BACKGROUND While most complications of cervical surgery are reversible,some,such as symptomatic postoperative spinal epidural hematoma(SEH),which generally occurs within 24 h,are associated with increased morbidity an...BACKGROUND While most complications of cervical surgery are reversible,some,such as symptomatic postoperative spinal epidural hematoma(SEH),which generally occurs within 24 h,are associated with increased morbidity and mortality.Delayed neurological dysfunction is diagnosed in cases when symptoms present>3 d postoperatively.Owing to its rarity,the risk factors for delayed neurological dysfunction are unclear.Consequently,this condition can result in irreversible neurological deficits and serious consequences.In this paper,we present a case of postoperative SEH that developed three days after hematoma evacuation.CASE SUMMARY A 68-year-old man with an American Spinal Injury Association(ASIA)grade C injury was admitted to our hospital with neck pain and tetraplegia following a fall.The C3-C7 posterior laminectomy and the lateral mass screw fixation surgery were performed on the tenth day.Postoperatively,the patient showed no changes in muscle strength or ASIA grade.The patient experienced neck pain and subcutaneous swelling on the third day postoperatively,his muscle strength decreased,and his ASIA score was grade A.Magnetic resonance imaging showed hypointense signals on T1 weighted image(T1WI)and T2WI located behind the epidural space,with spinal cord compression.Emergency surgical intervention for the hematoma was performed 12 h after onset.Although hypoproteinemia and pleural effusion did not improve in the perioperative period,the patient recovered to ASIA grade C on day 30 after surgery,and was transferred to a functional rehabilitation exercise unit.CONCLUSION This case shows that amelioration of low blood albumin and pleural effusion is an important aspect of the perioperative management of cervical surgery.Surgery to relieve the pressure on the spinal cord should be performed as soon as possible to decrease neurological disabilities.展开更多
Objective： To investigate whether human dendritic cells （DC） derived from peripheral blood mononuclear cells （PBMC）, which were pulsed by heat shock protein 70 （HSP70） isolated from human bladder tumor cell lin...Objective： To investigate whether human dendritic cells （DC） derived from peripheral blood mononuclear cells （PBMC）, which were pulsed by heat shock protein 70 （HSP70） isolated from human bladder tumor cell lines of E J, were able to induce peptide specific cytotoxic T-lymphocytes （CTL） response in vitro and give the experimental foundation for the future clinical trials of immunotherapy in bladder tumor. Methods： The E J-derived HSP70 co-cultured with DC from the healthy volunteers＇ PBMC, along with the crude lysate （the supematant before HSP70 purification） from EJ cells were used as the experimental groups and DC not pulsed by any tumor cells antigen were the blank control. The autologous T-lymphocytes were added into the above various DC groups, and after incubation, the stimulation indexes （SI） and interferon-y （IFN-γ） were detected to evaluate the immune activities of various DC groups. The killing effects of CTL to target cells, EJ and Hela cells, were determined with 51^Cr releasing test. Results： Both DC/HSP70 and DC/the crude lysate could effectively activate CTL in vitro and kill target cells EJ. The killing effect of DC/HSP70 to EJ was much stronger than DC/the crude lysate （the supernatant before HSP70 purification） （P 〈 0.05）. DC without any tumor cell antigens had a lower killing power to EJ. Meanwhile, DC/ HSP70 had little killing power to Hela non-relevant to bladder tumor histopathologically as compared with EJ cells （P 〈 0.05）. Conclusion： The DC pulsed by HSP70 derived from the autologous tumor cells could induce a peptide complexes specific CTL response to tumor cells, and the CTL response induced by the DC/HSP70 was stronger, which display the basis of the possible clinical application of DC/HSP70 for bladder tumor.展开更多
BACKGROUND The literature on thyrotoxicosis caused by excessive ingestion of exogenous thyroid hormone is limited,and most cases reported have involved pediatric clinical studies.CASE SUMMARY A 21-year-old woman initi...BACKGROUND The literature on thyrotoxicosis caused by excessive ingestion of exogenous thyroid hormone is limited,and most cases reported have involved pediatric clinical studies.CASE SUMMARY A 21-year-old woman initially presented with palpitation and chest tightness after an overdose of levothyroxine(10 mg).The patient transiently lost consciousness and developed atrial fibrillation during hospitalization.We used propylthiouracil to decrease the peripheral conversion of T4 to T3 and inhibit the synthesis of endogenous thyroxine,propranolol to control heart rate,hydrocortisone to correct severe thyrotoxicosis,and hemoperfusion to increase levothyroxine clearance.The patient recovered and was discharged.CONCLUSION For patients with thyrotoxicosis after taking excess levothyroxine,it is critical to monitor vital signs and initiate effective treatment.展开更多
