[Abstract] Tolerance is a state in which the human body is less responsive to changes in internal environmental status caused by drugs or other factors. Tolerance is a biological phenomenon, a natural consequence of the action of drugs or chemical factors. Altered organismal tolerance status often leads to the development of multiple autoimmune diseases. Autoimmune thyroiditis (AIT) is a particular type of autoimmune disease, and is exactly the result of an altered immune tolerance of the thyroid gland to a series of "redundant" antigen-antibody binding reactions that produce specific or non-specific inflammation leading to tissue destruction of the thyroid gland. In recent years, a variety of somatic cell therapies have been developed for the purpose of improving the body's tolerance, partially used in the clinical treatment of autoimmune diseases such as systemic lupus erythematosus, multiple sclerosis and Crohn's disease, etc. Such somatic cells that can regulate tolerance are called tolerogenic cells. The present paper will focus mainly on the specific autoimmune diseases such as AIT, discuss the promising therapeutic implications of tolerogenic cells for this group of diseases, and provide a summary of relevant studies. Hopefully, it will provide new research directions for the treatment of the disease.

OBJECTIVETo study the identification method of Pterocephalus hookeri.

METHODThe microscopical, Physicochemical and TLC methods were used.

RESULT AND CONCLUSIONThe convenient and effective identification methods for P. hookeri were established, which provide basis for its quality standard and development.

Chromatography, Thin Layer ; Drugs, Chinese Herbal ; analysis ; Magnoliopsida ; anatomy & histology ; chemistry ; Pharmacognosy ; Plant Leaves ; anatomy & histology ; chemistry ; Plant Roots ; anatomy & histology ; chemistry ; Plants, Medicinal ; anatomy & histology ; chemistry ; Quality Control

Sixty healthy Sprague-Dawley male rats were used and divided randomly into control group (group C), cadmium loading group with medium dose (group M) and cadmium loading group with high dose (group H). Groups C, M and H were orally dosed daily with 0, 5 and 10 mg/kg of cadmium for over 6 weeks. Effects of cadmium loading on testis and endocrine function of reproduction in male rats were studied. The results showed that the zinc content decreased slightly in testis and plasma, and the cadmium concentration increased significantly in the testis of groups M and H; while the plasma levels of cadmium and zinc had no obvious difference as compared with those of group C; daily sperm production in the testis of group H decreased markedly during week 3 of cadmium loading, and was significantly lower in groups M and H as compared to that in group C during week 6; alkaline phosphatase (ALP) in group H and lactate dehydrogenase-X (LDH-X) in groups M and H were markedly lower compared to those of group C; plasma testosterone (T) level in both cadmium loading groups decreased and was low or significantly lower than that in group C; follicle stimulating hormone (FSH) and luteinizing hormone (LH) levels had no apparent difference between the three groups. It is suggested that the gradual accumulation of cadmium in testis tissue induced by chronic cadmium loading results in changes in some enzyme activity, a decrease in sperm production, and defect of endocrine function activity in the testis.
Alkaline Phosphatase ; drug effects ; Animals ; Cadmium ; blood ; Cadmium Chloride ; administration & dosage ; toxicity ; Follicle Stimulating Hormone ; blood ; Isoenzymes ; drug effects ; L-Lactate Dehydrogenase ; drug effects ; Luteinizing Hormone ; blood ; Male ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Reproduction ; drug effects ; Spermatogenesis ; drug effects ; Testis ; enzymology ; pathology ; Testosterone ; blood

OBJECTIVETo observe the effect and safety of autologous cultured skin fibroblasts transplantation for treating depressed facial skin defects.

METHODSA total of 19 patients were treated from Jan, 2010 to Oct, 2010. Autologous skin fibroblasts were separated from postauricular skin biopsy or resected skin tissue in other surgeries such as blepharoplasty. They were cultured and expanded with exclusive method. Cells (2 x 10(7)/ml) within three passages were injected intradermally at the site of skin depression three times at one-month interval. Adverse events were observed and recorded. Clinical effects were evaluated and graded by two unrelated physicians before and 6 months after the first injection.

RESULTSCells from 16 patients were successfully cultured at the first time. The other 3 patients underwent a second harvest. A total amount of 6 x 10(8) cells could be reached within three passages in 45 days. 16 out of 19 patients accomplished the whole course of this study. Minor adverse events were observed in two patients including small ulcer caused by over injection in one patient and slightly redness and swelling in the other. The redness disappeared after a week without any treatment. No serious complications were observed. Significant difference was noticed between the scores obtained before and after the treatment.

CONCLUSIONSFrom this study, neither serious complications nor excessive cell proliferation or scar formation was found after cell injection. The effect of using autologous fibroblast transplantation was obvious and long-lasting, which provides a new choice for the treatment of depressed facial skin defects.

