腓动脉穿支螺旋桨皮瓣在小腿足踝创面修复中的应用

目的探讨腓动脉穿支螺旋桨皮瓣在小腿足踝皮肤软组织缺损创面修复中的应用。 方法2018年10月至2020年4月,采用腓动脉穿支螺旋桨皮瓣修复小腿足踝创面29例,其中车祸伤19例,机器绞伤7例,皮肤肿瘤3例。术前采用便携式超声多普勒探测仪定位穿支位置,根据创面设计腓动脉穿支螺旋桨皮瓣,皮瓣切取面积8 cm×4 cm～20 cm×8 cm,转移修复创面。随访观察受区及供区的外形及足踝功能,评价临床应用的美学效果。 结果术后皮瓣均成活,患者均获随访,随访时间6～18个月,平均11个月。小腿供瓣区无凹陷、破溃,小腿外形无改变,留有线状瘢痕,不影响整体外观,皮瓣质地良好、色泽正常,皮瓣与周围皮肤无明显色差。 结论腓动脉穿支螺旋桨皮瓣血供可靠,不牺牲主干血管,不需取皮植皮,是修复小腿足踝中小面积皮肤软组织缺损的良好皮瓣之一。     

穿支蒂腓浅神经营养血管皮瓣修复外踝部皮肤缺损

目的　报道利用穿支蒂腓浅神经营养血管皮瓣修复对外踝部皮肤软组织缺损。 方法 利用便携式多普勒超声仪,在创缘周围探测腓动脉发出的穿支,以其中最合适的穿支为旋转点及血管蒂,沿腓浅神经轴线切取穿支蒂皮瓣逆向转位修复外踝部伴有肌腱及骨外露的创面。 结果　本组9例,男6例,女3例;年龄20～45岁,平均32岁;皮肤软组织缺损面积为3 cm×5 cm～7 cm×11 cm;皮瓣切取面积为4 cm×6 cm～8 cm×12 cm。皮瓣存活良好,颜色正常,修复效果好。平均随访两个月,患者步态正常,无疼痛,但其中2例患者抱怨小腿外侧区及足背有麻木感。 结论　穿支蒂腓浅神经营养血管皮瓣设计灵活,切取方便,血供可靠,适于修复外踝部的皮肤软组织缺损创面,是一种皮神经营养血管皮瓣与穿支蒂皮瓣相结合的优良皮瓣。     

踝管动脉穿支小腿皮瓣修复足部软组织缺损

目的 总结踝管动脉穿支皮瓣修复足部的软组织缺损效果。 方法 在踝管动脉穿支解剖学研究的基础上,2005年6月至2013年6月间临床采用踝管动脉穿支皮瓣修复足部的软组织缺损36例,致伤原因：车祸伤24例,砸伤12例。损伤部位：足背14例,足内侧22例,软组织缺损范围为5 cm×3 cm~16.5 cm×10.0 cm。皮瓣切取面积最小为6.0 cm×4.0 cm,最大为本组皮瓣切取范围为7 cm×5 cm~18 cm ×12 cm,远端蒂旋转点位于平内踝。 结果 临床修复36例,创面Ⅰ期愈合33例,Ⅱ期愈合3例。所有病例经5~15个月随访,皮瓣色泽正常,外形与功能改善满意,供区创面植皮愈合良好,对功能无不良影响。 结论 踝管动脉穿支皮瓣,可以修复足部远侧创面,效果好。     

胫后动脉踝上穿支皮瓣修复足踝部创面

目的　报道胫后动脉踝上穿支皮瓣修复足踝部创面的临床效果。 方法　对13例足踝部创面的患者,采用胫后动脉踝上穿支皮瓣转位修复术,其中足背创面5例,足跟部创面3例,踝部创面5例。4例急诊外伤创面伴有骨、肌腱外露者急诊修复。5例急诊创面采用VSD负压吸引后亚急诊行皮瓣修复, 4例为术后皮肤坏死,二期行皮瓣修复。皮肤缺损面积为1.5 cm×2.0 cm~7.0 cm×14.0 cm,切取皮瓣面积为2.5 cm×3.5 cm~8.0 cm×15.0 cm。 结果 本组13例皮瓣全部成活,供区植皮均成活。术后随访时间6~18个月,平均10个月。皮瓣质地接近周围皮肤,外观无臃肿。供区皮肤直接缝合者,术后瘢痕较小;供区植皮者,无明显瘢痕增生。踝关节活动良好,患肢均可负重行走。 结论　采用胫后动脉踝上穿支皮瓣转位修复足踝部创面,具有手术操作简单、安全的特点,是一种较好的术式。     

