Follicle-stimulating hormone (FSH) is synthesized and secreted by the anterior pituitary, which binds to its receptors expressed on the membrane of Sertoli cells in the testis to bring about spermatogenesis. With the development of DNA sequencing technology, FSH SNPs rs10835638 and FSHR SNPs rs6165, rs6166, and rs1394205 were detected, which might directly affect the expression of FSH and activity of FSHR, resulting in male spermatogenic dysfunction. This review focuses on the relationship of FSH and FSHR gene polymorphisms with male infertility.
Follicle Stimulating Hormone ; genetics ; Humans ; Infertility, Male ; genetics ; Male ; Polymorphism, Single Nucleotide ; Receptors, FSH ; genetics ; Sertoli Cells ; Spermatogenesis ; Testis

Objective To investigate symptom characteristics and their their prevalence in terminally ill patients with ovarian carcinoma.Methods A retrospective study was carried out based on clinical data of 98 terminally ill patients with ovarian carcinoma who died in our hospital during January 1995 to December 2004.Fifteen most common symptoms were analyzed with a focus on the followings:symptom incidence,survival time after symptom occurrence,regularity of symptom cluster,and common causes of death.Fifteen symptoms were:pain,cachexia,pleural effusion and ascites,dyspnea,fever,intestinal obstruction,renal failure,bone marrow depression,lung infection,hemorrhage,deep venous thrombosis (DVT),intestinal or pancreatic fistula,mycotic infection,jaundice and emergency conditions.Results (1)The most prevalent symptom was pleural effusion and ascites(63%),followed by pain(60%), cachexia(59%),dyspnea(52%)and intestinal obstruction(49 %).(2)The symptom which lasted longest survival time was mycotic infection(77 days),followed by intestinal or pancreatic fistula(75 days), intestinal obstruction(67 days),pain(60 days)and eachexia(60 days).Symptoms such as bone marrow depression,renal failure,dyspnea and emergency conditions were comparatively critical associated with shorter survival times(14,13,12,7 days,respectively).(3)Terminal symptoms occurred typically in clusters,with 4.9?1.5 symptoms per case.Of 98 cases,84 cases(86%)had 4 or more symptoms,with the median survival time of 63 days from the last day of anti-cancer therapy,and a slow death process.The remaining 14 cases(14%)with 3 or fewer symptoms survived only 25 days,of which 10 cases(71%)died of emergency diseases.The survival time for two groups was significantly different(P

A phytochemical investigation on the aerial parts of a Tibetan medicine Meconopsis horridula, by solvent extraction, repeated chromatographies on silica gel, Sephadex LH-20, and preparative TLC techniques, led to the isolation of 9 compounds. By spectroscopic analysis and comparison of its 1H and 13C-NMR data with those in literatures, their structures were identified as oleracein E(1), N-( trans-p-coumaroyl) tyramine (2), chrysoeriol (3), apigenin (4), hydnocarpin (5), p-coumaric acid glucosyl ester (6), stigmast-5-ene-3beta-ylformate (7), 3beta-hydroxy-7alpha-ethoxy-24beta-ethylcholest-5-ene (8), and beta-sitosterol (9), respectively, among which compounds 6-8 were isolated from the genus for the first time,and 1,3 were isolated from the species for the first time. A MTT method was applied to evaluate the cytotoxic activity of compounds 14 against the human hepatocellular liver carcinoma cell line (HepG2), and compound 1 showed significant cytotoxicity against HepG2,with its inhibitory rate of 52.2% at 10 micromol x L(-1).
Medicine, Tibetan Traditional ; Molecular Structure ; Papaveraceae ; chemistry ; Plant Extracts ; chemistry ; Spectrometry, Mass, Electrospray Ionization

OBJECTIVETo study the protective effect of lidocaine against lung injury after hemorrhagic shock in rabbits.

METHODSEighteen healthy rabbits were randomly divided into 3 groups (n=6), namely lidocaine group (group L), hemorrhagic shock group (group H) and control group (group C). Hemorrhagic shock model was established in rabbits in groups L and H, and the venous blood samples were collected for measurement of plasma malondialdehyde (MDA) and superoxidedismutase (SOD) before phlebotomy (T0), 2 h after hemorrhagic shock (T1) and 2 h after resuscitation (T2). Blood samples were also taken for measurement of MDA and SOD at the same time points in group C. The wet to dry weight ratio of the lung (W/D) was measured at T2.

RESULTSMDA level was significantly lower while SOD level significantly higher in group L than in group H (P<0.05). The W/D ratio in group L was reduced significantly as compared with that in group H (P<0.05).

CONCLUSIONLidocaine can remarkably alleviate lung injury after hemorrhagic shock by inhibiting MDA production and increasing SOD content.

Animals ; Disease Models, Animal ; Lidocaine ; pharmacology ; Lung ; drug effects ; metabolism ; Lung Injury ; prevention & control ; Malondialdehyde ; blood ; Rabbits ; Shock, Hemorrhagic ; drug therapy ; Superoxide Dismutase ; blood

OBJECTIVETo investigate the effect of propofol at doses for different anesthesia depths on γ-aminobutyric acid (GABA) in different cerebral regions at propofol uptake equilibrium in dogs.

