Biomedical subjects

J Guo

Publications and source records attributed to J Guo.

At least 199 records · Page 11Linked to original sources

PubMed1999

Theoretical and experimental CD of conformationally flexible complex molecules-application to ouabain pentanaphthoate and analogs.

Theoretical calculation of circular dichroic exciton-coupled spectra of ouabain 1,19,2',3',4'-pentanaphthoate and its analogs was executed by a combination of conformational analysis with molecular mechanics and quantum-chemical calculation. Most of the calculated CD spectra show good agreement with the corresponding experimental data, which suggests that the method may be generalized for applications to other conformationally flexible natural products. The CD calculation was then used to evaluate the plausibility of "fortuitous CD cancellation," which was observed in the microscale naphthoylation study of hypothalamic inhibitory factor, a presumed ouabain isomer from bovine hypothalamus.

Animals↗

PubMed1999

Study on IL-4, IL-5 and IL-10 in liver and bone marrow of mice infected with Schistosomiasis Japonica.

To compare Th2 cytokines levels in livers and bone marrow of mice infected with Schistosomiasis Japonica and understand their implication, ABC immunohistochemical staining technique and multimedia pathologic pictures analysis were used to detect the IL-4, IL-5 and IL-10 derived from livers and bone marrow of infected mice. Results showed that in the livers of infected mice, IL-4, IL-5 and IL-10 were obviously increased over time. The level of IL-4 was increased most among the 3 indicators. In bone marrow of infected mice, however, even though IL-4 was slowly increased over time, it was lower than that of livers in 10th and 12th week. The level of IL-5 was higher than that of livers during 12th weeks. Before 10th weeks IL-10 was elevated. After 12th week IL-10 was decreased and obviously lower than that of livers. It is concluded that in mice infected with Schistosomiasis Japonica, the immune response occurred mainly in the liver. Therefore, in bone marrow, IL-5 showed obvious auto-secretion. It might be related to its biological ability to induce B cell division and eosinophil differentiation.

Animals↗

PubMed1999

Effects of sphingosine 1-phosphate on pacemaker activity in rabbit sino-atrial node cells.

The effects of sphingosine 1-phosphate (S-1-P) on pacemaker activity and underlying membrane currents were studied in isolated rabbit sino-atrial (SA) node cells. S-1-P (0.1 microM) reversibly increased the cycle length of spontaneous pacemaker activity from 560 to 1434 ms, and hyperpolarized the maximal diastolic potential (MDP) from -67 to -70 mV. In voltage-clamp experiments, S-1-P (1 microM) activated a pertussis toxin-sensitive, inwardly-rectifying, time-independent K+ current (I(K,ACh)) that had a reversal potential of -88 mV (K+ equilibrium potential -86 mV). S-1-P (1 microM) had no measurable effect on the L-type Ca2+ current (I(Ca,L)) or the hyperpolarization-activated inward current (I(f)) under basal conditions. In the presence of the beta-adrenergic agonist, isoproterenol (ISO, 0.1 microM), S-1-P (1 microM) reversed the ISO-induced increase in pacing rate, hyperpolarized the MDP and decreased the ISO-induced enhancement of both I(Ca,L) (from 171 to 118% of control) and I(f) (from 211 to 135% of control). These results demonstrate that under basal conditions S-1-P can significantly slow spontaneous pacing in rabbit SA node cells mainly due to activation of a background, inwardly-rectifying K+ current. In the presence of ISO, S-1-P also slows the spontaneous pacing rate due to activation of the same K+ current, as well as inhibition of I(Ca,L) and I(f).

Acetylcholine↗

PubMed1999

Synthesis, characterization and antitumor activity of copper(II) complex with nicotinamido-4-bis(2-chloroethyl)aminobenzaldimine.

