A Chinese patient with the clinical features of Parkinson's disease contains a single copy of octarepeat deletion in PRNP case report.

Insertion or deletion of single copy of octapeptide repeat (OR) in human PrP protein are considered as polymorphism, while of insertions of more numbers of OR and deletion of two copies of OR are associated with genetic prion diseases.Here, we reported a 58-year-old female patient who displayed clinical manifestations of Parkinson's disease (PD) but contained deletion mutation of single copy of OR in one PRNP allele. The patient complained involuntary tremor of left upper limb for 18 months and her symptoms aggravation for 6 months at the time referring to Chinese National CJD surveillance system. The tremor was pronounced at rest, exacerbated by stress and disappear during sleep. Her symptoms were partially relieved after receiving medicament for PD. Neurological examination recorded involuntary movement of left hand and gear-like muscle tension of left upper limb. Coordination movement reported positive of Romberg sign and unstable in heel-keen test. EEG recorded a mild abnormality, but without periodic sharp wave complexes (PSWC). MRI showed a mild write matter demyelination. CSF protein 14-3-3 was negative. PRNP sequencing revealed heterozygosity of single copy deletion on ORs (R1-2-3-4/R1-2-2-3-4).No family history of neurodegenerative disease was recorded. Such case with a single copy of OR deletion in PRNP displaying the feature of PD is rarely reported in Chinese mainland.

Novel Perbutyrylated Glucose Derivatives of (-)-Epigallocatechin-3-Gallate Inhibit Cancer Cells Proliferation by Decreasing Phosphorylation of the EGFR: Synthesis, Cytotoxicity, and Molecular Docking.

Lung cancer is one of the most commonly occurring cancer mortality worldwide. The epidermal growth factor receptor (EGFR) plays an important role in cellular functions and has become the new promising target. Natural products and their derivatives with various structures, unique biological activities, and specific selectivity have served as lead compounds for EGFR. D-glucose and EGCG were used as starting materials. A series of glucoside derivatives of EGCG (7-12) were synthesized and evaluated for their in vitro anticancer activity against five human cancer cell lines, including HL-60, SMMC-7721, A-549, MCF-7, and SW480. In addition, we investigated the structure-activity relationship and physicochemical property-activity relationship of EGCG derivatives. Compounds 11 and 12 showed better growth inhibition than others in four cancer cell lines (HL-60, SMMC-7721, A-549, and MCF), with IC50 values in the range of 22.90-37.87 µM. Compounds 11 and 12 decreased phosphorylation of EGFR and downstream signaling protein, which also have more hydrophobic interactions than EGCG by docking study. The most active compounds 11 and 12, both having perbutyrylated glucose residue, we found that perbutyrylation of the glucose residue leads to increased cytotoxic activity and suggested that their potential as anticancer agents for further development.

Synthesis, antitumor activity, and molecular docking of (-)-epigallocatechin-3-gallate-4ß-triazolopodophyllotoxin conjugates.

Two new (-)-epigallocatechin-3-gallate-4ß-triazolopodophyllotoxin conjugates (7 and 8) were synthesized and evaluated for biological activity. Compound 8 showed highly potent anticancer activity against A-549 cell line with IC50 of 2.16 ± 1.02 µM, which displayed the highest selectivity index value (SI = 14.5) in A-549 cells. Molecular docking indicated that compound 8 could bind with the active site of Top-II. Therefore, compound 8 might be a promising candidate for further development.

Rhodium-Catalyzed Direct Bis-cyanation of Arylimidazo[1,2-α]pyridine via Double C-H Activation.

An efficient Cp*Rh(III)-catalyzed selective bis-cyanation of arylimidazo[1,2-α]pyridines with N-cyano-N-phenyl-p-methylbenzenesulfonamide via N-directed ortho double C-H activation has been developed. The reaction proceeds with broad functional group tolerance to furnish various cyanated imidazopyridines in high yields. The current methodology exhibits unique characteristics, including high bis-cyanation selectivity, operational convenience, and gram-scale production.

A large outbreak of acute gastroenteritis caused by the human norovirus GII.17 strain at a university in Henan Province, China.

