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Objective To study the distribution and drug resistance of pathogens in patients with lung cancer,and analyze the prevention strategies. Methods A total of 312 cases of lung cancer patients with infection treated in our hospital from January 2017 to January 2021 were selected as the research objects.The lower respiratory tract secretions,urine and feces were collected for pathogen culture and drug sensitivity test;the distribution and drug resistance of pathogens were analyzed,and the corresponding prevention strategies were formulated. Results Of the 312 patients, 165 (52.88%) had respiratory tract infection, 79 (25.32%) had oropharyngeal infection, and 68 (21.80%) had urinary tract infection.The highest proportion was respiratory infection.Among the 312 patients,398 pathogens were detected of which 212 Gram-positive bacterias (53.27%)were found of which Staphylococcus epidermidis(15.58%)and Staphylococcus aureus(13.07%)accounted for a relatively high proportion. Among 175 Gram-negative strains,Klebsiella pneumoniae(15.94%)and E.coli (10.05% ) accounted for a large proportion.The resistance rate of Gram-positive bacteria,such as Staphylococcus epidermidis and Staphylococcus aureus,to amikacin,gentamicin and penicillin,was more than 50%,which was sensitive to vancomycin. Gram negative bacteria such as Klebsiella pneumoniae and E.coli have high resistance to common antibiotics,and the drug resistance rate to cefepime and cefazolin is more than 50%,and sensitive to imipenem/cilastatin and imipenem/cilastatin.Among 11 fungi,4 cases were resistant to fluconazole , 36.36%,3 to itraconazole,27.27%,0 to ketoconazole and voriconazole,0.00%. Conclusion The distribution and drug resistance of pathogenic bacteria in patients with lung cancer infection in our hospital have certain characteristics,in which Gram-positive bacteria are mainly Staphylococcus epidermidis and Staphylococcus aureus,Gram-negative bacteria are mainly Klebsiella pneumoniae and Escherichia coli,and there are also a small number of fungal infections.Therefore,we should strengthen the monitoring of etiology and drug resistance,and strengthen the management of hospital disinfection Drug sensitivity results of patients,rational use of antibiotics,so as to improve the treatment effect and reduce the risk of infection.
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Objective To investigate the effects of surgical trauma on synaptic structure in hippocampal CA3 area in aged rats.Methods Fifty-six healthy SD rats aged 18 months were randomly divided into 3 groups: control group (group C, n = 8) , anesthesia group (group A, n = 24) , and operation group (group O, n - 24) . Anesthesia was performed with intraperitoneal ketamine 40 mg/kg but no operation was carried out in group A. Anesthesia was also performed with intraperitoneal ketamine 40 mg/kg, and splenectomy was performed after loss of righting reflex in group O. Eight animals from group A and O selected on 1, 3, and 7 d after anesthesia or operation respectively underwent Morris water maze test for assessment of the cognitive function. The animals were . then decapitated. Hippocampal CA3 area was isolated for examination with electron microscope and the synaptic structure in the polymorphic layer of hippocampal CA3 area was measured. Results Compared to group C and A, the times of passing through the original platform and number of synapses were significantly reduced, the width of synaptic cleft was significantly increased, the thickness of the postsynaptic density was significantly decreased, the length of the active zones was significantly shortened, and the curvature of the synaptic interface and percentage of perforated synapses were significantly decreased at T_(1,2), ( P < 0.05 or 0.01) , but no significant change was found in the indices mentioned above at T_3 in group O(P > 0.05). Compared to group C, the latency and swimming distance were significantly prolonged at T_1 in group A and at T_(1,2) in group O ( P < 0.01) . Compared to group A, the latency at T_(1,2) and the swimming distance at T_2 were significantly prolonged in group O ( P < 0.05) . Conclusion Surgical trauma can induce early postoperative cognitive impairment through changing synaptic structure in hippocampal CA3 area in aged rats.
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Objective To investigate the effect of NR2B antisense oligonucleotide on naloxone-induced withdrawal responses in morphine-dependent rats. Methods Famale SD rats weighing 230-270 g were anesthetized with intraperitoneal pentobarhital 60 mg/kg. Intrathecal (IT)catheter was placed at L3,4 interspace.Thirty-two rats in which FT catheter was successfully placed were randomly divided into 4 groups ( n = 8 each) : group C control; group MD morphine dependence; group AO NR2B antisense oligonucleotide (aNR2B) and group SO NR2B sense oligonucleotide (sNR2B) . In group MD, AO, SO chronic morphine dependence was induced by increasing doses of subcutaneous morphine for 6 days. The initial dose of morphine was 10 mg/kg twice a day and was increased by 10 mg/kg twice every other day and reached 50 mg/kg on the 6th day. In group AO and SO IT aNR2B or sNR2B 15 nmol was administered simultaneously with subcutaneous morphine. Morphine withdrawal responses was induced by IT naloxone 4 mg/kg and scored based on the responses (0 = normal; higher scores signify severer responses) . The weight loss was calculated.The expression of NR1, NR2A and NR2B mRNA in hippocampus was determined by RT-PCR. Results The morphine withdrawal syndrome and weight loss were significantly incresed in group MD, AO and SO, while NR2B mRNA expression in hippocampus was up-regulated in group MD and SO compared with group C. The morphine withdrawal syndrome and weight loss were significantly decreased, NR2A mRNA expression in hippocampus was up-regulated and NR2B mRNA expression was down-regulated in group AO compared with group MD. There was no significant difference in NR1 mRNA expression between the 4 groups . Conclusion NR2B antisense oligonucleotide can suppress morphine withdrawal responses through the regulation of NMDA receptor level and construction in hippocampus.
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Objective To investigate the role of nitric oxide(NO)in the spinal cord sensitization in a rat model of neuropathic pain.Methods Thirty-two male adult Wistar rats weighing 200-300 g were randomly divided into 4 groups with 8 animals in each group:group Ⅰ sham operation;group Ⅱ L-NAME pretreatment + sham operation;group Ⅲ CCI and group Ⅳ L-NAME pretreatment + CCI.Neuropathic pain was induced by chronic constrictive injury(CCI).The animals were anesthetized with intraperitoneal pentobarbital 40 mg/kg.The right sciatic nerve was exposed and 4 loose ligatures were placed on the sciatic nerve at 1 mm intervals with 3-0 silk thread.In group Ⅰ and Ⅱ the sciatic nerve was exposed but not ligated.In group Ⅲ and Ⅳ L-NAME 250 μg in normal saline 10 μl was injected into subarachnoid space over 30 seconds at 15 min before sham operation or CCI.The paw-withdrawal threshold to nociceptive thermal stimuli(PWTT)was measured before operation(baseline)and on the 3rd day after operation.Four rats in each group were killed on the 4th and 7th day after operation,and lumbar segment of the spinal cord(L4-5)was removed for determination of expression of pCREB in the dorsal horn of spinal cord by immuno-histochemical technique.Results The paw-withdrawal threshold to nociceptive thermal stimuli(PWTT)was significantly decreased on the 3rd day after operation as compared with the baseline before operation in all 4 groups.The PWTT on the 3rd day after operation was significantly higher in group Ⅰ,Ⅱ and Ⅳ than in CCI group(group Ⅲ),but there was no significant difference in the PWTT after operation among the 3 groups(Ⅰ,Ⅱ,Ⅳ).The expression of pCREB in the dorsal horn neurons of spinal cord was significantly upregulated in CCI group (Ⅲ) as compared with the other 3 groups.Conclusion Spinal cord NO induces hyperalgesia in neuropathic pain through release of pCREB in spinal cord dorsal horn.