Nicotinamido-4-bis(2-chloroethyl)aminobenzaldimine (NBAB) was synthesized and characterized by elemental analysis, IR and 1H NMR spectra. The complex of Cu(NBAB)2(NO3)2 was prepared in ethanol and characterized by elemental analysis, conductivity, cyclic voltammetry, IR, UV-Vis, fluorescence, CD and EPR spectra. The characteristic data suggest that the complex has an elongated octahedral structure, and NBAB behaves as bidentate in the keto form. The antitumor activities of NBAB and the complex against L1210 murine leukemia and K562 were investigated with both the MTT method and the colony formation test. The results in vitro indicate that antitumor activities of NBAB are superior to 2,2'-chlorodiethylamine hydrochloride (nitrogen mustard) for L1210, and inferior to nitrogen mustard for K562, but the antitumor activities of the complex for both cell lines are superior to nitrogen mustard.

Animals↗

PubMed1999

The prolonged hematologic effects of a single injection of PEG-rHuMGDF in normal and thrombocytopenic mice.

A single injection of > or =10 microg/kg PEG-rHuMGDF in mice causes a dose-dependent increase in circulating platelets beginning on day 3 and peaking on days 5-6. The mean platelet volume and platelet distribution width at doses > or =100 microg/kg initially increase in a dose-dependent fashion and later decrease. However, the mean platelet volume does not change when platelets are incubated with PEG-rHuMGDF in vitro. The number of marrow megakaryocytes increases in a dose-dependent fashion as early as day 1 and peaks on day 3. Marrow megakaryocyte colony-forming units (CFU-Meg) do not increase on days 1-3 at a dose of 100 microg/kg (a dose that increases platelet numbers two- to threefold and may be clinically relevant), but the relative frequency of high ploidy megakaryocytes and the proportion of large marrow megakaryocytes (29-50 microm in diameter) increases. After a dose of 1,000 microg/kg the percentage of megakaryocytes in mitosis peaks at 24-48 hours and the percentage of megakaryocytes incorporating BrdU is maximal at 48 hours, the relatively delayed peak of BrdU incorporation most likely representing endomitosis. The relative frequency of type II and III megakaryocytes peaks on days 3 and 4, respectively. Pharmacokinetic analysis of PEG-rHuMGDF shows peak serum concentrations at 2-4 hours and a terminal half-life of 11.4+/-2.5 hours. A single injection of PEG-rHuMGDF ameliorates carboplatin-induced megakaryocytopenia and thrombocytopenia in a dose-response dependent fashion. In conclusion, a single injection of PEG-rHuMGDF increases megakaryocyte and platelet production in normal and myelo-suppressed mice.

Acetylcholinesterase↗

PubMed1999

Rarity of autoantibodies to a major autoantigen, thyroid peroxidase, that interact with denatured antigen or with epitopes outside the immunodominant region.

The nature of the autoantibody repertoire to the dominant autoantigen in human autoimmune thyroid disease is controversial. There is evidence that autoantibodies to thyroid peroxidase (TPO) interact with overlapping conformational epitopes in an immunodominant region and binding to denatured (DN) protein is decreased. Contrary data demonstrate TPO autoantibody reactivity with DN-TPO or polypeptide fragments. However, none of the TPO-specific, human monoclonal autoantibodies isolated to date preferentially recognize denatured autoantigen. We therefore searched an immunoglobulin gene phage display library for human autoantibodies that bind TPO denatured by reduction and alkylation (DN-TPO). Thyroid-infiltrating B cells from a typical TPO autoantibody-positive patient were the source of mRNA for library construction. Surprisingly, the library enriched after panning on DN-TPO, as well as a panel of individual clones, preferentially bound native (N)-TPO. Of 13 clones selected using DN-TPO or N-TPO, 12 clones recognized the TPO immunodominant region. Moreover, regardless of selection with N-TPO or DN-TPO, their heavy and light chains were encoded by similar VDJ and Vkappa combinations. One clone (DN4), isolated using DN-TPO, did not interact with the TPO immunodominant region and its H chain derives from a different VH gene. Although DN4 binds specifically to TPO, its affinity is low, unlike the high affinities of other human TPO autoantibodies. In conclusion, human monoclonal autoantibodies that preferentially recognize denatured TPO could not be isolated from an immunoglobulin gene library despite selection with denatured protein. Our findings demonstrate the bias of the human B cell repertoire towards recognition of an immunodominant region on the conformationally intact form of a major thyroid autoantigen.

