Objective To investigate the correlative factors that affect the outcome of pregnancy complicated with burn injuries and to provide the treatment proposal for the pregnant women with vary gestational age. Methods Retrospective analysis of 13 cases of burn injuries during pregnancy was made. Results All patients required standard treatment to heal the burn injuries. During the first trimester, abortions occurred in two of the four patients; Abortions occurred in two and premature labour occurred in one of the nine patients who were injured during their second or third trimester. Conclusion Abortions or premature labour appeared during pregnancy as complications of the treatment of burn injuries. Enough fluid therapy in time in early phase of burn is necessary for mother survival and placental perfusion.

Objective To determine whether tissue factor(TF) is present in the amniotic fluid of normal term pregnancy. Methods Tissue factor antigen levels in amniotic fluid, blood plasma, centrifugal supernatant and sediment of 16 normal term pregnancies were detected with immunoenzymatic method(ELISA). Results Tissue factor antigen levels in the blood plasma, the whole amniotic fluid, the centrifugal supernatant and the sediment were [(31?9) ng/L0, [(404?186) ng/L], [(348?177) ng/L] and [(1360?639) ng/L], respectively. Tissue factor antigen concentrations in three states of the amniotic sediment(P

BACKGROUND:Hyperpyrexia can induce a wide range of cel apoptosis in organisms, but no study has introduced the mechanism of heat stress-induced neuronal apoptosis.
OBJECTIVE:To observe the effect of nuclear factor kappa B (NF-κB) signal pathway on heat stress-induced neuronal apoptosis through reactive oxygen species.
METHODS:Heat stress model was established in the cel incubator. Heat stress group of cel s were incubated at 39,41,43℃for2hours,whilecontrolgroupofcelswereincubatedat37 ℃in5% CO2 for 2 hours. Apoptosis was analyzed by flow cytometry using Annexin V-FITC/PI staining. The expression levels of caspase-3 and p-NF-κB65 were determined by western blot analysis. The amounts of intracel ular reactive oxygen species were assayed by DCFH staining. In addition, the effect of MnTMPyP and PTDC on heat stress-induced apoptosis was also studied.
RESULTS AND CONCLUSION:39 ℃ heat stress had no impact on the apoptosis, 41 ℃ heat stress induced a smal amount of apoptosis (10.19%), and 43 ℃ heat stress triggered a large amount of apoptosis (43.02%). The expression of caspase-3 and p-NF-κB65 was increased, in a temperature-dependent manner. In addition, both MnTMPyP and PTDC significantly decreased the heat stress-induced apoptosis and expression of caspase-3 and p-NF-κB65. Experimental findings indicate that, the increase of intracel ular reactive oxygen species may induce neuronal apoptosis, and NF-κB participates in the heat stress-induced neuronal apoptosis as the intermedial signal pathway.

Objective To investigate the effects of different doses of estradiol on apoptosis of T lymphocytes from spleens in ovariectomized mice and explore the possible mechanisms.Methods The mice splenic T lymphocytes were isolated and divided into ten groups: young group, sham- ovariectomized group, ovariectomized group, ovariectomized plus estradiol(10-11, 10-10, 10-8 and 106groups, ovariectomized plus estradiol (10-10mol/L) plus 1CI182 780 (10-7tool/L) group, ovariectomized plus estradiol(10-10mol/L) plus 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine(MPP, 10-6mol/L) group, ovariectomized plus estradiol(10-10mol/L) plus pyrroline dithiocarbamate(PDTC, 10-6mol/L) group. The apoptosis rates were determined by flow eytometry using Annexin V-FITC/ PI and the protein levels of ERa, ERβ, Bax, Bcl-2 and P65 were detected by Western blot. Results The apoptosis rate of ovariectomized group was(19. 4±2.5)%, which was higher than that of young group [(14.6±2.4%) 3 and sham-ovariectomized group [p (14.5±2.3)%], and the levels of Bcl-2 and nuclear P65 were lower than the young group [(0. 25±0. 05, 0. 09±0. 01) vs. (0. 40± 0.07,0. 15±0. 02), P<0.01]. The ovariectomized plus estradiol (10-10tool/L) group had lower apoptosis rate and higher Bcl-2 and P65 levels compared to the ovariectornized group[(16.6±1.8)% vs.(19.4±2.5)%,P<0.05;0.36±0.03 vs. 0.25～0.05, 0.14±0.01 vs. 0.09±0.01, P< 0. 01)], while the ovariectomized plus estradiol(10-8mol/L, 10-6tool/L) groups had higher apoptosis rates than the ovariectomized group[(22. 55±2. 5)% vs. (19. 4±2. 5)% ,P<0. 05;(27.8±3.1)% vs. (19.4 4±2. 5)%,P<0. 01, respectively]. The 2protein levels of ERa and ERβ of ovariectomized group were 0. 23±k0.01 and 0. 22±0. 03, respectively, which were lower than those of young((0. 27±0. 02) and (0. 29±0.04)] and sham-ovariectomized group [(0. 28±0. 03) and (0. 29±0.02)]. The ovariectomized plus estradiol(10-1110-1010-8tool/L) groups had higher while ovariectomized plus estradiol(10-6mol/L) group had lower ERα and ERβ protein levels (0. 09±0. 01,0. 14±0.02) than the ovariectomized group(P<0. 01). There was no significant difference between ovariectomized plus estradiol(10-10mol/L) plus ICI182 780 group or ovariectomized plus estradiol(10-10tool/L) plus PDTC group and ovariectomized group [(19.4±1.6)% vs. (19.4±2. 5)%, (21.0±2. 9)% vs. (19.4d±2. 5)%, P>0. 05). There were also no significant difference between ovariectomized plus estradiol(10-10mol/L) plus MPP group and ovariectomized plus estradiol (10-10mol/L) grou p[(16.9±2.2)% vs. (16.6±1.8)%, P>0.05]. Conclusions The ovariectomy of mice leads to increased apoptosis rates of splenic T lymphocytes. The effects of estradiol on the apoptosis of T lymphocytes in ovariectomized mice are dependent on doses: physiological dose of estradiol inhibits while higher dose of estradiol exacerbats the apoptosis of T lymphocytes in ovariectomized mice.Physiological dose of estradiol may act on Rice T lymphocytes via ERβ and NFkB signaling.