BACKGROUND: Human noroviruses are a major cause of viral gastroenteritis and are the main etiological agents of acute gastroenteritis outbreaks. An increasing number of outbreaks and sporadic cases of norovirus have been reported in China in recent years. There was a large acute gastroenteritis outbreak at a university in Henan Province, China in the past five years. We want to identify the source, transmission routes of the outbreak by epidemiological investigation and laboratory testing in order to provide the effective control measures. METHODS: The clinical cases were investigated, and analysed by descriptive epidemiological methods according to factors such as time, department, grade and so on. Samples were collected from clinical cases, healthy persons, the environment, water, and food at the university. These samples were tested for potential bacteria and viruses. The samples that tested positive for norovirus were selected for whole genome sequencing and the sequences were then analysed. RESULTS: From 4 March to 3 April 2015, a total of 753 acute diarrhoea cases were reported at the university; the attack rate was 3.29%. The epidemic curve showed two peaks, with the main peak occurring between 10 and 20 March, accounting for 85.26% of reported cases. The rates of norovirus detection in samples from confirmed cases, people without symptoms, and environmental samples were 32.72%, 17.39%, and 9.17%, respectively. The phylogenetic analysis showed that the norovirus belonged to the genotype GII.17. CONCLUSIONS: This is the largest and most severe outbreak caused by genotype GII.17 norovirus in recent years in China. The GII.17 viruses displayed high epidemic activity and have become a dominant strain in China since the winter of 2014, having replaced the previously dominant GII.4 Sydney 2012 strain.

[Sources and Characteristics of Regional Background PM1 in North China During the Autumn and Winter Polluted Period].

The campaign of investigating the chemical compositions and particle size distributions of NR-PM1(non-refractory PM1) was conducted by using a High Resolution Time of Flight Aerosol Mass Spectrometer(HR-ToF-AMS) at the Shangdianzi(SDZ) regional atmospheric background site(117.07°E, 40.39°N), northeast of Beijing, from October 17th 2015 to January 27th 2016. The results showed that organics was the main component of PM1, and the proportion of nitrate was higher than that of sulfate in autumn and winter. The mean mass-resolved size distributions for the main components displayed accumulation mode. The wider organic peak shape and larger nitrate peak size indicated that the organics contributed to both small and large particles at the beginning of the particle formation, growth and aging processes, while most of nitrate particles preferred to grow into large particles during the aging process. The ratios of elements between OM and OC, O/C and H/C were calculated as 1.91, 0.58 and 1.58 respectively. The slope of Van Krevelen diagram of organic aerosols during polluted episode was -0.21, whose oxidation state was higher than those of other city sites. Nitrate was the major contributor of NR-PM1 during the polluted period, while organics was significantly higher than that during clean period. The results of back trajectories analysis demonstrated that the air masses were complex during the pollution episode. The northwest wind from central Inner Mongolia and Siberia dominated the clean episodes, which was conducive to the spread of pollutants.

The Features of Genetic Prion Diseases Based on Chinese Surveillance Program.

OBJECTIVE: To identify the features of Chinese genetic prion diseases. METHODS: Suspected Creutzfeldt-Jakob disease (CJD) cases that were reported under CJD surveillance were diagnosed and subtyped using the diagnostic criteria issued by the WHO. The general information concerning the patient, their clinical, MRI and EEG data, and the results of CSF 14-3-3 and PRNP sequencing were carefully collected from the database of the national CJD surveillance program and analyzed using the SPSS 11.5 statistical software program. RESULTS: Since 2006, 69 patients were diagnosed with genetic prion diseases and as having 15 different mutations. The median age of the 69 patients at disease onset was 53.5 years, varying from 19 to 80 years. The majority of patients displaying clinical symptoms were in the 50-59 years of age. FFI, T188K gCJD and E200K were the three most common subtypes. The disease appeared in the family histories of 43.48% of the patients. The clinical manifestations varied considerably among the various diseases. Patients who carried mutations in the N-terminus displayed a younger age of onset, were CSF 14-3-3 negative, had a family history of the condition, and experienced a longer duration of the condition. The clinical courses of T188K were significantly shorter than those of FFI and E200K gCJD, while the symptoms in the FFI group appeared at a younger age and for a longer duration. Moreover, the time intervals between the initial neurologist visit to the final diagnosis were similar among patients with FFI, T188K gCJD, E200K gCJD and other diseases. CONCLUSION: The features of Chinese genetic prion diseases are different from those seen in Europe and other Asian countries.

