Biomedical subjects
Publications and source records attributed to J Shen.
In this paper are reviewed the research reports on biomaterials used in recent years in the field of tissue engineering for cartilage regeneration. The preparation of these biomaterials are also discussed. Finally, ideas are proposed to solve the problems in the field of cartilage tissue engineering.
OBJECTIVE: To study prospectively the enhancement features of multi-phase scan of dynamic MRI and spiral CT in the diagnosis of small hepatocellular carcinoma (SHCC) and to discuss the cause of dynamic MRI being superior to spiral CT. METHODS: Multi-phase contrast scanning of dynamic MR and spiral CT were done in 53 SHCC patients. The lesions were proved by surgery and pathology. The arterial-phase, portal venous-phase and delayed phase scan of spiral CT were carried out after the pre-contrast scanning of the entire liver. MRI was performed with SE sequence and FMPSPGR sequence dynamic multi-phase contrast scans. RESULTS: Seventy-six lesions were found in 53 patients. Sixty-nine lesions and 54 lesions were enhanced obviously in MR and spiral CT arterial-phase scans. The typical enhancement patterns of SHCC in the arterial-phase, portal venous-phase and delayed phase scan of MRI and spiral CT were hyper-hypo-hypointense (dense) and hyperintense (hyperdense), -isointense (isodense) and -hypointense (hypodense). Atypical enhancement patterns were hyperintense (hyperdense), -hyperintense (hyperdense), -hyperintense (hyperdense), -hyperintense (hyperdense), -isointense (isodense), -isointense (isodense) and -hypointense- (hypodense), -hypointense (hypodense) and -hypointense (hypodense). CONCLUSION: Both dynamic MRI and spiral CT multi-phase contrast scanning are able to demonstrate the enhancement features of SHCC, with arterial-phase scan of MRI being superior to spiral CT in reflecting the hypervascular characterization of SHCC. Combined with SE sequence in characterizing the SHCC, MRI is better than spiral CT.
OBJECTIVE: Taking GST M1 as an example to introduce analytic method of interaction models between the polymorphism(s) of metabolic gene(s) and environmental exposure in stomach cancer susceptibility. METHODS: Using community-based case-control design, combined with molecular biological techniques (PCR) and multiple variables logistic regression models, we analyzed 112 intestinal types of stomach cancer cases with endoscopy and pathology diagnosis in the Yangzhong City Hospital during January 1997 and December 1998. A total of 675 controls were selected from persons who had no history of digestive system cancers. RESULTS: After adjustment of confounding variables with both GST M1 null genotype and history of ever tobacco smoking, the results showed a significant types of 4 gene-environment interaction. Interaction index (gamma) value was 3.38 and OR(eg) value was 8.40, suggesting that a super multiplicative interaction occurred. The results also showed that GST M1 null genotype had a high exposure-gene effect interaction with tobacco smoking (pack year), while gamma values were 0.995, 2.085 and 2.157 respectively. A low exposure-gene effect interaction was found in GST M1 null genotype with the amount of (kg x year) alcohol consumption while gamma values were 1.01 and 0.97 respectively. CONCLUSION: Logistic regression model can be used to evaluate gene-environment interaction and dose-response of exposure-gene effect.
