AlM: To explore the different ages of congenital nasolacrimal duct obstruction in infants, take different treatment methods at different times.
METHODS:The 87 cases of 102 children were divided into three different age groups: the first group of 25d-3mo of age 21 cases 26 eyes; The second group >3mo-7mo 31 cases 36 eyes;The third group >7-24mo of age 35 cases 40 eyes. For the first group of infants, the implementation of the lacrimal sac nasolacrimal duct massage + eye drops; for the second group of infants, carry lacrimal pressure washing treatment; for the third group of infants, the implementation of the nasolacrimal duct probing treatment.
RESULTS: The first group of children through the nasolacrimal duct sac massage + drops tobramycin eye drops treatment unobstructed 12, the cure rate was 46. 2%;The second group of children through pressurized irrigation treatment lacrimal patency by 33, the cure rate was 91. 7%; The third group of children through the nasolacrimal duct probing unobstructed 36 treatment, the cure rate was 90. 0%. The second and third group were better than the first group (χ2=15. 71, P<0. 01;χ2=15. 27, P<0. 01);the treatment effect of the second and third groups was no significant difference (χ2=0. 02, P>0. 05).
CONCLUSlON:lnfants with congenital nasolacrimal duct obstruction should distinguish between ages, taking different treatments, in order to obtain a better therapeutic effect, and lacrimal pressure washing is the preferred way of treating infants with congenital nasolacrimal duct obstruction.

Objective To study the feature of MRI in ureter transitional cell carcinoma,to evaluate the diagnostic value in transitional cell carcinoma of ureter with MRI.Methods Heavily T_2-weighted fast spin echo pulse sequence,fat suppression pulse and MR urography(MRU)were performed.The MRI finding of the ureter transitional cell carcinoma were anlysed in 32 cases and were discssed with the review of literature.Results Fifteen lesions were located at the upper portionof the ureter,7 at mid portion and 10 at lower portion.Each case presented urinary obstruction,distention and uretal hydrocele.21 retrograde urleropyelogrhpy of nodular shaperal irregular,11 irregular the ureteral wall,10 dilate the ureter in 21 cases,11 infitrative lesion to grow in location,9 lymphanode to enlarge in surrounding of major arterial of abdominal and renal out in 11 cases.17—72 mm length the lesion,39 mm average,6—50 mm width the leion,17 mm average.Hypointense on T_1 WI and hyperintense on T_2 WI image in 23 cases,hyperintense on both T_1 WI and T_2 WI image in 5 cases,hypointense on T_1 WI and isointense on T_2 WI image in 2 case, slightly hypointense on both T_1 WI and T_2 WI images in 2 case.Ninteen homogeneous and 13 non homogeneous of signal in lesion,22 reliable and 5 suspicious diagnosis and 5 misdiagnosis in MRI. Conclusion The location,the shape,the spectrum of the tumor and change of surrounding tiessue were clear cuted in MRI,but further research in confirmation of the diagnosis.

Adenoids ; diagnostic imaging ; pathology ; Child ; Child, Preschool ; Female ; Humans ; Hypertrophy ; Magnetic Resonance Imaging ; Male ; Radiographic Image Enhancement ; methods ; Tomography, Spiral Computed ; methods

Objective To analyze the genetic phenotypes of Nantong Han population and evaluate the application value of 17 Y-STR loci in Nantong population.Methods The peripheral blood samples were collected from 343 unrelated Nantong Han males and the genomic DNA were extracted by Chelex-100 method.Genotyping was performed using the AmpF(l)STR YfilerTM Kit.The results were compared with other 12 Han populations,including Anhui,Jiangsu,Jiangxi,Shandong,Shanghai,Zhejiang (1),Lanzhou,Nanyang,Luzhou,Mudanjiang,Shanxi and Zhejiang (2),and 9 minority populations (Mongol,Xibe,Tibetan in Lhasa,Tibetan in Qinghai,Kazak,Uighur,Manchu,Paiwan in Taiwan and Tujia).Results A total of 327 different haplotypes were found in 17 Y-STR loci in Nantong Han population.The haplotype diversity (HD) was 0.999 7.The R,value between Nantong Han and other Chinese populations ranged from-0.000 6 to 0.263 5.The multidimensional scaling results showed that Nantong Han population had no significant differences between most of the Han populations,but had significant differences between most of Chinese minority populations.Conclusion Seventeen Y-STR loci can be a powerful tool for forensic application because of its high polymorphism in Nantong Han population.

