恩替卡韦联合胸腺肽α1治疗慢性乙型肝炎疗效研究

目的：观察和比较恩替卡韦联合胸腺肽α1治疗HBeAg阳性慢性乙型肝炎的疗效。方法：选取我院58例HBeAg阳性慢性乙型肝炎患者分成联合组和对照组。联合组28例,初始同时使用恩替卡韦及胸腺肽αl24周,之后停胸腺肽αl继续用恩替卡韦至48周。对照组30例,单用恩替卡韦0．5mg／d,48周。定期检测ALT复常率,HBVDNA转阴率,HBeAg／抗HBe血清转换率,肝纤维化组合,Fibroscan评分两组在治疗结束时进行疗效评价。结果：24周时两组ALT复常率无差异显著性（P〉0．05）,联合组和对照组HBVDNA阴转率在24周、48周时均差异有显著性（P〈0．05）。联合组与单用组HBeAg血清转换率在第24周、48周时,两组比较差异均有显著性（P〈0．05）。肝纤维化组合各指标（HA,LN,PIIIP,Ⅳ型胶原）,Fibroscan评分两组治疗48周后比较差异均有显著性（P〈0．05）,且两组治疗前后差异联合组更显著。治疗过程中,未发现明显副作用。结论：恩替卡韦联合胸腺肽d1治疗HBeAg阳性慢性乙型肝炎,安全性与耐受性良好,联合组在ALT复常率,HBeAg血清转换率和HBVDNA转阴率,抗肝纤维仲韵井种P昂荽楫干蕈闱凰巷卡韦组．     

瑞巴派特四联疗法对幽门螺杆菌阳性消化性溃疡患者血清氧化应激指标和胃蛋白酶原的影响

摘要 目的：观察瑞巴派特四联疗法治疗幽门螺杆菌（Hp）阳性消化性溃疡的疗效及对患者血清氧化应激指标和胃蛋白酶原的影响。方法：选取2020年7月至2021年12月期间广西壮族自治区胸科医院收治的Hp阳性消化性溃疡患者（n=100）,按照随机数字表法分为联合组（50例,瑞巴派特四联疗法）、对照组（50例,标准四联疗法）。对比两组疗效、量表评分、血清氧化应激指标、胃蛋白酶原（PG）、不良反应发生率、Hp根除率、复发率。结果：联合组的临床总有效率高于对照组（P<0.05）。联合组的消化性溃疡愈合率高于对照组（P<0.05）。治疗后,联合组胃食管反流性疾病症状频率量表（FSSG）各项评分、临床症状各项评分低于对照组（P<0.05）。治疗后,联合组血清丙二醛（MDA）低于对照组,血清谷胱甘肽过氧化物酶（GSH-PX）、超氧化物歧化酶（SOD）高于对照组（P<0.05）。治疗后,联合组胃蛋白酶原（PG）Ⅰ、PGⅡ低于对照组（P<0.05）。两组不良反应总发生率组间对比无差异（P>0.05）。联合组的Hp根除率高于对照组,复发率低于对照组（P<0.05）。结论：瑞巴派特四联疗法治疗Hp阳性消化性溃疡患者,可有效促进溃疡愈合,缓解临床症状,改善机体应激状态和胃蛋白酶原水平,提高Hp根除率,减少不良反应及复发情况。     

胃苏颗粒联合四联疗法对幽门螺杆菌相关性消化性溃疡患者血清炎性因子、胃肠激素及生活质量的影响

摘要 目的：探讨胃苏颗粒联合四联疗法对幽门螺杆菌（Hp）相关性消化性溃疡患者血清炎性因子、胃肠激素及生活质量的影响。方法：选取2018年3月~2019年12月期间我院收治的Hp阳性消化性溃疡患者124例,根据奇偶数字法将患者分为对照组、联合组,各62例。对照组给予四联疗法,联合组给予胃苏颗粒联合四联疗法,疗程均为4周。对比两组疗效、Hp根除率、炎性因子水平、胃肠激素水平、生活质量及不良反应。结果：联合组Hp根除率、临床总有效率高于对照组（P<0.05）。联合组治疗4周后SF-36量表各维度评分较对照组更高（P<0.05）。联合组治疗4周后血清降钙素原（PCT）、白介素-6（IL-6）、超敏C反应蛋白（hs-CRP）水平低于对照组（P<0.05）。联合组治疗4周后胃泌素（GAS）、胃动素（MTL）低于对照组（P<0.05）。两组不良反应发生率对比差异无统计学意义（P>0.05）。结论：胃苏颗粒联合四联疗法治疗Hp相关性消化性溃疡患者,可有效改善患者体内血清炎性因子及胃肠激素水平,并提高其生活质量和Hp根除率,疗效优于单纯四联疗法。     

