Stimulated emission of a microcavity dressed exciton and suppression of phonon scattering.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to H Cao.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Intraspinal air has been described in patients undergoing diagnostic lumbar puncture and epidural analgesia, as a manifestation of degenerative disk disease, and after less common mechanisms, such as blunt trauma [1], strenuous exercise [2], and pelvic trauma [3]. We report a case of spinal epidural emphysema incidentally noted on CT after placement of a thoracostomy tube.
Explore the source record for details and available documents.
Immunocytochemistry with a monoclonal antiepidermal growth factor (anti-EGF) receptor antibody directed against the extracellular domain which can inhibit ligand binding to the receptors showed that nuclei of choriocarcinoma JEG-3 cells and normal placental trophoblasts were distinctly immunostained for EGF receptors. This finding led us to investigate the structure and function of nuclear EGF receptors. Western immunoblotting revealed that cell membranes, isolated intact pure nuclei, and nuclear membranes contain a 170-kilodalton EGF receptor protein. Covalent receptor cross-linking demonstrated that the 170-kilodalton receptor protein in nuclei and nuclear membranes can bind [125I]EGF just as in cell membranes, and that this binding is inhibited by excess unlabeled EGF. As in cell membranes, the addition of EGF resulted in an increased receptor autophosphorylation in the nuclei and nuclear membranes. In addition, the activated receptor kinase stimulated, and in some cases inhibited, tyrosine phosphorylation of a number of lower molecular size proteins, especially in nuclei and nuclear membranes. Although the identity of these proteins is not known, none of them could bind [125I]EGF. The addition of EGF to isolated nuclei resulted in a time-dependent specific transcriptional inhibition of hCG/LH receptor gene. In summary, our data demonstrating the presence of functional nuclear EGF receptors are novel, potentially important, and go against the traditional concepts of growth factors action. The nuclear receptors have the capacity to transduce signals from EGF and may mediate intracrine and paracrine actions of EGF in the regulation of trophoblast functions.
The biosynthesis of human chorionic gonadotrophin (hCG) is a hallmark endocrine function of human choriocarcinoma cells. The present study investigated the consequences of greatly diminishing this synthesis in JAR cells by stably transfecting them with pRSV-antisense hCG-alpha cDNA expression vector. The vector directs the synthesis of antisense hCG-alpha subunit mRNA which would then bind to sense hCG-alpha subunit mRNA, thus blocking its translation and consequently dimer hCG protein synthesis. The transfection with pRSV-antisense hCG-alpha cDNA resulted in a dramatic decrease in hCG secretion as compared with untransfected parental cells or those transfected with an empty vector used for the selection of clones. The decreased secretion was due to a decreased synthesis which in turn was due to a fall in steady-state hCG-alpha and -beta subunit mRNA levels. The decrease of hCG-beta subunit transcripts was unexpected and it was not due to contamination of antisense hCG-alpha cDNA construct with hCG-beta sequence. The transcription of hCG-alpha and -beta subunit genes was not altered in transfected cells suggesting that increased degradation was responsible for decreased steady-state hCG subunit mRNA levels. Despite the decreased hCG levels, the transfected cells maintained normal hCG receptor levels, responded to epidermal growth factor stimulation of hCG synthesis and secretion and grew at the same rate as the control parental cells and those transfected with an empty vector.
Explore the source record for details and available documents.
PURPOSE: To transplant human fetal retinal pigment epithelium (RPE) into the subretinal space of rabbits and monkeys as an organized monolayer without artificial support. METHODS: The method involves dissecting small patches of cultured RPE monolayers in sheets (1 to 5 mm2), sucking them into a glass pipette and injecting them into the subretinal space after producing a bleb detachment of the neural retina. RESULTS: These patches unfold and survive as a quasi-monolayer under the reattached neural retina intimately associated with the host photoreceptors and phagocytizing host outer segment material. Graft rejection is observed in most rabbits at 1 month but not in monkeys at 3 months after transplantation. CONCLUSIONS: Monolayer patches of cultured human fetal RPE can be transplanted to the subretinal space, where they survive in contiguity with healthy host outer segments. In primates, but not in rabbits, host-graft rejection does not occur for at least 2 to 3 months.
Veto cells are cells which suppress self directed cytotoxicity (CTX) regardless of the strain of origin of the cytotoxic effector cell. The mechanism by which veto cells inhibit self directed CTX is largely unknown. We have previously described the emergence of a veto cell in murine chronic graft versus host (CGVH) disease both in vivo and in vitro. Using an in vitro system in which veto cells are induced, we now report that a soluble factor is also induced which is capable of suppressing CTX. This cytotoxicity suppressing factor (CsF) is heat labile and has a molecular weight above 50 kD. The factor prevents the emergence of a cytotoxic effector cell. but is largely ineffective once the effector cell has functionally emerged. CsF is irreversible and is not restricted in its ability to inhibit anti-self CTX.
