二甲双胍、阿卡波糖及西格列汀治疗2型糖尿病合并非酒精性脂肪性肝病的疗效

目的比较二甲双胍、阿卡波糖及西格列汀治疗2型糖尿病合并非酒精性脂肪性肝病(nonalcoholicfattyliverdisease,NAFLD)患者的临床效果。方法选择2016年9月到2018年9月于宝鸡市第二人民医院就诊的2型糖尿病合并NAFLD患者240例,采用随机数字表将其分为阿卡波糖组、西格列汀组及二甲双胍组,每组80例。所有患者均给予饮食控制及运动指导,二甲双胍组服用二甲双胍0.5g/次,3次/d;阿卡波糖组服用阿卡波糖50mg/次,3次/d;西格列汀组服用西格列汀100mg/次,1次/d;3组患者均治疗6个月。检测3组患者空腹血糖(fastingplasmaglucose,FPG)、餐后2h血糖(2 h postprandial blood glucose,2hPG)、糖化血红蛋白(glycosylated hemoglobin,HbA1c)、空腹胰岛素水平(fasting insulin,FIns)、胰岛素抵抗指数(homeostasis model assessment-insulin resistanceindex,HOMA-IR)、血清脂联素(adiponecti,ADN)、丙氨酸氨基转移酶(alanine aminotransferase,ALT)、天冬氨酸氨基转移酶(aspartateaminotransferase,AST)、γ-谷氨酰转肽酶(γ-glutamyl transpeptidase,γ-GT)、肝脂肪含量及受控衰减参数(controlled attenuation parameters,CAP);统计3组患者治疗期间不良反应(包括头疼、腹泻、恶心及低血糖)发生率。结果治疗前,二甲双胍组、阿卡波糖组及西格列汀组患者的性别[男性:43(53.75%)vs 41(51.25%)vs 40(50.00%)]、年龄[(51.24±5.15)岁vs(51.13±5.11)岁vs(51.08±5.10)岁]、糖尿病病程[(4.37±0.43)年vs(4.26±0.43)年vs(4.42±0.44)年]、轻度脂肪肝比例[33(41.25%)vs 31(38.75%)vs 35(43.75%)]、FPG [(7.43±0.74)mmol/L vs(7.59±0.76)mmol/L vs(7.52±0.75)mmol/L]、2h PG [(12.34±1.21)mmol/L vs(12.34±1.23)mmol/L vs(12.25±1.22)mmol/L]、HbA1c [0.0821±0.0082 vs 0.0843±0.0084 vs 0.0836±0.0083]、FIns [(10.55±1.06)m IU/L vs(10.39±1.04)mIU/L vs(10.46±1.05)mIU/L]、AST [(67.18±6.72)U/L vs(67.05±6.71)U/L vs(67.23±6.72)U/L]、ALT [(56.24±5.62)U/L vs(56.11±5.61)U/L vs(56.38±5.64)U/L]、γ-GT [(62.18±6.21)U/L vs(61.89±6.19)U/L vs(62.05±6.20)U/L]、HOMA-IR [3.50±0.52 vs 3.51±0.53 vs 3.50±0.52]、ADN[(456.38±45.64)ng/mlvs(452.95±45.29)ng/mlvs(454.67±45.46)ng/ml]、肝脂肪含量[(13.17±2.32)%vs(13.06±2.31)%vs(13.14±2.31)%]及CAP [(274.38±27.44)dB/m vs(275.16±27.52)dB/m vs (273.08±27.31)dB/m]的差异无统计学意义(P 0.05)。治疗后,二甲双胍组、阿卡波糖组及西格列汀组患者FPG [(6.42±0.64)mmol/L vs(6.11±0.61)mmol/L vs(5.66±0.56)mmol/L]、2h PG [(10.38±1.04)mmol/L vs(9.42±0.95)mmol/L vs(8.77±0.88)mmol/L]、HbA1c [0.0749±0.0074 vs 0.0679±0.0068 vs 0.0631±0.0063]、FIns [(9.43±0.94)mIU/L vs(9.11±0.91)mIU/L vs(8.52±0.85)mIU/L]、HOMA-IR [2.70±0.40 vs 2.47±0.35 vs 2.14±0.30]、ADN[(582.49±58.25)ng/ml vs(643.62±64.36)ng/ml vs(748.39±74.84)ng/ml]、AST [(44.59±4.46)U/L vs(40.36±4.04)U/L vs(36.14±3.61)U/L]、ALT [(42.58±4.26)U/L vs(40.33±4.03)U/L vs(38.79±3.88)U/L]、γ-GT [(45.38±4.54)U/L vs(40.83±4.08)U/L vs(35.46±3.55)U/L]、肝脂肪含量[(10.26±1.03)%vs(8.77±0.88)%vs(7.15±0.72)%]及CAP [(250.23±25.02)d B/m vs(241.63±24.16)d B/m vs(233.09±23.31)dB/m],差异有统计学意义(P均0.05)。西格列汀组FPG、2h PG、HbA1c、FIns、HOMA-IR、AST、ALT、γ-GT、肝脂肪含量及CAP值水平均显著低于其他2组,ADN水平高于其他2组,差异有统计学意义(P均0.05)。二甲双胍组、阿卡波糖组和西格列汀组患者不良反应发生率分别为17.50%(14/80)、13.75%(11/80)、11.25%(9/80),差异无统计学意义(χ~2=1.300,P=0.522)。西格列汀组患者治疗后FPG、2hPG、HbA1c、 FIns、HOMA-IR、ADN、AST、ALT、γ-GT、肝脂肪含量和CAP均显著低于治疗前(P均0.001)。结论西格列汀治疗2型糖尿病合并NAFLD疗效较好且可有效改善肝功能。     

