PubMed Health⌕ Search

Biomedical subjects

J M Zhang

Publications and source records attributed to J M Zhang.

At least 19 recordsLinked to original sources

Troponin T measurement can predict persistent left ventricular dysfunction in peripartum cardiomyopathy.

OBJECTIVE: To determine whether measurement of cardiac troponin T (cTnT) concentration in newly diagnosed peripartum cardiomyopathy (PPCM) can be used to predict persistent left ventricular dysfunction after a 6-month follow-up. PATIENTS AND METHODS: This was a prospective, multiple-centre clinical trial that studied 106 patients with newly diagnosed PPCM surviving over 6 months. cTnT concentration was measured within 2 weeks of the onset of PPCM. RESULTS: Serum cTnT concentration was negatively correlated with left ventricular ejection fraction (LVEF) at follow-up (LVEF, r = -0.518, p = 0.0001). Analysis by receiver operator characteristic curve yielded an area under the curve of 0.764 (95% CI 0.669 to 0.860, p = 0.0001, vs null hypothesis value 0.5) for cTnT, and a cTnT concentration cut off of >0.04 ng/ml, predicting persistent left ventricular dysfunction with a sensitivity of 54.9% and a specificity of 90.9%. Among 106 recruited patients, there were 33 patients with cTnT concentrations >0.04 ng/ml and 73 patients with cTnT concentrations < or =0.04 ng/ml. After a 6-month follow-up, there was significantly smaller LVEF (35.42% (13.04% vs 50.16% (10.48%, p = 0.0001) and more persistent left ventricular dysfunction (84.8% vs 31.5%, OR = 12.17 (95% CI 4.17 to 35.57), p = 0.001) in patients with cTnT >0.04 ng/ml than in patients with cTnT < or =0.04 ng/ml. CONCLUSION: Serum cTnT concentration measured within 2 weeks of the onset of PPCM was correlated negatively with LVEF at follow-up. This marker offers a simple, quick, inexpensive, non-invasive method for predicting a persistent LVEF of < or =50%. A cTnT concentration of >0.04 ng/ml predicted persistent left ventricular dysfunction with a sensitivity of 54.9% and a specificity of 90.9%.

Adult↗

Genetic engineering of Periplaneta fuliginosa densovirus as an improved biopesticide.

The smoky-brown cockroach (Periplaneta fuliginosa) densovirus (PfDNV) has previously shown potential in urban pest control. To improve its efficacy as a biopesticide, the genome of PfDNV was engineered by inserting the insect-specific toxin gene BmKIT1 in the open reading frame encoding the major structural proteins. A green fluorescent protein (GFP) marker was tagged to the BmKIT1 at its C-terminus for in vivo imaging using Confocal laser scanning microscopy (CFSM). Using a virion rescue strategy, the genomes of recombinant and wild-type (wt) PfDNV were then cotransfected in P. fuliginosa nymphs. Reverse transcription PCR (RT-PCR) showed that the inserted BmkIT1 genes were expressed in the P. fuliginosa nymphs 48 h after cotransfection. CFSM and transmission electron microscopy also confirmed the generation of virus particles and expression of BmKIT1-GFP fusion protein in the cotransfected nymphs. The recombinant viruses remained infective to P. fuliginosa nymphs in feeding tests. Using the LT(50) bioassay method, the coninfection of the recombinant and wt PfDNV killed the P. fuliginosa nymphs approximate 32% faster than wt PfDNV only. This is the first report showing the improvement of engineered densovirus for the potential application of biopesticide.

Animals↗

Mechanical hyperalgesia in rats with chronic perfusion of lumbar dorsal root ganglion with hyperglycemic solution.

In diabetes, chronic systemic hyperglycemia is associated with pain and other symptoms of peripheral neuropathy. Evaluation of mechanisms causing these symptoms is complicated because of the overlap between the systemic effects of hyperglycemia and its toxic effects within the peripheral nervous system. To address this problem we developed a technique for chronic local in vivo perfusion of rat lumbar dorsal root ganglion (DRG) with a hyperglycemic solution. Osmotic pumps were filled with 30 mM glucose in physiological buffer and implanted in normal adult rats. The output of the catheter attached to the pump was positioned in a hole drilled through the right transverse process of the L(5) vertebrae to perfuse the corresponding DRG. Repetitive tests of foot withdrawal to mechanical stimuli have shown that chronic hyperglycemia localized to the L(5) DRG causes hyperalgesia in the hind limb innervated by perfused ganglion but not in the contralateral limb. Control experiments (DRG perfusion with 5 mM glucose or 5 mM glucose+25 mM mannitol solution) have shown that hyperglycemia-induced hyperalgesia can not be attributed to surgery-related injury or hyperosmolality of the ganglion-perfusing solution. These data demonstrate direct functional toxicity of hyperglycemia in the peripheral nervous system. This technique provides a new approach for in vivo study of chronic effects of physiologically active factors on DRG neuron function.