腓动脉穿支腓肠神经营养血管皮瓣修复足踝部软组织缺损

目的 探讨腓动脉穿支腓肠神经营养血管皮瓣逆行转移修复足踝部软组织缺损的临床治疗效果。 方法　2011年11月~2014年3月,运用以腓动脉穿支腓肠神经营养血管皮瓣逆行转移修复足踝部软组织缺损31例。软组织缺损部位：踝前部12例,外踝部10例,足跟部9例。软组织缺损面积 1.0 cm×0.8 cm～18.0 cm×10.0 cm,切取皮瓣面积 2.5 cm×7.0 cm~21.0 cm×12.0 cm,供区直接闭合或游离皮片覆盖。 结果 术后31例皮瓣29例全部成活,2例皮瓣远端局部表层皮肤坏死,经换药治疗后愈合。平均随访19个月,所有患者伤口愈合良好,皮瓣负重区无破溃,皮瓣色泽、质地良好。恢复穿鞋、行走功能。 结论　该皮瓣切取简单,血供可靠,不牺牲主要血管,修复效果满意。腓动脉穿支腓肠神经营养血管皮瓣是修复足踝部软组织缺损的理想选择。     

腘动脉外侧皮支单蒂皮瓣或联合腓动脉穿支双蒂皮瓣游离移植修复手足创面

目的 探讨腘动脉外侧皮支单蒂皮瓣或联合腓动脉穿支双蒂皮瓣游离移植修复手足皮肤软组织缺损的临床效果。方法 回顾性研究。纳入2013年3月—2020年6月东莞市长安新安医院手足显微外科收治的手足皮肤缺损伴肌腱、骨骼外露患者21例,其中男19例、女2例,年龄16~65岁（平均37.8岁）。手部创面8例,足部创面13例;软组织缺损面积3.5 cm×5.5 cm~10.0 cm×14.0 cm。观察患者术后皮瓣成活情况,采用英国医学研究会颁布的感觉功能恢复分级评价标准评估患者皮瓣感觉功能恢复情况,采用笔者参考皮瓣功能7项检查制定的皮瓣外观功能10项检查表进行皮瓣外观功能综合评价。结果 21例患者术后皮瓣全部成活。采用腘动脉外侧皮支单蒂皮瓣游离移植修复13例、腘动脉外侧皮支联合腓动脉穿支双蒂皮瓣游离移植修复8例,皮瓣切取面积4.0 cm×6.5 cm~10.0 cm×16.0 cm,供区创面直接缝合或植皮覆盖。术后随访6~36个月,皮瓣质地良好,厚薄适中,两点间辨别觉13~25 mm;皮瓣外观功能综合评价：优7例、良11例、可3例,优良率为85.7％。小腿供区无功能性影响。结论 腘动脉外侧皮支单蒂皮瓣或联合腓动脉穿支双蒂皮瓣游离移植修复手足创面,皮瓣血供有保障,成活率高,是修复手足软组织创面的有效术式之一。     