二甲双胍对急性肺损伤细胞凋亡、迁移和上皮-间质转化的影响及机制研究

目的 探讨二甲双胍对急性肺损伤细胞凋亡、迁移和上皮-间质转化(EMT)的影响及机制。方法本实验时间为2022年6—11月。将人肺泡上皮细胞(A549细胞)分为对照组、过氧化氢(H₂O₂)组、2.5 mmol/L二甲双胍组、5.0 mmol/L二甲双胍组、10.0 mmol/L二甲双胍组、SB203580组，对照组不做任何干预；H₂O₂组加入400μmol/L H₂O₂作用24 h，以构建急性肺损伤细胞模型；2.5 mmol/L二甲双胍组、5.0 mmol/L二甲双胍组、10.0 mmol/L二甲双胍组在H₂O₂组基础上分别加入2.5、5.0、10.0 mmol/L二甲双胍进行干预；SB203580组在H₂O₂组基础上加入10.0 mmol/L p38丝裂原活化蛋白激酶(p38 MAPK)信号通路抑制剂——SB203580进行干预，选取细胞活力最佳时的药物浓度进行后续实验...     

二甲双胍抑制2型糖尿病大鼠脂肪组织胎球蛋白A表达的研究

目的探讨二甲双胍对T2DM大鼠外周血及脂肪组织胎球蛋白A(FetA)的影响。方法40只SD大鼠分为普食组(NC组)、T2DM组、二甲双胍治疗组(MET组)及胰岛素治疗组(INS组),每组各10只。高脂高糖饮食联合小剂量STZ建立T2DM大鼠模型,MET组予二甲双胍灌胃,INS组皮下注射胰岛素使其血糖与MET组基本保持一致。16周龄时ELISA检测血清FetA浓度,Western blot法检测脂肪单磷酸腺苷激活蛋白激酶(AMPK)、核转录因子(NF-κB)及FetA的表达,RT-qPCR法检测脂肪NF-κB及FetA mRNA的表达。结果 T2DM组血清FetA较NC组升高[(11.26±1.76)vs(23.99±4.64)ng/ml,P0.05],脂肪AMPK表达降低[(0.68±0.17)vs(0.11±0.03),P0.05],NF-κB及其mRNA表达升高[(0.53±0.07)vs(0.86±0.14),(1.00±0.10)vs(2.42±0.47),P0.05],FetA及其mRNA表达增多[(0.40±0.07)vs(0.66±0.11),(1.07±0.09)vs(1.98±0.27),P0.05]。与T2DM组比较,MET组血清FetA降低[(23.99±4.64)vs(17.37±3.25)ng/ml,P0.05],脂肪AMPK表达升高[(0.11±0.03)vs(0.49±0.80),P0.05],NF-κB及其mRNA表达减少[(0.86±0.14)vs(0.61±0.09),(2.42±0.47)vs(1.51±0.37),P0.05],FetA及其mRNA表达降低[(0.66±0.11)vs(0.47±0.06),(1.98±0.27)vs(1.25±0.16),P0.05]。与T2DM组比较,INS组各指标变化差异无统计学意义(P0.05)。结论二甲双胍降低T2DM大鼠外周血FetA的浓度,可能通过AMPK-NF-κB抑制脂肪组织FetA来表达。     