[Epidemiological analysis of imported malaria prevalence in Luoyang City from 2010 to 2013].

OBJECTIVE: To understand the epidemiological characteristics of imported malaria in Luoyang City, so as to provide the evidence for malaria prevention and control in this city. METHODS: The Epidemic situation data from network reports, as well as the case survey and the epidemiological investigation data of imported malaria were collected and analyzed in Luoyang City from 2010 to 2013. RESULTS: A total of 98 imported malaria cases were reported in Luoyang City from 2010 to 2013, including 35 cases of vivax malaria, 57 cases of falciparum malaria, 4 cases of ovale malaria and 2 cases of quartan malaria. All the cases were confirmed by laboratory detection. Seventy-one cases (72.44%) returned from African countries, and 27 (27.55%) cases returned from Southeast Asian countries. The majority cases were young man, and 78.57% of the cases were diagnosed by different levels of centers for disease control and prevention. There was no significant seasonal variation in onset time. The median time from onset to seeing doctor was 6 days. CONCLUSIONS: The epidemic situation of imported malaria is quite serious in Luoyang City. It is necessary to further strengthen the professional training and multi-sectoral cooperation, and take effective pre- vention and control measures to reduce the hazard of imported malaria.

Rare V180I mutation in PRNP gene of a Chinese patient with Creutzfeldt-Jakob disease.

Abstract Here, we reported a Chinese case of Creutzfeldt-Jakob disease (CJD) with a rare mutation in the prion protein gene (PRNP) leading to an exchange of amino acid from valine (V) to isoleucine (I) at codon 180 (V180I). The 72 year-old Chinese women started with gradual memory loss. On admission, she did not present special abnormality during clinical examinations except bradykinesia in her lower extremities. Myoclonic jerks and increased muscle tone were noticed 3 months after the onset. No periodic activity was recorded at electroencephalography (EEG) and 14-3-3 protein was negative in the cerebrospinal fluid (CSF) sample. Brain diffusion weighted images (DWI) demonstrated high signal intensities in bilateral frontal, parietal, temporal and occipital cortices, especially on the left hemisphere, and high signal intensities were also seen in the left caudate nucleus and the putamen. The patient had no family history of similar symptoms. Her general condition was gradually deteriorative, but the patient was still alive when we performed the follow-up 12 months after onset.

Clinical, histopathological and genetic studies in a family with fatal familial insomnia.

We compared clinical data from two related Chinese patients with fatal familial insomnia (FFI) and collected information about their pedigree. The clinical features in the two cases were similar and included initial progressive insomnia and sympathetic activation, which persisted throughout the clinical course. A total of 135 members of this family, across seven generations, were retrospectively investigated. Eleven family members, including the two FFI cases, were found to have died with similar neurological problems. Analysis of PRNP in 32 family members revealed eleven carrying the D178N allele, including the two FFI patients. Spongiform degeneration in brains was not found, but gliosis was obvious in the thalamus of the two cases at postmortem. Proteinase K-resistant prion protein (PrP) was not found in proband's brain by immunohistochemistry, but observed in some areas of brain for both cases by PrP-specific Western blot. Investigation of the pedigree has led to the identification of an additional 9 family members who had similar clinical symptoms and 9 currently healthy individuals with the D178N mutation.

[Studies on heredity rule of the first genealogy regarding fatal familial insomnia in Henan province].

OBJECTIVE: To investigate the epidemiological, genealogic characteristic, familial history of the families with fatal familial insomnia, its clinical and pathological features as well as the heredity rule of related genes. METHODS: 135 familial members of 7 eras were studied. Vein blood samples from patients as well as from some familial members were collected. PRNP gene was studied with PCR, its serial was determined and then authenticated with Nsp I . Brain tissue was obtained for neuropathological test and PrP(Sc) test with Western blot method. RESULTS: Clinical symptoms of the 2 diagnosed cases were typical. 11 familial members died of similar neural disease. 32 samples of their familial members, codon at D178N of PRNP of 11 members was mutated, with mutation rate as 34.38% while D129N showed as methionine. Brain tissue of both probands denaturalized into spongiform and the nerve fiber was absent but PrP(Sc) protein was identified. CONCLUSION: Genealogy was described in the family with fatal familial insomnia since the patients had typical clinical symptoms and pathological characteristics. It seemed necessary to confirm cases of fatal familial insomnia and their genealogy with epidemiological data and to investigate its gene characteristics as well as with neuropathological and Western blot tests.

