ABSTRACT
Objective:To analyze the risk factors of carbapenem-resistant Klebsiella pneumoniae (CRKP) infection in intensive care unit (ICU) patients and to construct a prediction model for infection. Methods:The clinical data of 204 patients with Klebsiella pneumoniae infection admitted in ICU of Jining First Hospital during January 2020 to December 2022 were retrospectively analyzed. Patients admitted during January 2020 to December 2021 were selected as model set ( n=150), and patients admitted during January to December 2022 were selected as validation set ( n=54). In model set, there were 59 cases infected with CRKP (CRKP group) and 91 cases infected with carbapenem-sensitive Klebsiella pneumonia (CSKP group). The risk factor of CRKP infection in ICU patients were analyzed with multivariate Logistic regression, based on which an infection prediction model was constructed. The predictive value of the model was evaluated by ROC, and verified in the validation group. Results:Multivariate Logistic regression analysis showed that empirical use of beta-lactam antibiotics( OR=6.985, 95 % CI 1.658-29.423, P=0.008), central vein catheterization( OR=7.486, 95 % CI 2.776-20.186, P<0.001)and tracheal intubation/incision( OR=10.695, 95 % CI 2.701-42.351, P=0.001)were risk factors for CRKP infection in ICU patients. The regression equation for predicting the risk of infection was -4.851+ empirical use of beta-lactam antibiotics×1.944+ central vein catheterization×2.013+ tracheal intubation/incision×2.370. The area under the ROC curve (AUC) of the model for predicting infection in the model group was 0.905, with sensitivity and specificity of 79.7% and 90.1%, respectively. The AUC of the model for predicting infection in validation group was 0.881, with sensitivity and specificity of 84.2% and 85.7%, respectively. Conclusion:The constructed infection prediction model in the study can effectively predict CRKP infection in ICU patients.
ABSTRACT
Background Lead (Pb) exposure impairs cognitive functions of children. Whether Pb exposure in different developmental stages induces long-term cognitive impairment, and whether chelation therapy could mitigate the cognitive impairment is rarely reported. Objective This experiment is designed to investigate effects of Pb exposure and chelation therapy during different developmental stages (breastfeeding, weaning, and early puberty periods) on mouse short-term and long-term cognitive functions. Methods C57BL/6 male mice in breastfeeding period, weaning period, and early puberty period (postnatal day 2, 21, and 41; PND 2, PND 21, and PND 41, n=30, respectively) were randomly divided into control, Pb exposure, and Pb+dimercaptosuccinic acid (DMSA) treatment groups (n=10 in each group). The control groups received standard food and deionized water. The Pb exposure mice received standard food and free drinking water containing Pb acetate (0.1% for dams, and 0.05% for pups). After receiving Pb acetate for 19 d, the Pb+DMSA treatment groups were given 1 mmol·kg−1·d−1 DMSA for 6 d with gastric infusion. Whole blood Pb levels were measured after DMSA treatment on experimental day 25. The effects on short-term cognitive function were tested in the Morris Water Maze task by the analyses of escape latency on PND 75−79, as well as target quadrant time and times of platform-crossing on PND 80. Hippocampal long-term potentiation of field excitatory postsynaptic potential (fEPSP) of mice on PND 365 was induced to demonstrate the effects on long-term cognitive function. Results The blood Pb levels among the Pb, Pb+DMSA, and control groups were statistically different for each developmental stage (Fbreastfeeding period=43.47, Fweaning period=228.6, Fearly period of puberty=274.2, all P<0.001). Compared to the counterpart control groups, blood Pb levels of the pb exposure groups (386.4, 265.0, and 178.1 μg·L−1 in breastfeeding period, weaning period, and early puberty period, respectively) were significantly higher for all stages. After the chelation therapy, the blood Pb significantly decreased for all stages (28.68, 47.29, and 20.93 μg·L−1 in the three periods, respectively, all P<0.001) and the Pb levels of the mice exposed in the breastfeeding period decreased most (by 92.58%, 82.15%, and 88.25% in the three periods, respectively, P<0.01). In the water maze task, the mice exposed to Pb in the breastfeeding period had a gentler decrease in escape latency (from 54.20 s on day 1 to 30.54 s on day 5, by 43.65 % decrease) than the control group (from 32.44 s on day 1 to 15.20 s on day 5, by 53.14 % decrease) (P<0.01) and a significant decrease in target quadrant time (P<0.05). After the chelation therapy, the escape latency of the DMSA-treated mice in the breastfeeding period (from 40.94 s on day 1 to 20.87 s on day 5, by 48.99 % decrease) was steeper than that of the Pb-exposed mice (P<0.05). The differences in the escape latency, target quadrant time, and times of platform-crossing were not significant between the Pb-exposed mice and the control mice in the weaning period and early period of puberty (all P>0.05). After the chelation therapy, such differences were also not significant compared with before therapy. Due to the small sample size, data were merged for different developmental stages in the long-term potentiation test. The amplitudes of fEPSP induced in the control, Pb-exposed, and DMSA treatment groups were significantly different (Fgroups=212.2, Ftime=11.36. P<0.001). The average fEPSP amplitude induced in the last 10 min recorded in the hippocampal slices in the Pb exposure group was significantly lower than that in the control group (P<0.05). After the DMSA treatment, no significant differences were observed in the fEPSP amplitudes between the Pb exposure group and the DMSA treatment group (P>0.05). When observing the fEPSP data by developmental stages, the fEPSP amplitude in the breastfeeding Pb-exposure group was 27.2% lower than that of the breastfeeding control group, while such changes were not obvious in the weaning period or in the early period of puberty. The fEPSP amplitude in breastfeeding DMSA treatment group was 44.3% higher than that of the breastfeeding Pb exposure group, while such changes were not observed in the weaning period or in early period of puberty. Conclusion Pb exposure during different developmental stages, especially in breastfeeding period, could affect short-term and long-term cognitive functions of mice. The harmful effects may be partially reversed by DMSA chelation therapy, especially being treated in breastfeeding period.
