Triple no loop Endobutton plate combined with Orthcord line for the treatment of acromioclavicular dislocation of Tossy type III / 中国骨伤

<p><b>OBJECTIVE</b>To explore the clinical effects of the triple no loop Endobutton plate combined with Orthcord line in treating acromioclavicular dislocation of Tossy type III.</p><p><b>METHODS</b>Between February 2011 and September 2013, 36 patients with acromioclavicular dislocation of Tossy type III were treated with triple no loop Endobutton plate and Orthcord line. There were 21 males and 15 females, aged from 9 to 48 years old with an average of (26.41±14.05) years. Couse of disease was from 2 to 7 days in the patients. The patients had the clinical manifestations such as shoulder pain, extension limited, acromioclavicular tenderness, positive organ point sign. Clinical effects were assessed by acromioclavicular scoring system.</p><p><b>RESULTS</b>Thirty six patients were followed up from 8 to 15 months with an average of (12.2±4.3) months. All incisions got primary healing. At the final follow up, all shoulder pain vanished, acromioclavicular joints without tenderness, negative organ point sign. No redislocation and steel plate loosening were found. According to the acromioclavicular scoring system, 31 cases obtained excellent results, 5 good.</p><p><b>CONCLUSIONS</b>The method of triple no loop Endobutton plate combined with Orthcord line for acromioclavicular dislocation of Tossy type III has advantage of less risk and complication, good functional rehabilitation and is an ideal method.</p>

The changes of monocarboxylate transporter-2 in spinal cord horn in a rat model of chronic inflammatory pain / 中国应用生理学杂志

<p><b>OBJECTIVE</b>To investigate the changes in the levels of monocarboxylate transporter-2 in spinal cord horn in a rat model of chronic inflammatory pain.</p><p><b>METHODS</b>Male SD rats weighting 180 - 220 g were randomly divided into two groups(n = 48): normal saline group (NS group), complete Freund's adjuvant group (CFA group). Rats were given injections of CFA 100 µl in left hind paw in group CFA, and an equal volume of saline was given injection in group NS. Mechanical withdraw threshold(MWT) and thermal withdraw latency(TWL) were measured at before injection(T0 and 3 h, 1 d, 3 d, 7 d, 14 d, and 21 d after injection(T1-7). Four rats were chosen from each group at T0-7 and sacrificed, and L4-5 segments of the spinal cord horn were removed for measurement of the expression of monocarboxylate transporter-2 by Western blot analysis.</p><p><b>RESULTS</b>In CFA group, mechanical hyperalgesia and allodynia appeared on the 3 h after CFA injection, then until the day 14. The expression of monocarboxylate transporter-2 in the spinal dorsal horn of rats in CFA group was significantly higher than that in normal control group at T1-6(P <0.05). The protein level of monocarboxylate transporter-2 was apparently correlated with MWT and TWL(P <0.01 and P <0.05) in CFA group.</p><p><b>CONCLUSION</b>The level of monocarboxylate transporter-2 in spinal dorsal horn is significantly increased in a rat model of chronic inflammatory pain and the change may involve in the formation and maintenance of central sensitization in spinal cord of chronic inflammatory uain.</p>

Progress in the fragment-based drug discovery / 药学学报

As an extension of the structure-based drug discovery, fragment-based drug discovery is matured increasingly, and plays an important role in drug development. Fragments in a small library, with lower molecular mass and high "ligand efficiency", are detected by SPR, MS, NMR, X-ray crystallography technologies and other biophysical methods. Then they are considered as starting points for chemical optimization with the guidance of structural biology methods to get good "drug-like" lead and candidate compounds. In this article, we reviewed the current progress of fragment-based drug discovery and detailed a number of examples to illustrate the novel strategies.

