OBJECTIVETo observe the effect of Guilingji Capsule (GC) on the fertility, liver functions, and serum lactate dehydrogenase (LDH) of adult male SD rats exposed by 900 MHz cell phone.

METHODSTotally 18 adult male SD rats and 36 adult female rats in child-bearing period were selected and randomly divided into three groups according to weight equilibrium principle, i.e., the normal group, the radiated group, and the GC group, 6 males and 12 females in each group. Male rats in the normal group and all female rats were not radiated. Male rats in the radiated group and the GC group received radiation for 4 h per day, lasting for 18 successive days. Rats in the GC group received GC suspension at the daily dose of 0. 15 g/kg by gastrogavage at the same time. Equal volume of normal saline was administrated to other male rats. Then male rats were mated with corresponding female rats from the 14th radiation night to the 18th radiation night in the ratio of 1:2. Male rats were killed following on the next morning of ending the radiation. Female rats were normally fed and then killed before delivery. The pregnant outcomes of female rats in responding groups (the rates of pregnancy and the number of death fetus, birth weight, body length, and tail length) were observed and compared. Serum alanine aminotransferase (ALT), aspartate transferase (AST), AST/ALT, and LDH levels of the male rats were detected by colorimetry. Histological and morphological changes of liver were observed by HE staining.

RESULTSCompared with the normal group, the pregnancy rates of female rats decreased and the number of death fetus increased, the serum LDH level obviously increased in the radiated group (P < 0.05). Serum levels of ALT, AST, and AST/ALT were no significantly changed in the radiated group. The hepatocyte nuclear atrophy and cytoplasm vacuolar degeneration appeared. Compared with the radiated group, the pregnancy rates increased, the number of death fetus dropped, and the serum level of LDH decreased in the GC group (P < 0.05). There was no obvious change in serum levels of ALT, AST, or AST/ALT. The hepatocyte nuclear atrophy and cytoplasm vacuolar degeneration were significantly attenuated. The histomorphological structures recovered to normal basically in the GC group.

CONCLUSIONSThe pregnancy rates could be decreased, the number of death fetus increased, histomorphological structures abnormal, and serum LDH level increased by exposure toy GSM 900 MHz cell phone. GC could prevent and treat the aforesaid lesion. But there was no statistical difference in serum ALT or AST levels.

Animals ; Cell Phone ; Drugs, Chinese Herbal ; pharmacology ; Female ; Fertility ; Lactate Dehydrogenases ; blood ; Liver ; drug effects ; Male ; Pregnancy ; Radiation ; Rats ; Rats, Sprague-Dawley

Aged ; Humans ; Lower Extremity ; Middle Aged ; Muscle, Skeletal/physiology* ; Vibration

Iodine, an essential component of the hormones produced by the thyroid gland, is widely but unevenly distributed in the earth's environment. Great difference exists in the iodine nutritional status of populations residing in different region. Both iodine deficiency and iodine excess can injure the thyroid gland. Iodine deficiency tigers endemic goiter, cretinism, and hyperthyroidism, while iodine excess can result in high iodine goiter, chronic lymphocytic thyroiditis, iodine-induced hyperthyroidism, and hypothyroidism; also, iodine deficiency or excess may affect the histological type of thyroid cancer. In 1996, China began to implement the universal salt iodization policy, which has basically eliminated the iodine deficiency disorders nationwide; however, it also caused the changes in the spectra of other thyroid diseases including iodine-induced hyperthyroidism, autoimmune thyroid disease, and papillary thyroid carcinoma. Individualized iodine nutritional status assessment for the populations, particularly those with thyroid diseases, will be beneficial.
China ; epidemiology ; Humans ; Iodine ; administration & dosage ; adverse effects ; deficiency ; Sodium Chloride, Dietary ; adverse effects ; Thyroid Diseases ; epidemiology ; etiology

Objective To investigate the better regimen of combined cyclophosphamide pulse therapy with corticosteroids in the treatment of Pemphigus. Methods Intravenous cyclophosphamide was given weekly in a dosage of 600 mg to those Pemphigus patients whose conditions couldn't be improved by corticosteroids (oral prednisone 1.2～1.5 mg/kg/d) alone. Results Ten patients with Pemphigus received weekly cyclophosphomide therapy in addition to corticosteroid. Patients conditions improved quickly, without side effects. Conclusions Cyclophosphamide weekly pulse therapy combined with corticosteroids is a good regimen in the treatment of Pemphigus.

OBJECTIVETo investigate the mechanisms of apoptosis induced in human hepatoma cell line SMMC7721 by plasmid pVHN constructed with Newcastle disease virus (NDV) HN gene.

METHODSTwenty-four h after transfection with liposome-plasmid pVHN complexes in vitro, the mortality rate of SMMC7721 cells was determined by MTT staining and flow cytometry (FCM) with PI staining. The alteration of mitochondrial trans-membrane potential of the cells was detected by FCM with rhodamine 123 staining. Cell genomic DNA was detected by agarose electrophoresis. The activation of caspase-3 was assayed by its substrate color reaction.

