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Biomedical subjects

J Cheng

Publications and source records attributed to J Cheng.

At least 433 records · Page 24Linked to original sources
PubMed1993

Locomotor-like rotation of either hip or knee inhibits soleus H reflexes in humans.

Human soleus H reflexes are depressed with passive movement of the leg. We investigated the limb segment origin of this inhibition. In the first experiment, H reflexes were evoked in four subjects during (1) passive pedaling movement of the test leg at 60 rpm; (2 and 3) pedaling-like flexion and extension of the hip and the knee of the test leg separately; and (4) stationary controls. In the second experiment, with the test leg stationary, the same series of movements occurred in the opposite leg. Rotation of the hip or the knee of the test leg significantly reduced mean reflex amplitudes (p < 0.01) to levels similar to those for whole-leg movement (mean H reflexes: stationary, 71%; test leg pedaling movement, 10%; knee rotation, 15%; hip rotation, 13% [all data are given as percentages of Mmax]). The angle of the stationary joint did not significantly affect the results. Rotation of the contralateral hip significantly reduced mean reflex magnitudes. Rotation of the contralateral knee had a similar effect in three of the four subjects. We infer that a delimited field of receptors induces the movement conditioning of both the ipsilateral and contralateral spinal paths. It appears that somatosensory receptor discharge from movement of the hip or knee of either leg induces inhibition as the foundation for the modulation of H reflexes observed during human movement.

Adult↗
PubMed1993

Expression of tissue factor, thrombomodulin, and E-selectin in baboons with lethal Escherichia coli sepsis.

Disseminated intravascular thrombosis is a frequent complication of endotoxic shock, and modulation of endothelial cell hemostatic properties has been proposed to play a role in its pathogenesis based on studies of endothelial cells in culture. This study examined the in vivo expression of tissue factor (TF) and thrombomodulin (TM) in a baboon model of lethal Escherichia coli sepsis using immunohistochemistry with monospecific antibodies. Expression of E-selectin (E-sel) was also determined as a marker of endothelial cell activation. Correlation of immunoreactivity with procoagulant activity in lipopolysaccharide-stimulated cultured human endothelial cells showed that immunohistochemistry was sufficiently sensitive to detect as little as 5% of the maximum in vitro endothelial cell TF response. Vascular endothelium of control animals expressed TM but had no detectable TF or E-sel. Following E. coli infusion, widespread E-sel expression and microvascular fibrin deposition was evident within 6 hours. However, expression of TF by endothelial cells became detectable only in the splenic microvasculature, where endothelial specificity of TF expression was confirmed by dual immunofluorescence of TF with von Willebrand's factor and with TM. In the spleen, there was a dissociation of expression of TF and E-sel, with marginal zone vessels being TF-positive and E-sel-negative, whereas sinusoidal endothelium was E-sel-positive but TF-negative. TM expression was unchanged from controls. Additionally, expression of TF by lung alveolar epithelial cells, splenic macrophages, and epithelial cells of the renal glomeruli was observed to be enhanced in septic animals. This study documents endothelial cell expression of TF in vivo in a relevant pathological setting. At the same time, compared with endothelial cells in culture, there is in vivo both significantly greater control of TF expression than expected, given the strong positive stimuli present in lethal E. coli septic shock and an unpredicted heterogeneity of activation responses.

Animals↗
PubMed1993

Hemodynamic and nonhemodynamic mechanisms of experimental pulmonary edema in rats and the effects of anisodamine and tetramethylpyrazine--estimation of blood gas analysis, RBC superoxide dismutase and prostaglandin E2 in plasma and bronchoalveolar lavage (Part 3).