苦参碱注射液对急性病毒性心肌炎的治疗作用

目的：观察苦参碱注射液治疗急性病毒性心肌炎（AVM）的临床疗效。方法：将AVM患者120例随机分为治疗组63例及对照组57例,对照组采用常规疗法,治疗组在对照组基础上给予苦参碱注射液治疗,连用2周。观察临床疗效。结果：治疗组总有效率90.5%,对照组总有效率73.7%,两组比较有显著性差异。治疗组治疗后血清肌酸磷酸激酶（CPK）、天冬氨酸转氨酶（AST）及血清乳酸脱氢酶（LDH）较对照组治疗后明显降低,差异有统计学意义（P〈0.05）。结论：苦参碱对急性心肌炎有良好疗效。     

晚期胃癌患者化疗中胸腺肽α1治疗疗效的临床研究

目的：探讨应用流式细胞仪（FCM）检测胃癌患者外周血免疫指标,以评价胸腺肽α1联合化疗对胃癌患者免疫功能的影响。方法：70例胃癌患者随机分为用药组和对照组。用药组35例采用胸腺肽α1＋化疗,对照组35例单用化疗,两组化疗方案相同。胸腺肽α1每次1.6mg,每周2次,连续4周（共8针）。28天为一疗程,共用2个疗程。采用FCM检测两组患者化疗前后外周血CD4、CD8、CD3＋CD4＋、CD3＋CD8＋免疫指标。结果：用药组CD4、CD8、CD3＋CD4＋、CD4/CD8均高于化疗前和对照组化疗后水平,均具有统计学意义（P〈0.05）。结论：胸腺肽α1配合化疗能提高患者的免疫功能,用FCM检测外周血免疫指标为临床观察肿瘤患者的免疫状态提供有效的依据。     

二甲双胍联合运动疗法干预妊娠期糖尿病患者的临床研究

摘要 目的：探讨二甲双胍联合运动疗法对妊娠期糖尿病（GDM）患者临床效果的影响。方法：将2020年3月到2022年3月北京航天总医院收治的89例GDM患者,按照抛掷硬币法随机分为组分为观察组（n=45）和对照组（n=44）。对照组口服盐酸二甲双胍片,观察组在对照组基础上加用运动疗法。对比两组患者的临床疗效、血糖指标、氧化应激指标、炎症因子水平、妊娠结局及不良反应。结果：治疗后观察组临床疗效总有效率93.33（42/45）高于对照组75.00%（33/44）（P<0.05）。治疗后两组患者空腹血糖（FPG）、餐后2 h血糖（2hPG）、糖化血红蛋白（HbAlc）均降低,且观察组显著低于对照组（均P<0.05）。治疗后两组超氧化物歧化酶（SOD）水平均升高且观察组显著高于对照组,丙二醛（MDA）、活性氧（ROS）水平均降低且观察组显著低于对照组（均P<0.05）。治疗后两组超敏C反应蛋白（hs-CRP）、肿瘤坏死因子（TNF-α、白细胞介素-6（IL-6）水平均降低且观察组水平显著低于对照组（均P<0.05）。观察组剖宫产、早产发生率低于对照组（均P<0.05）。治疗期间两组患者不良反应事件总发生率无差异（P>0.05）。结论：二甲双胍联合运动疗法能有效控制GDM患者血糖水平,优化氧化应激指标,降低炎症因子水平,改善妊娠结局,且具有一定的安全性。     