OBJECTIVE: To explore whether there existed spatial and familial aggregation in gastric cancer in Yangzhong City of Jiangsu Province. METHODS: Using the data collected from cancer incidence registry and report system in Yangzhong City and newly designed investigation for double Y nuclear family, a genetic epidemiological study was conducted in 448 nuclear pedigrees with gastric cancer and 437 control pedigrees, involving 5 242 family members. RESULTS: Chi square test of goodness-of-fit for Poisson distribution showed there was difference between real incidence rate of gastric cancer in all townships and towns in Yangzhong and expected distribution, with chi(2) = 191.07, P < 0.001. The highest rate was in Sanyao, Changhong and Youfang townships, which was 2.2 times higher as that in the areas with low-incidence rate. Prevalence rate of gastric cancer was significantly higher in the siblings (5.42%) and parents (8.65%) of the probands, than that in siblings and parents of their spouses (4.94% and 3.20%, respectively). Prevalence rate of gastric cancer in the offspring with both parents suffered from gastric cancer was the highest, 22.58%. Test for goodness-of-fit of binominal distribution showed that there was significant difference between observed number and expected number of pedigrees with gastric cancer, with P < 0.0001. CONCLUSION: There was not only significantly spatial aggregation of gastric cancer in Yangzhong City, but also familial aggregation, which coincided with a mode of multi-genetic inheritance based on preliminary results and laid a foundation for exploring the difference in gentic susceptibilities and environmental factors for gastric cancer in Yangzhong City.
OBJECTIVE: To study the effects of sodium butyrate on proliferation, differentiation and apoptosis of immortalized esophagus epithelial cells. METHODS: SHEE, an immortalized human fetal esophageal epithelial cell line induced by HPV18 E6E7, was cultivated in culture flasks and 24-well plates. Two experiment groups of cultured cells were treated with 1 and 5 mmol/L of sodium butyrate respectively for 4 days, and one group of untreated cells set aside as control. The numbers of cloned cells were calculated. The ultra-structure of SHEE cells was examined by transmission electron microscopy (TEM). The cell cycle and number of apoptotic cells were measured by flow cytometry, Ki-67 and cytokeratin of cells were detected by immunohistochemistry method and F-actin of cells labeled with phalloidin was examined by laser confocal scanning microscopy. RESULTS: Colony formations showed a significant decrease in the 2 experiment groups after 4 days of culture (P < 0.01). In the 1 mmol/L group, the cells at S phase were diminished and arrested at G(0)/G(1) phase. Compared with control group, Ki-67 positive cells were found decreased, while F-actin and cytokeratin were increased. Apoptotic cells in 5 mmol/L group were increased markedly. CONCLUSIONS: Sodium butyrate may induce SHEE cells growth arrest, differentiation and apoptosis. The effects depend on sodium butyrate concentration and time of exposure. Whether it can be used in combination with other anticancer drugs should be further studied.
OBJECTIVE: To study the effect of Bcl-2 on the cortical neurons of primary cultured mice with HSV-1 infection. METHODS: Analysis of the expression of Bcl-2 on the cortical neurons of primary cultured fetal mice in vitro infected with HSV-1 for 11 hours or exposed to sorbitol for 5 hours was made by flow cytometry and Western blotting. RESULTS: The Bcl-2 of the cultured neurons undergoing HSV-1 infection expressed upregulating compared with the mock untreated neurons. The Bcl-2 protein of HSV-1 infected and exposed to sorbitol neurons expressed upregulating compared with the control group. The Bcl-2 protein of the primary cultured 3 day cells expressed higher than that of the primary cultured 7 day cells. The higher neurovirulence, the higher expression of Bcl-2. CONCLUSIONS: Bcl-2 might protect the primary cultured cortical neurons of fetal mice from apoptosis where infected with HSV-1, and thereby the lifespan of host cells may be prolonged.
OBJECTIVE: To evaluate the therapeutic methods of sensorineural hearing loss with iron deficiency anemia and their effects. METHOD: Sixty-eight Wistar rats were randomly divided into 3 groups: Group A (iron deficiency group A) 24 rats, group B (iron deficiency group B) 24 rats and group C (control group) 20 rats. Group A and B were fed with iron deficiency diet for 6 weeks. By analyzing ABR and DPOAE, hearing loss was detected in group A and B. Then, group A was given iron supplementation diet and hyperbaric oxygen therapies, and group B was given iron supplementation diet only. RESULT: The auditory thresholds and period latencies (PL) of I waves of ABR and DPOAE amplitude in 2 kHz and 3 kHz within group A and B were significantly different before and after treatment (P < 0.05). But the effects of treatment between these two groups had not significant differences (P > 0.05). CONCLUSION: It suggested that good results can be obtained by early iron supplementation in iron deficiency hearing loss cases. Hyperbaric Oxygen therapy may not be necessary.
