An analysis of the variations and clinical applications of the lateral circumflex femoral artery.

BACKGROUND: Identifying the arterial variation of the lateral circumflex femoral artery (LCFA) is a vital step in planning surgical and radiological approach. The aim of the study was to evaluate the variations and discuss the clinical correlates of the LCFA. MATERIALS AND METHODS: Fifty eight adult cadavers (male 45, female 13) with 115 usable sides were used to assess and classify the origin and branches of the LCFA. Also its external diameter, distance from mid-inguinal ligament to sites of origin from the profunda femoris artery or femoral arteries. RESULTS: There were seven types of LCFA variations in this sample. We classified them as types A to G, of which type A was normal, that is, the one showing a single LCFA arising from the profunda femoris artery. Nearly 50.43% of the sample had type B-G variations, each having 13, 10, 23, 4, 4, and 3 cases, accounting for 11.30%, 8.70%, 20.00%, 3.48%, 3.48%, and 2.61%, respectively. CONCLUSIONS: There are many variant types in the LCFA. To avoid iatrogenic injuries, clinicians must have a sound understanding of the variation types of this important blood vessel.

The impact of low-intensity extracorporeal shock wave therapy on testicular function in adult rats.

BACKGROUND: Low-intensity extracorporeal shock wave therapy (Li-ESWT) has been introduced as a treatment for penile diseases. Its impact on testicular function during treatment remains unknown. OBJECTIVES: To clarify whether Li-ESWT impairs testicular function during the treatment of penile diseases by investigating the impact of Li-ESWT on testosterone synthesis and spermatogenesis in adult rats. MATERIALS AND METHODS: Twenty-four male Sprague-Dawley rats were equally divided into the following three groups: control group, 1.6 BAR group, and 3.2 BAR group. Rats in the experimental groups were treated with Li-ESWT at different energy levels (300 shocks at 1.6 BAR or 3.2 BAR, 2 Hz frequency) three times a week for 3 weeks. The control group did not receive any treatment during the same period of time. One day after the last shock wave treatment, serum and testicular tissue testosterone concentrations were measured, and sperm quality was assayed. Histologic examination of the testes and quantitative real-time PCR were performed. RESULTS: Testosterone levels in both the serum and testicular tissue did not change after Li-ESWT exposure. The expression levels of steroidogenic enzymes (steroidogenic acute regulatory protein (StAR), cytochrome P450 cholesterol side-chain cleavage enzyme (P450scc), and 3ß-hydroxysteroid dehydrogenase (3ß-HSD)) were not impacted by Li-ESWT. The 3.2 BAR group showed a significantly lower sperm count and lower expression of synaptonemal complex protein 3 (SYCP3) in testicular tissue than the control group. No significant differences in sperm quality or SYCP3 expression were observed between the control group and the 1.6 BAR group. CONCLUSION: Li-ESWT exposure at 3.2 BAR inhibited spermatogenesis and decreased sperm quality, which indicated that male patients with a desire to preserve fertility should undergo low-energy Li-ESWT or other treatment modalities.

[Analysis on the novel compound heterozygous mutation Fâ ª of a patient with hereditary factor â ª deficiency].

Objective: To investigate the clinical phenotype and genotype characteristics of a Chinese hereditary factor Ⅺ deficiency pedigree. Methods: The activated partial thromboplastin time (APTT), prothrombin time (PT), FⅪ activity (FⅪ: C) were measured by clotting method using automatic coagulation analyzer. The FⅪ antigen (FⅪ: Ag) was assayed by enzyme-linked immunosorbent assay (ELISA). Fifteen exons of F11 from the proband and his pedigree members were amplified by polymerase chain reaction (PCR), then sequenced. Pymol software was used to analyze the novel mutations. Results: APTT, FⅪ: C and FⅪ: Ag of proband was 74.2 s, 4.0% and 2.9%, respectively. For his older sister, APTT, FⅪ: C and FⅪ: Ag was 67.1 s, 3.0% and 1.8%, respectively. APTT, FⅪ: C and FⅪ: Ag of healthy controls were 34.5 s, 100.0% and 100.0%. FⅪ: C of proband's father, mother and brother were 72.0%, 62.0%, and 78.0%, respectively. FⅪ: Ag of them were 50.0%, 43.0%, and 51.8%, respectively. The other coagulant parameters of the proband and his pedigree were all in the normal range. Sequence analysis showed two heterozygous gene mutations in F11 of the proband and his older sister. One was a deletion of T at nucleotide 1 491 in exon 12, resulting in a frameshift. A substitution of leucine 465 by tryptophan and a terminal coden after 7 amino acid: F11NM_13142c.1491delT (p.Leu465Trp.fs*7). The other was a G to A substitution at nucleotide 1 815 in exon 15, resulting in a substitution of glycine 573 by aspartic acid: F11 NM_13142c.1815G>A (p.Gly573Asp). F11NM_13142c.1491delT (p.Leu465Trp.fs*7) heterozygotes were found both in the proband's father and his brother while p. Gly573Asp heterozygote was only found in his mother. F11 of the proband's uncle was wild. Conclusion: The novel compound heterozygous mutations of F11NM_13142c.1491delT (p.Leu465Trp.fs*7) and F11 NM_13142 c. 1815G>A (p.Gly573Asp) are responsible for FⅪ deficiency to the proband, which induced the decrease of FⅪ: C and FⅪ: Ag.