Anisodamine (ADM, 654-2, 30 mg/kg) and tetramethylpyrazine (TMP, 120 mg/kg) have shown an apparent preventive effect on pulmonary edema (PE). In this study, the nonhemodynamic mechanism was studied: The dynamic changes of PaO2, O2Sat, PaCO2, and blood pH were measured, and RBC superoxide dismutase (SOD) and plasma and bronchoalveolar lavage (BAL) PGE2 levels were estimated. It was concluded that ADM and TMP exerted inhibitory effects on the hypoxic state. The ability of ADM and TMP to adjust RBC SOD and PGE2 levels may be one of the preventive mechanisms of the drugs.

Animals↗
PubMed1993

[Clinical application of extraperitoneal ovarian transposition in cervical cancer].

Ten young patients with cervical cancer were treated by extraperitoneal ovarian transposition. All patients received pelvic irradiation post operatively. Sex hormone were analysed after treatment. 10 cervical cancer patients who were irradiated only were analysed as control. Our data suggested that extraperitoneal ovarian transposition has definite significance for reserving ovarian function in young patients with cervical cancer and improve the quality of operation. This operation is chiefly suited for young patients with early cervical cancer who were operated extra-peritoneally, also for young patients who are irradiated alone or before operation.

Adult↗
PubMed1992

The genetic basis of epidermolytic hyperkeratosis: a disorder of differentiation-specific epidermal keratin genes.

Epidermolytic hyperkeratosis (EH) is a skin disease characterized by keratin filament clumping and degeneration in terminally differentiating epidermal cells. We have discovered that the genetic basis for EH resides in mutations in differentiation-specific keratins. Two of six distinct incidences of EH had a keratin 10 (K10) point mutation in a highly conserved arginine. Remarkably, this same residue is mutated in the basal epidermal K14 in three incidences of another skin disease, epidermolysis bullosa simplex (EBS). By genetic engineering, gene transfection, and 10 nm filament assembly, we show that this mutation is functionally responsible for the keratin filament clumping that occurs in basal (EBS) or suprabasal (EH) cells. These studies strengthen the link between filament perturbations, cell fragility, and degeneration first established with EBS. They also suggest a correlation between filament disorganization and either cytokinesis or nuclear shape, giving rise to the seemingly binucleate cells typical of EH.

Amino Acid Sequence↗
PubMed1992

Transcriptional regulation of human apolipoprotein genes ApoB, ApoCIII, and ApoAII by members of the steroid hormone receptor superfamily HNF-4, ARP-1, EAR-2, and EAR-3.

Apolipoproteins B, CIII, and AII are synthesized primarily in the liver and intestine and play an important role in lipid and cholesterol metabolism. It was previously shown that the cis-acting elements (BA1 (-79 to -63), CIIIB (-87 to -63), and AIIJ (-740 to -719) present in the regulatory regions of the human apoB, apoCIII, and apoAII genes, respectively, are recognized by common transcription factors present in hepatic nuclear extracts. This report shows that four members of the steroid receptor superfamily, ARP-1, EAR-2, EAR-3, and HNF-4, bind specifically to the regulatory elements BA1, CIIIB, and AIIJ. Dissociation constant measurements showed that ARP-1, EAR-2, and HNF-4 bind to elements BA1 and CIIIB with similar affinities (Kd 1-3 nM). Cotransfection experiments in HepG2 cells revealed that ARP-1, EAR-2, and EAR-3 repressed the BA1, CIIIB, and AIIJ element-dependent transcription of the reporter gene constructs and the transcription driven by homopolymeric promoters containing either five BA1 or two CIIIB elements. In contrast, HNF-4 activated transcription of reporter genes containing the elements BA1, CIIIB, and AIIJ and reversed the ARP-1-mediated repression of the apoB and apoCIII genes. These results suggested that the opposing transcription effects observed between HNF-4 and ARP-1 may be due to competition for binding to the same regulatory element. Mutations which affected the binding of HNF-4 to elements BA1 and CIIIB affected its ability to activate transcription of the apoB and apoCIII reporter genes, respectively. Transcriptional activation by HNF-4 depended on the presence of elements II (-112 to -94) and III (-86 to -62) of the apoB and H (-705 to -690), I (-766 to -726), and J (-792 to -779) of the apoCIII promoters, indicating that transcriptional activation of apoB and apoCIII genes by HNF-4 requires the synergistic interaction of factors binding to these elements. The finding that HNF-4, ARP-1, EAR-2 and EAR-3 can regulate the expression of the apoB, apoCIII, and apoAII genes suggest that these nuclear hormone receptors may be an important part of the signal transduction pathways modulating lipid metabolism and cholesterol homeostasis.