OBJECTIVE: To explore the clinical manifestations and therapeutic effects of treating chronic suppurative otitis media with two terms tympanoplasty. METHOD: 36 patients were retrospectively analyzed. The criterions of success are air room in middle ear, intact eardrum and decrease of A-B gape in audiometry. RESULT: 32 cases of all patients got successful effects, 4 cases failed. The main cause of failure is to fail forming air room in middle ear. CONCLUSION: The two term's tympanoplasty can save the residual hearing in most patient. But it is difficult to get successful result if more mucous membrane in the middle ear disappeared.
OBJECTIVE: To investigate the characteristics of tone burst transmission of the middle ear implant(MEI). METHODS: Ten adult rabbits with normal hearing were used. A silver ball electrode was placed at the round window membrane to measure cochlear microphonics (CM) when sounds were presented before and after the implantation of the MEI. The tone burst was the acoustic stimulus. RESULTS: Frequency response functions without and with the MEI in rabbit model were calculated, and their amplitude-frequency curves ranging from 0.5 to 6 kHz resembled each other in shape with gain factors about 15 dB at the frequencies above 1 kHz. CONCLUSION: The results of this study indicated that the frequency response of the device fitted the speech transmission and it had high fidelity with little noise.
OBJECTIVE: To evaluate the results of TSRH instrumentation in the correction of coronal, sagittal and rotational deformity of scoliosis. METHODS: From January 1998 to December 1999, thirty-two consecutive patients (6 males, 26 females)with scoliosis underwent anterior or posterior spinal instrumentation and fusion using TSRH instrumentation. Of these cases, 21 were idiopathic scoliosis and 11 were congenital scoliosis. The average age at surgery was 16.4 years (range, 11 approximately 45 years). The mean Cobb angle at surgery was 71.2 degrees range, 44 degrees approximately 125 degrees) in the coronal plane, and 49. degrees range, 16 degrees aprroximately 67degrees in the sagittal plane. Rotational deformity (Nash-Moe) ranged from I to III degree. Preoperative apical translation averaged 4.8 cm (range, 3 approximately 9 cm). RESULTS: The average follow-up duration was 13.3 months (range, 10 approximately 24 months). At the final follow-up, the mean Cobb angle in the coronal plane was 26.6 (range, 10 degrees approximately 73 degrees), with a 63.8% of improvement. Sagittal alignment was well maintained with a mean Cobb angle of 28 degrees (range, 10 degrees approximatelky 45 degrees). The average correction of rotation of the apical vertebra was I degree. The average apical translation was 1.6 cm (range, 0.5 approximately 5.0 cm) representing a correction rate of 66, 7%. Complication was noted in two cases with an incidence of 3.1%, one case had superficial infection and the other one had lower hook dislocation. There was no neurologic deficit and pseudoarthrodesis in this series. CONCLUSION: TSRH instrumentation is an effective and convenient three-dimensional correction system with a lower rate of complication, which can not only correct the coronal and rotational deformity, but maintain the sagittal alignment as well.