Thermal characterization of lowly Nd3+ doped disordered Nd:CNGG crystal.

Thermal properties of a lowly Nd(3+)-doped disordered Nd:CNGG crystal have been symmetrically investigated. At room temperature, the specific heat, thermal diffusion coefficient and density were determined to be 0.595 J/g.K, 1.223 mm(2)/s and 4.718 g/cm(3), corresponding the thermal conductivity of 3.43 W/m.K. By measuring the thermal lens at different pump power, the thermal-optical coefficient was calculated to be 9.2x10(-6) K(-1) for the first time to our knowledge. All the thermal properties recovered that this material can be used in the moderate and even high pump power.

Dual-wavelength synchronously mode-locked Nd:CNGG laser.

We have experimentally demonstrated a dual-wavelength synchronously mode-locked Nd:CNGG laser based on the semiconductor saturable absorber mirror technique. Mode locking was achieved simultaneously on two gain bands of the crystal that have a central wavelength separation of 2.4 nm. The fundamental mode-locked pulse train has a repetition rate of 88 MHz and pulse duration of 5 ps, with an average output power of approximately 90 mW. Autocorrelation measurements show that each of the synchronously mode-locked pulses consists of a train of quasi-periodic beat pulses with a 660 fs pulse width and a 0.63 THz repetition rate.

Hypermethylation of hepatic Gck promoter in ageing rats contributes to diabetogenic potential.

AIMS/HYPOTHESIS: Hepatic glucokinase (GCK) is a key enzyme in glucose utilisation. Downregulation of its activity is associated with insulin resistance and type 2 diabetes mellitus. However, it is unknown whether hepatic Gck expression is influenced by age and is involved in ageing-mediated diabetes, and whether the degree of methylation of the hepatic Gck promoter is correlated with the transcription of Gck. To address the question, we evaluated hepatic Gck transcription and promoter methylation in young (14 weeks), adult (40 weeks) and aged (80 weeks) rats. METHODS: Hepatic glycogen, Gck expression and the kinase activity of GCK were measured in three age groups. The CpG methylation status was determined by both bisulphite direct sequencing and clone sequencing of the PCR amplificates of Gck promoter. The causal relationship between Gck methylation and mRNA expression was confirmed by treating rat primary hepatocytes with 5-aza-2'-deoxycytidine (5-Aza-CdR). RESULTS: We have shown an age-associated decline in hepatic glycogen, Gck expression levels and the kinase activity of hepatic GCK. The eleven CpG sites studied displayed age-related progressive methylation changes in hepatic Gck promoter, which were confirmed by two methods: direct and clone sequencing. After 5-Aza-CdR treatment of rat primary hepatocytes, there was a fourfold increase in Gck expression. CONCLUSIONS/INTERPRETATION: Our results demonstrate that an age-related increase in methylation is negatively associated with hepatic Gck expression, suggesting that DNA methylation could be involved in increasing age-dependent susceptibility to hepatic insulin resistance and diabetes. Thus, the epigenetic modification of the hepatic Gck promoter may represent an important marker for diabetogenic potential during the ageing process.

Passively Q-switched Yb3+:YCa4O(BO3)3 laser with InGaAs quantum wells as saturable absorbers.

A diode-pumped Yb:YCOB laser at 1086 nm is passively Q switched by using InGaAs quantum wells as saturable absorbers and utilizing the Bragg mirror structure as an output coupler. With an absorbed pump power of 9.2 W the laser produces pulses of 100 ms duration with average pulse energy of as much as 165 microJ at a pulse repetition rate of 7 kHz.

