Objective To observe the effects of vitamin C (VC) and E (VE) on the uhrastrueture of liver, kidney and brain tissue of fluorosis rats. Methods One hundred and twenty Wistar rats were chosen as the experimental animals and were divided into 9 groups randomly. The control group were given distilled water and the fluoride exposed group were given distilled water containing sodium fluoride 150 mg/L. The throe VC-fluoride exposed groups were given VC orally in a dose of 50,100,150 mg·kg-1.d-1, respectively, and the three VE-fluoride exposed groups were given VE of 25,50,75 mg·kg-1·d-1, respectively. The VC-VE-fluoride exposed group were given VC of 100 mg·kg-1·d-1and VE of 50 mg·kg-1·d-1at the same time of high fluoride water intake. The rats were sacrificed after 9 months and the ultrastructure changes on liver, kidney and brain tissues of each group were observed under transmission electron microscope(TEM). Results The uhrastrueture of liver, kidney and brain showed pathologic changes in the rats that drank water containing high eoneentrations of sodium fluoride. ①Edema of hepatocytes, smeared mitochontria and nuclear matrix, lipid droplet in eytoplasm of hepatocytes, margination of nueleohs as well as obvious swelling of liver sinusoidal endothelial were observed in fluoride exposed group. ② There were marginafion of heterochromatin, expansion of cell space and endoplasmic reticulum in the kidney after the exposure to excess fluoride.③Signifieant changes were found on glial eells on the brain, including cell swelling, increase and marginafion of heterochromatin in the fluoride exposure group. There were no significant uhrastrueture changes in the VC or VE intervention group, while the VC-VE-fluoride exposure group was almost the same as the control group. Conclusions Fluoresis may cause damage on liver, kidney and brain in rats. VC and VE, alone or combined, have protective effects, and the combined supplementation was stronger than single supplementations.

OBJECTIVETo discuss the clinical effects of open reduction and internal fixation (ORIF) for treatment of patients with Lisfranc injury combined the second metatarsal base comminuted fracture.

METHODSFrom March 2007 to June 2012, 7 patients with Lisfranc injury combined the second metatarsal base comminuted fracture were treated including 5 males and 2 female aged from 22 to 51 years old (means 42 years), 4 of sprain and 3 of traffic injury. According Myerson classification, there was 1 case of type A, 3 of type B and 3 of type C. Kirschner wire was used to fix Lisfranc ligament placing from the medial cuneiform bone to the second metatarsal base during the operation. After the operation American Orthopaedic Foot and Ankle Society (AOFAS) criteria system were applied to evaluate the foot and ankle function. Preoperative and postoperative AP, lateral and oblique X-ray and CT scan were collected for radiographic evaluation.

RESULTSAll patients were followed up from 12 to 20 months (16.8 months in average). According to AOFAS criteria system, 3 cases were excellent result,3 good, 1 fair. All the wounds were primary healing without skin necrosis, infection, Kirschner loose,broken, or other complications.

CONCLUSIONKirschner wire had good clinical efficacy for fixing Lisfranc ligament injury with the second metatarsal base comminuted fracture, and could avoid arthrodesis.

Adult ; Bone Wires ; Female ; Humans ; Male ; Metatarsal Bones ; injuries ; surgery ; Middle Aged ; Tarsal Joints ; injuries ; surgery ; Wound Healing

OBJECTIVETo detect hot point mutations of ATP7B gene in Hunan Han patients with Wilson' disease (WD).

METHODSThe genomic DNA of 22 WD patients was extracted and exons 5, 8, 12, 13 were amplified by PCR. Screening for the mutations was done by direct sequencing and analysed by BLAST.

RESULTSFifteen of the 22 patients were found with mutations. Ten heterozygous Arg778Leu (2273G --> T) mutations were found in exon 8, all of them were accompanied with 2250C --> G polymorphism (Leu770Leu). Seven patients were found with 2855G --> A (Arg952Lys) polymorphism (4 heterozygous and 3 homozygous), 3 of them had Arg778Leu mutation in exon 8 and one with heterozygous mutation Gly943Asp (2828G --> A) in exon 12 simultaneously. Only one patient was found with heterozygous Pro992Leu (2975C --> T) mutation in exon 13. No mutations were found in exon 5.

CONCLUSIONArg778Leu is the hot point mutation of ATP7B gene in Hunan Han patients with Wilson' disease while exon 5 is not.