二甲双胍在高海拔地区糖尿病治疗中的安全性研究

高海拔地区初诊糖尿病患者61例,个体化治疗基础上全部加用二甲双胍1.5g/d治疗14 d.平均海拔2 260米和2 780米两地区(海拔差580米),氧分压相差3.5 mm Hg(1 mm Hg=0.133 kPa),初发糖尿病患者在治疗前血乳酸水平即高于正常值.高海拔地区中青年组及老年组治疗前血乳酸水平均较高[(3.90±0.85对3.65±0.70)、(4.67±0.80对3.69±0.78)mmol/L,均P＜0.05],中青年组糖尿病患者加用二甲双胍14 d后血乳酸水平未显著上升[(4.50±0.50和3.79±0.62)mmol/L,P＞0.05],老年组糖尿病患者加用二甲双胍14 d后血乳酸水平明显上升[(5.59±0.55和5.27±0.43)mmol/L,P＜0.05].因此,在高原地区的老年糖尿病患者应慎用或避免使用二甲双胍.     

二甲双胍分别联合利拉鲁肽及甘精胰岛素治疗2型糖尿病的临床观察

目的观察单纯使用二甲双胍血糖控制不佳的2型糖尿病患者分别联合利拉鲁肽及甘精胰岛素治疗的临床疗效与安全性。方法纳入2012年2月至2013年5月在北京军区总医院内分泌科门诊就诊的单纯使用二甲双胍超过3个月血糖控制不佳[糖化血红蛋白(Hb A1c)7%]的2型糖尿病患者40例,其中男性28例,女性12例,年龄34~70岁,平均年龄(51.5±7.3)岁。所有患者在继续服用盐酸二甲双胍片(≥1500 mg/d)的基础上,随机分为两组,利拉鲁肽组和甘精胰岛素组,每组各20例。分别联合应用利拉鲁肽及甘精胰岛素治疗12周后,比较两组患者治疗前后Hb A1c、空腹血糖、餐后2 h血糖、血脂、体质指数(BMI)及低血糖等不良反应的发生情况。结果与治疗前比较,利拉鲁肽组治疗后BMI[(28.32±0.35)kg/m2 vs.(26.75±1.10)kg/m2]、空腹血糖[(10.23±2.14)mmol/L vs.(7.06±1.09)mmol/L]、餐后2小时血糖[(14.68±4.43)mmol/L vs.(9.35±1.84)mmol/L]、低密度脂蛋白胆固醇[(2.76±0.97)mmol/L vs.(2.05±0.97)mmol/L]下降,差异有统计学意义(P均0.05);Hb A1c[(8.84±1.15)%vs.(7.34±0.66)%]下降,差异有显著统计学意义(P0.01)。与治疗前比较,甘精胰岛素组治疗后空腹血糖[(9.78±1.06)mmol/L vs.(6.72±1.58)mmol/L]下降,差异有统计学意义(P均0.05);Hb A1c也[(8.34±0.48)%vs.(7.44±0.28)%]下降,差异有显著统计学意义(P0.01)。与甘精胰岛素组治疗后比较,利拉鲁肽组治疗后低密度脂蛋白胆固醇降低,差异有统计学意义(P0.05)。两组患者治疗期间均未发生低血糖,利拉鲁肽组有3例出现轻微胃肠道反应,甘精胰岛素组无胃肠道反应。结论单纯使用二甲双胍3个月后血糖控制不佳的2型糖尿病患者联合应用利拉鲁肽及甘精胰岛素治疗安全有效,利拉鲁肽值得临床推广应用。     

