RESUMO
Objective:To explore the serum levels of copper and zinc and the application value of the ratio in assessing disease activity in patients with inflammatory bowel disease (IBD).Methods:From March 2019 to April 2020, 200 patients with IBD hospitalized at the Department of Gastroenterology of the First Affiliated Hospital of Anhui Medical University were selected by prospective random direct sampling method, including 100 patients with Crohn′s disease (CD) and 100 patients with ulcerative colitis (UC). The Crohn′s disease activity index (CDAI) and the modified Mayo score were used to evaluate the disease activity of CD patients and UC patients. In the same period 100 healthy individuals in the routine physical examination were selected as healthy control group. The serum levels of copper and zinc of the healthy control group, the CD group and the UC group were determined by atomic absorption spectrometry. The levels and the ratio of serum copper to zinc of three groups were compared. The ratio of serum copper to zinc of CD patients and UC patients with different disease activity were compared. The correlation between the ratio of serum copper to zinc and IBD activity indexes were analyzed, which included fecal calprotectin (FC), C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), CDAI and Mayo score. Receiver operating characteristic curve was drawn to analyze the value of the ratio of serum copper to zinc, CRP and ESR in predicting disease activity of patients with IBD. Independent sample t test, least significant difference- t test and Pearson correlation analysis were performed for statistical analysis. Results:The serum copper levels and the ratio of serum copper to zinc of the CD group and the UC group were both higher than that of the healthy control group, however the serum zinc levels were lower than that of the healthy control group ( (32.27±7.69) and (29.80±9.68) mol/L vs. (20.16±6.67) mol/L; 2.81±1.57 and 2.29±1.09 vs. 0.68±0.36; (14.64±7.11) and (15.65±8.17) mol/L vs. (34.29±16.40) mol/L), and the differences were statistically significant ( t=2.81, 5.87, 1.47, 7.21, 1.73 and 2.56, all P<0.05). Among CD patients, the the ratio of serum copper to zinc of patients at remission stage (29 cases), mild activity stage (23 cases), moderate activity stage (30 cases) and severe activity stage (18 cases) was 2.61±1.43, 2.75±1.35, 3.15±2.37 and 4.17±1.77, respectively, and the ratios of serum copper to zinc of patients at mild activity stage, moderate activity stage and severe activity stage were all higher than that of patients at the remission stage, and the differences were statistically significant ( t=3.41, 7.92 and 5.84, all P<0.05). There were statistically significant differences in the ratios of serum copper to zinc between patients at mild activity stage and moderate activity stage, severe activity stage, and between patients at moderate activity stage and severe activity stage ( t=5.82, 6.23 and 3.45, all P<0.05). Among UC patients, the ratio of serum copper to zinc of patients at remission stage (10 cases), mild activity stage (30 cases), moderate activity stage (45 cases) and severe activity stage (15 cases) was 1.52±0.44, 1.74±0.58, 2.38±0.83 and 3.80±1.19, respectively, the ratio of serum copper to zinc of patients at moderate activity stage was higher than that of patients at remission stage and mild activity stage, and the ratio of serum copper to zinc of patients at severe activity stage was higher than those of patients at remission stage, mild activity stage and moderate activity stage, and the differences were statistically significant ( t=7.92, 5.83, 3.21, 9.54 and 2.83, all P<0.05). There was no statistically significant difference in serum copper to zinc ratio between patients at remission and at mild activity stage ( P>0.05). The ratio of serum copper to zinc of CD patients was positively correlated with FC and CRP ( r=0.697 and 0.586, P=0.014 and 0.001), however was not correlated with ESR or CDAI score (both P>0.05). The ratio of serum copper to zinc of UC patients was positively correlated with FC, ESR and Mayo score ( r=0.488, 0.452 and 0.331, P=0.001, P<0.01 and P=0.041), however was not correlated with CRP ( P>0.05). The cut-off value of the ratio of serum copper to zinc, CRP and ESR for the diagnosis of CD activity was 1.76, 8 mg/L and 20 mm/1 h, respectively. Among them, ESR was the most effective in the diagnosis of CD activity with an area under the curve (AUC) value of 0.830, and to the sensitivity and specificity was 69.0% and 86.2%, respectively. The cut-off value of the ratio of serum copper to zinc, CRP and ESR for the diagnosis of UC activity was 1.63, 8 mg/L and 20 mm/1 h, respectively; among which the the ratio of serum copper to zinc had the highest efficacy in the diagnosis of UC activity, with an AUC value of 0.862, sensitivity and specificity of 73.0% and 90.9%, respectively. Conclusion:The the ratio of serum copper to zinc is correlated with the disease activity of IBD, which may become a new auxiliary indicator for the evaluation of disease activity.
