羟基喜树碱合用PF方案治疗食管癌术后肺转移68例临床观察

目的 观察羟基喜树碱（HCPT）联合PF方案治疗食管癌术后肺转移的疗效及可行性。方法 HCPT10mg，5-FU500mg／m2，DDP20mg／m^2，第1～5天静滴，21天重复为一周期，完成2周期后评价疗效。结果 全组68例，无CR,PR38例，有效率55．9％。毒副作用主要表现为消化道反应、血液毒性和脱发，均能耐受。结论 羟基喜树碱（HCPT）联合PF方案治疗食管癌术后肺转移疗效确切，且毒副反应可耐受，价格适中，值得推广。     

奈达铂联合多西他赛治疗晚期食道癌的临床观察

目的：观察奈达铂联合多西他赛治疗晚期食道癌的近期疗效及不良反应。方法：将80例晚期食道癌患者随机分为治疗组和对照组,每组40例,治疗组：采用奈达铂联合多西他赛治疗,其中奈达铂25mg／（m2·d）第1～3天给予;对照组：采用顺铂联合多西他赛治疗,其中顺铂25mg／（m2·d）第1～3天给予,两组均在第1天给予多西他赛75mg／m2,21天为1个周期。化疗2个周期后按WHO标准评价疗效及毒副作用。结果：治疗组完全缓解2例,部分缓解14例,稳定18例,进展6例,有效率为40．0％（16／40）;对照组完全缓解2例,部分缓解16例,稳定16例,进展6例,有效率45．0％（18／40）,两组有效率比较差异无统计学意义（P〉0．05）。治疗组和对照组消化道不良反应分别为10．0％和30．0％;肾毒性分别为0和15．0％,血小板下降分别为30．0％和5．0％,差异有统计学意义（P〈0．05）;白细胞减少分别为70．0％和65．0％,差异无统计学意义（P〉0．05）。结论：奈达铂联合多西他赛方案与顺铂联合多西他赛方案治疗晚期食道癌的疗效相近,在毒副作用方面多西他赛联合奈达铂方案耐受性良好,具有优势。     

卡培他滨联合紫杉醇治疗晚期转移性宫颈癌的临床研究

目的探讨观察紫杉醇联合希罗达对比紫杉醇联合顺铂治疗晚期转移性宫颈癌的疗效及不良反应。方法对2003年7月至2006年12月本院确诊晚期转移性宫颈鳞癌患者52人双盲随机分为两组,试验组（n=26）121服希罗达每日1650mg／m^2,连服1～14d,紫杉醇80mg／m^2静脉滴注,第1天应用,每3周为1周期,连用2-4周期;对照组（n=26）顺铂20mg／m^2静脉注射,第1～5天,紫杉醇80mg／m^2静脉滴注,第1天应用,每3周为1周期,连用2-4周期,治疗结束2周后评价疗效。结果试验组可评价26例,有效率46．15％（12／26）,中位生存时间11．6月,1年生存率43．33％（13／26）;安全性方面Ⅲ反应占38．4％（9／26）,Ⅳ反应占15．4％（4／26）．主要为手足综合征、骨髓抑制和消化道毒性。对照组疗效可评价26例,有效率42．31％（11／26）,中位生存时间11．9月,1年生存率43．33％（13／26）;安全性方面Ⅲ反应占34．4％（10／26）,Ⅳ反应占17．2％（5／26）,主要为脱发、消化道毒性、骨髓抑制。结论希罗达联合紫杉醇对晚期转移性宫颈癌的疗效与紫杉醇联合顺铂疗效相当．但是不良反应较轻。     

紫杉醇联合草酸铂、卡培他滨三药方案治疗晚期转移性鼻咽癌的临床研究

目的探讨紫杉醇联合草酸铂、卡培他滨三药方案治疗晚期转移性鼻咽癌的疗效及不良反应。方法2002年1月至2005年1月，110例晚期转移性鼻咽癌病人入组：试验组55例患者．第1天应用紫杉醇135mg／m^2、草酸铂130mg／m。静脉滴注，口服卡培他滨1650mg／m^2／d，连服l-14d，每3周为一个周期，连用2-4个周期；对照组55例患者，第1-5天应用DDP 20mg／m^2、5-Fu 0．5g／m^2静脉注射，3周为一个周期，连用2-4个周期；治疗结束2-4周后评价疗效。结果试验组疗效可评价55例，对照组疗效可评价53例。试验组与对照组有效率分别为（CR＋PR）50．9％（28例）和32．1％（17例），两者差异有统计学意义（P〈0．05）。试验组和对照组中位生存时间为10．6个月和8．6个月，两者差异有统计学意义（t〈0．05）。安全性方面：试验组Ⅳ反应主要为手足综合征8例（14．5％）、骨髓抑制2例（3．6％）和消化道毒性4例（7.3％）；对照组Ⅳ反应主要为消化道毒性8例（15.1％）、骨髓抑制2例（3.8％）。结论紫杉醇联合草酸铂、卡培他滨三药方案对晚期转移性鼻咽癌的疗效较DDP＋5-Fu有优势，且不良反应可以耐受。     