六味地黄丸对2型糖尿病患者血糖控制及血清炎症因子表达的影响

目的分析六味地黄丸对2型糖尿病患者血糖控制及血清炎症因子表达的影响。方法选取2015年10月—2017年10月该院收治的102例2型糖尿病患者的处方作为观察对象,应用随机数字表法将其分两组,观察组与对照组分别51例。对照组采用二甲双胍治疗,观察组采用六味地黄丸联合二甲双胍治疗。对比两组血糖及血清炎症因子水平变化。结果观察组治疗后2 h PG[(8.04±1.16)mmol/L]、FPG[(6.24±1.24)mmol/L]、HbA1c[(6.01±1.41)%]均较对照组低[(9.57±1.29)mmol/L、(7.74±1.19)mmol/L、(7.23±1.37)%],且治疗后IL-6[(55.54±10.51)ng/L]、IL-8[(5.02±0.64)ng/L]、TNF-α[(1.24±0.18)ng/L]低于对照组[(63.47±10.49)、(6.37±0.58)、(1.47±0.21)ng/L],差异有统计学意义(P0.05)。结论六味地黄丸应用于2型糖尿病患者的治疗中,能有调节患者血糖水平,降低炎症反应。     

甘精胰岛素联合二甲双胍治疗2型糖尿病的效果评价

目的探讨治疗2型糖尿病中应用甘精胰岛素联合二甲双胍的效果。方法对该院2018年2月—2019年2月收治的2型糖尿病68例患者为研究对象,对患者按照随机分组,对照组34例患者应用二甲双胍联合中性低精蛋白新胰岛素治疗,观察组给予患者甘精胰岛素联合二甲双胍治疗,比较两组疗效及血糖变化。结果观察组总有效率94.12%;对照组总有效率82.35%,差异有统计学意义(P0.05)。治疗后,观察组空腹血糖、餐后2 h血糖、糖化血红蛋白分别为(5.54±1.18)mmol/L、(7.24±2.18)mmol/L、(6.08±1.02)mmol/L;对照组分别为(6.78±1.58)mmol/L、(8.72±2.81)mmol/L、(7.38±1.21)mmol/L,差异有统计学意义(P0.05)。结论甘精胰岛素联合二甲双胍治疗2型糖尿病效果显著,值得临床应用。     

2型糖尿病大鼠胸主动脉磷酸化p38丝裂素活化蛋白激酶蛋白表达及利拉鲁肽对其干预作用的研究

目的探讨p38丝裂素活化蛋白激酶(MAPK)与糖尿病大血管病变的关系及利拉鲁肽对其的干预作用。方法 24只Wistar大鼠分为正常对照组(NC)和实验组(EXP)。EXP组予高糖高脂饮食联合小剂量STZ腹腔注射建立T2DM大鼠模型。将成模大鼠随机分为糖尿病组(DM)和利拉鲁肽组(LIR),每组各7只。LIR组予利拉鲁肽(100μg/kg,2次/d)皮下注射,共8周;DM组和NC组予等量生理盐水皮下注射。实验结束后,测定各组相关指标;HE染色观察胸主动脉形态,免疫组织化学法检测胸主动脉磷酸化p38MAPK、核因子-κB(NF-κB)和单核细胞趋化蛋白-1(MCP-1)蛋白表达水平。结果 HE染色可见DM组胸主动脉呈动脉粥样硬化表现。DM组胸主动脉磷酸化p38MAPK、NF-κB和MCP-1蛋白表达水平较NC组升高(P=0.000),LIR组较DM组降低(P=0.017)。Spearman相关分析显示,胸主动脉磷酸化p38 MAPK与NF-κB、MCP-1蛋白表达呈正相关。DM组血糖、TG、TC、LDL-C、血清细胞间黏附分子-1(ICAM-1)、血管内皮黏附分子-1(VCAM-1)、NF-κB水平较NC组升高(P=0.000),较LIR组降低(P0.01)。结论在大鼠实验中,p38MAPK信号通路参与了糖尿病大血管病变的发生;利拉鲁肽可能通过下调血管p38MAPK磷酸化水平、抑制炎症反应、调脂等发挥了对糖尿病大血管病变的保护作用。     