Amino Acid Sequence↗

PubMed1999

Intraventricular haemorrhage and its prognosis, prevention and treatment in term infants.

The purpose of this study was to investigate the prognosis of intraventricular haemorrhage (IVH) in term infants and its prevention and treatment. The authors diagnosed IVH in full-term newborns by using computerized tomography (CT) or cranial ultrasonography (US). The results of CT or US were reviewed and the grade of haemorrhage was determined by an independent radiologist using Papile's criteria. All the infants were examined on the first day of their life by a paediatrician and judged to be full term. Survivors were examined between age 2 and 10 years at the Child Development Clinic by a Developmental Paediatrician using the Gesell scales and a standard neurologic examination. The results showed that three of 36 infants (8 per cent) died; complications of pregnancy were present in 17 mothers (47 per cent); nine women tested negative for platelet antigen 1 and their infants exhibited alloimmune thrombocytopenia. Age at diagnosis ranged from in utero to 28 days. Clinical presentation included feeding intolerance, irritability, jaundice, fever, and restlessness. Of the nine children with grade IV IVH, three died and six survivors were severely handicapped. Overall, 22 (67 per cent) of 33 survivors had no or mild handicap. The results of this study suggest that severity of haemorrhage was of prognostic value. Perinatal alloimmune thrombocytopenia turned out to be the single most important cause of severe haemorrhage and poor outcome. Identification and treatment of these infants must begin in utero if we are to prevent IVH and its complications in this group of patients.

Cerebral Hemorrhage↗

PubMed1999

Increased type 1 fimbrial expression among commensal Escherichia coli isolates in the murine cecum following catabolic stress.

Although indigenous bacteria intimately colonize the intestinal mucosa, under normal conditions the intestinal epithelial cell is free of adherent bacteria. Nonetheless, commensal bacteria such as Escherichia coli adhere to and translocate across the intestinal epithelium in association with a number of pathologic states including hemorrhagic shock, immunosuppression, traumatic tissue injury, and lack of enteral feedings. The adhesins involved in the adherence of indigenous E. coli to the intestinal epithelium in vivo following catabolic stress are unknown. We have developed a mouse model to study the bacterial adhesins which mediate the increased intestinal adherence of E. coli after partial hepatectomy and short-term starvation. Our studies demonstrated that hepatectomy and starvation in the mouse were associated with a 7,500-fold increase in the numbers of E. coli bacteria adhering to the cecum. In addition, erythrocyte agglutination studies, as well as immunostaining of fimbrial preparations and electron micrographs of the bacteria, revealed that surface type 1 fimbriae were more abundant in the commensal E. coli harvested from the ceca of the stressed mice. These E. coli isolates adhered to a mouse colon cell line and injected cecal loops in a mannose-inhibitable manner, which suggests a role for type 1 fimbriae in the adherence of the E. coli isolates to the cecum in vivo following host catabolic stress.

Adhesins, Escherichia coli↗

PubMed1999

Molecular requirements for human immunodeficiency virus type 1 plus-strand transfer: analysis in reconstituted and endogenous reverse transcription systems.

