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Biomedical subjects

M Zhou

Publications and source records attributed to M Zhou.

At least 325 records · Page 18Linked to original sources
PubMed1993

Pentoxifylline restores cardiac output and tissue perfusion after trauma-hemorrhage and decreases susceptibility to sepsis.

BACKGROUND: Although pentoxifylline produces various beneficial effects in a preheparinized model of hemorrhagic shock, it was unknown whether this agent restores the depressed cardiac output (CO) and tissue perfusion in a nonheparinized model of trauma-hemorrhage and resuscitation and, if so, whether it decreases the susceptibility to sepsis after hemorrhage. METHODS: After laparotomy (i.e., induction of trauma), rats were bled to and maintained at a mean arterial pressure of 40 mm Hg until 40% of the maximum shed blood volume was returned in the form of Ringer's lactate. The animals were then resuscitated with Ringer's lactate, four times the volume of shed blood. Pentoxifylline (50 mg/kg body weight) or normal saline solution was infused intravenously more than 95 minutes during and after resuscitation. At 1.5 and 4 hours after resuscitation, CO, tissue perfusion, and plasma liver enzyme levels were determined. Sepsis was induced by cecal ligation and puncture at 20 hours after hemorrhage, and the necrotic cecum was excised 10 hours thereafter. RESULTS: CO and tissue perfusion in the liver, kidney, spleen, and small intestine decreased significantly after hemorrhage and resuscitation. Pentoxifylline treatment, however, restored the depressed CO and tissue perfusion. The elevated liver enzyme levels were also significantly reduced by pentoxifylline treatment. Moreover, pentoxifylline prevented the increased mortality of posthemorrhaged rats subjected to sepsis. CONCLUSIONS: Because pentoxifylline restored the depressed CO and tissue perfusion and decreased the susceptibility to sepsis, this agent appears to be a useful adjunct to crystalloid resuscitation after trauma and hemorrhage, even in the absence of blood resuscitation.

Alanine Transaminase↗
PubMed1993

Expression of myeloperoxidase mRNA by leukemic cells from childhood acute lymphoblastic leukemia.

The frequency of acute lymphoblastic leukemia (ALL) expressing the myeloperoxidase (MPO) gene and other myeloid-associated characteristics was determined in 26 (20 B-lineage, six T-lineage) children at diagnosis. All cases were diagnosed as ALL by standard morphological and cytochemical criteria. In the 26 cases, leukemic blast cells from four B-lineage and two T-lineage ALL patients were simultaneously expressing myeloid-associated antigens. By Northern blot analysis, MPO mRNA was detected in leukemic cells from five out of six cases expressing both lymphoid and myeloid antigens, and from four out of 16 B-lineage and one out of four T-lineage ALL without myeloid antigens. There was no detectable MPO protein or enzymatic activity in the leukemic cells of these cases as examined by immunocytochemistry and cytochemistry. MPO mRNA expression in ALL cells was significantly associated with age < 1 year: leukemic blast cells from all five infant ALL patients expressed MPO mRNA, compared to five out of 21 ALL patients > 1 year of age whose leukemic cells were MPO mRNA(+) (p < 0.01). These results suggest that MPO gene transcription in the absence of translation may characterize a recently described subset of pediatric ALL patients who also express myeloid markers, and may serve as a useful marker for this entity.

Adolescent↗
PubMed1993

Preparation and evaluation in vitro and vivo of copoly (lactic/glycolic) acid microspheres containing norethisterone.

Poly (lactic/glycolic) acid (PLGA) microspheres containing 20% norethisterone (NET) were prepared and the preparation methodology was optimised. The microspheres showed a slow and steady release pattern up to more than 96 hours in 27.5 wt% ethanol solution. In vivo performance of the microspheres indicated that a single intramuscular injection of 80 mg of microspheres could significantly prolong the duration of estrus suppression up to 45 days in rats. In addition, the studies on the stability of microspheres showed that there was no significant change both in the NET content of microspheres and the NET release rate in vitro after storage for one year.

Animals↗
PubMed1993

Lipoperoxidative damage in experimental rabbits with atherosclerosis.