AIM: To investigate whether the gene variants in MYOC and ABCA1 are associated with primary angle-closure glaucoma(PACG) and anterior chamber depth(ACD) and axial length(AL) in samples from northern China. METHODS: Th...AIM: To investigate whether the gene variants in MYOC and ABCA1 are associated with primary angle-closure glaucoma(PACG) and anterior chamber depth(ACD) and axial length(AL) in samples from northern China. METHODS: The present case-control association study consisted of 500 PACG patients and 720 unrelated controls. Each participant was genotyped for eleven single nucleotide polymorphisms(SNPs) in MYOC and ABCA1 genes(rs12076134, rs183532, rs235875 and rs235913 in MYOC, rs2422493, rs2487042, rs2472496, rs2472493, rs2487032, rs2472459 and rs2472519 near ABCA1) using an improved multiplex ligation detection reaction(iMLDR) technique. The genetic association analyses were performed by PLINK using a logistic regression model. The association between genotypes and ocular biometric parameters was performed by SPSS using generalized estimation equation. Bonferroni corrections wereimplemented and the statistical power was calculated by the Power and Sample Size Calculation. RESULTS: Two SNPs rs183532 and rs235875 as well as a haplotype TTC in MYOC were nominally associated with PACG despite the significance was lost after Bonferroni correction. No association was observed between ABCA1 and PACG, neither did the association between these variants and ACD as well as AL. CONCLUSION: The present study suggests MYOC and ABCA1 do not play a part in the pathogenesis of PACG as well as the regulation of ocular biometric parameters in a northern Chinese population. Further investigations with large sample size are needed to verify this consequence.展开更多
The generation of reactive oxygen species(ROS)at the tumor site to induce destruction is emerging as a novel strategy for cancer treatment,which involves photodynamic therapy(PDT).Nevertheless,tumors typically create ...The generation of reactive oxygen species(ROS)at the tumor site to induce destruction is emerging as a novel strategy for cancer treatment,which involves photodynamic therapy(PDT).Nevertheless,tumors typically create a hypoxic environment and are equipped with an endogenous antioxidant defense system that could potentially impede the efficiency of the therapeutic approach.To overcome these drawbacks,herein,a tumor microenvironment-responsive the ND-PAA-CD-Ce6@MnO_(2)(NPCC@M)delivery system was fabricated by disulfide bond coupling chlorin e6(Ce6)to nanodiamond(ND)and further wrapped by MnO_(2)nanosheets to facilitate PDT.The use of disulfide bond not only stabilizes Ce6 in the blood circulation to prevent premature leakage,but also destroys the antioxidant barrier of overexpressed glutathione(GSH)in tumor cells.Moreover,the outer MnO_(2)was rapidly degraded by the endogenous hydrogen peroxide(H_(2)O_(2))in the acidic pH and GSH within the tumor cells,which leads to an abundance of O_(2)and while increases the level of 1O_(2)under laser irradiation.The results eventually broke the redox homeostasis and attenuate hypoxia,thereby inducing apoptosis and necrosis of tumor cells.Detailed in vitro and in vivo biological effect has revealed a good biosafety profile and a high tumor suppression effect.Such a novel ND-based system with tumor microenvironment-modulating capability to elevate oxygen content and promote GSH consumption in tumor cells opens new opportunities for enhanced ROS treatment paradigms.展开更多
Objective This study aimed to investigate the molecular mechanisms responsible for fluconazole resistance in clinical isolates of this pathogenic yeast.Methods A total of 41 Candida tropicalis strains were collected f...Objective This study aimed to investigate the molecular mechanisms responsible for fluconazole resistance in clinical isolates of this pathogenic yeast.Methods A total of 41 Candida tropicalis strains were collected from the clinical laboratory of Taiyuan City Central Hospital.Antifungal susceptibility testing was performed by ATB FUNGU 3 method.The 14 α-demethylase (ERG11) gene in all clinical isolates of Candida tropicalis were amplified by PCR,and their nucleotide sequences were determined in order to detect point mutations.Likewise,efflux transporters (CDR1 and MDR1) and ERG11 genes were tested by semiquantitative reverse transcription-polymerase chain reaction (RT-PCR) for their expression in Candida tropicalis cells at the mRNA level.Results The fluconazole-resistant rate of 41 Candida tropicalis was 12.2%.The amino acid substitutions in ERG11p of R245K,Y221F and V362I were found in fluconazole-resistant isolates.And no amino acid substitution was detected in fluconazole-susceptible ones.The mRNA level of CDR1,MDR1 and ERG11 genes in fluconazole-resistant isolates all showed overexpression compared with fluconazole-susceptible ones.Conclusions Missense mutations in ERG11 gene associated with overexpression of CDR1,MDR1 and ERG11 gene seemed to be responsible for the acquired fluconazole resistance of these clinical isolates.展开更多