Animals↗

Autocrine regulation of norepinephrine transporter expression.

The norepinephrine transporter (NET) is a neurotransmitter scavenger and site of drug action in noradrenergic neurons. The aim of this study was to identify mechanisms that regulate NET expression during the development of quail (q) sympathetic neuroblasts, which develop from neural crest stem cells. Neurotrophin-3 (NT-3) and transforming growth factor beta1 (TGF-beta1) cause an increase of qNET mRNA levels in neural crest cells. When combined, the growth factors are additive in increasing qNET mRNA levels. Both NT-3 and TGF-beta1 are synthesized by neural crest cells. Onset of NET expression precedes the onset of neural crest stem cell emigration from the neural tube. In older embryos, qNET is expressed by several crest-derived and noncrest tissues. The data show that qNET expression in presumptive sympathetic neurons is initiated early in embryonic development by growth factors that are produced by neural crest cells themselves. Moreover, the results support our previous observations that norepinephrine transport contributes to the regulation of the differentiation of neural crest stem cells into sympathetic neurons.

Animals↗

Huperzine A, a nootropic alkaloid, inhibits N-methyl-D-aspartate-induced current in rat dissociated hippocampal neurons.

Huperzine A, a nootropic alkaloid isolated from a Chinese herb, has been proposed as one of the most promising agents to treat Alzheimer's disease. Recently, the agent was found to inhibit the N-methyl-D-aspartate (NMDA) receptors in rat cerebral cortex in addition to causing an inhibitory effect on acetylcholinesterase. In the present study, the mechanisms underlying NMDA receptor inhibition were investigated using whole-cell voltage-clamp recording in CA1 pyramidal neurons acutely dissociated from rat hippocampus. Huperzine A reversibly inhibited the NMDA-induced current (IC(50)=126 microM, Hill coefficient=0.92), whereas it had no effect on the current induced by alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate or kainate. The effect was non-competitive, and showed neither 'voltage-dependency', nor 'use-dependency'. The IC(50) values of huperzine A were neither altered by changing the concentrations of glycine (2-0.2 microM) and pH (7.4-6.7) in the external solution, nor by addition of Zn(2+) (5 microM) and dithiothreitol (5 mM) to the external solution. However, addition of spermine (200 microM) to the external solution caused a parallel shift to the right of the huperzine A concentration-response curve. From these we suggest that huperzine A acts as a non-competitive antagonist of the NMDA receptors, via a competitive interaction with one of the polyamine binding sites. The potential relevance of NMDA receptor antagonist activity of huperzine A to the treatment of Alzheimer's disease is discussed.

Alkaloids↗

Topical application of acidic bupivacaine to the lumbar ganglion induces mechanical hyperalgesia in the rat.

UNLABELLED: To investigate the neurologic mechanisms of acidic local anesthetic-induced low back pain in humans, we administered bupivacaine and buffered saline at acidic or alkalinized pH at the L5 dorsal root ganglion (DRG) of rats via a hole drilled through the transverse process covering the DRG. Behavioral changes were tested before and after bupivacaine or saline administration. Results indicate that acute single-dose infusion of the DRG with bupivacaine (0.5%) at acidic pH (5.5) induced ipsilateral mechanical hyperalgesia that lasted for 7 days. Acute infusion of alkalinized bupivacaine (pH 7.2), however, caused only minor hyperalgesia that lasted <3 days. Similar results were obtained when bupivacaine was replaced with saline. Alternatively, chronic delivery of acidic saline to the DRG via a subcutaneously implanted osmotic pump resulted in a significant decrease in the withdrawal threshold on the ipsilateral hind paw that lasted for 10 days. In rats receiving chronic treatment of the DRG with alkalinized saline, mechanical hyperalgesia lasted for only 3 days. The results demonstrated that acidic bupivacaine deposited at the DRG causes pain and hyperalgesia when the effects of the local anesthetic have dissipated. These findings may explain the limited therapeutic effects of some acidic local anesthetics used for management of cancer-related and chronic back pain. IMPLICATIONS: Acidic bupivacaine administered at the L5 lumbar ganglion causes pain and hypersensitivity of the hind paw in the rat. These findings may explain the limited therapeutic effects of some acidic local anesthetics used for treatment of cancer-related and chronic back pain.