We purified and characterized a novel RIP (ribosome inactivating protein), Luffin-S from the seeds of Luffa cylindrica. Different from Luffin-A and B, which are RNA N-glycosidases with molecular weights of 27 and 28 kDa, respectively, Luffin-S has an M.W. of only approx. 10 kDa, much smaller than any other RIPs so far investigated. Its abundant resources, toxicity similar to TCS in a cell-free protein synthesis system and unique mechanism as phosphodiesterase, like alpha-sarcin, promisingly make it a potential toxic moiety of immunotoxin.
Human retinal pigmented epithelium (RPE) can be cultured by removing small patches of this layer from the choroid of the fetal eye. Such RPE patches give rise to healthy, epithelioid monolayers in vitro within 1-2 weeks without contamination from retinal or choroidal cells. The viability and proliferative capacity of these cultures is independent of the initial polarity of the patch. These RPE monolayers develop apical/basal polarity and a basal lamina and rest on a field of collagen fibers; they are capable of phagocytizing outer segments. A patch can be lifted off a confluent monolayer and transferred to another culture dish without risking the viability of either the old or the new culture. This provides a means of transplanting an organized, polarized patch of human RPE from one place to another.
Systemic acquired resistance (SAR) is a nonspecific defense response in plants that is associated with an increase in the endogenous level of salicylic acid (SA) and elevated expression of pathogenesis-related (PR) genes. To identify mutants involved in the regulation of PR genes and the onset of SAR, we transformed Arabidopsis with a reporter gene containing the promoter of a beta-1,3-glucanase-encoding PR gene (BGL2) and the coding region of beta-glucuronidase (GUS). The resulting transgenic line (BGL2-GUS) was mutagenized, and the M2 progeny were scored for constitutive GUS activity. We report the characterization of one mutant, cpr1 (constitutive expressor of PR genes), that was identified in this screen and shown by RNA gel blot analysis also to have elevated expression of the endogenous PR genes BGL2, PR-1, and PR-5. Genetic analyses indicated that the phenotype conferred by cpr1 is caused by a single, recessive nuclear mutation and is suppressed in plants producing a bacterial salicylate hydroxylase, which inactivates SA. Furthermore, biochemical analysis showed that the endogenous level of SA is elevated in the mutant. Finally, the cpr1 plants were found to be resistant to the fungal pathogen Peronospora parasitica NOCO2 and the bacterial pathogen Pseudomonas syringae pv maculicola ES4326, which are virulent in wild-type BGL2-GUS plants. Because the cpr1 mutation is recessive and associated with an elevated endogenous level of SA, we propose that the CPR1 gene product acts upstream of SA as a negative regulator of SAR.
The gene for black-ear coat colour pattern, commonly found among cattle of tropical origin, was observed in 809 animals of four breeds of local cattle in southern China. Gene frequencies for Tf, Hb and Alb demonstrated that these groups of cattle were quite divergent from Bos taurus. These breeds of cattle are thought to be descended from ancient Chinese cattle. At the same time certain influences observed in coat colour may be derived from Bali cattle.
Epidermal growth factor (EGF) stimulates the secretion of hCG in choriocarcinoma cells. However, the molecular mechanisms involved in this EGF action have never previously been investigated. The present study investigated them as well as EGF regulation of the hCG/LH (LH) receptor gene in JEG-3 human choriocarcinoma cells. The JEG-3 cells contain multiple EGF receptor messenger RNA (mRNA) transcripts and a single 170-kilodalton immunoreactive receptor protein. The human EGF can bind to the receptor protein and stimulate the receptor autophosphorylation as well as the phosphorylation of four other membrane proteins. Culturing JEG-3 cells with recombinant human EGF resulted in a dose- and time-dependent increase in hCG secretion. The maximal effect was seen at 100 ng/ml EGF, with a time lag of about 5 h. Tyrosine kinase, but not protein kinase-C or protein kinase-A, signaling was involved in the EGF action to increase hCG secretion. The EGF-induced increase in hCG secretion was not due to an increase in cell number or differentiation into multinuclear syncytia. EGF treatment resulted in a dose- and time-dependent increase in steady state levels of hCG alpha and hCG beta mRNAs. This increase was due to the stabilization of subunit mRNA transcripts. The increase in subunit mRNAs preceded the increase in hCG secretion. The EGF treatment resulted in a dose- and time-dependent decrease in steady state levels of the hCG/LH receptor mRNA transcripts. The decrease was due to a transcriptional inhibition of receptor gene. EGF treatment paradoxically stabilized hCG/LH receptor protein. In summary, EGF treatment up-regulates hCG subunits gene expression and down-regulates hCG/LH receptor mRNAs involving transcriptional and posttranscriptional mechanisms in JEG-3 human choriocarcinoma cells.
