Ultrasound-guided core-needle biopsy for peripheral pulmonary lesions: a systematic review and meta-analysis.

AIM: To evaluate the diagnostic value and safety of ultrasound-guided core-needle biopsy for peripheral pulmonary lesions (PPLs). MATERIALS AND METHODS: PubMed, EMBASE, and the Cochrane Library for relevant were searched for studies published up to June 2022. The diagnostic accuracy of US-guided percutaneous transthoracic needle biopsy (PTNB) for the diagnosis of PPLs was evaluated using pooled sensitivity, specificity, diagnostic odds ratio (DOR), positive and negative likelihood ratios (PLR and NLR), and the area under the summary receiver operating characteristic curves value (SROC). RESULTS: The search included 12 original studies (3,830 procedures). For US-guided PTNB, the pooled sensitivity and specificity for the diagnosis of PPLs were 0.93 (95% confidence interval [CI]: 0.91-0.94) and 0.99 (95% CI: 0.96-1.00), respectively. The pooled estimates of the PLR, NLR, and DOR were 134.88 (95% CI: 24.88-731.74), 0.07 (95% CI: 0.06-0.09), and 1,814.95 (95% CI: 333.62-9,873.76), respectively. The area under the SROC curve was 0.95 (95% CI: 0.93-0.97). The overall complication rate was 3.6% (136 of 3,830), including self-limited haemoptysis and asymptomatic pneumothorax, and only six cases of pneumothorax requiring chest tube drainage and one case of severe bleeding were reported. CONCLUSIONS: US-guided core-needle biopsy is an excellent diagnostic tool for PPLs, with high accuracy and excellent technical performance and safety.

[Evaluation and analysis of anxiety, depression and quality of life in vasomotor rhinitis].

Objective: To evaluate the mental state and quality of life in patients with vasomotor rhinitis (VMR) before and after treatment, and to provide guidance for improving the overall health of VMR patients. Methods: Two hundred and twenty VMR patients (VMR group, 118 males, 102 females; aged from 18 to 72 years old), three hundred and twenty allergic rhinitis (AR) patients (AR group, 178 males, 142 females; aged from 18 to 79 years old) from January 2016 to September 2019 were selected in the otolaryngology clinic of Affiliated Hospital of Guizhou Medical University, four hundred and twenty-three healthy people (control group, 243 males, 180 females; aged from 19 to 70 years old) were selected in physical examination center at the same time by continuous enrollment method, symptom check list (SCL-90), self-rating anxiety scale (SAS) and self-rating depression scale (SDS) were used to evaluate the mental state of VMR patients before and after treatment, and 12-item short form health survey version 2.0 (SF-12v2) was used to evaluate their quality of life, statistical data were collected and analyzed by ANOVA and t-test. Results: The scores of eight factors (physical function, role physical function, general health, vitality, role-emotional, mental health) of SF-12v2 in VMR patients before treatment were lower than that of posttreatment, that of AR patients and the control group, the differences were significant (all P<0.05), the scores of somatization, obsession, depression, anxiety and psychosis in SCL-90 in VMR patients before treatment were significantly higher than that of posttreatment, that of AR patients and the control group (all P<0.05), the SAS and SDS in VMR patients before treatment (51.28±16.32; 53.28±18.55) were significantly higher than that of posttreatment (38.53±13.21; 39.35±13.34), that of AR patients (42.23±14.32; 43.32±13.78) and the control group (29.78±10.07;33.46±10.55; t(SAS) were 9.007, 6.813 and 20.59; t(SDS) were 9.043, 7.154 and 17.260, all P<0.05). Conclusion: VMR patients generally suffer from psychological damage, which seriously affects the quality of life of the patients. On the basis of routine treatment, we should attach more importance to the negative psychology of VMR patients and intervene when necessary.