Objective To investigate renal histopathological changes and cli ni cal characteristics in 20 women with preeclamptic nephropathy or gestational pro teinuria.Methods Between 1999 and 2002, 20 women who suffered from preeclampsia or proteinuria during pregnancy underwent postpartum renal biopsies from fifth d ay to third month after delivery. One woman repeated her renal biopsy half year later. Each biopsy specimen was divided into three parts,and processed and stain ed for conventional light microscopy(LM), immunohistology (IH) and electron micr oscopy (EM) examination. The clinicopathological data were studied and women wer e followed up after discharge for a long time. Results Sixteen of 20 women were diagnosed as preeclampsia, whose altered glomeruli demonstrated a typical endoth elial lesion (endotheliosis), and mild to moderate proliferation of mesangial ce lls. IH revealed either negative or mild IgG、IgM and C3 deposits. Focal glomeru losclerosis (FGS) was observed in one of 16 cases, whose microproteinuria (0 49 g/24 h) lasted for more than one year, meanwhile the proteinuria of other 15 wo men disappeared completely within 3～6 months after delivery. Besides, one was I gA nephropathy (IgAN) complicated preeclamptic nephropathy, whose proteinuria de creased obviously after delivery, but remained microhematuria, and endothelial l esion disappeared in repeat biopsy after half year. One was IgAN and received a treatment of adrenocorticosteroid and immunosupressive agents because of macropr oteinuria. One was mild mesangial proliferative glomerulonephritis presenting co nstant microhematuria and microproteinuria. One was typeⅠmembranous nephropathy , whose proteinuria decreased remarkably after delivery as well. Conclusions Ren al histopathological changes of preeclampsis are typical endothelial lesion, and often recover completely within 6 months after delivery. Recovery may be delaye d in the case of FGS accompanied. Pregnancy may aggravate primary renal damage w hich will be improved after delivery. Postpartum renal biopsy is safe and benefi cial to early diagnosis, treatment and prognosis.

Objective To investigate the relationship between serum pregnancy associated plasma protein A (PAAA‐A) ex‐pression and gene polymorphism with the severity of coronary lesions in the patients with coronary heart disease (CHD) .Methods Ninety‐eight patients with CHD in the Nanyang Municipal Central Hospital were selected as the observation group and divided into single vessel lesion group and multiple vessel lesion group according to coronary angiographic results .Ninety‐eight individuals un‐dergoing healthy physical examination were selected as the control group .The venous blood was collected at the visiting hospital in the observation group and at the physical examination in the control group for detecting the serum PAPP‐A protein level by ELISA .PAPP‐A gene and IVS6+ 95 polymorphism were analyzed by adopting polymerase chain reaction restriction fragment length polymorphism(PCR‐RELP) .Results Compared with the control group ,peripheral blood PAPP‐A protein level in the obser‐vation group was significantly increased(P<0 .05) ,moreover the PAPP‐A protein level in the multiple vessel lesion group was sig‐nificantly higher than that of the single vessel lesion group (P<0 .05) .The peripheral blood PAPP‐A level was positively correlated with the severity of CHD .Three genotypes existed in PAPP‐A gene IVS6+95 locus ,including CG heterozygous ,homozygous CC and GG homozygous type .The CC homozygous allele frequency in the patients with multiple vessel lesion was higher than that in the patients with single vessel lesion (P<0 .05) .Conclusion The PAPP‐A protein level and IVS6+95 polymorphism have a close relation with the severity of coronary lesions in patients with CHD .CC genotype may be one of genetic susceptibility gene markers in the patients with CHD .