胃苏颗粒联合四联疗法对Hp阳性慢性萎缩性胃炎患者血清胃肠激素和胃黏膜COX-2、NF-κB表达的影响

摘要 目的：观察胃苏颗粒联合四联疗法对幽门螺杆菌（Hp）阳性慢性萎缩性胃炎（CAG）患者血清胃肠激素和胃黏膜氧化酶-2（COX-2）、核转录因子-κB（NF-κB）表达的影响。方法：选取2017年7月~2019年6月期间中国人民解放军总医院第二医学中心消化内科收治的Hp阳性CAG患者120例,根据信封抽签法将患者分为观察组（60例,胃苏颗粒联合四联疗法）、对照组（60例,四联疗法）,均治疗2周。观察两组疗效、Hp根除率、胃肠激素和胃黏膜COX-2、NF-κB表达,观察两组治疗方案的药物安全性。结果：观察组的临床总有效率和Hp根除率均高于对照组（P<0.05）。观察组治疗2周后胃泌素（GAS）、胃动素（MTL）水平低于对照组,胃泌素-17（G-17）水平高于对照组（P<0.05）。观察组治疗后3个月的胃黏膜COX-2、NF-κB表达低于对照组（P<0.05）。两组不良反应发生率对比无差异（P>0.05）。结论：Hp阳性CAG患者采用四联疗法联合胃苏颗粒治疗,可有效控制患者胃肠激素水平,降低胃黏膜COX-2、NF-κB表达,疗效确切,且不良反应发生风险较低。     

酪酸梭菌活菌胶囊联合四联疗法对幽门螺杆菌阳性胃溃疡患者血清炎症因子、胃肠激素和胃蛋酶原亚群的影响

摘要 目的：探讨酪酸梭菌活菌胶囊联合四联疗法对幽门螺杆菌（Hp）阳性胃溃疡患者血清炎症因子、胃肠激素和胃蛋酶原亚群的影响。方法：选择天津市中医药研究院附属医院于2017年2月~2020年3月期间收治的Hp阳性胃溃疡患者100例,按信封抽签法随机分为对照组（50例,采用四联疗法治疗）、观察组（50例,采用酪酸梭菌活菌胶囊联合四联疗法治疗）。对比两组患者疗效、血清炎症因子、胃肠激素、胃蛋酶原亚群、Hp根除率及不良反应。结果：治疗4周后,观察组患者的总有效率为92.00%（46/50）,高于对照组患者的70.00%（35/50）（P＜0.05）。观察组治疗4周后白介素-6（IL-6）、肿瘤坏死因子-α（TNF-α）、降钙素原（PCT）、C反应蛋白（CRP）水平低于对照组（P<0.05）。观察组治疗4周后胃泌素（GAS）低于对照组,胃动素（MTL）高于对照组（P<0.05）。观察组治疗4周后胃蛋白酶原Ⅰ（PGⅠ）、胃蛋白酶原Ⅱ（PGⅡ）水平较对照组更低（P<0.05）。对比两组不良反应发生率无差异（P>0.05）。观察组的Hp根除率为94.00%（47/50）,较对照组的72.00%（36/50）更高（P<0.05）。结论：酪酸梭菌活菌胶囊联合四联疗法治疗Hp阳性胃溃疡患者,可取得显著疗效,提高Hp根除率,改善血清炎症因子、胃肠激素和胃蛋酶原亚群,且安全性较好。     

悬吊训练疗法联合生物反馈电刺激对产后压力性尿失禁患者盆底功能和尿流动力学的影响

摘要 目的：观察悬吊训练疗法联合生物反馈电刺激对产后压力性尿失禁（PSUI）患者盆底功能和尿流动力学的影响。方法：选择2019年7月~2021年8月期间我院接收的PSUI患者96例,符合要求的患者根据信封抽签法分为对照组（48例）和研究组（48例）。对照组患者接受悬吊训练疗法,研究组患者接受悬吊训练疗法联合生物反馈电刺激,对比两组疗效、盆底功能指标和尿流动力学指标,观察两组尿垫试验漏尿量、国际尿失禁咨询委员会尿失禁问卷简表（ICI-Q-SF）问卷评分。结果：研究组的临床总有效率高于对照组（P<0.05）。治疗1个月后,两组24 h尿垫试验漏尿量和ICI-Q-SF问卷评分降低,且研究组低于对照组（P<0.05）。研究组治疗1个月后盆底肌力改善效果优于对照组（P<0.05）。两组治疗1个月后最大尿道闭合压力（MUCP）、功能尿道长度（LES）、腹压漏尿点压（ALPP）、与最大尿流率（Qmax）升高,且研究组高于对照组（P<0.05）。结论：PSUI患者经悬吊训练疗法联合生物反馈电刺激干预,可有效改善临床症状,促进盆底功能和尿流动力学恢复,效果显著。     

