OBJECTIVE: To explore the forensic pathological features of death caused by anaphylactic shock. METHODS: One hundred and forty-two death cases of anaphylactic shock were retrospectively analyzed. The IgE level in the serum of anaphylactic shock cases were statistically compared with that of 62 non-anaphylactic shock cases. RESULTS: Most cases (77.46%) of anaphylactic shock death occurred in the medical institutes, with intravenous drug administration accounting for 53.53% of anaphylactic shock death. β-Lactam antibiotics, glucocorticoid and herbal medications were responsible for a significant proportion of such cases. Although characteristic histopathological changes were absent in vast majority of these anaphylactic shock cases, the differences of IgE levels in the serum between anaphylactic shock group and non-anaphylactic shock group were statistically significant (P<0.05). CONCLUSION Combined information including clinical data, autopsy results, IgE level, and other specific test results should be evaluated together in the forensic pathological diagnosis of anaphylactic shock.
Anaphylaxis ; Autopsy ; Cause of Death ; Forensic Pathology ; Humans ; Infusions, Intravenous ; Retrospective Studies ; Serum

Twenty Newcastle disease virus(NDV)strains were isolated from diseased chicken and geese in field outbreaks during 2005 and 2006 in some regions of Jiangsu and Guangxi,and the antigenic analysis of the all NDV isolates had been done based on the reaction spectrum with a panel of monoclonal antibodies to the HN glycoprotein.The entire ORFs encoding HN protein of these NDV isolates were amplified by RT-PCR successfully,cloned and sequenced.The resultant sequences of HN genes of 13 isolates of chicken origin and 7 isolates of goose origin were gained and analyzed.The results of reaction spectrum showed that there were some distinct differences in the antigenic epitopes among the 20 NDV isolates.And the sequences revealed that the coding regions of the HN genes of these isolates all consisted of 1716 nt characteristic of virulent strains of NDV,coding for 571 amino acids.Neucleotides sequence homology were found to be from 94.8%to 100%among 18 NDV isolates of genotypeⅦ,and the neucleotides sequence homology between all the isolates and the other genotypeⅦstrains of recent years in China ranged from 92.1%to 99.6%.The deduced amino acid sequences and the receptor-binding regions of HN proteins between the NDV isolates of chicken origin and of goose origin were compared and analyzed.The results showed that some unique amino acid substitutions were found in the genome of the NDV isolates,and the close genetic similarity provided evidence for epidemiological linkage between the NDV isolates of chicken origin and of goose origin in the same period.

AIMTo explore the effects of gentamicin ototoxicity on the expression of heat shock protein 70 in guinea pigs cochlea.

METHODSWe used immunohistochemistry staining and image quantitative analysis system, combined with auditory brainstem response (ABR) measurement to investigate the change on the expression of HSP70 in guinea pigs cochlea of gentamicin ototoxicity.

RESULTSThe levels of HSP70 immunoreactivity in guinea pigs cochlea of experimental animals were high including Corti's organ, stria vascularis, medial spiral limbus, spiral ganglion cells and the threshold of ABR was in high correlation with the expression of HSP70 ([ r] > 0.8, P < 0.01).

CONCLUSIONGentamicin can induce expression of HSP 70 in guinea pigs cochlea and protect hearing function.

Animals ; Cochlea ; drug effects ; physiopathology ; Gentamicins ; toxicity ; Guinea Pigs ; HSP70 Heat-Shock Proteins ; metabolism ; Heat-Shock Response ; drug effects

To examine the significance of heat shock protein 70 mRNA in ototoxicity resulted from gentamicin (GM), twenty healthy albino guinea pigs (200-250 g) of either sex with a positive Prier reflex were divided into two groups randomly. In GM group the animals received 100 mg/kg GM daily by intraperitoneal injection for 10 d. In saline control group the animals received 2.5 ml/kg saline daily by intraperitoneal injection for 10 d. Auditory brainstem response (ABR) thresholds were recorded in each animal before and 1 d after GM or saline administration. After the second ABR measurement, the expression of HSP70 mRNA in guinea pig cochlea was observed with in situ hybridization and image quantitative analysis system. The results showed that the threshold of ABR in the GM group was significantly higher than that of the saline control (P< 0.001). The expression of HSP70 mRNA was more intensive in stria vascularis, spiral ligament and spiral ganglion cells in the GM group than that of the saline control group. These results suggest that administration of gentamicin can induce the expression of HSP 70 mRNA in guinea pig cochlea, and that this effect may protect hearing function from ototoxicity.
Animals ; Cochlea ; metabolism ; Evoked Potentials, Auditory, Brain Stem ; physiology ; Female ; Gentamicins ; toxicity ; Guinea Pigs ; HSP70 Heat-Shock Proteins ; biosynthesis ; genetics ; Male ; RNA, Messenger ; biosynthesis ; genetics ; Random Allocation

