大学生的睡眠质量与抑郁、焦虑的关系

目的:探讨大学生的睡眠质量与抑郁、焦虑症状严重程度的关系。方法:选取580名大学生,采用匹兹堡睡眠量表(PSQI)、抑郁自评量表(SDS)、焦虑自评量表测试(SAS)分别测查其睡眠质量以及抑郁、焦虑症状严重程度。SDS标准分≥53分为抑郁组,53分为无抑郁组;SAS标准分≥50分为焦虑组,50分为无焦虑组。结果:PSQI总分与SDS得分、SAS得分正相关(r=0.58、0.47,均P0.01)。得到抑郁组39例、无抑郁组488例,焦虑组147例、无焦虑组380例;其中抑郁症状的大学生PSQI总分高于无抑郁症状者[(9.2±2.2)vs.(5.5±2.2),P0.01],有焦虑症状的大学生PSQI总分高于无焦虑症状者[(7.2±2.6)vs.(5.3±2.1),P0.01];且PSQI总分对SDS得分和SAS得分的主效应均有统计学意义(F=22.64、14.00,均P0.01)。PSQI总分与SDS得分正向关联(β=0.58,P0.01),对SDS得分解释率为33.4%;PSQI总分与SAS得分正向关联(β=0.47,P0.01),对SAS得分的解释率为22.1%。结论:大学生睡眠质量是衡量抑郁、焦虑严重程度的重要指标。     

监狱警察睡眠及情绪状况调查

目的:了解监狱警察睡眠和焦虑、抑郁情绪的现状。方法:用匹兹堡睡眠质量指数(PSQI)、焦虑自评量表(SAS)和抑郁自评量表(SDS)对广东省监狱管理局的2093名监狱警察进行调查。结果:监狱警察PSQI均分为7．10±3．68,40．71％的监狱警察存在睡眠问题。SAS分为41．64±7．66,焦虑症状发生率为11．94％;SDS分为45．11±8．01,抑郁症状发生率为26．99％。男警PSQI得分高于女警(7．2±3．6／6．7 ±3．9,t=2．1,P<0．05)。35岁以上监狱警察SAS、SDS的标准分及焦虑症状发生率高于≤35岁的警察 (14．0％,11．1％,X2=18．77,P=0．000)。监区警察的PSQI得分高于行政人员(7．3±3．6／6．5±3．7．P< 0．05),行政人员睡眠问题发生率低于后勤人员、监区警察(34．4％、41．5％、42．1％,P<0．05)。PSQI分与SAS总分、SDS总分的相关系数为0．23、0．36(P<0．05)。结论:监狱警察的睡眠质量问题和焦虑、抑郁情绪比较严重,不同工作岗位、年龄及男女监狱警察的睡眠、焦虑、抑郁状况不同。     

护士睡眠质量与焦虑抑郁情绪的相关研究

目的探讨护士的睡眠质量和焦虑、抑郁情绪状况及其相互关系。方法用匹兹堡睡眠质量指数（PSQI）,焦虑自评问卷（SAS）和抑郁自评问卷（SDS）对某医院的护士的睡眠及焦虑抑郁情绪进行了调查。结果 PSQI总均分为7.86±4.03,睡眠障碍发生率为51.3%;46.8%的护士有焦虑情绪,45.3%的护士有抑郁情绪。PSQI总分与SAS总分,SDS总分均有显著性相关（r=0.36,P〈0.01;r=0.29,P〈0.01）。结论睡眠质量与焦虑抑郁情绪有密切的关系,相互影响。     

大学生睡眠质量与焦虑抑郁状况及其相关性分析

目的 分析睡眠障碍与焦虑、抑郁的相关性,以期为改善大学生睡眠质量提供一定参考依据。方法 2018年3月应用匹兹堡睡眠量表（PSQI）、焦虑自评量表（SAS）和抑郁自评量表（SDS）对我校4个专业827名大学生进行睡眠质量和心理状态评估。结果 827名大学生PSQI平均总分为（5.73±2.41）分,SAS平均总分为（43.83±9.11）分,SDS平均总分为（41.93±7.71）分。高年级学生、医学类大学生PSQI、SAS、SDS总分高于低年级学生、非医学类大学生PSQI、SAS、SDS总分,差异具有统计学意义（P＜0.05）;PSQI≥8大学生的SDS得分和SAS得分高于5≤PSQI≤7大学生、高于PSQI≤4大学生,SAS≥50分大学生的PSQI总分高于SAS＜50分大学生的PSQI总分,SDS≥53分大学生的PSQI总分高于SDS＜53分大学生的PSQI总分,差异具有统计学意义（P＜0.05）。结论 我校大学生睡眠质量不容乐观,睡眠质量与焦虑、抑郁情绪关系密切,应引起学校管理者及老师的重视。     

