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This report presents a case of a male infant, aged 32 days, who was admitted to the hospital due to 2 days of bloody stools and 1 day of fever. Upon admission, venous blood samples were collected, which appeared pink. Blood biochemistry tests revealed elevated levels of triglycerides and total cholesterol. The familial whole genome sequencing revealed a compound heterozygous variation in the LPL gene, with one variation inherited from the father and the other from the mother. The patient was diagnosed with lipoprotein lipase deficiency-related hyperlipoproteinemia. Acute symptoms including bloody stools, fever, and bloody ascites led to the consideration of acute pancreatitis, and the treatment involved fasting, plasma exchange, and whole blood exchange. Following the definitive diagnosis based on the genetic results, the patient was given a low-fat diet and received treatment with fat-soluble vitamins and trace elements, as well as adjustments to the feeding plan. After a 4-week hospitalization, the patient's condition improved and he was discharged. Follow-up showed a decrease in triglycerides and total cholesterol levels. At the age of 1 year, the patient's growth and psychomotor development were normal. This article emphasizes the multidisciplinary diagnosis and treatment of familial hyperlipoproteinemia presenting with symptoms suggestive of acute pancreatitis, including bloody ascites, in the neonatal period.
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Humains , Nourrisson , Mâle , Maladie aigüe , Ascites , Cholestérol , Hyperlipoprotéinémie de type I/génétique , Hyperlipoprotéinémies , Lipoprotein lipase/génétique , Pancréatite , TriglycérideRésumé
Objective To understand the epidemiological characteristics of syphilis in Songjiang District of Shanghai from 2007 to 2017, and provide evidence for further improvement in the prevention and control measures. Methods Descriptive analysis was performed on the syphilis case data in Songjiang District from 2007 to 2017. Results In 2007-2017, a total of 8 546 cases of syphilis were reported in Songjiang District, with an average annual incidence of 48.23/100 000.The overall incidence showed a U-shaped upward trend, with the highest incidence in 2016 (68.17/100 000);the average annual incidence decreased by 6.13/100 000 from 2007 to 2010, whereas increased by 5.64/100 000 from 2011 to 2017.Syphilis was characterized as follows:1) The epidemic was dominated by the cases with local household registration, latent syphilis (51.84%), reported in June-September, aged 20-59 years (81.24%).The cases in the age group over 60 years showed a significant upward trend.2) In the local syphilis cases, there were more men than women, and the sex ratio was 1.3 : 1 (especially the sex ratio in the stage 1 and stage 2 syphilis was 1.73 : 1).In the foreign cases from other provinces, there were less men than women, and the sex ratio was 0.6 : 1. 3) In the primary syphilis cases, there were more men (35.50%) than women (20.98%), while more female cases in the latent syphilis and secondary syphilis cases.Local primary and secondary cases were mainly in the age group of 30 to 59 years (59.06%).The cases from other provinces were mainly 20 to 49 years old (85.24%). Conclusion The incidence of syphilis in Songjiang District is increasing.As primary syphilis are more likely to be male and young adults, we should strength the surveillance, establish standardized diagnosis and treatment of syphilis, advocate sexually transmitted diseases prevention and treatment and safe sexual behavior, and also promote active screening in women and the elderly for further control of syphilis.
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AIM:To investigate the effect of microRNA(miR)-381-3p on neuronal injury in the hippocampus of depressive rats and the possible regulatory mechanism.METHODS:The rat model of depression was established by sub-cutaneous injection of corticosterone and the model rats received fluoxetine treatment.The body weight,open field test and biochemical indexes were measured for judging the therapeutic effect of fluoxetine.The expression of miR-381-3p,brain-derived neurotrophic factor(BNDF),Bcl-2 and Bax in the hippocampus was determined.The cultured neonatal rat hipp-ocampal neurons were pre-transfected with miR-381-3p inhibitor and then incubated with corticosterone.The cell viability, and the expression of miR-381-3p, BNDF, Bcl-2 and Bax were detected.The targeted regulatory role of miR-381-3p in BDNF was verified by luciferase reporter assay.RESULTS:Compared with depression group,fluoxetine increased the body weight,the number of cross-field activities and the content of norepinephrine,inhibited the expression of miR-381-3p and promoted the expression of BNDF in the hippocampus.miR-381-3p silencing reversed the effect of corticosterone,resulting in the increase in the survival rate of hippocampal neurons, upregulation of BDNF and Bcl-2, and downregulation of Bax expression.miR-381-3p targeted the regulation of BNDF expression.CONCLUSION: Silencing miR-381-3p protects rat hippocampal neurons from corticosterone injury,and its mechanism may be related to the upregulation of BNDF expression.
