Perception of Labial Size and Objective Measurements-Is There a Correlation? A Cross-Sectional Study in a Cohort Not Seeking Labiaplasty

IntroductionPoor genital self-image is a common phenomenon leading to an increasing interest in female genital surgery over the last years.AimThe aim was to correlate objective measurements of the labia minora with the individual subjective perception of the labial size.MethodsIn a cross-sectional study with 200 premenopausal women (median age 33.5 years) presenting for gynecological issues other than vulvar diseases, labial width and length were measured, and psychological and physical complaints were assessed. Multivariable logistic regression analyses were performed to identify factors that influenced self-reported complaints and subjective perception of labia size.Main Outcome MeasureThe main outcome measure was labial appearance (width and length in mm, color), subjective perception of the labial size, and complaints.ResultsThe median width of the labia minora was 19.0 mm (interquartile range = 12.6–27.5), and the median length was 35.5 mm (interquartile range = 27.8–48.9). The objective size of the labia was significantly associated with womens' subjective perception of the labial size, but not with self-reported complaints. Nearly one-third of the women (n = 53, 27%) reported complaints of their labia minora which were mainly physical (n = 41, 77%) or a combination of physical and psychological problems (n = 9, 17%), while only a small group reported experiencing only psychological complaints (n = 3, 6%). Predictors of complaints were previous cosmetic surgery and the subjective perception of the labia size. The latter was significantly associated with discomfort during intercourse and when visiting a sauna and by labia minora that protruded over the labia majora.Clinical ImplicationsCutoff values to define labial hypertrophy and to justify labial reduction surgery should be avoided.Strength & LimitationsThis is a large sample of labial measurements in women not seeking labiaplasty. Standardized and validated questions regarding quality of life, sexuality, and body image could have provided more insight into psychological aspects.ConclusionThese data demonstrate the variability of labial anatomy and its perception.Widschwendter A, Riedl D, Freidhager K, et al. Perception of Labial Size and Objective Measurements-Is There a Correlation? A Cross-Sectional Study in a Cohort Not Seeking Labiaplasty. J Sex Med 2020;17:461–469.     

益气逐瘀方对缺氧诱导乳鼠心肌细胞凋亡及miR-24/Bim通路的影响

目的研究益气逐瘀方(参元丹)对缺氧诱导乳鼠心肌细胞凋亡及miR-24/Bim通路的影响。方法分离并培养乳鼠心肌细胞,建立心肌细胞缺氧模型,Lipofectamine2000转染miR-24 mimic/inhibitor至心肌细胞,实验分为正常组、缺氧组、参元丹组、参元丹+miR-24 mimic组、参元丹+miR-24 inhibitor组,治疗组予参元丹含药血清干预。比色法检测心肌细胞培养基上清液LDH、CPK活性,MTT法检测心肌细胞存活率,Annexin V/PI双染流式细胞术检测心肌细胞凋亡,qRT-PCR检测心肌细胞miR-24、Bim mRNA表达。结果与低氧组相比,参元丹组、参元丹+miR-24 mimic组、参元丹+miR-24 inhibitor组均能显著降低细胞培养基上清液LDH、CPK活性(P<0.05),提高心肌细胞存活率(P<0.05),降低心肌细胞凋亡(P<0.05),升高心肌细胞miR-24 mRNA表达(P<0.05),降低Bim mRNA表达(P<0.05);治疗组之间比较,参元丹+miR-24 mimic组作用更显著(P<0.05)。结论益气逐瘀方参元丹能够减轻缺氧诱导乳鼠心肌细胞损伤及细胞凋亡,其作用机制可能与其上调miR-24表达,同时抑制其靶基因Bim mRNA表达有关。     

体外转染Cyclin A2基因对原代大鼠心肌细胞增殖的影响

目的探讨体外转染细胞周期素A2(Cyclin A2)基因对原代大鼠心肌细胞增殖的影响,为心脏再生提供细胞学依据。方法 SD乳鼠12只,分离、培养、鉴定原代乳鼠心肌细胞并分为3组,实验组:转染带有强化绿色荧光蛋白(GFP)和Cyclin A2基因的重组腺病毒(Ad-Cyclin A2-GFP);空病毒组:转染不含目的基因带有GFP的重组腺病毒(Ad-Null-GFP);阴性对照组:未做转染处理,仅加入等量的培养基。利用GFP示踪技术,评估原代心肌细胞转染效率;转染后的细胞继续体外培养3~5d,利用免疫荧光技术分别检测Cyclin A2、磷酸化组蛋白H3(H3P)、心肌肌钙蛋白-T(c Tn T)。结果 1.荧光GFP示踪表明原代心肌细胞的转染效率高达(97±0.74)%;2.免疫荧光标记显示,空病毒组和对照组结果相似;心肌细胞特异性标记蛋白c Tn T分布于细胞质,原代心肌细胞纯度高达(95±0.62)%;心肌细胞Cyclin A2主要在胞核内聚集,少数分布于细胞质。H3P为核蛋白在细胞核内分布。3.转染Cyclin A2后,实验组H3P阳性率明显高于空病毒组和对照组,差异具有统计学意义(P0.05);实验组可见大量多核细胞,以双核为主,伴少量3核细胞。结论腺病毒作为转染载体对原代心肌细胞有很好的侵染效率;Cyclin A2超表达促进原代心肌细胞形成双核。     

