股骨远端去旋转截骨联合内侧髌股韧带重建术治疗复发性髌骨脱位的早期疗效

目的探讨股骨远端去旋转截骨（derotational distal femoral osteotomy，DDFO）联合内侧髌股韧带（medial patellofemoral ligament，MPFL）重建术治疗股骨前倾角（femoral anteversion angle，FAA）过大（≥30°）的复发性髌骨脱位的早期疗效。方法2017 年 6 月—2019 年 8 月，收治 17 例 FAA≥30° 的复发性髌骨脱位患者，均行 DDFO 联合 MPFL 重建术治疗。男 5 例，女 12 例，年龄 14～22 岁，平均 17.7 岁。髌骨脱位 2～8 次，平均 3.6 次。病程 2～7 年，平均 4.6 年。膝关节恐惧试验均为阳性。术前疼痛视觉模拟评分（VAS）以及 Lysholm 评分、Tegner 评分、Kujala 评分分别为（4.2±1.1）、（47.8±8.1）、（3.6±1.1）、（56.8±5.7）分，影像学测量 FAA、股骨远端外侧机械角（mechanical lateral distal femoral angle，mLDFA）、外侧髌骨移位值（lateral patella displacement，LPD）、胫骨结节-股骨滑车间距（tibial tuberosity-trochlear groove distance，TT-TG）分别为（34.9±3.4）°、（85.8±3.0）°、（13.7±3.8）mm、（23.1±2.1）mm。结果患者切口均Ⅰ期愈合，无膝关节僵硬、感染及髌骨再次脱位等并发症发生。患者均获随访，随访时间 13～25 个月，平均 17.7 个月。影像学复查显示，1 例截骨不愈合，经二次手术翻修加强固定后愈合；其余患者截骨均于术后 3～4 个月完全愈合。末次随访时，膝关节恐惧试验均为阴性；FAA、mLDFA、LPD 以及 TT-TG 分别为（15.6±2.7）°、（83.0±2.1）°、（5.0±2.6）mm、（20.5±2.5）mm，VAS 评分、Lysholm 评分、Tegner 评分以及 Kujala 评分分别为（2.4±1.4）、（93.4±7.8）、（6.8±1.5）、（89.0±8.0）分，上述指标与术前比较差异均有统计学意义（P<0.05）。 结论DDFO 联合 MPFL 重建术治疗 FAA 过大（≥30°）的复发性髌骨脱位可获得良好早期疗效，膝关节疼痛明显减轻、功能明显改善。     

改性壳聚糖基导电复合材料神经导管的体内降解及组织相容性观察

目的探讨改性壳聚糖基导电复合材料神经导管的体内降解及组织相容性，以期为组织工程神经构建提供新的支架材料。方法采用微乳液聚合法合成纳米聚吡咯（polypyrrole，PPy），与壳聚糖共混后注入定制的成管模型，冷冻干燥及脱酸后，制成改性纳米 PPy/壳聚糖复合材料导管（记作 CP 导管）；再经不同程度乙酰化（乙酰化反应时间分别为 30、60、90 min）改性，制备不同乙酰度的 CP 导管（记作 CAP1、CAP2、CAP3 导管）。各导管予红外光谱、扫描电镜进行表征，使用四探针电导仪测定电导率。取 30 只雌性 SD 大鼠，于背部左、右侧各制备 4 个皮下筋膜隧道，分别植入上述导管。术后 2、4、6、8、10、12 周取材，大体观察导管形态及完整性、扫描电镜观察导管微观结构、测量导管降解率，以观察导管体内降解性能；行 HE 染色及抗巨噬细胞免疫荧光染色，观察导管体内组织相容性。结果经表征证实乙酰化改性后的各导管 1 562 cm^–1左右的酰胺Ⅱ谱带增强，表示壳聚糖乙酰化改性成功。各导管均具备导电性能，组间电导率差异无统计学意义（P>0.05）。扫描电镜观察示各导管表面相对光滑、结构致密，无明显差异。导管植入体内后，随时间延长均出现一定程度塌陷，其中 CAP3 导管尤为明显；亦出现不同程度质量丢失，且乙酰化度越高，质量变化越大（P<0.05）。扫描电镜观察示植入 12 周后材料出现较多孔隙，且随着乙酰化度增加，孔隙呈增大趋势。组织学观察显示术后早期各导管均有较多巨噬细胞、淋巴细胞浸润，随着植入时间延长，淋巴细胞有所减少、成纤维细胞增多、胶原纤维增生明显。 结论不同乙酰度的改性壳聚糖基导电复合材料神经导管均有较好的体内生物相容性、可导电、可降解，且降解性与乙酰度相关，有望为组织工程神经构建提供一种新的支架材料。     