伊立替康或多西他赛联合奥沙利铂治疗晚期非小细胞肺癌的临床观察

目的：观察伊立替康或多西他赛联合奥沙利铂治疗晚期非小细胞肺癌（NSCLC）的近期疗效及毒副作用。方法1晚期非小细胞肺癌68例中,伊立替康联合奥沙利铂组（A组）36例,采用伊立替康100mg／m2,第1、8天;奥沙利铂130mg／m2,第2天,静脉滴注。多西他赛联合奥沙利铂组（B组）32例,采用多西他赛75mg／m2,第1天;奥沙利铂130mg／m2,第2天,静脉滴注。21天为1周期,连用2周期后评定疗效。结果：A组和B组有效率分别为41．67％和31．25％,两组差异无统计学意义（P〉0．05）。A组迟发性腹泻和胆碱性综合征发生率明显高于B组（P〈0．01）,但A组粒细胞减少发生率明显低于B组（P〈0．05）。结论：伊立替康或多西他赛联合奥沙利铂治疗晚期非小细胞肺癌有较好的疗效,不良反应可以耐受,安全性好,可以考虑作为晚期非小细胞肺癌治疗方案之一。     

吉西他滨联合奈达铂治疗复发性上皮性卵巢癌的疗效观察

目的：观察吉西他滨联合奈达铂治疗复发性上皮性卵巢癌的近期疗效和毒副反应。方法：复发性上皮性卵巢癌32例,按前次铂类化疗至本次化疗时间间隔分为铂类耐药组（≤6个月,14例）和铂类敏感组（〉6个月,18例）。采用吉西他滨1000mg／m。,静脉滴注30rain,d1、d8;奈达铂80mg／m2,静脉滴注2h,d1;21d为一个周期,每2个化疗周期后评价疗效。结果：32例患者共接受153个化疗周期,总有效率59．38％（19／32）;铂类敏感组有效率61．11％（11／18）,铂类耐药组有效率57．14％（8／14）,两组间有效率比较差异无统计学意义（P〉0．05）。两组毒副反应程度均较轻,主要为骨髓抑制。结论：吉西他滨联合奈达铂治疗复发性上皮性卵巢癌是有效的二线化疗方案。     

多西紫杉醇联合替吉奥治疗晚期胃癌的临床观察

目的观察多西紫杉醇联合替吉奥治疗晚期胃癌的临床疗效及不良反应。方法将84例晚期胃癌患者随机分为实验组和对照组,每组42例。试验组接受多西紫杉醇75mg／m2静脉滴注,第1天,替吉奥80mg／m2,分2次,餐后口服。第1,14天,21d为1个周期,至少化疗2个周期;对照组化疗方案为顺铂25mg／m2,静脉滴注,第1～3天,醛氢叶酸钙200mg／m2,静脉滴注,第l～5天,5一氟尿嘧啶500mg／m2,第l～5天（在cF之后）,28d为1个周期,至少化疗2个周期。评价两组疗效及不良反应。结果试验组有效率为57．1％,中位疾病进展时间9．3个月,中位生存期14．3个月,1、2年生存率分别为57．1％和21．4％;对照组有效率为42．9％,中位疾病进展时间6．1个月,中位生存期10．2个月,1、2年生存率分别为38．1％和9．5％。两组疗效差异有统计学意义（P〈0．05）。主要毒副反应为骨髓抑制和胃肠道反应,大部分患者可耐受。结论多西紫杉醇联合替吉奥治疗晚期胃癌的近期疗效好,且不良反应可以耐受,值得进一步研究。     

