腹腔镜阑尾切除术残端荷包包埋61例

目的总结腹腔镜阑尾切除术残端荷包包埋的手术经验。方法回顾分析2009年7月至2010年6月施行的61例腹腔镜阑尾切除术,术中阑尾残端均行荷包包埋,阐述手术的经验体会。结果 61例腹腔镜阑尾切除术残端荷包包埋均成功完成,无一例发生副损伤及并发症。结论腹腔镜下阑尾残端荷包包埋是安全可行的,不增加患者的手术费用,值得推广。     

一种保留哺乳功能的乳头内陷矫正术研究

目的:探索一种保留育龄期孕前患者哺乳功能的乳头内陷矫正方法。方法:临床纳入乳头内陷程度为Ⅰ型、Ⅱ型的孕前育龄患者各60例,随机分为Ⅰ型手术组、Ⅰ型对照组、Ⅱ型手术组及Ⅱ型对照组各30例。手术组孕前进行手术,并佩戴矫正器6个月,对照组不予手术处理。同时以乳头发育正常的30例孕前育龄者作为正常组。纳入成功妊娠、生产并尝试哺乳患者,统计乳头高度,母乳喂养情况,乳头皲裂及乳腺炎的发生情况。结果:对于Ⅰ型和Ⅱ型患者,手术组术后即刻及孕晚期,其乳头高度相对术前及对照组均有显著性改善(P0.01),母乳喂养4个月成功率显著提高(P0.05),乳头皲裂和乳腺炎的发生率显著降低(P0.05),且除Ⅱ型患者的术后乳头高度外,与正常组比较差异无统计学意义(P0.05)。结论:对于Ⅰ型及Ⅱ型乳头内陷,佩戴乳头内陷矫正器除可增加乳头高度外,可在保留哺乳功能的同时,降低产后乳头皲裂和乳腺炎发生率。     

Optic nerve injury demonstrated by MRI with STIR sequences

We studied nine patients with optic nerve injury associated with closed head trauma by magnetic resonance imaging (MRI) with short inversion time inversion recovery (STIR) sequences on 11 occasions from 4 days to 14 years after the injury: three studies were within 17 days and eight over 4 months to 14 years. MRI revealed abnormal high signal in 10 of the 11 injured nerves. MRI 4 days after the injury showed no abnormality.     

磁共振流入反转恢复序列在布-加综合征中的诊断价值

目的：探讨1.5T MR 扫描仪流入反转恢复(IFIR)序列诊断布-加综合征(BCS)的可行性。方法选取45例 MRI 影像资料齐全、经外科手术或介入治疗确诊的 BCS,比较 IFIR 序列与 DSA 诊断 BCS 的一致性。结果45例患者中,IFIR 序列正确诊断40例(88.9%),其中Ⅰa 型10例,Ⅰb 型14例,Ⅱ型10例,Ⅲ型6例;DSA 正确诊断41例(91.1%),其中Ⅰa 型8例,Ⅰb 型14例,Ⅱ型13例,Ⅲ型6例;两者诊断正确率差异无统计学意义(P>0.05),Spearman 相关分析,具有高度一致性(r=0.853,P<0.001);但两者在Ⅰa 型和Ⅱ型的分型上差异有统计学意义(P <0.05)。结论1.5T MR IFIR 序列诊断 BCS 与 DSA 有较高的一致性,可作为术前筛查的可靠方法。     

楔形真皮乳腺瓣法矫正重度乳头内陷

目的探讨矫正女性重度乳头内陷的手术治疗新方法。方法设计乳晕去表皮楔形真皮乳腺瓣,双侧楔形瓣翻转180°交叉重叠置于乳头基部,以支撑乳头和缩小乳头颈部直径。应用不可吸收的缝线分层严密缝合创口,消除乳头可能回缩的空间,缩窄乳头颈部皮肤。结果2002年7月至2008年12月,采用该方法共治疗35例先天性或复发性重度乳头内陷患者,全部病例术后伤口均愈合良好,无血肿、感染等并发症。术后随访3个月至2年,切口瘢痕不明显,乳头高度及外形满意,无复发。结论楔形真皮乳腺瓣法是矫正重度乳头内陷和术后复发的一种较好的手术治疗方法,尤其对防止乳头内陷的术后复发具有良好效果。     

去表皮乳晕双菱形组织瓣内翻充填矫治乳头内陷

目的探讨乳头内陷的治疗方法。方法应用去表皮双菱形乳晕真皮瓣与乳腺腺体组织瓣内翻充填治疗先天性乳头内陷,松解短缩的乳腺导管及纤维束,将组织瓣由乳头下方的隧道内穿出作为支撑组织。结果8例患者随访半年至2年,形态均良好,其中1例术后正常哺乳。结论该术式是矫正乳头内陷的较好方法之一,效果确切,不易复发。     