计算流体力学在组织工程中的应用进展

目的综述计算流体力学（computational fluid dynamics，CFD）在组织工程中的应用进展。方法广泛查阅 CFD 应用于组织工程的相关文献，主要对 CFD 用于生物反应器设计改良或优化、模拟体外组织再生过程中的流体动力学和细胞生长动力学等方面进行综述。结果CFD 的模拟预测能力可为生物反应器的设计优化和体外组织工程组织培养提供重要的指导作用，且结合实验研究能进一步提高模型预测结果的准确性。结论CFD 作为新兴和有效的研究工具，已在组织工程中展现出独特优势并取得显著进展，但更全面、准确地模拟组织再生全过程仍需进一步研究。     

β Chain deficiency in three patients with dysfunctional C8 molecules

Structural and functional studies were performed on a dysfunctional C8 molecule present in the serum of two siblings and an unrelated individual. The C8 in these three sera exhibited a pattern of partial immunologic identity with C8 in normal serum but was devoid of functional activity. The C8 was immunoprecipitated from the three sera and from a control serum with an antihuman C8 antiserum and analyzed by SDS-PAGE using highly purified human C8 as a reference. A selective absence of a band of 62,000 mol. wt was observed in the immunoprecipitates from the sera containing dysfunctional C8. Experiments performed with the purified α-γ and γ subunits showed that the hemolytic activity of the C8 deficient sera could be reconstituted by the addition of the β chain but not the α-γ dimer. Binding of the dysfunctional C8 to C$\text{567}$ was excluded by the following observations: (1) EAC 1–7 treated with the C8 deficient sera and then washed could not be lysed after the addition of the β subunit and C9; and (2) the abnormal molecules did not interfere with the consumption of normal C8 by the soluble complex SC5b-7.     

Einflu\ eines Β1-Rezeptorenblockers auf die Plasmaspiegel des atrialen natriuretischen Peptids bei Patienten mit essentieller Hypertonie unter Ergometerbelastung

Summary In order to investigate the behaviour of atrial natriuretic peptide (ANP) in untreated mild to moderate essential hypertension and the influence of blood pressure normalisation by a ₁-receptor blocker a study was conducted in groups of normotensive and hypertensive middle aged subjects. 10 normal subjects and 10 patients with essential hypertension (WHO I–II) without any medication and on betaxolol monotherapy were studied at rest and during graded exercise. In addition the response of ANP, cyclic guanosine monophosphate (cGMP) and the renin-aldosterone-system was investigated.Normal subjects and hypertensive patients did not differ in ANP levels at rest and also responded with a comparable exercise dependent increase at all workload levels. A steady decrease of ANP was noticed during the recovery period in both groups. After-blocker treatment in the hypertensive patients ANP concentrations significantly rose, both at rest and more pronounced during exercise. cGMP reacted in a similar way but showed a more inert response. A counter-regulatory behaviour between ANP and PRA or aldosterone, as seen under volume shifts, could not be detected. These findings demonstrate that plasma ANP is not altered in untreated essential hypertension. Increased ANP levels in ₁-blocker treatment may contribute to its blood lowering effect.