RESUMO
Objective:To evaluate the deformity changes in the treatment of congenital clubfoot in infants by ultrasound, and to explore its clinical application value.Methods:Seventeen infants with congenital clubfoot treated in the Department of Pediatric Orthopaedics of the Third Affiliated Hospital of Zhengzhou University from March 2020 to June 2021 and 27 normal infants in the same period were selected. The distance between medial malleolus and scaphoids (MM-N distance) of all feet was measured by ultrasound. The distance from the tangent line of the lateral edge of calcaneus to the midpoint of the lateral edge of the chondroid bone (C-C distance), medial soft tissue thickness and tibial calcaneal angle were measured by ultrasound. The data before, after treatment and during follow-up were statistically analyzed.Results:A total of 88 feet of 44 infants were evaluated. The mean number of cast was 4.7±1.1, the follow-up time was (96.9±59.3)days. The MM-N distance, C-C distance and posterior tibial calcaneal angle in the clubfoot group were improved after treatment and at the last follow-up, and the differences were statistically significant (all P<0.01). During the treatment, 1 case had false correction, and 2 cases recurred in the last follow-up. Conclusions:Ultrasound can clearly display the medial, dorsal, lateral and posterior articular structures of normal and clubfoot, and can observe the deformity changes of clubfoot during the correction process, which can provide guidance for the clinical treatment of clubfoot.
RESUMO
Objective To evaluate the effect of sevoflurane on activation of nuclear factor kappa B (NF-κB) during brain injury induced by hemorrhagic shock (HS) in pigs.Methods Thirty-two adult male Bama miniature pigs,aged 6 months,weighing 22-25 kg,were divided into 4 groups (n=8 each) using a random number table:sham operation group (group Sham),HS group,sevoflurane preconditioning group (group Sev-Pre) and sevoflurane postconditioning group (group Sev-Post).The animals were anesthetized,and tracheostomized and mechanically ventilated.In group Sham,the bilateral femoral arteries and internal jugular veins were only cannulated.HS was induced by removing 40％ of blood volume within 15 min (30 ml/kg) via the right femoral artery and maintaining at this level for 1 h before resuscitation in HS,Sev-Pre and Sev-Post groups.In group Sev-Pre,2％ sevoflurane was inhaled for 30 min,and then HS was induced.In group Sev-Post,2％ sevoflurane was inhaled for 30 min starting from the time point immediately after HS was induced.Immediately before establishment of the model and at 30,60,90,120,180 and 240 min of HS (T1-6),blood samples from the jugular vein were collected for determination of serum interleukin-1beta (IL-1β) and tumor necrosis factor-alpha (TNF-α) concentrations by enzymelinked immunosorbent assay.At 4 h of HS,the rats were sacrificed,and brains were removed for microscopic examination of hippocampal CA1 region (using haematoxylin and eosin staining) and for determination of the expression of NF-κB in nucleoprotein (by Western blot).Results Compared with group Sham,the concentrations of serum IL-1β and TNF-α were significantly increased at T2-6,and the expression of NF-κB in nucleoprotein in hippocampal CA1 region was up-regulated in HS,Sev-Pre and Sev-Post groups (P＜0.05).Compared with group HS,the concentrations of serum IL-1β and TNF-α were significantly decreased at T3-6,and the expression of NF-κB in nucleoprotein in hippocampal CA1 region was down-regulated in Sev-Pre and Sev-Post groups (P＜0.05).There were no significant differences between group SevPre and group Sev-Post in concentrations of serum IL-1β and TNF-α and expression of NF-κB in nucleoprotein in hippocampal CA1 region (P＞0.05).The pathologic changes were significantly attenuated in SevPre and Sev-Post groups as compared with group HS.Conclusion The mechanism by which sevoflurane attenuates brain injury induced by HS may be related to inhibition of NF-κB activation and reduction of inflammatory responses in pigs.