circRNA＿100395通过结合miR-31-5p抑制心肌细胞肥大相关基因的表达

目的:探讨环状RNA(circRNA)₁00395对心肌细胞肥大表型的影响及其作用机制。方法:通过RT-qPCR检测健康器官捐献者(n=8)与心衰患者(n=14)心肌组织中circRNA₁00395及其宿主基因Kelch蛋白样家族成员20(KLHL20)的表达水平。原代分离、培养乳小鼠心室肌细胞(NMVCs),分别感染对照病毒(rAd-GFP)和circRNA₁00395重组腺病毒(rAd-circRNA₁00395)24 h,探究circRNA₁00395对心肌肥大相关的β-肌球蛋白重链(β-MHC)、骨骼肌α-肌动蛋白(ACTA1)及心房钠尿肽(ANP)表达的影响。采用鬼笔环肽染色检测circRNA₁00395对血管紧张素II(Ang II)处理的NMVCs肥大反应的影响。通过双萤光素酶报告基因实验及RNA pull-down实验验证微小RNA-31-5p(miR-31-5p)与circRNA₁00395的结合作用。通过转染miR...     

肝细胞生长因子对心肌细胞肥大的影响

目的 探讨肝细胞生长因子（HGF）在培养新生大鼠心肌细胞肥大中的作用。方法 原代心肌细胞中进行，分对照组和不同浓度HGF组（1ng／mL、10ng／mL、100ng／mL），采用放射性同位素3H-leu掺入法检测培养心肌细胞蛋白质合成速率。应用荧光定量PCR方法检测HGF对培养心肌细胞肥大相关基因ANF、B-MHC表达的影响。结果 HGF（1ng／mL、10ng／mL、100ng／mL）作用心肌细胞24h后可明显增加心肌细胞3H—leu的掺入量，分别增高2．15、4．66、2．51倍，与对照组比较有显著性差异（P〈0．01，0．01，0．01）；并可诱导心肌细胞ANF和B-MHC表达增加，ANFmRNA表达增加平均为（2．63±0．04，4．32±0．08，3．91±0．05），分别增高1．61、3．32、2．91倍，与对照组（1±0．00）比较有显著性差异（P〈0．01，0．01，0．01）；B-MHCmRNA表达增加平均为（2．14±0．03，2．81±0．07，2．42±0．06），分别增高1．10、1．82、1．41倍，与对照组比较有显著性差异（P〈0．01，0．01，0．01）；上述结果表明1ng／mL已经起作用，10ng／mL作用最强，100ng／mLHGF有所下降。结论 肝细胞生长因子可促进心肌细胞蛋白质合成速率和心肌细胞ANF、B-MHC表达增加，它可直接促进心肌细胞的肥大。     

维持性血液透析与腹膜透析患者左心室功能及相关因素分析

目的针对维持性肾脏替代治疗患者左心室功能情况及相关因素进行分析。方法将264例患者按不同肾脏替代治疗方式分为血液透析组（A组）和腹膜透析组（B组）,并常规检测血肌酐（SCr）、尿素氮（BUN）、血浆白蛋白（Alb）、血红蛋白（Hb）、血钙、血磷、血总胆固醇（TC）、甘油三酯（TG）、高密度脂蛋白胆固醇（HDL-C）、低密度脂蛋白胆固醇（LDL-C）、血全段甲状旁腺激素（iPTH）,超敏C反应蛋白（hs-CRP）;高压液相方法检测血浆同型半胱氨酸（Hey）;利用超声心动检查评价左心室功能。结果2组中,A组Hb、TG高于B组（P〈0．05）,而BUN低于B组（P〈0．05）;B组左心室舒张功能异常发生率高于A组（P〈0．01）;A组室间隔厚度、后壁厚度低于B组,而左室舒张末内径、左室收缩末内径及舒张早期和舒张晚期二尖瓣121最大血流速度之比（E／A）及射血分数（EF）高于B组,但只有舒张早期和舒张晚期二尖瓣口最大血流速度之比（E／A）有统计学差异（P〈0．01）;多因素Logistic回归分析显示,Alb、尿酸（UA）、hs—CRP、血钙、血磷水平是。肾脏替代治疗患者左室收缩功能障碍的危险因素;而年龄及收缩压与舒张压是其患者左室舒张功能障碍的危险因素。结论不同肾脏替代治疗方式下,患者左心室舒张功能异常发生率存在差异,纠正低蛋白血症,增加透析剂量,控制血压,减轻心脏负荷,纠正钙磷水平可能有助于改善其患者左心室功能异常。     

