OBJECTIVE: To observe the effects of Jianpi Yishen Recipe (JPYSR), a compound Chinese herbal medicine, on recurrence, metastasis and life span of mice transplanted with proventriculus squamous carcinoma cells after tumorectomy. METHODS: JPYSR was orally administered to 615 mice transplanted with proventriculus squamous carcinoma cells in the palma of left hind limb after tumorectomy. The local tumor recurrence, lung metastasis and life span of the mice were evaluated and compared with those of the 5-FU-treated mice and untreated mice. RESULTS: The pulmonary metastasis rate was 94.4% and the recurrence rate was 94.44% in untreated group. The pulmonary metastasis rate was 68.4%, the inhibition rate of pulmonary metastasis was 27.5%, the recurrence rate was 78.95%, and the inhibition rate of tumor recurrence was 65.35% in JPYSR-treated group. The average and median life spans were obviously prolonged in JPYSR-treated group, as compared with those in untreated group. The life-prolonging rate was 100%. CONCLUSION: JPYSR can effectively inhibit the local recurrence and pulmonary metastasis of the transplanted proventriculus squamous carcinoma in mice after tumorectomy, and prolong the life span.

Objective To investigate the role of human herpesvirus type 7 (HHV-7) in the development of drug eruptions.Methods Venous blood samples were collected from 35 patients with mild drug eruptions at acute stage,15 patients with severe drug eruptions at both acute stage and remission stage,as well as 50 healthy human controls.PCR was performed to detect HHV-7 DNA in peripheral blood mononuclear cells (PBMCs),and enzymelinked immunosorbent assay (ELISA) to determine the titer of anti-HHV-7 IgM antibody in serum.Statistical analysis was carried out by t test,one way analysis of variance,Chi-square test and q test.Results The detection rate of HHV-7 DNA was significantly higher in these patients with drug eruptions than in the healthy controls (82.00％ (41/50) vs.62.00％ (31/50),x2 =4.96,P ＜ 0.05),different among patients with severe drug eruptions (93.33％ (14/15)),patients with mild drug eruptions (77.14％ (27/35)) and the healthy controls (x2 =6.32,P ＜ 0.05),higher in the patients with severe drug eruptions than in the healthy controls (q =3.50,P ＜ 0.05),but not significantly different between the patients with severe drug eruptions at acute stage and those at remission stage (73.33％(11/15),P ＞ 0.05).The anti-HHV-7 IgM antibody titer was significantly increased in the patients with drug eruptions compared with the healthy controls ((69.319 0 ± 25.289 7) ng/L vs.(59.785 3 ± 22.438 2) ng/L,t =1.99,P ＜ 0.05),but no significant difference was observed among the patients with severe drug eruptions (74.340 7 ±31.411 2) ng/L),patients with mild drug eruptions ((65.479 1 ± 21.326 1) ng/L) and healthy controls (P ＞ 0.05) or between HHV-7 DNA-positive patients ((63.748 1 ± 27.239 1) ng/L) and-negative patients ((65.580 2 ± 36.258 4) ng/L,P ＞ 0.05).Conclusions Active HHV-7 infection exists in patients with drug eruptions,and may be associated with the development and aggravation of this entity.

Objective To understand the current status of malaria prevalence,its impacts and malaria transmission trends in Jiangsu Province.MethodsThe malaria incidence,and its symptoms,mosquito preventive measures,Anopheles density,mosquito biting rates and related factors were investigated in malaria epidemic villages as surveillance sites such as Guanshan Town of Suining County,Tangzhang Town of Tongshan County,Tianganghu town of Sihong County,Qiuji Town of Xuyi County and Zhangzhu Twon of Yixing City.ResultsIn 2006,the bednet coverage was 20.29% and bednet-using rate was 34.32% in 27903 residents of 7921 households of 15 administrative villages.In 2005,750 Anopheles sinensi were captured from 50 bednets in the early morning,the human biting ratio was 0.17/person per night,and in 2006,1927 Anopheles sinensi were captured from 50 bednets in the early morning,human biting ratio was 0.38/person per night.The average blood smear checking rate was 2.72%(6089 people)and the average positive rate was 0.48%(29 plasmodium positive individuals).ConclusionThe lower blood smear microscopy testing,few positive rates of febrile patients and increased Anopheles sinensis density were the main factors of malaria relapses in the area of the North Huaihe River in Jiangsu Province.