RESUMO
Objective To evaluate the effect of monosialoganglioside (GM-1) on hippocampal protein kinase B (Akt) /glycogen synthase kinase 3β (GSK-3β) signaling pathway in the rats undergoing cardiopulmonary bypass (CPB).Methods Eighteen healthy male Sprague-Dawley rats, aged 6 months, weighing 400-500 g, were randomly divided into 3 groups (n =6 each) using a random number table:control group (group C), CPB group and GM-1 group.GM-1 20 mg/kg was added to the priming solution in group GM-1, while the equal volume of normal saline was given in group CPB.At 3 h after termination of CPB, blood samples were taken from the jugular vein for determination of plasma neuron-specific enolase (NSE) and S-100β protein concentrations using enzyme-linked immunosorbent assay.After blood sampling, the rats were sacrificed, and the hippocampi were isolated for microscopic examination of the ultrastructure of the hippocampal neurons (with electron microscope), and for detection of neuronal apoptosis (with light microscope) and phosphorylation of Akt and GSK-3β (by Western blot).Results Compared with group C, the concentrations of plasma NSE and S-100β protein, and the number of apoptotic neurons were significantly increased in CPB and GM-1 groups, the phosphorylation of Akt and GSK-3β was decreased in group CPB, and the phosphorylation of Akt and GSK-3β was increased in group GM-1 (P＜0.05).Compared with group CPB, the concentrations of plasma NSE and S-100β protein, and the number of apoptotic neurons were significantly decreased, the phosphorylation of Akt and GSK-3β was increased (P＜0.05), and the pathological changes were reduced in group GM-1.Conclusion GM-1 can reduce apoptosis in hippocampal neurons through activating Akt/GSK-3β signaling pathway, thus mitigating CPB-induced brain injury in rats.
RESUMO
Objective To evaluate the effect of sevoflurane on brain injury in pigs with hemorrhagic shock (HS).Methods Twenty-four adult male Bama miniature pigs, aged 6 months, weighing 22-25 kg, were equally and randomly divided into 3 groups using a random number table: sham operation group (group Sham) , group HS, and sevoflurane group (S group).In group Sham, the bilateral femoral arteries and internal jugular vein were only punctured.The animals were anesthetized with iv propofol 3.0 mg/kg, tracheostomized and mechanically ventilated.The right femoral artery was cannulated for blood-letting.HS was induced by blood-letting (40％ blood volume within 15 min), and it was then maintained for 1 h after the end of blood-letting to induce brain injury.In group S, 2％ sevoflurane was inhaled for 30 min after successful establishment of the model.Immediately before establishment of the model (T0) , and at 30, 60,90, 120, 180 and 240 min after HS (T1-6) , blood samples were collected from the internal jugular vein for determination of interleukin-1beta (IL-1β) and tumor necrosis factor-alpha (TNF-α) concentrations in serum (by enzyme-linked immunosorbent assay), and neuron-specific enolase (NSE) and S-100β protein concentrations in serum (using double antibody sandwich method).Results Compared with group Sham, the serum IL-1β, TNF-α, NSE and S-100β protein concentrations were significantly increased at T2-6 in HS and S groups (P＜0.05).Compared with group HS, the serum IL-1β, TNF-α, NSE and S-100β protein concentrations were significantly decreased at T3-6 in group S (P＜ 0.05).Conclusion Sevoflurane can mitigate brain injury in pigs with HS, and the mechanism is associated with inhibition of inflammatory responses.
