Objective To explore the relationship between family environment and parental rearing patterns and adolescent schizophrenia , for the prevention of adolescent mental and provide scientific basis of schizophrenia . Methods In adolescent patients with schizophrenia in 101 cases( case group ) ,101 cases of the other without a histo-ry of psychosis patients as control group ,using the family environment scale ,EMBU for two groups of patients quality of life evaluation,non conditional Logistic regression analysis of related factors were analyzed .Results Intimacy, emotion expression,entertainment and father emotional warmth and understanding (F1) was a protective factor(OR=0.643,95%CI=0.235~0.863,P=0.01;OR=0.582,95%CI=0.168~0.906,P=0.01;OR=0.478,95%CI=0.174~0.834,P=0.01),but the contradiction,the father punished severely(F2),father′s refusal and denial(F5) and mother′s over interference(M2) as a risk factor(OR=1.535,95%CI=1.096~2.187,P=0.01;OR=1.516, 95%CI=1.097~2.096,P<0.01;OR=1.375,95%CI=1.034~1.989,P=0.01;OR=1.347,95%CI=1.272~1.915,P<0.01).Conclusion Good family environment and parental rearing pattern can reduce the incidence of schizophrenia .

A case of cytomegalovirus infection with skin lesions as the primary manifestation is reported.A 46-year-old female patient presented with a 3-month history of painful perioral blisters and erosions,and a 6-week history of erythema,blisters and erosions on the left ann.The patient was ever diagnosed with systemic lupus erythematosus and lupus nephritis 12 years prior to the presentation.Systemic lupus erythematosus was exacerbated 5 months prior to this presentation,and glucocorticoids and mycophenolate mofetil were administered.Skin examination revealed irregularly shaped perioral blisters with erosions and crusts,localized patchy erythema with erosion in the center on the flexor aspect of the left forearm,erythema and blisters on the left upper arm,and multiple petechiae and ecchymoses on the abdomen.Histopathological examination of the skin lesion on the left upper limb showed epidermal necrolysis with scattered viral inclusion bodies.Immunohistochemical examination revealed positive staining for cytomegalovirus antigen in giant cells in the necrolytic epidermis.Cytomegalovirus DNA was detected in exudates from lesions.However,cytomegalovirus DNA was not detected in the serum in the initial test,but became positive (8.04 × 103 copies/ml) 1 week later.In addition,anti-cytomegalovirus IgG antibodies were detected in the serum.The patient was diagnosed with cutaneous cytomegalovirus infection.Affter the treatment with both oral and topical ganciclovir,the lesions were improved gradually,followed by severe pulmonary infection,and the patient was finally died of multiple organ failure.

Objective To report a pedigree with tyrosinemia type Ⅱ,and to analyze its causative mutations.Methods Clinical data were obtained from a 10-year-old male proband with tyrosinemia type Ⅱ,and analyzed retrospectively.Blood and urine samples were collected from 19 persons in 3 generations of the pedigree,and the amino acid level was detected in these samples.Genomic DNA was extracted from all of the 19 family members,and mutations in the tyrosine aminotransferase (TAT) gene were detected.Results The patient developed photophobia at 2 months after birth,and the symptom was gradually aggravated after that.At the age of 6 years,ocular pain and photophobia occurred.At the age of 8 years,linear keratotic plaques occurred on his fingertips and soles of both feet,with obvious tenderness.Ophthalmic examination showed no obvious abnormalities in corneal staining or ocular fundus.Skin examination showed multiple linear keratotic plaques on the fingers and soles of both feet.The serum tyrosine level was 825.64 μmol/L,and the level of p-hydroxyphenyllactic acid in urine was 161.4 μmol/L.Genetic testing showed 2 novel mutations,including c.236G ＞ A at position 236 in exon 2 of the TAT gene causing the substitution of glycine by glutamic acid (p.Gly79Glu),and c.1141G ＞ T at position 1141 in exon 10 of the TAT gene leading to the formation of a premature termination codon instead of glutamic acid (p.Glu381*).The proband was the only patient in the family.Some members in the patrilineal family carried the mutation c.1141G ＞ T (p.Glu381*),and some in the maternal family carried the mutation c.236G ＞ A (p.Gly79Glu).Conclusion This is the first case of tyrosinemia type Ⅱ reported in the domestic population,and 2 novel heterozygous mutations were identified in the TAT gene,which may lead to the occurrence of tyrosinemia type Ⅱ in the patient.