FHIT (fragile histidine triad) gene at chromosome 3p14.2 usually expresses at a very low level in human tissue and cells. A high frequency of abnormalities in FHIT gene has been demonstrated in various cancers. FHIT is proposed as a putative tumor-suppressor gene. To evaluate the expression of the FHIT gene in various leukemias, bone marrow or peripheral blood samples from 98 leukemia patients were tested by RT-PCR: 38 from patients with AML-[M(2)(9), M(3)(12), M(4)(8), M(5)(9)], 16 with ALL, and 34 with CML-[CP(20), AP(4), BC(10)] of various FAB types, as well as 10 patients with other hematological malignancies. To detect a deletion in sequencing the FHIT gene, the representative aberrant PCR products were cloned and then sequenced. The results showed that 22/38 (58%) patients with AML, 9/16 (56%) patients with ALL and 19/34 (56%) patients with CML were detectable of aberrant FHIT mRNA transcripts or deletion of FHIT. In 6 (16%) AML patients, 3 (19%) ALL patients, and 5 (15%) CML patients, the wild-type product was absent. Some patient's samples - 6 (42%) AML, 6 (38%) ALL, and 14 (41%) CML revealed aberrant FHIT transcripts in addition to a normal-sized band. Samples from healthy donors (PB, n = 12; BM, n = 5) did not indicate any abnormal expression. Eleven isolated fragments from various patterns of FHIT gene expression were investigated using cDNA sequencing. Sequence analysis revealed deletion of exon 4-8, exon 5-8, and exon 5-6 in various leukemias, as well as the deletion of the full FHIT gene sequence. The fused transcripts included: exon 3 and exon 9, exon 3 and exon 7, exon 4 and exon 9, exon 5 and exon 7. Sequence analysis of aberrant fragments present in samples from an AML and a CML patients was detected for point mutations and insert mutations located in exons 2, 8 and 10, plus a variety of aberrant transcripts. Deletion or aberrant FHIT mRNA transcripts in 50/98 (51%) leukemia patients were found. All samples with aberrant FHIT lacked gene product. A Kaplan-Meier plot of survival in patients with AML in relation to FHIT expression revealed that aberrance or loss of FHIT gene significantly correlated with a low clinical remission rate and poor overall survival.
Acid Anhydride Hydrolases ; genetics ; Base Sequence ; Gene Deletion ; Humans ; Leukemia ; genetics ; metabolism ; Lymphocytes ; metabolism ; Molecular Sequence Data ; Mutation ; Neoplasm Proteins ; genetics ; Polymerase Chain Reaction ; RNA, Messenger ; analysis

Differentiation, the stepwise specialization of cells, and transdifferentiation, the apparent switching of one cell type into another, capture much of the stem cell spotlight. But dedifferentiation, the developmental reversal of a cell before it reinvents itself, is an important process too. In multicellular organisms, cellular dedifferentiation is the major process underlying totipotency, regeneration and formation of new stem cell lineages. In humans, dedifferentiation is often associated with carcinogenesis. The study of cellular dedifferentiation in animals, particularly early events related to cell fate-switch and determination, is limited by the lack of a suitable, convenient experimental system. The classic example of dedifferentiation is limb and tail regeneration in urodele amphibians, such as salamanders. Recently, several investigators have shown that certain mammalian cell types can be induced to dedifferentiate to progenitor cells when stimulated with the appropriate signals or materials. These discoveries open the possibility that researchers might enhance the endogenous regenerative capacity of mammals by inducing cellular dedifferentiation in vivo.
Animals ; Cell Differentiation ; Cells, Cultured ; Epidermal Growth Factor ; physiology ; Humans ; Regeneration ; Salamandridae ; physiology ; Serum ; physiology ; Thrombin ; pharmacology

OBJECTIVETo observe the effect of neferine on Collagen-I, TIMP-1 and MMP-2 expressions and protein secretion of hepatic stellate cells.

METHODThe hepatic stellate cell line HSC-T6 was cultured in vitro, and then randomly divided into 5 groups: the control group, the platelet-derived growth factor (PDGF) group and PDGF + neferine (2, 6, 10 micromol x L(-1)) groups. All of the groups were cultured for 48 h, and their cells were collected to extract mRNA and detect Collagen-I, TIMP-1 and MMP-2 expressions with RT-PCR. Their cell supernatants were also collected to determine the protein content of three factors with ELISA.

RESULTCompared with the control group, PDGF could remarkably increase the Collagen-I, TIMP-1 and MMP-2 expressions and protein secretion of hepatic stellate cells. Compared with the PDGF group, PDGF + neferine (6, 10 micromol x L(-1)) groups showed a notable decrease in the Collagen-I and mRNA expression and protein secretion along with the increase in the concentration, whereas the PDGF + neferine (2 micromol x L(-1)) group showed no significant change in the Collagen-I and mRNA expression and protein secretion. Compared with the PDGF group, three PDGF + neferine groups showed no notable change in MMP-2 expression and protein secretion.

CONCLUSIONNeferine can inhibit the Collagen-I, TIMP-1 and mRNA protein expression and protein secretion of PDGF-induced HSCs along with the increase in the concentration, but with not remarkable effect on the MMP-2 expression and secretion.