Efficient diode-pumped actively Q-switched Nd:YAG/BaWO4 intracavity Raman laser.

Barium tungstate (BaWO4) is employed to achieve efficient stimulated Raman scattering conversion in a compact diode-pumped actively Q-switched Nd:YAG laser. With an incident pump power of 9.2 W, 1.56 W of 1181 nm first-Stokes average output power was generated at a pulse repetition rate of 20 kHz, corresponding to an optical-to-optical conversion efficiency of 16.9%.

Stimulation by melittin of Na+-Ca2+ exchange current in ventricular myocytes of guinea pigs.

AIM: To study the mechanism of calcium overload induced by melittin in myocytes. METHODS: Whole cell patch-clamp technique was applied for recording the currents. RESULTS: Mel 0.05, 0.1 micromol/L increased the peak amplitude of I(Na) (nA) from -2.1+/-0.8 to -3.2+/-1.0 (n=7, P < 0.05) and -3.7+/-1.5 (n=7, P < 0.05) respectively at testing potential of -40 mV. Mel 0.05, 0.1, 0.2 micromol/L had no significant effect on I(Ca), but enhanced I(Na-Ca) (pA) from 53+/-21 to 427+/-256 (n=5, P < 0.05), 349+/-147 (n=5, P<0.01) and 320+/-97 (n=5, P < 0.05) respectively at a testing potential of +50 mV. CONCLUSION: The stimulating effect of Mel on I(Na-Ca) rather than the effect on I(Ca) contributes to the calcium overload of myocytes.

Inhibitory effect of melittin on Na+,K+-ATPase from guinea pig myocardial mitochondria.

AIM: To investigate the effect of melittin (Mel) of Na+,K+-ATPase activity and it's kinetic mode of action on guinea pig myocardial mitochondria. METHODS: Effect of Mel on heart mitochondrial Na+,K+-ATPase activity was determined with colorimetry method. RESULTS: Mel inhibited Na+,K+-ATPase in a concentration and time dependent manner, IC50 was 2.60 micromol/L. Kinetic studies of interaction between Mel and K+, Na+, ATP revealed that inhibitory effect of Mel was competitive with K+, but not with Na+ and ATP. CONCLUSION: Mel polypeptide potently inhibits Na+,K+-ATPase, possibly by binding to the K+ site.

Effects of melittin on isolated papillary muscles of guinea pig.

AIM: To investigate the effect of melittin (Mel) on papillary muscles of guinea pigs. METHODS: Contraction of papillary muscles were examined by conventional method and action potentials (AP) were recorded by standard glass microelectrode technique. RESULTS: Mel (0.5, 3 micromol/L) significantly increased the contractility of guinea pig papillary muscles while 5 micromol/L exerted dual action with a transient decrease followed by an increase of the contractility. Mel shortened the functional refractory period (FRP) at concentrations of 0.5, 3, and 5 micromol/L and increased the automaticity induced by adrenaline (Adr) at 3 and 5 micromol/L. Mel shifted the duration-intensity curve upward at 3 micromol/L. It shortened the action potential duration (APD) of fast action potential (FAP), decreased the action potential amplitude (APA) and resting potential (RP) at 0.5 and 3 micromol/L. As to slow action potential (SAP), Mel 0.8 micromol/L shortened APD20 and APD50, and decreased APA and RP. CONCLUSION: Mel increased the contractility and automaticity of papillary muscles, shortened the FRP, decreased the excitability, shortened the APD, and decreased APA and RP of AP.

Sodium nitroprusside-induced seizures and adenosine release in rat hippocampus.

In the present study, we examined the effects of nitric oxide (NO)-related compounds, i.e. sodium nitroprusside (NO donor), diethyldithiocarbamate (NO trapper) and dithiothreitol (superoxide radical scavenger) on release of aspartate and adenosine from rat hippocampus using electrophysiological and microdialysis methods. Perfusion with 0.05 or 0.5 mM sodium nitroprusside significantly reduced high K(+)-evoked release of aspartate during high K(+) perfusion. Perfusion with 0.5 mM sodium nitroprusside always induced seizures and significantly increased release of aspartate and adenosine during washout of sodium nitroprusside. Diethyldithiocarbamate (5 mM) reversed the effects of sodium nitroprusside. Dithiothreitol (1 mM) significantly reduced the increase in adenosine release by sodium nitroprusside. These findings indicate that adenosine release is closely related to development of seizures, which are triggered by an increase in both NO itself and in part peroxynitrite, which results in reaction with superoxide radicals.

