OBJECTIVETo study the changes of platelet in May-Hegglin anomaly (MHA) and the molecular pathogenesis mechanism.

METHODSPeripheral blood was drawn from the MHA proband, her father and her uncle. Platelet count and morphology were examined by automatic blood cell counter and microscopy, respectively. The platelet membrane protein was examined by flow cytometry. Membrane antibodies were determined by ELISA. PCR was used to amplify the exons 25, 31 approximately 32, 38 and 40 of the MYH 9 gene in the MHA patient and her diseased father. Furthermore, PCR products were sequenced, a specific point mutation was identified and inclusions (Dohle's body) in the neutrophil was detected by indirect immunofluorescence technique.

RESULTSIt was proved that in MHA patients, platelet count was higher by cell counter than by microscope (P < 0.01). Giant platelet was 94% but platelet membrane proteins (CD41, CD61, CD42A, CD42b) were in normal range. Membrane antibodies was undetectable. An A5521G mutation (GAG-->AAG) in the exon 38 was found in the proband and her diseased father, resulting in a characteristic change of NMMHC-A1841 (Glutamic acid-->Arginine), which was not found in other members of the family and in normal controls. Spindle-like inclusions with fluorescence were clearly displayed in neutrophil cytoplasm.

CONCLUSIONThe molecular pathogenesis mechanism of May-Hegglin anomaly is the mutation in MYH 9 gene.

Adult ; Base Sequence ; Blood Platelets ; metabolism ; pathology ; DNA Mutational Analysis ; Enzyme-Linked Immunosorbent Assay ; Female ; Flow Cytometry ; Granulocytes ; metabolism ; pathology ; Humans ; Inclusion Bodies ; metabolism ; pathology ; Male ; Molecular Motor Proteins ; genetics ; Mutation ; Myosin Heavy Chains ; genetics ; Pedigree ; Platelet Count ; Platelet Membrane Glycoproteins ; metabolism ; Thrombocytopenia ; blood ; genetics ; pathology

OBJECTIVETo study the clinical significance of changes of serum myocardial enzymes in patients with acute carbon monoxide poisoning.

METHODSTo determine the dynamic changes of the activity of myocardial enzymes and ECG in 62 patients with acute CO poisoning.

RESULTSIn patients with acute CO poisoning 5 kinds of myocardial enzymes begin to increase within 24 hours, the activities of aspartate aminotransferase (AST), creatine phosphokinase (CPK), lactic dehydrogenase (LDH), alpha-hydroxybutyrate dehydrogenase (alpha-HBDH), CPK isoenzyme (CK-MB) were (20.2 +/- 12.3), (151.6 +/- 91.8), (146.8 +/- 50.4), (154.8 +/- 47.7), (13.8 +/- 8.1) U/L respectively, while those in control group were (12.1 +/- 6.7), (90.6 +/- 17.3), (118.7 +/- 13.5), (89.9 +/- 27.9), (5.9 +/- 3.3) U/L respectively. There was significant difference between two groups (P < 0.01); 3 d later, the activities of 5 enzymes were still increased [(21.3 +/- 12.3), (105.8 +/- 51.4), (144.8 +/- 51.4), (159.8 +/- 35.4), (16.2 +/- 9.1) U/L respectively]. 7 and 12 d later, the activities of alpha-HBDH and CK-MB were still higher than those of control (P < 0.01). LDH(1) and LDH(2) increased to peak value in 24 h after poisoning (35.3 +/- 5.8), (43.8 +/- 5.7) U/L vs (24.8 +/- 3.9), (36.9 +/- 4.3) U/L, P < 0.01. The abnormal rate of serum LDH(1) was 78.7%, LDH(2) 58.3%, LDH 45.2%, CK-MB 37.1%, alpha-HBDH 33.6% and the abnormal rate of ECG was less than 10%.

CONCLUSIONAcute carbon monoxide poisoning may cause myocardial injury. Determination of serum myocardial enzymes may contribute to showing myocardial injury, early diagnosis and treatment, results of treatment and prognosis.