Objective:To investigate the effect of suspended leukocyte poor red blood cell transfusion on hemeoxygenase-1 (HO-1) expression and T lymphocyte subsets in peripheral blood of patients with myelodysplastic syndrome.Methods:50 cases of MDS patients treated in Shandong Blood Center from January 2016 to December 2019 were selected as the research object. According to the different infusion of blood components, they were randomly divided into the observation group and the control group, with 25 cases in each group.The patients in the observation group were treated with s suspended leukocyte poor red blood cell transfusion, and the patients in the control group were treated with washing red blood cell infusion.The level of HO-1, interleukin-6 (IL-6) and TNF-α and the T cell subset such as CD 3+, CD 4+, CD 8+ and CD 4+/CD 8+ in the serum before and after transfusion were tested by enzyme linked immunosorbent assay and flow cytometry, respectively. Results:There was no statistically significantdifference in the level of HO-1, IL-6 and TNF-α in the serum of the two groups before transfusion ( P>0.05); After transfusion, TNF-α in the serum of the observation group significantly decreased, compared with that in control group: (152.10 ± 21.89) ng/L vs. (201.14 ± 28.90) ng/L, (1.34 ± 0.45) ng/L vs. (2.89 ± 1.01) ng/L. However, the HO-1 significantly increased: (78.91 ± 15.74) μg/L vs. (58.99 ± 13.33) μg/L, andthe difference was statistically significant ( P<0.05). There was nostatistically significantdifference in the immunologic functions of the two groups before transfusion ( P>0.05); After transfusion, CD 4+/CD 8+of the observation group both significantly increased, compared with that inthe control group: (49.11 ± 19.13)% vs. (47.13 ± 12.84)%, (25.23 ± 10.80)% vs. (21.09 ± 12.28)%, (24.74 ± 10.84)% vs. (21.88 ± 11.18)%, 1.02 ± 0.25 vs. 0.96 ± 0.20, and the difference was statistically significant ( P<0.05). Conclusions:The expression level of HO-1 in peripheral blood and immune function of patients with myelodysplastic syndrome can be improved by suspended leukocyte poor red blood cell transfusion.

OBJECTIVETo confirm the genetic diagnosis of two patients with ring chromosome 22 syndrome and investigate the mechanism underlying the formation of r(22) and potential genetic causes for the clinical phenotypes.

METHODSCytogenetic and molecular analyses using standard G-banding, fluorescence in situ hybridization and single nucleotide polymorphism array (SNP array) were performed.

RESULTSFor case 1, the karyotype was 46,XY,r(22)(p11q13). SNP array has identified a 7.0 Mb heterozygous deletion at 22q13.2q13.33. For case 2, the karyotype was 46,XY,r(22)(p11q13)[84]/45,XY,-22[6]; SNP array has detected a heterozygous microdeletion of 1.6 Mb at 22q13.33.

CONCLUSIONWith combined application of genetic testing, 2 cases of r(22) syndrome were diagnosed, which has improved the understanding of the genotype-phenotype correlation of r(22).

Child, Preschool ; Chromosome Banding ; Chromosomes, Human, Pair 22 ; genetics ; Genetic Testing ; Humans ; Male ; Nerve Tissue Proteins ; genetics ; Oligonucleotide Array Sequence Analysis ; Polymorphism, Single Nucleotide ; Ring Chromosomes

OBJECTIVETo identify the small supernumerary marker chromosomes (sSMC) and guide the genetic counseling and medical treatment in two patients with Turner syndrome.

METHODSHigh resolution GTG and C banding, SRY amplification by PCR and fluorescence in situ hybridization (FISH) on metaphase chromosomes were performed to the two patients.