The extent of lipoperoxidation in experimental rabbits with atherosclerosis was determined dynamically during the experimental period of 65 days. Lipoperoxide (LPO) levels and selenium-dependent glutathions peroxidase (SeGSHPx) activities in liver, aorta, heart muscle, plasma erythrocyte (RBC) and platelet were examined on the 65th day. The results showed that the potential anti-lipoperoxidation in the atherosclerotic rabbits was decreased significantly, and the tissues were suffered from lipoperoxidative damage. It seems that there is a close relationship between lipoperoxidative damage and the development of atherosclerosis.

Animals↗
PubMed1993

Alterations in circulating blood volume during polymicrobial sepsis.

Although a great deal is known concerning the pathophysiology of sepsis, it is not clear whether circulating blood volume (CBV) is altered under such conditions. To study, this, rats were subjected to sepsis by cecal ligation and puncture (CLP). Immediately after CLP or sham operation, the animals received 3 ml/100 g body weight normal saline subcutaneously. CBV was determined by using in vivo indocyanine green (ICG) clearance at 2, 5, 10, or 20 hr after CLP or sham operation. This technique does not require any blood sampling. Serum glutamic pyruvic transaminase (SGPT) and glutamic oxaloacetic transaminase (SGOT) were assayed enzymatically as indicators of hepatocyte damage. Hepatic microcirculation was assessed at a selected time point (10 hr post-CLP) by using laser Doppler flowmetry and colloidal carbon infusion techniques. The results indicate that CBV, as determined by ICG clearance, remained unchanged up to 10 hr following the onset of sepsis (i.e., early sepsis) but decreased significantly at 20 hr after CLP (late sepsis). However, systemic hematocrit increased significantly at 5, 10, and 20 hr after CLP, indicating that plasma volume decreased at those time points. This suggests that there may be limitations in accurately assessing CBV at 5 and 10 hr after CLP, i.e., during the hyperdynamic circulatory state of sepsis, using the ICG clearance method. Moreover, SGPT and SGOT levels increased significantly at 10 hr, and the levels increased further at 20 hr post-CLP. In contrast, microvascular blood flow and carbon-perfused areas in the liver were significantly increased at 10 hr post-CLP.

Alanine Transaminase↗
PubMed1992

Human HSP27 is phosphorylated at serines 78 and 82 by heat shock and mitogen-activated kinases that recognize the same amino acid motif as S6 kinase II.

The intracellular concentration of the 27-kDa mammalian heat shock protein, HSP27, increases several-fold after heat and other metabolic stresses and is closely associated with the acquisition of thermotolerance. Posttranslational modifications may also affect the function of HSP27. Heat shock of HeLa cell cultures, or treatment with arsenite, phorbol ester, or tumor necrosis factor, caused a rapid phosphorylation of preexisting HSP27 and the appearance of three phosphorylated isoforms, HSP27 B, C, and D. Digestion with trypsin and fractionation of the peptides by reverse phase high performance liquid chromatography revealed three 32P-labeled phosphopeptides. Microsequence analysis identified peak I as Ala76-Leu77-Ser78-Arg79 and peak II as Gln80-Leu81-Ser82-Ser83-Gly84-Val85- Ser86-Glu87-Ile88-Arg89; peak III contained the undigested peptide pair Ala76-Arg89. Ser82 was the major site and Ser78 the minor site of phosphorylation. Mutant proteins with Ser78 or Ser82 altered to glycine or Ser78-Ser82 double mutants were phosphorylated to reduced extents in vivo after heat or arsenite treatment. Ser78 and Ser82 (and Ser15) occur in the sequence motif RXXS, which is recognized by ribosomal protein S6 kinase II. Mitogenic stimulation of serum-deprived, Go-arrested Chinese hamster cells with serum, thrombin, or fibroblast growth factor also stimulated phosphorylation of HSP27 Ser78 and Ser82, and mitogenic stimulation and heat shock activated protein kinase activities that phosphorylated HSP27 and protein S6 in vitro. These results suggest that HSP27 may exert phosphorylation-activated functions linked with growth signaling pathways in unstressed cells. A homeostatic function at this level could protect cells from adverse effects of signal transduction systems which may be activated inappropriately during stress.

Amino Acid Sequence↗
PubMed1992

Protective effects of preheparinization on the microvasculature during and after hemorrhagic shock.