Adult ; Cells, Cultured ; Cicatrix ; therapy ; Face ; abnormalities ; Female ; Fibroblasts ; transplantation ; Humans ; Male ; Middle Aged ; Skin ; cytology ; Transplantation, Autologous ; Treatment Outcome ; Young Adult

Objective To explore the effect and indication of splenectomy in liver transplantation.Methods From January 2001 to April 2006,260 patients underwent piggyback orthotopic liver transplantation(PBOLT),and 28 patients had undergone combined PBOLT and splenectomy(splenectomy group).These patients were compared to 56 randomly selected non-splenectomy patients from the same transplant period,meaningly two controls were se- lected for every non-spleneetomy case.Two groups were analyzed with respect to rate of infection and survival rate, as well as biopsy-proven acute allograft rejection within 30 days after transplantation.Results Rate of infection in the splenectomy group was higher than that in the non-splenectomy patients(85.7% vs 55.4%,P

OBJECTIVETo assess the association between serum 25-hydroxyvitamin D [25(OH)D] levels at birth and bronchopulmonary dysplasia (BPD) in preterm infants.

METHODSThis study recruited preterm infants with gestational age of below 34 weeks who were born between January 2014 and December 2016. These preterm infants were classified into two groups: BPD and control. The association between serum 25(OH)D levels at birth and BPD was analyzed.

RESULTSSerum 25(OH)D levels in the BPD group was significantly lower than those in the control group [(37±17 nmol/L vs 47±20 nmol/L; P<0.05), and the rate of vitamin D deficiency was significantly higher than those in the control group (90.2% vs 74.0%; P<0.05). The level of serum 25(OH)D was negatively correlated with the incidence of BPD (r=-0.201, P=0.001).

CONCLUSIONSVitamin D deficiency at birth may be associated with BPD in preterm infants, but need to be further studied by multivariate analysis.

Bronchopulmonary Dysplasia ; blood ; etiology ; Female ; Humans ; Infant, Newborn ; Infant, Premature ; blood ; Male ; Vitamin D ; analogs & derivatives ; blood ; Vitamin D Deficiency ; complications

OBJECTIVEA stable primary breast cancer model in liver-specific insulin-like growth factor 1 (IGF-1) deficient (LID) mice and control mice was established. To screen apoptosis related genes expression in different serum IGF-1 levels by gene chip and flow cytometry.

METHODSThe LID mice and control mice were used. Induction of breast cancer was achieved by using the 7,12-dimethylbenz(a) anthracene. Ginsenoside Rg3 was used to interfering therapy treatment. The incidence of breast cancer in every group was compared, and expression of apoptosis associated genes was detected by gene chip and flow cytometry.

RESULTSThe incidence of tumor in none ginsenoside Rg3 injected control mice was 66.7%. The incidence of tumor in ginsenoside Rg3 injected LID mice was 12.0% which was significantly lower than any other group (P < 0.05). The apoptosis percentage in none ginsenoside Rg3 injected control mice was (2.7 +/- 0.7)%. The apoptosis percentage in ginsenoside Rg3 injected LID mice was (14.0 +/- 1.7)%. The results of gene chip indicated that in contrast to LID mice, LTA, LTB, TNF-alpha, TRAIL, TRANCE, BLK, BOK, CASP8, TRAF5, and APAF1 genes were down-regulated, and LTBR, TRAF4 genes were up-regulated in the breast cancer tissues of control mice. Application of ginsenoside Rg3 therapy could change the expression of these genes.

CONCLUSIONSCirculating IGF-1 levels play a role in the onset and development of breast cancer. Degrade serum IGF-1 level is able to promote apoptosis by affecting the expression of a series of apoptosis related genes consequently inhibit the growth of breast cancer. There was a synergistic effect with the application of ginsenoside Rg3.

Animals ; Apoptosis ; Breast Neoplasms ; metabolism ; pathology ; Cell Proliferation ; Disease Models, Animal ; Female ; Insulin-Like Growth Factor I ; genetics ; metabolism ; Mice ; Mice, Knockout ; Oligonucleotide Array Sequence Analysis

OBJECTIVEMutations in NPHS2 mapped to 1q25-q31 and encoding podocin, which is exclusively expressed in glomerular podocytes, are responsible for autosomal recessive familial steroid-resistant nephrotic syndrome (SRNS) with minor glomerular abnormalities or focal segmental glomerulosclerosis. Different groups from European and North American countries have screened NPHS2 mutations in familial SRNS with recessive inheritance, documenting a mutation detection rate of 45% - 55% in families. This study aimed to examine mutations in the NPHS2 gene in Southern Chinese Han ethnic group patients with familial SRNS.

METHODSGenomic DNA from 3 probands from Southern Chinese Han families with autosomal recessive SRNS, and their siblings and parents was isolated and analyzed for all eight exons, exon-intron boundaries and promoter of NPHS2 using the polymerase chain reaction and direct sequencing.

RESULTSNo mutation of NPHS2 in all eight exons and exon-intron boundaries was identified in the 3 probands. However, a polymorphism of 954T > C in exon 8 was detected in all the 3 probands and some controls, and 5 variants of NPHS2 promoter, -1709G > A, -1000A > T, -670C > T, -116C > T and -51G > T, were identified in some patients and controls, indicating that these variants are polymorphisms. One heterozygous variant of NPHS2 promoter, -1715A > G, was also identified in one proband and her mother whose urinalyses were normal, whereas it was not found in any of the 50 controls. There was no significant difference in the allelic frequencies of -1709G > A, -1000A > T, -670C > T, -116C > T and -51G > T polymorphisms between the patients and controls.