[Analysis for clinical and genetic characteristics of a sporadic FFI case].

OBJECTIVE: To report and study a case of sporadic family fatal insomnia (SFFI) on its. METHODS: Investigate clinical characteristics and family disease history of a suspect FFI patient. His clinical characteristic was analyzed, he and his 14 family members genomic DNA was extracted by standard techniques from their and blood detected with polymerase chain reaction (PCR) method and DNA sequencing to find out his prion protein (PrP) gene mutation. The patient's CSF was detected with Western-Blot method for 14-3-3 brain protein. RESULTS: The patient was diagnosed as an sporadic FFI by his developed sleep disturbance and changes in sleep-awake rhythm, motor abnormalities, mental disorder, dementia, autonomic dysfunction; his family history; his 14-3-3 brain protein-positive (CSF) and analysis results of his PrP gene (codon point mutation D178N and methionine homozygosity at position 129M/M). Suggesting that in the future to identify CJD and FFI patients, screening should focus on clinical symptoms and laboratory results. The PrP gene of 14 family members did not appear Mutation, and there is no person suffering from the same disease. CONCLUSIONS: The case was diagnosed as a sporadic familial fatal insomnia. Analysis of suspicious patients' genomic DNA for PrP gene mutation might be very important for FFI diagnosis because there exist many difficulties in clinical laboratory evaluation. This patient might be the first SFFI patient reported in China and the case finding might have momentousness in clinical and basical study.

[Surveillance on Rickettsia in epidemic areas of scrub typhus in Xinyang areas of Henan].

OBJECTIVE: To understand the epidemic status of Rickettsia in Xinyang areas of Henan province. METHODS: Samples including liver, spleen, kidney from mouse and chigger mites from Xinyang areas and serum samples were detected by nested-polymerase chain reaction (PCR) and indirect immunofluorescence assay (IFA). RESULTS: In 62 viscus samples from mice organs, the positive rates were 16.13%, 8.06% and 6.45% for Orientia tsutsugamushi, R. typhii and Spotted fever group rickettsiae respectively. In blood clots samples from mice, the positive rates were 8.06%, 6.45% and 1.61 % for O. tsutsugamushi, R. typhii and Spotted fever group rickettsiae respectively. Three out of 26 mouse serum samples were positive for the predicted fluorexcent intensity O. tsutsugamushi. CONCLUSION: Using nested-PCR and IFA methods, O. tsutsugamushi, R. typhii and Spotted fever group rickettsiae were detected in the captured mice living in Xinyang areas of Henan province. Results showed that there were intensive natural reserviors of Rickettsia in Henan province, suggesting that the risk of outbreak of Rickettsia in these areas was high.

Study on the pathophysiologic basis of classification of 'spleen' deficiency in chronic gastritis.

BACKGROUND: Most of the studies on traditional Chinese medicine (TCM) 'spleen' deficiency syndrome in the recent 30 years were conducted only on the basis of single functional index, neglecting the study on the pathophysiologic internal relationship between spleen deficiency syndrome and gastric diseases in modern medicine. But it was at the subcellular molecular biological level that we explored the pathophysiologic basis of classification of spleen deficiency in chronic gastritis by detecting the bioactive substances in gastric mucosa nuclei and mitochondria. METHODS: By means of optical microscope, scanning electron microscope (SEM), transmission electron microscopy (TEM) and histochemical staining, we conducted histopathological, subcellular ultrastructural analysis and nuclei and mitochondrial ultrastructural analysis of gastric mucosa of 188 spleen deficiency patients and of 42 voluntary blood donors. At the same time, bioactive substances were measured by means of X-ray energy dispersive analysis system (EDAX) image analysis system, radioimmunoassay method and chemiluminescence method. RESULTS: The content of cAMP, superoxide dismutase (SOD), Zn and Cu in gastric mucosa, and the content of Zn and Cu in mitochondria decreased progressively in order of groups: healthy control (HC), spleen Qi deficiency without organic lesion (F-SQD), spleen Yang deficiency without organic lesion (F-SyangD), disease without symptoms group, spleen Qi deficiency with organic lesion (G-SQD), spleen Yang deficiency with organic lesion (G-SyangD), spleen Yin deficiency (SyinD) and spleen deficiency with Qi stagnation (SDQS), chronic spleen deficiency gastritis (CSG) and chronic atrophic gastritis (CAG); decreased in order of HC, intestinal metaplasia (IM)Ia, IMIb, IMIIa and IMIIb, P < 0.05. The content of DNA, Zn and Cu in nuclei progressively increased in order mentioned above, P < 0.05. CONCLUSIONS: The quantitative changes of gastric mucosal cAMP, SOD, Zn, Cu, of mitochondrial Zn, Cu and of nuclear DNA, Zn and Cu are not only the substance base on which the lesion of gastric mucosa tissue structure occurs, but also the substance base on which spleen deficiency is classified. G-SQD and G-SyangD were more likely to be found in low-grade or middle-grade CSG and CAG, while SyinD and SDQS in middle-grade or high-grade CSG, CAG and IMIIb.