Animals↗
PubMed1992

Basement membranes in adenoid cystic carcinoma. An immunohistochemical study.

Tissue samples from 30 patients with adenoid cystic carcinoma and 20 with adenocarcinoma of salivary gland origin were studied by immunohistochemical staining with specific antibodies to the four macromolecules that are present in normal basement membranes: type IV collagen, laminin, heparan sulfate proteoglycan, and entactin. In the adenoid cystic carcinoma samples, the four proteins were localized in different types of extracellular matrices in the tumor, namely pseudocystic spaces, hyaline stroma, and around tumor cell nests. The staining intensity was enhanced by pretreatment with hyaluronidase. The tumor cells of adenoid cystic carcinoma showed a tendency to proliferate with individual cells in contact with the basement membrane and to infiltrate through basement membrane-rich tissues, such as peripheral nerves, blood vessels, and skeletal muscles. In contrast, only circumferential staining of tumor cell nests was obtained in adenocarcinoma samples. The results suggest that adenoid cystic carcinoma is a tumor with affinity for basement membranes, and this basic feature is reflected in its histology and presumably in its biologic behavior. Immunostaining with antibodies to basement membrane proteins appears to be useful for differential diagnosis of some types of these two carcinomas.

Adenocarcinoma↗
PubMed1992

Kappa 3 opiate receptor binding in the mouse and rat.

Previous work examining the binding of [3H]naloxone benzoylhydrazone (NalBzoH) in calf brain has identified a novel binding site, kappa 3. In mice and rats NalBzoH elicits an analgesic response which can clearly be differentiated from classical mu, delta or kappa 1 mechanisms and which is pharmacologically consistent with a kappa 3 receptor mechanism of action. In the current studies we demonstrate the presence of kappa 3 sites in both mouse and rat brains. The selectivity of the kappa 3 sites for opioids clearly discriminated it from traditional mu, kappa 1, kappa 2 or delta receptors. In the rat, the density of kappa 3 sites increased 2.5-fold from age 2 days to 21 days, after which it remained relatively stable. Among a number of brain regions in the rat, the density of kappa 3 sites varied dramatically. Highest levels were present in the hypothalamus, thalamus, striatum and midbrain with very low levels in the cerebellum. Intermediate levels were present in cortex, brain stem and spinal cord. Together, these studies support the presence of kappa 3 receptors in both mouse and rat brain which are very similar to those previously reported in calf brain.

Animals↗
PubMed1992

Molecular analysis of Saccharomyces cerevisiae chromosome I. On the number of genes and the identification of essential genes using temperature-sensitive-lethal mutations.

Previous analyses of Saccharomyces cerevisiae chromosome I have suggested that the majority (greater than 75%) of single-copy essential genes on this chromosome are difficult or impossible to identify using temperature-sensitive (Ts-) lethal mutations. To investigate whether this situation reflects intrinsic difficulties in generating temperature-sensitive proteins or constraints on mutagenesis in yeast, we subjected three cloned essential genes from chromosome I to mutagenesis in an Escherichia coli mutator strain and screened for Ts- lethal mutations in yeast using the "plasmid-shuffle" technique. We failed to obtain Ts- lethal mutations in two of the genes (FUN12 and FUN20), while the third gene yielded such mutations, but only at a low frequency. DNA sequence analysis of these mutant alleles and of the corresponding wild-type region revealed that each mutation was a single substitution not in the previously identified gene FUN19, but in the adjacent, newly identified essential gene FUN53. FUN19 itself proved to be non-essential. These results suggest that many essential proteins encoded by genes on chromosome I cannot be rendered thermolabile by single mutations. However, the results obtained with FUN53 suggest that there may also be significant constraints on mutagenesis in yeast. The 5046 base-pair interval sequenced contains the complete FUN19, FUN53 and FUN20 coding regions, as well as a portion of the adjacent non-essential FUN21 coding region. In all, 68 to 75% of this interval is open reading frame. None of the four predicted products shows significant homologies to known proteins in the available databases.