CONCLUSIONNPHS2 mutations are not a major cause of familial steroid-resistant nephrotic syndrome in Southern Chinese Han ethnic group included in the study.

Adolescent ; Asian Continental Ancestry Group ; genetics ; Child ; Child, Preschool ; Female ; Gene Frequency ; Humans ; Infant ; Intracellular Signaling Peptides and Proteins ; genetics ; Male ; Membrane Proteins ; genetics ; Mutation ; Nephrotic Syndrome ; ethnology ; genetics ; Pedigree

OBJECTIVEHemolytic uremic syndrome (HUS) is a common primary disease that can cause acute renal failure in childhood. Renal disease is the most important long-term complication in patients who survived the acute stage of HUS. Use of angiotensin-converting enzyme inhibitors (ACEI) and a restricted protein intake may be beneficial to the patients. However, it is not established whether such patients should be treated with steroids and immunosuppressors. The present study aimed to probe into the benefit of using steroid and immunosuppressor in patients after acute stage of HUS.

METHODSThe subjects included 17 patients (aged 9 months to 15 years, 12 males, 5 females) with HUS. Thirteen patients recovered from the acute stage of HUS, and underwent continuative treatment and follow-up. All the patients were treated with ACEI and early restriction of protein intake. Additionally, 2 children manifested as glomerulonephritis, one was treated with triperygium glycosides. Other 11 children who manifested as nephrotic syndrome were treated with prednisone, among them 5 children had no response or had incomplete response to prednisone, for these children short-term high dose cyclophosphamide or methylprednisolone pulse treatment were added; in 3 of the children short-term high dose methylprednisolone treatment was applied additionally for membranoproliferative glomerulonephritis and/or focal segmental glomerulosclerosis and crescentic glomerulonephritis.

RESULTSAfter follow-up for 2 months to 8 years, 4 patients with milder disease recovered, their blood pressure, renal function and urinalysis became normal, but 1 patient had recurrence. Among 9 patients with severe disease, 6 maintained normal blood pressure, recovered renal function and urinalysis, the other 3 patients failed to comply with treatment protocol and died during the 3rd, 9th and 13th month. The remainder (4 cases) gave up therapy and died on the 27th to 48th days of the course.

CONCLUSIONThe treatment applied in this study could improve the prognosis of patients after acute phase of HUS evidently by using the steroid and immuno suppressor according to clinical classification and pathological findings. It is recommended that triperygium glycosides is beneficial to children with glomerulonephritis, proteinuria and hematuria after acute stage of HUS. Adjustment of therapeutic schedule based on pathological findings after renal biopsy is helpful. To the patients with progressive renal failure who have no response to the steroid and immunosuppressors, steroid and immunosuppressor should be discontinued and dialysis treatment should be applied. Protocol compliance is also an important factor.

Acute Disease ; Adolescent ; Angiotensin-Converting Enzyme Inhibitors ; therapeutic use ; Child ; Child, Preschool ; Combined Modality Therapy ; Diet, Protein-Restricted ; Drug Therapy, Combination ; Female ; Follow-Up Studies ; Hemolytic-Uremic Syndrome ; diet therapy ; drug therapy ; physiopathology ; Humans ; Immunosuppressive Agents ; therapeutic use ; Infant ; Male ; Prognosis ; Steroids ; therapeutic use ; Treatment Outcome

OBJECTIVETo investigate the effect of p38 mitogen-activated protein kinase (p38MAPK) on the expression of COX-2 and caspase-3 in the substania nigra (SN) of mice with MPTP-induced Parkinson disease (PD).

METHODSC57BL/CN mice were treated with MPTP to prepare a subacute PD model, and their behavioral changes following the treatment were observed. Immunohistochemistry and Western blotting were performed to detect the expression of tyrosine hydroxylase (TH), COX-2 and phosphorylation of P38MAPK in the SN and their changes following treatment with SB203580, a specific inhibitor of P38MAPK.

RESULTSThe 7-day model group showed typical symptoms of PD with decrements of TH-positive neurons and TH protein level in the SN of the midbrain by about 65% and 75%, respectively (P<0.01). In the 3-day model group, the COX-2-, caspase-3- and phosphorylated P38MAPK-immunoreactive cells and their protein levels in the SN increased markedly with obvious loss of TH-positive neurons. Administration of SB203580 obviously lessened the above changes (P<0.01).

CONCLUSIONP38MAPK regulates the inflammation and apoptosis in the SN of the mouse model of subacute PD, and SB203580 may provide some neuroprotective effect.

Animals ; Caspase 3 ; genetics ; metabolism ; Cyclooxygenase 2 ; genetics ; metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Parkinson Disease ; metabolism ; Signal Transduction ; Substantia Nigra ; metabolism ; p38 Mitogen-Activated Protein Kinases ; metabolism