Objective To observe the effect of small dosage of perphenazine(2～6 mg)on psychotic symptoms of senile dementia.Methods 31 senile cases with psychotic symptoms after dementia(Alzheimer disease or vascular dementia)accepted small dosage of perphenazine in addition of the conventional therapy.They were assessed with Sadoz Clinical Assessment Geriatric(SCAG)and Treatment Emergent Symptom Scale(TESS).Results The score decreased 50%～75%(markedly improved)in 2 cases,25%～50%(improved)in 22 cases,lower than 25%(no improved)in 7 cases.Some mild emergent symptoms have been observed.Conclusion Small dosage of perphenazine is safe and effective in treating psychotic symptoms of senile dementia.

Objective:To explore social support and personality characteristic of patients with clinically chronic pains to provide a new idea for clinical psycho-intervention.Method:45 patients with clinically chronic pains were evaluated by the Symptom Checklist(SCL-90),EPQ and SSRS,and compared with the control group.Results:Somatization,interpersonal sensitivity,anxiety,fear and psychotic factors have significant differences from those of the control group when being compared(p

To observe the clinical efficacy of nicorandil for treating the patient with cardiac syndrome X (CSX) and its impact on vascular endothelial function. Methods: A total of 140 CSX patients were randomly divided into 2 groups: Control group, the patients received conventional anti-angina therapy and Nicorandil group, based on conventional anti-angina therapy, the patients received additional oral nicorandil treatment. n=70 in each group. All patients received resting emission computed tomography (ECT) and treadmill exercise ECG stress test (TET). Blood levels of endothelin (ET-1), high-sensitivity C-reactive protein (hs-CRP) and nitric oxide (NO) were examined before and 3 months after treatment. Results: Compared with pre-treatment condition, the attack frequency of angina pectoris and positive rate of ECT were decreased after treatment in both groups, P<0.05; in Nicorandil group, the suspicious positive rate and positive rate of TET were reduced after treatment, P<0.05. Compared with Control group, Nicorandil group had the much lower suspicious positive rate and positive rate of TET after treatment, P<0.05. Blood tests indicated that compared with pre-treatment condition, ET-1 and hs-CRP were decreased, NO was increased after treatment in both groups, all P<0.05; blood levels of ET-1, hs-CRP and NO were different between 2 groups after treatment, all P<0.05. Conclusion: Nicorandil could inhibit inflammatory factors, elevate endothelial function and therefore improve micro vascular angina symptoms, increase exercise tolerance obviously.

ABSTRACT:Objective To investigate the distributional characteristics of anaphylactogens in prurigo nodularis (PN)patients so as to provide clinical basis for selecting the method of allergy test.Methods We divided 262 PN patients into four groups and then used skin-prick (5 4 patients ),skin-patch (5 0 patients ),serum IgE allergen detection (56 patients)and serum IgG allergen detection (102 patients)to analyze anaphylactogen positive rate and their distribution differences in PN.Results For skin-prick test in 54 PN patients,the detection rates of platanus orientalis,artemisia argyi,poplar,dust mite,dirt mite,cod,peanut and tomato were higher than those in the control group (P<0.05 ).For skin-patch test in 50 PN patients,the detection rates of nickel sulfate,flavor compounds,black rubber,and carba mix were higher than those in the control group (P<0.05).For serum IgE test in 5 6 PN patients,the detection rates of house dust,scandent hop,cat/dog hair,bug,penicillium/neurospora and mutton were higher than those in the control group (P<0.05).For serum IgG test in 102 PN ones,the detection rates of crab,shrimp,beef and cod were higher than those in the control group (P<0.05).Conclusion Skin-prick test and serum IgE detection have high application values in PN patients.Serum IgG detection is of certain importance in adjusting PN patients’diet structure while skin-patch test applied in PN needs further exploration.

Objective:To identify the pathogenic gene mutations in a family with early onset severe retinal dystrophy (EOSRD).Methods:A retrospective clinical study. One patient and three family members from a Han of EOSRD who were diagnosed at Henan Eye Hospital in August 2018 were included in the study. After the detailed history of the patients was collected, all participants underwent best corrected visual acuity (BCVA), slit-lamp, fundus biomicroscopy with the slit lamp, untra-widefield fundus color photography, spectral-domain optical coherence tomography (SD-OCT) and full-field electroretinography (ff-ERG). The subject’s peripheral venous blood of 5 ml was collected and the whole genome DNA was extracted. A genetic eye disease capture chip containing 441 disease-causing genes was used for targeted capture and enrichment of high-throughput sequencing, and Sanger sequencing was performed for the clear pathogenic mutation sites; the analysis software was used for bioinformatics analysis of the mutation sites.Results:A 6-year-old female proband developed poor night vision in both eyes after 1 year old. The BCVA of both eyes were 0.1. The color of the optic disc was slightly lighter; the diameter of the retinal vessels was slightly reduced, and extensive pigment changes can be seen in the retina outside the vascular arch. SD-OCT examination showed that the outer membrane, ellipsoid zone and chimera zone in the central fovea of both eyes were unclear and intermittent. The visual area outside the fovea was neuroepithelial outer plexiform layer, outer nuclear layer, outer membrane, ellipsoid zone. The chimera zone gradually disappeared, and the thickness of the pigment epithelial layer was not uniform. In ff-ERG examination, the functions of the binocular cone and rod system were severely decreased. The results of genetic testing showed that there were c.921C>A homozygous mutations in the Tubby-like protein (TULP1) gene of the proband, and c.3121C>T and c.3488G>A compound heterozygous mutations in the cyclic nucleotide gated channel beta 1 (CNGB1) gene. Amino acid conservation analysis results showed that the above three mutation sites were highly conserved in multiple species; bioinformatics analysis results showed that TULP1 gene c.921C>A (p.Cys307*) had translation termination in the protein conserved region, CNGB1 gene c.3121C>T (p.Arg1041Trp) and c.3488G>A (p.Gly1163Glu) had amino acid polarity changes in the protein conserved region, which led to major changes in the protein spatial structure.Conclusion:TULP1 gene c.921C>A homozygous mutation, CNGB1 gene c.3121C>T and c.3488G>A compound heterozygous mutation are the mutation sites of this EOSRD family.