METHODSTwelve 12-18-month-old healthy hybrid dogs weighing 10-12 kg were randomly divided into light anesthesia group (n=6) and deep anesthesia group (n=6) with a single bolus dose of propofol (5.5 and 7.0 mg/kg, respectively) completed in 15 s followed by intravenous propofol infusion at a constant rate (55 and 70 mg·kg(-1)·h(-1), respectively). Blood samples (2 ml) were taken from the internal carotid artery and jugular vein to measure plasma propofol concentrations 50 min after the start of the infusion. The dogs were then sacrificed and tissues were taken from different brain regions and the cervical cord to measure GABA concentrations using high-pressure liquid chromatography (HPLC).

RESULTSThe plasma propofol concentrations in internal carotid artery and jugular vein were similar in both light anesthesia group (3.00 ± 0.31 and 3.10 ± 0.51 µg/ml, respectively, P>0.05) and deep anesthesia group (6.41 ± 0.05 and 6.40 ± 0.11 µg/ml, respectively, P>0.05). GABA concentrations in the brain regions were significantly higher in deep anesthesia group than in light anesthesia group (P<0.05). The dorsal thalamus and hypothalamus showed greater GABA variations [(83.83 ± 2.230%) and (85.83 ± 1.72)%] compared to other brain regions at different anesthesia depths (P<0.05).

CONCLUSIONSIn both groups, plasma propofol concentrations in the internal carotid artery and internal jugular vein reach equilibrium at 50 min of propofol infusion. The variation of GABA is associated with the anesthesia depth of propofol, and GABA variation in the dorsal thalamus and hypothalamus plays an important role in propofol anesthesia.

Anesthetics, Intravenous ; pharmacokinetics ; Animals ; Brain ; metabolism ; Dogs ; Female ; Male ; Propofol ; blood ; pharmacokinetics ; gamma-Aminobutyric Acid ; metabolism

OBJECTIVETo observe the regional distribution of propofol in canine spinal cord under noxious stimulation.

METHODSTwelve healthy hybrid dogs (12-18 months old, weighing 10-12 kg) were randomly divided into control group (n=6) and stimulation group (n=6). All the dogs were anesthetized with a single bolus dose of propofol (7 mg/kg) in 15 seconds followed by propofol infusion at a constant rate of 70 mg/kg/h via the great saphenous vein of the right posterior limb. In the stimulation group, the tails of the dogs were clamped for 5 min after 45 min of propofol infusion. Blood samples were taken from the internal carotid artery and internal jugular vein at 50 min after propofol infusion to detect plasma propofol concentrations by high-pressure liquid chromatography (HPLC). The dogs were then immediately sacrificed by decapitation and the frontal horn, posterior horn, intermediate zone, frontal funiculus, posterior funiculus and lateral funiculus of the spinal cord were dissected for determination of propol content by HPLC.

RESULTSThe plasma concentrations of propofol in the internal carotid artery and internal jugular vein were 5.07-/+0.23 and 5.03-/+0.10 microg/ml in the stimulation group, respectively showing no significant differences from those in the control group (5.09-/+0.03 and 5.08-/+0.03 microg/ml, P>0.05). In the control group, the propofol concentration was 5.09-/+0.08 microg/g in the frontal horm, 5.10-/+0.08 microg/g in the posterior horn, 5.05-/+0.19 microg/g in the intermediate zone, 5.06-/+0.14 microg/g in the frontal funiculus, 5.06-/+0.15 microg/g in the posterior funiculus and 5.06-/+0.41 microg/g in the lateral funiculus, showing no significant differences (P>0.05). The propofol concentrations in the frontal horn (7.65-/+0.47 microg/g) and posterior funiculus (7.06-/+0.82 microg/g) in the stimulation group were significantly higher than those in the other spinal cord tissues (P<0.05) and those in the control group (P<0.05).

CONCLUSIONAt 50 min after intravenous injection of propofol at a constant rate of 70 mg/kg/h, plasma propofol concentrations in the internal carotid artery and internal jugular vein reaches equilibrium with a balanced distribution in all the spinal cord regions. Propofol concentration can be higher in the frontal horn and posterior funiculus under noxious stimulation.

Animals ; Dogs ; Female ; Male ; Nociceptors ; drug effects ; physiology ; Pain ; physiopathology ; Physical Stimulation ; Propofol ; administration & dosage ; pharmacokinetics ; pharmacology ; Random Allocation ; Spinal Cord ; metabolism

OBJECTIVETo find out the relationship between mutation of ATP7B gene promoter region and pathogenesis of Wilson disease(WD).

METHODSTwo of 48 WD patients presented C-->T base substitution mutations at the position -183. DNA sequences of the promoter region from normal and mutant samples were separated. The fragments containing the promoter region were cloned upstream of the luciferase. Luciferase activity was analyzed.

RESULTSThe luciferase activity of reporter gene containing normal sequence of ATP7B gene promoter region did not show significant difference as compared with that of reporter gene containing mutant promoter(n=3, P > 0.05).