Despite the fact that trauma patients are not heparinized at the time of injury, most models of hemorrhagic shock involve heparinization before the initiation of hemorrhage. To determine whether preheparinization has any effects on the microvasculature of organs during or after hemorrhage, rats (with and without preheparinization) were bled to a mean arterial blood pressure (BP) of 40 mm Hg. In two groups, this pressure was maintained by withdrawing additional blood until BP could no longer be maintained at 40 mm Hg (maximal bleedout, MB). In another two groups, the BP was maintained at 40 mm Hg until 40% of the MB volume was returned in the form of lactated Ringer's solution. The rats were then resuscitated with four times the volume of MB with lactated Ringer's. At MB or immediately after resuscitation, colloidal carbon black was rapidly infused and the liver, kidney, and spleen were excised, fixed, and sectioned. In additional animals, blood samples for platelet counts and total body fibrinogen estimates were taken before hemorrhage and at MB or at the end of resuscitation. The results indicate that at MB, microvascular patency in the kidney and liver was significantly depressed in the nonheparinized rats but not depressed in the preheparinized rats. This protective effect of heparin is not directly attributable to its anticoagulant properties, since there were no differences in the consumption of platelets or fibrinogen between the nonheparinized and preheparinized groups. Although the microvascular patency improved with resuscitation in the nonheparinized group, the glomeruli counts and perfusion of the spleen remained significantly lower than in the preheparinized group.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

ATP-MgCl2 restores renal microcirculation following trauma and severe hemorrhage.

Although ATP-MgCl2 enhances the recovery of renal function after ischemia and reperfusion, it is not known whether this agent has any beneficial effects on renal microcirculation and function in a nonheparinized model of trauma and severe hemorrhage. To study this, a midline laparotomy was performed (i.e., trauma induced) and the rats were bled to and maintained at a mean arterial pressure of 40 mmHg (1 mmHg = 133.32 Pa) until 40% of the maximum shed blood volume was returned in the form of Ringer's lactate (RL) solution. Animals were then resuscitated with 4 times the volume of the shed blood in the form of RL. ATP-MgCl2, 50 mumol/kg body weight, or an equivalent volume of saline, was infused intravenously during and following resuscitation. Renal microcirculation was examined by using colloidal carbon infusion and laser Doppler flow-metry. Glomerular filtration rate (GFR) was assessed with [3H]inulin clearance and cardiac output (CO) was determined by dye dilution technique. The results indicate that the depressed renal microcirculation following hemorrhage and resuscitation was restored by ATP-MgCl2 treatment. GFR was significantly higher in ATP-MgCl2-treated than saline-treated rats. ATP-MgCl2 also increased urine output, restored the decreased CO, and prevented the occurrence of renal edema after hemorrhage and resuscitation. Thus, ATP-MgCl2 appears to be a useful adjunct to crystalloid resuscitation following trauma and severe hemorrhagic shock even in the absence of blood resuscitation.

Adenosine Triphosphate↗
PubMed1992

Differential alterations in microvascular perfusion in various organs during early and late sepsis.

Although cellular dysfunction occurs very early in sepsis, it remains controversial whether this is solely due to a decrease in tissue perfusion. Recent studies have indicated that while active hepatocellular function was depressed, hepatic surface microvascular blood flow (MBF) increased in early sepsis but decreased in late sepsis as produced by cecal ligation and puncture (CLP). However, it is not known whether microvascular hyperperfusion in early sepsis and microvascular hypoperfusion in late sepsis are common events in other organs under such conditions. To study this, rats were subjected to sepsis by CLP, after which these and the corresponding shams received 3 ml/100 g body wt normal saline. Microvascular perfusion and MBF in various tissues were assessed by colloidal carbon infusion and laser-Doppler flowmetry, respectively, at 5 h (i.e., early sepsis) or 20 h (late sepsis) after CLP or sham operation. Carbon-perfused areas were quantitated by an Optomax image analyzer. The results indicate that the carbon-perfused areas and MBF in the liver, renal cortex, spleen, and small intestinal serosa (only MBF) increased significantly 5 h after CLP. In late sepsis, however, the carbon-perfused areas and MBF were found to be significantly decreased. A highly linear relationship was observed between the changes of carbon-perfused areas and MBF during sepsis in the tested organs. Thus the microvascular responses in the fluid-resuscitated sepsis model are characterized by hyperperfusion in the early stage and hypoperfusion in the late stage of sepsis in the tested tissues. The cellular dysfunctions observed during the early stage of sepsis are, therefore, not due to any reduction in tissue perfusion.

