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Z Li

Publications and source records attributed to Z Li.

At least 937 records · Page 52Linked to original sources
PubMed1998

Rhesus macaques infected with macrophage-tropic simian immunodeficiency virus (SIVmacR71/17E) exhibit extensive focal segmental and global glomerulosclerosis.

We previously showed that inoculation of rhesus macaques with molecularly cloned lymphocytetropic simian immunodeficiency virus (SIVmac239) results in SIV-associated nephropathy (SIVAN) and that the glomerulosclerotic lesions were associated with the selection of macrophagetropic (M-tropic) variants (V. H. Gattone et al., AIDS Res. Hum. Retroviruses 14:1163-1180, 1998). In the present study, seven rhesus macaques were inoculated with M-tropic SIVmacR71/17E, and the renal pathology was examined at necropsy. All SIVmacR71/17E-infected macaques developed AIDS, and most developed other systemic complications, including SIV-induced encephalitis and lentivirus interstitial pneumonia. There was no correlation between the length of infection (42 to 97 days), circulating CD4(+) T-cell counts, and renal disease. Of the seven macaques inoculated with SIVmacR71/17E, five developed significant mesangial hyperplasia and expansion of matrix and four were clearly azotemic (serum urea nitrogen concentration of 40 to 112 mg/dl). These same five macaques developed focal segmental to global glomerulosclerotic lesions. Increased numbers of glomerular CD68(+) cells (monocytes/macrophages) were found in glomeruli but not the tubulointerstitium of the macaques inoculated with SIVmacR71/17E. All macaques had glomerular deposits of immunoglobulin G (IgG), IgM, and tubuloreticular inclusions, and six of seven had IgA deposition. However, there was no correlation between the presence of circulating anti-SIVmac antibodies, immunoglobulin deposition, and glomerular disease. Tubulointerstitial infiltrates were mild, with little or no correlation to azotemia, while microcystic tubules were evident in those with glomerulosclerosis or azotemia. The four most severely affected macaques were positive for diffuse glomerular immunostaining for viral core p27 antigen, and there was intense staining in the glomeruli of the two macaques with the most severe glomerulosclerosis. Viral sequences were isolated from glomerular and tubulointerstitial fractions from macaques with severe glomerulosclerosis but only from the tubulointerstitial compartment of those that did not develop glomerulosclerosis. Interviral recombinant viruses generated with env sequences isolated from glomeruli confirmed the M-tropic nature of the virus found in the glomeruli. The correlation between the increased number of CD68(+) cells (monocytes/macrophages) in the glomeruli, the localization of p27 antigen in the glomeruli, and the glomerular pathology confirms and extends our previous observations of an association between glomerular infection and infiltration by M-tropic virus and SIVAN.

AIDS-Associated Nephropathy↗
PubMed1998

Oral immunization of macaques with attenuated vaccine virus induces protection against vaginally transmitted AIDS.

The chimeric simian-human immunodeficiency virus SHIVKU-1, bearing the envelope of human immunodeficiency virus type 1 (HIV-1), causes fulminant infection with subtotal loss of CD4(+) T cells followed by development of AIDS in intravaginally inoculated macaques and thus provides a highly relevant model of sexually transmitted disease caused by HIV-1 in human beings. Previous studies using this SHIV model had shown that the vpu and nef genes were important in pathogenesis of the infection, and so we deleted portions of these genes to create two vaccines, DeltavpuDeltanefSHIV-4 (vaccine 1) and DeltavpuSHIVPPc (vaccine 2). Six adult macaques were immunized subcutaneously with vaccine 1, and six were immunized orally with vaccine 2. Both viruses caused infection in all inoculated animals, but whereas vaccine 1 virus caused only a nonproductive type of infection, vaccine 2 virus replicated productively but transiently for a 6- to 10-week period. Both groups were challenged 6 to 7 months later with pathogenic SHIVKU-1 by the intravaginal route. All four unvaccinated controls developed low CD4(+) T-cell counts (<200/microliter) and AIDS. The 12 vaccinated animals all became infected with SHIVKU-1, and two in group 1 developed a persistent productive infection followed by development of AIDS in one. The other 10 have maintained almost complete control over virus replication even though spliced viral RNA was detected in lymph nodes. This suppression of virus replication correlated with robust antiviral cell-mediated immune responses. This is the first demonstration of protection against virulent SHIV administered by the intravaginal route. This study supports the concept that sexually transmitted HIV disease can be prevented by parenteral or oral immunization.