Diminutive Incision Acromioplasty Assisted with Arthroscopy in the Treatment of Chinese Patients with Subacromial Impingement Syndrome / Acromioplastia de Incisión Diminuta Asistida con Artroscopia en el Tratamiento de Pacientes Chinos con Síndrome de Pinzamiento Subacromial

ABSTRACT Background: Many causes can lead to shoulder pain and subacromial impingement syndrome (SIS) is the most frequently recorded disorders. The aim of this study was to evaluate the clinical effects of diminutive incision acromioplasty assisted with arthroscopy for the treatment of Chinese patients with subacromial impingement syndrome. Subject and Methods: Twenty-two patients with 24-painful shoulders subacromial impingement syndrome were enrolled. All painful shoulders were in Grades II (8) and III (16) according to Neer's classification. Detailed physical examination was performed. Conventional radiography and subsequent magnetic resonance imaging (MRI) of the shoulder region of all patients were done. The University of California at Los Angeles Shoulder (UCLA) score system was used for all patients to evaluate their satisfaction after surgery. The preoperative recordings of the UCLA scores were collected and all enrolled cases including 24-painful shoulders were available for follow-up in 1, 3, 6, 12 months after surgery. Results: According to the UCLA scoring system, the symptom of all painful shoulders were improved after one year postoperatively. The average score before surgery from 15.4 points increased to 31.2 points postoperatively, showing a statistical difference (p < 0.05). Conclusions: A diminutive incision acromioplasty assisted with arthroscopy is a reliable approach to treat Chinese patients with subacromial impingement syndrome. All painful shoulders were obviously improved in one year after surgery.

ABSTRACT Antecedentes: Muchas causas pueden provocar dolor de hombro y síndrome de compresión subacromial (SIS) es el trastorno más frecuentemente registrado. El objetivo de este estudio fue evaluar la clínica. Efectos de la acromioplastia con incisión diminuta asistida con artroscopia para el tratamiento de Pacientes chinos con síndrome de pinzamiento subacromial. Sujeto y métodos: Se incluyeron veintidós pacientes con síndrome de afectación subacromial de 24-hombros dolorosos. Todos los hombros dolorosos estaban en Grados II (8) y III (16) de acuerdo con la clasificación de Neer. Se realizó examen físico detallado. Se realizaron radiografías convencionales y, posteriormente, imágenes de resonancia magnética (IRM) de la región del hombro de todos los pacientes. El sistema de puntuación de la Universidad de California en Los Angeles Shoulder (UCLA) se utilizó para que todos los pacientes evaluaran su satisfacción después de la cirugía. Los registros preoperatorios de las puntuaciones de UCLA se recopilaron y todos los casos incluidos, incluidos 24-hombros dolorosos, estaban disponibles para el seguimiento en 1, 3, 6 y 12 meses después de la cirugía. Resultados: De acuerdo con el sistema de puntuación de UCLA, el síntoma de todos los hombros dolorosos mejoró después de un año después de la operación. La puntuación promedio antes de la cirugía de 15.4 puntos aumentó a 31.2 puntos después de la operación, mostrando una diferencia estadística (p < 0.05) Conclusiones: Una acromioplastia de incisión diminuta asistida con artroscopia es un enfoque confiable para tratar a pacientes chinos con síndrome de pinzamiento subacromial. Todas las lesiones dolorosas se mejoraron obviamente en un año después de la cirugía.

[Study on the expression of epidermal growth factor receptor protein during benzo(a)pyrene induced carcinogenesis].

Objective: To explore the expression of epidermal growth factor receptor(EGFR) protein during benzo(a)pyrene (BaP) induced carcinogenesis. Methods: This study, we firstly utilized immunofluorescence assay and Western-blot to examine EGFR expression of the BaP which was constructed previously by project team induced malignant transformation human bronchial epithelial cell (BTC) and the control (16HBE cell). Then, we selected 36 healthy SD rats, divided into two groups according to simple random method, 18 rats each group. The constructed rat lung neoplasm model induced by pulmonary injection of BaP (10 mg/ml of BaP solution in 0.2 ml corn oil), contrast group use 0.2 ml corn oil, lung tissue was collected and the EGFR expression of lung tissue was detected by immunofluorescence assay and Western blot. T analysis was used to test the different of EGFR between two groups. Results: Immunofluorescence analysis showed that the EGFR expression in BTC was significantly higher than 16HBE cell. Meanwhile, Western blot also was used to confirmed this result, the relative expression of EGFR protein in the rats of the model group the control group were 1.04±0.13 and 2.32±0.12, respectively, and the difference was statistically significance (t=12.39, P<0.001). In vivo, well-defined tumor was found in the rat with pulmonary injection of BaP, and the lung showed diffuse alveolar septal thickening, alveolar wall destruction and pulmonary alveoli fusion, which suggested that the rat lung neoplasm model was constructive successfully. Furthermore, we found the EGFR expression of lung was increased dramatically in the rat lung neoplasm model by immunofluorescence detection and Western blot. The relative expression of EGFR protein in the rats of the model group the control group were 0.21±0.03 and 1.30±0.07, respectively, and the difference was statistically significance (t=12.84, P<0.001). Conclusion: Expression of EGFR protein was increased during BaP carcinogenesis, and EGFR may play an important role in the carcinogenesis of BaP.