二甲双胍对草酸钙诱导的人肾小管上皮细胞HK-2氧化应激及炎症反应调节作用观察

目的 观察二甲双胍对草酸钙诱导的人肾小管上皮细胞HK-2氧化应激及炎症反应的调节作用。方法 将HK-2细胞随机分成对照组、草酸钙组、二甲双胍组1、二甲双胍组2、PDTC组，其中对照组给予无血清DMEM培养基，草酸钙组加入浓度为100μg/m L的草酸钙晶体悬浮液，二甲双胍组1加入浓度为100μg/m L的草酸钙晶体悬浮液和1.20 mmol/L的二甲双胍晶体悬浮液，二甲双胍组2加入浓度为100μg/m L的草酸钙晶体悬浮液和0.80 mmol/L的二甲双胍晶体悬浮液，PDTC组加入浓度为100μg/m L的草酸钙晶体悬浮液和100 mmol/L的NF-κB特异性抑制剂PDTC晶体悬浮液。各组细胞继续培养6 h，采用比色法检测细胞上清液中丙二醛（MDA），采用Elisa法检测细胞上清液中单核细胞趋化蛋白-1(MCP-1)蛋白，采用RT-PCR法检测细胞中NF-κB、MCP-1 mRNA。结果 对照组、草酸钙组、二甲双胍组1、二甲双胍组2、PDTC组细胞上清液中MDA含量分别为（0.21±0.02）、（1.62±0.09）、（1.04±0.01）、（1.27±0.12）、（0.83±0.0...     

吡格列酮和二甲双胍联合诺和灵30R治疗2型糖尿病疗效分析

目的探索吡格列酮和二甲双胍联合诺和灵30R治疗2型糖尿病疗效。方法选取2015年4月—2017年4月期间该院收治的100例2型糖尿病患者,将其抽签化分组,两组各有50例,对照组和观察组分别采用二甲双胍+诺和灵30R治疗和吡格列酮+二甲双胍+诺和灵30R治疗。结果观察组患者的CHOL(6.05±0.39)mmol/L、LDL-C(10.05±2.46)mmol/L、hs-CRP(2.51±0.98)mg/mL、BMI(26.05±1.44)kg/m~2、2 hPG(8.14±1.36)mmol/L、FBG(6.42±0.69)mmol/L、HbA1c(6.05±1.05)%、低血糖发生率(2.00%)、血糖达标时间(7.05±2.96)d、胰岛素用量(38.48±3.52)U均优于对照组(P0.05)。结论吡格列酮+二甲双胍+诺和灵30R治疗2型糖尿病患者效果显著。     

