Posterior spinal cord block: a dosimetric study

To determine the optimal width of a midline posterior spinal block (MPSB) (to avoid delivering too great a dose to the cord and too small a dose to adjacent tissue), the authors determined with magnetic resonance (MR) imaging normal ranges of cord depth and width and correlated them with film dosimetric data. In 59 randomly selected patients there was a wide range for both depth and width. The average depths of the anterior and posterior surfaces of the cord were 6.7 cm +/- 1.4 and 5.4 cm +/- 1.3, respectively. The average cord width was 1.6 cm +/- 0.4. Optimal cord block width as a function of cord width was determined for a 6-MV photon beam. The optimal cord block width at the surface (half-value layer [HVL] thickness = 6) varied from 1.5 to 3.0 cm for cord widths of 0.8-2.4 cm, which correspond to two standard deviations from the average. There was no significant dependence on depth of the cord. For optimal treatment outcome, the MPSB width may have to be determined for each patient individually.     

麝香保心丸对内皮素-1诱导原代培养的人脐动脉血管平滑肌细胞增殖的影响

目的:观察麝香保心丸(SXBXW)对内皮素-1(ET-1)诱导原代培养的人脐动脉血管平滑肌细胞(VSMCs)增殖作用的影响。方法:建立ET-1刺激原代培养人脐动脉VSMCs增殖的细胞模型,设对照组、ET-1组、ET-1+SXBXW0.25g/L组、ET-1+SXBXW0.5g/L组、ET-1+SXBXW1.0g/L组和ET-1+SXBXW2.0g/L组,采用MTT法测定ET-1和SXBXW对细胞增殖的影响;用台盼蓝拒染和乳酸脱氢酶检测方法观察不同浓度的SXBXW对VSMCs的毒性作用;用流式细胞术观察ET-1和SXBXW对VSMCs增殖周期的影响。结果:与对照组相比,ET-1可显著促进VSMCs的增殖,一定剂量的SXBXW能够有效地抑制ET-1诱导的VSMCs细胞增殖,呈剂量依赖性;SXBXW抑制细胞增殖,但对活细胞数目和乳酸脱氢酶释放量均没有影响,提示对VSMCs无毒性作用。ET-1能够刺激VSMCs从G1期进入S期,从而促进细胞增殖,而SXBXW能抑制这一作用。结论:SXBXW能够有效抑制ET-1诱导的VSMCs增殖作用,其作用机制可能与其抑制细胞周期从G1期进入S期有关。     

Evidence that the retroviral DNA integration process triggers an ATR-dependent DNA damage response

Caffeine is an efficient inhibitor of cellular DNA repair, likely through its effects on ATM (ataxia telangiectasia mutated) and ATR (ATM and Rad3-related) kinases. Here, we show that caffeine treatment causes a dose-dependent reduction in the total amount of HIV-1 and avian sarcoma virus retroviral vector DNA that is joined to host DNA in the population of infected cells and also in the number of transduced cells. These changes were observed at caffeine concentrations that had little or no effect on overall cell growth, synthesis, and nuclear import of the viral DNA, or the activities of the viral integrase in vitro. Substantial reductions in the amount of host-viral-joined DNA in the infected population, and in the number of transductants, were also observed in the presence of a dominant-negative form of the ATR protein, ATRkd. After infection, a significant fraction of these cells undergoes cell death. In contrast, retroviral transduction is not impeded in ATM-deficient cells, and addition of caffeine leads to the same reduction that was observed in ATM-proficient cells. These results suggest that activity of the ATR kinase, but not the ATM kinase, is required for successful completion of the viral DNA integration process and/or survival of transduced cells. Components of the cellular DNA damage repair response may represent potential targets for antiretroviral drug development.     

Celiac artery stenting: a new strategy for patients with pancreaticoduodenal artery aneurysm associated with stenosis of the celiac artery