Pot1 OB-fold mutations unleash telomere instability to initiate tumorigenesis.

Chromosomal aberrations are a hallmark of human cancers, with complex cytogenetic rearrangements leading to genetic changes permissive for cancer initiation and progression. Protection of Telomere 1 (POT1) is an essential component of the shelterin complex and functions to maintain chromosome stability by repressing the activation of aberrant DNA damage and repair responses at telomeres. Sporadic and familial mutations in the oligosaccharide-oligonucleotide (OB) folds of POT1 have been identified in many human cancers, but the mechanism underlying how hPOT1 mutations initiate tumorigenesis has remained unclear. Here we show that the human POT1's OB-folds are essential for the protection of newly replicated telomeres. Oncogenic mutations in hPOT1 OB-fold fail to bind to single-stranded telomeric DNA, eliciting a DNA damage response at telomeres that promote inappropriate chromosome fusions via the mutagenic alternative non-homologous end joining (A-NHEJ) pathway. hPOT1 mutations also result in telomere elongation and the formation of transplantable hematopoietic malignancies. Strikingly, conditional deletion of both mPot1a and p53 in mouse mammary epithelium resulted in development of highly invasive breast carcinomas and the formation of whole chromosomes containing massive arrays of telomeric fusions indicative of multiple breakage-fusion-bridge cycles. Our results reveal that hPOT1 OB-folds are required to protect and prevent newly replicated telomeres from engaging in A-NHEJ mediated fusions that would otherwise promote genome instability to fuel tumorigenesis.

Repair of critical-sized bone defects with anti-miR-31-expressing bone marrow stromal stem cells and poly(glycerol sebacate) scaffolds.

The repair of critical-sized defects (CSDs) is a significant challenge in bone tissue engineering. Combining the use of progenitor cells with gene therapy represents a promising approach for bone regeneration. MicroRNAs play important roles in most gene regulatory networks, regulate the endogenous expression of multiple growth factors and simultaneously modulate stem cell differentiation. Our previous study showed that knocking down miR-31 promotes the osteogenesis of bone marrow stromal stem cells (BMSCs). To investigate the therapeutic potential of cells engineered to express anti-miR-31 for CSD repair, lentiviral vectors encoding negative control, miR-31 precursor and anti-sense sequences were constructed and transduced into osteo-inductive BMSCs. The expression of osteogenic-specific genes, alkaline phosphatase activity and Alizarin Red S staining were investigated to evaluate the effects of miR-31 on the cell fate of BMSCs over a 3-week period. In addition, miR-31-modified BMSCs seeded on poly(glycerol sebacate) (PGS) scaffolds were used to repair 8 mm critical-sized calvarial defects in rats. The results showed that miR-31 suppression significantly increased the expression of osteogenic-specific genes in vitro at the mRNA and protein levels, and that robust new bone formation with high local bone mineral density was observed in the anti-miR groups in vivo. Moreover, the PGS scaffolds carrying anti-miR-31-expressing BMSCs exhibited good biocompatibility and a high regeneration rate (~60%) within in vivo bone defects. Our results suggest that miR-31 gene delivery affects the potential of BMSCs for osteogenic differentiation and bone regeneration and that PGS is a potential substrate for genetically modified, tissue-engineered bone in the repair of large bone defects.

Induction of retinal ganglion-like cells from fibroblasts by adenoviral gene delivery.