内踝上穿支皮瓣修复足踝部皮肤缺损

目的　报道以内踝上胫后动脉为蒂的穿支皮瓣修复足踝部皮肤软组织缺损的临床效果。 方法　2003年2月～2010年2月,对22例足踝部皮肤软组织缺损患者,采用以内踝上胫后动脉为蒂的穿支皮瓣修复术。皮瓣面积10 cm×7 cm～15 cm×11 cm,供区采用下腹部全厚皮片植皮。 结果　术后22例患者皮瓣均一期成活,供区伤口一期愈合。经随访6～36个月,平均随访12个月。皮瓣质地优良,外观不臃肿,感觉恢复S2~S3+,足部行走功能恢复满意。供区植皮者植皮区松软,外观可,无瘢痕挛缩。 结论　内踝上以胫后动脉为蒂的穿支皮瓣修复足踝部皮肤软组织缺损,具有解剖恒定,手术操作安全、简便,可满足踝部部创面覆盖的需要。     

血流桥接型股前外侧皮瓣修复下肢主干血管及软组织缺损创面

目的　探讨应用血流桥接型股前外侧皮瓣修复下肢皮肤、软组织缺损创面的临床效果。 方法　2014年8月~2016年12月,对12例下肢皮肤、软组织缺损伴骨或内固定外露患者,男8例,女4例,年龄7~66岁,应用血流桥接型股前外侧皮瓣移植修复小腿创面8例、踝部创面3例、足部创面1例,血管缺损长度为6~15 cm（平均10 cm）,将旋股外侧动脉降支主干近、远端分别与受区动脉近、远端进行端-端吻合,皮瓣切取面积5 cm×6 cm~32 cm×19 cm,供区直接缝合或以全厚皮片植皮修复。 结果　术后12例皮瓣全部成活,其中1例皮瓣边缘部分坏死,经换药后疤痕愈合,1例皮瓣术后1 d 出现血管危象,经探查后成活,皮瓣均未见静脉回流不足的表现,术后随访3~24个月(平均8个月),术后桥接血管血流通畅,皮瓣质地优良。 结论　血流桥接型股前外侧皮瓣不牺牲受区主干血管,同时实现覆盖创面的目的,是修复下肢皮肤、软组织缺损的理想方法。     

游离膝降动脉穿支皮瓣在足部软组织缺损中的应用

目的　总结应用游离膝降动脉穿支皮瓣修复足部软组织缺损的方法和临床效果。 方法　自2014年3月至2016 年12月,应用游离膝降动脉穿支皮瓣修复足部皮肤缺损8例,皮瓣面积7.0 cm×9.0 cm至9.0 cm×20.0 cm,5例以膝降动脉主干为蒂,3例以肌皮穿支为蒂。 结果　8例皮瓣全部成活,随访3~10个月,平均8个月,皮瓣的色泽、弹性、外观质地良好。 结论　膝降动脉穿支皮瓣血管蒂恒定,血管口径大小适中,皮瓣质地厚薄适中,是修复手足部皮肤缺损较适用的方法。     

游离腓肠内侧动脉穿支皮瓣在四肢创面修复中的临床应用

目的 探讨游离腓肠内侧动脉穿支皮瓣(MSAPF)在四肢创面修复中的临床应用效果。方法 回顾性研究。纳入2013年10月—2020年3月徐州仁慈医院手外科41例应用MSAPF修复四肢皮肤软组织缺损患者的临床资料,其中男24例、女17例,年龄16~58岁(平均42.4岁),机器绞伤26例、重物砸伤7例、车祸伤5例、电锯切割伤3例。皮肤软组织缺损面积为4.0 cm×3.5 cm～10.0 cm×8.0 cm,皮瓣切取面积5.0 cm×4.5 cm～12.0 cm×10.0 cm。术中发现穿支血管变异3例(7.3%)。采用疗效满意度评分表,依据患者术后创面愈合、皮瓣感觉、皮瓣温度、皮瓣形态及供区瘢痕,进行疗效满意度评价。结果 本组41例患者中,除3例术后发生血管危象外,余皮瓣完全成活,未发生感染、坏死等并发症。3例皮支血管变异者,经向后外侧寻找穿支,重新调整皮瓣位置,成功完成修复。患者均获得随访3~18个月,平均11.2个月,皮瓣外形良好、质地柔软,其中1例二期行肌腱松解术时做了皮瓣修薄。本组患者的疗效满意度为5~10分,患者均对治疗效果表示满意。结论 MSAPF是修复四肢中小面积皮肤软组织缺损的理想方式,针对穿支血管变异者,经恰当处理,也可成功切取小腿后区皮瓣。     