AIDS Vaccines↗
PubMed1998

Effect of cleavage mutants on syncytium formation directed by the wild-type fusion protein of Newcastle disease virus.

The effects of Newcastle disease virus (NDV) fusion (F) glycoprotein cleavage mutants on the cleavage and syncytium-forming activity of the wild-type F protein were examined. F protein cleavage mutants were made by altering amino acids in the furin recognition region (amino acids 112 to 116) in the F protein of a virulent strain of NDV. Four mutants were made: Q114P replaced the glutamine residue with proline; K115G replaced lysine with glycine; double mutant K115G, R113G replaced both a lysine and an arginine with glycine residues; and a triple mutant, R112G, K115G, F117L, replaced three amino acids to mimic the sequence found in avirulent strains of NDV. All mutants except Q114P were cleavage negative and fusion negative. However, addition of exogenous trypsin cleaved all mutant F proteins and activated fusion. As expected for an oligomeric protein, the fusion-negative mutants had a dominant negative phenotype: cotransfection of wild-type and mutant F protein cDNAs resulted in an inhibition of syncytium formation. The presence of the mutant F protein did not inhibit cleavage of the wild-type protein. Furthermore, evidence is presented that suggests that the mutant protein and the wild-type protein formed heterooligomers. By measuring the syncytium-forming activity of the wild-type protein at various ratios of expression of mutant and wild-type protein, results were obtained that are most consistent with the notion that the size of the functionally active NDV F protein in these assays is a single oligomer, likely a trimer. That a larger oligomer, containing a mix of both wild-type and mutant F proteins, has partial activity cannot, however, be ruled out.

Animals↗
PubMed1998

Adenovirus type 12-induced fragility of the human RNU2 locus requires p53 function.

Adenovirus type 12 (Ad12) infection of human cells induces four chromosomal fragile sites corresponding to the U1 small nuclear RNA (snRNA) genes (the RNU1 locus), the U2 snRNA genes (RNU2), the U1 snRNA pseudogenes (PSU1), and the 5S rRNA genes (RN5S). Ad12-induced fragility of the RNU2 locus requires U2 snRNA transcriptional regulatory elements and viral early functions but not viral replication or integration, or chromosomal sequences flanking the RNU2 locus. We now show that Ad12 cannot induce the RNU1, RNU2, or PSU1 fragile sites in Saos-2 cells lacking the p53 and retinoblastoma (Rb) proteins but that viral induction of fragility is rescued in these cells when the expression of wild-type p53 or selected hot-spot mutants (i.e., V143A, R175H, R248W, and R273H) is restored by transient expression or stable retroviral transduction. We also observed weak constitutive fragility of the RNU1 and RNU2 loci in cells belonging to xeroderma pigmentosum complementation groups B and D (XPB and XPD) which are partially defective in the ERCC2 (XPD) and ERCC3 (XPB) helicase activities shared between the repairosome and the RNA polymerase H basal transcription factor TFIIH. We propose a model for Ad12-induced chromosome fragility in which interaction of p53 with the Ad12 E1B 55-kDa transforming protein (and possibly E4orf6) induces a p53 gain of function which ultimately perturbs the RNA polymerase II basal transcription apparatus. The p53 gain of function could interfere with chromatin condensation either by blocking mitotic shutdown of U1 and U2 snRNA transcription or by phenocopying global or local DNA damage. Specific fragilization of the RNU1, RNU2, and PSU1 loci could reflect the unusually high local concentration of strong transcription units or the specialized nature of the U1 and U2 snRNA transcription apparatus.

Adenoviruses, Human↗
PubMed1998

A tandem array of minimal U1 small nuclear RNA genes is sufficient to generate a new adenovirus type 12-inducible chromosome fragile site.

