Analysis of Consistency between Forensic Psychiatry Identification Diagnosis and Clinical Diagnosis of 1 369 Cases / 法医学杂志

Objective To explore the consistency between identification diagnosis and pre-identification clinical diagnosis of patients with mental disorder undergoing forensic psychiatry identification. Methods The identification data of 1 369 appraised individuals who underwent criminal responsibility identification carried out by the Forensic Institute of Second Affiliated Hospital of Jining Medical University from 2014 to 2017 were collected retrospectively using self-designed investigation data sorting table. A comparative analysis of the mental disorder diagnosis results of expert opinion and past clinical diagnosis results was made. Results Among 1 369 appraised individuals, 964 cases （70.4%） were identified and diagnosed with mental disorder and 405 cases （29.6%） without mental disorder. Among the former, 63.3% （610 cases） were clinically diagnosed, which was higher than 43.2% （175 cases, P<0.05） in the latter. Among the various mental disorders that had been identified and diagnosed, patients with hysteria, stress, and neurosis had the highest proportion of clinical diagnoses （86.7%）, while patients with mental retardation had the lowest proportion of clinical diagnoses （9.6%）. Schizophrenia had the highest overall consistency rate of identification diagnosis and clinical diagnosis （98.4%）, while personality and behavior disorder had the lowest （33.3%）. The overall consistency rate between clinical diagnosis and identification diagnosis of the mental disorder group was 84.1%, and the Kappa value was 0.759. Compared with clinical diagnosis, the consistency rate between inpatient diagnosis and identification diagnosis was higher （85.9%, P<0.05）. Conclusion In forensic psychiatry identification that provides data of past clinical diagnosis and treatment, a high consistency between identification diagnosis and clinical diagnosis of the appraised individual who is identified and diagnosed with mental disorder exists. Clinical diagnosis （especially the inpatient diagnosis） has a relatively good reference value for forensic psychiatry identification.

The effect of iodine excess on bone metabolism in experimental autoimmune thyroiditis rats / 中国地方病学杂志

Objective To explore the effect of iodine excess on bone metabolism in experimental autoimmune thyroiditis (EAT) rats. Methods We selected 36 female Lewis rats with body weight of (131 ± 15)g,and divided them into 3 groups randomly: control group, EAT group and EAT + high iodine group, assuring 12 rats in every group. These rats were fed fodder with different concentration of iodine(0.9,0.9, 18.0 mg/kg), and rats in EAT group and EAT + high iodine group were immunized with pig thyroglobulin(pTG) and complete Freund's adjuvant(CFA) to create EAT model. After two weeks, the pathological changes of the thyroid tissues were observed,and the serum thyroid autoantibody[thyroglobulin antibody(TGAb) and thyroid microsomal antibody(TMAb)], the thyroid hormone levels[triiodo thyronine(T3) and thyrine(T4)] and some relevant data of bone metabolism[bone gla protein (BGP), tartrate-resistant acid phosphatase (TRAP), C-terminal propeptide of type Ⅰ procollagen (PICP),C-terminal telopeptide of type Ⅰ collagen (ICTP), insulin-like growth factor- 1 ( IGF- 1 ), osteoprotegerin (OPG) and receptor activator of NF-κB ligand (RANKL)] were measured. Results Inflammatory cell infiltration and local follicular structural damage were observed in the thyroid tissues of EAT rats in EAT group and EAT + high iodine group, and the pathological changes of EAT + high iodine group were mainly thyroid follicular expansion and integration. The level of serum TGAb, TMAb, T3 and T4 of EAT rats in EAT group and EAT + high iodine group[ (63.01 ± 12.36)%, (60.62 ± 11.24)%, (3.78 ± 1.43), (125.12 ± 16.00)pmol/L and (75.00 ± 15.44)%,(72.15 ± 15.00)%, (3.69 ± 0.91 ), (149.40 ± 20.67)pmol/L] were higher than those of the control group[ (4.47 ±1.04)%, (5.73 ± 1.01 )%, (0.75 ± 0.12), (76.91 ± 9.30)pmol/L, all P ＜ 0.05], and the level of serum TGAb,TMAb and T4 of EAT rats in EAT + high iodine group were higher than those of the EAT group(all P ＜ 0.05).The level of serum BGP, PICP and IGF- 1 in EAT group[ ( 1.70 ± 0.31 ), ( 11.31 ± 1.52) μg/L, (0.31 ± 0.06 ) mg/L]were lower than those of the control group[ (8.60 ± 0.33), (14.28 ± 3.10)μg/L, (1.16 ± 0.02)mg/L, all P ＜0.05], and the level of serum TRAP, ICTP, OPG and RANKL[ ( 19.88 ± 3.60)ng/L, (2.43 ± 0.82), (22.36 ± 2.80),( 1.35 ± 0.23 )μg/L] were higher than those of the control group[ ( 14.57 ± 3.56)ng/L, (0.50 ± 0.20), (1.61 ± 0.34),(0.10 ± 0.02)μg/L, all P ＜ 0.05]; compared with EAT group, the level of PCIP and OPG in EAT + high iodine group [ (8.03 ± 1.84), ( 16.80 ± 3.79)μg/L] were obviously decreased(all P ＜ 0.05). Conclusions The reinforcement of differentiation and maturation of osteoblast in the EAT rats results in the increasing of bone resorption. The activity of osteoblast and osteoclast of the EAT rats are inhibited by excessive iodine, showing a low conversion-type osteoporosis.

