Forensic parameters and population analysis of 21 autosomal STR loci in the Wuhu Han population from Anhui Province, East China.

BACKGROUND: At present, there are no available genetic data on the AGCU EX22 Kit from the Wuhu Han population. AIM: This study investigates the applicability of the AGCU EX22 kit, designed for the Chinese population for forensic analysis and population genetics of the Wuhu Han population. SUBJECTS AND METHODS: Bloodstains from 1565 unrelated healthy individuals in Wuhu city, Anhui Province, were collected for analysis. The AGCU EX22 kit was used for amplification, and capillary electrophoresis was used to separate the amplification products. Allele frequencies and forensic parameters were determined. The Wuhu Han population was compared to 10 reference populations through genetic distance, a phylogenetic neighbor-joining tree and principal component analysis. RESULTS: In total, 281 alleles and 1187 genotypes were observed. No significant deviations from Hardy-Weinberg equilibrium at any locus were found after Bonferroni's correction. The 21 autosomal short tandem repeat (STR) genetic markers exhibited high informativeness and polymorphism. The cumulative power of discrimination and power of exclusion were 0.999999999999999999999999913380 and 0.999999996752339, respectively. Population comparisons revealed a genetic affinity between Wuhu Han and southern Han populations, except for the Guangdong Han population, which aligned with the traditional geographical division in China. CONCLUSION: The AGCU EX22 Kit, containing 21 STR loci, is suitable for forensic application and population genetics studies in the Wuhu Han population.

Construction and evaluation of DNA vaccine encoding Crimean Congo hemorrhagic fever virus nucleocapsid protein, glycoprotein N-terminal and C-terminal fused with LAMP1.

Crimean-Congo hemorrhagic fever virus (CCHFV) can cause severe hemorrhagic fever in humans and is mainly transmitted by ticks. There is no effective vaccine for Crimean-Congo hemorrhagic fever (CCHF) at present. We developed three DNA vaccines encoding CCHFV nucleocapsid protein (NP), glycoprotein N-terminal (Gn) and C-terminal (Gc) fused with lysosome-associated membrane protein 1 (LAMP1) and assessed their immunogenicity and protective efficacy in a human MHC (HLA-A11/DR1) transgenic mouse model. The mice that were vaccinated three times with pVAX-LAMP1-CCHFV-NP induced balanced Th1 and Th2 responses and could most effectively protect mice from CCHFV transcription and entry-competent virus-like particles (tecVLPs) infection. The mice vaccinated with pVAX-LAMP1-CCHFV-Gc mainly elicited specific anti-Gc and neutralizing antibodies and provided a certain protection from CCHFV tecVLPs infection, but the protective efficacy was less than that of pVAX-LAMP1-CCHFV-NP. The mice vaccinated with pVAX-LAMP1-CCHFV-Gn only elicited specific anti-Gn antibodies and could not provide sufficient protection from CCHFV tecVLPs infection. These results suggest that pVAX-LAMP1-CCHFV-NP would be a potential and powerful candidate vaccine for CCHFV.

ISG20L1 acts as a co-activator of DAPK1 in the activation of the p53-dependent cell death pathway.

Our previous studies have revealed that GADD45α is a liable proapoptotic protein, which undergoes MDM2-dependent constitutive ubiquitylation and degradation in resting cancer cells. Under chemotherapeutic agent (such as arsenite, 5-Fu and VP-16) exposure, DAPK1 functions as a novel p53 (also known as TP53) kinase, which induces phosphorylation of p53 at Ser15 and transactivates the p53 target Ets-1, to synergistically repress IKKß-dependent MDM2 stability, and ultimately removes the inhibitory effect of MDM2 on GADD45α, resulting in GADD45α accumulation and cell apoptosis. In the current study, we show that there is a strong induction of ISG20L1 (also known as AEN) expression in several cancer cell lines under exposure of arsenite and other chemotherapeutic agents. Surprisingly, although originally identified as a transcriptional target of p53, ISG20L1 induction was not controlled by p53. Instead, ISG20L1 functioned as upstream activator of p53 by interacting with DAPK1, and plays an essential role in promoting DAPK1-p53 complex formation and the subsequent activation of Ets-1/IKKß/MDM2/GADD45α cascade. Therefore, our findings have revealed novel function of ISG20L1 in mediating cancer cell apoptosis induced by chemotherapeutic agents via modulating activation of the DAPK1- and p53-dependent cell death pathway.