We have developed a reconstituted system which models the events associated with human immunodeficiency virus type 1 (HIV-1) plus-strand transfer. These events include synthesis of plus-strand strong-stop DNA [(+) SSDNA] from a minus-strand DNA donor template covalently attached to human tRNA3Lys, tRNA primer removal, and annealing of (+) SSDNA to the minus-strand DNA acceptor template. Termination of (+) SSDNA synthesis at the methyl A (nucleotide 58) near the 3' end of tRNA3Lys reconstitutes the 18-nucleotide primer binding site (PBS). Analysis of (+) SSDNA synthesis in vitro and in HIV-1 endogenous reactions indicated another major termination site: the pseudouridine at nucleotide 55. In certain HIV-1 strains, complementarity between nucleotides 56 to 58 and the first three bases downstream of the PBS could allow all of the (+) SSDNA products to be productively transferred. Undermodification of the tRNA may be responsible for termination beyond the methyl A. In studies of tRNA removal, we find that initial cleavage of the 3' rA by RNase H is not sufficient to achieve successful strand transfer. The RNA-DNA hybrid formed by the penultimate 17 bases of tRNA still annealed to (+) SSDNA must also be destabilized. This can occur by removal of additional 3'-terminal bases by RNase H (added either in cis or trans). Alternatively, the nucleic acid chaperone activity of nucleocapsid protein (NC) can catalyze this destabilization. NC stimulates annealing of the complementary PBS sequences in (+) SSDNA and the acceptor DNA template. Reverse transcriptase also promotes annealing but to a lesser extent than NC.

DNA, Single-Stranded↗

PubMed1999

A mouse monoclonal antibody to a thyrotropin receptor ectodomain variant provides insight into the exquisite antigenic conformational requirement, epitopes and in vivo concentration of human autoantibodies.

We used the secreted TSH receptor (TSHR) ectodomain variant TSHR-289 (truncated at amino acid residue 289 with a 6-histidine tail) to investigate properties of TSHR autoantibodies in Graves' disease. Sequential concanavalin A and Ni-chelate chromatography extracted milligram quantities of TSHR-289 (approximately 20-40% purity) from the culture medium. Nanogram quantities of this material neutralized the TSH binding inhibitory activity in all 15 Graves' sera studied. We generated a mouse monoclonal antibody (mAb), 3BD10, to partially purified TSHR-289. Screening of a TSHR complementary DNA fragment expression library localized the 3BD10 epitope to 27 amino acids at the N-terminus of the TSHR, a cysteine-rich segment predicted to be highly conformational. 3BD10 preferentially recognized native, as opposed to reduced and denatured, TSHR-289, but did not interact with the TSH holoreceptor on the cell surface. Moreover, mAb 3BD10 could extract from culture medium TSHR-289 nonreactive with autoantibodies, but not the lesser amount (approximately 25%) of TSHR-289 molecules capable of neutralizing autoantibodies. Although the active form of TSHR-289 in culture medium was stable at ambient temperature, stability was reduced at 37 C, explaining the mixture of active and inactive molecules in medium harvested from cell cultures. In conclusion, studies involving a TSHR ectodomain variant indicate the exquisite conformational requirements of TSHR autoantibodies. Even under "native" conditions, only a minority of molecules in highly potent TSHR-289 preparations neutralize patients' autoantibodies. Therefore, Graves' disease is likely to be caused by even lower concentrations of autoantibodies than previously thought. Finally, reciprocally exclusive binding to TSHR-289 by human autoantibodies and a mouse mAb with a defined epitope suggests that the extreme N-terminus of the TSHR is important for autoantibody recognition.

Animals↗

PubMed1999

Evidence for genetic transmission of thyroid peroxidase autoantibody epitopic "fingerprints".

Autoimmune thyroid disease is characterized by the tendency to cluster in families and by IgG class autoantibodies to antigens such as thyroid peroxidase (TPO). The epitopes recognized by polyclonal serum autoantibodies can be quantitatively fingerprinted using four recombinant human TPO autoantibodies (expressed as Fab) that define A and B domain epitopes in an immunodominant region. To determine whether these fingerprints are genetically transmitted, we analyzed fingerprints of 63 members of 7 multiplex Old Order Amish families and 17 individuals from 4 Hashimoto thyroiditis families. Inhibition of serum autoantibody binding to [125I]TPO by the recombinant Fab was used to assess recognition of the TPO immunodominant region (4 Fab combined) and recognition of domain A or B (individual Fab). Complex segregation analysis was performed using a unified model (POINTER). For the 4 Fab combined inhibition phenotype, the no transmission model was rejected (chi2(4) = 20.67; P < 0.0032), and the most parsimonious model includes a major gene effect. More importantly, evidence for genetic transmission was obtained for the phenotype defined by the ratio of inhibition by subdomain Fab B1:B2. Thus, for this ratio (reflecting recognition of the B domain), the no transmission model was rejected chi2(4) = 63.59; P < 0.000008). Moreover, the polygenic hypothesis could be rejected, but not the major locus hypothesis, suggesting that major genes might be involved in familial transmission of this trait. In conclusion, our findings suggest that autoantibody recognition of the TPO immunodominant region and the TPO B domain is genetically transmitted. These data may open the way to the identification by candidate analysis or positional cloning of at least one gene responsible for the development of Hashimoto's thyroiditis.