Human gestational trophoblastic neoplasms overexpress hCG/LH receptors. Whether this overexpression is a reflection of a loss of self-regulation of hCG biosynthesis was investigated using JAR human choriocarcinoma cells. The results show that exogenous hCG did not affect steady state hCG alpha and hCG beta mRNA or dimer hCG protein levels in JAR cells. The JAR cells, however, responded to 8-bromo-cAMP with an increase in hCG alpha mRNA levels, suggesting that cAMP-mediated regulation of the hCG subunit genes was intact in the cells. Disruption of receptor function by a receptor antibody, which resulted in an increase in hCG alpha mRNA levels and hCG secretion in normal trophoblasts, had no effect on JAR cells. Unlike normal trophoblasts, which contain a predominant receptor transcript of 1.8 kilobases (kb), with minor higher molecular size (7.5 and 5.4 kb) transcripts occasionally seen, JAR cells contain a higher abundance of multiple transcripts (7.5, 5.4, 3.5, and 1.8 kb), with the predominant transcript being 5.4 kb. In addition, although normal trophoblasts contain an 80-kilodalton receptor protein, JAR cells contain only a 50-kilodalton hCG/LH receptor isoform. In contrast to the effects of exogenous hCG on normal placental tissue in vitro, it was unable to down-regulate receptor transcripts or receptor protein in JAR cells. In summary, JAR cells lack the ability to self-regulate hCG biosynthesis. This loss could explain how hCG can reach very high levels in gestational trophoblastic disease compared to those in normal pregnancy.
Carotid bodies are sensory organs for monitoring arterial oxygen and CO2. Previous studies have shown that chemoreceptor tissue contains substance P (SP) and exogenously administered SP augments chemosensory discharge. In the present study, we examined the physiological importance of SP in carotid body chemoreception by using a selective nonpeptide SP [neurokinin (NK) 1] receptor antagonist CP-96,345. In experiments performed on anesthetized cats, sensory discharge was recorded from the carotid body in situ. To control for alterations in blood flow, additional studies were conducted on the carotid body in vitro. In in vivo studies, close carotid body (intraarterial) administration of CP-96,345 attenuated the sensory response to hypoxia in a dose-dependent manner with 73% of the response abolished at doses of 0.3-0.6 mg/kg. Comparable doses of the (2R,3R)-enantiomer had no effect on hypoxia-induced excitation, indicating that the effect of CP-96,345 was not due to nonspecific action. In contrast, the carotid body response to high CO2 was not affected by CP-96,345, implying that only the hypoxic response is mediated by NK-1 receptor and confirming that the effect of the SP antagonist was not due to nonspecific actions. Marked attenuation of the sensory response to hypoxia was also obtained in the carotid body in vitro, suggesting that the effects of the NK-1 antagonist were not secondary to cardiovascular changes. These results demonstrate that CP-96,345 attenuates or abolishes the chemosensory response to hypoxia but not to CO2 and suggest that SP mediates the hypoxia-induced sensory excitation in the cat carotid body via NK-1 receptor activation.
Explore the source record for details and available documents.
Four genes, closely linked to major histocompatibility complex (MHC) class II genes, have been identified in humans, mice, and rats and are thought to be involved in the generation and transport of endogenous immunogenic peptides for the MHC class I antigen-processing pathway. The Tap-1 and Tap-2 genes presumably encode a heterodimeric protein complex responsible for transporting endogenous immunogenic peptides to the lumen of the endoplasmic reticulum. The Lmp-2 and Lmp-7 gene products are two subunits of the large cytosolic proteasome complex possibly involved in generation of endogenous peptides. To study the genetic polymorphism of the Lmp-2 gene, we used a published cDNA sequence as a consensus sequence and PCR-amplified, cloned, and sequenced the Lmp-2 gene from 12 inbred mouse strains. We found three amino acid variants, LMP-2d, LMP-2b, and LMP-2q, which partially correlated with restriction fragment length polymorphism variants identified with Southern blots. Allelic polymorphism of the Lmp-2 gene may be involved in peptide selection, leading to autoimmune disease susceptibility.