Objective To analyze the clinical manifestations and gene mutations of rare causes of primary adrenal insufficiency (PAI) in childhood.Methods The clinical features,laboratory tests and gene mutation of 13 patients with PAI in our hospital from September 2010 to August 2017 were analyzed retrospectively.Patients with congenital adrenal hyperplasia,X-linked adrenoleukodystrophy with neurological onset or a clear family history,and autoimmune adrenal insufficiency were excluded.Results The median age of 13 cases (12 males,1 female) was 3 years and 10 months.Medical history or clinical manifestations on the first visit included hyperpigmentation,electrolyte imbalance/salt-wasting crisis,gastrointestinal symptoms,and fatigue,etc.All developments of external genitalia were normal.All cases presented with decreased serum cortisol and increased ACTH levels.Some of the cases showed decreased aldosterone level and plasma renin activity,while 17α-hydroxyprogesterone,testosterone,and androstenedione were in the normal range.Part of cases revealed delayed bone age and adrenal atrophy.Three gene mutations were detected in 13 patients,including NR0B 1 gene (9/13),ABCD 1 gene (3/13),and CYP 11A 1 gene (1/13).NR0B1,and ABCD1 gene mutations were pathogenic mutations,consistent with clinical characteristics.CYP11A1 gene mutation was heterozygote,which cannot fully explain the clinical features.Conclusion PAI in childhood presents common clinical manifestations of adrenal insufficiency,e.g.hyperpigmentation and electrolyte imbalance/sah-wasting crisis,but without specificity.Gene mutational analysis is necessary for precise diagnosis and prognosis estimation.NR0B1 and ABCD1 gene mutations were common in childhood with rare causes of PAI.

ObjectiveTo explore the clinical features and causative genes of short stature children with unknown etiology， providing evidence for precise clinical diagnosis and treatment. MethodsThe study recruited children with suspected but undiagnosed short stature from the pediatric endocrinology department in our hospital between January 2018 and August 2022. A retrospective analysis was performed on the clinical manifestations， laboratory test and whole exome sequencing （WES） results. Causative genes were classified and analyzed according to different pathogenic mechanisms. ResultsA total of 48 children （30 boys and 18 girls） were enrolled， aged 7.73 ± 3.97 years， with a height standard deviation score （ HtSDS） of -3.63 ± 1.67. Of the patients， 33 （68.8%） suffered from facial anomalies， 31 （64.6%） from skeletal abnormalities， 26 ［54.2%， 61.5% of whom born small for gestational age （SGA）］ from perinatal abnormalities， 24 ［50.0%， 87.5% of whom with growth hormone （GH） peak concentration below normal］ from endocrine disorders and 21（43.8%） had a family history of short stature. Laboratory tests showed that GH peak concentration following stimulation test was （9.72 ± 7.25） ng/mL， IGF-1 standard deviation score was -0.82 ± 1.42， the difference between bone age and chronological age was -0.93 ± 1.39 years. Of the 25 cases with mutant genes found by WES， 14 （56.0%） had pathogenic mutation， 6 （24.0%） likely pathogenic mutation， and 5 （20.0%） mutation of uncertain significance. Pathogenic and likely pathogenic variants were identified in 14 genes， including 10 affecting intracellular signaling pathways （PTPN11， RAF1， RIT1， ARID1B， ANKRD11， CSNK2A1， SRCAP， CUL7， SMAD4 and FAM111A） and 4 affecting extracellular matrix （ECM） components or functions （ACAN， FBN1， COL10A1 and COMP）. ConclusionsA rare monogenic disease should be considered as the possible etiology for children with severe short stature accompanied by facial anomalies， disproportionate body types， skeletal abnormalities， SGA， GH peak concentration below normal and a family history of short stature. WES played an important role in identifying the monogenic causes of short stature. This study indicated that affecting growth plate cartilage formation through intracellular signaling pathways and ECM components or functions was the main mechanism of causative genes leading to severe short stature in children. Further research may help discover and study new pathogenic variants and gene functions.