[Different meanings of Long(stranguria) in medicaland historical books in Han Dynasty].

The word "long (stranguria)" is seen both in historical and medical works in the Han Dynasty, but with much different meanings. In medical books, including Nei jing(Inner Canon), Wu shi er bing fang(Prescriptions for Fifty-two Diseases), and Wu wei yi jian(Medical Bamboo slips of Wuwei), Long refers to incontinence of urination. However, in historical books, Long is usually expressed as "pi long" , referring to different conditions, including lame, fatigue, and disability, all congenital or acquired renal deficient illness. It is also seen in unearthed documents as fei ji (disability) and "du long" , referring to congenital or postnatal severe diseases resulting in disability to do anything. Together with orphan, widow, widower, senility, and poverty without relatives for existence, all weak communities need to be supported and saved.

Reversal of cisplatin resistance in non-small cell lung cancer stem cells by Taxus chinensis var.

Drug resistance in cells is a major impedance to successful treatment of lung cancer. Taxus chinensis var. inhibits the growth of tumor cells and promotes the synthesis of interleukins 1 and 2 and tumor necrosis factor, enhancing immune function. In this study, T. chinensis var.-induced cell death was analyzed in lung cancer cells (H460) enriched for stem cell growth in a defined serum-free medium. Taxus-treated stem cells were also analyzed for Rhodamine 123 (Rh-123) expression by flow cytometry, and used as a standard functional indicator of MDR. The molecular basis of T. chinensis var.-mediated drug resistance was established by real-time PCR analysis of ABCC1, ABCB1, and lung resistance-related protein (LRP) mRNA, and western blot analysis of MRP1, MDR1, and LRP. Our results revealed that stem cells treated with higher doses of T. chinensis var. showed significantly lower growth inhibition rates than did H460 cells (P < 0.05). The growth of stem and H460 cells treated with a combination of T. chinensis var. and cisplatin was also significantly inhibited (P < 0.05). Rh-123 was significantly accumulated in the intracellular region and showed delayed efflux in stem cells treated with T. chinensis var. (P < 0.05), compared to those treated with verapamil. T. chinensis var.-treated stem cells showed significant downregulation of the ABCC1, ABCB1, and LRP mRNA and MRP1, MDR1, and LRP (P < 0.05) compared to H460 cells. Thus, T. chinensis var.-mediated downregulation of MRP1, MDR1, and LRP might contribute to the reversal of drug resistance in non-small cell lung cancer stem cells.

Silicon photonic wire biosensor array for multiplexed real-time and label-free molecular detection.

We demonstrate a silicon photonic wire waveguide biosensor array chip for the simultaneous monitoring of different molecular binding reactions. The chip is compatible with automated commercial spotting tools and contains a monolithically integrated microfluidic channel for sample delivery. Each array sensor element is a 1.8-mm-long spiral waveguide folded within a 130 microm diameter spot and is incorporated in a balanced Mach-Zehnder interferometer with a near temperature independent response. The sensors are arranged in a 400 microm spacing grid pattern and are addressed through cascaded 1x2 optical power splitters using light from a single input fiber. We demonstrate the real-time monitoring of antibody-antigen reactions using complementary and mismatched immunoglobulin G receptor-analyte pairs and bovine serum albumin. The measured level of detection for each sensor element corresponds to a surface coverage of less than 0.3 pg/mm(2).

[Inhibitory effect of paeonol on lipid peroxidational reaction and oxidational decorate of low density lipoprotein].

OBJECTIVE: To observe the effects of paeonol(Pae) on lipid peroxidational reaction and oxidational decorate of low density lipoprotein(LDL). METHOD: The rat model of hyperlipidaemia was established by feeding high lipid diet with cholesterol for 6 weeks. The contents of malondialdehyde(MDA) and oxidized low density lipoprotein(OX-LDL) were measured by thiobarbituric acid reactive substance(TBA) method and sandwich method of enzyme-linked immunosorbent assay for detection of polyclone antibody. LDL of serum in healthy person was separated by improve precipitate method. RESULTS: Pae(300, 150 mg.kg-1) could reduce significantly the levels of MDA of serum, aorta and liver; Pae(300 mg.kg-1) decreased obviously the content of OX-LDL of plasma; Pae(1,000, 200, 40 micrograms.ml-1) refrained markedly the course of oxidational decorate of LDL of serum in healthy person. CONCLUSION: Pae could reduce the levels of MDA and OX-LDL in hyperlipidaemia rats, and refrain the oxidational decorates of LDL of serum in healthy person.

DNaseY: a rat DNaseI-like gene coding for a constitutively expressed chromatin-bound endonuclease.

