardial breakthrough sites and activation sequence. Normal breakthrough in the basal anterolateral left ventricular epicardium was absent in all four patients. Two patients had breakthrough in the apical region of the anterolateral left ventricle. In the other two this region was activated from wave fronts emerging in the right ventricle and inferior left ventricle. The latest site of left ventricular activation was the basal segment of the anterolateral wall, a site never found to be the latest activated in our previously studied patients without conduction defects. This site was activated during or slightly after the terminal portion of the QRS complex. It is concluded that marked left axis deviation in patients with coronary artery disease reflects delayed activation of the basal anterolateral left ventricle, and is consistent with the presence of block or delay in the anterior "fascicle" of the left bundle branch.

Adult↗
PubMed1979

Epicardial activation of the intact human heart without conduction defect.

To describe the epicardial ventricular activation sequence in the intact human heart, we obtained epicardial maps from 11 patients with normal QRS undergoing open heart surgery. Epicardial breakthrough (EBT), defined as the emergence of a radially propagating epicardial wavefront, occurred in three to five sites in each patient, and was earliest in the anterior right ventricle, 7--25 msec (mean 17 msec) after the onset of the QRS in all patients. Subsequent EBT occurred in the inferior right ventricle (10 sites in 10 patients), in the anterolateral left ventricle (13 sites in 10 patients), and the inferior left ventricle (eight sites in seven patients). Latest epicardial activation (LEA), defined as the latest site of recordable epicardial activity, occurred in the basal segments in all patients, anteriorly in the right ventricle in five patients, and inferiorly in six patients, four on the right and two on the left. LEA occurred 63--96 msec (mean 77 msec) after the onset of the QRS, and was recorded within 20 msec of the end of the QRS in all patients. Sequence of epicardial activation reflected a fusion process among the wavefronts. This descriptive and quantitative data should provide a suitable basis for comparison of abnormal ventricular activation sequences in patients undergoing surgery for preexcitation or ventricular tachycardia.

Adult↗
PubMed1979

Incidence and site of atrioventricular block in patients with chronic bifascicular block.

Four hundred fifty-two patients with chronic bifascicular block and initially intact atrioventricular (AV) conduction were detected, studied, and prospectively followed between January 1970 and March 1978. There were 360 males and 92 females, ages 18--93 years (mean +/- SD, 62 +/- 15 years). Follow-up ranged from 29-2804 days (mean 1066 +/- 97 days). AV block (2 degrees or 3 degrees) developed in 29 patients, nine with apparent cause and spontaneously in 20. Cumulative annual incidence of all heart block for 1--5 years was, respectively, 4%, 5.9%, 8.7%, 10.1% and 11.3%, and for spontaneous block was 2%, 3.1%, 5.2%, 6.7%, and 7.1%. Sites of spontaneous block were probably or definitely AV nodal in ten, His bundle in one, and trifascicular in nine. Cumulative incidence of AV block in surviving bifascicular block patients is 11% at 5 years, with 7% reflecting spontaneous block. The probable or definite site of AV block varies and is trifascicular in less than half of the patients. The small incidence of trifascicular block probably explains the difficulty in predicting this complication with electrophysiological studies.

Adolescent↗
PubMed1979

Congenital abnormalities of the conduction system in two patients with tachyarrhythmias.

Serial sections of the conduction system (CS) were performed in two patients with recurrent tachyarrhythmias. Case 1, a 34-year-old female who had dual atrioventricular (AV) nodal pathways with recurrent paroxysmal supraventricular tachycardia, committed suicide. Autopsy revealed an abnormally formed atrial septum with insertion of eustachian valve on the AV part of the pars membranacea. The intercuspid portion of the pars membranacea was muscular. The AV node was located adjacent to the membranous part of the ventricular septum rather than the central fibrous body. In addition, there was an accessory anterior AV node on the parietal wall of the right atrium. Case 2, a 13-year-old boy with history of recurrent ventricular tachycardia, died suddenly. CS revealed a right-sided, markedly septated bundle. The first part of right bundle branch was divided into three parts, which later joined together. Both cases showed fatty infiltration of the atrial septum, more than normal for the age of the patients. The relationship of the recurrent tachyarrhythmias to the congenital abnormalities in the CS in the two cases and the fatty infiltration is reviewed.

Adolescent↗
PubMed1979

Effects of atropine on induction and maintenance of atrioventricular nodal reentrant tachycardia.

The electrophysiologic effects of atropine were studied in 14 patients with dual atrioventricular (AV) nodal pathways and recurrent paroxysmal supraventricular tachycardia (PSVT). During PSVT, all patients used a slow pathway (SP) for antegrade and fast pathway (FP) for retrograde conduction. Atropine enhanced both SP antegrade and FP retrograde conduction, shown by a decrease in paced cycle lengths (atrial and ventricular) producing AV and ventriculoatrial block. Five patients had induction of sustained PSVT before and after atropine. Seven patients failed to induce or sustain PSVT before atropine, because of retrograde FP refractoriness. All seven had induction of sustained PSVT after atropine due to facilitation of FP retrograde conduction. Two patients had only single atrial echoes before atropine, reflecting SP antegrade refractoriness. After atropine, sustained PSVT was inducible in one, and nonsustained in the other, PSVT cycle length could be compared in seven patients before and after atropine and decreased from 383 +/- 25 to 336 +/- 17 (p less than 0.05). Thus, in patients with dual AV nodal pathways, atropine facilitated SP antegrade and FP retrograde conduction, shortened cycle length of PSVT and potentiated ability to sustain PSVT.

Adult↗