Effect of Weikangfu granule on the physiopathologic figure of precancerosis of gastric mucosa in patients of chronic gastritis with Pi-deficiency syndrome.

OBJECTIVE: To study the physiopathologic basis of Weikangfu Granule (WKFG) in treating precancerosis of gastric mucosa in patients of chronic gastritis with Pi-deficiency syndrome (CG-PDS). METHODS: One hundred and fifteen patients of CG-PDS who suffered from intestinal metaplasia (IM) and atypical hyperplasia (ATHP) of gastric mucosa, were divided into two groups. The treated group (n = 61) was treated by WKFG with its ingredients modified according to the syndrome type of patients. The control group (n = 54) was treated with Weishu granule. The histopathological and subcellular ultrastructural changes were detected by optical microscope, screening electronic microscope, transmission electronic microscope and histochemical staining; the nuclear and mitochondrial ultrastructure of gastric mucosa were analyzed with energy dispersion X-ray analyser and image analysis system. And the changes of cAMP, lipid peroxide (LPO), superoxide dismutase (SOD) before and after treatment in the treated group were measured and compared with those of the health control group consisting of 15 volunteers. RESULTS: The symptomatic and pathological therapeutic effect in the treated group were significantly superior to those in the control group (P < 0.05). The contents of Zn, Cu, cAMP, SOD and (3)H-TdR LCT in gastric mucosa of the treated group before treatment were all lower than those of the healthy control group, yet all these indexes markedly increased after treatment, while serum LPO level, which increased before treatment was lowered after treatment. All the changes showed statistical significance (P < 0.05 or P < 0.01). CONCLUSION: WKFG can reverse IM and ATHP in patients of CG-PDS, and the effect may be realized by way of increasing the level of Zn, Cu, cAMP and SOD in gastric mucosa, promoting cell differentiation, enhancing cellular immunity and reducing oxygen free radicals and lipid peroxidation.

Study on the pathological basis of classification of spleen deficiency in chronic gastritis.

BACKGROUND: Spleen in Traditional Chinese Medicine (TCM) is not actually the spleen in the anatomic sense designated in western medicine because its functions basically belong to the physiological category of digestive system in modern medicine, and it represents a macroscopic concept of digestion, absorption and nutrition metabolism. Spleen deficiency syndrome refers to the clinical phenomena such as hypofunction of digestion, absorption and nutrition metabolism. By integrating TCM with modern medicine, this paper is intended to explore the pathological basis of classification of spleen deficiency in chronic gastritis. METHOD: By means of optical microscope, scanning electron microscope (SEM), transmission electron microscope (TEM) and histochemical staining, we conducted histopathological and subcellular ultrastructural (nuclei and mitochondrial) analysis of gastric mucosa of 188 patients of spleen deficiency, and that of 42 voluntary blood donors without clinical symptoms. RESULTS: The gastric mucosa of patients with spleen Qi deficiency (SQD) and spleen yang deficiency (SyangD) could either be affected by organic lesion (type G-occurring on the basis of chronic superficial gastritis (CSG), chronic atrophic gastritis (CAG)) or unaffected (type F-chiefly belonging to functional indigestion); spleen yin deficiency (SyinD) and spleen deficiency with Qi stagnation (SDQS) both occurred on the basis of CSG and CAG; and the degree of mucosa inflammatory cells infiltration, the degree of decrease in glands propria, and the incidence of IMIIb in CSG and CAG were more serious than those of G-SQD and G-SyangD, P < 0.05 - 0.01. CONCLUSION: Spleen deficiency syndrome is likely to occur on the basis of organic lesion of gastric mucosa (disease with symptoms of both CSG or CAG and spleen deficiency symptoms), as well as on the basis of inorganic lesion of gastric mucosa (nondisease with symptoms, which is, despite spleen deficiency symptoms, there is no CSG or CAG). Besides, the clinical phenomenon of disease without symptoms (despite CSG or CAG, there is no spleen deficiency symptoms) occurres because of such factors as genetic diathesis and compensation. The lesion degree of CSG or CAG and the incidence of IMIIb of SyinD and SDQS are more serious than those CSG and CAG of G-SQD and G-SyangD.