Central nervous system neurons fail to regenerate after birth, which greatly hampers the effective treatment of many neurodegenerative diseases. Neurons differentiated from induced pluripotent stem cells have been considered a possible option for cell-based therapies. Recent discoveries have revealed that fibroblasts can be directly converted into neurons without a transition through a pluripotent state. This approach might serve as a more efficient and convenient method for the cellular therapy of neurodegenerative diseases. Currently, several types of neurons have been directly generated from fibroblasts, including dopamine neurons, motor neurons and neural progenitor cells. In our study, by screening a series of candidate genes, we found that the adenovirus-mediated transduction of Ascl1, Brn3b and Ngn2 can directly convert mouse fibroblasts to retinal ganglion-like cells. The induced retinal ganglion-like cells co-express multiple retinal ganglion cell markers, and exhibit membrane properties of functional neurons. The reprogramming mediated by adenoviruses occurs much sooner than that mediated by lentiviruses. Furthermore, the induced retinal ganglion-like cells that are produced via adenoviral gene delivery are free of exogenous gene integration. Retinal ganglion-like cells that are induced by adenoviruses demonstrate great potential applicability in clinical therapy and provide a novel platform for the research of retinal degenerative diseases.

SP600125, a JNK inhibitor, suppresses growth of JNK-inactive glioblastoma cells through cell-cycle G2/M phase arrest.

SP600125 is a well studied inhibitor of c-Jun N-terminal kinase (JNK). Its direct biochemical effects on JNK-inactive tumor cells are usually ignored. In this study, we investigated the effects of SP600125 on JNK-inactive U251 human glioblastoma cells. Our results demonstrate that, 20 microM or more SP600125 can induce significant cell growth inhibition and cell-cycle G2/M phase arrest in U251 cells. Interestingly, we also found that SP600125 can stop the duplicated chromosomes from separating into two cells and the karyokinesis progression. Our study opened up a new perspective for further studies involved in JNK inhibitors or anti-glioma therapy.

Improvement of glucose tolerance by rhein with restored early-phase insulin secretion in db/db mice.

AIMS: In the present study, we investigated whether rhein exerted hypoglycemic action and rhein's effect on the pancreatic ß cell in db/db mice. MATERIALS AND METHODS: Thirty 4-week-old db/db mice were randomized to treatment with rhein (120 mg/kg) (no.=15) and placebo (1% natrium cellulose solution) (no.=15) for 8 weeks, respectively. Fifteen age-matched non-diabetic littermates db/m mice treated with placebo were studied as non-diabetic control. After an 8-week treatment, ip glucose tolerance test (IPGTT) and arginine tolerance test were performed. Area under curve (AUC) of insulin levels in IPGTT was calculated to evaluate insulin secretory function. Immunohistochemical staining of insulin was performed to estimate ß cell mass. TUNEL assay was performed to determine ß cell apoptosis. Islet isolation and perifusion were performed to evaluate kinetics of insulin release in vitro, especially first-phase insulin. RESULTS: Compared with control group, AUC of glucose concentrations significantly decreased in the rhein-treated group (p<0.05). Simultaneously, AUC of insulin levels increased in the rhein-treated group (p<0.05), especially in the first 30 min after glucose load. Perifusion showed that the rhein-treated group manifested a significantly increase of first-phase insulin secretion. Immunohistochemical study and TUNEL assay showed that rhein treatment greatly preserved ß cell mass and inhibited ß cell apoptosis. CONCLUSIONS: Rhein treatment significantly improved glucose- dependent and independent insulin secretion by preservation of ß cell mass and inhibition of ß cell apoptosis in db/db mice. The characteristics of rhein may make it a novel therapeutic means for preventing from or curing diabetes in the near future.

Improved glucose-stimulated insulin secretion by intra-islet inhibition of protein-tyrosine phosphatase 1B expression in rats fed a high-fat diet.