Psychological status prior coronary angiography in patients with and without coronary artery disease / 中华心血管病杂志

<p><b>OBJECTIVE</b>To compare the prior coronary angiography (CAG) psychological status in chest pain patients with and without coronary artery disease (CAD).</p><p><b>METHODS</b>Ninety-nine patients with chest pain and scheduled for CAG were selected by cluster sampling method. The mental status was measured by Hamilton Anxiety Rating Scale (HAMA) and Hamilton Depression Rating Scale-17 (HAMD-17) 24 hours before CAG, and the risk factors for CAD were also determined.</p><p><b>RESULTS</b>There were 43 patients with HAMA score > or = 14, 18 patients with HAMD-17 score > or = 14 and 16 patients with both scores > or = 14. CAD was diagnosed in 46 patients by CAG. HAMA score was significantly higher in patients without CAD than patients with CAD (14.1 +/- 7.1 vs. 11.1 +/- 6.7, P < 0.05).</p><p><b>CONCLUSIONS</b>Incidences of anxiety and depression were high in chest pain patients prior CAG and incidence of anxiety prior CAG was significantly higher in chest pain patients without CAD compared to chest pain patients with CAD.</p>

Prehospital delay time and mortality in patients with acute myocardial infarction / 中华心血管病杂志

<p><b>OBJECTIVE</b>To determine the relationship between prehospital delay time (PDT) and other associated factors on mortality in patients with acute myocardial infarction.</p><p><b>METHODS</b>We retrospectively analyzed factors associated with mortality in 580 patients with acute myocardial infarction presented to the Emergency Ward and Emergency Intensive Care Unit (EICU) of Beijing Anzhen Hospital from March 2004 to March 2006 (428 males, average age: 60.7 +/- 12.9 years). The patients were divided to 3 groups according various therapies: thrombolysis, PCI/CABG or symptomatic medication groups.</p><p><b>RESULTS</b>The median PDT was 130 min. Thrombolysis, PCI/CABG and medical therapy were applied in 122 (21.0%), 266 (45.9%) and 192 (33.1%) patients respectively. PDT was significantly longer in patients receiving medical therapy (290.9 min +/- 3.4 min) compared to patients treated with thrombolysis (104.5 min +/- 2.3 min) and PCI/CABG (119.1 min +/- 2.3 min, all P < 0.05). The overall mortality rate was 5.3% (31/580) and all occurred in patients with medical therapy group mostly due to irreversible ventricular fibrillations. Old age (OR = 1.047, P = 0.004), diabetes mellitus (OR = 2.159, P = 0.02) and PDT (OR = 2.159, P = 0.023) are independent predict factors for mortality.</p><p><b>CONCLUSION</b>Coronary Revascularisation by thrombolysis, PCI or CABG early post acute myocardial infarction is the key issue for reducing mortality in patients with acute myocardial infarction.</p>

cAMP response-element binding protein participates in the phosphorylated extracellular signal-regulate kinase mediated neuropathic pain / 生理学报

It has been reported that extracellular signal-regulate kinase (ERK) is involved in the modulation of nociceptive information and central sensitization produced by intense noxious stimuli and/or peripheral tissue inflammation. Few studies have explored the relationship between ERK and cAMP response-element binding protein (CREB) in neuropathic pain after nerve injury, such as chronic constriction injury (CCI) of the sciatic nerve. In the present study, CCI model was employed to investigate the activation of ERK on the expression of phosphorylated CREB (pCREB) in chronic neuropathic pain. Lumbar intrathecal catheters were chronically implanted in male Sprague-Dawley rats. The left sciatic nerve was loosely ligated proximal to the sciatica's trifurcation at around 1.0- mm intervals with 4-0 silk suture. Mitogen-activated protein kinase kinase (MEK) inhibitor U0126 and phosphorothioate-modified antisense oligonucleotides (ODN) were intrathecally administered one day before and three consecutive days after CCI. Thermal and mechanical nociceptive thresholds were assessed with the paw withdrawal lantency (PWL) to radiant heat and von Frey filaments respectively. The expression of pCREB and Fos were assessed by both Western blot and immunohistochemical analysis. The results showed that intrathecal injection of U0126 or ERK antisense ODN attenuated significantly CCI-induced mechanical and thermal hyperalgesia. Correlating with behavior results, the injection also markedly suppressed the increase of CCI-induced pCREB and c-Fos expression. The results obtained suggest that CREB participates in the pERK-mediated neuropathic pain.