First report of wild tomato mosaic virus infecting chilli pepper in China.

Chilli pepper is an important economic crop and virus diseases are constraints on its production. In 2018, disease surveys were conducted at a 15-ha chilli pepper plantation in Dehong, southwest of Yunnan Province, China. Throughout the chilli pepper growing season from March to September, pepper plants developed three different virus-like symptoms on leaves, including mosaic, yellow mottle and shrinkage (Fig. S1). Based on observation of virus-like symptomatic phenotypes, the field surveys indicated that the disease incidence ranged from 30% in March to a peak 100% in July, resulting in a significant loss of pepper fruit from 30 to 100% depending on plot of the field. Potyvirus-like filamentous particles, around 11*760 nm, were observed under electron microscopy in the sap of symptomatic leaves (Fig. S1). To further determine the viral species in these samples, total RNA was extracted from three symptomatic samples using a Trans ZolUp Plus RNA Kit (Trans Gene, Beijing, China). Complementary DNA (cDNA) was synthesized using oligo (dT) and M-MLV reverse transcriptase (Promega, Madison, Wisconsin, USA) according to the manufacturer's instructions, and the polymerase chain reaction (PCR) was performed using degenerate primers specific to genus Potyvirus targeting HC-Pro region (HPFor: 5-TGYGAYAAYCARYTIGAYIIIAAYG-3; HPRev: 5-GAICCRWAIGARTCIAIIACRTG-3) (Ha et al. 2008) under the following conditions: an initial denaturation at 94°C for 4min, 30 cycles of denaturation at 94°C for 30 s, annealing at 56°C for 30 s, extension at 72°C for 30s, and a 10min final extension at 72°C. An expected 683-bp DNA fragment was amplified and cloned into the pMD 18-T Vector (Takara, Japan) for sequencing. Sequence analysis using BLAST revealed that the amplicons of phenotype I (Fig. S1a) shared highest nucleotide identity (85.6%) with wild tomato mosaic virus (WTMV) isolate from Vietnam (GenBank no. DQ851495) while the amplicons of phenotype III (Fig. S1c) showed the highest nucleotide identity (93%) with chilli veinal mottle virus (ChiVMV) isolate from Sichuan, China. (GenBank no. MK405594). Amplicons of phenotype II included both sequence of above WTMV and ChiVMV, indicating co-infection of phenotype II (Fig. S1b). Phenotype I sample was used for mechanical inoculation on chilli pepper as described previously (Yang et al.2013). After ten days, virus-like symptoms similar to phenotype I were observed on leaves, and WTMV infection, but not ChiVMV infection, was confirmed by RT-PCR tests on inoculated pepper plants (Fig. S1 e, f). To further ascertain the incidence of these two viruses in the field, primers WT-F: 5'-GTTGTTGAATGTGGTTTAGTT-3' and WT-R: 5'-AGATGTGCTTTGGAAGCGACC-3' were designed based on the WTMV sequence (GenBank no. DQ851495) to amplify a 476 bp product, and primers Ch-F/Ch-R (Ch-F: 5'-AAAGAAGAACAAGCGACAGAA-3', Ch-R: 5'-CATCACGCAAATATTCAAAGC-3') were designed based on ChiVMV sequence (GenBank no. MK405594.1) to amplify a 332 bp product. RT-PCR was conducted on 31 field-collected samples, and amplicons of expected sizes, 476bp and 332bp, corresponding to WTMV and ChiVMV, respectively, were obtained and sequenced to verify their identity. The results (Fig. S2) showed that 71% (22/31) of the samples tested positive for WTMV, 90% (28/31) tested positive for ChiVMV, and 65% (20/31) were co-infected with the two viruses. The WTMV was first reported infecting wild tomatoes in Vietnam in 2008 (Ha et al. 2008), and later reported in China in Nicotiana tabacum (Sun et al. 2015), Solanum nigrum (Zhang et al. 2019), and wild eggplant (Zhang et al. 2014). To our knowledge, this is the first report of WTMV infection on chilli pepper under natural conditions. Our study revealed that the chilli pepper disease in Dehong was caused by single or co-infection of WTMV and ChiVMV. It is necessary to find effective methods to control these two viruses.

Selective degradation of IKKα by autophagy is essential for arsenite-induced cancer cell apoptosis.