Animals ; Benzylisoquinolines ; pharmacology ; Cells, Cultured ; Collagen Type I ; analysis ; genetics ; Drugs, Chinese Herbal ; pharmacology ; Hepatic Stellate Cells ; chemistry ; drug effects ; Matrix Metalloproteinase 2 ; analysis ; genetics ; Rats ; Tissue Inhibitor of Metalloproteinase-1 ; analysis ; genetics

OBJECTIVE To investigate the neuroprotective effect and possible mechanisms of lute-olin-7-O-β-D-glucuronide (LGU) against focalcerebral ischemic injury. METHODS The focal cerebral ischemic injury model was established by middle cerebral artery occlusion (MCAO). Male Sprague Dawley rats were randomly divided into sham group,model group(MCAO),LGU group(0.24,0.72 and 2.16 mg·kg-1)and positive control group(Edaravone at 5 mg·kg-1).LGU was injected intravenously 30 min after MCAO.Neurological severity score,infarct volume and brain water content were detected 24 h after MCAO and the levels of Na+-K+ATPase,Ca2+ATPase,TNF-α and IL-1β were detected to explore the possible mechanisms.For the therapeutic time window test,LGU(0.72 mg·kg-1)was injected intrave-nously 0.5, 2, 4, 6, 8, 10 and 12 h respectively after MCAO. To evaluate motion behavior, LGU were injected intravenously 30 min after MCAO and once per day during detection period. The changes of motor coordination were detected by rotating rod method and grip strength analysis, and the changes of gaits were detected using DigiGait Imaging System. RESULTS LGU improved the neurological severity score, infarct volume ratio and brain water content. The therapeutic time window of LGU for cerebral infarction and brain edema was at least 6 h and for neurological dysfunction was 12 h.LGU also prolonged the latency on rotarod, increased the forelimb tension and improved 8 gait parameters, including stance duration,stride length,stance width,paw area,paw area variability,gait symmetry,ataxia coefficient and tau propulsion.Furthermore,LGU increased Na+-K+-ATPase and Ca2+-ATPase levels in the cortex and hippocampus in the ischemic side,reduced the levels of TNF-α and IL-1β in the serum. CONCLUSION LGU has a significant neuroprotective effect against cerebral ischemic injury via improving energy metabolism and reducing inflammation.

Objective To explore the genetic interactions between angiotensin-convertingenzyme (ACE) I/D and methylenetetrahydrofolate reductase (MTHFR) C677T genotypes in middlecerebral artery stenosis (MCAS) among the asymptomatic residents in Foshan area of China. MethodsUsing a cluster sampling method, 2500 subjects were randomly selected from the residential communitiesof Rongqi town of Foshan area, Guangdong Province. By means of epidemiological questionnaire survey,physical examination, examination of the biochemical markers and transcraniai color Doppler (TCD), 897eligible subjects (306 males and 591 females) were selected from this population and subsequentlydivided into MCAS group and control group according to the TCD results. ACE and METHFR genepolymorphism analyses were conducted using amplified fragment length polymorphism-polymerase chainreaction (AFLP-PCR) and PCR-restriction fragment length polymorphism (PCR-RFLP). Chi-square test, t test, Mann-Whitney test and logistic regression analysis were used to analyze the data. ResultsGender, age, waist-to-hip ratio (WHR) and Ⅱ+CC genotype distribution in the subjects with MCAS weresignificantly different from those in the control subjects. Logistic regression analysis identified age andACE Ⅱ+ MTHFR CC genotype as the independent factors that affected MCAS. Conclusion There aregenetic interactions between ACE I/D and MTHFR C677T genotypes, and the ACE Ⅱ+MTHFR CCgenotype is an independent genetic factor for protection against MCAS in the asymptomatic residents inFoshan area of China.

OBJECTIVETo study apoptosis and gene FasL expression induced by carbon disulfide in sertoli cells of male rats.

METHODSSertoli cells were exposed to different concentrations of CS(2) (0, 0.36, 0.72, 1.44 micromol/ml) for 24 hours. Survival rate, apoptosis rate, expression level of gene FasL were measured using MTT, FCM, and RT-PCR methods respectively.

RESULTSSertoli cell survival rate decreased as the concentration of CS(2) increased. The survival rate (73.34% +/- 1.39%) was significantly lower than the control group (99.98% +/- 5.48%) when the concentration of CS(2) > or = 1.44 micromol/ml (P < 0.05). Apoptosis rate increased as the CS(2) concentration increased. Apoptosis rate (7.93% +/- 0.43%) was significantly higher when the concentration of CS(2) > or = 1.44 micromol/ml (P < 0.05). Expression level of the FasL significantly increased as the concentrations of CS(2) (P < 0.05).

CONCLUSIONCS(2) is cytotoxic to sertoli cells. It could cause apoptosis of sertoli cells.

Animals ; Apoptosis ; drug effects ; Carbon Disulfide ; toxicity ; Cell Line ; Cell Survival ; Fas Ligand Protein ; metabolism ; Male ; Rats ; Sertoli Cells ; drug effects ; metabolism ; Testis ; cytology