We report a new strategy—celiac artery stenting—to relieve stenosis of the celiac arterial root. This was performed in two patients with pancreaticoduodenal artery (PDA) aneurysm associated with a stenotic celiac arterial root. The first patient was a 66-year-old man complaining of abrupt onset of upper abdominal pain. Abdominal computed tomography revealed a huge retroperitoneal hematoma behind the duodenum, and superior mesenteric artery (SMA) angiography demonstrated an aneurysm arising from inferior pancreaticoduodenal artery and celiac arteriography showed a stenotic celiac arterial root. Transcatheter embolization of the aneurysm was tried, but failed. Because of his unstable hemodynamics, emergent laparotomy with resection of the aneurysm was performed. Fourteen days after the operation, percutaneous transluminal angioplasty with celiac arterial stenting was done. The patient was discharged 2 days later, and has had no further bleeding episode for 3 years. The second patient was a 46-year-old woman, who also complained of acute upper abdominal pain. Abdominal computed tomography disclosed a huge retroperitoneal hematoma, and selective SMA angiography demonstrated an aneurysm arising from the inferior pancreaticoduodenal artery, and celiac arteriography showed a stenotic celiac arterial root. Because angiography showed no active bleeding from the aneurysm, percutaneous transluminal angioplastic stenting of the stenotic celiac artery was performed. She was discharged 5 days later and has had no further bleeding episode for 2 years. Celiac arterial stenting, as shown in our two patients, could be easily and safely employed in patients with PDA aneurysm associated with a stenotic celiac arterial root to release the stenosis of the celiac arterial root and to prevent further possible bleeding.     

Thoracic aortic aneurysm with aortobronchial fistula: a thirteen-year experience

PURPOSE: This study investigated the causes of aortobronchial fistula, clinical features, diagnostic modalities, and prognostic factors. PARTICIPANTS: A retrospective analysis of 17 patients with aortobronchial fistula secondary to thoracic aortic aneurysm was studied. METHODS: Retrospective chart review was used. RESULTS: Atherosclerosis (47.1%), infection (23.5%), and previous thoracic vascular surgery (17.6%) accounted for most causes. Most patients (94.1%) experienced at least 1 episode of hemoptysis. Chest computer tomography is the most useful tool and revealed hematoma or consolidation around the aneurysm in more than half of our patients. Bronchoscopy and aortoangiogram frequently did not demonstrate an aortobronchial fistula. The 6 patients in the surgery group all survived, in contrast to 100% mortality in the non-surgery group. The average interval between initial presentation of hemoptysis and surgical intervention in the surgery group is 68 days, in contrast to 170 days between initial presentation of hemoptysis and death in the non-surgery group. CONCLUSIONS: A high index of suspicion will decrease delayed diagnosis. Early diagnosis and emergent surgery are 2 prognostic factors for survival.     

Skeletal muscle dihydropyridine-sensitive calcium channel (CACNA1S) gene mutations in chinese patients with hypokalemic periodic paralysis

BACKGROUND: Thyrotoxic periodic paralysis (TPP), familial periodic paralysis (FPP), and sporadic periodic paralysis (SPP) are common causes of hypokalemic periodic paralysis and have similar clinical presentations, thus possibly sharing the identical mutations. METHODS: We analyzed the role of the three known CACNA1S gene mutations (R528H, R1239H, and R1239G) in Chinese patients, including two FPP families, 36 TPP patients, 12 SPP patients, and their relatives. Fifty unrelated healthy subjects were also studied. Genomic DNA was prepared from the peripheral blood of all patients, their family members, and healthy subjects. Mutations of the CACNA1S gene were screened using polymerase chain reaction-based restriction analysis. RESULTS: Two FPP families had the R528H point mutation, but with incomplete penetrance occurring more commonly in men than in women. Only one SPP patient had a de novo mutation (R528H). None of the TPP patients had mutations in the three hot spots. CONCLUSION: Patients with FPP have R528H mutations in the CACNA1S gene. Only a few patients with SPP may share similar mutations with FPP. TPP patients do not carry any of the three known gene mutations.     

Genetics of Somatic Mammalian Cells: Lethal Antigens as Genetic Markers for Study of Human Linkage Groups

The antigen that causes killing of at least 98% of a human cell population treated with a 1% solution of a specific rabbit antiserum in the presence of complement is a sensitive genetic marker. The rapid loss of human chromosomes in human-Chinese hamster cell hybrids makes possible a convenient test of linkage relationships with this marker. Hybrid clones with and without the lethal antigen were isolated and analyzed. In 76 clones and subclones studied, 41 carried both the lethal antigen and the lactic dehydrogenase-A marker, 35 carried neither, and no clones contained only one of the two markers. In contrast to this clear demonstration of linkage, absence of linkage was found between the lethal antigen and the following markers: Lactic dehydrogenase B, NAD-dependent malic dehydrogenase, NADP-dependent malic dehydrogenase, glucose-6-phosphate dehydrogenase, phosphoglucomutase, glutamate oxaloacetate transaminase, indophenol oxidase, glucose phosphate isomerase, proline, inositol, hypoxanthine B, and glycine A. This lethal antigen appears to be carried on a single human autosome.