CONCLUSIONNo influence of C-->T base substitution mutations on the activity of promoter was observed in study. The results suggest that WD pathogenesis relates little to the mutations of the promoter region in Chinese.

Adenosine Triphosphatases ; genetics ; Adolescent ; Adult ; Base Sequence ; Cation Transport Proteins ; genetics ; Cell Line, Tumor ; Child ; Copper-transporting ATPases ; DNA Mutational Analysis ; Female ; Hepatolenticular Degeneration ; genetics ; Humans ; Luciferases ; genetics ; metabolism ; Male ; Middle Aged ; Mutation ; Promoter Regions, Genetic ; genetics ; Young Adult

OBJECTIVETo study the inhibitory effect of (-)-epigallocatechin-3-gallate (EGCG) on cancer cells line HCT-8 and HT29 and its influence on the expression of HES1 and JAG1.

METHODSColorectal cancer cells line HCT-8 and HT29 were cultured in vitro and treated with different concentrations of EGCG(10 mg/L, 20 mg/L, 35 mg/L). The inhibition of proliferation was tested by MTT analysis. Influence of EGCG on the cell apoptosis and cell cycle of HCT-8 and HT29 were detected with flow cytometry, and gene expression of HCT-8 and HT29 after EGCG treatment with real-time polymerase chain reaction.

RESULTSEGCG affected the proliferation and apoptosis of HCT-8 and HT29. The inhibition rates of the three different concentrations of EGCG were(28.894±5.076)%, (34.903±1.794)%, and (39.028±0.105)% on HCT-8, and (14.682±4.244)%, (22.429±3.847)%, and (29.840±5.076)% on HT29. EGCG caused G(2)/M phase arrest and M phase transition in HCT-8 cell line, and S phase arrest and G2 phase transition in HT29 cell line. EGCG down-regulated HES1 gene expression in both cell lines, however, the differences were not statistically significant(both P>0.05). EGCG upregulated JAG1 gene expression in both cell lines, however only the difference in HCT-8 was statistically significant(0.201±0.018 vs. 0.440±0.077, P=0.029).

CONCLUSIONSEGCG can significantly inhibit the proliferation of HT29 cells and HCT-8 cells by changing cell cycle and inducing cell apoptosis. The mechanism may be related to the upregulation of JAG1 gene expression.

Apoptosis ; drug effects ; Basic Helix-Loop-Helix Transcription Factors ; metabolism ; Calcium-Binding Proteins ; metabolism ; Catechin ; analogs & derivatives ; pharmacology ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Colorectal Neoplasms ; pathology ; Flow Cytometry ; HT29 Cells ; Homeodomain Proteins ; metabolism ; Humans ; Intercellular Signaling Peptides and Proteins ; metabolism ; Jagged-1 Protein ; Membrane Proteins ; metabolism ; Serrate-Jagged Proteins ; Transcription Factor HES-1

BACKGROUNDPulmonary embolism, a potentially fatal event, occurs more frequently in cancer patients than in the general population. To offer an accurate diagnosis and effective treatment to such patients in China, we analyzed the incidence rate and clinical features of pulmonary embolism in patients with solid tumor hospitalized in the Peking Union Medical College (PUMC) Hospital.

METHODSA retrospective analysis was made of the hospitalized patients with solid malignancies complicated with pulmonary embolism who had been admitted into the PUMC Hospital from January 2002 to December 2008.

RESULTSThe incidence of pulmonary embolism in hospitalized patients with solid malignancies was 0.27% (120/43 967). The median age at diagnosis was 57.5 years. The male to female ratio was 1.0:1.4 (49:71). Patients with non-small-cell lung cancer (NSCLC) constituted the largest proportion of the 120 patients (37.5%), followed by patients with breast (9.2%), ovarian (8.3%), pancreatic (6.7%), and liver cancer (6.7%). Eighty patients (66.7%) had stage IV cancer. Bone was the most common site of distant metastasis (46.3%). D-dimer level was elevated in 90.9% of the 66 tested patients. The incidence of bleeding due to anti-coagulation therapy was 3.6%. Thirty-six (30.0%) of the 120 patients had concurrent deep venous thrombosis in the lower extremities. Seventeen patients developed acute pulmonary embolism within 2 weeks after surgery, 3 of whom died suddenly. Four patients presented with deep venous thrombosis and 1 with pulmonary embolism prior to the identification of malignancy.

CONCLUSIONSPatients with cancer of the lung, ovarian, breast, pancreas, and liver are more likely to be complicated with pulmonary embolism than those with other types of solid tumors. Patients with distant metastasis are at a higher risk of pulmonary embolism. Pulmonary embolism without concurrent deep venous thrombosis is more frequently observed than concurrence of both disorders in the clinical setting.

Adolescent ; Adult ; Aged ; Aged, 80 and over ; Anticoagulants ; therapeutic use ; Child ; Child, Preschool ; Female ; Heparin ; therapeutic use ; Humans ; Male ; Middle Aged ; Neoplasms ; classification ; complications ; diagnosis ; drug therapy ; Pulmonary Embolism ; diagnosis ; drug therapy ; etiology ; Young Adult