Three layer functional model and energy exchange concept of aging process

Relying on a certain degree of abstraction, we can propose that no particular distinction exists between animate or living matter and inanimate matter. While focusing attention on some specifics, the dividing line between the two can be drawn. The most apparent distinction is in the level of structural and functional organization with the dissimilar streams of ‘energy flow’ between the observed entity and the surrounding environment. In essence, living matter is created from inanimate matter which is organized to contain internal intense energy processes and maintain lower intensity energy exchange processes with the environment. Taking internal and external energy processes into account, we contend in this paper that living matter can be referred to as matter of dissipative structure, with this structure assumed to be a common quality of all living creatures and living matter in general. Interruption of internal energy conversion processes and terminating the controlled energy exchange with the environment leads to degeneration of dissipative structure and reduction of the same to inanimate matter, (gas, liquid and/or solid inanimate substances), and ultimately what can be called ‘death.’ This concept of what we call dissipative nature can be extended from living organisms to social groups of animals, to mankind. An analogy based on the organization of matter provides a basis for a functional model of living entities. The models relies on the parallels among the three central structures of any cell (nucleus, cytoplasm and outer membrane) and the human body (central organs, body fluids along with the connective tissues, and external skin integument). This three-part structural organization may be observed almost universally in nature. It can be observed from the atomic structure to the planetary and intergalactic organizations. This similarity is corroborated by the membrane theory applied to living organisms. According to the energy nature of living matter and the proposed functional model, the decreased integrity of a human body's external envelope membrane is a first cause of the structural degradation and aging of the entire organism. The aging process than progresses externally to internally, as in single cell organisms, suggesting that much of the efforts towards the restoration and maintenance of the mechanisms responsible for structural development should be focused accordingly, on the membrane, i.e., the skin. Numerous reports indicate that all parts of the human body, like: bones, blood with blood vessels, muscles, skin, and so on, have some ability for restoration. Therefore, actual revival of not only aging tissue of the human body's membrane, but the entire human body enclosed within, with all internal organs, might be expected. We assess several aging theories within the context of our model and provide suggestions on how to activate the body's own anti-aging mechanisms and increase longevity. This paper presents some analogies and some distinctions that exist between the living dissipative structure matter and inanimate matter, discusses the aging process and proposes certain aging reversal solutions.     

Unusual responses of nocturnal pineal melatonin synthesis and secretion to swimming: Attempts to define mechanisms

Abstract: The effect of swimming at night on rat pineal melatonin synthesis was compared with that of light exposure at night. Rats were forced to swim at 0030 hr (lights out at 2000 hr) and sacrificed by decapitation 15 and 30 min later, immediately after swimming. Other groups of animals were exposed to white light (650μW/cm²) for 15 and 30 min at same time. Swimming caused a rapid and highly significant drop in the melatonin content in the pineal gland; however, the activity of N-acetyltransferase (NAT), the supposed rate limiting enzyme in the melatonin production, was not changed. Despite the drop in pineal melatonin levels, serum concentrations of the indole remained elevated in the rats that swam. In contrast, melatonin levels in the pineal and serum of light exposed rats fell precipitously, accompanied by a significant suppression of NAT activity. Since we anticipated that the strenuous exercise associated with swimming may induce release of artrial natriuretic peptide (ANP) from the heart, which in turn could cause the release of pineal melatonin, in a second study we injected physiological saline intravenously to stretch the cardiac muscle and release ANP. Three milliliters of normal saline was injected during the day into the jugular vein of anesthetized rats that were pretreated with isoproterenol to stimulate pineal melatonin production. Animals were killed 15 min after the saline injection, and pineal NAT activity and pineal melatonin levels were measured. The saline injections caused no alteration in the elevated levels of either NAT or melatonin. These data suggest that the disparity in pineal NAT activity (which was high) and pineal melatonin (which was low), in animals swum at night, may not be caused by ANP which is released during strenuous exercise such as swimming.     

The immunoneuroendocrine role of melatonin

Abstract: A tight, physiological link between the pineal gland and the immune system is emerging from a series of experimental studies. This link might reflect the evolutionary connection between self-recognition and reproduction. Pinealectomy or other experimental methods which inhibit melatonin synthesis and secretion induce a state of immunodepression which is counteracted by melatonin. In general, melatonin seems to have an immunoenhancing effect that is particularly apparent in immunodepressive states. The negative effect of acute stress or immunosuppressive pharmacological treatments on various immune parameters are counteracted by melatonin. It seems important to note that one of the main targets of melatonin is the thymus, i.e., the central organ of the immune system. The clinical use of melatonin as an immunotherapeutic agent seems promising in primary and secondary immunodeficiencies as well as in cancer immunotherapy. The immunoenhancing action of melatonin seems to be mediated by T-helper cell-derived opioid peptides as well as by lymphokines and, perhaps, by pituitary hormones. Melatonin-induced-immuno-opioids (MHO) and lymphokines imply the presence of specific binding sites or melatonin receptors on cells of the immune system. On the other hand, lymphokines such as -γ-interferon and interleukin-2 as well as thymic hormones can modulate the synthesis of melatonin in the pineal gland. The pineal gland might thus be viewed as the crux of a sophisticated immunoneuroendocrine network which functions as an unconscious, diffuse sensory organ.     