Administration, Topical↗

Effects of bupivacaine and ropivacaine on high-voltage-activated calcium currents of the dorsal horn neurons in newborn rats.

BACKGROUND: Local anesthetics, such as bupivacaine, have been reported to block calcium currents in primary sensory neurons and to interfere with the release of neurotransmitters in central nervous system neurons. However, it is unknown whether local anesthetics affect the calcium current activity of central nervous system neurons. METHODS: Using a traditional whole cell voltage clamp technique, effects of bupivacaine and ropivacaine on high-voltage-activated calcium currents (HVA-Ic(a)) were investigated in enzymatically dissociated dorsal horn neurons of neonatal rats. Calcium currents were evoked by testing pulses from a holding potential of -90 to 0 mV. RESULTS: Bupivacaine significantly reduced HVA-Ic(a) in a dose-dependent manner. The peak HVA-Ic(a) decreased by 24.5+/-2.5, 32.0+/-6.8, 59.4+/-6.2, 88.3+/-1.5, and 91.6+/-1.1% in response to 10, 30, 50, 100 and 200 microM bupivacaine, respectively. Unlike bupivacaine, ropivacaine markedly increased HVA-Ic(a) at lower concentrations (< 50 microM) but decreased HVA-Ic(a) at higher concentrations (> or = 50 microM). The percent increases in peak HVA-Ic(a) induced by 10 and 30 microM ropivacaine were 95+/-19.1 and 41.6+/-8.3%, respectively. The percent decreases in response to 50, 100, and 200 microM ropivacaine were 21.1+/-2.1, 63.2+/-6.0 and 79.1+/-7.6%, respectively. Results indicate that the inhibitory potency of ropivacaine on HVA-Ic(a) was significantly lower than that of bupivacaine at the same concentrations. CONCLUSIONS: The current study showed that bupivacaine inhibited HVA-Ic(a) recorded from dorsal horn neurons and that ropivacaine increased HVA-Ic(a) at lower concentrations but decreased HVA-Ic(a) at higher concentrations. The inhibitory potency of ropivacaine was lower than that of bupivacaine. Inhibition of calcium currents of central nervous system neurons may be related to the systemic neurotoxic effects of local anesthetics (e.g., convulsions, seizures).

Amides↗

Case report: MR findings of malignant melanoma of the vagina.

We report a case in which malignant melanoma of the vagina showed some MR signal changes after radiotherapy. Before radiotherapy, the tumour had slightly high signal intensity on T(1) weighted images and was enhanced after gadolinium-DTPA administration. After radiotherapy, the signal intensity of the tumour increased conspicuously on both T(1) weighted images and fat suppression T(1) weighted images.

Contrast Media↗

[Pollen morphology of bee plants in Changbai Mountain area].

OBJECTIVE: To develop and utilize the bee plants and bee products in Changbai Mountain area, the representative area of alpine plants in northeast China featuring abundant resources of bee plants. METHOD: The pollen of bee plants was observed and studied by LM and SEM. RESULT: The pollen is morphologically oblate, suboblate, spheroidal and prolate. The external sculpture is commonly reticulate, striate and echinulate. CONCLUSION: Plant pollen identification criteria have been furnished for the development of bee plant resources as well as the inspection of bee products in Changbai Mountain area.

Animals↗

Behavior of lanthanides in countercurrent chromatography using dihexyl-N,N-diethylcarbamoyl methylene phosphonate as stationary phase.

Counter-current chromatography is a real liquid-liquid chromatography. The retention volume of the solute can be calculated from the batch distribution ratio in organic separations. In the separations of metal ion, there are several complex and dissociation reactions involved in the two phases, and the retention volume cannot be always predicted from the batch distribution ratio. A mass transfer model is proposed in this paper and an expression of V(R) is derived. The retention volume of metal ion is determined not only by the batch distribution ratio but also by the mechanism of the extraction reaction. When 25% dihexyl-N,N-diethylcarbamoyl methylenephosphonate in cyclohexane is used as stationary phase and 2.91 mol/l HNO3 as mobile phase, the dynamic distribution ratios obtained from the chromatogram are not equal to but proportional to the batch distribution coefficients. These results are in agreement with the theoretical expression.

