酪酸梭菌活菌散治疗婴幼儿秋冬季腹泻的临床疗效观察

目的观察酪酸梭菌活菌散治疗婴幼儿秋冬季腹泻的临床疗效。方法将120例秋冬季腹泻的患儿随机分为酪酸梭菌活菌散治疗组和对照组,对照组60例患儿单用蒙脱石散,1.5g/次,3次/d;酪酸梭菌活菌散治疗组60例患儿先服用蒙脱石散,剂量同上,间隔2h后,加服酪酸梭菌活菌散,1袋/次,3次/d,疗程为3~7d或治愈为止;在此基础上,两组患儿均给予补液(纠酸、维持水电解质及酸碱平衡)、退热等治疗。观察两组患儿腹泻治疗效果(包括大便性状恢复正常时间、呕吐消失时间和总有效率)及不良反应发生情况。结果酪酸梭菌活菌散治疗组显效率为81.7%,总有效率为100.0%,对照组显效率为28.3%,总有效率为90.0%,酪酸梭菌活菌散治疗组明显高于对照组,且差异均有统计学意义(χ2=4.385,P0.05);酪酸梭菌活菌散治疗组第3天大便次数相比对照组明显减少[治疗组(1.88±0.88)次/d,对照组(3.28±1.80)次/d,t=5.395,P0.05)],大便恢复正常时间明显短于对照组[治疗组(3.67±1.31)d,对照组(4.8±1.09)d,t=5.158,P0.05)],呕吐消失时间也明显短于对照组[治疗组(2.9±0.99)d,对照组(4.02±1.34)d,t=4.894,P0.05)]。结论酪酸梭菌活菌散治疗婴幼儿秋冬季腹泻的临床疗效显著,且未见不良反应发生,值得临床推广。     

酪酸梭菌活菌散与蒙托石散间隔联用治疗婴幼儿病毒性腹泻疗效观察

目的观察和评价酪酸梭菌活菌散与蒙脱石散间隔应用治疗婴幼儿病毒性腹泻的临床疗效。方法将130例病毒性腹泻患儿随机分为观察组和对照组。观察组65例,先冲服蒙脱石散,1.5～3 g/次,3次/d,冲服蒙脱石散2 h后再服用酪酸梭菌活菌散,0.5 g/次,3次/d,疗程3～7 d;对照组65例,单独应用蒙脱石散治疗,观察疗效和不良反应。结果观察组总有效率为96.9%,对照组总有效率为72.3%,差异有统计学意义(P<0.01),观察组在缩短热退时间、大便性状恢复正常时间和平均住院时间及第3天的大便次数减少均优于对照组(P<0.01)。结论酪酸梭菌活菌散与蒙脱石散间隔联用治疗婴幼儿病毒性腹泻疗效显著,且未见不良反应,值得临床推广应用。     

酪酸梭菌活菌散治疗婴幼儿病毒性腹泻疗效观察

目的观察和评价酪酸梭菌活菌散治疗婴幼儿病毒性腹泻的临床疗效。方法将200例病毒性腹泻患儿随机分为观察组和对照组。观察组120例,服用酪酸梭菌活菌散,首次1 000 mg,以后500 mg/次,4次/d,疗程3~7 d,对照组80例,应用蒙脱石散治疗,观察疗效和不良反应。结果观察组总有效率为92.5%,对照组总有效率为71.25%,差异有统计学意义(P<0.01)。结论酪酸梭菌活菌散治疗婴幼儿病毒性腹泻疗效显著,且未见不良反应,值得临床推广应用。     

酪酸梭菌活菌散与制霉菌素片联用治疗婴幼儿鹅口疮的疗效观察

目的观察和评价酪酸梭菌活菌散与制霉菌素片联用治疗婴幼儿鹅口疮的临床疗效。方法将97例鹅口疮患儿随机分为观察组和对照组,观察组47例,在涂抹制霉菌素片的基础上服用酪酸梭菌活菌散,0.5g/次,3次/d,疗程28 d,对照组50例,单独制霉菌素片,观察复发率和不良反应。结果观察组的总复发率为8.5%,显著低于对照组的30%(P<0.05)。结论酪酸梭菌活菌散与制霉菌素片联用治疗婴幼儿鹅口疮预防复发疗效显著,且未见不良反应,值得临床推广应用。     