医学生睡眠质量与焦虑抑郁情绪关系的调查分析

目的探讨医学生睡眠质量与焦虑抑郁情绪的相关性,并对影响睡眠质量的有关因素进行分析。方法以匹兹堡睡眠质量指数(PSQI)、焦虑自评量表(SAS)、抑郁自评量表(SDS)为评价工具,采用分层整群抽样方法,调查某医学高等专科学校1~3年级医学生睡眠障碍的发生率及分布特征。结果医学生睡眠障碍的发生率为14.73%,男生(6.85%)女生(7.88%)间无显著性差异。19.52%的学生有抑郁情绪,男女生分别为8.22%和11.30%(P<0.05)。14.73%的学生存在焦虑,并且10.27%的学生焦虑、抑郁情绪并存。PSQI总分与SAS、SDS得分均呈显著正相关。回归分析表明,影响PSQI总分的因素依次为睡眠效率、睡眠障碍、入睡时间、睡眠质量、日间功能、催眠药物、睡眠时间。结论焦虑、抑郁情绪是影响医学生睡眠质量的重要因素,提高医学生的心理素质,增强其适应环境的能力,对于保持良好的健康状态是十分重要的。     

铁路职工睡眠质量与焦虑、抑郁相关研究

目的探讨铁路职工的睡眠质量、焦虑、抑郁及其相互关系。方法采用分层整群随机抽样的方法，抽取302名济南铁路分局铁路职工。对所抽样本进行匹兹堡睡眠质量指数（PSQI）、焦虑自评量表（SAS）、抑郁自评量表（SDS）的调查。结果PSQI、SAS、SDS得分分别为5.61±2.93,40.2±10.2和45.3±10.0；睡眠质量问题、焦虑及抑郁症状的发生率分别为21.9%,18.7%和35.2%。PSQI总分与焦虑、抑郁得分呈显著正相关（P＜0.0001）。结论焦虑、抑郁是影响铁路职工睡眠质量的重要因素,主管部门应重视职工的睡眠问题，重视心理卫生知识宣传，合理安排作息时间，减少影响因素，提高铁路职工的工作和生活质量。     

新型冠状病毒肺炎患者的自我效能感在负性情绪与睡眠质量间的中介作用

目的:探讨新型冠状病毒肺炎患者的负性情绪与睡眠质量之间的关系,以及自我效能感在负性情绪和睡眠质量间的中介作用。方法:对60例新冠肺炎患者采用自编一般人口学资料调查表、焦虑自评量表(Self-Rating Anxiety Scale, SAS)、抑郁自评量表(Self-Rating Depression Scale, SDS)、匹兹堡睡眠质量指数(Pittsburgh sleep quality index, PSQI)、一般自我效能感量表(General Self-Efficacy Scale, GSES)进行问卷调查。结果:新冠肺炎患者的焦虑症状检出率为33.3%,抑郁症状检出率为50.0%,睡眠障碍检出率为56.7%。SAS、SDS、PSQI评分分别为(44.96±13.51)分、(50.06±14.60)分和(6.98±4.69)分。新冠肺炎患者的负性情绪负向预测自我效能感(β=-0.47,P0.001),自我效能感负向预测睡眠质量(β=-0.49,P0.001),负性情绪正向预测睡眠质量(β=0.43,P0.001)。新冠肺炎患者的自我效能感水平在负性情绪与睡眠质量间起部分中介作用,效应量为34.89%。结论:新冠肺炎患者的自我效能感在负性情绪和睡眠质量间起部分中介作用,负性情绪可以直接和通过自我效能感的部分中介作用影响睡眠质量。     

综合医院护理人员睡眠质量与抑郁焦虑状况的相关性

目的:了解综合医院护理人员睡眠质量与抑郁焦虑状况的关系,为改善护理人员的睡眠质量提供参考。方法:采用匹兹堡睡眠指数量表(PSQI)、抑郁自评量表(SDS)、焦虑自评量表(SAS)对109名综合医院护理人员进行测评。结果:本组护理人员PSQI总分及各因子分均高于正常人群(U=5.76~15.33,P0.01),且41.3%(45/109)护理人员PSQI总分大于7分,远高于正常人群(χ2=69.11,P0.001);本组护理人员的SDS总分和SAS总分均高于我国常模(U=12.12,12.39;P0.01);SAS总分和SDS总分均与PSQI总分呈正向相关(r=0.534,0.897;P0.01)。结论:综合医院护理人员的睡眠质量较差,改善其抑郁焦虑状况有助于睡眠质量的改善。     