Objective To comprehensively evaluate the risk factors of aplastic anemia, and provide scientific evidence for the primary prevention of aplastic anemia. Methods The published Papers were searched by"aplastic anemia" "case control study" and"risk factors" as key words collected from Chinese National Knowledge Infrastructure, Chinese VIP journal database, PubMed, Cochrane library and Clinical Trial and other databases, ranged from the creation date of each database to September 2017 .A meta-analysis of studies on risk factors was performed to calculate the pooled odd ratios (ORs) with 95％ confidence intervals (CIs) with Software Stata 14.0. Results The database search resulted in the identification of 1, 094 articles. After screening, 22 case-control studies were included in the study with 16 factors. Ten risk factors were showed statistically significant differences, including paint exposure (OR=3.82, 95％ CI: 1.68-8.66), chloramphenicol (OR=3.21, 95％ CI: 1.98-5.20), benzene exposure (OR=2.94, 95％ CI: 2.11-4.11), glue exposure (OR=2.56, 95％CI: 1.28-5.12), history of hepatitis (OR=2.54, 95％ CI: 1.94-3.34) , hair dye exposure (OR=2.37, 95％ CI: 1.08-5.22) , pesticides exposure (OR=1.98, 95％ CI: 1.60-2.45), β-lactam (OR=1.77, 95％ CI: 1.03-3.06), sulfonamides (OR=1.64, 95％ CI:1.03-2.61) and fuel/oil exposure (OR=1.53, 95％ CI: 1.25-1.87) , and high economic income (OR=0.52, 95％ CI:0.43-0.63) is the protective factor. Conclusion The meta-analysis of case-control studies suggests that the risk factors of aplastic anemia mainly including four aspects: drug use, past history, socioeconomic status and occupational or environmental exposure to chemical toxic substances.

OBJECTIVETo elucidate the effect of inflammation and coronary atherosclerotic plaque destabilization in the pathogenesis of acute coronary syndromes (ACS).

METHODSTwenty-eight patients with ACS and 13 patients with stable angina pectoris (SA) were examined by intravascular ultrasound (IVUS). Coronary plaque morphology and areas in culprit lesions were analyzed. The serum levels of hs-CRP, MMP-9, TIMP-1, sCD40L were also measured.

RESULTSSoft plaques were dominant in culprit lesions of ACS patients (71.4%, 20/28), and hard plaques were dominant in culprit lesions of SA patients [76.9% (10/13), P = 0.004]. At the culprit site, plaque area, plaque burden and remodeling index were all significantly larger in culprit lesions of ACS patients than those of SA patients (all P < 0.05). Positive remodeling was more frequent in ACS patients than in SA patients, whereas negative remodeling was more frequent in SA patients (P < 0.05). The serum levels of hs-CRP, MMP-9, sCD40L were higher in ACS group compared with SA group (P < 0.05, respectively). Moreover, hs-CRP level was positively correlated with MMP-9 (r = 0.671, P = 0.000) and sCD40L (r = 0.494, P = 0.008), respectively, in ACS patients. There was no difference in TIMP-1 between two groups (P = 0.234).

CONCLUSIONSThese results suggest that structurally vulnerable plaques are essential element in the pathogenesis of ACS and inflammation might play an important role in plaque vulnerability.

Acute Coronary Syndrome ; blood ; diagnostic imaging ; pathology ; Aged ; C-Reactive Protein ; metabolism ; CD40 Ligand ; blood ; Coronary Artery Disease ; diagnostic imaging ; pathology ; Female ; Humans ; Inflammation ; Male ; Matrix Metalloproteinase 9 ; blood ; Middle Aged ; Tissue Inhibitor of Metalloproteinase-1 ; blood ; Ultrasonography, Interventional

OBJECTIVETo study the molecular mechanisms of protein C (PC) deficiency caused by PC gene mutations of C64W, F139V and K150 deletion (K150d).

METHODSWild-type and mutant PC cDNA expression plasmids (PCwt, PC C64W, PC F139V, PC K150d) were constructed and transfected into COS-7 cells or CHO cells respectively for in vitro expression study and immunofluorescent assay. Fluorescent real-time PCR was used to detect the expression of PC mRNA, protein degradation inhibition and endo-beta-N-acetylglucosaminidase H (Endo H) digestion experiments to explain the mutant protein degradation pathway and its localizations inside the cells.

RESULTSPC C64W was not secreted from the cells and was gradually degraded inside the cells. There was partial secretion of PC F139V, most of the protein molecule was not secreted and degraded intracellularly. Mutant PC K150d was secreted normally from the cells. Fluorescent realtime PCR analysis of total mRNA from transfected cells showed no reduction of the mutant PC mRNA expression compared with that of wild-type PC mRNA. Protein degradation inhibition experiments showed that mutants PC C64W and PC F139V were degraded intracellularly through the proteasome pathway. Endo H digestion experiments and immunofluorescence results suggested that mutant PC molecules were located mainly in pre-Golgi apparatus.

CONCLUSIONSImpaired secretion and degradation intracellularly of the mutants might be the molecular mechanisms of PC deficiency caused by C64W and F139V mutations. K150 deletion mutation might not affect the secretion of the mutant.