17-β estradiol attenuates ovariectomy-induced changes in cardiomyocyte contractile function via activation of AMP-activated protein kinase

Menopause increases the risk of cardiometabolic diseases in women. This circumstance is usually attributed to a deficiency in circulating estrogen levels although the underlying mechanism remains elusive. Given the pivotal role of AMP-activated protein kinase (AMPK) in the regulation of energy metabolism and cardiac function, this study was designed to examine the role of AMPK in estrogen deficiency and replacement-exerted cardiomyocyte responses. Adult female WT and AMPK kinase dead (KD) mice were subjected to bilateral ovariectomy (OVX) or sham operation. A cohort of ovariectomized mice received 17β-estradiol (E2) (40 μg/kg/day, i.p.) for 6 weeks. Mechanical and intracellular Ca²⁺ properties were evaluated including peak shortening (PS), time-to-PS (TPS), time-to-90%-relengthening (TR₉₀), and maximal velocity of shortening/relengthening (±dL/dt). Levels of AMPK, Akt JNK, ACC, SERCA, membrane Glut4, AS160 and PGC-1α were assessed using Western blot. OVX significantly decreased PS, ±dL/dt and intracellular Ca²⁺ rise in responsible to electric stimulus, prolonged TR₉₀ and intracellular Ca²⁺ decay without affecting TPS and resting intracellular Ca²⁺, the effects of which were reconciled by E2 replacement. Western blot analysis depicted that OVX suppressed phosphorylation of Akt AMPK and ACC although it promoted JNK phosphorylation, the effects of which were mitigated or significantly attenuated by E2 treatment in WT but not KD mice. Moreover, OVX procedure downregulated SERCA2a and membrane Glut4 while inhibiting AS160 phosphorylation without affecting PGC-1α levels. In vitro study revealed that E2 corrected cardiomyocyte contractile dysfunction elicited by OVX in cardiomyocytes from WT but not the AMPK kinase dead mice. Taken together, these data suggest that E2 treatment ameliorates estrogen deficiency-induced changes in cardiac contractile function possibly through an AMPK-dependent mechanism.     

Midkine-a通过限制心肌细胞总数的方式阻碍斑马鱼胚胎心脏生长

目的 探讨一种可溶性的外分泌因子Midkine-a在斑马鱼胚胎心脏发育过程中的功能。方法 在整体胚胎上做Midkine-a RNA的原位杂交实验;利用原有的转基因斑马鱼系Tg (pMidkine-a:EGFP),动态观察胚胎从出生到心脏发育成形这一段时间心脏荧光表达情况;将原有的转基因斑马鱼体系 Tg (phsp:Midkine-a:EGFP) 胚胎进行热休克而过表达Midkine-a,观察胚胎心脏表型;利用Tg (pcmlc2:dsRed)鱼系胚胎的心肌细胞核带有红色荧光,能进行单个心脏心肌细胞计数这一特点,将杂合的Tg (phsp:Midkine-a:EGFP)鱼系与纯合的Tg (pcmlc2:dsRed)鱼系交配,以得到Tg (phsp:Midkine-a:EGFP/pcmlc2:dsRed)的杂合胚胎,对其进行热休克而过表达Midkine-a,计算每个胚胎心脏内心肌细胞的总数; 用吗啉寡聚核苷酸 （Morphonino,MO）阻碍新生胚胎内的Midkine-a mRNA 表达,观察胚胎心脏表型。结果 原位杂交试验证实Midkine-a在胚胎48hpf （hours post fertilization, 受精后小时,用来标记斑马鱼胚胎年龄）大时表达于心脏;转基因Tg (pMidkine-a:EGFP)胚胎在72hpf时其EGFP表达于心脏;Tg(phsp:Midkine-a:EGFP) 胚胎在过表达Midkine-a后心脏变小;吗啉寡聚核苷酸敲除Midkine-a对胚胎心脏发育无影响;最后在Tg (phsp:Midkine-a:EGFP/pcmlc2:dsRed)鱼系胚胎内过表达Midkine-a导致其单个心脏内心肌细胞数目变少,与其小心脏外形吻合。结论 Midkine-a在斑马鱼胚胎发育过程中表达于胚胎心脏;过表达Midkine-a导致胚胎心脏内心肌细胞总数减少及心脏变小;敲除Midkine-a则对胚胎心脏发育无影响。