Adult ; Carbon Monoxide Poisoning ; blood ; enzymology ; Creatine Kinase ; blood ; Creatine Kinase, MB Form ; Female ; Humans ; Hydroxybutyrate Dehydrogenase ; blood ; Isoenzymes ; blood ; L-Lactate Dehydrogenase ; blood ; Male ; Middle Aged ; Myocardium ; enzymology

This study was aimed to investigate the effect of recombinant mutant human TNF-related apoptosis-inducing ligand (rmhTRAIL) combined with As(2)O(3) on inducing apoptosis of adriamycin-resistant leukemia cell line K562/A02 (mdr-1(+)). The morphologic changes of cells treated with rmhTRAIL were observed by inverted microscope, taking adriamycin-sensitive cell line K562 (mdr-1(-)) as control; the inhibitory rate of cell proliferation after being treated with rmhTRAIL, As(2)O(3) alone or combined was assayed by MTT method; the apoptosis peaks of K562/AO2 and K562 were quantitatively detected by flow cytometry with PI staining after being treated with rmhTRAIL, As(2)O(3) alone or in combination. The results indicated that the inhibition effect of rmhTRAIL and As(2)O(3) in combination on K562/AO2 and K562 cells was higher than that of riTRAIL and As(2)O(3) alone (p < 0.01), rmhTRAIL combined with As(2)O(3) had synergistic effect in killing K562/AO2 and K562 cells by king's formula. The apoptosis rates of K562/AO2 and K562 cells were 34.93 +/- 0.10% and 10.53 +/- 0.16% (p < 0.01), as well as 5.95 +/- 0.07%, and 3.50 +/- 0.01% (p < 0.05), 50.95 +/- 0.91% and 20.75 +/- 0.95% (p < 0.05) respectively when their cells were treated by rmhTRAIL and As(2)O(3) alone. The apoptosis rate in K562/AO2 group was higher than that in K562 group. It is concluded that rmhTRAIL can induce K562/A02 and K562 cell apoptosis; rmhTRAIL combined As(2)O(3) had synergistic effects; the efficacy of on rmhTRAIL or As(2)O(3) inducing K562/AO2 cell apoptosis is higher than that on their parental cell line K562.
Apoptosis ; drug effects ; Arsenicals ; pharmacology ; Doxorubicin ; pharmacology ; Drug Resistance, Multiple ; drug effects ; Drug Resistance, Neoplasm ; drug effects ; Drug Synergism ; Humans ; K562 Cells ; Oxides ; pharmacology ; Recombinant Proteins ; pharmacology ; TNF-Related Apoptosis-Inducing Ligand ; pharmacology

The main causes of death for paraquat poisoning are irreversible pulmonary fibrosis, respiratory failure and even multiple organ failure. Currently, the main clinical treatment methods are gastric lavage, catharsis, blood purification and symptomatic supportive treatment, but the effectiveness is not satisfactory. It has made some progress in clinical treatment of paraquat poisoning and the study of molecular mechanisms at home and abroad. The article simply reviews in the clinical treatment of pulmonary fibrosis induced by paraquat poisoning such as blood purification, antioxidants, glucocorticoid, Chinese medicine treatment, and the molecular mechanism research such as epithelial-mesenchymal transition, Wnt/β- catenin pathway, the NF-κB pathway and Akt-Nrf-2 pathways.

Objective:To observe clinical efficacy of Lung-toxin dispelling formula No.1 treating patients of corona virus disease 2019(COVID-19) type severe/type extremely severe, and summarize experiences of diagnosis and treatment. Method:Collected and analyzed clinical informations of patients of COVID-19 type severe/type extremely severe, treated with Lung-toxin dispelling formula No.1, who were hospitalized in central hospital in Zhumadian and the first affiliated hospital of Henan university of traditional Chinese medicine from 31^st January to 27^th February. Result:All patients had positive epidemiological history, major symptoms were fever, cough, tachypnea, weakness and sore heavy muscles, combined with bad appetite and diarrhea. The median age was 59, median time from onset to getting worse was 9 days, ground glass opacity, lamellar, nodular high density shadow were mostly displayed in both lungs， lesions progressedfaster. After treatment with Lung-toxin dispelling formula No.1 combined with western medicine, the median time of PCR-NAD-test from positive to negative was 16 days, the median hospitalization days were 20 days, all patients were cured and discharged. Conclusion:Lung-toxin dispelling formula No.1 had certain clinical efficiency in treating patients of COVID-19 type severe/type extremely severe, further large sample clinical verification is needed.