Study on the classification of chronic gastritis at molecular biological level.

AIM: To explore the pathophysiologibasis for the fact that patients with digestive tract symptoms do not necessarily have gastric mucosal pathology and those without clinical symptoms do not necessarily have no gastric mucosal pathology. METHODS: The ultrastructure, trace elements, cAMP, DNA, SOD and LPO in the gastric mucosa and its epithelial cells of 188 patients without organic lesions of heart, lung, liver, gallbladder, pancreas, kidney or intestine and basically histopathological normal persons (F) were detected synchronously by SEM, TEM, EDAX, Image analysis system RIA and (3)H-TdR Lymphocyte Transfer Test. RESULTS: The content of Zn, Cu, cAMP and (3)H-TdR LCT in gastric mucosa and the content of Zn, Cu, DNA and LPO in gastric mucosa epithelial nuclei of each group were shown as belows: Normal control (4.1+/-1.0, 5.2+/-0.8, 15.9+/-1.5, 1079.7+/-227.4, 7.6+/-0.4, 58.4+/-0.3, 12.6+/-2.7, 2.6+/-0.6); CSG without symptoms group (3.7+/-1.2, 5.1+/-1.8, 15.6+/-0.9, 924.5+/-234.9, 7.8+/-0.3, 58.6+/-0.4, 13.0+/-3.1, 2.9+/-0.4); CAG without symptoms group (3.3+/-1.0, 4.8+/-0.9, 14.9+/-0.7, 887.7+/-243.6, 7.8+/-0.3, 58.7+/-0.3, 14.3+/-2.8, 3.1+/-0.4); F type with symptoms group (3.5+/-1.4, 4.5+/-1.0, 15.7+/-1.4, 932.1+/-2449.3, 7.9+/-0.4, 58.7+/-0.5, 13.5+/-4.6, 2.9+/-0.7); CSG with symptoms group (2.8+/-1.9, 4.0+/-1.5, 14.2+/-1.8, 867.3+/-240.5, 8.1+/-0.5, 58.9+/-0.5, 15.2+/-3.2, 4.2+/-0.7); CAG with symptoms group (2.0+/-1.8, 3.4+/-1.5, 13.4+/-1.8, 800.9+/-221.8, 8.6+/-0.4, 59.3+/-0.5, 16.5+/-3.1, 4.5+/-0.6). The contents of Zn, Cu in mitochonondria and SOD in gastric mucosa of each group were shown as belows: Normal control group (9.2+/-0.5, 58.3+/-0.3, 170.5+/-6.1), CSG without symptoms group (8.9+/-0.5, 58.2+/-0.3, 167.2+/-5.3), CAG without symptoms group (8.8+/-0.4, 57.5+/-0.2, 166.1+/-4.2); F type with symptoms group (8.9+/-0.5, 58.0+/-0.3, 167.9+/-5.7), CSG with symptoms group (8.6+/-0.5, 57.8+/-0.3, 163.3+/-5.6); CAG with symptoms group (8.3+/-0.4, 57.5+/-0.3, 161.2+/-4.3). There were significant differences in these cases, P<0.05-0.001. There were synchronous changes of gastric mucosa epithelial cellular ultrastructure. The "background lesions" (focal atrophic gastritis, focal intestinal metaplasia, micro-ulcer) in nonfocal gastric mucosa of all groups had significant differences (P<0.05-0.001). CONCLUSION: Disease with symptoms, disease without symptoms, nondisease with symptoms occur on the basis of the quantitative changes of gastric mucosa epithelial cellular ultrastructure and related bioactive substances.