Adenosine Triphosphatases ; genetics ; Adolescent ; Asian Continental Ancestry Group ; genetics ; Cation Transport Proteins ; genetics ; Child ; Copper-transporting ATPases ; DNA ; genetics ; DNA Mutational Analysis ; Exons ; Hepatolenticular Degeneration ; ethnology ; genetics ; Humans ; Mutation

BACKGROUNDMany studies have suggested that angiotensin II (Ang II) and its receptors may be involved in the development of asthma. However, the expression of angiotensin II receptors (AGTR) is not clear in the lung tissue of chronic asthmatics. This study was designed to determine the relationship between airway remodeling, dysfunction and the expression of AGTRs in a rat model of asthma.

METHODSRats were sensitized with ovalbumin (OVA) for 2 weeks. Sixty minutes before an inhalation challenge, the rats were pretreated either with valsartan (15, 30, 50 mg x kg(-1) x d(-1)) or saline intragastrically. Then the rats received an OVA challenge for 30 alternative days. Acetylcholine (Ach)-induced bronchoconstriction was measured after the final antigen challenge. White cell counts in bronchoalveolar lavage fluid (BALF) and morphological changes in the airways were then assessed. The levels of transforming growth factor-beta 1 (TGF-beta(1)) and platelet-derived growth factor (PDGF) in BALF were detected by ELISA. The levels of AGTR1 and AGTR2 mRNA and protein in lung tissues were measured by RT-PCR and Western blotting.

RESULTSAGTR1 mRNA and protein levels in repeatedly OVA-challenged rats were significantly increased as compared with negative controls. The AGTR1 mRNA expression versus white cell counts of BALF and airway wall thickness (mainly in small airways) in lungs of chronic antigen-exposed rats were positively correlated. Valsartan decreased the level of AGTR1 in repeatedly OVA-challenged rats. However, AGTR2 mRNA and protein levels in the OVA-challenged rats and high-dose valsartan-treated rats (50 mg x kg(-1) x d(-1)) were also increased. Valsartan significantly decreased inflammatory cell accumulation and attenuated Ach-evoked bronchoconstriction in repeatedly antigen-challenged rats. Valsartan also decreased allergen-induced structural changes in rat airway (including total airway wall thickness and smooth muscle area) and the levels of TGF-beta(1) and PDGF in BALF.

CONCLUSIONSAGTR1 expression is potentially associated with airway remodeling and dysfunction in asthma. Ang II and AGTR1 may participate in airway inflammation and airway remodeling of chronic antigen-exposed rats. Valsartan, a AGTR1 antagonist, could inhibit AGTR1 expression and partially inhibits structural airway changes as well as airway inflammation in chronic OVA-exposed rats.

Angiotensin II Type 1 Receptor Blockers ; pharmacology ; Angiotensin Receptor Antagonists ; Animals ; Asthma ; chemically induced ; genetics ; metabolism ; Blotting, Western ; Bronchoalveolar Lavage Fluid ; chemistry ; Enzyme-Linked Immunosorbent Assay ; Gene Expression ; drug effects ; Lung ; drug effects ; metabolism ; pathology ; Male ; Ovalbumin ; Platelet-Derived Growth Factor ; metabolism ; Rats ; Rats, Wistar ; Receptor, Angiotensin, Type 1 ; genetics ; metabolism ; Receptor, Angiotensin, Type 2 ; genetics ; metabolism ; Receptors, Angiotensin ; genetics ; metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Tetrazoles ; pharmacology ; Transforming Growth Factor beta1 ; metabolism ; Valine ; analogs & derivatives ; pharmacology ; Valsartan

OBJECTIVETo investigate miRNA-221 expression in human colorectal carcinoma (CRC) cells and the effects of miR-221-specific inhibitor on the proliferation and apoptosis of CRC cells.

METHODSFour human CRC cell lines (HT-29, Lovo, SW-480, and CaCO2) were examined for miRNA-221 expression using real-time Q-PCR. The specific 2,-methoxy-modified RNA oligonucleotides of miR-221 (anti-miR-221) were synthesized and transfected into Caco2 cells via liposome, and the changes in the expression of miR-221 in the cells were detected by real-time Q-PCR. The proliferation and apoptosis of the transfected CRC cells were detected using MTT assay and flow cytometry.

RESULTSThe 4 human CRC cells showed significantly upregulated expression of miR-221 compare with HUVECs (P<0.01). The miR-221-specific inhibitor, anti-miR-221, significantly inhibited the expression of miR-221 in Caco2 cells and suppressed the cell proliferation, causing also obvious cell apoptosis (P<0.01).

CONCLUSIONThe miR-221-specific inhibitor shows potent inhibitory effect on the growth of CRC cells, suggesting its value as a potential anti-tumor candidate for treatment of CRC.