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Abkürzungsverzeichnis ANP atriales natriuretisches Peptid - ALD Aldosteron - C_In Inulin Clearance - cGMP zyklisches Guanosinmonophosphat - irANP immunoreaktives atriales natriuretisches Peptid - PAH Paraaminohippursäure - PRA Plasma-Renin-Aktivität - RAA-System Renin-Angiotensin-Aldosteron-System - RBF renaler Blutflu - RIA Radioimmunoassay - RVR renaler Gefä\widerstand     

Sympathoinhibition by rilmenidine in conscious rabbits: involvement of α2-adrenoceptors

Summary Cardiovascular and sympathetic nervous system effects of the mixed ₂-adrenoceptor and imidazoline receptor agonist rilmenidine were studied in conscious rabbits chronically instrumented for the recording of the firing rate of renal sympathetic fibers. Separate experiments were carried out on pithed rabbits with electrically stimulated (2 Hz) sympathetic outflow. Drugs were administered intravenously in a cumulative manner.In conscious rabbits, rilmenidine 0.1, 0.3 and 1.0 mg kg^–1 dose-dependently lowered blood pressure, renal sympathetic nerve activity, heart rate and the plasma concentration of noradrenaline and adrenaline. The effect on blood pressure and plasma catecholamines was maximal after 0.3 mg kg^–1 whereas heart rate and renal sympathetic nerve activity decreased further after rilmenidine 1.0 mg kg^–1. Yohimbine 0.1 and 0.5 mg kg^–1, when injected subsequently, attenuated and at the higher dose abolished all effects of rilmenidine. The effects of rilmenidine were also antagonized by the ₂-adrenoceptor antagonist 2-(2,3-dihydro-2-methoxy-1,4-benzodioxin-2-yl)-4,5-dihydro-1H-imidazole HCl (RX821002; 0.1 and 0.5 mg kg^–1). Yohimbine 0.1 and 0.5 mg kg^–1 did not attenuate or attenuated only slightly the decrease of heart rate and renal sympathetic nerve activity produced by infusion of vasopressin. In pithed rabbits with electrically-stimulated sympathetic outflow, yohimbine 0.1 submaximally and yohimbine 0.5 mg kg^–1 maximally increased the plasma noradrenaline concentration.The experiments show by direct measurement of sympathetic nerve firing and plasma catecholamines that rilmenidine causes sympathoinhibition in conscious rabbits, presumably through central sites of action. The antagonism by yohimbine, at doses which are selective for ₂-adrenoceptors (vs. imidazoline receptors), demonstrates the involvement of ₂-adrenoceptors in the sympatho-inhibition.Correspondence to: B. Szabo at the above address     

Urinaryα 1 as an index of proximal tubular function in early infancy

Urinary ₁-microglobulin (U-A₁M) was measured in healthy term infants on days 1, 4, 7, 14, 28, 90 and 180 of life. U-A₁M was high until day 14 and declined thereafter. It was significantly correlated with urinary ₂-microglobulin (U-B₂M) throughout the study, but not with serum A₁M on days 1 or 7. Similar to U-B₂M, U-A₁M in the clinically stable term infants with intrauterine growth retardation (n=4–7) was not elevated on days 1–7. In the sick infants who needed immediate resuscitatio at birth (n=4–8), U-A₁M as well as U-B₂M was high on days 1–7 and then decreased to normal levels, suggesting that U-A₁M can be used as a sensitive marker of acute proximal tubular damage and its recovery. These observations indicate that U-A₁M is a useful index of proximal tubular function in early infancy.     

Recent advances in understanding the pathogenesis of the hemolytic uremic syndromes

One of the requirements for an agent to cause hemolytic uremic syndrome (HUS) is its ability to injure endothelial cells. Shiga-like toxin (SLT) can do this. SLT is produced byEscherichia coli andShigella dysenteriae serotype 1; both have been implicated as causes of typical HUS. Endothelial cells have receptors (GB₃) for SLT and the toxin can inhibit eukaryotic protein synthesis, thereby causing cell death. Glomerular endothelial cell injury or death results in a decreased glomerular filtration rate and many of the perturbations seen in HUS. It is no longer certain that hemolysis is the result of a microangiopathy. Cell injury results in release of von Willebrand multimers; if these are ultra-large, thrombosis may ensue. There is also increasing evidence that neutrophils have a role in the pathogenesis of typical HUS.Streptococcus pneumoniae can also cause HUS and care must be taken to avoid giving plasma to patients withS. pneumoniae-associated HUS. There is compelling evidence that types of HUS are inherited by autosomal recessive and autosomal dominant modes. Patients with autosomal recessive HUS may have recurrent episodes. Mortality and morbidity rates are high for the inherited forms.