Schizophrenia in a North Swedish geographical isolate, 1900–1977. Epidemiology, genetics and biochemistry

Over 200 schizophrenic patients belonging to three major and interrelated pedigree complexes have been investigated over the past 30 years in a North Swedish geographically isolated population, presently numbering about 6,000. An intensive investigation of a number of biochemical correlates and genetic markers in a few selected families belonging to one of the major pedigrees has indicated new strategies for the current research program.
Schizophrenia, as defined operationally, is significantly associated with decreased activities of two enzymes (1) blood platelet monoamine oxidase, (2) plasma dopamine-β-hydroxylase, and (3) with the genetic marker Gc² (group specific antigen). Both enzymes are subject to genetic variation. A positive score for linkage between schizophrenia and low plasma DBH activity has been calculated, but, so far, available data are insufficient for discrimination between linkage and partial contribution of genetically controlled low plasma DBH to the pathogenesis of the disease. Alternatively, both mechanisms could be involved.
As a model for continued research, schizophrenia is explained as based on a double dominant-recessive genotype (Aabb), representing a vulnerability which in about 50 % of cases develops into clinical schizophrenia. It is suggested that the dominant mutation (A) operates on or affects MAO activity, and that the recessive genotype (bb) is instrumental in low variates of DBH activity and very likely such variates within the normal range of physiological variation. Moreover, it is suggested that the combined effects of MAO- and DBH-reduced efficiency on the metabolism of e.g. dopamine could be an essential pathogenic mechanism for the schizophrenic illness which is segregating in this population.     

The dominant diseases of modernized societies as omega-3 essential fatty acid deficiency syndrome: Substrate beriberi

About 1900, modern food selection and processing caused widespread $\text{epidemics}$ of the B vitamin deficiency diseases of beriberi and pellagra which, for genetic reasons, often expressed as different diseases ranging from bowel and heart disease to dermatoses and psychoses. But the B vitamins merely help convert essential fatty acids (EFA) into the prostaglandin (PG) tissue regulators and it now turns out that, through hydrogenation, milling and selection of w3-poor southern foods, we have also been systematically depleting, by as much as 90%, a newly discovered trace Nordic EFA (w3) of special importance to primates and sole precursor of the PG3(4) series, even as a concurrent fiber deficiency increases body demand for EFA. Since substrate EFA is processed by many B vitamin catalysts, an EFA deficiency will mimic a $\text{panh}$ypovitaminosis B, i.e., a mixture of $\text{substrate}$ beriberi and $\text{substrate}$ pellagra resembling vitamin beriberi and pellagra but exhibiting as even more diverse $\text{endemic}$ disease. This would consitute a second stage of the Modern Malnutrition and explain why some workers now hold the dominant diseases of modermized societies to be new, nutritionally based, pellagraform yet lipid-related and to range, once again, from heart disease to psychosis. It is an assumption that our dominant diseases are unrelated to each other or are merely revealed by our diagnostic acumen and therapeutic success; and that hydrogenating millions of tons of food oils annually, to destroy the rancidity producing w3-EFA, is safe for $\text{primates}$. Extensive beriberiform disease is reported here in 32 typical cases taken from medical practice which responds strikingly to linseed oil supplements (60% w3-EFA) in confirmation of identical results in Capuchins.     

The universal muscular chain reaction,muscle spasm,Torsions, ruptures and extravasations. Chameleons of pathology and some manifestations of simple muscular disorders

Most bodily functions require the coordinated actions of complementary and supplementary paired muscle groups. Where this essential muscular cooperation is lacking, hollow organs may burst and others become literally screwed up, giving rise to many similar spastic diseases such as Torticollis, Twisted ovarian cyst, Torsion of the Testis, Volvulus of the intestines, Varicose Veins, Megacolon, Aortamegaly, Scoliosis, Erb's Palsy, Peyronie's Disease, Main-en-Griffe, Undescended Foot (Pes Cavus), Talipes, Strabismus. Spasm is “panenepidemic” and unclassified examples of Torsion Dystonia and Dyskinesia really are as common as debt and taxes.     