Apoptosis ; drug effects ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Colorectal Neoplasms ; pathology ; Humans ; MicroRNAs ; antagonists & inhibitors ; metabolism

Long-segment lichen sclerosus (LS) urethral stricture is a challenge for urologists. Limited data are available for surgeons to make a surgical decision between Kulkarni and Asopa urethroplasty. In this retrospective study, we investigated the outcomes of these two procedures in patients with LS urethral stricture. Between January 2015 and December 2020, 77 patients with LS urethral stricture underwent Kulkarni and Asopa procedures for urethroplasty in the Department of Urology, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine (Shanghai, China). Of the 77 patients, 42 (54.5%) underwent the Asopa procedure and 35 (45.5%) underwent the Kulkarni procedure. The overall complication rate was 34.2% in the Kulkarni group and 19.0% in the Asopa group, and no difference was observed ( P = 0.105). Among the complications, no statistical difference was observed in the incidence of urethral stricture recurrence ( P = 0.724) or glans dehiscence ( P = 0.246) except for postoperative meatus stenosis ( P = 0.020). However, the recurrence-free survival rate between the two procedures was significantly different ( P = 0.016). Cox survival analysis showed that antiplatelet/anticoagulant therapy use ( P = 0.020), diabetes ( P = 0.003), current/former smoking ( P = 0.019), coronary heart disease ( P < 0.001), and stricture length ( P = 0.028) may lead to a higher hazard ratio of complications. Even so, these two techniques can still provide acceptable results with their own advantages in the surgical treatment of LS urethral strictures. The surgical alternative should be considered comprehensively according to the patient characteristics and surgeon preferences. Moreover, our results showed that antiplatelet/anticoagulant therapy use, diabetes, coronary heart disease, current/former smoking, and stricture length may be contributing factors of complications. Therefore, patients with LS are advised to undergo early interventions for better therapeutic effects.
Male ; Humans ; Urethral Stricture/etiology* ; Retrospective Studies ; Constriction, Pathologic/surgery* ; Lichen Sclerosus et Atrophicus/surgery* ; Treatment Outcome ; Urologic Surgical Procedures, Male/methods* ; China ; Urethra/surgery* ; Postoperative Complications/etiology* ; Mouth Mucosa ; Diabetes Mellitus/etiology* ; Anticoagulants ; Coronary Disease

OBJECTIVETo investigate the expression of microRNA-221 (miR-221) and CDKN1C/P57 in colorectal carcinoma (CRC) and adjacent non-cancerous tissues. The effect of miR-221-specific inhibitor on cell proliferation and apoptosis in CRC cells was also assessed.

METHODSThe expression of miR-221 was detected by real-time RT-PCR. CDKN1C/P57 mRNA and corresponding protein expression pattern were detected by semi-quantitative RT-PCR and Western-blot. The specific 2'-methoxy-modified RNA oligonucleotide of miR-221(miRNA inhibitor,anti-miR-221) was designed, synthesized and transfected into Caco2 cell by liposome. Finally, the status of CRC cell proliferation and apoptosis were detected by MTT assay and flow cytometry.

RESULTSThe expression of miR-221 was significantly up-regulated in CRC tissues as compared to the adjacent non-cancerous tissues(2.041±1.401 vs. 0.806±0.341, P<0.01). There was no significant difference in CDKN1C/P57 mRNA expression between CRC and non-cancerous tissues, whereas CDKN1C/P57 protein markedly decreased in CRC (3.019±1.708 vs. 0.972±0.316, P<0.01). miR-221-specific inhibitor significantly enhanced CDKN1C/P57 protein expression, inhibited proliferation of CRC cells and induced apoptosis of CRC cells(P<0.01).

CONCLUSIONSmiR-221 inhibits CDKN1C/P57 expression by post-transcriptional gene silencing to promote CRC development and progression. miR-221-specific inhibitor potentially inhibits the growth of CRC cells. Therefore, it may be a new target for the biologic therapy for CRC.

Adult ; Aged ; Apoptosis ; genetics ; Caco-2 Cells ; Cell Line, Tumor ; Cell Proliferation ; Colorectal Neoplasms ; genetics ; metabolism ; pathology ; Cyclin-Dependent Kinase Inhibitor p57 ; genetics ; metabolism ; Female ; Humans ; Male ; MicroRNAs ; genetics ; Middle Aged ; RNA Interference

OBJECTIVETo prepare the PrP specific monoclonal antibodies (mAbs) that can be used for the detection of mammalian prions and study of pathogenesis of prion diseases.

METHODSSeveral BALB/c mice were immunized with recombinant hamster prion protein (HaPrP). Three hybridoma cell lines designated as B7, B9, and B10, secreting monoclonal antibodies against HaPrP, were established by hybridoma technique. The mAbs reactivities were evaluated with ELISA, Western blot, and immunohistochemistry.