Sodium nitroprusside-induced seizure and taurine release from rat hippocampus.

We have recently reported that the nitric oxide (NO) donor, sodium nitroprusside (SNP), induces seizures which are associated with an increase in the basal release of aspartate and glutamate from rat hippocampus (Kaku et al., 1998). In order to determine whether taurine release occurs with SNP-induced seizures, we examined the effects of NO-related compounds, i.e., the NO trapper, diethyldithiocarbamate (DETC), the superoxide radical scavenger, dithiothreitol (DTT), the xanthine oxidase inhibitor, oxypurinol and the guanylyl cyclase inhibitor, 1H-(1,2,4)oxadiazole(4,3-a)quinoxalin-1-one (ODQ), on SNP-induced seizures and in vivo taurine release from rat hippocampus using microdialysis. Perfusion with 0.5mM SNP provoked seizures and significantly increased taurine release, with the increase in release occurring primarily during reperfusion with artificial cerebrospinal fluid lacking SNP. Perfusion with 5mM DETC significantly abolished the SNP-induced seizures and reduced taurine release during and after perfusion with the drugs. Perfusion with 1mM DTT significantly reduced both the frequency of the SNP-induced seizures and taurine release during and after perfusion with the drugs. Perfusion with 1 mM oxypurinol or 0.5 mM ODQ did not reduce the frequency of the SNP-induced seizures, but tended to decrease taurine release during and after perfusion with the drugs. These results demonstrate that SNP-induced seizures are triggered by an increase in both NO and peroxynitrite and are related to an increase in taurine release from rat hippocampus.

Biphasic manner of melittin on isolated guinea pig atria.

AIM: To investigate the effect of melittin (Mel) on isolated guinea pig atria. METHODS: The effect of Mel on the contraction and heart rate of isolated guinea pig atria at different concentrations was determined. RESULTS: Mel at a lower concentration (0.1-0.8 mumol.L-1) enhanced the contraction of left atria in a concentration-dependent manner; but at a higher concentration (1.6-12.8 mumol.L-1) it exerted an inhibitory effect. At 0.1-30 mumol.L-1 it was found to increase heart rate of right atria. In addition, verapamil (Ver) 0.3 mumol.L-1 was found to depress the effect of Mel. CONCLUSION: Mel possesses a biphasic effect on left atria and a positive chronotropic effect on right atria. Its mechanism might be related with Ca2+ channel.

Blocking effects of heteroclitin D and gomisin J on L-type calcium channels in ventricular cells of guinea pig.

AIM: To study the effects of heteroclitin D (HD) and gomisin J (GJ), two lignans from Kadsura medicinal plants, on L-type calcium channels in ventricular cells of guinea pig. METHODS: The calcium currents were measured by whole-cell patch-clamp recording technique. RESULTS: HD 1 and 10 mumol/L decreased the L-type calcium current from (770 +/- 155) to (482 +/- 104) and (384 +/- 85) pA, respectively. GJ 10 mumol/L inhibited calcium current from (822 +/- 169) to (436 +/- 143) pA. Neither HD nor GJ affected the steady-state activation curve. But they had impact on steady-state inactivation curve. HD 10 mumol/L changed the half inactivation voltage (V0.5) from -22.7 to -40.9 mV, and slope factor (kappa) from 10.2 to 20.6 (n = 4 cells from 3 guinea pigs, P < 0.05). GJ 10 mumol/L changed the V0.5 from -17.7 to -33.3 mV, and kappa from 15.9 to 27.8 (n = 5 cells from 3 guinea pigs, P < 0.05). CONCLUSION: HD and GJ inhibited L-type calcium channels.

Effect of melittin on potassium currents and action potential in ventricular myocytes of guinea pig.