ABSTRACT
Objective@#Predefining the most effective treatment for patients with depressive disorders remains a problem. We will examine the differential brain regions of gray matter (GM) in major depressive disorder (MDD) patients and the relationship between changes in their volume and the efficacy of early antidepressant treatment using magnetic resonance imaging (MRI). @*Methods@#159 never-medicated patients with first-episode MDD and 53 normal control subjects (NCs) were enrolled. The brains were scanned by MRI and measured with the 17-item Hamilton Depression Rating Scale (HAMD-17) at baseline and after 2 weeks of treatment with selective serotonin reuptake inhibitor (SSRI)s, and the non-responder group and responder group were obtained. The patients were analyzed by voxel-based morphological (VBM) and SPSS software. Receiver operator characteristics (ROC) analysis was performed for the difference between the responder group and the non-responder group in the differential brain regions, and Pearson correlations were computed between volume size and HAMD score reduction rate. @*Results@#Smaller GM volume of the right superior temporal gyrus (STG), and the orbital parts of the right medial frontal gyrus and right inferior frontal gyrus were observed in MDD versus the NCs. The non-responder group demonstrated a significant volume reduction at the right STG compared with the responders, but no corresponding change in orbital part of right medial frontal gyrus and right inferior frontal gyrus. ROC analysis showed that Accuracy=71.2%. There was a positive correlation between the STG gray matter volume and the HAMD-17 score reduction rate (r=0.347, p=0.002). @*Conclusion@#The study results confirmed the local changes in brain structure in MDD and may initially predict the early treatment response produced by SSRIs as antidepressants.
ABSTRACT
Objective To explore the characteristics of cognitive impairment and its influence factors in first-epi?sode depression patients with sleep disorder. Methods Three hundred and eighteen patients with first-episode depres?sion and two hundreds and forty-three healthy controls were recruited. The patients were divided into two group accord?ing to the sleeping situation: 202 patients with sleep disorder and 116 patients without. The Repeatable Battery for the Assessment of Neuropsychological Status (RBANS) was used to evaluated the cognitive function of all subjects, including immediate memory, visual span, speech function, attention and delayed memory. The 17 item Hamilton Depression Scale (HAMD-17) was used to evaluate patients’symptoms. Results The scores of immediate memory, visual span, speech function, delayed memory and the whole scale in the depression patients with sleep disorder were significantly lower than the patients without sleep disorder and the controls (P<0.05). Compared with the controls, the patients without sleep disor?der had lower scores of immediate memory, language function, delayed memory and the whole scale (P<0.05). Multiple linear regression showed that in the depression patients with sleep disorder, the RBANS score was related with the cogni?tive factors in HAMD (β=6.29, P=0.04);immediate memory was related with age (β=-0.24, P=0.04);visual span was re?lated with sleeping factor in HAMD (β=2.33, P=0.01);speech function was related with marriage (β=-5.74, P=0.01) and sleeping factor in HAMD (β=-1.20, P=0.03). In the depression patients with sleep disorder, speech function of RBANS was related with age (β=-0.32, P=0.04);attention was related with retardation factor in HAMD (β=2.52, P=0.01). Con?clusion The first-episode depression patients with sleep disorders have cognitive function damage in many aspects. The depressive symptoms (sleep changes, cognitive disorders, retardation and so on), age and marital status may be the influ?encing factors on cognitive impairment in first-episode depression patients with sleep disorder.
ABSTRACT
Objective To observe the effects of Hedan tablet on cytokines and oxidation factors in APOE-/-mouse, and to explore its effect on atherosclerosis and to explore its behind mechanism. Methods APOE-/-mice (n=50) were randomly divided into control group, model group, low dose Hedan tablet treatment group, high dose Hedan tablet treatment group and simvastatin treatment group. Mice in control group were given normal feed while mice in other groups were fed with high cho?lesterol diet. Hedan or Simvastatin was administrated intra-gastrically while normal saline was given to model group in the same route. After 12 weeks, mice were sacrificed to observe the mRNA level of tumor necrosis factor-α(TNF-αmRNA) in aorta by RT-PCR. Mean while, serum levels of interleukin-1 (IL-1), interleukin-10 (IL-10), malonaldehyde (MDA) and su?peroxide dismutase (SOD) were determined in different groups. Results Compared with control group, TNF-αmRNA tran?scription level as well as serum levels of IL-1 and MDA significantly increase while serum levels of IL-10 and SOD de?creased remarkably in model group, (P<0.01). Compared with model group, mRNA levels of TNF-αas well as serum levels of IL-1 and MDA were significantly decreased while serum levels of IL-10, SOD were greatly increased in low dose and high dose Hedan tablet treatment groups as well as in simvastatin treatment group (P<0.01). Conclusion Hedan tablet inhibit the formation of atherosclerosis through its anti-oxidation role and anti-inflammation role.