Infection of human cells with adenovirus serotype 12 (Ad12) induces metaphase fragility of four, and apparently only four, chromosomal loci. Surprisingly, each of these four loci corresponds to a cluster of genes encoding a small abundant structural RNA: the RNU1 and RNU2 loci contain tandemly repeated genes encoding U1 and U2 small nuclear RNAs (snRNAs), respectively; the PSU1 locus is a cluster of degenerate U1 genes; and the RN5S locus contains the tandemly repeated genes encoding 5S rRNA. These observations suggested that high local levels of transcription, in combination with Ad12 early functions, can interfere with metaphase chromatin packing. In support of this hypothesis, we and others found that an artificial tandem array of transcriptionally active, but not inactive, U2 snRNA genes would generate a novel Ad12-inducible fragile site. Although U1 and U2 snRNA are both transcribed by RNA polymerase II and share similar enhancer, promoter, and terminator signals, the human U1 promoter is clearly more complex than that of U2. In addition, the natural U1 tandem repeat unit exceeds 45 kb, whereas the U2 tandem repeat unit is only 6.1 kb. We therefore asked whether an artificial array of minimal U1 genes would also generate a novel Ad12-inducible fragile site. The exogenous U1 genes were marked by an innocuous U72C point mutation within the U1 coding region so that steady-state levels of U1 snRNA derived from the artificial array could be quantified by a simple primer extension assay. We found that the minimal U1 genes were efficiently expressed and were as effective as minimal U2 genes in generating a novel Ad12-inducible fragile site. Thus, despite significant differences in promoter architecture and overall gene organization, the active U1 transcription units suffice to generate a new virally inducible fragile site.

Adenoviruses, Human↗
PubMed1998

Simian-human immunodeficiency virus (SHIV) containing the nef/long terminal repeat region of the highly virulent SIVsmmPBj14 causes PBj-like activation of cultured resting peripheral blood mononuclear cells, but the chimera showed No increase in virulence.

SIVsmmPBj14 is a highly pathogenic lentivirus which causes acute diarrhea, rash, massive lymphocyte proliferation predominantly in the gastrointestinal tract, and death within 7 to 14 days. In cell culture, the virus has mitogenic effects on resting macaque T lymphocytes. In contrast, SIVmac239 causes AIDS in rhesus macaques, generally within 2 years after inoculation. In a previous study, replacement of amino acid residues 17 and 18 of the Nef protein of SIVmac239 with the corresponding amino acid residues of the Nef protein of SIVsmmPBj14 yielded a PBj-like virus that caused extensive activation of resting T lymphocytes in cultures and acute PBj-like disease when inoculated into pig-tailed macaques. This study suggested that nef played a major role in both processes. In this study, we replaced the nef/long terminal repeat (LTR) region of a nonpathogenic simian-human immunodeficiency virus (SHIV), SHIVPPc, with the corresponding region from SIVsmmPBj14 and examined the biological properties of the resultant virus. Like SIVsmmPBj14, SHIVPPcPBjnef caused massive stimulation of resting peripheral blood mononuclear cells (PBMC), which then produced virus in the absence of extraneous interleukin 2. However, when inoculated into macaques, the virus failed to replicate productively or cause disease. Thus, while these results confirmed that the nef/LTR region of SIVsmmPBj14 played a major role in the activation of resting PBMC, duplication of the cellular activation process in macaques may require a further interaction between nef and the envelope glycoprotein of simian immunodeficiency virus because SHIV, containing the envelope of human immunodeficiency virus type 1, failed to cause activation in vivo.

Animals↗
PubMed1998

Role of skeletal muscle in thiazolidinedione insulin sensitizer (PPARgamma agonist) action.

