ABSTRACT
Mori Cortex is the dry root bark of Moras alba L. and usually used in clinical practice. It is sweet and cold in nature, and enters the lung meridian. With effects in purging lung and relieving asthma, and inducing diuresis to reduce edema, it is mainly used to treat lung heat, asthma, cough, swelling, urine deficiency and facial skin edema. In clinic, it is mainly used for the treatment of respiratory system, urinary infection and diabetes mellitus. In recent years, great progress has been made in studies on the pharmacological effects of Mori Cortex. The literatures on the pharmacological effects of Mori Cortex in recent years were reviewed and summarized in this paper. Mori Cortex has antitussive, anti-inflammatory, hypoglycemic, cardiovascular, antiviral, anticancer, immunoregulatory, antioxidation and anti-allergy and other pharmacological effects, in addition to antitussive, expectorant, antiasthmatic and other traditional effects. Total flavones have a strong pharmacological activity. These extended studies provide valuable reference for the further development of Mori Cortex. This paper summarizes the pharmacological effects of Mori Cortex, proposes the key directions of further studies, and provides the beneficial reference for better development and utilization of Mori Cortex.
ABSTRACT
<p><b>OBJECTIVE</b>To confirm the diagnosis of a Wolf-Hirschhorn syndrome by family study using both cytogenetic and molecular genetic techniques.</p><p><b>METHOD</b>G-band karyotyping was performed for all the 6 members in the family. Multiplex ligation-dependent probe amplification (MLPA) was used to detect the chromosome abnormality for the proband, his father and brother. Microarray comparative genomic hybridization (Array-CGH) was carried out to map the exact chromosomal breakpoints for the proband.</p><p><b>RESULT</b>The proband presented with a typical face, delayed growth and hypotonia in Wolf-Hirschhorn syndrome. His G-band karyotype was 46, XY, der(4)t(4;8) (p16.2; p23.1)pat. MLPA showed 4pter loss and 8pter gain. Array-CGH revealed an XY male with a 3.781 Mb deletion of 4p16.3-p16.2 and a 6.760 Mb duplication of 8p23.3-p23.1. The proband's brother has mental retardation and skeletal abnormalities. His G-band karyotype was 46, XY, der(8)t(4;8)(p16.2;p23.1)pat. MLPA showed 4pter gain and 8pter loss. The proband's father had normal phenotype with a balanced translocation of 46, XY, t(4;8)(p16.2;p23.1)pat. MLPA showed a normal result. The proband's grandfather showed a normal phenotype with a balanced translocation 46, XY, t(4;8)(p16.2;p23.1). The other members in the family showed normal phenotypes with normal karyotypes.</p><p><b>CONCLUSION</b>The proband has features of Wolf-Hirschhorn syndrome with partial monosomy 4p and partial trisomy 8p. The proband's brother has a partial trisomy 4p and partial monosomy 8p. The derived chromosomes are inherited from paternal balanced translocation t(4;8)(p16.2;p23.1).</p>