OBJECTIVE: To clone complete EcoRII restriction endonuclease gene (ecoRIIR) and methyltransferase gene (ecoRIIM) in one vector and to analyze the coordinating expression of this whole R-M system. METHODS: Unidirectional deletion subclones were constructed with ExoIII. ecoRIIR/ M genes were preliminarily located in the cloned fragment according to the enzyme activities of subclones. Exact deletion sites were determined by sequencing, and transcriptional start sites were determined by S1 mapping. RESULTS: The DNA fragment which was cloned into pBluescript SK + contained intact ecoRIIR gene and ecoRIIM gene, and two transcriptional start sites of ecoRIIR gene were determined. 132bp to 458bp from 3'end of ecoRIIR gene are indispensable to enzyme activities and deletion of 202bp from 3' end of ecoRIIM gene made enzyme lose the capability in DNA protection to resist specific cut with EcoRII endonuclease (EcoRII. R). Deletion of the coding and flanking sequences of one gene did not affect the expression of the other gene, and the recombinants only containing ecoRIIR gene appeared to be lethal to dcm+ host. CONCLUSION: ecoRIIM gene linking closely to ecoRIIR gene is very important for the existence of the R-M system in process of evolution, but the key to control EcoRII R-M order may not exist in transcriptional level .
OBJECTIVE: To evaluate the histological response and biocompatibility of implanted domestic bio-degradable PDLLA membranes in vivo. METHODS: The domestic biodegradable PDLLA membranes and non-degradable ePTFE membranes were in pairs placed subcutaneously in surgical incision made in the dorsum of rats. The tissue responses to these materials were observed histologically at 1, 2, 4, 8 and 12 weeks after placement. RESULTS: The tissue responses of the two kinds of materials were similar to the non-specific reaction mainly infiltrated with lymphocytes, plasmocytes, macrophages, and foreign body giant cells. The polymorphonuclears and foreign body giant cells infiltrated round the ePTFE membranes existed for a relatively long period, in contrast to that of PDLLA membranes. CONCLUSION: Domestic PDLLA membranes with good biocompatibility will be adapted to making GTR into a single step procedure.
CONTEXT: High-dose chemotherapy poses considerable challenges to emesis management. Although prior studies suggest that acupuncture may reduce nausea and emesis, it is unclear whether such benefit comes from the nonspecific effects of attention and clinician-patient interaction. OBJECTIVE: To compare the effectiveness of electroacupuncture vs minimal needling and mock electrical stimulation or antiemetic medications alone in controlling emesis among patients undergoing a highly emetogenic chemotherapy regimen. DESIGN: Three-arm, parallel-group, randomized controlled trial conducted from March 1996 to December 1997, with a 5-day study period and a 9-day follow-up. SETTING: Oncology center at a university medical center. PATIENTS: One hundred four women (mean age, 46 years) with high-risk breast cancer. INTERVENTIONS: Patients were randomly assigned to receive low-frequency electroacupuncture at classic antiemetic acupuncture points once daily for 5 days (n = 37); minimal needling at control points with mock electrostimulation on the same schedule (n = 33); or no adjunct needling (n = 34). All patients received concurrent triple antiemetic pharmacotherapy and high-dose chemotherapy (cyclophosphamide, cisplatin, and carmustine). MAIN OUTCOME MEASURES: Total number of emesis episodes occurring during the 5-day study period and the proportion of emesis-free days, compared among the 3 groups. RESULTS: The number of emesis episodes occurring during the 5 days was lower for patients receiving electroacupuncture compared with those receiving minimal needling or pharmacotherapy alone (median number of episodes, 5, 10, and 15, respectively; P<.001). The electroacupuncture group had fewer episodes of emesis than the minimal needling group (P<.001), whereas the minimal needling group had fewer episodes of emesis than the antiemetic pharmacotherapy alone group (P =.01). The differences among groups were not significant during the 9-day follow-up period (P =.18). CONCLUSIONS: In this study of patients with breast cancer receiving high-dose chemotherapy, adjunct electroacupuncture was more effective in controlling emesis than minimal needling or antiemetic pharmacotherapy alone, although the observed effect had limited duration. JAMA. 2000;284:2755-2761.