Thiazolidinedione (TZD) insulin sensitizers are specific agonists of peroxisome proliferator activated receptor (PPAR)gamma. However, their mechanism of action and the in vivo target tissue(s) that mediate insulin sensitization remain poorly defined. Although PPARgamma messenger RNA expression has been reported in skeletal muscle, the expression of PPARgamma within myocytes in intact muscle tissue has not been examined. An antipeptide PPARgamma antibody was generated; immunohistochemistry was then used to demonstrate that PPARgamma is present within nuclei of myocytes [in both skeletal (white and red fibers) and cardiac tissue (rodent and human)]. The effect of insulin sensitizer treatment on muscle insulin action was studied using ob/ob mice after 4 days dosing with a potent (6 nM PPARgamma Kd) TZD (10 mg/kg x day). 2-deoxyglucose (2-DOG) uptake was then assessed in freshly isolated soleus muscles from lean vs. ob/ob vs. TZD-treated ob/ob mice. In lean mouse muscles, 2-DOG uptake was stimulated by 82%, 95%, 165% (with 25, 100, 2000 microU/ml insulin); muscles from ob/ob were severely insulin resistant (<80% stimulation with 2000 microU/ml insulin). Muscles from TZD-treated ob/ob displayed a normal insulin response with 100 (71%) or 2000 (158%) microU/ml insulin. Additional studies were performed using ZDF rats treated with/without TZD for 7 days. In vivo 2-DOG glucose uptake into soleus, gastrocnemius, and diaphragm muscles was measured during euglycemic-hyperinsulinemic clamp. Compared with lean rats, muscle 2-DOG uptake in ZDF was reduced by 52% (soleus) or 71% (diaphragm). Partial (40-60%) normalization of the reduced 2-DOG uptake was evident in TZD-treated ZDF rats. In contrast to the effect of in vivo treatment on muscle insulin action, preincubation of isolated soleus muscles from naive lean or ob/ob mice for 5 h with 100 nM TZD did not affect insulin-stimulated 2-DOG uptake. We conclude: 1) PPARgamma is expressed in myocytes within skeletal and cardiac muscle. 2) In vivo activation of PPARgamma by treatment of insulin-resistant mice/rats with a potent TZD corrects impaired muscle insulin action. 3) The lack of a direct effect on muscle after 5 h in vitro TZD incubation suggests that changes in insulin action may require a longer duration of PPARgamma activation or that improved muscle insulin sensitivity may result from an indirect in vivo effect of PPARgamma activation (e.g. changes in systemic lipid metabolism).

Animals↗
PubMed1998

L-CAM expression induces fibroblast-epidermoid transition in squamous carcinoma cells and down-regulates the endogenous N-cadherin.

SCC9 cells, derived from a squamous carcinoma of the tongue, were shown to lack E-cadherin but express alpha- and beta-catenins and N-cadherin. These cells also lack plakoglobin expression, do not assemble desmosomes and exhibit the typical morphology and growth properties of transformed cells. The N-cadherin expressed in SCC9 cells has properties similar to other classical cadherins, including interactions with the catenins. We transfected SCC9 cells with a full-length cDNA for L-CAM (liver cell adhesion molecule), the functional chicken homologue of E-cadherin. The exogenously expressed L-CAM formed complexes with catenins and the cytoskeleton and induced a morphological transition from fibroblastoid to epithelioid, conferred density-dependent growth inhibition, increased aggregation ability, and increased synthesis and stability of alpha- and beta-catenins. Coincident with these phenotypic changes, we detected a significant reduction in the level of endogenous N-cadherin, primarily as a result of rapid degradation of this protein in L-CAM-expressing cells. These results show the abnormal expression of N-cadherin in these transformed epidermoid cells, demonstrate the dynamics of the relationship between two cadherins, and provide a model system for the functional analysis of the tumor suppressor activity of E-cadherin in carcinomas.

Cadherins↗
PubMed1998

Antipyretic activity of gingyo-san, a traditional medicine, in influenza virus-infected mice.

Gingyo-san is composed of 10 crude drugs and used as a traditional antipyretic medicine for the treatment of the common cold and influenza virus infection. In a murine intranasal influenza infection model, fever produced by the infection has been demonstrated to be reduced by suppressing interferon-induced interleukin (IL)-1 alpha production. Thus, we focused on the serum level of IL-1 alpha which produces such novel antipyretic activity, and evaluated the relationship between defervescence and the suppression of IL-1 alpha production by Gingyo-san in influenza virus-infected mice. Fever was produced in the infected mice 33-44 h after infection. Oral administration of a hot water-extract of Gingyo-san (8.9-12.5 mg/0.25 ml/mouse x 3 per day) significantly reduced fever production and suppressed the rise in IL-1 alpha production to the level in uninfected mice. No apparent toxicity by Gingyo-san was observed in infected mice. When the hot water-extract of each 10 of the crude components of Gingyo-san (an unknown amount extracted from 6.25 mg/0.25 ml/mouse x 3 per day for Saigae Tataricae Cornu and 3.5 mg/0.25 ml/mouse x 3 per day for the other 9) was orally administered to infected mice, 6 showed significant antipyretic activity. Of these 6, Saigae Tatricae Cornu significantly suppressed the rise in IL-1 alpha production to the basal level while the other 5 did not affect serum IL-1 alpha. Thus, of the 10 crude components of Gingyo-san, Saigae Tataricae Cornu simultaneously exhibited antipyretic and IL-1 alpha-regulatory activities. The novel antipyretic action of Gingyo-san may be mainly mediated by Saigae Tataricae Cornu which regulates the elevated serum IL-1 alpha level produced by influenza infection.