参苓白术散加减联合酪酸梭菌活菌散治疗小儿腹泻疗效观察

目的观察和评价参苓白术散加减联合酪酸梭菌活菌散治疗小儿腹泻的临床疗效。方法选取玉田县医院60例患有腹泻的儿童,随机分成观察组和对照组。对照组给予补液纠正水、电解质紊乱等常规治疗,观察组在常规治疗基础上服用参苓白术散加减联合酪酸梭菌活菌散,其中酪酸梭菌活菌散剂量为0．5g/次,3次／d,急性腹泻疗程为3～7d,慢性腹泻疗程为14～21d,观察疗效。结果观察组显效率为63．3％,有效率为33．3％,总有效率为96．6％;对照组显效率为46．7％,有效率为30．O％,总有效率为76．7％,两组比较差异有统计学意义（P〈0．05）,观察组疗效明显优于对照组。结论参苓白术散加减联合酪酸梭菌活菌散治疗小儿腹泻疗效显著,能迅速恢复肠道菌群平衡和肠道生理功能,值得临床推广。     

酪酸梭菌活菌散治疗小儿病毒性腹泻疗效观察

目的观察和评价酪酸梭菌活菌散（商品名：宝乐安）治疗小儿轮状病毒性腹泻的临床疗效。方法将93例轮状病毒性腹泻患儿随机分为观察组和对照组,观察组46例,给予酪酸梭菌活菌散,0．5g/次,3次／d;对照组47例,给予利巴韦林15mg／（kg·d）,分2次肌内注射或加入10％GS250ml中静脉滴注。疗程均为3—7d,观察疗效和不良反应。结果观察组总有效率为95．7％,轮状病毒转阴率为89．2％;对照组总有效率为76．6％,轮状病毒转阴率为65．8％,差异有显著性（P〈0．05）。2组均未见不良反应。结论酪酸梭菌活菌散治疗小儿轮状病毒性腹泻疗效显著,且未见不良反应,值得临床推广应用。     

酪酸梭菌活菌散联合抗菌药治疗小儿急性细菌感染性腹泻临床疗效观察

目的观察和评价酪酸梭菌活菌散（商品名：宝乐安）联合抗菌药治疗小儿急性细菌感染性腹泻临床疗效。方法将60例急性细菌感染性腹泻患儿随机分为观察组和对照组,观察组30例,对照组30例,2组均给予口服抗菌药及对症支持治疗。其中观察组在服用抗菌药2h后服用酪酸梭菌活菌散,0.5g/次,3次/d;对照组只给予抗菌药及对症支持治疗,不用酪酸梭菌活菌散。对2组总有效率及体温、大便恢复正常时间进行统计分析。结果观察组总有效率为96.7%,对照组总有效率为83.3%,2组相比差异具有非常显著性（P〈0.01）;观察组体温、大便恢复正常时间均显著短于对照组（P〈0.01）。结论酪酸梭菌活菌散联合抗菌药治疗小儿急性细菌感染性腹泻的疗效,优于单用抗菌药,值得临床推广应用。     

利水健脾解毒汤灌肠联合酪酸梭菌活菌散治疗婴幼儿轮状病毒肠炎疗效观察

目的探讨利水健脾解毒汤灌肠联合酪酸梭菌活菌散口服治疗婴幼儿轮状病毒肠炎的临床疗效。方法将82例的患轮状病毒肠炎婴幼儿随机分为治疗组42例与对照组40例,两组患儿均给予常规治疗,治疗组给予利水健脾解毒汤灌肠及酪酸梭菌活菌散口服,对照组静滴利巴韦林,观察患儿治疗一疗程(3 d)临床疗效和轮状病毒转阴率。结果治疗组总有效率为90.47%,轮状病毒转阴率为71.43%,对照组分别为52.50%、32.50%。治疗组总有效率及轮状病毒转阴率均显著高于对照组(P0.01),2组患儿均未出现不良反应。结论利水健脾解毒汤灌肠及酪酸梭菌活菌散口服治疗婴幼儿轮状毒肠炎疗效显著,安全性高,是治疗婴幼儿轮状病毒肠炎的有效方法。     