Two catalytic subunits of the IKK complex, IKKα and IKKß, trigger NF-κB activation as well as NF-κB-independent signaling events under both physiological and pathological conditions. Here we identified the NF-κB-unrelated cytoprotective function of IKKα in promoting autophagy by triggering p53 transactivation and upregulation of its downstream autophagic mediator, DRAM1, in the arsenite-treated hepatoma cells, which responses depended on IKKα kinase activity. Furthermore, IKKα triggered p53/DRAM1-dependent autophagy by inducing CHK1 activation and CHK1/p53 interaction. Interestingly, after provoking autophagy, IKKα could be specifically recognized by the autophagic machinery via directly binding with LC3B, resulting in selective degradation of IKKα by autophagy. Unexpectedly, the selectivity of autophagic sequestration towards IKKα was mediated by novel mechanism independent of the classical LC3-interacting regions (LIRs) within IKKα, while C-terminal arm of LIR was involved in mediating IKKα/LC3B interaction. Taken together, we conclude that IKKα attenuates arsenite-induced apoptosis by inducing p53-dependent autophagy, and then selective feedback degradation of IKKα by autophagy contributes to the cytotoxic response induced by arsenite.

Transcriptional repression of IKKß by p53 in arsenite-induced GADD45α accumulation and apoptosis.

Our previous studies revealed that GADD45α is a liable protein, which undergoes MDM2-dependent constitutive ubiquitination and degradation in resting HepG2 hepatoma cells. Arsenite exposure induces ribosomal stress responses mediated by the ribosomal protein S7, which can block MDM2 activity and result in GADD45α accumulation and cell apoptosis. In the present study, we found that one of the catalytic subunits of IκB kinase (IKK), IKKß, exerted a novel IKKα- and NF-κB-independent function in stabilizing MDM2 and therefore contributed to ubiquitination-dependent degradation of GADD45α in resting HepG2 cells. Arsenite stimulation induced transactivation of p53, which formed a complex with its downstream target, Ets-1, and then synergistically repressed IKKß transcription, reduced MDM2 stability, and ultimately removed the inhibitory effect of MDM2 on GADD45α induction. In addition, DAPK1 functioned as an upstream protein kinase triggering p53/Ets-1-dependent IKKß and MDM2 reduction and GADD45α accumulation, thus promoting apoptosis in HepG2 cells. Subsequent studies further revealed that the activation of the DAPK1/p53/Ets-1/IKKß/MDM2/GADD45α cascade was a common signaling event in mediating apoptosis of diverse cancer cells induced by arsenite and other tumor therapeutic agents. Therefore, we conclude that data in the current study have revealed a novel role for IKKß in negatively regulating GADD45α protein stability and the contribution of p53-dependent IKKß reduction to mediating cancer cell apoptosis.

TP53-dependent autophagy links the ATR-CHEK1 axis activation to proinflammatory VEGFA production in human bronchial epithelial cells exposed to fine particulate matter (PM2.5).

ABSTARCT Epidemiological and clinical studies have increasingly shown that fine particulate matter (PM2.5) is associated with a number of pathological respiratory diseases, such as bronchitis, asthma, and chronic obstructive pulmonary disease, which share the common feature of airway inflammation induced by particle exposure. Thus, understanding how PM2.5 triggers inflammatory responses in the respiratory system is crucial for the study of PM2.5 toxicity. In the current study, we found that exposing human bronchial epithelial cells (immortalized Beas-2B cells and primary cells) to PM2.5 collected in the winter in Wuhan, a city in southern China, induced a significant upregulation of VEGFA (vascular endothelial growth factor A) production, a signaling event that typically functions to control chronic airway inflammation and vascular remodeling. Further investigations showed that macroautophagy/autophagy was induced upon PM2.5 exposure and then mediated VEGFA upregulation by activating the SRC (SRC proto-oncogene, non-receptor tyrosine kinase)-STAT3 (signal transducer and activator of transcription 3) pathway in bronchial epithelial cells. By exploring the upstream signaling events responsible for autophagy induction, we revealed a requirement for TP53 (tumor protein p53) activation and the expression of its downstream target DRAM1 (DNA damage regulated autophagy modulator 1) for the induction of autophagy. These results thus extend the role of TP53-DRAM1-dependent autophagy beyond cell fate determination under genotoxic stress and to the control of proinflammatory cytokine production. Moreover, PM2.5 exposure strongly induced the activation of the ATR (ATR serine/threonine kinase)-CHEK1/CHK1 (checkpoint kinase 1) axis, which subsequently triggered TP53-dependent autophagy and VEGFA production in Beas-2B cells. Therefore, these findings suggest a novel link between processes regulating genomic integrity and airway inflammation via autophagy induction in bronchial epithelial cells under PM2.5 exposure.