Calibration↗

Cardioprotective effects of FK409, a nitric oxide donor, after isolated rat heart preservation for 16 hours.

BACKGROUND: We examined the cardioprotective effects of FK409, a nitric oxide donor, after isolated rat heart preservation. METHODS: FK409 was administered to the hearts in pretreatment (FK409-1 group), during ischemia (FK409-2), or during reperfusion (FK409-3). The combined nitrate and nitrite level, coronary flow, cardiac function, coronary vasodilatory response, creatine kinase (CK), and myocardial water content were evaluated after the hearts had been preserved in University of Wisconsin solution at 0 degrees C for 16 hours. RESULTS: The release of nitrate and nitrite increased in reperfusion between the 20-to-40-second measurement and the measurement at 40 minutes, and the recovery of cardiac function was significantly improved in the FK409 groups. The coronary vasodilatory response to acetylcholine chloride was enhanced in the FK409-1 and FK409-2 groups. CK release decreased in FK409 groups after 15 minutes in reperfusion. CONCLUSIONS: This study suggests that FK409 has the best protective effect on cardiac function and coronary endothelial function when it is administered in the ischemic period, a less protective effect when administered during pretreatment, and the least protective effect when FK409 is given during reperfusion after heart preservation for 16 hours.

Acetylcholine↗

Perfusion of the mechanically compressed lumbar ganglion with lidocaine reduces mechanical hyperalgesia and allodynia in the rat.

The rat L(5) dorsal root ganglion (DRG) was chronically compressed by inserting a hollow perforated rod into the intervertebral foramen. The DRG was constantly perfused through the hollow rod with either lidocaine or normal saline delivered by a subcutaneous osmotic pump. Behavioral evidence for neuropathic pain after DRG compression involved measuring the incidence of hindlimb withdrawals to both punctate indentations of the hind paw with mechanical probes exerting different bending forces (hyperalgesia) and to light stroking of the hind paw with a cotton wisp (tactile allodynia). Behavioral results showed that for saline-treated control rats: the withdrawal thresholds for the ipsilateral and contralateral paws to mechanical stimuli decreased significantly after surgery and the incidence of foot withdrawal to light stroking significantly increased on both ipsilateral and contralateral hind paws. Local perfusion of the compressed DRG with 2% lidocaine for 7 days at a low flow-rate (1 microl/h), or for 1 day at a high flow-rate (8 microl/h) partially reduced the decrease in the withdrawal thresholds on the ipsilateral foot but did not affect the contralateral foot. The incidence of foot withdrawal in response to light stroking with a cotton wisp decreased significantly on the ipsilateral foot and was completely abolished on the contralateral foot in the lidocaine treatment groups. This study demonstrated that compression of the L(5) DRG induced a central pain syndrome that included bilateral mechanical hyperalgesia and tactile allodynia. Results also suggest that a lidocaine block, or a reduction in abnormal activity from the compressed ganglia to the spinal cord, could partially reduce mechanical hyperalgesia and tactile allodynia.

Anesthetics, Local↗

Direct inhibition of G(1) cdk kinase activity by MyoD promotes myoblast cell cycle withdrawal and terminal differentiation.

MyoD has been proposed to facilitate terminal myoblast differentiation by binding to and inhibiting phosphorylation of the retinoblastoma protein (pRb). Here we show that MyoD can interact with cyclin-dependent kinase 4 (cdk4) through a conserved 15 amino acid (aa) domain in the C-terminus of MyoD. MyoD, its C-terminus lacking the basic helix-loop-helix (bHLH) domain, or the 15 aa cdk4-binding domain all inhibit the cdk4-dependent phosphorylation of pRb in vitro. Cellular expression of full-length MyoD or fusion proteins containing either the C-terminus or just the 15 aa cdk4-binding domain of MyoD inhibit cell growth and pRb phosphorylation in vivo. The minimal cdk4-binding domain of MyoD fused to GFP can also induce differentiation of C2C12 muscle cells in growth medium. The defective myogenic phenotype in MyoD-negative BC3H1 cells can be rescued completely only when MyoD contains the cdk4-binding domain. We propose that a regulatory checkpoint in the terminal cell cycle arrest of the myoblast during differentiation involves the modulation of the cyclin D cdk-dependent phosphorylation of pRb through the opposing effects of cyclin D1 and MyoD.