AIM: To examine the effects of melittin (Mel), the major component of bee venom, on delayed rectifier K+ current (Ik), inward rectifier K+ current (Ikl) and action potential (AP) in guinea pig ventricular myocytes. METHODS: Ik, Ikl, and AP were recorded using the whole-cell patch-clamp technique. RESULTS: The action potential duration (APD) was shortened by Mel in a concentration-dependent manner. Mel 0.05, 0.1, 0.2 mumol.L-1 shortened APD50 from (520 +/- 55) to (459 +/- 91) (n = 5, P > 0.05), (385 +/- 102) (n = 5, P < 0.01), and (281 +/- 81) ms (n = 5, P < 0.01), respectively; and APD90 from (613 +/- 96) to (536 +/- 93) (n = 5, P > 0.05), (467 +/- 96) ms (n = 5, P < 0.01), and (354 +/- 95) ms (n = 5, P < 0.01), respectively. Mel increased the amplitude of Ik also in a concentration-dependent manner. Mel 0.05, 0.1, 0.2 mumol.L-1 increased Ik from (295 +/- 109) to (371 +/- 142) (n = 5, P < 0.05), (467 +/- 180) (n = 5, P < 0.05), (552 +/- 248) pA (n = 5, P < 0.05), respectively at testing potential of + 40 mV. But no significant effect of Mel on Ikl was observed at these concentrations. CONCLUSION: Mel significantly increased Ik in a concentration-dependent manner which contributed to shortening of APD.

7-Nitroindazole reduces nitric oxide concentration in rat hippocampus after transient forebrain ischemia.

We investigated the effects of 7-nitroindazole, a specific inhibitor of neuronal nitric oxide (NO) synthase, on NO concentration and on blood flow in rat hippocampus after transient forebrain ischemia which was induced by 4-vessel occlusion for 10 min. NO concentration was measured directly by an NO-selective electrode method. Hippocampal blood flow was also estimated by laser Doppler flowmetry. 7-Nitroindazole [0 (vehicle), 12.5, 25, 50 or 100 mg/kg] was administered intraperitoneally 20 min before ischemia. 7-Nitroindazole at any dose used did not affect basal NO levels before ischemia. 7-Nitroindazole (25, 50 and 100 mg/kg) reduced the NO concentration significantly during post-ischemic early reperfusion. Before 10 min of ischemia and during post-ischemic early reperfusion, there were no significant differences in hippocampal basal blood flow and reactive hyperemia between vehicle- and 7-nitroindazole-treated groups. These results demonstrate that the neuronal NO synthase inhibitor, 7-nitroindazole, can effectively inhibit NO synthesis in rat hippocampus during post-ischemic early reperfusion.

Somatostatin receptor subtype 2 knockout mice are refractory to growth hormone-negative feedback on arcuate neurons.

The pulsatile nature of GH release is apparently regulated by alternating sequential changes in two hypothalamic hormones, GH releasing hormone (GHRH) and somatostatin. Entrainment of this pulsatility appears to involve GH-mediated negative feedback. Recently a new receptor involved in GH release was cloned. Activation of this receptor by GH-releasing peptides and MK-0677 initiates and amplifies GH pulsatility and is associated with increased Fos immunoreactivity and electrical activity in GHRH containing arcuate neurons. We show that pretreating mice with GH blocks activation of these neurons by MK-0677. Similarly, octreotide inhibited the action of MK-0677. To determine whether this GH-mediated negative feedback on GHRH neurons was direct, or by GH stimulation of somatostatin release from periventricular neurons, we selectively inactivated the gene for one of the five specific somatostatin receptor subtypes (subtype 2). In the knockout mice, both GH and octreotide failed to inhibit MK-0677 activation of arcuate neurons. GH did, however, increase Fos immunoreactivity in the periventricular nucleus, consistent with GH stimulation of somatostatin release from periventricular neurons. Thus, GH-mediated negative feedback involves signaling between periventricular and arcuate neurons with the signal being transduced specifically through somatostatin subtype 2 receptors.

Anti-lipid peroxidation of gomisin J on liver mitochondria and cultured myocardial cells.

AIM: To study the influences of gomisin J on lipid peroxidation and calcium paradox. METHODS: Using two in vitro models of rat liver mitochondria membrane lipid peroxidation (LPO) and cultured myocardial cells. RESULTS: Gomisin J inhibited Fe2+/ascorbic acid and ADP/NADPH-induced LPO with IC50 (95% confidence limits) 5.5 (4.5-6.7) and 4.7 (2.8-7.8) mumol.L-1, respectively, when cultured myocardial cells preincubated with Ca(2+)-free medium for 2 min were incubated with normal medium containing Ca2+, a marked increase of malondialdehyde (MDA) formation occurred and gomisin J 10 mumol.L-1 protected myocardial cells through decreasing MDA formation. CONCLUSION: Gomisin J inhibits LPO in rat liver mitochondria and protects cultured myocardial cells from being injured by calcium paradox.