BACKGROUND: Insulin resistance of pancreatic ß-cell itself may be a potential link between systemic insulin resistance and impaired insulin secretion in Type 2 diabetes. Protein tyrosine phosphatase 1B (PTP1B) dephosphorylates tyrosine residues in insulin receptors (IR) and IR substrate (IRS) proteins, and thereby inhibits insulin signaling. Thus the impact of PTP1B expression on ß-cell insulin pathway may affect insulin secretory function. AIM: The aim of the present study was to investigate the effects of intra-islet inhibition of PTP1B expression on glucose-stimulated insulin secretion and potential mechanisms in rats fed a high-fat diet (HFD). MATERIALS AND METHODS: Twenty 10-week-old Sprague Dawley rats were randomly assigned to a regular diet (RD) or a HFD for 8 weeks. At the end of the 8th week, fasting glucose, fasting insulin concentration and lipid profile were measured and an oral glucose tolerance test was done after 12-h fast. Then islet isolation was performed for static incubation and perifusion. Recombinant adenoviruses containing siPTP1B (Ad-siPTP1B), or siControl (Ad-siControl) sequences were constructed using AdEasy™ system. Islets were transfected and then assigned to the Ad-siPTP1B group, the Ad-siControl group, and mock control group. Real-time RT-PCR and Western blot were used to evaluate the expression level of PTP1B. Western blot of glucose transporter 2 (GLUT-2) and glucokinsase were also done to investigate the ß-cell glucose-sensing apparatus. Islets were incubated with Krebs-Ringer bicarbonate containing 2.8 mmol/l glucose then 16.7 mmol/l glucose to evaluate glucose-stimulated insulin secretion (GSIS). Islet perifusion was also performed to evaluate kinetics of insulin release in vitro. RESULTS: HFD rats manifested modest glucose intolerance compared with RD group. And PTP1B expression in isolated islets of rats in the HFD group was higher than that of the RD group. GSIS was impaired in islets of HFD rats (2.3±0.5-fold as basal for HFD vs 8.1±1.3-fold for RD; p<0.05). Ad-siPTP1B treatment resulted in 73% decrease in PTP1B mRNA levels and 61% decrease in PTP1B protein compared with islets treated with Ad-siControl (p<0.05). Simultaneously, PTP1B inhibition resulted in 4.7±0.8-fold increase of GSIS from basal (vs 1.9±0.1-fold for Ad-siControl, p<0.05). Perifusion showed notable improvement of first-phase insulin secretion by AdsiPTP1B treatment. Significant decrease of both GLUT-2 (by 49.8%) and glucokinase (GCK, by 43.7%) were found in the HFD group when compared with the RD group, while up-regulation of both GLUT-2 (by 98%) and GCK (by 62%) was achieved after PTP1B inhibiton by Ad-siPTP1B. CONCLUSIONS: Intra-islet PTP1B is an important physiological regulator of glucose-induced insulin release and the characteristics of PTP1B inhibitors in insulin secretion could make it a potential novel therapeutics for protection of ß-cell secretory function in Type 2 diabetes.

Space radiation damage in ZnO induced by subthreshold electrons: defect identity and optical degradation.

Space radiation damage in ZnO induced by subthreshold electrons was studied through reflectance spectra, electron paramagnetic resonance, and photoluminescence. Owing to the vacuum freezing treatment, perturbed singly ionized zinc vacancies (V'(Zn)⁻), chemisorbed species, and electrons in the conduction band and/or bound to shallow donor levels were observed. V'(Zn)⁻ is due to the ionization and the ionization-induced diffusion processes and is most likely responsible for the 420-nm absorption band. These results also support that the green luminescence in ZnO is related to zinc vacancies.

The long-term effect of autologous endothelial progenitor cells from peripheral blood implantation on infarcted myocardial contractile force.

This study was designed to evaluate the long-term effect of endothelial progenitor cell (EPC) implantation in acute myocardial infarction in Sprague-Dawley rats after ligation of the left anterior descending coronary artery. Autologous EPCs from peripheral blood were purified and implanted into an acute myocardial infarct site. Specimens and muscle strip were harvested at 3 and 6 weeks, and at 6, 8 and 12 months for contractile force assessment and, by immunohistology, for expression of vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF) and factor VIII. Expression of VEGF and bFGF, and microvessel counts and contractile force in the cell implantation group were significantly higher than in the control group up to 8 months after implantation. Beyond 8 months following implantation, however, no further improvement occurred. The EPCs showed an ability to improve contractile performance in infarcted myocardium by means of angiogenesis and vasculogenesis, and the results seemed to persist long-term.

Mutagenesis of the regulatory domain of phenylalanine hydroxylase.