益生菌联合三联疗法治疗小儿幽门螺杆菌相关性胃炎的疗效及对炎性因子的影响

摘要 目的：探讨益生菌联合三联疗法治疗小儿幽门螺杆菌（HP）相关性胃炎的疗效及对炎性因子的影响。方法：选取2017年1月~2018年6月期间我院收治的HP相关性胃炎患儿93例,根据乱数表法将患儿分为研究组（n=47）、对照组（n=46）,对照组患儿给予三联疗法治疗,研究组在对照组的基础上联合益生菌治疗,比较两组患儿临床疗效、临床症状总评分、炎性因子、HP根除率、不良反应发生率及复发率。结果：治疗1个月后,研究组的临床总有效率为87.23%（41/47）,高于对照组的69.57%（32/46）（P<0.05）。两组治疗2周后、1个月后的临床症状总评分及治疗1个月后血清肿瘤坏死因子-α（TNF-α）、超敏C反应蛋白（hs-CRP）、白介素-6（IL-6）水平均下降（P＜0.05）,且研究组低于对照组（P<0.05）。研究组HP根除率高于对照组（P<0.05）。两组不良反应发生率及复发率比较无差异（P>0.05）。结论：益生菌联合三联疗法治疗小儿HP相关性胃炎的疗效确切,可改善患儿的临床症状,降低炎性因子水平,且用药安全性较好。     

Rapid induction of thymosin beta 4 in concanavalin A-stimulated thymocytes by translational control

The expression of thymosin beta 4, an ubiquitous peptide of high cellular content, was studied in concanavalin A-stimulated rat thymocytes within the first 3 h after activation of the cells. An early 6.3-fold increase of the peptide occurred after 1 h of stimulation amounting to 0.4% of the total cellular protein. This increase coincided with that of thymosin beta 4 biosynthesis measured by [35S]methionine incorporation. The share of thymosin beta 4 synthesis in total protein synthesis 1 h after addition of concanavalin A amounts to 1% but no elevation of the corresponding mRNA was observed. These data suggest that a translational control mechanism is involved in this rapid induction. Consequently, actinomycin D did not inhibit thymosin beta 4 induction in contrast to cycloheximide. The peaks of maximal thymosin beta 4 levels and biosynthesis were followed by rapid decreases of these parameters suggesting a function of thymosin beta 4 in the early phase of T cell activation.     

Solid phase synthesis of thymosin beta 9

Thymosin beta 9, a 41 residue thymic polypeptide, has been synthesized by a solid phase method. A modification of the low HF method was used to deprotect and cleave the peptide from the resin. Thymosin beta 9 was then obtained in analytically pure form by a one-step purification procedure in 32% yield. The activity of thymosin beta 9 in the terminal deoxynucleotidyl transferase assay was greater than calf thymus fraction 5, but comparable to thymosin beta 4. In contrast to thymosin alpha 1, neither beta 4 nor beta 9 was active in the rosette inhibition assay.     

Retinoic Acid Regulates Thymosin β Levels in Rat Neuroblastoma Cells

A small acidic polypeptide, termed thymosin beta 10, has been identified and is present in the nervous system of the rat by the ninth day of gestation. Thymosin beta 10 levels rise during the remaining days of life in utero, and then decline to nearly undetectable values between the second and fourth week post partum. The present study investigates the possible developmental signals and mechanisms that might regulate the expression of thymosin beta 10 during neuroembryogenesis. Many cell lines derived from tumors of the central nervous system express thymosin beta 10, as well as its homologue gene product, thymosin beta 4. Because some of these cell lines respond to exogenously applied agents by increasing their apparent state of differentiation, we have determined whether thymosin beta 10 levels are coordinately modulated. In several neuroblastomas, including the B103 and B104 lines, retinoic acid elicits a time- and dose-dependent increase in the content of thymosin beta 10, but not that of thymosin beta 4. The increase in thymosin beta 10 polypeptide is associated with a marked increase in the specific mRNA encoding this molecule. The mRNA for thymosin beta 4 is unaffected by retinoic acid. This is in contrast with the situation in vivo, where the expression of both genes decreases after birth. Other agents that influence the morphology of B104 cells, such as phorbol esters and dibutyryl cyclic AMP, have no influence on beta-thymosin levels. A range of steroids, which like retinoids act upon nuclear receptors, was also inactive. The stimulatory action of retinoic acid is detectable within 4 h, and thymosin beta 10 peptide levels continue to rise for at least 4 days. The influence of the isoprenoid is fully reversible and exhibits structural specificity. We believe that this culture system is mimicking the early rising phase of thymosin beta 10 levels in brain and that endogenous retinoids may be candidate physiological regulators of this gene.     