Rare recombination events generate sequence diversity among balancer chromosomes in Drosophila melanogaster

Multiply inverted balancer chromosomes that suppress exchange with their homologs are an essential part of the Drosophila melanogaster genetic toolkit. Despite their widespread use, the organization of balancer chromosomes has not been characterized at the molecular level, and the degree of sequence variation among copies of balancer chromosomes is unknown. To map inversion breakpoints and study potential diversity in descendants of a structurally identical balancer chromosome, we sequenced a panel of laboratory stocks containing the most widely used X chromosome balancer, First Multiple 7 (FM7). We mapped the locations of FM7 breakpoints to precise euchromatic coordinates and identified the flanking sequence of breakpoints in heterochromatic regions. Analysis of SNP variation revealed megabase-scale blocks of sequence divergence among currently used FM7 stocks. We present evidence that this divergence arose through rare double-crossover events that replaced a female-sterile allele of the singed gene (sn^X2) on FM7c with a sequence from balanced chromosomes. We propose that although double-crossover events are rare in individual crosses, many FM7c chromosomes in the Bloomington Drosophila Stock Center have lost sn^X2 by this mechanism on a historical timescale. Finally, we characterize the original allele of the Bar gene (B¹) that is carried on FM7, and validate the hypothesis that the origin and subsequent reversion of the B¹ duplication are mediated by unequal exchange. Our results reject a simple nonrecombining, clonal mode for the laboratory evolution of balancer chromosomes and have implications for how balancer chromosomes should be used in the design and interpretation of genetic experiments in Drosophila.Balancer chromosomes are genetically engineered chromosomes that suppress crossing over with their homologs and are used for many purposes in genetics, including construction of complex genotypes, maintenance of stocks, and estimation of mutation rates. Balancers typically carry multiple inversions that suppress genetic exchange or result in the formation of abnormal meiotic products if crossing over does occur (Fig. 1A); for example, single crossovers inside the inverted segment create acentric or dicentric chromosomes that will fail to segregate properly during meiosis or large deletions or duplications that will likely result in inviable gametes (1, 2). Balancers also often carry recessive lethal or sterile mutations to prevent their propagation as homozygotes as well as dominant markers for easy identification. First developed for use in Drosophila melanogaster, balancer chromosomes remain some of the most powerful tools for genetic analysis in this species (3).Open in a separate windowFig. 1.Consequences of a single or double crossover between a WT X chromosome and an X chromosome carrying a single inversion, In(1)dl-49. Euchromatin is shown in blue, heterochromatin is shown in gray, and centromeres are depicted as circles. Thin white lines mark locations of inversion breakpoints, and yellow crosses/thin lines mark locations of crossover events. (A) A single crossover event within the inverted segment results in the formation of chromosomes with deletions and zero (acentric) centromeres or duplications and two (dicentric) centromeres, neither of which will segregate properly during meiosis. (B) A double crossover within an inverted segment results in intact chromosomes with one centromere that will segregate properly during meiosis.Despite their widespread use, very little is known about the organization of Drosophila balancer chromosomes at the molecular level. Since their original syntheses decades ago, balancers have undergone many manipulations, including the addition or removal of genetic markers. Moreover, rare recombination events can cause spontaneous loss of deleterious alleles on chromosomes kept over balancers in stock, as well as loss of marker alleles on balancer chromosomes themselves (3). Likewise, recent evidence has shown that sequence variants can be exchanged between balancer chromosomes and their wild type (WT) homologs via gene conversion during stock construction or maintenance (4, 5). Thus, substantial variation may exist among structurally identical balancer chromosomes owing to various types of sequence exchange.To gain insight into the structure and evolution of balancer chromosomes, we have undertaken a genomic analysis of the most commonly used X chromosome balancer in D. melanogaster, First Multiple 7 (FM7). We have focused on FM7 because this X chromosome balancer series lacks lethal mutations and thus can be easily sequenced in a hemizygous or homozygous state. In addition, the FM7 chromosome has been shown to pair normally along most of its axis with a standard X chromosome, providing a structural basis for possible exchange events (6). Moreover, although details of how early balancers in D. melanogaster were created are not fully recorded, the synthesis and cytology of the FM7 series is reasonably well documented (3).The earliest chromosome in the FM7 series, FM7a, was constructed using two progenitor X chromosome balancers, FM1 and FM6, to create a chromosome carrying three inversions—In(1)sc⁸, In(1)dl-49, and In(1)FM6—relative to the WT configuration (7, 8) (Fig. 2A). Subsequently, a female-sterile allele of singed (sn^X2) was introduced onto FM7a to create FM7c, which prevents the loss of balanced chromosomes carrying recessive lethal or female-sterile mutations (9). More recently, versions of FM7a and FM7c have been generated that carry transgene insertions that allow the determination of balancer genotypes in embryonic or pupal stages (10–14).Open in a separate windowFig. 2.Structure of the FM7 balancer chromosome. Euchromatin is shown in blue, and heterochromatin is shown in gray. (A) Schematic view of the organization of WT and FM7 X chromosomes. FM7 contains three inversions—In(1)sc⁸, In(1)dl-49, and In(1)FM6—relative to WT. The six breakpoint junctions for the three inversions are numbered 1–6 and are shown in detail in B. (B) Location and organization of inversion breakpoints in FM7. Each inversion has two breakpoints that can be represented as A/B and C/D in the standard WT arrangement and as A/C and B/D in the inverted FM7 arrangement, where A, B, C, and D represent the sequences on either side of the breakpoints. Locations of euchromatic breakpoints are on Release 5 genome coordinates, and the identity of the best BLAST match in FlyBase is shown for heterochromatic sequences. Primers used for PCR amplification are shown above each breakpoint; details are provided in Methods and Datasets S2 and S3. Forward and reverse primers are named with respect to the orientation of the assembled breakpoint contigs, not the orientation of the WT or FM7 X chromosome.To identify the inversion breakpoints in FM7 balancers and to study patterns of sequence variation that may have arisen since the origin of the FM7 series, we sequenced genomes of eight D. melanogaster stocks carrying the FM7 chromosome (four FM7a and four FM7c). We discovered several megabase-scale regions in which FM7c chromosomes differ from one another, which presumably arose via double-crossover (DCO) events from balanced chromosomes (Fig. 1B). These DCOs eliminate the female-sterile sn^X2 allele in the centrally located In(1)dl-49 inversion and are expected to confer a fitness advantage to sn⁺ chromosomes, either by allowing propagation of sn⁺ FM7 as homozygotes in females or by sn⁺ FM7 males outcompeting sn^X2 FM7 males in culture. We found that loss of the sn^X2 allele is common in FM7c chromosomes by screening other FM7c-carrying stocks at the Bloomington Drosophila Stock Center. We also identified the breakpoints of the B¹ duplication carried on FM7, and found direct molecular evidence for the role of unequal exchange in the origin and reversion of the B¹ allele (15–19). Our results provide clear evidence that the common assumption that balancers are fully nonrecombining chromosomes is incorrect on a historical timescale, and that substantial sequence variation exists among balancer chromosomes in circulation today.     