'Very sore nights and days': the child's experience of illness in early modern England, c.1580-1720

Sick children were ubiquitous in early modern England, and yet they have received very little attention from historians. Taking the elusive perspective of the child, this article explores the physical, emotional, and spiritual experience of illness in England between approximately 1580 and 1720. What was it like being ill and suffering pain? How did the young respond emotionally to the anticipation of death? It is argued that children’s experiences were characterised by profound ambivalence: illness could be terrifying and distressing, but also a source of emotional and spiritual fulfilment and joy. This interpretation challenges the common assumption amongst medical historians that the experiences of early modern patients were utterly miserable. It also sheds light on children’s emotional feelings for their parents, a subject often overlooked in the historiography of childhood. The primary sources used in this article include diaries, autobiographies, letters, the biographies of pious children, printed possession cases, doctors’ casebooks, and theological treatises concerning the afterlife.     

Guidelines for the Validation and Use of Immunoassays for Determination of Introduced Proteins in Biotechnology Enhanced Crops and Derived Food Ingredients

Recent advancements in agricultural biotechnology have created a need for analytical techniques to determine introduced proteins in crops enhanced through modern biotechnology techniques. These proteins are expressed in plant tissues and may be present in food ingredients. Immunoassays are ideally suited for protein detection and may be used as both quantitative and threshold methods. Microplate ELISA and lateral flow devices are two of the most commonly used immunoassay formats for agricultural biotechnology applications. This paper provides general background information and a discussion of criteria for the validation and application of immunochemical methods to the analysis of proteins introduced into plants and food ingredients using biotechnology methods. It is the result of a collaborative effort of members of the Analytical Environmental Immunochemical Consortium. This collaborative effort represents the combined expertise of several organizations to reach consensus on establishing guidelines for the validation and use of immunoassays. Further, the paper offers developers and users a consistent approach to adopting the technology as well as aid in producing accurate and meaningful results.     

Ultracryotomy: development and application (with examples from the yeast cytology) (author's transl)

The preparation steps usually necessary for obtaining ultrathin frozen sections of biological material (chemical prefixation, enclosing, cryoprotective treatment, freezing, sectioning, and post-staining the sections for transmission electron microscopy) are submitted to a critical analysis. The application of cryo-ultramicrotomy, in particularly for cytochemical purposes, is reviewed. Fundamental considerations of chemical prefixation and poststaining are supported by examples from yeast cytology. Furthermore, the efficiency of the cryo-ultramicrotomy (electron optical resolution of ultrastructural details) is demonstrated on yeast cells and protoplasts.     