A rat gene, designated DNaseY, encoding a 36 kDa endonuclease was identified and cloned. Sequence analysis of the cDNA showed it to be the rat homologue of human DNAS1L3. The DNaseY gene product had 42% identity to DNaseI, including conserved critical active site residues, the essential disulfide bridge, the calcium binding domain, and a signal peptide, as well as 2 of the 3 signature boxes. Significantly, DNaseY had 2 nuclear localization signals and was more basic (pI 9.5) than DNaseI (pI 4.8). The DNaseY gene contained a number of exons similar to that of DNaseI, separated by much larger introns, resulting in a gene of >17 kb compared to <4 kb gene of DNaseI. The 36 kDa DNaseY gene product was catalytically inactive but was converted to an active 33 kDa endonuclease following processing of the hydrophobic signal peptide. Antibody generated against peptides representing the predicted amino acid sequence of DNaseY cross-reacted with a 33 kDa nuclear protein which possessed endonucleolytic activity. The enzyme was active over a broad pH range (optimum pH 7-8), was Ca2+/Mg2+-dependent, was inhibited by Zn2+, and was capable of both single- and double-stranded DNA cleavage, producing DNA fragments with 3'-OH ends. Furthermore, the DNaseY gene was expressed constitutively in all cells and tissues tested, but it was not transcriptionally up-regulated in apoptotic cells. All these features were consistent with a role in the early stages of apoptotic DNA fragmentation.

GABA induces GABAergic MSCs in cultured embryonic rat thalamic neurons.

Application of 0.1-10 microM GABA in the vicinity of cultured embryonic rat thalamic neurons recorded with patch pipettes in the presence of 2 microM TTX induced or increased the frequency of miniature synaptic currents (MSCs) that reversed polarity at the Cl- equilibrium potential. These MSCs were blocked by the GABAA receptor antagonist bicuculline and exhibited exponential decay kinetics that closely paralleled those estimated from fluctuation analysis of Cl- channels activated pharmacologically by applying 1-10 microM GABA to the same cells. We conclude that the MSCs are mediated by GABA. Application of the GABAA receptor agonist muscimol activated Cl- current but failed to induce GABAergic MSCs while submicromolar concentrations of GABA evoked GABAergic MSCs but did not activate Cl- channels. The GABAB receptor agonist (-)baclofen did not mimic GABA in inducing MSCs. Induction of GABAergic MSCs by GABA required extracellular Ca2+. Verapamil and Co2+, which block voltage-dependent calcium channels, completely blocked GABA-induced MSCs independent of their effects on the direct activation of a Cl- current response. The results indicate that GABA can trigger GABAergic Cl(-)-dependent MSCs in a Cao(2+)-dependent manner. The mechanism may involve a novel receptor and/or signal transduction pathway.

Exogenous GABA persistently opens Cl- channels in cultured embryonic rat thalamic neurons.

We recorded whole-cell Cl- currents in cultured embryonic rat thalamic neurons by brief applications of GABA or the structural analogue muscimol. In 17 of 141 neurons (12%) the Cl- current persisted for a minute or more after the pipette was removed from the bath. Cl- current never persisted after muscimol exposure even in those cells exhibiting persistent GABA-activated currents (PGC). The half decay times (T50) of PGCs were exponentially and asymptotically related to the duration of GABA exposure and could be interrupted or completely aborted by low-pressure application of saline. PGCs were insensitive to membrane potential, to Tiagabine, a nipecotic acid analogue known to block GABA uptake, and persisted in Cao(2+)-free medium. Fluctuation analysis revealed that PGCs exhibited inferred Cl- channel properties whose kinetic components and estimated average elementary conductance showed no significant difference from those estimated during GABA exposure. The relative contribution of low frequency components was consistently reduced and that of high frequency components modestly increased during PGC compared to those recorded during GABA exposure. Taken together, the results suggest the existence of a superficial compartment in these embryonic neurons that can momentarily accumulate and release exogenous GABA.

Tetrandrine, a Ca++ antagonist: effects and mechanisms of action in vascular smooth muscle cells.

Tetrandrine, an alkaloid extracted from the Chinese medicinal herb Radix stephania tetrandrae, has traditionally been used to treat hypertension. In the present study, the effect of tetrandrine on vascular smooth muscle was investigated by using the rat tail artery as a model of a resistance vessel. Tetrandrine relaxes the tension in tail artery helical strips produced by depolarization with 60 mM KCl. Further studies show that tetrandrine inhibits the KCl-induced intracellular Ca++ increase and L-type voltage-dependent Ca++ channel currents, suggesting that tetrandrine relaxes the vessel via inhibition of Ca++ influx through Ca++ channels. Tetrandrine also inhibits norepinephrine (NE)-induced vasocontraction in the presence of extracellular Ca++. It does not, however, inhibit NE-induced vasocontraction in the absence of extracellular Ca++. Tetrandrine also inhibits the NE-induced intracellular Ca++ increase in the presence of extracellular Ca++ and has no effect on the NE-induced intracellular Ca++ increase in the absence of extracellular Ca++. This suggests that tetrandrine also blocks NE-induced Ca++ influx but not NE-induced Ca++ release from the intracellular Ca++ stores. Furthermore, tetrandrine inhibits thapsigargin-induced intracellular Ca++ concentration increase, suggesting that, in addition to blocking Ca++ influx, tetrandrine also may interfere with the interaction between thapsigargin and Ca++ adenosine triphosphatase.

