Congenital malformations and other reproductive losses in goats due to poisoning by Poincianella pyramidalis (Tul.) L.P. Queiroz (=Caesalpinia pyramidalis Tul.).

In the semiarid region of Brazil, in areas with vegetation composed mainly of Poincianella pyramidalis, several cases of congenital malformation and reproductive losses were observed in goats and sheep from 2012 to 2014. To determine the teratogenic effect of P. pyramidalis, two groups of eight goats each were used. Goats from Group 1 received fresh P. pyramidalis, harvested daily, as the only roughage during the whole breeding and pregnancy period. Goats in Group 2 (control) received Cynodon dactylon (tifton) hay free choice. Ultrasound examination for pregnancy diagnosis was performed every 28 days. Four goats from Group 1 were pregnant on day 28 but not on day 56, suggesting embryonic death or abortion. Another goat from Group 1 died at day 70 of pregnancy, and the fetuses exhibited micrognathia. The other three goats bore six kids, three of which showed bone malformations in the limbs, spine, ribs, sternum, and head, including arthrogryposis, scoliosis and micrognathia. One kid also showed hypoplasia of the left pulmonary lobes. In the control group, all goats bore a total of 13 kids and none of them exhibited malformations. These results demonstrated that P. pyramidalis causes congenital malformations and other reproductive losses in goats.

Change of selenium in environment and risk of adolescent idiopathic scoliosis: a retrospective cohort study.

OBJECTIVES: Scoliosis is the disease which has a long history over one century. However, the pathogenesis remains unclear at present. To demonstrate the effect of different selenium content in environment on the morbidity of adolescent idiopathic scoliosis (AIS). METHODS: Retrospective cohort study (follow-up from 1997 to 2009): compare the difference morbidity between high selenium group and the normal selenium group of AIS. PATIENTS: 9998 cases from three areas in China were participated in this study. There is different selenium content in these three areas. RESULTS: High selenium levels were significant associated with the AIS morbidity. While low selenium level had no significant correlation with the AIS morbidity. CONCLUSIONS: This study confirmed that high selenium content in the environment was one of risk factors for idiopathic scoliosis. We speculated that the excessive growth of the spine and the spinal cord asynchronous growth effect were key factors that high selenium content in the environment leads to scoliosis.

High selenium may be a risk factor of adolescent idiopathic scoliosis.

The pathogenesis of adolescent idiopathic scoliosis (AIS) remains little understood. Previous work has shown that guppy fish is an ideal animal model of idiopathic scoliosis which has similar epidemiological and morphological characteristic with AIS. However, some research speculated that the high-selenium environment could also induce idiopathic-type scoliosis of fish. We believe that the high-selenium related deformity of spine and guppy curveback syndrome may have the same pathogenesis. And high selenium may be a risk factor of AIS.

Chronic effects of dietary selenium on juvenile Sacramento splittail (Pogonichthys macrolepidotus).

The chronic effects of dietary selenium (Se) exposure in juvenile Sacramento splittail (Pogonichthys macrolepidotus) were investigated in the laboratory. A total of 960 (40 fish per tank, 3 tanks per diet) 7-month-old juvenile splittail were fed one of eight Purified-Casein diets supplemented with selenized yeast for 9 months in a flow-through system. These diets contained the following: 0.4 (control), 0.7, 1.4, 2.7, 6.6, 12.6, 26.0, and 57.6 mg of Se kg(-1) dry weight. Survival, Se tissue concentration, growth, gross morphology, and liver histopathology were assessed at 5- and 9-month of exposure. Mortalities occurred only in the two highest Se treatments and were accounted for 8.3 and 18.3% at 5-month and 10.0 and 34.3% at 9-month, respectively. Liver and muscle Se concentration were significantly correlated with dietary Se concentration. Fish exposed to 0.4-12.6 mg of Se kg(-1) diets had reached equilibrium in liver Se concentration by 5 month. Splittail fed diets at concentrations > or =26.0 mg of Se kg(-1) had not reached equilibrium in liver, and muscle Se concentrations and grew significantly slower (p < 0.05) at 5- and 9-month exposure. Se-induced deformities were observed in fish fed > or =2.7 mg of Se kg(-1) diets at 5-month and in fish fed > or =0.7 mg of Se kg(-1) diets at 9-month. Fish fed 26.0 and 57.6 mg of Se kg(-1) diets had higher liver lesion scores at 5-month while fish fed 6.6 and 57.6 mg of Se kg(-1) diet had higher liver lesion scores at 9-month. Results indicate that survivals, growth, changes of tissue Se concentrations, and histopathology of juvenile splittail were dose-dependent, but their response thresholds to dietary Se concentrations differed and depended on treatment concentrations and duration of exposure. Chronic exposure to 6.6 mg of Se kg(-1) diet induced deleterious health effects that can potentially impact survival of juvenile splittail.

Deflazacort in Duchenne muscular dystrophy: a comparison of two different protocols.

We compare the long-term benefits and side effects of deflazacort using two treatment protocols from Naples (N) and Toronto (T). Boys with Duchenne muscular dystrophy between the ages of 8 and 15 years and who had four or more years of deflazacort treatment were reviewed. Diagnostic criteria included males with proximal muscle weakness evident before 5 years, increased serum creatine kinase and genetic testing and/or a muscle biopsy consistent with Duchenne muscular dystrophy. Thirty-seven boys were treated with protocol-N using deflazacort at a dose of 0.6 mg/kg per day for the first 20 days of the month and no deflazacort for the remainder of the month. Boys with osteoporosis received daily vitamin D and calcium. Deflazacort treatment started between 4 and 8 years of age. Thirty-two were treated with protocol-T using deflazacort at a dose of 0.9 mg/kg per day, plus daily vitamin D and calcium. Treatment started between 6 and 8 years of age. All boys were monitored every 4-6 months. The results were compared with age-matched controls in the two groups (19 for protocol-N and 30 for protocol-T). For the boys treated with protocol-N, 97% were ambulatory at 9 years (control, 22%), 35% at 12 years (control, 0%), 25% at 15 years (control, 0%). For the 32 boys treated with protocol-T, 100% were ambulatory at 9 years (control, 48%), 83% at 12 years (control, 0%) and 77% at 15 years (control, 0%). No aids or leg braces were used for ambulation. In boys 13 years and older, a scoliosis of >20 degrees developed in 30% of the boys on protocol-N, 16% on protocol-T and 90% of controls. For protocol-N, no cataracts were observed while in protocol-T, 30% of boys had asymptomatic cataracts that required no treatment. Fractures occurred in 19% (control 16%) of boys on protocol-N and 16% (control, 20%) of boys on protocol-T. This report illustrates: (a) the importance of collaborative studies in developing treatment protocols in Duchenne muscular dystrophy and (b) the long-term beneficial effects of deflazacort treatment in both protocols. However, the protocol-T seems to be more effective and frequently is associated with asymptomatic cataracts.