Ultrastructure and molecular biological changes of chronic gastritis, gastric cancer and gastric precancerous lesions: a comparative study.

AIM: To carry out a comparative study on ultrastructure and molecular biological changes of chronic gastritis (CG), gastric cancer (GC) aand gastric precancerous lesions. METHODS: By the use of histochemical staining, SEM with EDAX, TEM with EDAX, image analysis technique, RIA and chemiluminescence method, gastric mucosa of 168 patients were synchronously analyzed in morphology, trace elements, DNA, cAMP, SOD, (3)H-TdR LCT and serum LPO were also done. RESULTS: The incidence of epithelial nucleoplasmic ratio >1, lobulated nuclei, inter-chromatin aggregation of granules, nucleolar hypertrophy, and the content of DNA, Zn, Cu in nuclei and serum LPO of each group were showed as belows: normal control group (0.0, 0.0, 6.7, 0.0, 12.6+/-2.7, 7.6+/-0.4, 58.4+/-0.3, 2.6+/-0.6), CSG group (5.7, 2.9, 7.4, 2.9, 15.2+/-3.1, 8.1+/-0.5, 58.9+/-0.5, 4.2+/-0.7), CAG group (31.3, 29.7, 45.3, 42.2, 16.5+/-3.1, 8.6+/-0.4, 59.3+/-0.5, 4.5+/-0.6), CA group (100.0, 100.0, 72.2, 50.0, 30.7+/-8.2, 8.8+/-0.3, 59.5+/-0.4, 6.8+/-1.6), ATP(++) group (61.5, 38.5, 23.1, 38.5, 23.5+/-8.9, 8.3+/-0.4, 59.1+/-0.4, 5.1+/-1.2), IM(++)+ATP(++)group (77.8, 55.5, 33.3, 44.4, 25.1+/-7.2, 8.4+/-0.5, 59.5+/-0.4, 6.5+/-1.1), IM(+++)+ATP(++) group (100.0, 100.0, 75.0, 62.5, 28.5+/-9.1, 8.9+/-0.5, 59.7+/-0.4, 7.6+/-0.7), IMII(b) group (100.0, 62.5, 75.0, 50.0, 27.3+/-10.3, 8.6+/-0.3, 59.5+/-0.4, 6.1+/-0.9); whereas the content of Zn, Cu in mitochondria and cAMP, SOD in gastric mucosa, and (3)H-TdR LCT of each group were showen as belows: normal control group (9.2+/-0.5, 58.3+/-0.3, 15.9+/-1.5, 170.5+/-6.1, 1079.7+/-227.4), CSG group (8.6+/-0.5, 57.8+/-0.3, 14.6+/-1.8, 163.3+/-5.6, 867.3+/-240.5), CAG group (8.3+/-0.4, 57.5+/-0.3, 13.4+/-1.8, 161.2+/-4.3, 800.9+/-221.8), CA group (8.9+/-0.4, 57.1+/-0.3, 10.2+/-3.9, 152.2+/-3.8, 325.7+/-186.8), ATP(++) group (9.1+/-0.4, 57.0+/-0.3, 12.4+/-1.8, 161.5+/-3.8, 642.9+/-174.3), IM(++)+ATP(++) group (8.6+/-0.4, 56.9+/-0.3, 12.0+/-2.3, 152.2+/-2.5, 326.3+/-160.3), IM(+++)+ATP(++) group (8.5+/-0.3, 56.8+/-0.2, 10.4+/-0.9, 147.4+/-2.6, 316.1+/-170.7), IMII(b) group (8.6+/-0.3, 56.9+/-0.3, 11.9+/-1.9, 150.0+/-2.8, 318.9+/-145.8), there were significant differences between groups (P<0.05-0.01). CONCLUSION: There was a significant difference between CG and GC in their ultrastructure and molecular biology. Only on the condition of changes of internal environment in combination with the harmful effect of external environment, chronic atrophic gastritis can then develop into gastric cancer. Hence it might have similar epithelial cell ultrastructure and molecular biological changes in ATP(++), IMII(b) and cancer, hence there were similar patterns of occurrence, development and transformation. Recognition of this trend might help to explore problems of prevention and cure.