Amino Acid Sequence↗
PubMed1992

Suppression of acute lymphoblastic leukemia by the human wild-type p53 gene.

Independent mutations in both alleles of the p53 tumor suppressor gene are a frequent finding in human T-cell acute lymphoblastic leukemia (T-ALL) cell lines and in the cells of some T-ALL patients in relapse. One major goal of studying the status of p53 (and other tumor suppressor genes) in human cancer is to facilitate the suppression of the tumorigenic phenotype through the restoration of the expression of the wild-type allele. While the efficient insertion of a suppressor into all cells of solid/metastatic human tumors may at present be impossible, insertion into leukemia cells may be feasible due to the accessibility of the leukemia cells in the body. To examine the feasibility of suppressing the tumorigenicity of human T-leukemia cells, the human T-ALL cell line Be-13, which lacks endogenous p53 protein, was infected with a recombinant retrovirus encoding the wild-type allele of human p53 (hwtp53). Expression of p53 reduced the growth rate of infected Be-13 cells in vitro, suppressed colony formation in methylcellulose cultures, and abrogated their tumorigenic phenotype in nude mice in vivo. These results suggest that suppression of the leukemic phenotype of relapse T-ALL-derived Be-13 cells is feasible. Acute leukemia cell suppression via high-efficiency infection with retroviruses encoding wtp53 may be feasible and beneficial in T-ALL cases as part of a bone marrow transplantation regimen in an effort to reduce the frequency of posttransplantation relapse.

Animals↗
PubMed1992

Separation of albumin from autologous plasma by heat.

A simplified technique has been developed to separate albumin from the plasma of a patient undergoing treatment with plasma exchange. This albumin can be returned to the patient to maintain colloid osmotic pressure without risk of transmitting disease. Patient plasma is obtained by apheresis. It is heated at 70 degrees C for 60 minutes to denature and remove autoantibodies, immune complexes, and abnormal globulins. The resulting low-concentration albumin solution (LCAS) retains its natural properties. Immunologic analysis by gel diffusion shows a reaction pattern of complete identity with that of human serum albumin. The albumin in LCAS is more than 90 percent of the remaining protein, as determined by scan of a cellulose acetate electrophoresis pattern. More than 97 percent of the albumin is in monomer form, as judged by polyacrylamide gel electrophoresis. No patient antibodies to neonantigens in the heat-treated albumin can be identified by double radial immunodiffusion. More than 80 percent of the plasma albumin is recovered in LCAS. LCAS is safe and efficient for use in plasma exchange.

Aluminum↗
PubMed1992

Immunohistochemical localization of progesterone receptor in human decidua of early pregnancy.

Rat monoclonal antibodies to human progesterone receptor were used for immunolocalization studies in human decidua of early pregnancy. Frozen sections of 42 specimens of decidua were stained by the peroxidase-antiperoxidase method (PAP). Progesterone receptor was localized exclusively in the nuclei of decidual and myometrial cells with no specific staining in the cytoplasm. In the decidualized endometrium, stroma were always positively stained. Smooth muscle, pericyte and endothelial cells of blood vessels were extensively stained. Glandular epithelia showed variation in staining, which was positive in the basal but very weak or negative in the superficial layer of the decidua. No specific staining could be detected in the control sections. Of special interest was the positive staining of the endothelium of decidual blood vessels, a finding which has not been reported previously. The cells of the inner lining of vessels that stained with the antiprogesterone receptor antibodies were also Factor VIII positive, thus confirming the endothelial nature of these cells. It is concluded from these results that endothelial cells from human first trimester decidua express progesterone receptors.