外企产线工人疲劳与情绪及睡眠质量的相关性研究

目的探讨外企产线工人疲劳与情绪状态及睡眠质量的相关性,以便有效的调节情绪和睡眠,缓解疲劳,为人力资源管理提供依据。方法采用随机整群抽样的方法,抽取某外企生产线工人586名,采用疲劳评定量表(FAI)、焦虑自评量表(SAS)、抑郁自评量表(SDS)及匹兹堡睡眠质量指数表(PSQI)对其进行测查。结果与常模比较,外企产线工人SAS和SDS总分均高于常模(t=3.37～5.75,P<0.01);疲劳严重程度、疲劳对环境特异性与焦虑、抑郁、睡眠紊乱及白天功能紊乱呈正相关(P<0.05或P<0.01);疲劳的心理后果与焦虑、抑郁及主观睡眠质量呈负相关(P<0.01),与睡眠紊乱、白天功能紊乱呈正相关(P<0.01);疲劳对休息、睡眠的反应与焦虑、抑郁、主观睡眠及睡眠持续性呈负相关(P<0.01);与睡眠紊乱呈正相关(P<0.01)。结论外企产线工人存有焦虑、抑郁情绪,其疲劳状况受焦虑、抑郁情绪及睡眠质量的影响。     

高校护生睡眠质量及与焦虑抑郁情绪的关系研究

目的调查高校护生的睡眠质量和影响因素，研究其与焦虑抑郁情绪的关系；为提高护生的睡眠质量提供依据。方法以睡眠状况自评量表（SRSS）、焦虑自评量表（SAS）以及自评抑郁量表（SDs）为评价工具，调查护生的睡眠质量及焦虑抑郁状况的发生率。结果①护生SRSS总分为23．30±5．658，与中国常模问的差异有统计学意义（Z=2．12，P〈0．05）。性别、担任班委否、恋爱否这3个因素影响护生睡眠质量；②护生的SAS、SDS总分分别为35．00±10．177和27．39±9．171；焦虑、抑郁症状的发生率分别为16．00％和21．00％；⑧相关分析表明，SRSS总分以及觉醒不足、入睡困难、睡眠不稳、早醒、恶梦夜惊和失眠后反应这6个因子的得分与SAS、SDS总分呈显著正相关；④回归分析表明，SRSS的10个因子中，入睡困难和恶梦夜惊被选入SAS回归模型；恶梦夜惊和睡眠不稳被选入SDS回归模型。结论高校护理专业学生的睡眠质量较差，性别、担任班委否、恋爱否以及焦虑抑郁情绪是影响护生睡眠质量的重要因素。     

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.     

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.     

What will studies of Fulani individuals naturally exposed to malaria teach us about protective immunity to malaria?

There are an estimated over 200 million yearly cases of malaria worldwide. Despite concerted international effort to combat the disease, it still causes approximately half a million deaths every year, the majority of which are young children with Plasmodium falciparum infection in sub-Saharan Africa. Successes are largely attributed to malaria prevention strategies, such as insecticide-treated mosquito nets and indoor spraying, as well as improved access to existing treatments. One important hurdle to new approaches for the treatment and prevention of malaria is our limited understanding of the biology of Plasmodium infection and its complex interaction with the immune system of its human host. Therefore, the elimination of malaria in Africa not only relies on existing tools to reduce malaria burden, but also requires fundamental research to develop innovative approaches. Here, we summarize our discoveries from investigations of ethnic groups of West Africa who have different susceptibility to malaria.     

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.     

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.     

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.     

Class II HLA in Georgia Caucasus Tbilisi Georgians and their Mediterranean ancestry: The Usko Mediterranean languages

Georgia (or Sakartvelo in its own language) is a South Caucasus Mts. country with its easternmost part is enigmatically named Iberia, like the Iberian Peninsula, which may refer to rivers “Kura” and “Ebro” or their valleys respectively. Most of their inhabitants speak Georgian which is included within Dene-Caucasian group and Usko-Mediterranean subgroup of languages. The latter includes Basque, Berber, ancient Iberian-Tartessian, Etruscan, Hittite, Minoan Lineal A and others. In the present paper, HLA class II -DRB1 and -DQB1 alleles has been studied and extended haplotypes calculated. Most frequent haplotypes are also of Mediterranean origin (i. e.: (A*02-B*51)-DRB1*11:01-DQB1*03:01, (A*02-B*51)-DRB1*13:01-DQB1*06:03, or (A*24-B*35)-DRB1*01:01-DQB1*05:01) and DA genetic distances show that closest world populations to Georgians are Mediterraneans. Georgians also show common extended haplotypes ((A*02-B*51)-DRB1*11:01-DQB1*03:01, (A*02-B*13)-DRB1*07:01-DQB1*02:01 and (A*03-B*35)-DRB1*11:01-DQB1*03:01) with Svan people, a secluded population in North Georgia mountains. We can conclude that Georgians belong to a very old Mediterranean substratum according to both linguistics (Usko Mediterranean languages) and HLA genetics.     

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.