RESUMO
At present,stroke has become one of the diseases seriously harming the human life and the quality of life with its high morbidity,disability,and mortality.Therefore,clinicians need to find more effective indicators to identify the clinical conditions and outcomes,and guide the treatment.Studies in recent years have suggested that the biological markers have important clinical value for guiding the treatment of stroke.
RESUMO
Objective To investigate the effect of monosialoganglioside GM1 on cardiopulmonary bypass (CPB)-induced inflammatory response in rats.Methods Twenty-four adult male Sprague-Dawley rats,weighing 350-450 g,were randomly divided into 3 groups (n =8 each):sham operation group (group S),group CPB and CPB + GMi group (group G).GM1 20 mg/kg was added to the priming solution in group G.While the equal volume of normal saline was given in group CPB.Blood samples were collected from the jugular vein at 3 h after termination of CPB for determination of plasma concentrations of neuron-specific enolase (NSE) and S-100β protein (by ELISA) and tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) (by radioimmunoassay).The hippocampi were isolated to detect the expression of hippocampal matrix metalloproteinase-9 (MMP-9) and IL-10 and NF-κB activity in hippocampal tissues by Western blot.Results Compared with group S,the plasma concentrations of NSE,S-100β protein,TNF-α and IL-6 and NF-κB activity were significantly increased,the expression of MMP-9 was up-regulated,and the expression of IL-10 was down-regulated in groups CPB and G (P ＜ 0.05).Compared with group CPB,the plasma concentrations of NSE,S-100β protein,TNF-α and IL-6 and NF-κB activity were significantly decreased,the expression of MMP-9 was down-regulated,and the expression of IL-10 was upregulated in group G (P ＜ 0.05).Conclusion The mechanism by which GM1 reduces the CPB-induced brain damage may be related to reduction of the central and systemic inflammatory response in rats.
RESUMO
Objective To investigate the effect of monosialoganglioside GM-1 on cardiopulmonary bypass (CPB)-induced brain injury in rats.Methods Twenty-seven adult male Sprague-Dawley rats,weighing 350-450 g,aged 15 months,were randomly divided into 3 groups (n=9 each): control group (C group),CPB group and GM-1 group.The animals were anesthetized with chloral hydrate,tracheostomized and mechanically ventilated.Right common carotid and right jugular vein were cannulated for closed-chest CPB.In groups CPB and GM-1,the rats underwent 1 h CPB.GM-1 20 mg/kg was added to the priming solution in group GM-1,while the equal volume of normal saline was given in group CPB.The animals were sacrificed at 3 h after termination of CPB or 3 h after the end of ventilation in group C,the brains were removed and the hippocampi isolated for microscopic examination and for determination of apoptosis (using TUNEL) and Bax and Bcl-2 protein expression (by immunohistochemistry and Western blot).Results Compared with group C,the number of apoptotic neurons and ratio of Bax/Bcl-2 were significantly increased,and the expression of Bcl-2 and Bax protein was up-regulated in groups CPB and GM-1 (P ＜ 0.05).Compared with group CPB,the number of apoptotic neurons and ratio of Bax/Bcl-2 were significantly decreased,the expression of Bax protein was down-regulated and the expression of Bcl-2 protein was up-regulated in group GM-1.The pathological changes were severe in group CPB and attenuated in group GM-1.Conclusion GM-1 can attenuate CPB-induced brain injury in rats and inhibition of the apoptosis in neurons may be involved in the mechanism.