Fluoxetine enantiomers as antagonists of p-chloroamphetamine effects in rats

The dextrorotatory enantiomer of fluoxetine was slightly more potent than the levorotatory enantiomer in antagonizing the depletion of brain serotonin by p-chloroamphetamine in rats. The time course of the depletion of brain serotonin at times out to 24 hr after the injection of p-chloroamphetamine was determined with or without simultaneous administration of one of the fluoxetine enantiomers. The dextrorotatory enantiomer prevented the depletion of brain serotonin at any time after p-chloroamphetamine. The levorotatory enantiomer prevented the initial depletion of brain serotonin at 2 and 4 hr, but by 8 hr brain serotonin concentration was decreased and by 24 hr the depletion of serotonin was almost as great as in rats treated with p-chloroamphetamine alone. The elevation of serum corticosterone that occurred acutely after injection of a low dose of p-chloroamphetamine was significantly antagonized by both enantiomers of fluoxetine, the dextrorotatory enantiomer being slightly more potent. In contrast, the lowering of DOPAC (3,4-dihydroxyphenylacetic acid) concentration in rat brain by p-chloroamphetamine was not antagonized by either enantiomer of fluoxetine, indicating this effect is not secondary to serotonin release by p-chloroamphetamine. The results are consistent with other evidence that both enantiomers of fluoxetine are potent inhibitors of serotonin uptake, the dextrorotatory enantiomer being longer-acting than the levorotatory enantiomer in rats.     

慢性病保健评估量表的汉化及条目评价

目的：汉化英文版的慢性病保健评估量表(assessment of chronic illness care,ACIC),并在湖南省试用进行文 化调试,以形成适合中国国情的慢性病保健评估量表。方法：根据WHO规定的量表翻译程序汉化英文版的ACIC,并 进行文化调试。对湖南省365名基层医疗卫生服务机构从事慢性病管理工作的人员进行调查,随机抽取183份有效问 卷,采用离散趋势法、G-P分析法、相关系数法、逐步回归分析法、Cronbach’s α法、因子分析法6种方法进行条目筛 选,用以评价量表条目。结果：6种方法评价C-ACIC量表条目显示：1)敏感性好,离散趋势法中每个条目的标准差均 大于2;G-P分析法中高低分两组进行t检验,差异有统计学意义(均P<0.001);2)代表性好,相关系数法中各条目与量 表总分、所属维度的总分的相关系数范围为0.588~0.916;3)内部一致性高,量表的总Cronbach’s α法为0.975,各维度 的范围为0.854~0.936;4)独立性强,因子分析中各条目的因子载荷均大于0.40,因子载荷范围为0.487~0.798;5)重要 性,逐步回归分析(α入=0.01,α出=0.05)中,34个条目均留在方程中。6种方法筛选条目结果保留了原英文版ACIC的7个 维度34个条目。结论：中文版C-ACIC量表保留了原英文版的ACIC的34个条目,且条目具有较好的敏感性、代表性、 内部一致性、独立性、重要性。     

Oral Contraceptive Therapy for Differentiating Ovarian Cysts

“Watchful waiting” to see whether an ovarian cyst in a woman of reproductive age will regress or disappear is perturbing to both patient and physician. Delay in differentiating between a functional and a nonfunctional cyst may be avoided if the physician remembers the pituitary-ovarian relationships in patients receiving an oral contraceptive agent. When a patient is not taking a contraceptive, estrogen-progestogen therapy can be used in an attempt to cause regression of the cyst.     

An Epizootiological Report of the Re‐emergence and Spread of a Lineage of Virulent Newcastle Disease Virus into Eastern Europe

A number of contemporary outbreaks of Newcastle disease (ND) in Israel, Turkey, Georgia and Bulgaria have all been caused by a very similar viruses related to lineage 5a (genotype VIIa). Comparison with published ND virus (NDV) sequences suggests that this virus strain originated in South‐East Asia and on introduction has circulated widely in backyard poultry in the Middle East and into Eastern Europe. An intracerebral pathogenicity index of 1.9 was obtained for a representative isolate from Bulgaria. In addition, the International Reference Laboratory for ND has characterized a molecular epidemiologically linked virus that has been reported to have caused disease in well‐vaccinated broiler chickens in Pakistan. In the 1990s, another strain from the 5a lineage NDV was introduced into Europe and spread across the continent causing numerous outbreaks up to 1999. Despite improved controls, including good diagnostic tests and widespread vaccination, in commercial poultry, the novel circulating NDV strains described here have been established widely in the region and represent an increased risk for similar disease outbreak events to reoccur within the EU.     