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This study aimed to establish a new propofol target-controlled infusion (TCI) model in animals so as to study the general anesthetic mechanism at multi-levels in vivo. Twenty Japanese white rabbits were enrolled and propofol (10 mg/kg) was administrated intravenously. Artery blood samples were collected at various time points after injection, and plasma concentrations of propofol were measured. Pharmacokinetic modeling was performed using WinNonlin software. Propofol TCI within the acquired parameters integrated was conducted to achieve different anesthetic depths in rabbits, monitored by narcotrend. The pharmacodynamics was analyzed using a sigmoidal inhibitory maximal effect model for narcotrend index (NI) versus effect-site concentration. The results showed the pharmacokinetics of propofol in Japanese white rabbits was best described by a two-compartment model. The target plasma concentrations of propofol required at light anesthetic depth was 9.77±0.23 μg/mL, while 12.52±0.69 μg/mL at deep anesthetic depth. NI was 76.17±4.25 at light anesthetic depth, while 27.41±5.77 at deep anesthetic depth. The effect-site elimination rate constant (ke0) was 0.263/min, and the propofol dose required to achieve a 50% decrease in the NI value from baseline was 11.19 μg/mL (95% CI, 10.25-13.67). Our results established a new propofol TCI animal model and proved the model controlled the anesthetic depth accurately and stably in rabbits. The study provides a powerful method for exploring general anesthetic mechanisms at different anesthetic depths in vivo.
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Animaux , Lapins , Anesthésiques intraveineux , Sang , Pharmacocinétique , Surveillance des médicaments , Perfusions veineuses , Modèles statistiques , Propofol , Sang , Pharmacocinétique , LogicielRésumé
<p><b>OBJECTIVE</b>To investigate the correlation of patients with thrombosis or prothrombotic status with hyperhomocysteinemia (HHcy), activated protein C-resistance(APCR) and gene polymorphism of coagulation factor V.</p><p><b>METHODS</b>Three hundred healthy voluteers were selected as controls, 223 cases of thrombosis (80 cases of cerebral infarction of CT, the MI of 82 cases of myocardial infarction, venous thrombosis of VTE 61 cases), 270 cases of patients with prothrombotic state (76 cases of pregnancy disease of PIH, 62 cases of chronic obstructive pulmonary disease (COPD), 60 cases of diabetes(DM) and 72 cases of cancer) were enrolled in this study. The plasma APCR and hyperhomocysteinemia were detected by APTT coagulation method and cycling enzyme method respectively, and restriction fragment length polymorphism(RFLP) were was used to detect the gene polymorphism of FV G1691-A, G1091-C and A1090-G in the patient and control groups.</p><p><b>RESULTS</b>APCR positive rate was 62.29% and 7.33%, and the positive hyperhomocysteinemia accounted for 68.42% and 10.00% respectively in the group of the patients with venous thrombosis and the normal control group. 3 cases of heterozygous FV gene mutations were found in the APCR-positive patients with venous thrombosis.</p><p><b>CONCLUSION</b>HHcy possitive rate of patients with venous thrombosis is signiticantly higher than that in control, the HHcy is one of the important causes resulting in thrombosis, the patients with venous thrombosis have proved to be with APCR, and the possitive APCR may be related with the coagulation factor V gene polymorphism.</p>