Formation and implications of a ternary complex of profilin, thymosin beta 4, and actin

Data from affinity chromatography, analytical ultracentrifugation, covalent cross-linking, and fluorescence anisotropy show that profilin, thymosin beta(4), and actin form a ternary complex. In contrast, steady-state assays measuring F-actin concentration are insensitive to the formation of such a complex. Experiments using a peptide that corresponds to the N terminus of thymosin beta(4) (residues 6-22) confirm the presence of an extensive binding surface between actin and thymosin beta(4), and explain why thymosin beta(4) and profilin can bind simultaneously to actin. Surprisingly, despite much lower affinity, the N-terminal thymosin beta(4) peptide has a very slow dissociation rate constant relative to the intact protein, consistent with a catalytic effect of the C terminus on conformational change occurring at the N terminus of thymosin beta(4). Intracellular concentrations of thymosin beta(4) and profilin may greatly exceed the equilibrium dissociation constant of the ternary complex, inconsistent with models showing sequential formation of complexes of profilin-actin or thymosin beta(4)-actin during dynamic remodeling of the actin cytoskeleton. The formation of a ternary complex results in a very large amplification mechanism by which profilin and thymosin beta(4) can sequester much more actin than is possible for either protein acting alone, providing an explanation for significant sequestration even if molecular crowding results in a very low critical concentration of actin in vivo.     

A novel β-thymosin from the sea urchin: extending the phylogenetic distribution of β-thymosins from mammals to echinoderms

The study of the phylogenetic distribution of the β-thymosin family is important to elucidate its biological function further. A new thymosin, designated as thymosin β₁₄, consisting of 40 amino acid residues and with a molecular weight of 4537 Da as determined by ion spray mass spectrometry, was isolated from the sea urchin. The N-terminus of this polypeptide is blocked by an acetyl group as found by matrix-assisted laser desorption mass spectrometric and amino acid analysis. The primary structure was elucidatd by Edman degradation of the HPLC-purified thymosin β₁₄ fragments produced by digestion with endoproteinase Asp-N and trypsin. Sequence comparison reveals that thymosin β₁₄ is 73% homologous to thymosin β₄, obtained from calf thymus. By isolating and characterising the structure of thymosin β₁₄ from the sea urchin, an invertebrate, substantial knowledge about the phylogenetic distribution and evolution of β-thymosins is gained. © 1997 European Peptide Society and John Wiley & Sons Ltd.     

Synthesis of an artificial gene coding for thymosin alpha1 and its expression in Escherichia coli as a hybrid with human tumor necrosis factor]

Chemical-enzymatic synthesis and cloning in Escherichia coli of an artificial gene encoding the immunoactive peptide thymosin alpha 1 have been carried out. Recombinant plasmids were constructed which contain fusion genes coding for hybrids of human tumour necrosis factor (TNF) and thymosin alpha 1 as N- or C-terminal part of the hybrid protein. In the C-terminal hybrid protein, TNF and thymosin alpha 1 are linked through a methionine residue, thus allowing for thymosin alpha 1 to be cleaved off the rest of the hybrid protein with cyanogen bromide. In case of the N-terminal hybrid protein, the linker between the thymosin alpha 1 and TNF sequences is the acid-labile dipeptide Asp-Pro. Expression of the hybrid genes in E. coli and properties of the recombinant proteins were studied. The N-terminal hybrid protein was secreted into periplasmic space, in contrast with the C-terminal hybrid protein, which formed insoluble aggregates inside bacterial cells. Procedures for the isolation of both hybrid proteins were developed. The N-terminal hybrid protein displayed full biological activity in the cytotoxic assay on the mouse fibroblast L-929 whereas the C-terminal hybrid protein proved to be much less active. Treatment of the hybrid protein TNF-thymosin alpha 1 with cyanogen bromide lead to a mixture of two polypeptides, from which thymosin alpha 1 was purified to homogeneity by simple chromatographic procedures.     