The regulatory domain of phenylalanine hydroxylase (PAH, EC ) consists of more than 100 amino acids at the N terminus, the removal of which significantly activates the enzyme. To study the regulatory properties controlled by the N terminus, a series of truncations and site-specific mutations were made in this region of rat PAH. These enzymes were expressed highly in Escherichia coli and purified through a pterin-conjugated Sepharose affinity column. The removal of the first 26 amino acids of the N terminus increased the activity by about 20-fold, but removal of the first 15 amino acids increased the activity by only 2-fold. Replacing serine-29 of rat PAH with cysteine from the same site of human PAH increased the activity by more than 4-fold. Mutation of serine to other amino acids with varying side chains: alanine, methionine, leucine, aspartic acid, asparagine, and arginine also resulted in significant activation, indicating a serine-specific inhibitory effect. But these site-specific mutants showed 30--40% lower activity when assayed with 6-methyl-5,6,7,8-tetrahydropterin. Stimulation of hydroxylase activity by preincubation of the enzyme with phenylalanine was inversely proportional to the activation state of all these mutants. Combined with recent crystal structures of PAH [Kobe, B. et al. (1999) Nat. Struct. Biol. 6, 442-448; and Erlandsen, H., Bjorgo, E., Flatmark, T. & Stevens, R. C. (2000) Biochemistry 39, 2208-2217], these data suggest that residues 16-26 have a controlling regulatory effect on the activity by interaction with the dihydroxypropyl side chain of (6R)-5,6,7,8-tetrahydrobiopterin. The serine/cysteine switch explains the difference in regulatory properties between human and rat PAH. The N terminus as a whole is important for maintaining rat PAH in an optimum catalytic conformation.

Detection of genetic alterations in mouse lung adenocarcinomas by two-dimensional gel electrophoresis.

DNA from 14 mouse lung adenocarcinomas and 7 normal lungs were examined by 2-dimensional gel electrophoresis (2-DGE) for genetic alterations. 2-DGE profiles from tumor samples were compared with those profiles from normal lung tissues through a computer-assisted color overlay system. Compared to the profiles in normal lung DNA, 6 spots were amplified and 16 spots were partially reduced in their intensity in tumors. Two spots were detectable only in tumor tissues. These altered spots indicate genetic changes in mouse lung tumor development. The identification of these genetic alterations is probably important in understanding mouse lung carcinogenesis.

[Expression of proteolytic enzymes of metastatic tumor cells and the effects of some influencing factors].

OBJECTIVE: To elucidate the types of proteolytic enzymes the dendritic cell sarcoma (DCS) cell expressed in vitro and the effects of modulating factors. METHODS: The proteolytic spots of DCS cells were examined, with ten different proteinase inhibitors, various antibodies and matrix. RESULTS: Aprotinin, EDTA-Na2 and pepstatin could inhibit the proteolysis of DCS cells respectively. Anti-ubiquitin antibody and anti-DCS antibody (1:200-1:100) showed no obvious inhibitory effects. DCS cells spread out fairly well but with no proteolysis. CONCLUSIONS: Under the conditions of our experiments the DCS cells had serine proteinase, metalloproteinase and aspartate proteinase activities. Antiubiquitin antibodies and anti-DCS antibodies showed no obvious influence on the proteolysis of DCS cells. DCS cells displayed different proteolysis status on different matrix.

[The effects of 6A8 cDNA transfection on biological behavior of tumor cells].

OBJECTIVE: To investigate the effects of antisense 6A8 cDNA on the malignant behavior of tumor. METHODS: Highly metastatic clonal variant CNE-2L2 from nasopharygeal carcinoma cell line(CNE-2Z) was transfected with antisense 6A8 cDNA or mock plasmid. Their adhesion, locomotion, proteolytic ability, in vitro invasion, in vivo growth and metastasis were comparatively studied with the wild CNE-2L2 cells. RESULTS: Antisense 6A8 cDNA transfected CNE-2L2 showed less adhesion to FN and LN, weakened locomotive ability and proteolytic ability, retarded in vivo growth and much less metastasis. CONCLUSION: Transfection of antisense 6A8 cDNA obviously decreased the malignant behavior of tumor cells.

Inhibition of metastasis to lung of a human nasopharyngeal carcinoma cell line CNE- 2L2 transfected with pRc/ CMV-antisense 6A8 cDNA in nude mice.

The growth of CNE-2L2 cell, a cloned line of human nasopharyngeal carcinoma with a high potentiality of metastasis to lung was inhibited to a certain extent after transfection with a recombinant antisense expression vector of a cDNA encoding a human alpha-mannosidase (pRc/CMV-antisense 6A8 cDNA) (the Genbank accession number of 6A8 cDNA is U37248) in comparison with that of the cell transfected with the Mock and of the wild cell. Two months after a subcutaneous inoculation of CNE-2L2 cell into the axilla of nude mice metastatic lesions in the lung were observed in 9/10 mice (90%) with grade III in 8 mice and grade II in one mouse in the wild cell group, in 6/8 mice (75 %) with grade III in one mouse, grade II in 2 mice and grade I in 3 mice in the Mock-transfection group, in only 3/10 mice (30%) with all grade I in pRc/CMV-antisense 6A8 cDNA-transfection group.

