Poncet病(病例报告及文献复习)

目的 探讨Poncet病的诊断与治疗。方法 通过病例报告及献复习，综述了Poncet病的发病机理、临床表现。结果 提高对Poncet病的认识。结论 临床上对风湿性或类风湿性关节炎病人均应与本病鉴别。     

rhGM—CSF对小鼠口腔粘膜损伤的防治作用

目的：观察rhGM-CSF对TMX致实验性小鼠口腔粘膜损伤的疗效。方法：按随机分组原则将501只昆明种小白鼠分成8组，分别在相应时间给予不同药物（MTX，CF或rhGM-CSF）的处理因素，于第1－10天光镜下观察小鼠口腔粘膜的病理改变和积分情况。结果：IDMTX致口腔粘膜损伤病变率（45％－63％）和积分率（19．4％－56％）较其它组高，且死亡率很低（小于5％）；IDMTX＋GM0（或GM2）组的口腔粘膜损伤病变率（30．53％和30．99％）和积分率（19．47％和17．25％）比IDMTX组（55．56％和36．31％）明显减少，且溃疡严重程度较轻，二者相差显著（P＜0．01）。结论：IDMTX致小鼠口腔粘膜损伤模型可以用于粘膜损伤的研究；rhGM-CSF可以减少MTX致小鼠口腔粘膜损伤，并促进粘膜损伤恢复。     

严重胸腹部闭合性联合伤致呼吸心跳停止成功救治1例

报告1例严重胸腹部闭合性联合伤所致的急性呼吸心跳骤停得到成功救治的病例。闭合性胸腹联合伤后,因病情可能发展,应随时注意复查胸片、血气等;若基层医院条件不够,应及时转往上级医院,以免延误患者的治疗。     

乳腺影像学报告及数据系统:超声良恶性病变鉴别诊断初探

1992年美国放射学会制定了乳腺影像学报告及数据系统(breast imaging reporting and data system,BI-RADS),2003年第四版修订时包括了超声诊断(BI-RADS-US)。本文旨在初步探讨BI-RADS-US对于乳腺良恶性病变鉴别诊断的能力。我们收集了2006年1月至2007年3月期间、获得病理诊断的乳腺占位性病变共69例72灶。均为女性,年龄14-83岁,平均41.6岁。首先根据一般的非BI-RADS标准,做出良恶性鉴别。然后用BI-RADS-US标准进行鉴别和分级(0-6级),其中2级和3级为良性和良性可能性大,4级为性质待定,5级为恶性可能性大。计算并比较上述两种方法的准确性、敏感性、特异性。结果在72病灶中,根据非BI-RADS标准,诊断为良性者40灶,符合病理诊断者38灶(95.0%),诊断为恶性者23灶,符合病理者18灶(78.3%);诊断为性质待定者9灶。根据BI-RADS-US标准和分级,2级和3级共有37灶,与病理结果符合者为36灶(97.2%);5级有31灶,与病理符合者为22灶(71.0%);4级有4灶。非BI-RADS和BI-RADS-US的准确性各为83.3%和81.9%(P=1.000),敏感性各为91.7%和95.8%(P=1.000),特异性各为79.2%和75.0%(P=0.754)。总之,第一版BI-RADS-US在乳腺良恶性病变鉴别诊断方面的初步应用表现出较高的敏感性,而与非BI-RADS方法比较则尚无明显差别。     

中西医结合治疗慢性鼻窦炎76例

目的观察中西医结合治疗慢性鼻窦炎的疗效．方法：对76例慢性鼻窦炎病人采用阿奇霉素，每次1粒（0．25g），替硝唑片每次1g口服，二者均一日1次，首剂量加倍，中成药藿胆丸每次服6克，一日两次，7天为一疗程，服药最长者2周。结果：显效56例（占73．7％），有效18例（占23．7％），无效2例（占2．6％），总有效率97．4％。结论：中西医结合治疗慢性鼻窦炎具有良好疗效。     