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This study aims to elucidate the mechanisms by which dexmedetomidine alleviates pulmonary edema in rats with acute lung injury induced by lipopolysaccharide (LPS). Male Wistar rats were randomly divided into five groups: normal saline control (NS) group, receiving intravenous 0.9% normal saline (5 mL/kg); LPS group, receiving intravenous LPS (10 mg/kg); small-dose dexmedetomidine (S) group, treated with a small dose of dexmedetomidine (0.5 μg · kg(-1) · h(-1)); medium-dose dexmedetomidine (M) group, treated with a medium dose of dexmedetomidine (2.5 μg · kg(-1) · h(-1)); high-dose dexmedetomidine (H) group, treated with a high dose of dexmedetomidine (5 μg · kg(-1) · h(-1)). The rats were sacrificed 6 h after intravenous injection of LPS or NS, and the lungs were removed for evaluating histological characteristics and determining the lung wet/dry weight ratio (W/D). The levels of tumor necrosis factor-alpha (TNF-α) and interleukin-1β (IL-1β) in the lung tissues were assessed by enzyme- linked immunosorbent assay (ELISA). The mRNA and protein expression levels of aquaporin-1 (AQP1) and aquaporin-5 (AQP5) were detected by RT-PCR, immunohistochemistry, and Western blotting. The lung tissues from the LPS groups were significantly damaged, which were less pronounced in the H group but not in the small-dose dexmedetomidine group or medium-dose dexmedetomidine group. The W/D and the concentrations of TNF-α and IL-1β in the pulmonary tissues were increased in the LPS group as compared with those in NS group, which were reduced in the H group but not in S group or M group (P<0.01). The expression of AQP1 and AQP5 was lower in the LPS group than in the NS group, and significantly increased in the H group but not in the S group or M group (P<0.01). Our findings suggest that dexmedetomidine may alleviate pulmonary edema by increasing the expression of AQP-1 and AQP-5.
Sujets)
Animaux , Mâle , Rats , Lésion pulmonaire aigüe , Traitement médicamenteux , Génétique , Anatomopathologie , Agonistes des récepteurs alpha-2 adrénergiques , Pharmacologie , Aquaporine-1 , Génétique , Allergie et immunologie , Aquaporine-5 , Génétique , Allergie et immunologie , Dexmédétomidine , Pharmacologie , Relation dose-effet des médicaments , Calendrier d'administration des médicaments , Régulation de l'expression des gènes , Injections veineuses , Interleukine-1 bêta , Génétique , Allergie et immunologie , Lipopolysaccharides , Poumon , Allergie et immunologie , Anatomopathologie , Taille d'organe , Oedème pulmonaire , Traitement médicamenteux , Génétique , Anatomopathologie , Rat Wistar , Transduction du signal , Transcription génétique , Facteur de nécrose tumorale alpha , Génétique , Allergie et immunologieRésumé
<p><b>AIM</b>To study the effect of acute fear stress on emotional behaviors, Hormone levels, and the expression and activation of cerebra Erk1/2 of rats in vivo.</p><p><b>METHODS</b>Fourty eight male SD rats were divided randomly into control group and stress group. Rats of stress group received 30 min' s acute stress including foot shock and white noise, and then the emotional behaviors were observed. The hormone level in plasm and brain was determined by spectrophotofluorometry and radioimmunoassay kit. In the following experiments, Western blot was performed to determine the expression and phosphorylation of extracellular signal-regulated protein kinase (Erk) of four different regions of the brain.</p><p><b>RESULTS</b>Rats tested after acute fear stress displayed substantial decreases in open-field activity, increases in resistance to capture, and increases in fright reaction (P < 0.01). The stress also resulted in significantly higher plasmic and cerebral noradrenaline, corticosteroid, 5-hydroxytryptamine levels, and lower adrenomedulin level in comparison with the control (P < 0.01) after stress. At the time point of 0 min and 30 min after stress, the phosphorylation of Erk1/2 were increased in all four brain regions examined (hippocampus, striatum, prefrontal cortex and cerebellum).</p><p><b>CONCLUSION</b>Acute fear stress can induce abnormalities of emotional behaviors, such as behavioral habits, anxiety and defense, startle and delayed adaptation to startle, as well as the alteration of hormone levels. The phosphorylation of Erk1/2 may play a role in the abnormality of emotional behaviors of rats induced by acute fear stress.</p>