酪酸梭菌二联活菌散防治婴幼儿肺炎继发腹泻116例疗效观察

目的 了解微生态制剂(酪酸梭菌二联活菌散)防治婴幼儿肺炎继发腹泻的疗效.方法 选取2008年1月至2010年12月收住清徐县第二人民医院呼吸科诊断为支气管肺炎继发腹泻的患儿共116例,随机分为2组,以住院期间抗生素治疗同时应用微生态制剂(酪酸梭菌二联活菌散)的患儿为治疗组60例,仅使用抗生素治疗的患儿为对照组56例,分别观察腹泻次数、大便性状、腹痛、止泻时间及大便镜检与大便培养正常时间及治疗有效率.结果 微生态制剂(酪酸梭菌二联活菌散剂)治疗组腹泻次数减少时间、大便性状变稠时间、腹泻停止时间明显短于对照组(P＜0.05),腹痛消失时间明显短于对照组(P＜0.01),治疗组临床症状消失时间明显比对照组短;治疗组大便镜检恢复正常时间明显短于对照组(P＜0.05),大便细菌培养恢复正常时间明显短于对照组(P＜0.01),2组患儿治疗效果比较,治疗组有效率为91.67％,对照组有效率为76.79％,经卡方检验x2=4.89,P＜0.05,差异有统计学意义,治疗组有效率明显高于对照组.结论 酪酸梭菌二联活菌散剂防治婴幼儿肺炎继发腹泻,能使腹泻时间缩短、疗效明显、方法简便,经济,易于患儿及父母接受.     

酪酸梭菌活菌散与抗菌药间隔序贯应用预防抗生素相关性腹泻疗效观察

目的观察和评价酪酸梭菌活菌散（商品名：宝乐安）与抗菌药间隔序贯应用治疗小儿肺炎预防抗生素相关性腹泻的临床疗效。方法将203例肺炎患儿随机分为预防组和对照组,预防组103例,对照组100例,2组均给予抗菌药及对症支持治疗。其中预防组在治疗的同时间隔2～3 h序贯使用酪酸梭菌活菌散,0.5 g/次,3次/d,出现腹泻继续服用;对照组不用酪酸梭菌活菌散预防,出现腹泻用酪酸梭菌活菌散治疗,0.5 g/次,3次/d。对2组继发腹泻的发生率、腹泻持续天数、肺炎治疗的总疗程、腹痛和脱水等症状和体征进行统计分析。结果预防组继发腹泻12例,发生率为11.7%,对照组继发腹泻57例,发生率为57.0%,2组相比差异具有非常显著性（P〈0.01）;预防组腹泻持续时间和治疗疗程显著短于对照组（P〈0.01）;预防组患儿腹痛和脱水等症状和体征发生率均少于对照组（P〈0.01）。结论酪酸梭菌活菌散与抗菌药间隔序贯应用治疗肺炎,能显著降低小儿抗生素相关性腹泻的发生率,预防性应用具有积极的临床意义。     

Role for dopamine in malonate-induced damage in vivo in striatum and in vitro in mesencephalic cultures