Discordance in HIV-1 viral loads and antiretroviral drug concentrations comparing semen and blood plasma

Objectives

For individuals not on antiretroviral therapy, the risk of heterosexual transmission of HIV appears negligible when blood plasma (BP) viral loads are <1500 HIV‐1 RNA copies/mL. It is not clear whether this observation can be extrapolated to individuals on highly active antiretroviral therapy (HAART). Because of differential tissue penetration, antiretroviral drug concentrations may be sufficient to maintain an undetectable viral load in the BP yet not achieve adequate levels to suppress HIV in the genital tract. Therefore, we wanted to correlate HIV viral loads and drug concentrations in semen plasma (SP) and BP.

Methods

Thirty‐three men were included. All were on combination antiretroviral therapy with an undetectable BP viral load for at least 1 year. Blood and semen samples were collected within 2 h of each other and tested for HIV RNA by the NucliSens QT (bioMerieux, St Laurent, QC, Canada) method; drug concentrations were determined by liquid chromatography tandem mass spectrometry.

Results

Two of the 33 patients (6.1%) with BP viral loads below detection had time‐matched HIV viral loads in SP ≥700 copies/mL. Both patients were on efavirenz, the SP concentrations of which were ≤10% of the levels in BP and well below the minimal therapeutic drug monitoring target concentration required to suppress HIV.

Conclusions

Because, at least in part, of poor drug penetration into the genital tract, an undetectable HIV viral load in the BP does not guarantee an undetectable viral load in semen. In view of this, caution should be taken in concluding that patients on HAART with suppressed viraemia are sexually non‐infectious.     

Energy recommendations for normal weight,overweight and obese children and adolescents: are different equations necessary?

In 2002/2005, separate energy requirement equations were generated by the Institute of Medicine's (IOM) Dietary Reference Intake process for normal weight and overweight/obese children and adolescents. The current paper questions the theoretical rationale of having two sets of equations (based solely on body-weight classification): when body weight is considered, overweight and obese children and adolescents do not seem to differ from their normal weight counterparts in energy expended for basal metabolism or physical activity tasks. However, energy needs for weight maintenance among overweight/obese girls were consistently higher when predicted using the equations for overweight/obese individuals compared with those developed for normal weight individuals. In contrast, among overweight/obese boys, they were consistently lower . Although the differences are within the variability of the estimates, even theoretical support for a higher energy intake (as occurs in girls) seems unwise because of the potential contribution to a higher body mass in children who are already at risk. It is the opinion of the authors that the IOM revisit the use of two separate equations and generate one set that is appropriate for all children and adolescents.     

Ischemia independent lesion evolution during focal stroke in rats

Lesion evolution during focal cerebral ischemia may depend on flow restrictions or on accumulation of toxic mediators within the infarct and expansion of these factors to the periinfarct region. So far, the precise contribution of flow dependent versus spreading-mediated impairment of viable periinfarct tissue has not been determined. Therefore, we measured lesion expansion, flow restrictions and glutamate distribution on serial brain sections at different time points after experimental focal ischemia.Permanent focal ischemia was induced by occlusion of the right middle cerebral artery in male rats and the flow reduction was subsequently measured at 1, 12 and 24 h using iodo[¹⁴C]antipyrine autoradiography. Additionally, the necrotic volume was determined on serial brain sections and the glutamate content was measured in tissue samples from adjacent microdissections.Twelve hours after focal ischemia no noteworthy viable areas with blood flow restrictions of 20-40 ml 100 g^− 1 min^− 1 existed but at 24 h the necrotic tissue exceeded the hemodynamically compromised region by 40 ± 21 mm³ (24%). Furthermore, at 12 and 24 h the glutamate content was elevated in areas surrounding the infarct.Relevant flow restrictions are detectable only during early stages of infarct maturation, whereas the propagation of secondary factors may be the predominant mechanism for delayed infarct evolution.