Different roles of the spinal protein kinase C alpha and gamma in morphine dependence and naloxone-precipitated withdrawal / 生理学报

Our previous studies showed that spinal neurons sensitization was involved in morphine withdrawal response. This study was to investigate the roles of spinal protein kinase C (PKC) alpha, gamma in morphine dependence and naloxone-precipitated withdrawal response. To set up morphine dependence model, rats were subcutaneously injected with morphine (twice a day, for 5 d). The dose of morphine was 10 mg/kg in the first day and was increased by 10 mg/kg each day. On day 6, 4 h after the injection of morphine (50 mg/kg), morphine withdrawal syndrome was precipitated by an injection of naloxone (4 mg/kg, i.p.). Chelerythrine chloride (CHE), a PKC inhibitor, was intrathecally injected 30 min before the administration of naloxone. The scores of morphine withdrawal symptom and morphine withdrawal-induced allodynia were observed. One hour after naloxone-precipitated withdrawal, Fos protein expression was assessed by immunohistochemical analysis and Western blot was used to detect the expression of cytosol and membrane fraction of PKC alpha and gamma in the rat spinal cord. The results showed that intrathecal administration of CHE decreased the scores of morphine withdrawal, attenuated morphine withdrawal-induced allodynia and also inhibited the increase of Fos protein expression in the spinal cord of morphine withdrawal rats. The expression of cytosol and membrane fraction of PKC alpha was significantly increased in the spinal cord of rats with morphine dependence. Naloxone-precipitated withdrawal induced PKC alpha translocation from cytosol to membrane fraction, which was prevented by intrathecal administration of CHE. During morphine dependence, but not naloxone-precipitated withdrawal, PKC gamma in the spinal cord translocated from cytosol to membrane fraction, and intrathecal administration of CHE did not change the expression of PKC gamma in the spinal cord of naloxone-precipitated withdrawal rats. It is suggested that up-regulation and translocation of PKC in the spinal cord contribute to morphine dependence and naloxone-precipitated withdrawal in rats and that PKC alpha and gamma play different roles in the above-mentioned effect.

Activation of the spinal extracellular signal-regulated kinase is involved in morphine dependence and naloxone-precipitated withdrawal response / 生理学报

Extracellular signal-regulated kinase (ERK), a mitogen-activated protein kinase (MAPK), transduces a broad range of extracellular stimuli into diverse intracellular responses. It has been reported that ERK is involved in the modulation of nociceptive information and central sensitization produced by intense noxious stimuli or peripheral tissue inflammation. Our previous studies showed that the spinal neurons sensitization was involved in morphine withdrawal response. This study was to investigate the role of the spinal ERK in morphine dependence and naloxone-precipitated withdrawal response. To set up morphine-dependent model, rats were subcutaneously injected with morphine (twice a day, for 5 d). The dose of morphine was 10 mg/kg on the first day and was increased by 10 mg/kg each day. On day 6, 4 h after the injection of morphine (50 mg/kg), morphine withdrawal syndrome was precipitated by an injection of naloxone (4 mg/kg, i.p.). Using anti-phospho-ERK (pERK) antibody, the time course of pERK expression was detected by Western blot. U0126, a mitogen-activated protein kinase kinase (MEK) inhibitor, or phosphorothioate-modified antisense oligonucleotides (ODN) was intrathecally injected 30 min or 36, 24 and 12 h before naloxone-precipitated withdrawal. The scores of morphine withdrawal symptom and morphine withdrawal-induced allodynia were observed. One hour after naloxone-precipitated withdrawal, pERK expression in the spinal dorsal horn was assessed by immunohistochemical analysis and Western blot was used to detect the expression of cytosolic and nuclear fraction of pERK in the rat spinal cord. The results showed that the expression of cytosolic and nuclear fraction of pERK, not non-phospho-ERK, in the spinal cord was gradually increased following the injection of morphine. When morphine withdrawal was precipitated with naloxone, the expression of the spinal pERK further increased. Intrathecal administration of U0126 or antisense ODN against ERK decreased the scores of morphine withdrawal, attenuated morphine withdrawal-induced allodynia and also inhibited the increase of pERK expression in the spinal cord of morphine withdrawal rats. These results suggest that activation of the spinal ERK is involved in morphine-dependent and naloxone-precipitated withdrawal response.