Animals ; CHO Cells ; COS Cells ; Cercopithecus aethiops ; Cricetinae ; Cricetulus ; Humans ; Mutation ; Plasmids ; genetics ; Protein C ; genetics ; Protein C Deficiency ; genetics ; Transfection

OBJECTIVETo identify the phenotype and gene mutation in two Chinese pedigrees with hereditary protein C deficiency.

METHODSThe plasma level of protein C activity (PC: A) , protein C antigen (PC: Ag), protein S activity (PS: A), and antithrombin activity (AT: A) of the probands and their family members were detected using chromogenic assay and ELISA, respectively. All of the nine exons and intron-exon boundaries of protein C gene were amplified by PCR and analyzed by direct sequencing of the probands. Restriction enzyme site analysis was used to confirm the mutation.

RESULTSThe plasma PC: A and PC: Ag for proband 1 was 1.2% and 0, respectively. Compound heterozygous mutations, C(TGC)64W (TGG) and F(TTC) 139V(GTC) , were identified in her, the former being inherited from the maternal side and the later the paternal side. Further genetic analysis showed that her husband ( II 8) had the heterozygous deletion mutation (K150 or 151 Del) in exon 7, her daughter had the same heterozygous deletion mutation and a F139V. The plasma PC: A and PC: Ag for proband 2 was 50. 3% and 1.9 mg/L, respectively. He had the heterozygous Lys150 or Lys151 deletion mutation, which was inherited from his father. Polymorphisms of C/T at position - 1654, A/G at - 1641 , and A/T at - 1476A/T in the promoter region of protein C were confirmed in all members of the two pedigrees, of which, proband 2 had homozygous CC/GG/TT. The F139V mutation was confirmed by restriction enzyme site analysis and polymorphism for this mutation was excluded. PS: A and AT: A were in normal range for all members.

CONCLUSIONCompound heterozygous mutation C64W and F139V of protein C gene lead to type I hereditary protein C deficiency for proband 1. K150 or 151 deletion mutation and polymorphism of CC/GG/TT might lead to type I hereditary protein C deficiency for proband 2. C64W is a novel mutation for protein C gene. F139V and K150 or 151 deletion mutation are reported for the first time in China.

Adult ; Asian Continental Ancestry Group ; genetics ; China ; Female ; Genotype ; Humans ; Male ; Mutation ; Pedigree ; Phenotype ; Polymorphism, Genetic ; Protein C Deficiency ; genetics

To study the genetic characteristics of 123 type II non-wild polioviruses isolated from acute flaccid paralysis (AFP) cases in mainland China in 2010, provide the scientific basis for maintaining the "polio-free" status, and the switching use of polio vaccine for China. VP1 gene was amplified by reverse transcription-polymerase chain reaction (RT-PCR) and the PCR products were then sequenced. The sequence results were analyzed with Sequencher 4.8, BioEdit 7.0.9 and MEGA 5.0. Of 65 strains, nt2909 was found to be a mutation hotspot, and also a neurovirulence determinant in VP1 region. During 2010, two vaccine-derived polioviruses (VDPVs) were isolated from Yunnan province, China and no wild poliovirus (WPV) was isolated. The epidemiological studies and laboratory results of the two VDPVs showed that they were newly discovered VDPVs because of the genetic difference from other VDPVs strains isolated in the world, implying the sensitive poliovirus surveillance network could timely detect the transmission of VDPVs and the importation of WPV.
Adolescent ; Adult ; Child ; Child, Preschool ; China ; Female ; Genotype ; Humans ; Male ; Phylogeny ; Poliomyelitis ; virology ; Poliovirus ; classification ; genetics ; isolation & purification ; Viral Proteins ; genetics ; Young Adult

Objective To analyze the risk of adverse drug events in pediatric clinical applications of tocilizumab versus inflixima.Methods Adverse event(AE)reporting data for tocilizumab versus infliximab in the U.S.Food and Drug Administration Adverse Event Reporting System database for the pediatric population from Q1 2013 to Q1 2023 were collected.AE risk signal mining was performed using the reporting odds ratio(ROR)method and the proportional reporting ratio(PRR)method.AEs were also classified and statistically analyzed according to the preferred system organ classification and preferred terminology(PT)of the International Dictionary of Medical Terminology.Results Data were extracted and cleaned to include 1 052 AE reports with 198 positive PT signals for tocilizumab as the suspected drug and 9 1 39 AE reports with 387 positive PT signals for infliximab as the suspected drug.The analyses suggested that the stronger positive risk signals for both drugs were focused on gastrointestinal disorders,infectious and invasive diseases,laboratory tests,musculoskeletal and connective tissue disorders,and blood,vascular,and lymphatic disorders.The risk signals for infliximab were focused on gastrointestinal disorders,infections,and infectious diseases,while the risk signals for tocilizumab were focused on the musculoskeletal muscle system.Conclusion Clinical use of both drugs in children has multi-system effects,tocilizumab may have effects on growth and development,and infliximab has effects on the gastrointestinal tract in children.