Regulation of environmental chemicals

Dibromochloropropane (1,2-dibromo-3-chloropropane, DBCP), a pesticide used widely for over 20 years to control nematodes on crops, turf and in nurseries, was banned by the United States Environmental Protection Agency (US EPA) in 1977 because of evidence of infertility in men and induction of a variety of tumors in laboratory animals. Despite the ban on the use of DBCP, this pesticide remains persistent in soil and continues to be detected as a groundwater contaminant in areas of past high use, in particular California's Central Valley. In this review, we present a critical evaluation of the available scientific literature on the potential for DBCP to affect cancer risk, including the results of animal cancer bioassays, human epidemiological studies and in vitro and in vivo genotoxicity studies. In addition, we provide updated information on DBCP chemistry and metabolism, production and past use, current regulations, its environmental fate, potential for human exposure and current remediation efforts. Results from long-term cancer bioassays in rodents show a statistically significant increase in the incidence of malignant and benign mammary gland tumors in female rats treated orally with DBCP compared to controls and some evidence of increased incidence of mammary fibroadenomas in DBCP low-dose treated female rats exposed by inhalation. Significantly increased incidence of tumors of the forestomach occurred in both sexes of rats and mice treated orally. Rats exposed to DBCP by inhalation showed significant increases in tumors of the tunica vaginalis in males; tumors of the pharynx and adrenal gland in females; and tumors of the tongue, nasal turbinate and nasal cavity in both sexes compared to controls. Male and female mice exposed to DBCP by inhalation experienced increased tumor incidence in the lungs and nasal cavity compared to controls. Significant increases in tumors of the lung and forestomach have also been reported in female mice treated by a dermal route. Although high mortality rates in both rat and mouse bioassays limited the ability to detect tumors late in life, the induction of a variety of tumors by multiple routes of exposure in two rodent species provides clear evidence of a DBCP tumorigenic response. In vitro, in vivo and human genotoxicity studies indicate that DBCP is capable of acting as a mutagen and clastogen. Few studies have been conducted to assess whether DBCP workplace or drinking water exposures affect cancer risk in humans. While case-control, cohort and ecological epidemiology studies have not found significant, positive associations between DBCP exposure and cancer in exposed populations, these studies have numerous limitations including small numbers of participants, a lack of control for confounding factors, lack of exposure information on DBCP and other chemicals and short follow-up times. Given the persistent nature of DBCP contamination in areas of past use, efforts should be made to continue remediation efforts and follow previously exposed populations for development of certain human cancers, including breast, ovarian, stomach, respiratory, oral and nasal cancers, among others.     

Ultrasonic Cavitation-Enabled Treatment for Therapy of Hypertrophic Cardiomyopathy: Proof of Principle

Ultrasound myocardial cavitation-enabled treatment was applied to the SS-16^BN rat model of hypertrophic cardiomyopathy for proof of the principle underlying myocardial reduction therapy. A focused ultrasound transducer was targeted using 10-MHz imaging (10 S, GE Vivid 7) to the left ventricular wall of anesthetized rats in a warmed water bath. Pulse bursts of 4-MPa peak rarefactional pressure amplitude were intermittently triggered 1:8 heartbeats during a 10-min infusion of a microbubble suspension. Methylprednisolone was given to reduce initial inflammation, and Losartan was given to reduce fibrosis in the healing tissue. At 28 d post therapy, myocardial cavitation-enabled treatment significantly reduced the targeted wall thickness by 16.2% (p?<0.01) relative to shams, with myocardial strain rate and endocardial displacement reduced by 34% and 29%, respectively, which are sufficient for therapeutic treatment. Premature electrocardiogram complexes and plasma troponin measurements were found to identify optimal and suboptimal treatment cohorts and would aid in achieving the desired impact. With clinical translation, myocardial cavitation-enabled treatment should fill the need for a new non-invasive hypertrophic cardiomyopathy therapy option.