RESULTSSignificant apoptosis was induced by transfection with plasmid pVHN into the cells for 24 h and the mortality rate was 50.0% (the mortality rate of control group was 5.2%). Genomic DNA was fragmented and mitochondrial trans-membrane potential was decreased, but caspase-3 activity increased.

CONCLUSIONSignificant apoptosis in SMMC7721 cells can be induced by NDV HN gene. Apoptosis may be resulted from the decrease of mitochondrial trans-membrane potential and activation of Caspase-3.

Apoptosis ; physiology ; Cancer Vaccines ; immunology ; Carcinoma, Hepatocellular ; pathology ; Caspase 3 ; metabolism ; Cell Line, Tumor ; HN Protein ; genetics ; Humans ; Liver Neoplasms ; pathology ; Newcastle disease virus ; genetics ; Transfection ; Vaccines, DNA ; immunology

OBJECTIVETo study the clinical value of muscle autograft denatured by microwave for repair of gap in removal of facial neuroma.

METHODSA case of patient with a larger facial nerve Schwann cell neuroma was reported. Based on the good results of our experimental research on rats recently, we completed the operation by transmastoid approach for removal of facial neuroma, and the gap of the nerve was repaired with muscle autograft denatured by microwave.

RESULTSThe patient was followed up for one year, and her facial function recovery on the affected side was satisfactory.

CONCLUSIONMuscle autograft denatured by microwave technique is convenient, highly efficient for repairing facial nerve gap after removal of facial neuroma.

Adult ; Facial Neoplasms ; complications ; surgery ; Facial Nerve ; physiology ; Facial Paralysis ; etiology ; surgery ; Female ; Follow-Up Studies ; Humans ; Microwaves ; Muscle, Skeletal ; transplantation ; Nerve Regeneration ; Neurilemmoma ; complications ; surgery ; Protein Denaturation ; Transplantation, Autologous

In order to elucidate the expression and molecular genetic background of ABO gene seven samples with ABO discrepancy further identified as bi-specific ABO gene were studied. All these samples were subjected to phenotyping by monoclonal and polyclonal antisera and were then genotyped by direct DNA sequencing and haplotype-sequencing at the exon 6 and 7 of ABO gene. As a result, six ABO dual-specific alleles were identified in Chinese population. An antigen expressed by these B (A) or Cis-AB individuals varied from very low level to the normal level, compared with common A blood group samples. In conclusion, molecular genetic backgrounds of two pairs out of four samples in all samples were the same, however, the ABO expression showed diverse.
ABO Blood-Group System ; genetics ; Asian Continental Ancestry Group ; genetics ; DNA Mutational Analysis ; Erythrocytes ; cytology ; enzymology ; metabolism ; Exons ; genetics ; Glycosyltransferases ; chemistry ; genetics ; Humans

OBJECTIVETo develop a novel scaffolding method for the copolymers poly lactide-co-glycolide acid (PLGA) to construct a three-dimensional (3-D) scaffold and explore its biocompatibility through culturing Schwann cells (SCs) on it.

METHODSThe 3-D scaffolds were made by means of melt spinning, extension and weaving. The queueing discipline of the micro-channels were observed under a scanning electronic microscope (SEM).The sizes of the micropores and the factors of porosity were also measured. Sciatic nerves were harvested from 3-day-old Sprague Dawley (SD) rats for culture of SCs. SCs were separated, purified, and then implanted on PLGA scaffolds, gelatin sponge and poly-L-lysine (PLL)-coated tissue culture polystyrene (TCPS) were used as biomaterial and cell-supportive controls, respectively. The effect of PLGA on the adherence, proliferation and apoptosis of SCs were examined in vitro in comparison with gelatin sponge and TCPS.

RESULTSThe micro-channels arrayed in parallel manners, and the pore sizes of the channels were uniform. No significant difference was found in the activity of Schwann cells cultured on PLGA and those on TCPS (P larger than 0.05), and the DNA of PLGA scaffolds was not damaged.

CONCLUSIONThe 3-D scaffolds developed in this study have excellent structure and biocompatibility, which may be taken as a novel scaffold candidate for nerve-tissue engineering.

Animals ; Biocompatible Materials ; Cell Adhesion ; Cell Proliferation ; Cell Separation ; Cells, Cultured ; Lactic Acid ; Microscopy, Electron, Scanning ; Polyglycolic Acid ; Rats ; Rats, Sprague-Dawley ; Schwann Cells ; cytology ; Tissue Engineering ; methods ; Tissue Scaffolds

BACKGROUNDNumerous studies have shown that reducing the level of tumor necrosis factor-alpha (TNFα) through the use of anti-TNF antibodies or soluble TNF receptor is a safe and efficacious treatment to inflammatory diseases such as rheumatoid arthritis. Therefore, novel approaches to achieve this outcome are desired. The aim of this study was to investigate the characterization of a small molecule inhibitor, Y316, which blocks TNF mRNA upregulation and TNF production by lipopolysaccharides (LPS) stimulated monocytes.

