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Acute lymphoblastic leukemia (ALL) is one of the frequently reported malignancies of childhood age. Earlier it was thought to be a fatal pathological state with no cure, but with advancements in medicine and science, new therapeutic approaches have resulted in better management and cure. However, one of the major hurdles in achieving a complete cure is the relapse of ALL at extra-medullary sites like the central nervous system (CNS). The present review article is focused on recent diagnostic avenues available for the detection of CNS disease during acute lymphoblastic leukemia (ALL) in young patients.

Multiple sclerosis (MS) is an inflammatory idiopathic autoimmune disease causing demyelination of central nervous system (CNS). The incidence of pediatric MS is relatively rare, affecting 0.2 to 0.64/100,000 subjects; cases with MS onset before age 10-12 years, account for less than 1% of all MS cases, while 2.7 to 10.5% of all MS cases worldwide are seen in children18 years of age, with a strong female preponderance. The disease course of MS varies from a benign type with relatively low level of disability after a long duration (15 years) of the disease, to a malignant type of MS with severe disability or even death within few months following onset. Diagnostic criteria for pediatric MS include ≥ 2 clinical events involving more areas of CNS inflammation in the absence of encephalopathy, separated by30 days, along with the involvement of brainstem. Pediatric MS generally presents relapsing-remittent form of MS, with majority of the patients recovering from the first attack. Major histocompatibility complex, more specifically, mutations in the human leukocyte antigen (HLA) DRB1*15 allele, are considered most important genetic factors that are contributory to the disease. Treatment choices for pediatric MS include many disease-modifying therapies (DMT) that are currently being used for adult MS and these are interferon-β 1a/1b (IFN-β1a/1b), glatiramer acetate, teriflunomide, dimethyl fumarate, alemtuzumab, etc. However, most of these have not gone through complete testing in randomized, placebo-controlled clinical trials for pediatric MS and are being prescribed off-label by clinicians. As these studies are progressing, it is important to address if these approaches of treating pediatric MS patients have any long-term impact on patients, in particular, physical, cognitive, developmental and social outcomes of the children.

To study the peripheral blood lymphocyte subsets in children with hemophagocytic lymphohistiocytosis (HLH) in acute period as well as remission period, and compare them with healthy children to investigate the significance of lymphocyte subsets in the diagnosis, treatment, and prognosis in children with HLH.From January 2009 to March 2014, 30 HLH patients were enrolled in this study. Among them, 20 were placed in the remission group, while 10 cases were placed in the death group. 6 cases died within 8 weeks due to the illness, and 4 cases died within 9 to 34 weeks. 30 children who were confirmed healthy after physical check-ups in the same period were enrolled in the control group. Peripheral blood was collected from both groups and lymphocyte subsets were studied using flow cytometry.The ratios of CD3+ T and CD8+ T cells increased in the HLH remission group and the death group, while CD4+, CD4+/CD8+ and CD3-CD16+CD56+NK ratios decreased. Difference detected in the proportion of CD19+ B cells was not statistically significant. By comparing lymphocyte subsets in the HLH acute period and the remission period in HLH patients we discovered that the differences in CD3+, CD8+, CD4+ and CD4+/CD8+, CD19+ B cells ratios were not statistically significant (p0.05). CD3-CD16+CD56+NK cells ratios in the remission period increased significantly.The lymphocyte subsets in children with HLH underwent obvious changes and there was an imbalance in cellular immunity. We believe that dynamic detection of changes may help us to evaluate the prognosis and the effect of the treatment.

Calcineurin inhibitor cyclosporine is widely used as an immunosuppressant in clinic. However, mounting evidence has shown that cyclosporine hinders tolerance induction by dampening Tregs. Therefore, it is of paramount importance to overcome this pitfall. Kaempferol was reported to inhibit DC function. Here, we found that kaempferol delayed islet allograft rejection. Combination of kaempferol and low-dose, but not high-dose, of cyclosporine induced allograft tolerance in majority of recipient mice. Although kaempferol plus either dose of cyclosporine largely abrogated proliferation of graft-infiltrating T cells and their CTL activity, both proliferation and CTL activity in mice treated with kaempferol plus low-dose, but not high-dose, cyclosporine reemerged rapidly upon treatment withdrawal. Kaempferol increased CD4+FoxP3+ Tregs both in transplanted mice and in vitro, likely by suppressing DC maturation and their IL-6 expression. Reduction in Tregs by low dose of cyclosporine was reversed by kaempferol. Kaempferol-induced Tregs exhibited both allospecific and non-allospecific suppression. Administering IL-6 abrogated allograft tolerance induced by kaempferol and cyclosporine via diminishing CD4+FoxP3+ Tregs. Thus, for the first time, we demonstrated that kaempferol promotes transplant tolerance in the presence of low dose of cyclosporine, which allows for sufficient Treg generation while minimizing side effects, resulting in much-needed synergy between kaempferol and cyclosporine.