Src/STAT3-dependent heme oxygenase-1 induction mediates chemoresistance of breast cancer cells to doxorubicin by promoting autophagy.

Chemotherapeutic resistance in breast cancer, whether acquired or intrinsic, remains a major clinical obstacle. Thus, increasing tumor cell sensitivity to chemotherapeutic agents will be helpful in improving the clinical management of breast cancer. In the present study, we found an induction of HO-1 expression in doxorubicin (DOX)-treated MDA-MB-231 human breast adenocarcinoma cells, which showed insensitivity to DOX treatment. Knockdown HO-1 expression dramatically upregulated the incidence of MDA-MB-231 cell death under DOX treatment, indicating that HO-1 functions as a critical contributor to drug resistance in MDA-MB-231 cells. We further observed that DOX exposure induced a cytoprotective autophagic flux in MDA-MB-231 cells, which was dependent on HO-1 induction. Moreover, upregulation of HO-1 expression required the activation of both signal transducer and activator of transcription (STAT)3 and its upstream regulator, protein kinase Src. Abrogating Src/STAT3 pathway activation attenuated HO-1 and autophagy induction, thus increasing the chemosensitivity of MDA-MB-231 cells. Therefore, we conclude that Src/STAT3-dependent HO-1 induction protects MDA-MB-231 breast cancer cells from DOX-induced death through promoting autophagy. In the following study, we further demonstrated the contribution of Src/STAT3/HO-1/autophagy pathway activation to DOX resistance in another breast cancer cell line, MDA-MB-468, which bears a similar phenotype to MDA-MB-231 cells. Therefore, activation of Src/STAT3/HO-1/autophagy signaling pathway might play a general role in protecting certain subtypes of breast cancer cells from DOX-induced cytotoxicity. Targeting this signaling event may provide a potential approach for overcoming DOX resistance in breast cancer therapeutics.

Analysis of miRNA expression profiling in human macrophages responding to Mycobacterium infection: induction of the immune regulator miR-146a.

OBJECTIVES: The regulatory mechanism of microRNA (miRNA) within macrophage innative response to Mycobacterium tuberculosis infection is not clear yet. METHODS: The expression profile of cellular miRNAs during Mycobacterium bovis BCG infection was analyzed by using microarray. The expression of miR-146a was evaluated in alveolar macrophages (AMs) of bronchoalveolar lavage solution from pulmonary tuberculosis (PTB) patients and healthy volunteers respectively. Inhibitor experiment and promoter analysis were used to investigate the pathway involved in the induction of miR-146a. Examination of miR-146a function in macrophages was performed by overexpression and inhibition of miR-146a. RESULTS: Among the altered miRNAs, 10 were downregulated whereas 8 were upregulated in M. bovis BCG-infected macrophage. MiR-146a was high expressed in cultured macrophage respond to M. bovis BCG but decreased in AMs of PTB patients, and stated a negative correlation with degree of smear-positive. Nuclear factor-κB pathway was required for the induction of miR-146a. Overexpression of miR-146a results in significant reduction of PTGS2 and enhanced the killing ability of THP-1 cells to intracellular M. bovis BCG, and miR-146a negatively regulated TNF-α release in feedback manner. CONCLUSIONS: Our findings suggest an important role of miR-146a in M. bovis BCG infection that helps to fine-tune the inflammation response of MTB infection.

MicroRNA-146a negatively regulates PTGS2 expression induced by Helicobacter pylori in human gastric epithelial cells.

BACKGROUND: Helicobacter pylori is a major human pathogenic bacterium in the gastric mucosa, but to date the regulatory mechanism of the H. pylori-induced inflammatory response is not clear. MicroRNAs have recently emerged as key post-transcriptional regulators of gene expression. We have previously reported that miR-146a negatively regulates the H. pylori-induced inflammatory response, but its molecular mechanism is just beginning to be explored. Our aim was to further explore the key targets of miR-146a and its role of regulation in H. pylori infection. METHODS: The potential targets of miR-146a were screened through bioinformatic approaches and identified by luciferase reporter assays and green fluorescent protein (GFP) repression experiments. Overexpression and inhibition of miR-146a were used to examine the impacts of miR-146a on its target gene, determined by quantitative real-time polymerase chain reaction (PCR) and western blotting. RESULTS: Prostaglandin endoperoxide synthase 2 (PTGS2) is a target gene of miR-146a, and miR-146a decreased PTGS2 expression by degradation of its mRNA, suggesting that the miR-146a-mediated inhibition is a post-transcriptional event. Furthermore, miR-146a and PTGS2 were significantly increased in H. pylori -infected human gastric epithelial cells. Overexpression of miR-146a resulted in significantly reduced PTGS2 production induced by H. pylori infection. CONCLUSIONS: These results suggest that miR-146a may be involved in negatively regulating H. pylori-induced PTGS2 expression in human gastric epithelial cells.