Type I collagen is composed of two chains, alpha1(I) and alpha2(I), encoded by two distinct genes, the alpha1(I) and alpha2(I) collagen genes, that are highly expressed in osteoblasts. In most physiological situations, alpha1(I) and alpha2(I) collagen expression is coregulated, suggesting that identical transcription factors control their expression. Here, we studied the role of Cbfa1, an osteoblast-specific transcription factor, in the control of alpha1(I) and alpha2(I) collagen expression in osteoblasts. A consensus Cbfa1-binding site, termed OSE2, is present at the same location in the alpha1(I) collagen promoter at approximately -1347 base pairs (bp) of the rat, mouse, and human genes. Cbfa1 can bind to this site, as demonstrated by electrophoretic mobility shift assay (EMSA) and supershift experiments using an anti-Cbfa1 antibody. Mutagenesis of the alpha1(I) collagen OSE2 at -1347 bp reduced the activity of a alpha1(I) collagen promoter fragment 2- to 3-fold. Moreover, multimers of this OSE2 at -1347bp confer osteoblast-specific activity to a minimum alpha1(I) collagen promoter fragment in DNA transfection experiments as well as in transgenic mice. An additional Cbfa1-binding element is present in the alpha1(I) collagen promoter of mouse, rat, and human at approximately position -372. This site binds Cbfa1 only weakly and does not act as a cis-acting activator of transcription when tested in DNA transfection experiments. Similar to alpha1(I) collagen, the mouse alpha2(I) collagen gene contains multiple OSE2 sites, of which one is conserved across multiple species. In EMSA, Cbfa1 binds to this site and multimers of this alpha2(I) OSE2 element confer osteoblast-specific activity to the minimum alpha1(I) collagen promoter in DNA transfection experiments. Thus, our results suggest that Cbfa1 is one of the positive regulators of the osteoblast-specific expression of both type I collagen genes.
BACKGROUND: Congenital long-QT syndrome (LQTS) is caused by mutations of genes encoding the slow component of the delayed rectifier current (LQT1, LQT5), the rapid component of the delayed rectifier current (LQT2, LQT6), or the Na(+) current (LQT3), resulting in ST-T-wave abnormalities on the ECG. This study evaluated the spectrum of ST-T-wave patterns and repolarization parameters by genotype and determined whether genotype could be identified by ECG. METHODS AND RESULTS: ECGs of 284 gene carriers were studied to determine ST-T-wave patterns, and repolarization parameters were quantified. Genotypes were identified by individual ECG versus family-grouped ECG analysis in separate studies using ECGs of 146 gene carriers from 29 families and 233 members of 127 families undergoing molecular genotyping, respectively. Ten typical ST-T patterns (4 LQT1, 4 LQT2, and 2 LQT3) were present in 88% of LQT1 and LQT2 carriers and in 65% of LQT3 carriers. Repolarization parameters also differed by genotype. A combination of quantified repolarization parameters identified genotype with sensitivity/specificity of 85%/70% for LQT1, 83%/94% for LQT2, and 47%/63% for LQT3. Typical patterns in family-grouped ECGs best identified the genotype, being correct in 56 of 56 (21 LQT1, 33 LQT2, and 2 LQT3) families with mutation results. CONCLUSIONS: Typical ST-T-wave patterns are present in the majority of genotyped LQTS patients and can be used to identify LQT1, LQT2, and possibly LQT3 genotypes. Family-grouped ECG analysis improves genotype identification accuracy. This approach can simplify genetic screening by targeting the gene for initial study. The multiple ST-T patterns in each genotype raise questions regarding the pathophysiology and regulation of repolarization in LQTS.