文摘BACKGROUND While most complications of cervical surgery are reversible,some,such as symptomatic postoperative spinal epidural hematoma(SEH),which generally occurs within 24 h,are associated with increased morbidity and mortality.Delayed neurological dysfunction is diagnosed in cases when symptoms present>3 d postoperatively.Owing to its rarity,the risk factors for delayed neurological dysfunction are unclear.Consequently,this condition can result in irreversible neurological deficits and serious consequences.In this paper,we present a case of postoperative SEH that developed three days after hematoma evacuation.CASE SUMMARY A 68-year-old man with an American Spinal Injury Association(ASIA)grade C injury was admitted to our hospital with neck pain and tetraplegia following a fall.The C3-C7 posterior laminectomy and the lateral mass screw fixation surgery were performed on the tenth day.Postoperatively,the patient showed no changes in muscle strength or ASIA grade.The patient experienced neck pain and subcutaneous swelling on the third day postoperatively,his muscle strength decreased,and his ASIA score was grade A.Magnetic resonance imaging showed hypointense signals on T1 weighted image(T1WI)and T2WI located behind the epidural space,with spinal cord compression.Emergency surgical intervention for the hematoma was performed 12 h after onset.Although hypoproteinemia and pleural effusion did not improve in the perioperative period,the patient recovered to ASIA grade C on day 30 after surgery,and was transferred to a functional rehabilitation exercise unit.CONCLUSION This case shows that amelioration of low blood albumin and pleural effusion is an important aspect of the perioperative management of cervical surgery.Surgery to relieve the pressure on the spinal cord should be performed as soon as possible to decrease neurological disabilities.
基金Supported by a grant from the National Natural Science Foundation of China (No. 3000754).
文摘Objective： To investigate whether human dendritic cells （DC） derived from peripheral blood mononuclear cells （PBMC）, which were pulsed by heat shock protein 70 （HSP70） isolated from human bladder tumor cell lines of E J, were able to induce peptide specific cytotoxic T-lymphocytes （CTL） response in vitro and give the experimental foundation for the future clinical trials of immunotherapy in bladder tumor. Methods： The E J-derived HSP70 co-cultured with DC from the healthy volunteers＇ PBMC, along with the crude lysate （the supematant before HSP70 purification） from EJ cells were used as the experimental groups and DC not pulsed by any tumor cells antigen were the blank control. The autologous T-lymphocytes were added into the above various DC groups, and after incubation, the stimulation indexes （SI） and interferon-y （IFN-γ） were detected to evaluate the immune activities of various DC groups. The killing effects of CTL to target cells, EJ and Hela cells, were determined with 51^Cr releasing test. Results： Both DC/HSP70 and DC/the crude lysate could effectively activate CTL in vitro and kill target cells EJ. The killing effect of DC/HSP70 to EJ was much stronger than DC/the crude lysate （the supernatant before HSP70 purification） （P 〈 0.05）. DC without any tumor cell antigens had a lower killing power to EJ. Meanwhile, DC/ HSP70 had little killing power to Hela non-relevant to bladder tumor histopathologically as compared with EJ cells （P 〈 0.05）. Conclusion： The DC pulsed by HSP70 derived from the autologous tumor cells could induce a peptide complexes specific CTL response to tumor cells, and the CTL response induced by the DC/HSP70 was stronger, which display the basis of the possible clinical application of DC/HSP70 for bladder tumor.
文摘BACKGROUND The literature on thyrotoxicosis caused by excessive ingestion of exogenous thyroid hormone is limited,and most cases reported have involved pediatric clinical studies.CASE SUMMARY A 21-year-old woman initially presented with palpitation and chest tightness after an overdose of levothyroxine(10 mg).The patient transiently lost consciousness and developed atrial fibrillation during hospitalization.We used propylthiouracil to decrease the peripheral conversion of T4 to T3 and inhibit the synthesis of endogenous thyroxine,propranolol to control heart rate,hydrocortisone to correct severe thyrotoxicosis,and hemoperfusion to increase levothyroxine clearance.The patient recovered and was discharged.CONCLUSION For patients with thyrotoxicosis after taking excess levothyroxine,it is critical to monitor vital signs and initiate effective treatment.