RESULTSThe mAbs produced by these cell lines reacted well with different recombinant hamster PrP proteins. Western blot analyses showed that mAbs B7 and B9 reacted with PrPSc from the scrapie-infected animals after proteinase K digestion with three glycosylated forms. The mAbs exhibited cross-reactivity with various PrPC from several other mammalian species, including humans and cattles. Immunohistochemistry assays confirmed that mAbs B7 and B9 could recognize not only extracellular but also intracellular PrPsSc.

CONCLUSIONThe mAbs of prion protein are successfully generated by hybridoma technique and can be applied for the diagnosis of prion associated diseases.

Animals ; Antibodies, Monoclonal ; immunology ; Blotting, Western ; Brain ; metabolism ; Cell Line, Tumor ; Cricetinae ; Enzyme-Linked Immunosorbent Assay ; Female ; Immunization ; Immunohistochemistry ; Mice ; Mice, Inbred BALB C ; PrPC Proteins ; genetics ; immunology ; PrPSc Proteins ; genetics ; immunology ; Recombinant Proteins ; immunology

OBJECTIVETo study the differential expression of four TRAIL receptors on bone marrow mononuclear cells (BMMNC) from multiple myeloma (MM) patients and myeloma cell line KM3 cells, to compare their altered expressions after chemotherapy and to explore the mechanisms by which TRAIL selectively kills tumor cells.

METHODSSemi-quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) and flow cytometry were used to investigate the expression of four TRAIL receptors on BMMNCs in 23 MM patients, KM3 cells and 15 controls, and the changes of their expression pattern after chemotherapy and after incubation of KM3 cells with sub-clinical concentration of doxorubicin.

RESULTSDR4 and DR5 were highly expressed on KM3 cells with no expression of DcR1 and DcR2. Expressions of DR4 and DR5 on BMMNCs from MM patients were higher and expression of DcR1 and DcR2 were lower than that of controls (P < 0.05). The expression of DR5 on MM and KM3 cells was up-regulated after chemotherapy and exposure to doxorubicin (P < 0. 05).

CONCLUSIONSThe expressions of four TRAIL receptors on myeloma cells and normal controls were different, which might account for the selective killing effect of TRAIL on MM cells. Up-regulated DR5 on KM3 cells after incubating with doxorubicin and after chemotherapy suggests the cytotoxic agents might enhance the apoptosis of MM cells.

Antineoplastic Agents ; pharmacology ; Cell Line, Tumor ; Cells, Cultured ; Doxorubicin ; pharmacology ; Female ; Flow Cytometry ; Gene Expression ; drug effects ; Humans ; Leukocytes, Mononuclear ; cytology ; drug effects ; metabolism ; Male ; Middle Aged ; Multiple Myeloma ; drug therapy ; genetics ; pathology ; Receptors, TNF-Related Apoptosis-Inducing Ligand ; biosynthesis ; genetics ; Reverse Transcriptase Polymerase Chain Reaction

OBJECTIVETo determine the distributions of six Helicobacter pylori (Hp)-specific antibodies in a high-risk population of gastric cancer (GC) and explore the relationship between Hp virulence factors and precancerous gastric lesions.

METHODSBased on the two intervention trials conducted in Linqu County, the seropositivities for CagA, VacA, GroEL, UreA, HcpC and GGT were assessed by recombinant immunoassay (recomLine) in 623 participants with H. pylori infection determined by (13)C-urea breath test ((13)C-UBT) and/or enzyme linked immunosorbent assay (ELISA).

RESULTSIn a total of 623 participants were detected by recomLine analysis, of which 594 were Hp-positive. The seropositivities rates of CagA, VacA, GroEL, UreA, HcpC and GGT were 84.0%, 38.2%, 66.7%, 17.7%, 58.8% and 42.8%, respectively. A total of 523 participants were determined as type I infection of Hp, accounting for 88.1%. Compared with superficial gastritis (SG), the infection rate of Hp type I was higher in the chronic atrophic gastritis (CAG) (P = 0.001).

CONCLUSIONSThe results of this population-based study suggest that the virulence factors of Hp may be related to the development of GC in a Chinese high-risk population. The recomLine analysis may serve as a tool for identification of Hp strains and prediction of high-risk population of GC.

Adult ; Antibodies, Bacterial ; blood ; Female ; Gastritis ; blood ; immunology ; microbiology ; Gastritis, Atrophic ; blood ; immunology ; microbiology ; Helicobacter Infections ; blood ; immunology ; Helicobacter pylori ; Humans ; Male ; Middle Aged ; Precancerous Conditions ; blood ; immunology ; microbiology ; Stomach Neoplasms ; blood ; immunology ; microbiology