METHODSPeripheral blood mononuclear cells (PBMC) from healthy volunteers were plated in 24-well plates and stimulated with LPS (1 µg/ml), phorbol-12-myristate-13-acetate (PMA) (100 ng/ml), zymosan (10 µg/ml) and Tsst (100 ng/ml). Supernatants were collected after 4-hour culture at 37°C, and quantitative determination of TNFα, interleukin-1β (IL-1β), IL-6, IL-8, IL-10 and IL-2 production in the supernatants was performed by colorimetric enzyme-linked immunosorbent assay (ELISA). Total RNA of PBMC was isolated and cytokine mRNA quantitation was performed by using a RNA level measuring kit (R & D Systems). PBMC were pretreated with Y316 (10 µmol/L, 1 µmol/L, 0.1 µmol/L, 0.01 µol/L and 0.001 µmol/L) or dimethyl sulfoxide at 37°C for 10 minutes, and then stimulated with LPS or PMA, protein concentrations of p44.42, IKBα, P38 and Jun NH2-terminal kinase were determined by Western blotting. Cyclic adenosine-3',5'-monophosphate (cAMP) of PBMC was measured by enzyme immunoassay kit (Amersham Pharmacia Biotech).

RESULTSY316 blocked TNF production and inhibited the upregulation of TNF mRNA levels in response to LPS, and also prevented the production of IL-1 and IL-6. In contrast, Y316 augmented the production of IL-10 in LPS-stimulated monocytes. Y316 failed to prevent the production of IL-2 and TNF in antigen-stimulated T cells, suggesting that its effects may be cell-type specific. Y316 prevented the phosphorylation and activation of the MAPK, ERK, and therefore appeared to mediate its effects on TNF by acting at an early point in the signaling cascade induced in response to LPS. There was no effect of Y316 on cAMP levels either alone or in the presence of LPS.

CONCLUSIONSY316 appears to be a small molecule inhibiting TNF production, which may act via a novel mechanism. Identification of the target of Y316 may lead to the development of alternative strategies for achieving selective cytokine inhibition.

Anti-Inflammatory Agents ; pharmacology ; Extracellular Signal-Regulated MAP Kinases ; metabolism ; Humans ; Interleukin-1 ; antagonists & inhibitors ; biosynthesis ; Interleukin-6 ; antagonists & inhibitors ; biosynthesis ; Lipopolysaccharides ; pharmacology ; Monocytes ; drug effects ; immunology ; Phosphorylation ; Tumor Necrosis Factor-alpha ; antagonists & inhibitors ; biosynthesis

OBJECTIVETo determine whether transforming growth factor betal (TGF-beta1)/Smad signaling pathway mediates p53-dependent apoptosis in hepatoma cell lines.

METHODSThree human hepatic carcinoma cell lines, HepG2, Huh-7, and Hep3B, were used in this study. TGF-beta1-induced apoptosis in hepatic carcinoma cell lines was analyzed using TUNEL assay. For identifying the mechanism of apoptosis induced by TGF-beta1, cell lines were transfected with a TGF-beta1-inducible luciferase reportor plasmid containing Smad4 binding elements. After transfection, cells were treated with TGF-beta1, then assayed for luciferase activity.

RESULTSThe apoptosis rate of HepG2 cell lines (48.51% +/- 8.21%) was significantly higher than control (12.72% +/- 2.18%, P <0.05). But TGF-beta1 was not able to induce apoptosis of Huh-7 and Hep3B cell lines. The relative luciferase activity of TGF-beta1-treated HepG2 cell lines (4.38) was significantly higher than control (1.00, P < 0.05). But the relative luciferase activity of TGF-beta1-treated Huh-7 and Hep3B cell lines less increased compared with control.

CONCLUSIONSHepG2 cells seem to be highly susceptible to TGF-beta1-induced apoptosis compared with Hep3B and Huh-7 cell lines. Smad4 is a central mediator of TGF-beta1 signaling transdution pathway. TGF-beta1/Smad signaling pathway might mediate p53-dependent apoptosis in hepatoma cell lines.

Apoptosis ; drug effects ; Carcinoma, Hepatocellular ; genetics ; metabolism ; pathology ; Cell Line, Tumor ; Genes, Reporter ; Genes, p53 ; Humans ; Liver Neoplasms ; genetics ; metabolism ; pathology ; Luciferases ; metabolism ; Plasmids ; Signal Transduction ; Smad4 Protein ; metabolism ; Transfection ; Transforming Growth Factor beta1 ; pharmacology