Studies suggest that acute and chronic opioids can regulate the cAMP-dependent protein kinase (PKA) signaling pathway and that changes in this pathway may be involved in opioid tolerance. In the present study, we examined the role of cAMP-PKA on mu-opioid receptor downregulation and tolerance in mice. Mice were injected intracerebroventricular (i.c.v.) and intrathecal (i.t.) once a day with an antisense oligodeoxynucleotide directed at the mRNA for the alpha catalytic subunit of mouse PKA. Controls were treated with saline or a mismatch oligodeoxynucleotide. On day 2 of treatment, mice were implanted s.c. with a 25-mg morphine pellet and an osmotic minipump infusing morphine (40 mg/kg/day) for 3 days. Other mice were implanted with an osmotic minipump infusing etorphine (125, 250 microg/kg/day) for 2 days. Control mice were implanted s.c. with inert placebo pellets. At the end of treatment, pumps and pellets were removed and mice tested for morphine or etorphine analgesia. Other mice were sacrificed and mu-opioid receptor binding assays conducted in whole brain. Both infusion doses of etorphine produced significant tolerance (ED(50) shift = 3.6 and 6.3-fold). The higher etorphine infusion produced downregulation of mu-receptor density ( approximately 30%) while the lower infusion dose of etorphine did not. Morphine treatment also produced significant tolerance in mice (ED(50) shift = 4.5-fold), but no receptor downregulation. Antisense to PKA partially blocked tolerance induced by the higher dose of etorphine, but had no effect on receptor downregulation. On the other hand, antisense to PKA completely blocked tolerance induced by morphine and the lower infusion dose of etorphine. The mismatch oligodeoxynucleotide had no effect on any measure. These results suggest that PKA has a limited role in opioid agonist-induced receptor downregulation. However, the partial block of tolerance for the high infusion dose of etorphine and the complete block of tolerance for morphine and the low infusion dose of etorphine suggests that PKA may play a critical role in tolerance that is "receptor-regulation-independent."
The vibrational spectroscopy of novel biliverdin compounds were studied by Fourier-transform Raman (FT-Raman) and infrared (FT-IR) spectroscopy. The effects of type, length and position of substituents at C(8) and C(12) or C(1) and C(19) of tetrapyrroles on FT-Raman and FT-IR spectra of these compounds, are discussed. The marker bands are developed in order to distinguish between etiobiliverdin and mesobiliverdin.
CD44 is a cell surface glycoprotein involved in cell adhesion during neurite outgrowth, leukocyte homing, and tumor metastasis. In the current study, we examined the regulation of this molecule 4 days after neural trauma in different forms of central and peripheral injury. Transection of the hypoglossal, vagus, or sciatic nerve led to the appearance of CD44-immunoreactivity (CD44-IR) on the surface of the affected motoneurons, their dendrites, and their axons. Fimbria fornix transection led to CD44-IR on a subpopulation of cholinergic neurons in the ipsi- and contralateral medial septum and diagonal band of Broca and colocalized with galanin-IR. Central projections of axotomized sensory neurons to the spinal cord (substantia gelatinosa, Clarke's column) also showed an increase in CD44-IR, which was abolished by spinal root transection. Nonneuronal CD44-IR was mainly restricted to sites of direct injury. In the crushed sciatic nerve, CD44-IR was found on the demyelinating Schwann cells and on infiltrating monocytes and granulocytes. Direct parasagittal transection of the cerebral cortex led to CD44-IR on resident astrocytes and on leukocytes entering the injured forebrain tissue. CD44-IR also increased on reactive retinal astrocytes and microglia after the optic nerve crush. Additional time points in the retina and hypoglossal nucleus (days 1, 2, and 14) and cerebral cortex (day 2) injury models also showed the same cell type pattern for the CD44-IR. Finally, polymerase chain reaction analysis confirmed the posttraumatic expression of CD44 mRNA and detected only the standard haematopoietic CD44 splice isoform both in direct and indirect brain injury models. Overall, the current study shows the widespread, graded appearance of CD44-IR on neurons and on nonneuronal cells, depending on the form of neural injury. Here, the ability of CD44 to bind to a variety of extracellular matrix and cell adhesion proteins and its common presence in different forms of brain pathology could suggest an important role for this cell surface glycoprotein in the neuronal, glial, and leukocyte response to trauma and in the repair of the damaged nervous system.