Male infertility is a complex multifactorial and polygenic disease, and genetic factors play an important role in its formation and development. Recently, the association between follicle stimulating hormone receptor (FSHR) gene polymorphisms and male infertility risk has attracted widespread attention due to the unique biological functions of FSH. The aim of this study was to further explore the associations between the Thr307Ala and Asn680Ser polymorphisms of the FSHR gene and male infertility. A case-control study of 212 infertile and 164 fertile men from North China was performed. FSHR polymorphism genotypes were obtained through direct DNA sequencing. A meta-analysis was also performed. In the single-site association analysis, no significant associations were identified between FSHR Thr307Ala and Asn680Ser polymorphisms and male infertility (P > 0.05). However, we found that the combined genotypic frequency of Thr/Ala + Asn/Asn was higher in infertile patients than in controls (6.6 vs 1.8%; odds ratio (OR) = 3.795; 95% confidence interval (CI): 1.072-13.434, P = 0.027). In the meta-analysis, there was also no evidence of FSHR polymorphism (rs 6165 and rs 6168) association with male infertility (P > 0.05). However, we found that the combined genotypes Thr/Thr + Asn/Asn had an increased risk of male infertility (OR = 1.238; 95%CI: 1.001-1.537, P = 0.049). Our studies further confirmed reports that there were no significant associations between the FSHR Thr307Ala and Asn680Ser polymorphisms and male infertility risk. However, a combined FSHR genotype showed significant association with male infertility.

In order to clarify the importance of nuclear IP(3)Rs in the development of myocardial hypertrophy, a hypertensive rat model was established by abdominal aortic constriction, and velocity and isopyknic gradient centrifugation was employed to fractionate the cardiac nuclei. The maximal number of binding sites (B(max)) and dissociation constant (Kd) of IP(3) to the nuclear envelopes were measured by [(3)H] IP(3) binding assay. The existence of IP(3)Rs on myocardial nuclear envelope was confirmed. [Ca(2+)] inhibited [(3)H] IP(3) binding to its receptors in cardiac nuclear envelopes in a concentration-dependent way. Phosphorylation by CaM and endogenous PKC decreased B(max) of nuclear IP(3) receptors. B(max) and Kd of nuclear IP(3)Rs were increased by 1.217 (P0.01) and by 2.149-fold (P0.01) respectively in hypertrophic myocardium as compared with those of the control. The above results suggest that IP(3)Rs exist in myocardial nuclei and are down regulated by CaM, PMA and free Ca(2+). The increase of the binding sites of IP(3)Rs in the nuclear envelopes and the decrease of their affinity might play importment roles in the development of overload induction of cardiac hypertrophy.

This paper reports one case with glucagonoma syndrome that resection of the primary glucagonoma in the pancreas was done. There was metastasis one in liver and lymph node. The definitive diagnosis was established by immunohistochemical analysis. The patient by immunohistochemical analysis. The patient remained well for 27 months and gained 5 kg of weight. Another experiences of diagnosis and treatment of 8 cases of malignant glucagonoma collected in chinese literature were reviewed. The clinical specialty of glucagonoma syndrome. diagnosis and management were discussed suggesting two points: on diagnosis the clinical specialty is a important clues: palliative primary tumor resection may be significant clinical improvement and prolonged survival.

From 1977 to 1987, six cases of heterotopic pancreas at the ampulla of Vater and the papilla were encountered. All patients were suffering from obstructive jaundice and misdiagnosed as having periampullary cancer and pancreaticoduodenectomy was done. The entity was rare and extremely difficult to diagnose even during exploration. The pathology, diagnosis and surgical treatment of this disease were discussed.

This paper presents an analysis of 35 GI epithelioid leiomyomas (leiomyoblastoma) including the authors' own 6 cases from 1975 to the end of 1987. Tumors were found in the stomach in 21 cases (60%), in the duodenum in 4 (11.2%), in the jejunum in 7 (19.8%), and in the ileum in 3 (8.5%). The male to female ratio was 1:1.2 ranging in ages from 11 to 68 with an average of 42. Of these, 82.8% were benign and 17.2% were malignant. No case was correctly diagnosed before the operation. Tumors were resected in 97.2% of the patients. In the author's opinion there should be two basic types of the tumor: benign and malignant, though the identification is often quite difficult. The mitosis, the size of primary tumor, the metastasis and recurrence of the tumor should all come into the consideration. Surgical resection of the tumor is the only effective treatment and all tumors should be treated as malignant.