Melatonin and photoperiodic time measurement: Seasonal breeding in the sheep

Abstract: Well-established circadian physiology supports the view that photoperiodic time measurement utilizes the coincidence between the presence of light and a photosensitive phase of a 'biological clock' to alter reproductive status—the so-called external coincidence model of seasonal breeding. In this review, we examine the mechanism whereby photoperiod interacts with presumed suprachiasmatic nuclei activity to allow endogenous melatonin to normally synchronize reproductive activity to the optimal time of year. The Romney Marsh sheep is particularly explored as an experimental model. It is suggested that the on/off activity of seasonal reproduction may be a robust mechanism able to be predictably manipulated by the judicious use of the light/dark cycle and exogenous melatonin, but firmly based on circadian principles.     

Response of rat pineal melatonin to calcium, magnesium, and lithium is circadian stage dependent

Abstract: Herein we documented the response of pineal melatonin production to electrolytes known to be effective on pineal function in view of a possible circadian stage dependence. We studied the release of melatonin by perifused rat pineal glands at 2 different circadian stages corresponding to the middle of the light and dark periods, i.e., respectively, 7 and 19 HALO (Hours After Light Onset, L:D = 12:12). The initial efflux rates were, as expected, much higher in the perifusates of glands removed from rats sacrificed during the dark phase than of those removed during the light phase. After 3 hr of perifusion, melatonin release reached similar levels which were found constant up to the 8th hr of perifusion, whatever the circadian stage. Perifusion of the glands with physiological concentrations for the rat of calcium (5.2 mmol/1) and magnesium (1.34 mmol/1) resulted in a stimulatory effect on the pineal glands removed from rats sacrificed in the middle of the dark period (19 HALO), whereas no effects were observed on the pineal glands removed from rats sacrificed during the light (7 HALO). Lithium (0.28 and 0.55 mmol/1) was ineffective on melatonin release in pineal glands removed 7 and 19 HALO. Our results show differences in the initial efflux rates of melatonin and in the response of perifused pineal glands to calcium and magnesium according to the circadian stage.     

Conservative management of perforated duodenal diverticulum： A case report and review of the literature

Duodenal diverticula are a relatively common condition. They are asymptomatic, unless they become complicated, with perforation being the rarest but most severe complication. Surgical treatment is the most frequently performed approach. We report the case of a patient with a perforated duodenal diverticulum, which was diagnosed early and treated conservatively with antibiotics and percutaneous drainage of secondary retroperitoneal abscesses. We suggest this method could be an acceptable option for the management of similar cases, provided that the patient is in good general condition and without septic signs.     

Changes in connexin43, the gap junction protein of astrocytes, during development of the rat pineal gland

Abstract: The abundance of gap junctions between rat pineal astrocytes formed by connexin43 (Cx43) was studied during development. Levels and distribution of Cx43 were measured by immunoblotting and indirect immunofluorescence, respectively. The amount of Cx43 in cells located within the gland was low until about the 7th postnatal day and increased to adult values between the 14th and 21st days postpartum. Although astrocytes, recognized by their vimentin immunoreactivity, were scarce before birth, they were abundant by the 7th postnatal day suggesting that the low levels of Cx43 found at this age corresponded to a low expression of this protein. Localization of the immunoreactivity to Cx43 and vimentin showed a close correlation, indicating that mature or immature pineal astrocytes form gap junctions made of Cx43. Since Cx43 levels attained their adult values at about the time the innervation and the functional state of the gland reached maturity (2–3 weeks after birth), it is proposed that astrocyte gap junctions are involved in the function of the adult rat pineal gland.