Analgesics, Non-Narcotic↗
PubMed1998

TPA induces a block of differentiation and increases the susceptibility to neoplastic transformation of a rat thyroid epithelial cell line.

The PC Cl 3 cell line is a well-characterized epithelial cell line of rat thyroid origin. This cell line retains in vitro the typical markers of thyroid differentiation: thyroglobulin (TG) synthesis and secretion, iodide uptake, thyroperoxidase (TPO) expression, and dependency on TSH for growth. Although the differentiated phenotype of thyroid cells has been relatively well described, the molecular mechanisms that regulate both differentiation and neoplastic transformation of thyroid cells still need to be investigated in detail. Protein kinase C (PKC), the target of tetradecanoylphorbol acetate (TPA), regulates growth and differentiation of several cell types. Here we show that treatment of PC Cl 3 cells with TPA induces an acute block of thyroid differentiation. TPA-treated PC Cl 3 cells are unable to trap iodide and the expression levels of thyroglobulin, TSH receptor, and TPO genes are drastically reduced by TPA treatment. This differentiation block is not caused by a reduced expression of one of the master genes of thyroid differentiation, the thyroid transcription factor 1 (TTF-1). TPA-treated PC Cl 3 cells display an increased growth rate indicating that, in addition to the differentiation block, TPA also significantly affects the growth regulation of thyroid cells. Finally, TPA treatment dramatically increases the number of transformation foci induced in PC Cl 3 cells by retroviruses carrying v-Ki-ras, v-Ha-ras, and v-mos oncogenes. These findings support the notion that the PKC pathway can influence proliferation, differentiation, and neoplastic transformation of thyroid cells in culture.

Animals↗
PubMed1998

Development of serial bio-shock tubes and their application.

OBJECTIVE: To design and produce serial shock tubes and further examine their application to experimental studies on blast injury. METHODS: Bio-medical engineering technique was used for the design and development of the serial shock tubes. One thousand four hundred and fifty nine animals (757 rats, 105 guinea pigs, 335 rabbits, 240 dogs and 22 sheep) were then used to test the wounding effects of the shock tubes. RESULTS: Three types of bio-shock tubes, that is, large-, medium- and small-scale shock tubes were made in our laboratory. The large-scale shock tube is 39 meters long; the inner diameter of the test section is 1 meter; and the maximum overpressure in the driving section is 10.3 MPa. A negative pressure could be formed by means of the reflected rarefactive wave produced by the end plate. The medium-scale shock tube is 34.5 meters long; the maximum overpressure in the driving section is 22 MPa; the test section is designed to be a knockdown, showing 5 basic types with inner diameter of 77 to 600 millimeters, which could be used for researches on overpressure, explosive decompression, underwater explosion, and so on. The small-scale shock tube is 0.5 meter long with the maximum endured overpressure of 68.6 MPa. Results from animal experiments showed that this set of shock tubes could induce various degrees of systemic or local blast injury in large or small animals. CONCLUSIONS: This set of bio-shock tubes can approximately simulate typical explosive wave produced by nuclear or charge explosion, and inflict various degrees of blast injury characterized by stability and reproducibility. Therefore, they can meet the needs of blast research on large and small animals.

Animals↗
PubMed1998

[Experimental study on delayed reinnervation of laryngeal adductor and abductor].

To investigate time of delayed reinnervated laryngeal muscle, 15 dogs were divided into two groups. The right recurrent laryngeal nerves of 10 dogs in experimental group were cut, and repaired at 4, 6, 8, 10 and 12 months intervals by transposition of the phrenic nerve to the recurrent laryngeal nerve after cutting and suturing the adductor branch to the main branch of ansa cervicalis. The right recurrent laryngeal nerves of 5 dogs in control group were cut, but did not repair. Laryngoscope, electromyography, contractile tension of laryngeal muscle and histologic studies were performed at six months postoperatively. The results showed that fair recovery of adduction and abduction was noted within ten months interval, and the effect of adduction was better than that of abduction. The effect decreased gradually with the denervated time increased. The conclusion demonstrated that delayed reinnervation of laryngeal muscle should be performed within ten months.

