ABSTRACT
ObjectiveSome studies reported that α7nAChR is closely related to the cognitive function. However, the elderly patients have become a high-risk group of postoperative cognitive dysfunction. The aim of this study was to explore the effect of sevoflurane inhalation on the cognitive function and the quantity of alpha 7nicotinic acetycholine receptors in the hippocampus of elderly model rats.MethodsAdult male Sprague-Dawley rats (N=72) were given subcutaneous injection of D-galactose on the neck for 6 weeks to establish elderly models. The model rats were divided into 4 groups randomly: control group (group Con, n=18) with 6h exposure carrier gas (2L/min Air+2L/min O2); Sevoflurane group (group Sev, n=18) with 6 h exposure to 3.2% sevoflurane through carrier gas. Sev+α7nAChR antagonist group (group Sev+M) injected with methyllycaconitine, after 24 h inhaled of 3.2% sevoflurane and carrier gas for 6 h. Sev+α7nAChR agonist group (group Sev+P, n=18) injected with PNU-282987, after 24 h inhaled of 3.2% sevoflurane and carrier gas for 6 h. Morris water maze experiments were conducted on 6 rats in each group 2 h, 1 week and 4 weeks after treatments, respectively. Every cycle after the behavioral test, the hippocampi were taken out. RT-qPCR method was used to detect α7nAChR mRNA expression. Western blotting was used to detect α7nAChR proteins expression.ResultsBehavioral test: compared with Con group at 2 h after awakening, indicators of working memory and spatial probe test in Sev group and Sev+M group decreased significantly (P0.05). RT-qPCR: compared with Con group at 2 h and 1 w after awakening, the expression of alpha 7nAChR mRNA in the other groups was down-regulated, while at 4 w it was up-regulated (P<0.05).Western blot: protein expression of alpha 7nAChR was down-regulated in the 2 h, 1 w Sev group and the Sev+M group after awakening, and up-regulated in the 4 w group after awakening (P<0.05).ConclusionInhalation of 3.2% sevoflurane for 6 h can cause 7nAChR metabolic disturbance in hippocampus of aging model rats and lead to a short-term (1 w) decline in learning and memory ability of the rats, but this effect is reversible. The PNU-282987 agonist can alleviate the temporary decrease of learning and memory caused by sevoflurane.
ABSTRACT
Polycystic ovary syndrome (PCOS) is the most common metabolic and endocrine disorder in women. However, there is no agreement concerning how to diagnose and treat PCOS worldwide. Three practice guidelines or consensuses, including consensus from the European Society of Human Reproduction and Embryology (ESHRE)/the American Society for Reproductive Medicine (ASRM) in Rotterdam, diagnosis criteria and consensus in China, and clinical practice guideline from the Endocrine Society (ES) in the United States are widely recognized. The present paper may provide some guidance for clinical practice based on a comparative analysis of the above three practice guidelines or consensuses.
Subject(s)
Adolescent , Adult , Female , Humans , Consensus , Hyperandrogenism , Infertility, Female , Insulin Resistance , Menstrual Cycle , Obesity , Polycystic Ovary Syndrome , Diagnosis , Psychology , Therapeutics , Practice Guidelines as TopicABSTRACT
<p><b>OBJECTIVE</b>To compare the mutation and single nucleotide polymorphism (SNP) of LNK gene between chronic myeloid leukemia(CML) and control groups, and to explore the relationship between LNK gene variation and the occurrence of CML.</p><p><b>METHODS</b>A total of 36 patients with CML were selected, 46 healthy persons were used as normal controls. DNA was extracted from bone marrow and peripheral blood, BCR/ABL1 fusion gene was detected by Q-PCR. The whole exon of LNK gene was amplified by PCR. The amplified sequences included the Rs3184504 (C/T) and Rs78894077 (A/C/G/T) affecting the expression of amino acids in LNK gene, and the Rs7973120 (A/T) unaffecting the expression of the amino acids. The mutations and SNP of LNK gene were analyzed by DNA sequencing.</p><p><b>RESULTS</b>Thirty-six cases of CML had BCR/ABL1 mutation, while no mutation was found in the control group. One case of CML had LNK heterozygous mutation (A300V), and the mutation rate was 2.8%, no mutation was seen in normal control group. Rs3184504: C/T allele frequency was 50%/50% in the control group, 94.4%/5.6% in the CML group, and the C allele in CML group was significantly higher than that in the control group; CC genotype accounted for 94.4% (P<0.01). Rs78894077: C/T allele in the control group was 9.8%/90.2%, in CML group was 16.7%/83.3%, the difference was not statistically significant(P>0.05); but CC genotype in CML group was very statistically significant higher than that in control group(P<0.01). Rs7973120: A/T allele frequency was 10.9%/89.1% in the control group, 25%/75% in the CML group, the LNK A allele in CML group was very significantly higher than that in control group (P<0.01).</p><p><b>CONCLUSION</b>CML patients have been confirmed to have LNK mutation; the SNPs of LNK are related with the development of CML, and the most CML patients carry the LNK Rs3184504 C allele and the Rs7973120 A allele.</p>