Hypo- und Hypermagnesämie aus kardiologischer Sicht

Zusammenfassung Eine Reihe pathologischer Zustände bedingen Magnesiummangel. Zustände mit Hypermagnesämie sind ebenfalls bekannt, doch wesentlich seltener. Für den Kardiologen beachtenswert ist, daß unter Therapie mit bestimmten Diuretica bei Herzinsuffizienz, bei Herzinfarkt, Kardiomyopathie, Digitalisintoxikation und bestimmten Herzrhythmusstörungen Hypomagnesämie beobachtet wurde. Leider kann in der klinischen Routine nur ein extracelluläres Magnesiumdefizit durch Serumbestimmungen gemessen werden; über Magnesiummangel einzelner Organe kann nichts ausgesagt werden. Hinweise für Magnesiummangel geben aber neben der Messung des Serumspiegels Anamnese, klinischer Befund, bestimmte EKG-Veränderungen wie auch evtl. Hypokalämie, ein Zustand, bei dem sich oft — besonders bei Aldosteronismus — parallele Veränderungen zeigten.Tierexperimente deuten darauf hin, daß infarktähnliche Läsionen unter Magnesiummangel entstehen, doch ob Herzinfarkt beim Menschen durch Magnesiummangel ausgelöst werden kann, ist noch ungeklärt. In Leichenherzen zeigte sich im Infarktgebiet neben Calciumakkumulation signifikanter Magnesiumverlust, wobei unklar blieb, ob sich Ursache oder Folge des Infarktes widerspiegelten. Falls ein ursächlicher Zusammenhang besteht, ist er im Myokardstoffwechsel selbst zu suchen, wie bei der Alkoholkardiomyopathie, wo myokardialer Magnesiummangel zumindest als pathogenetischer Teilfaktor anerkannt wird. Andererseits versucht man aber auch Beziehungen zwischen Atherosklerose, Blutgerinnung und Hypomagnesämie herzustellen, in der Meinung, daß Magnesiummangel auch über den coronaren Pathomechanismus des Herzinfarktes wirken könnte. Sicher scheint, daß gewisse EKG-Veränderungen und Herzrhythmusstörungen durch einen irritierten Magnesiumhaushalt bedingt sein können, da sie bei Gabe bzw. Entzug von Magnesium verschwinden. Daß Magnesiummangel die Glykosidtoleranz verringert, wird tierexperimentell bestätigt. Unter Hypomagnesämie bewirkt Acetylstrophanthidin eher und länger Rhythmusstörungen als ohne, außerdem lassen diese sich durch Magnesiumgaben eliminieren. Da in gewissen Fällen spontane und digitalisinduzierte Herzrythmusstörungen durch Magnesiuminjektionen beseitigt wurden, scheint Magnesium als Therapeuticum angebracht. Einsatz verschiedener Magnesiumsalze bei Angina pectoris, degenerativen Herzerkrankungen und Herzinsuffizienz ohne geprüften und offensichtlich gestörten Magnesiumhaushalt ist fragwürdig, weil keine eindeutigen klinischen Erfolgsbeweise vorliegen. Immerhin mag es aber larvierte, durch Serumbestimmungen nicht erfaßbare Mangelzustände geben. Allgemein erscheint es aus kardiologischer Sicht ratsam, den Magnesiumhaushalt zu überwachen und in entsprechenden Fällen auszugleichen, um möglichen Myokardläsionen oder fatalen Herzrhythmusstörungen entgegenzuwirken.     

HLA in North Colombia Chimila Amerindians

HLA-A,-B,-C,-DRB1 and -DQB1 alleles have been studied in Chimila Amerindians from Sabana de San Angel (North Colombian Coast) by using high resolution molecular typing. A frequent extended haplotype was found:HLA-A*24:02-B*51:10-C*15:02-BRB1*04:07-DQB1*03:02 (28.7%) which has also been described in Amerinndian Mayos Mexican population (Mexico, California Gulf, Pacific Ocean). Other haplotypes had already been found in Amerindians from Mexico (Pacific and Atlantic Coast), Peru (highlands and Amazon Basin), Bolivia and North USA. A geographic pattern according to HLA allele or haplotype frequencies is lacking in Amerindians, as already known. Also, five new extended haplotypes were found in Chimila Amerindians. Their HLA-A*24:02 high frequencies characteristic is shared with aboriginal populations of Taiwan; also, HLA-C*01:02 high frequencies are found in New Zealand Maoris, New Caledonians and Kimberly Aborigines from Australia. Finally, this study may show a model of evolutionary factors acting and rising one HLA allele frequency (-A*24:02), but not in others that belong to the same or different HLA loci.     

The case for allele‐specific recognition by the TCR

There is a sharp difference in how one views TCR structure–function–behaviour dependent on whether its recognition of major histocompatibility complex‐encoded restriction elements (R) is germline selected or somatically generated. The generally accepted or Standard model is built on the assumption that recognition of R is by the V regions of the αβ TCR, which is not driven by allele specificity, whereas the competing model posits that recognition of R is allele‐specific. The establishing of allele‐specific recognition of R by the TCR would rule out the Standard model and clear the road to a consideration of a competing construct, the Tritope model. Here, the case for allele‐specific recognition (germline selected) is detailed making it obvious that the Standard model is untenable.