Autoantibodies↗

PubMed1999

Cellular thyroid peroxidase (TPO), unlike purified TPO and adjuvant, induces antibodies in mice that resemble autoantibodies in human autoimmune thyroid disease.

Autoantibodies to several protein antigens in human autoimmunity interact with a restricted range of epitopes, whereas diverse epitopes are recognized by antibodies induced in animals using antigen and adjuvant. To examine the basis for this difference, we compared the qualitative nature of antibodies developing in AKR/N mice injected with purified thyroid peroxidase (TPO) and adjuvant or with TPO expressed on major histocompatibility complex (MHC) class II+ fibroblasts. Mice injected with purified TPO had higher TPO antibody levels than TPO+/class II+ fibroblast-treated mice. Despite lower titers, recipients of TPO+/class II+ cells developed very high affinity antibodies (Kd = approximately 10(-10) M), comparable with those of human TPO autoantibodies and about 10-fold higher than those in purified TPO plus adjuvant-immunized mice. Moreover, more than 90% of TPO antibodies in TPO+/class II+ fibroblast-injected mice, compared with only approximately 50% in TPO plus adjuvant-immunized mice, were to the immunodominant region recognized by patients' autoantibodies. Consistent with this epitopic restriction, TPO+/class II+ fibroblast-injected mice had TPO antibody epitopic fingerprints similar to those of human autoantibodies. In conclusion, mice injected with TPO+/class II+ fibroblasts, but not those injected with purified TPO and adjuvant, develop antibodies closely resembling autoantibodies in human disease. These observations indicate that some animal models based on conventional immunization may not be representative of human diseases with a major humoral component.

Adjuvants, Immunologic↗

PubMed1999

Isolation and characterization of monoclonal antibodies directed against novel components of macrophage phagosomes.

In order to identify novel proteins associated with various stages of macrophage phagocytosis, we have generated monoclonal antibodies that recognize phagosomes. Purified Fc receptor-mediated phagosomes, isolated by feeding IgG-conjugated magnetic beads to LPS-primed murine peritoneal macrophages, were used as the immunogen. An immunofluorescence screen was used to isolate and single-cell clone approximately 150 monoclonal antibodies that recognize mouse macrophage phagosomes as well as labeling other cellular components in patterns which are frequently distinct from those observed with previously characterized phagosome-associated proteins. Predominant morphological categories (in addition to phagosome labeling) include staining of one or more of the following: cytoskeletal patterns, vesicular patterns and plasma membrane localization. In this paper, we describe the antibody screen, preliminary characterization of the antibodies and our identification of the antigens for three representative monoclonal antibodies. These antibodies identify a plasma membrane associated receptor (Mac-1, a subunit of the complement receptor), an actin binding protein (coronin-2) and a vesicular protein (amphiphysin II). Some of the antibodies recognize many cell types, whereas other antibodies are apparently macrophage specific as assessed by flow cytometry and histology. Remarkably, several of the antibodies cross-react with the phagocytic slime mold, Dictyostelium discoideum, recognizing phagosomes and other cellular elements as assessed by immunofluorescence and immunoblots. These results indicate that macrophage phagocytosis has both conserved ancestral features and unique specialized aspects associated with the role of these phagocytes in immunity.