吉西他滨联合顺铂治疗复发或难治性非霍奇金淋巴瘤

目的评价吉西他滨联合顺铂治疗复发或难治性非霍奇金淋巴瘤的疗效和安全性。方法15例复发或难治性淋巴瘤接受吉西他滨联合顺铂方案化疗：吉西他滨1000mg／m^2第1天和第8天，顺铂25mg／m^2第1～3天，21d为1个周期。结果15例患者中CR4例（26．7％），PR6例（40．0％），SD4例（26．7％），PD1例（6．6％），完全缓解率66．7％，毒性反应主要为血液学毒性和恶心呕吐反应。结论吉西他滨联合顺铂方案是治疗复发或难治性非霍奇金淋巴瘤安全、有效的化疗方案。     

泰索帝联合顺铂与吉西他滨联合顺铂治疗非小细胞肺癌的临床观察

目的 探讨泰索帝联合顺铂与吉西他滨联合顺铂治疗非小细胞肺癌（NSCLC）的疗效、生存期及毒副作用。方法 28例经组织学或细胞学确诊的未曾治疗的晚期非小细胞肺癌（NSCLC），随机分为泰索帝联合顺铂（DC）治疗组（14例）、吉西他滨联合顺铂治疗组（GC）（14例）。结果 DC组有效率为42．85％（CR2例，PR4例），一生存率57．1％，中位生存期（MST）8．5个月，TTP 5．05个月，中位缓解期（MRT）9．5个月。GC组有效率为38．46％（CRI例，PR4例），一生存率38．5％，中位生存期（MST）8个月，TTP 3．89个月，中位缓解期（MRT）8．26个月。WHO血液学毒性评价，Ⅲ／Ⅳ度中性粒细胞下降，DC组：21．4％，GC组：为15．4％；Ⅲ／Ⅳ度血小板减少，DC组：7．1％，GC组：15．4％；Ⅲ／Ⅳ度血红蛋白下降，DC组：7．1％，GC组：7．7％；Ⅱ-Ⅳ度感觉神经病变发生率：DC组：14．3％；GC组：7．7％，；胃肠道反映，Ⅱ／Ⅲ呕吐发生率DC组：（14．3％）明显优于GC组：（53．8％）（P〈0．05）。结论 DC、GC方案对非小细胞肺癌，显示了相似的有效率，中位生存期及1年生存率。DC组胃肠道反应，Ⅱ／Ⅲ呕吐发生率明显低于GC组，为耐受性较好的治疗晚期NSCLC化疗方案。     

GP方案同步放疗治疗Ⅲ期非小细胞肺癌的临床研究

目的观察和评价吉西他滨联合顺铂（GP）同步放疗治疗Ⅲ期非小细胞肺癌的耐受性和近期疗效。方法42例Ⅲ期非小细胞肺癌患者随机分为2组，放疗组21例先采取常规前后野对穿照射，剂量40Gy后改为调强适形放射治疗，包括原发灶和转移淋巴结，25～30Gy／10～12次，总剂量为65～70Gy。同步放化疗组的放射治疗同单纯放疗组，化疗采用吉西他滨1g／m^2第1、8天静脉滴注，顺铂30mg／m^2·d，第1～3天静脉滴注，21d为1个化疗周期。化疗共4～6个周期。结果同步放化疗组与单纯放疗组总有效率分别为85．7％和57．1％，两组差异有统计学意义。同步放化疗组1、2、3年生存率为66．7％、33．3％、23．8％，单纯放疗组1、2、3年生存率为38．1％、14．3％、9．5％，两组差异有统计学意义（P〈0．05）。两组的不良反应除骨髓抑制和消化道反应外无显著性差异。结论GP方案同步放疗治疗Ⅲ期非小细胞肺癌患者耐受性良好。疗效满意，远期疗效有待进一步观察。     

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 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.     

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.     

Environmental risk factors and their role in the management of atopic dermatitis

Introduction: The etiology of atopic dermatitis (AD) is multifactorial with interaction between genetics, immune and environmental factors.

Areas covered: We review the role of prenatal exposures, irritants and pruritogens, pathogens, climate factors, including temperature, humidity, ultraviolet radiation, outdoor and indoor air pollutants, tobacco smoke exposure, water hardness, urban vs. rural living, diet, breastfeeding, probiotics and prebiotics on AD.

Expert commentary: The increased global prevalence of AD cannot be attributed to genetics alone, suggesting that evolving environmental exposures may trigger and/or flare disease in predisposed individuals. There is a complex interplay between different environmental factors, including individual use of personal care products and exposure to climate, pollution, food and other exogenous factors. Understanding these complex risk factors is crucial to developing targeted interventions to prevent the disease in millions. Moreover, patients require counseling on optimal regimens for minimization of exposure to irritants and pruritogens and other harmful exposures.     