Amino Acid Sequence↗

Evolutionary conservation of MyoD function and differential utilization of E proteins.

The formation of striated muscle in both vertebrates and invertebrates involves the activity of the MyoD family of basic-helix-loop-helix (bHLH) transcription factors. The high degree of evolutionary conservation of MyoD-related proteins, both in the sequence of their bHLH domains and in their general developmental expression patterns, suggests that these factors are also conserved at the level of function. We have addressed this directly using MyoD and E protein factors from vertebrates, Drosophila, and Caenorhabditis elegans. Various MyoD and E factor combinations were tested for their ability to interact in vitro and to function in vivo in the myogenic conversion of 10T12 mouse fibroblasts. We found that the ability of different homo- and heterodimers to bind DNA in vitro was an accurate measure of biological activity in vivo. A second assessment of conserved function comes from the ability of these factors to rescue a C. elegans hlh-1 (CeMyoD) null mutation. We found that both Drosophila and chicken MyoD-related factors were able to rescue a C. elegans CeMyoD loss-of-function mutation. These results demonstrate a remarkable degree of functional conservation of these myogenic factors despite differences in E-protein interactions.

Amino Acid Sequence↗

Coupling of the cell cycle and myogenesis through the cyclin D1-dependent interaction of MyoD with cdk4.

Proliferating myoblasts express the muscle determination factor, MyoD, throughout the cell cycle in the absence of differentiation. Here we show that a mitogen-sensitive mechanism, involving the direct interaction between MyoD and cdk4, restricts myoblast differentiation to cells that have entered into the G0 phase of the cell cycle under mitogen withdrawal. Interaction between MyoD and cdk4 disrupts MyoD DNA-binding, muscle-specific gene activation and myogenic conversion of 10T1/2 cells independently of cyclin D1 and the CAK activation of cdk4. Forced induction of cyclin D1 in myotubes results in the cytoplasmic to nuclear translocation of cdk4. The specific MyoD-cdk4 interaction in dividing myoblasts, coupled with the cyclin D1-dependent nuclear targeting of cdk4, suggests a mitogen-sensitive mechanism whereby cyclin D1 can regulate MyoD function and the onset of myogenesis by controlling the cellular location of cdk4 rather than the phosphorylation status of MyoD.

Animals↗

Multicentre trial on the efficacy and toxicity of single-dose samarium-153-ethylene diamine tetramethylene phosphonate as a palliative treatment for painful skeletal metastases in China.

A multicentre trial was organized in China as part of an international coordinated research project to study the efficacy and toxicity of single-dose samarium-153 ethylene diamine tetramethylene phosphonate (EDTMP) as a palliative treatment for painful skeletal metastases. One hundred and five patients with painful bone metastases from various primaries were treated with 153Sm-EDTMP at a dose of 37 MBq/kg(group I) or 18.5 MBq/kg (group II). The effects were evaluated according to change in daily analgesic consumption, pain score, sum of effect product (SEP), Physician's Global Assessment (PGA), blood counts, and organ function tests conducted regularly for 16 weeks. Fifty-eight of 70 patients in group I and 30 of 35 in group II had a positive response, with SEPs of 22.29+/-14. 47 and 20.13+/-13.90 respectively. Of 72 patients who had been receiving analgesics, 63 reduced their consumption. PGA showed that the Karnofsky score (KS) increased from 58.54+/-25.90 to 71.67+/-26. 53, indicating improved general condition, but the difference was not significant. Among subgroups of patients, only those with breast cancer showed a significant change in the Karnofsky score after treatment. Inter-group differences were found for net change in KS between patients with lung and patients with breast cancer, and between patients with lung and patients with oesophageal cancer. Seventeen patients showed no response. No serious side-effects were noted, except for falls in the white blood cell (nadir 1.5x10(9)/l) and platelet (nadir 6.0x10(10)/l) counts in 44/105 and 34/105 cases, respectively. Ten patients had an abnormal liver function test. Response and side-effects were both independent of dose. In conclusion, 153Sm-EDTMP provided effective palliation in 83.8% of patients with painful bone metastases; the major toxicity was temporary myelosuppression. Further studies are needed to identify better ways of determining the appropriate dose in the individual case and the efficacy of treatment.

Analgesics, Non-Narcotic↗