Defects in mitochondrial energy metabolism have been implicated in the pathology of several neurodegenerative disorders. In addition, the reactive metabolites generated from the metabolism and oxidation of the neurotransmitter dopamine (DA) are thought to contribute to the damage to neurons of the basal ganglia. We have previously demonstrated that infusions of the metabolic inhibitor malonate into the striata of mice or rats produce degeneration of DA nerve terminals. In the present studies, we demonstrate that an intrastriatal infusion of malonate induces a substantial increase in DA efflux in awake, behaving mice as measured by in vivo microdialysis. Furthermore, pretreatment of mice with tetrabenazine (TBZ) or the TBZ analogue Ro 4-1284 (Ro-4), compounds that reversibly inhibit the vesicular storage of DA, attenuates the malonate-induced DA efflux as well as the damage to DA nerve terminals. Consistent with these findings, the damage to both DA and GABA neurons in mesencephalic cultures by malonate exposure was attenuated by pretreatment with TBZ or Ro-4. Treatment with these compounds did not affect the formation of free radicals or the inhibition of oxidative phosphorylation resulting from malonate exposure alone. Our data suggest that DA plays an important role in the neurotoxicity produced by malonate. These findings provide direct evidence that inhibition of succinate dehydrogenase causes an increase in extracellular DA levels and indicate that bioenergetic defects may contribute to the pathogenesis of chronic neurodegenerative diseases through a mechanism involving DA.     

Scurvy in capybaras bred in captivity in Argentine

In order to determine if the absence of vitamin C in the diet of capybaras (Hydrochoerus hydrochaeris) causes scurvy, a group of seven young individuals were fed food pellets without ascorbic acid, while another group of eight individuals received the same food with 1 g of ascorbic acid per animal per day. Animals in the first group developed signs of scurvy-like gingivitis, breaking of the incisors and death of one animal. Clinical signs appeared between 25 and 104 days from the beginning of the trial in all individuals. Growth rates of individuals deprived of vitamin C was considerably less than those observed in the control group. Deficiency of ascorbic acid had a severe effect on reproduction of another population of captive capybaras. We found that the decrease in ascorbic acid content in the diet affected pregnancy, especially during the first stages. The results obtained suggest that it is necessary to supply a suitable quantity of vitamin C in the diet of this species in captivity.     

Changes in lactate dehydrogenase activity in chicken tissues in hyperthyreosis in ontogenesis

The lactate dehydrogenase activity in reactions of lactate oxidation and synthesis was studied in subfractions of the chicken brain, heart and liver at the embryonal, early postembryonal and adult stages of development after thyroxine administration. It has been shown that during embryogenesis thyroxine predominantly enhanced the rate of lactate oxidation in the mitochondrial tissues. A marked increase in the lactate synthesis was found in cytoplasm of the adult chicken tissues. Specificity of enzyme activity alterations was detected in the chicken brain during ontogenesis after thyroxine administration.     

SSTR5 ablation in islet results in alterations in glucose homeostasis in mice

Somatostatin (SST) peptide is a potent inhibitor of insulin secretion and its effect is mediated via somatostatin receptor 5 (SSTR5) in the endocrine pancreas. To investigate the consequences of gene ablation of SSTR5 in the mouse pancreas, we have generated a mouse model in which the SSTR5 gene was specifically knocked down in the pancreatic beta cells (betaSSTR5Kd) using the Cre-lox system. Immunohistochemistry analysis showed that SSTR5 gene expression was absent in beta cells at three months of age. At the time of gene ablation, betaSSTR5Kd mice demonstrated glucose intolerance with lack of insulin response and significantly reduced serum insulin levels. Insulin tolerance test demonstrated a significant increase of insulin clearance in vivo at the same age. In vitro studies demonstrated an absence of response to SST-28 stimulation in the betaSSTR5Kd mouse islet, which was associated with a significantly reduced SST expression level in betaSSTR5Kd mice pancreata. In addition, betaSSTR5Kd mice had significantly reduced serum glucose levels and increased serum insulin levels at 12 months of age. Glucose tolerance test at an older age also indicated a persistently higher insulin level in betaSSTR5Kd mice. Further studies of betaSSTR5Kd mice had revealed elevated serum C-peptide levels at both 3 and 12 months of age, suggesting that these mice are capable of producing and releasing insulin to the periphery. These results support the hypothesis that SSTR5 plays a pivotal role in the regulation of insulin secretion in the mouse pancreas.