[Phenomenon of intrinsic rhythm of luteinizing hormone release from isolated anterior pituitary gland of female rat].

The intrinsic nature of rthymic release of luteinizing hormone (LH) of isolated human and rat anterior pituitary gland reported independently by Macro Gambacciani and Xie in 1987 can be more directly demonstrated by a computer programme of Time Series-HSY Hidden Periodic Analytic Approach for continuous monitoring the LH output of the perfusate from a perfusion system with in vitro anterior pituitary of SD female rat. The results are as follows: (1) Under various reproductive conditions the average frequency (min/cycle) and amplitude (ng/ml) of the intrinsic rhythm of LH release were quite different: In proestrous group the frequency and amplitude were the highest, being intermediate in the ovariectomized group and lowest in the lactation group. (2) The intrinsic rhythm of LH release could be changed by either peptide or steroid hormones. In proestrous group with 30 min of gonadotropin-releasing hormone (GnRH), stimulation would reduce both frequency and amplitude. In case of lactation, the frequency was unchanged, but amplitude lowered, while in the ovariectomized rat pituitary, the 30 min GnRH stimulation decreased the frequency of release only. The intrinsic rhythm of the LH release could also be influenced by steriod hormones (Ru486 and Anordrin). With 120 min before removal of the anterior pituitary gland the rats receiving i.m. injection of Ru486 (2 mg/kg bw) or Anordrin (2 mg/kg), the results showed that Ru486 decreased frequency, while Anordrin decreased only the frequency to a less extent, both without amplitude affected. (3) Verapamil and EGTA added to the perfusion system did not abolish but only decreased the rhythmic phenomenon by using proestrous pitutary. This suggests that participation of Ca2+ may take place in the intrinsic release of LH. The above results indicated that the intrinsic rhythm of LH release of isolated anterior pituitary gland is different from various reproductive hormonal conditions and capable of being modified by exogenous hormones. The physiological function of the intrinsic rhythm of LH release of anterior pituitary gland remains to be elucidated.

Detection of genomic alterations in human cervical cancer by two-dimensional gel electrophoresis.

Two-dimensional gel electrophoresis was used to comprehensively scan the whole genome of 6 cervical intraepithelial neoplasia (CIN) lesions, 7 cervical squamous cell carcinomas, 1 cervical adenosquamous cell carcinoma, and 2 cervical adenocarcinomas for multiple genetic alterations, such as DNA amplification, chromosome deletion, loss of heterozygosity, and chromosome translocation, as compared with the paired normal tissues. DNA spot analysis of the genomic 2-dimensional gels was performed by a computer color overlay system and by spot recognition software allowing for objective spot comparison and quantitation. Nine spots were found to be amplified in the cervical carcinomas while two amplified spots were detected in the CIN III lesions. Fourteen DNA spots were either reduced in their intensity or absent in cervical carcinomas as compared to their normal paired tissues. Reduction of intensity in 6 spots was observed in the 5 CIN III lesions. These genetic alterations may represent changes in cancer genes that are associated with human cervical carcinogenesis. Further characterization of these alterations may be significant to the understanding of cervical tumorigenesis and to the development of biomarkers for clinical trials in cancer chemoprevention.

[Chemosensitivity testing of fresh human gastrointestinal cancers using AgNOR assay].

The argyrophilic staining of nucleolar onganizer region (AgNOR), a simple colorimetric test, has been adapted for chemosensitivity testing of human gastric and colorectal cancers. Seven different chemotherapeutic agents were tested. The drug sensitivity was measured and compared according to the decrease rate of AgNOR granules between control tumor cells and tumor cells treated with antitumor drugs. Only 3 of 10 cases of advanced gastric carcinoma were sensitive to one antitumor agent. Most colorectal carcinoma cases (18/20) were sensitive to at least one antitumor agent. The sensitive sequence of antitumor agents we have had in this study was relative to clinic. The method and characteristics of AgNOR assay as a chemosensitivity test was introduced. It's value is being observed.