基金Supported by the National Natural Science Foundation of China(No.81460093)the Ningxia Nature Science Funding from the Department of Science and Technology of Ningxia Hui Autonomous Region(No.NZ16194)
文摘AIM: To investigate whether the gene variants in MYOC and ABCA1 are associated with primary angle-closure glaucoma(PACG) and anterior chamber depth(ACD) and axial length(AL) in samples from northern China. METHODS: The present case-control association study consisted of 500 PACG patients and 720 unrelated controls. Each participant was genotyped for eleven single nucleotide polymorphisms(SNPs) in MYOC and ABCA1 genes(rs12076134, rs183532, rs235875 and rs235913 in MYOC, rs2422493, rs2487042, rs2472496, rs2472493, rs2487032, rs2472459 and rs2472519 near ABCA1) using an improved multiplex ligation detection reaction(iMLDR) technique. The genetic association analyses were performed by PLINK using a logistic regression model. The association between genotypes and ocular biometric parameters was performed by SPSS using generalized estimation equation. Bonferroni corrections wereimplemented and the statistical power was calculated by the Power and Sample Size Calculation. RESULTS: Two SNPs rs183532 and rs235875 as well as a haplotype TTC in MYOC were nominally associated with PACG despite the significance was lost after Bonferroni correction. No association was observed between ABCA1 and PACG, neither did the association between these variants and ACD as well as AL. CONCLUSION: The present study suggests MYOC and ABCA1 do not play a part in the pathogenesis of PACG as well as the regulation of ocular biometric parameters in a northern Chinese population. Further investigations with large sample size are needed to verify this consequence.
基金the Central Government Guiding Local Science and Technology Development(grant No.YDZX20191400002477)the Shanxi Province Natural Science Foundation(grant No.202203021221003)+2 种基金Shanxi Province Patent Transformation Project(grant No.202304015)CIRP Open Fund of Radiation Protection Laboratories(grant No.CIRP-CAEA20220203)Interdisciplinary Construction Project of Shanxi University(grant No.113541028).
文摘The generation of reactive oxygen species(ROS)at the tumor site to induce destruction is emerging as a novel strategy for cancer treatment,which involves photodynamic therapy(PDT).Nevertheless,tumors typically create a hypoxic environment and are equipped with an endogenous antioxidant defense system that could potentially impede the efficiency of the therapeutic approach.To overcome these drawbacks,herein,a tumor microenvironment-responsive the ND-PAA-CD-Ce6@MnO_(2)(NPCC@M)delivery system was fabricated by disulfide bond coupling chlorin e6(Ce6)to nanodiamond(ND)and further wrapped by MnO_(2)nanosheets to facilitate PDT.The use of disulfide bond not only stabilizes Ce6 in the blood circulation to prevent premature leakage,but also destroys the antioxidant barrier of overexpressed glutathione(GSH)in tumor cells.Moreover,the outer MnO_(2)was rapidly degraded by the endogenous hydrogen peroxide(H_(2)O_(2))in the acidic pH and GSH within the tumor cells,which leads to an abundance of O_(2)and while increases the level of 1O_(2)under laser irradiation.The results eventually broke the redox homeostasis and attenuate hypoxia,thereby inducing apoptosis and necrosis of tumor cells.Detailed in vitro and in vivo biological effect has revealed a good biosafety profile and a high tumor suppression effect.Such a novel ND-based system with tumor microenvironment-modulating capability to elevate oxygen content and promote GSH consumption in tumor cells opens new opportunities for enhanced ROS treatment paradigms.
文摘Objective This study aimed to investigate the molecular mechanisms responsible for fluconazole resistance in clinical isolates of this pathogenic yeast.Methods A total of 41 Candida tropicalis strains were collected from the clinical laboratory of Taiyuan City Central Hospital.Antifungal susceptibility testing was performed by ATB FUNGU 3 method.The 14 α-demethylase (ERG11) gene in all clinical isolates of Candida tropicalis were amplified by PCR,and their nucleotide sequences were determined in order to detect point mutations.Likewise,efflux transporters (CDR1 and MDR1) and ERG11 genes were tested by semiquantitative reverse transcription-polymerase chain reaction (RT-PCR) for their expression in Candida tropicalis cells at the mRNA level.Results The fluconazole-resistant rate of 41 Candida tropicalis was 12.2%.The amino acid substitutions in ERG11p of R245K,Y221F and V362I were found in fluconazole-resistant isolates.And no amino acid substitution was detected in fluconazole-susceptible ones.The mRNA level of CDR1,MDR1 and ERG11 genes in fluconazole-resistant isolates all showed overexpression compared with fluconazole-susceptible ones.Conclusions Missense mutations in ERG11 gene associated with overexpression of CDR1,MDR1 and ERG11 gene seemed to be responsible for the acquired fluconazole resistance of these clinical isolates.