HLA genes in Amerindians from Mexico San Vicente Tancuayalab Teenek/Huastecos

Huastecos or Teenek Amerindians are presently living at North East Mexico (San Luis Potosi State). They have probably one of the most ancient culture of Mexico and Central America together with Mayas and Olmec groups with which also show close relationships. Proximity to Atlantic Ocean/Mexican Gulf originated that Spaniards had very early contact with them at about 1519 CE or before. In the present paper we have aimed to study HLA gene profile which may be useful for HLA and disease epidemiology and transplant programs in Teeneks. HLA-DRB1*04:07, -DRB1*14:06 and -DRB1*04:11 have been found in high frequency like in other Amerindian groups. High frequency typical Amerindians HLA extended haplotypes have been found, such as A*02-B*35-DRB1*04:07-DQB1*03:02; A*68-B*39-DRB1*04:07-DQB1*03:02 and A*02-B*39-DRB1*04:07-DQB1*03:02; also new haplotypes have been described, like A*02-B*52-DRB1*04:11-DQB1*03:02, A*68-B*35-DRB1*14:02-DQB1*03:01 and A*68-B*40-DRB1*16:02-DQB1*03:01. Genetic proximity is observed not only to linguistically close Mayans, but also to Mazatecans, Mixtecans and Zapotecans, who speak an altogether different languages; it shows once more that genes and languages do not correlate. This population was greatly diminished after European contact between 1500 and 1600 years CE; in fact, North and South America First Inhabitants population was brought from 80 down to 8 million people because of diseases (i.e.: measles, smallpox or influenza), slavery and war.     

État de l’art : nouveaux anticoagulants et transfusion

Direct oral anticoagulants (DOAC) are indicated for stroke prevention in atrial fibrillation and for the prevention and treatment of venous thromboembolism. As any anticoagulant, they are associated with a bleeding risk. Management of DOAC-induced bleeding is challenging. Idarucizumab, antidote for dabigatran, is currently available and is part of the therapeutic strategy, whereas antidotes for anti-Xa agents are under development. Activated or non-activated prothrombin concentrates are proposed, although their efficacy to reverse DOAC is uncertain. We propose an update on DOAC-associated bleeding management, integrating the availability of idarucizumab and the critical place of DOAC concentration measurements.     

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.     

Renal dysplasia and asplenia in two sibs

A family is reported in which two sibs, one male and the other female, both died within 24 hours of birth with enlarged polycystic kidneys. Postmortem histology in the second child showed gross renal dysplasia. In both children the pancreas was enlarged, nodular and cystic but the liver appeared macroscopically normal. In the second child, histological examination confirmed pancreatic fibrosis with cystic dilation of ducts, but showed portal fibrosis with bile duct proliferation in the liver.
This combination of findings is very reminiscent of those in a girl and her brother reported by Ivemark et al. (1959). The children reported here also showed absence or hypoplasia of the spleen, cardiac anomalies and other features of the Ivemark syndrome (Ivemark 1955), a quite different, usually sporadic, congenital disorder. It is suggested that the children described here have a distinct lethal congenital disorder, probably inherited in an autosomal recessive manner.     

The universal muscular chamber. A basic unit of the genitourinary, cardiovascular, gastro-intestinal, skeletal, cutaneous, respiratory and other systems, endocameral hypertension; and spasm, the key to their idiopathic diseases and arthropathies

Starting with the integument, we see many organs are contractile sacs or multiples thereof, which tubes or bags constitute the major part of the entire body. Recognition of this basic unit and its characteristics sheds new light, individually and collectively, on many disorders previously considered unrelated. Muscular tears and perforations develop in the walls of these chambers, being no way peculiar to those organs, wherein, hydrochloric acid occurs. So, it is not necessary to explain the absence of excessive acid from patients who exhibit holes in the gastric, uterine, aortic, duodenal, rectal, pulmonary, retina, and other walls. Muscle, not acid is the great common factor relating idiopathic disorders in the gastrointestinal tract to each other and to similar diseases in other systems. When the units are linked together, the lesions tend to appear as arthropathies, i.e. at the joints. Rephrasing common-place observations, frees us from conventional, conceptual cul-de-sacs. An observation is only as good as its interpretation, so all possibilities must be considered, otherwise, we will remain blinded by our misconceptions.