MicroRNA-146a modulates TGF-ß1-induced phenotypic differentiation in human dermal fibroblasts by targeting SMAD4.

During wound healing and tissue repair the dermal fibroblast-to-myofibroblast transdifferentiation plays an important role, transforming growth factor-ß1 (TGF-ß1) is considered to be the main stimuli factor of transdifferentiation. MicroRNAs (miRNAs) have recently emerged as key post-transcriptional regulators of gene expression. The involvement of miRNAs and their roles in TGF-ß1-induced myofibroblast transdifferentiation remains to be determined in detail. The current study found that the expression of miR-146a was upregulated in human dermal fibroblasts cells in response to TGF-ß1 stimulation in dose-dependent manner by quantitative RT-PCR. Bioinformatic analyses predict that signaling effectors mothers against decapentaplegic protein 4 (SMAD4) is a miR-146a target gene. Luciferase assay demonstrated that miR-146a mimics suppressed SMAD4 3'-UTR reporter construct activity. Furthermore, miR-146a overexpression in dermal fibroblast did not decrease target mRNA levels, but significantly reduced target protein expression. In addition, dermal fibroblasts transfected with miR-146a mimics exhibited attenuated TGF-ß1 -induced α-smooth muscle actin (α-SMA) expression compared with the control. This study demonstrated that miR-146a may function as a novel negative regulator to modulate myofibroblast transdifferentiation during TGF-ß1 induction by targeting SMAD4.

[Comparison of four imaging examinations of shoulder joint injury in forensic expertise].

OBJECTIVE: To compare the value of four imaging examinations, including the X-ray, CT, MRI and gas-iodine double contrast CT analyses, in the forensic expertise of shoulder joint injury. METHODS: Imaging data of shoulder joint injury, by the X-ray, CT, MRI and gas-iodine double contrast CT were retrieved and analyzed. RESULTS: The correct diagnosis rates of fracture and soft tissue injury by X-ray, CT and MRI were 52.8%, 72.0% and 63.2%, as well as 0.0%, 32.9% and 82.5%, respectively. The correct diagnosis rate of soft tissue injury by gas-iodine double contrast CT was 100%. CONCLUSION: X-ray is a useful screening method, CT is better for diagnosis of fracture, and MRI is fit for diagnosis of soft tissue injury. Gas-iodine double contrast CT can reflect not only the soft tissue injury but also its severity. Thus, combined application of X-ray, CT, MRI and gas-iodine double contrast CT can provide important imaging information for forensic expertise in shoulder joint injury.

[Forensic clinical analysis on 25 cases of traumatic cerebral infarction].

OBJECTIVE: To investigate characteristics of forensic clinical identification on traumatic cerebral infarction(TCI). METHODS: Twenty-five cases of TCI were analyzed retrospectively, including the general situation, location of infarction and clinical feature. RESULTS: TCI occurred primarily in children and elderly. All the cases had definite cerebral trauma which was located mainly in the regions of basal ganglia-internal capsule, frontal, temporal and parietal cerebral cortex. CONCLUSION: The consequence of TCI has direct correlation with location of cerebral infarction. More attention should be paid to this issue in forensic practice.

[Effects of triptolide on hypothalamic-pituitary-adrenal axis of rats].