Animals↗
PubMed1992

Antitumor activity of siwenmycin: a novel anthracycline antibiotic.

A novel anthracycline antibiotic, siwenmycin, isolated from the culture of Streptomyces galilaeus var. siwenesis, was examined for its antitumor activities against P388, K562, B16-F10, HeLa, HEp-2 and Lewis lung carcinoma cell lines. The results showed that siwenmycin was effective against P388, K562, HeLa and HEp-2 tumor cell lines in vitro, and significantly inhibited the growth of the Lewis lung carcinoma cell line in vivo. Siwenmycin could also suppress spontaneous and artificial pulmonary metastases of B16-F10 and Lewis lung carcinoma cell lines in C57BL/6 mice. The inhibitory effect of siwenmycin on spontaneous pulmonary metastasis of Lewis lung carcinoma in C57BL/6 mice was even stronger than that of adriamycin (ADM), which is, at present, commonly used in clinical practice. Furthermore, the double-labeling test used in this study has verified that siwenmycin can inhibit cellular RNA synthesis at about one tenth the concentration required to inhibit DNA synthesis to the same degree, indicating that the antitumor mechanism of siwenmycin also differs from that of ADM. The acute toxicity of siwenmycin was very low, and it was as effective in vivo as in vitro, suggesting that this newly found antibiotic should be studied for possible clinical antitumor applications.

Aclarubicin↗
PubMed1992

The effect of recombinant GM-CSF and G-CSF on the bone marrow cells of children with acute lymphoblastic leukemia.

Colony stimulating factors (CSFs) are glycoprotein hormones that regulate growth and differentiation of hematopoietic progenitor cells. Their use to stimulate granulocyte precursors during periods of neutropenia in patients with acute myeloid leukemia (AML) is limited by their concomitant stimulation of the proliferation of myeloblasts. The effects of these agents on leukemic lymphoblasts is not entirely known. We have investigated the in vitro effects of granulocyte-CSF (G-CSF) and granulocyte/macrophage-CSF (GM-CSF) on leukemic cells from children with acute lymphoblastic leukemia (ALL). DNA synthesis of bone marrow cells from 22 children with ALL, either at diagnosis or in relapse, was examined with and without CSFs. Proliferative potential was also tested in a clonogenic assay with 13 bone marrow specimens. These factors did not stimulate the growth of ALL cells in either assay. Our results indicate that G-CSF and GM-CSF should be able to stimulate granulocyte proliferation without enhancing leukemic proliferation during periods of neutropenia in children with ALL.

Bone Marrow↗
PubMed1992

[The effect of 211At labelled monoclonal antibody against gastric cancer on DNA, RNA and protein synthesis in gastric cancer cell].

By means of nuclide precursor incorporation, the effects of 211At labelled monoclonal antibody against gastric cancer (211At-3H11McAb) on DNA, RNA and protein synthesis in gastric cancer cell were studied. The results show that 211At-3H11McAb and Na211At-3 inhibit 3H-TdR, 3H-UR and 3H-Leu incorporation, especially 3H-UR incorporation, into gastric cancer cell at 3.7 x 10(4)Bq and 1.85 x 10(5)Bq; the inhibiting rates depend on concentration. The DNA biosynthesis in gastric cancer cell gradually recover after the drug is removed, suggesting that the drug should exert an inhibiting action on DNA biosynthesis in tumor cell through interference of DNA metabolism.

Antibodies, Monoclonal↗
PubMed1992

[Influence of moxibustion on TXA2 and PGI2 in plasma of rat infected epidemic hemorrhagic fever virus (EHFV)].

In this paper, the model of rat infected EHFV was made and the influence of moxibustion on TXA2 and PGI2 in its plasma was observed. The results show that the content of TXA2 increased and PGI2 decreased in rat significantly after the abdominal inoculation of EHFV, and the content of TXA2 decreased and PGI2 increased markedly in rat infected EHFV to normal level after treatment with moxibustion, suggesting that the regulative function of moxibustion on TXA2 and PGI2 is one of its nerve-endocrine-immune regulations to the body, and there is an important significance. This study provides an important reference for mechanism exploration of moxibustion preventing and treating EHF.

6-Ketoprostaglandin F1 alpha↗