Animals↗

PubMed1999

Dual signaling and ligand selectivity of the human PTH/PTHrP receptor.

Parathyroid hormone (PTH) activates PTH/PTH-related peptide-related receptors (PTHRs) to stimulate both adenylyl cyclase (AC) and phospholipase C (PLC). How these parallel signals mediate specific cellular and tissue responses to PTH, such as the complex anabolic versus catabolic actions of PTH on bone, remains unsettled. Previous studies of PTHR signaling and function employed mainly rodent or other cell lines that express endogenous PTHRs and, possibly, alternate species of PTH receptors. To preclude confounding effects of such receptors, we stably expressed recombinant human PTHRs (hPTHRs) at different levels of surface density in LLC-PK1 porcine renal epithelial cells that lack endogenous PTH responsiveness. hPTH(1-34) induced concentration-dependent activation of both AC and PLC via transfected hPTHRs. Maximal intensity of each signal increased with receptor density, but more hPTHRs were required for PLC than for AC activation. Coupling to AC was saturated at receptor densities too low to detect sustained PLC activation. hPTH(3-34), found by others to be a PLC/protein kinase C (PKC)-selective peptide in rat cells, did not activate PLC via human (or rat) PTHRs under conditions (1 microM peptide, 106 hPTHRs/cell) where hPTH(1-34) stimulated PLC severalfold. Other cellular responses that require PKC activation in these cells, such as sodium-dependent phosphate transport and cAMP-independent secretion of plasminogen activator, were induced by PTH(1-34) but not by hPTH(3-34) or hPTH(7-34). We conclude that amino-truncated PTH analogs reported to activate PKC cannot directly activate phosphatidylinositol-specific PLC via the human or rat PTHR and therefore that PTH receptors may access alternate, PLC-independent pathways of PKC activation in some target cells. The relative intensity of AC and PLC signaling via the hPTHR may be strongly regulated by changes in its surface expression.

Adenylyl Cyclases↗

PubMed1999

The nucleolar targeting signal (NTS) of parathyroid hormone related protein mediates endocytosis and nucleolar translocation.

Previous work has identified the parathyroid hormone-related protein (PTHrP) nucleolar targeting signal (NTS) as both necessary and sufficient for localization of PTHrP to the nucleus and nucleolus of a variety of cells where it is believed to participate in the regulation of cell proliferation, differentiation, and apoptotic cell death. The mechanism whereby a secreted peptide, such as PTHrP, gains access to the nuclear compartment remains a question of debate. The current work examines the possibility that exogenous PTHrP is internalized and transported to the nuclear compartment by a mechanism that is dependent on preservation of the PTHrP NTS. Transiently expressed, PTHrP(1-141) was detected at the cell surface as well as in the cytoplasmic and nuclear compartments of COS-1 cells. Deletion of the NTS, or mutation of the conserved GxKKxxK motif within the NTS, effectively prevented both cell-surface binding and nuclear/nucleolar accumulation of PTHrP(1-141). A biotinylated peptide corresponding to the PTHrP NTS (PTHrP-NTS-biotin) was internalized and translocated to the nucleus and nucleolus in a time-, temperature-, and concentration-dependent manner, whereas a peptide representing a similar bipartite NTS from Nucleolin was not. Internalization and nucleolar targeting of PTHrP-NTS-biotin were indistinguishable in CFK2 cells, which express the common PTH/PTHrP receptor, and in 27m21 cells, which do not. In addition, pretreatment with a saturating dose of synthetic PTHrP(74-113) was capable of abrogating nucleolar accumulation of the PTHrP-NTS peptide, whereas pretreatment with PTHrP(1-34) or PTHrP(67-86) was not. These observations demonstrate that binding of exogenous, full-length PTHrP to the cell surface is mediated through a conserved motif embedded in the NTS and suggest that internalization and nucleolar targeting of an NTS peptide are mediated through binding to a cell surface protein distinct from the PTH/PTHrP receptor. In total, the data support the hypothesis that secreted PTHrP(1-141) can be endocytosed and targeted to the nucleolus through a mechanism that is dependent on preservation of a core motif within the PTHrP NTS.