Isolation of a gametophyte-specific cDNA encoding a lipoxygenase from the red alga Porphyra purpurea.

A cDNA clone encoding a lipoxygenase was obtained from a subtracted cDNA library specific for the gametophyte of Porphyra purpurea. The amino acid sequence of the P. purpurea lipoxygenase is most similar to the sequences of animals and plants in the iron-binding, catalytic region located in the C-terminal half of the enzymes. Northern hybridization confirmed that the gene represented by this cDNA is expressed only in the gametophyte.

Calpastatin gene in human testis.

Antibodies present in a serum obtained from an infertile woman interacted with a 17.5 kD glycoprotein (BS-17 component) extracted from human sperm by Western blot. Polyclonal antibodies were raised against the BS-17 component and used to identify positive staining clones from a human testis lambda gt11 expression library. The cDNA encoding the BS-17 component was isolated and its nucleotide sequence determined. The BS-17 cDNA contained 758 nucleotides with an open reading frame of 558 nucleotides encoding a polypeptide consisting of 186 amino acids. The BS-17 cDNA showed 99.7% homology in 758 nucleotides overlap with the 3' terminus of the gene coding calpastatin and 99.5% identity in 186 amino acid overlap with the carboxyl terminus of calpastatin. The BS-17 component of human sperm corresponds to the carboxyl terminus of calpastatin. This conclusion is supported by the finding that the polyclonal antibodies also interacted with a 84 kD protein corresponding to the M(r) of calpastatin.

Tetrandrine inhibits both T and L calcium channel currents in ventricular cells.

Tetrandrine, a putative Ca2+ channel blocker, is extracted from the Chinese medicinal herb, Radix stephania tetrandrae. In the present study, the whole-cell version of the patch clamp technique was used to investigate the effects of tetrandrine on both T and L calcium channel currents in primary cultured neonatal rat ventricular cells. We show that tetrandrine inhibits both T and L calcium channel currents in ventricular cells. This inhibition of inward Ca2+ currents is concentration dependent and reversible. Tetrandrine does not shift the I-V relationship of the calcium currents. These results clearly demonstrate that tetrandrine acts as a calcium channel antagonist in ventricular cells. Previous data show that tetrandrine may be regarded as a wide-spectrum calcium channel antagonist.

Biochemical and cellular aspects of the anticancer activity of selenium.

Aberrant differentiation is a frequent hallmark of tumors, suggesting that modulators for differentiation and proliferation play a role in multistage carcinogenesis and that their use can also be exploited in cancer chemoprevention and therapy. We have demonstrated that selenium (Se) may be a modulator for the differentiation and proliferation of tumor cells. Evidence has been obtained that Se exerts the following effects: reversing changes of biochemical phenotypes toward normal levels, including reduction of cGMP level and cAMP-dependent protein kinase isozyme type I; increase in cAMP level and cAMP-dependent protein kinase isozyme type II, and altering membrane properties. Furthermore, we have obtained support for this hypothesis utilizing experiments on cultured human liver cell lines. It is demonstrated that Se can lead to the following changes: a. reduction of mitotic index; b. increase in the adhesiveness of cells; c. decrease in confluent saturation density and induction of an early contact inhibition; and d. decrease in tumorigenicity. For the purpose of comparison, the effects of Se on the normal counterparts was also studied. Contrary to what was observed above, there was no significant change in both biochemical and cellular aspects of normal cells treated analogously.

[Level of cyclic AMP-dependent protein kinase isozyme in normal liver and hepatoma tissue and the effect of sodium selenite].

Sodium selenite in normal saline was administered intraperitoneally (1 mg/kg) into mice bearing ascitic hepatocarcinoma for 4 days. The cyclic AMP-dependent protein kinase isozymes (type I and type II) in normal liver and hepatocarcinoma cells were separated and assayed. The results show that the level of type I/II is markedly higher in hepatocarcinoma than in the normal liver cells. Sodium selenite is able to reduce it towards the normal level. Further analysis shows that the chief function of sodium selenite is to reduce the raised level of type I/II in hepatocarcinoma cells which, in fact, is due to the increase of total amount of type I cyclic AMP-dependent protein kinase. This paper presents the speculation that one of the mechanisms of the inhibitory effect of sodium selenite on carcinogenesis may be due to the selective action of this compound on the cyclic AMP-dependent protein kinase isozymes in tumor cells, thus inhibiting cancer cell division and facilitating differentiation and reversion.