OBJECTIVE: To observe the effects of triptolide on the hypothalamic-pituitary-adrenal axis (HPAA) of rats in light of morphological and functional changes. METHODS: Thirty Sprague-Dawley (SD) male rats were randomized into 3 groups and given 2% propylene glycol, mixture of propylene glycol and prednisone acetate or compounds of propylene glycol and triptolide by gavage, respectively, for consecutive 7 weeks. Determination in the 3 groups was conducted concerning the contents of blood plasma cortisol (COR), adrenocorticotropic hormone (ACTH) and corticotropin-releasing hormone (CRH) besides measurement of the rats' body weight, coefficient of the adrenal gland and observation of the histopathological changes in fascicular zone of adrenal cortex. Immunohistochemical staining technique was used to detect the expression of ACTH in pituitary in the 3 groups. RESULTS: (1) The content of COR in the groups of triptolide and prednisone acetate appeared lower and serum ACTH showed no significant difference, but CRH in the group of triptolide was augmented as compared with the control group (P < 0.05). (2) The rats' weight in the groups of triptolide and prednisone acetate was declined, and yet, the coefficient of the adrenal gland remained no significant change in comparison with the controls. HE staining and electron microscopy examination revealed thinned and constricted zona fasciculata in adrenal gland in the rats of triptolide and prednisone acetate, with hypofunction. ACTH expression in the group of triptolide was higher than that of the control group (P < 0.05). CONCLUSION: Morphologically and functionally, the findings suggest that long-term use of triptolide may result in atrophied cortex and hypofunction of the adrenal gland, leading to augmented production and secretion of CRH and ACTH from respective hypothalamic and pituitary.

[The pathological observation of acute intoxication by Alangium Chinese in mice].

OBJECTIVE: To investigate the pathological change of mice organ intoxicated by Alangium Chinese and its poisoning mechanism. METHODS: Mice were intoxicated by gavage with extract of Alangium Chinese. Then the histopathologic examination was made for evaluating the pathological changes in the organs of the poisoned mice by HE staining. RESULTS: The main pathological changes included alveolar hemorrhage, pulmonary interstitial hemorrhage, sinus hepaticus expansion and congestion, hepatocyte edema, subarachnoid hemorrhage, congestion and hemorrhage of other organs. CONCLUSION: The main target organs or tissue of Alangium Chinese are the lungs, liver and vascular smooth muscle. There is correlation between the toxic effect and the dosage.

[The value of TNFalpha testing in evaluation of death due to drug anaphylactic shock].

OBJECTIVE: To analyze the changes of the serum TNFalpha level in cadavers of drug anaphylactic shock(DAS) and to explore the significance of the TNFalpha testing in evaluation of death caused by DAS. METHODS: The level of serum TNFalpha from cardiac blood was determined by double antibody-sandwich ELISA method. RESULTS: The level of TNFalpha in the experimental group was (131.6+/-9.4) pg/mL, while the level in the infectious diseases control group and the normal control group were (87.3+/-6.4) pg/mL and (17.2+/-4.5) pg/mL, respectively. There was statistically significant difference among the groups (P<0.05). CONCLUSION: The serum TNFalpha level may be used as one of the indexes for evaluation of death caused by highly suspected drug anaphylactic shock.

An improved method for refolding recombinant decay accelerating factor for therapeutic studies.

Decay accelerating factor (DAF) is a very potent complement regulatory protein which holds promise for clinical usage. Here we report on an improved procedure for refolding both rat and human DAF over-expressed in Escherichia coli. It was shown that 50-70% of the inclusion body could be refolded to soluble active protein. This method excludes the use of L-arginine, which is expensive, and can be used to prepare a large quantity of recombinant DAF for therapeutic studies.

(E)-4-[(4-Amino-5-bromo-pyridin-3-yl)-iminometh-yl]phenol.

In the mol-ecule of the title compound, C(12)H(10)BrN(3)O, the pyridine and benzene rings are oriented at a dihedral angle of 34.93 (3)°. Intra-molecular N-H⋯N and N-H⋯Br hydrogen bonds result in the formation of two non-planar five-membered rings. In the crystal structure, inter-molecular O-H⋯N and N-H⋯O hydrogen bonds link the mol-ecules to form a three-dimensional network.

[Apoptosis in myocardial cells after macleaya cordata total alkaloids poisoning in rats].

OBJECTIVE: To observe pathological changes and apoptosis in rats myocardial cells after Macleaya cordata total alkaloids poisoning, and to provide some references for Macleaya cordata total alkaloids poisoning detection. METHODS: An experimental model of Macleaya cordata total alkaloids poisoning was established, and the technology of TUNEL staining was used.The results were analyzed by computer image analysis competitive system. RESULTS: Quantities of apoptosis in myocardial cells in poisoning groups were much more than those in the control groups at different tages (P<0.01). In addition the quantities of apoptosis were different after different poisoning duration. CONCLUSION: Although clinical symptoms was not obvious and could not be detected by poison analysis. Pathological changes induced by Macleaya cordata total alkaloids could be found through the apoptosis detection.