Adult↗
PubMed1992

Cachexia and graft-vs.-host-disease-type skin changes in keratin promoter-driven TNF alpha transgenic mice.

Tumor necrosis factor alpha (TNF alpha) orchestrates a wide range of effects that combat severe infections in animals. At lower levels, TNF alpha plays an important protective role in stimulating chemotaxis and antimicrobial activity of neutrophils, macrophages, and eosinophils. During chronic illness, TNF alpha secretion can be elevated markedly, giving rise to cachexia, hemorrhage, necrosis and, ultimately, death. Although TNF alpha may mediate many of its effects through macrophages, 30% of TNF alpha injected into animals concentrates in the skin. In recent years, it has been shown that keratinocytes can be induced to synthesize TNF alpha. To explore the role of TNF alpha synthesis in keratinocytes, we used a keratin-14 (K14) promoter to target human TNF alpha expression in the epidermis and other stratified squamous epithelia of transgenic mice. Most mice expressing the K14-TNF alpha transgene stopped gaining weight within 1 week postbirth, and exhibited retarded hair growth. In the skin, adipose production was profoundly inhibited, whereas signs of fibrosis and immune infiltration were evident in the dermis. Over time, the epidermis exhibited an increased stratum corneum, as signs of necrosis began to appear in the skin. Within 3-5 weeks, the mice displayed features characteristic of cachexia and necrosis. Our results suggest that TNF alpha expression by keratinocytes not only plays a role in inflammatory and graft-versus-host-disease-like responses in the skin, but also in other tissues, apparently by virtue of stratified squamous epithelial-derived TNF alpha entering the bloodstream. Our results have enabled the first evaluation of many of the effects of TNF alpha in transgenic animals.

Animals↗
PubMed1992

Primary malignant lymphoma of the salivary gland: a tumor of mucosa-associated lymphoid tissue.

The clinical, morphologic and immunohistochemical features of 10 cases of the low-grade mucosa-associated lymphoid tissue (MALT) lymphoma of salivary glands are described. Although the initial histologic diagnosis in nine of these cases was myoepithelial sialadenitis, the diagnosis of primary salivary gland MALT lymphoma was based on the demonstration of light chain restriction and on morphologic characteristics. Histologic study showed a characteristic cytology, which included centrocytoid cells (composed of small centrocytes and monocytoid B cells) and a varying degree of plasma cell differentiation; the occurrence of epithelial or acinar invasion by neoplastic centrocytoid cells; and the presence of reactive lymph follicles among the neoplastic cells. Furthermore, multinucleate giant cells resembling Warthin-Finkeldey cells were detected in seven cases. In the light of these findings, cases previously diagnosed as myoepithelial sialadenitis require careful assessment and nine out of 32 cases are, in reality, examples of primary salivary gland MALT lymphomas. Immunohistochemical analysis of paraffin sections revealed the following characteristic immunophenotype of MALT lymphoma: L26, KiB3 and LN2 positive, and a monotypic immunoglobulin pattern (predominantly IgM/kappa). It was of interest that salivary gland parenchyma, infiltrated by neoplastic centrocytoid cells, reacted with LN3 for cells expressing human leukocyte antigen-DR (HLA-DR) antigens. Whereas salivary gland epithelia devoid of a neoplastic invasion were invariably negative for LN3. This suggests a lymphocyte-mediated role in salivary epithelial HLA-DR expression. It appears that HLA-DR expression is an inducible phenomenon in MALT lymphomas of salivary gland.

Adult↗