The early induction of the actin-sequestering peptide thymosin beta 4 in thymocytes depends on the proliferative stimulus

The expression of the actin-sequestering peptide, thymosin beta 4, was analyzed in proliferating rat thymocytes, activated by diverse stimuli, during the early G1 phase and the S phase. In the presence of concanavalin A a 6.3-fold increase of thymosin beta 4 occurred already after 1 h of stimulation without elevation of the corresponding mRNA level. In contrast, during the S phase the increase of thymosin beta 4 (2.5-fold) was accompanied by a higher mRNA level, but did not exceed the growth related increase of total protein. Stimulation with a crosslinked antibody against rat T cell antigen receptor or stimulation with phorbol 12-myristate 13-acetate (PMA) and Ca(2+)-ionophore A23187, separately or in combination, did not lead to the marked increase of the thymosin beta 4 concentration in the early G1 phase but resulted in elevated thymosin beta 4 peptide and mRNA levels during the S phase. It therefore appears that protein kinase C activation and a rise in cytoplasmic Ca(2+)-concentration are not exclusively responsible for the stimulation of thymosin beta 4 specific translation in thymocytes. This assumption was reinforced by the observation that inhibition of the protein kinase C activity by 1-(5-isoquinolinylsulfony)-2-methylpiperazine (H-7) did not affect the cellular thymosin beta 4 content 1 h and 48 h after concanavalin A (Con A) stimulation.     

Thymosin beta10 inhibits cell migration and capillary-like tube formation of human coronary artery endothelial cells

Thymosin beta10 is a cytoplasm G-actin sequestering protein whose functions are largely unknown. To determine the direct effects of exogenous thymosin beta10 on angiogenic potentials as endothelial cell migration and capillary-like tube formation, human coronary artery endothelial cells (HCAECs) were incubated with increasing doses of thymosin beta10 (25-100 ng/ml). By using a modified Boyden chamber assay, thymosin beta10 inhibited cell migration in a dose- and time-dependent manner with the maximal effect being a 36% reduction at 100 ng/ml as compared to controls (P < 0.01). In addition, thymosin beta10 (100 ng/ml) significantly inhibited the capillary-like tube-formation of HCAECs on Matrigel, showing a 21% reduction of the total tube length as compared to negative controls (P < 0.01). Furthermore, by using real time PCR analysis, thymosin beta10 significantly decreased mRNA levels of vascular endothelial growth factor (VEGF), VEGF receptor-1 (VEGFR-1) and integrin alphaV after 24 h treatment in HCAECs. By contrast, thymosin beta4 significantly increased HCAEC migration. These results indicate that thymosin beta10, but not thymosin beta4, have direct inhibitive effects on endothelial migration and tube formation that might be mediated via downregulation of VEGF, VEGFR-1 and integrin alphaV in HCAECs. This study suggests a potential therapeutic application of thymosin beta10 to the diseases with excessive angiogenesis such as cancer.     

Isolation and characterization of thymosin beta 9 Met from pork spleen

We have identified a new thymosin beta 4-like peptide in pork spleen. The new peptide (12 mg) and thymosin beta 4 (33 mg) were isolated from 230 g of spleen by solid phase extraction, preparative isoelectric focusing, and HPLC. The new peptide was termed thymosin beta 9 Met to indicate its close relationship to thymosin beta 9 from calf. The only difference from thymosin beta 9 is the substitution of leucine by methionine at position 6. This peptide replaces thymosin beta 10 which is the minor thymosin beta 4-like peptide in most mammals, e.g., in man, rat, mouse, cat, and rabbit. The structure was determined by amino acid analysis, tryptic digestion, and carboxypeptidase digestion. Pork spleen contains 192 micrograms of thymosin beta 4 and 117 micrograms of thymosin beta 9 Met per gram of tissue.     

Primary structure of thymosin beta 12, a new member of the beta-thymosin family isolated from perch liver.

A new polypeptide termed thymosin beta 12 has been isolated from perch liver and its primary structure elucidated. This polypeptide contains 43 amino acid residues with a molecular weight of 4822 Da. The content of thymosin beta 12 from perch liver has been determined as 43 micrograms/g of tissue. The amino-terminal end of this polypeptide is blocked by an acetyl group as deciphered by fast-atom bombardment mass spectrometric analysis. Sequence analysis reveals that thymosin beta 12 is 79% homologous to thymosin beta 4, an immunomodulator which was originally isolated from calf thymus. Thymosin beta 12 also shows 84% sequence homology to thymosin beta 11, a beta 4 analog which replaces beta 4 in two species of bony fish, oscar and rainbow trout. The evolutionary implication of such results will be discussed. The isolation of a new beta 4-related peptide from perch liver which differs from beta 11 indicates that beta-thymosin peptides are widely distributed in lower vertebrate classes.