RESULTSThe karyotypes of the two patients were 45, X [29]/46,X, +mar[31] and 45,X[71]/46,X, +mar[29] respectively. SRY test indicated SRY-positive for patient 1, whose sSMC was originated from chromosome Y. The karyotype was confirmed as 45,X[29]/46,X,idic(Y)(q10)[31]. ish idic(Y)(q10)(RP11-115H13x2) (SRY+) by FISH. While in patient 2, the sSMC was originated from chromosome X, whose karyotype was determined as 45, X[71]/46,X, r(X)(p11.23q21)[29]. ish r(X) (p11.23q21)(AL591394.11xAC092268.3).

CONCLUSIONUsing cytogenetic and molecular cytogenetic analyses, we have identified the sSMCs in two patients with Turner syndrome, which was helpful to the clinical diagnosis and treatment.

Adolescent ; Child ; Chromosomes, Human, X ; genetics ; Chromosomes, Human, Y ; genetics ; Female ; Genetic Markers ; Humans ; In Situ Hybridization, Fluorescence ; Karyotyping ; Turner Syndrome ; genetics

OBJECTIVE: To explore the genetic basis for a child with multiple malformations. METHODS: A child who had presented at Shanxi Provincial Children's Hospital in February 2021 was selected as the study subject. Clinical data of the patient was collected, and whole exome sequencing (WES) was carried out to screen pathogenic variants associated with the phenotype. Candidate variant was validated by Sanger sequencing of her family members. RESULTS: The child had normal skin, but right ear defect, hemivertebral deformity, ventricular septal defect, arterial duct and patent foramen ovale, and separation of collecting system of the left kidney. Cranial MRI showed irregular enlargement of bilateral ventricles and widening of the distance between the cerebral cortex and temporal meninges. Genetic testing revealed that she has harbored a heterozygous variant of NM_178014.4: c.217A>G (p.Met73Val) in the TUBB gene, which was unreported previously and predicted to be likely pathogenic based on the guidelines from the American College of Medical Genetics and Genomics (ACMG). The child was diagnosed with Complex cortical dysplasia with other brain malformations 6 (CDCBM6). CONCLUSION CDCBM is a rare and serious disease with great genetic heterogeneity, and CDCBM6 caused by mutations of the TUBB gene is even rarer. Above finding has enriched the variant and phenotypic spectrum of the TUBB gene, and provided important reference for summarizing the genotype-phenotype correlation of the CDCBM6.
Humans ; Child ; Female ; Abnormalities, Multiple ; Blood Group Antigens ; Family ; Malformations of Cortical Development/genetics* ; Brain ; Mutation

Chronic high-salt diet-associated renal injury is a key risk factor for the development of hypertension. However, the mechanism by which salt triggers kidney damage is poorly understood. Our study investigated how high salt (HS) intake triggers early renal injury by considering the ‘gut-kidney axis’. We fed mice 2% NaCl in drinking water continuously for 8 weeks to induce early renal injury. We found that the ‘quantitative’ and ‘qualitative’ levels of the intestinal microflora were significantly altered after chronic HS feeding, which indicated the occurrence of enteric dysbiosis. In addition, intestinal immunological gene expression was impaired in mice with HS intake. Gut permeability elevation and enteric bacterial translocation into the kidney were detected after chronic HS feeding. Gut bacteria depletion by non-absorbable antibiotic administration restored HS loading-induced gut leakiness, renal injury and systolic blood pressure elevation. The fecal microbiota from mice fed chronic HS could independently cause gut leakiness and renal injury. Our current work provides a novel insight into the mechanism of HS-induced renal injury by investigating the role of the intestine with enteric bacteria and gut permeability and clearly illustrates that chronic HS loading elicited renal injury and dysfunction that was dependent on the intestine.
Animals ; Bacteria ; Bacterial Translocation ; Blood Pressure ; Drinking Water ; Dysbiosis ; Enterobacteriaceae ; Gastrointestinal Microbiome ; Gene Expression ; Hypertension ; Intestines ; Kidney ; Mice* ; Microbiota ; Permeability ; Risk Factors