Identifying Range-of-Motion Deficits and Talocrural Joint Laxity After an Acute Lateral Ankle Sprain

ContextApproximately 72% of patients with an ankle sprain report residual symptoms 6 to 18 months later. Although 44% of patients return to activity in less than 24 hours after experiencing a sprain, residual symptoms should be evaluated in the long term to determine if deficits exist. These residual symptoms may be due to the quality of ligament tissue and motion after injury.ObjectiveTo compare mechanical laxity of the talocrural joint and dorsiflexion range of motion (DFROM) over time (24 to 72 hours, 2 to 4 weeks, and 6 months) after an acute lateral ankle sprain (LAS).DesignCross-sectional study.SettingAthletic training research laboratory.Patients or Other ParticipantsA total of 108 volunteers were recruited. Fifty-five participants had an acute LAS and 53 participants were control individuals without a history of LAS.Main Outcome Measure(s)Mechanical laxity (talofibular interval and anterior talofibular ligament length) was measured in inversion (INV) and via the anterior drawer test. The weight-bearing lunge test was conducted and DFROM was measured. The data were analyzed using repeated-measures analysis of variance, independent-samples t tests, and 1-way analysis of variance.ResultsOf the 55 LASs, 21 (38%) were grade I, 27 (49%) were grade II, and 7 (13%) were grade III. Increases were noted in DFROM over time, between 24 and 72 hours, at 2 to 4 weeks, and at 6 months (P < .05). The DFROM was less in participants with grade III than grade I LASs (P = .004) at 24 to 72 hours; INV length was greater at 24 to 72 hours than at 2 to 4 weeks (P = .023) and at 6 months (P = .035) than at 24 to 72 hours. The anterior drawer length (P = .001) and INV talofibular interval (P = .004) were greater in the LAS group than in the control group at 6 months.ConclusionsDifferences in range of motion and laxity were evident among grades at various time points and may indicate different clinical responses after an LAS.