Animals↗
PubMed1998

[Experimental study of the architecture of skin following tension traction and wound closure].

The experiment performed on domestic pig, was designed to investigate the architecture of the stretching skin and the effect of tension traction on the wound closure. An 7 cm x 3.5 cm was drawn at a standard position. Drawing horizontal and vertical lines on the traction area, points of 1 cm apart were tattooed on the lines. A traction force measuring device was used to draw the wound edges together. Measurements of the distances between the points were made. An 7 cm x 10 cm wound was made on identical sites of each hind leg. In the experiment the traction tension was applied on the edges of wound immediately after the wound debridement. The results showed the stretched distance in the two areas was 5-7 times the width of the wound. The gain of skin from traction was 61-89 percent in the width of the wound. The wounds from traction five days could be closed 5 days after traction. It was concluded that the skin which could be used for traction was abundant. Wound closure with the skin traction technique had many advantages, such as rapid decreasing the size of wound and early closing of wound.

Animals↗
PubMed1998

[Analysis of the causes of vascular crisis following anastomosis of small vessel and its prophylaxis and treatment].

In order to find out the causes, diagnosis, and the prevention and treatment of vascular crisis following anastomosis of small vessels, 314 cases vascular crisis from 1985 to 1997, were analyzed, in which 152 cases, suffered from tissue necrosis either total or partial, making up 48.4%. One hundred and forty-four cases underwent conservative treatment occupying 45.8% and 104 cases had tissue necrosis, occupying 68.4%. Operative exploration was done on 170 cases, occupying 54.1% and 48 cases of them suffered from necrosis, which made up 31.6% of all necrotic cases. Eighty-six cases were followed up by regular visits, ranging from 40 days to 7 years, with the finding that those who had regained normal circulation after vascular crisis recovered as well as those without crisis, and among those who did not regain normal circulation but survived with the help of collateral circulation after vascular crisis, they were usually cases of bad union, healing of wound, persistent swelling, different degree of tissue atrophy, poor recovery of sensation. It was concluded that proper use of vascular anastomosis technique and prophylactic measures preventing postoperative vascular spasm were extremely important, in the prevention of development of vascular crisis following anastomosis of small vessels. If vascular crisis did not respond well to conservative treatment, prompt surgical exploration should be undertaken.

Adolescent↗
PubMed1998

[Experimental study on the effect of Chinese traditional medicine "bone growth fluid" in the change of trace elements in bone lengthening area].

In order to study the effect of Chinese traditional medicine, "Bone Growth Fluid", on bone formation in bone lengthening, the limb lengthening model was made on goat to observe bone formation in the distracted area, and the content of the trace elements was determined. The bone-lengthening operation was carried out on the upper metaphysis of left tibia. The animals were divided into two groups following operation. From 2nd day afteroperation, "Bone Growth Fluid", 10 ml per kilogram body weight, was given daily to goats in the experimental group, and same amount of normal saline was given to goats in another group as control. The results showed-that new bone formation and bone remodeling in the experimental group appeared earlier than that in the control group, and the content of the trace elements was also improved. So Chinese Traditional medicine, "Bone Growth Fluid", could accelerate the accumulation of the trace elements in callus on the distracted sites and it might play some role in the promotion of osteogenesis and bone remodeling in bone lengthening.

Animals↗
PubMed1998

Effect of radix Salviae miltiorrhizae on the gene expression of nitric oxide synthase in ischemic rat brains.

The effect of Radix Salviae Miltiorrhizae (RSM) on the gene expression of nitric oxide synthase (NOS) in rat brains during ischemia was studied with in situ hybridization and the results were analyzed with IBAS 2000 Image Analysis System. It was found that NOS gene expression of cerebral cortex and caudate-putamen was markedly increased in 24 hours in ischemia group (P < 0.01). In RSM-treated rats, although the NOS gene expression of ischemic side was also increased as compared with contralateral cortex and caudate-putamen, it was significantly lower in RSM-treated rats than those of the controls (P < 0.05, P < 0.01). The present study indicates that RSM can partly inhibit NOS gene expression of cerebral cortex and caudate-putamen during ischemia. This may be one of the protective mechanisms of RSM on cerebral ischemia.

Animals↗