Amino Acid Sequence↗

PubMed1999

Balance of Th1/Th2 cytokines in thyroid autoantibody synthesis in vitro.

Thyroid-infiltrating lymphocytes spontaneously synthesize IgG class thyroid autoantibodies while blood lymphocytes require activation to produce the same autoantibodies. Surprisingly, the stimulus commonly used to induce autoantibodies by blood lymphocytes, Pokeweed mitogen (PWM), inhibits autoantibody synthesis by thyroid lymphocytes. To address this dichotomy, we investigated the Th1: Th2 cytokine balance in relation to thyroid peroxidase (TPO) autoantibody production in cultures of thyroid, lymph node and blood lymphocytes. The characteristic PWM effect on TPO autoantibody production by thyroid and blood lymphocytes (10 day cultures) was confirmed. Cytokine measurements in these cultures revealed that PWM increased IFN-gamma production by thyroid, lymph node and blood lymphocytes. However, PWM enhanced IL-4 levels in lymphocytes from blood and lymph node but not in thyroid lymphocytes. Moreover, the IL-4: IFN-gamma ratios in short- and long-term cultures were higher for PBMC and lymph node lymphocytes than for thyroid lymphocytes. In summary, PWM shifts the cytokine balance towards Th2 for blood lymphocytes and towards Th1 for thyroid lymphocytes. The shift towards Th1 in the target organ is associated with reduced autoantibody synthesis. Our observations suggest that "immune deviation" towards Th2 as a form of therapy in Graves' disease could project the patient from the frying pan into the fire.

Autoantibodies↗

PubMed1999

[Inhibitory effect of glycyrrhizin on NF-kappa B binding activity in CCl4 plus ethanol induced liver cirrhosis in rats].

OBJECTIVE: To investigate the effects of Potenlini on nuclear factor-kappa B (NF-kappa B) binding activity in the livers of animals models with liver cirrhosis, and to delineate the molecular mechanism of the bioactivities of Potenlini. METHODS: Male SD rats were randomly allocated into a normal control group, a model control group, and a Potenlini group. Rats in the latter two groups were treated with CCl4 and Ethanol solution in order to induce chronic liver injury. Rats in Potenlini group were given Potenlini treatment at the same time. All rats were killed at the 9th week after CCl4 administration. Serum and liver specimens were collected, serum ALT activities and histological findings were assessed. Nuclear extracts from liver tissues were prepared and gel retardation assays were performed for the evaluation of NF-kappa B activity. RESULTS: (1) Serum ALT levels were significantly reduced in rats treated with Potenlini compared with those in rats of the model control group, which had dramatically increased ALT levels. (2) Histologically, liver steatosis and fibrosis were severe in the rats of the model group, but were significantly improved in rats of the Potenlini group. (3) NF-kappa B binding activity was markedly increased in the liver specimens taken from the rats of the model control group in comparison with the binding of normal livers, but the binding levels were nearly normal in the livers of the Potenlini group. CONCLUSION: Potenlini can inhibit the NF-kappa B binding activity in CCl4 and ethanol induced chronic liver injury, and that may partially be the mechanism by which Potenlini protects liver from hepatotoxin-induced liver injury and cirrhosis.

Alanine Transaminase↗

PubMed1999

A parallel study on the effects in treatment of impotence by tonifying the kidney with and that without improving blood circulation.

141 cases of functional impotence of the kidney-deficiency type were treated by tonifying the kidney. On them, 103 cases at the same time were treated by improving blood circulation and the other 38 cases by the former only. As a result the total effective rate and the markedly effective rate in the former were 84.46% and 46.60% respectively; but in the latter, 60.55% and 13.15%. A significant difference was found in Ridit analysis (P < 0.05), indicating that method of tonifying the kidney with improving blood circulation is much better than by simply tonifying the kidney alone.

Adult↗