Genetic polymorphisms of 9 non-combined of DNA index system short tandem repeat loci in Guangdong Han population / 中华医学遗传学杂志

<p><b>OBJECTIVE</b>To investigate the genetic polymorphisms and their forensic application of 9 non-combined of DNA index system (CODIS) short tandem repeat(STR) loci in Guangdong Han population.</p><p><b>METHODS</b>DNA samples from 500 unrelated individuals were extracted and amplified with fluorescence labeled multiplex PCR system. PCR products were separated and genotyped with capillary electrophoresis.</p><p><b>RESULTS</b>One hundred and fifteen alleles and 160 genotypes were observed in the 9 STR loci, respectively. The heterozygosity was 0.824-0.884, the discrimination power (DP) was 0.925-0.969 and the polymorphism information content (PIC) was 0.77-0.86, respectively. The distribution met the Hardy-Weinberg equilibrium (P > 0.05). The total discrimination power was 1.00 x 10(-13), the combined probability of exclusion for trio-paternity testing was 0.999989488. The combined probability of exclusion for duo-paternity testing was 0.873436.</p><p><b>CONCLUSION</b>The 9 STR loci are powerful and reliable for personal identification and paternity testing. They can be used as supplementary loci in fatherless (motherless) testing or cases with mutation events.</p>

Endogenous danger signals trigger hepatic ischemia/reperfusion injury through toll-like receptor 4/nuclear factor-kappa B pathway / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Restoration of blood flow to the ischemic liver lobes may paradoxically exacerbate tissue injury, which is called hepatic ischemia/reperfusion injury (IRI). Toll-like receptor 4 (TLR4), expressed on several liver cell types, and the nuclear factor-kappa B (NF-kappaB) signaling pathway are crucial to mediating hepatic inflammatory response. Because IRI is essentially a kind of profound acute inflammatory reaction evoked by many kinds of danger signals, we investigated TLR4/NF-kappaB signaling pathway activation in a murine model of partial hepatic IRI.</p><p><b>METHODS</b>Wild-type mice (WT, C3H/HeN) or TLR4 mutant mice (C3H/HeJ) were subjected to 45 minutes of partial hepatic ischemia followed by 1 hour, 3 hours of reperfusion. Sham group accepted the same procedure without the obstruction of blood supply. At the end of reperfusion, the compromise of liver function and the histological change of liver sections were measured as the severity of liver injury. The level of endotoxin in the portal vein was measured by limulus assay. NF-kappaB activation was determined by electrophoretic mobility shift assay (EMSA). The levels of tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta) in systemic blood after hepatic IRI were assessed by enzyme-linked immunosorbent assay (ELISA).</p><p><b>RESULTS</b>The compromise of liver function and the morphological injuries in mutant mice were relieved more markedly than those in WT mice after partial hepatic IRI. NF-kappaB activation in WT mice was stronger than that in TLR4 mutant mice, and both were stronger than those in the sham operated mice (P < 0.01). Endotoxin in each group was undetectable. The levels of TNF-alpha and IL-1beta in systemic blood were elevated in both strains, but lower in the sham operated group. These mediators were significantly decreased in TLR4 mutant mice compared with those in WT mice (P < 0.01).</p><p><b>CONCLUSIONS</b>The TLR4/NF-kappaB signaling pathway may mediate hepatic IRI triggered by endogenous danger signals. Inhibition of the TLR4/NF-kappaB pathway may be a potential therapeutic target for attenuating ischemia/reperfusion-induced tissue damage in some clinical settings.</p>

Activation of Kupffer cell TLR2 signaling pathway during hepatic ischemia/reperfusion injury process in mice and it's significance / 中华肝脏病杂志

<p><b>OBJECTIVE</b>To study changes of TLR2 signaling pathway expression in Kupffer cells during the process of hepatic ischemia/reperfusion in a mice model and the mechanism of TLR2 signaling pathway participating in hepatic ischemia/reperfusion injury.</p><p><b>METHODS</b>BALB/c mice were divided into 3 groups: sham operation (SH), ischemia/reperfusion (I/R) and GdCl3 treatment (Gd) groups. After 4 h of reperfusion, the expression of TLR2 mRNA and membrane TLR2 protein were analyzed in ischemic lobes of the livers, and in Kupffer cells isolated from ischemic lobes. The expression of NF-kappaB in ischemic lobes was also examined. Levels of endotoxin, ALT and TNFalpha were measured at the same time point.</p><p><b>RESULTS</b>The expressions of TLR2 mRNA and protein in both ischemic hepatic lobes and Kupffer cells isolated from ischemic lobes were increased in the I/R group compared to those in the SH group, as well as the expression of NF-kappaB in ischemic lobes, which was down regulated by intravenous GdCl3 treatment. Levels of ALT and TNFalpha in the portal vein were higher in the I/R group than in the SH group, which also were decreased with treatment of GdCl3. The level of endotoxin in the three groups remained constant.</p><p><b>CONCLUSION</b>TLR2 signaling pathway in Kupffer cells is activated during the process of hepatic ischemic/reperfusion injury. The activation of TLR2 signaling pathway in Kupffer cells may play a role in this process.</p>