Combined radiation-trauma injury is mainly observed in radiation treatment of cancer and radiation injury with traumatic patients. The prominent problem of combined radiation-trauma injury is delayed or prolonged wound healing. The mechanism of the impaired wound healing is complicated, and the current effective treatment method are limited. This paper reviews the mechanism and treatment of this impaired wound healing, including the cellular depletion, stromal cell dysfunction, aberrant collagen deposition, microvascular damage, as well as the targeted therapies for the impaired wound healing such as stem cell repletion, antioxidant therapy, transforming growth factor beta-1 ( TGF-β1 ) modulation, and implantable biomaterials. This paper is designed to provide a reference for further deep research on the mechanism and treatment of radiation-trauma injury.

Objective:To determine the pathogenic gene mutation in a family with incomplete congenital quiescent night blindness (CSNB) of Schubert-Bornschein type.Methods:A retrospective clinical study. In February 2021, one patient and his parents and elder brother from a Han Chinese incomplete CSNB of Schubert-Bornschein type family diagnosed by clinical and genetic examination at Henan Provincial People's Hospital were included in the study. The patient’s medical history, family history were inquired; best corrected visual acuity (BCVA), color vision, fundus color photography, full-field electroretinogram (ERG), and frequency domain optical coherence tomography (OCT) were examined in detail. Five ml of the subject’s peripheral venous blood was collected and the whole genome DNA was extracted. The genomic DNA of the subject was library constructed, and all-exon probes were polymerized for capture. The suspected pathogenic mutation site was verified by Sanger, and the pathogenicity of the gene mutation site was determined by parallel bioinformatics analysis.Results:The BCVA of both eyes of the proband (Ⅱ2) was 0.4; the color vision test could not recognize the red color. Fundus examination showed no obvious abnormalities. The retina thickness in the macular area of both eyes was slightly thinned. ERG examination of the whole field showed that the amplitude of ERG b wave was significantly reduced under the stimulation of binocular dark adaptation 3.0 and showed a negative waveform. The mother of the proband (Ⅰ2) had normal BCVA, color vision, fundus color photography, and frequency domain OCT examination. The full-field ERG examination showed that the amplitude of each eye reaction was slightly reduced, and the amplitude of the dark adaptation shock potential was significantly reduced. Genetic testing showed that the proband (Ⅱ2) had a c.1761dupC hemizygous mutation in exon 14 of the voltage-dependent calcium channel α1F subunit gene ( CACNA1F gene). The results of protein sequence homology analysis showed that the site was highly conserved in multiple species; the results of bioinformatics analysis showed that the CACNA1F gene c.1761dupC (pY588fs) subsequently had a frameshift mutation and became a stop at position 10. Codons appear translational termination in the conserved regions of the protein. According to the standards and guidelines of the American College of Medical Genetics and Genomics, the mutation was judged to be a possible pathogenic variant. The mother of the proband (Ⅰ2) was a carrier of this site mutation. The clinical and genetic test results of the father and elder brother of the proband were not abnormal. Conclusion:CACNA1F gene c.1761dupC is the pathogenic mutation site of the Schubert-Bornschein type incomplete CSNB family.

Objective:To identify the pathogenic gene mutations in a family with Leber congenital amaurosis (LCA).Methods:In October 2018, 1 patient and 3 normal family members from a LCA family was enrolled in this retrospective study. Detailed medical history of proband was obtained and fixation test, cycloplegic refraction, slit-lamp, fundus color photography and full-field ERG were performed. And other family members underwent BCVA, refraction slit-lamp, fundus biomicroscopy with the slit lamp, fundus color photography and full-field ERG. The family was investigated with a specific hereditary eye disease enrichment panel which contained 441 known pathogenic genes and based on targeted exome capture technology first to indentify the potential pathogenic genes and mutations. Then the potential pathogenic mutations were conformed by Sanger sequencing. Finally, the results were analyzed via bioinformatics analysis.Results:The proband showed no trace object from childhood, but had obvious photophobia and nystagmus. No positive changes were found in the anterior segment, vitreous and retina in both eyes. Both cone and rod system function decreased significantly in full-field ERG in both eyes. Gene tests showed the proband carried both RPGRIP1 c.1635dupA and c.3565C> T, which composited a heterozygous mutation. Bioinformatics analysis showed RPGRIP1 c.1635dupA was a pathogenic mutation, and RPGRIP1 c.3565C> T which was a novel potential pathogenic mutation in LCA.Conclusion:The compound heterozygous mutation, c.1635dupA and c.3565C> T in RPGRIP1 may be responsible for the pathogenesis in this Chinese Han LCA pedigree.