No Abstract Available.
Cytotoxins* ; Gram-Positive Bacteria* ; Perforin*

No Abstract Available.
Cytotoxins* ; Gram-Positive Bacteria* ; Perforin*

As a growing number of surgeons are perforining cataract extraction by phacoernulsification and the continuous curvilinear capsulorhexis [CCC] has rapidly increased in popularity as the anterior capsulotomy technique, its advantages have been reported recently. But its complications induced by capsular contraction after ccc have been noted, and so we have studied the change in anterior capsular opening area and refractive error after ccc. One surgeon performed cataract extraction using ccc and phacoernulsification, and implanted posterior chamber IOL [optic size 5. 5mm, Pharmacia 812A] in the bag in 48 eyes, and we measured the area of anterior capsular opening and refractive error [spherical equivalent] at I week and 3 months after operation. The average percentage of anterior capsular shrinkage rate at 3 months was 14.8% and showed statistically significant difference [P<0.05], but. had not correlation with initial ccc size. The average refractive change at 3 months was 0. 2D hyperopic shift but did not show statistically significant difference.
Capsulorhexis* ; Cataract Extraction ; Perforin ; Phacoemulsification ; Refractive Errors

No Abstract Available.
Cytokines* ; Perforin* ; Shwartzman Phenomenon* ; Vibrio vulnificus* ; Vibrio*

No abstract available.
Apoptosis* ; Caspase 3* ; Endothelial Cells* ; Perforin* ; Vibrio vulnificus* ; Vibrio*

OBJECTIVETo introduce the clinical manifestations and laboratory tests of adult onset of primary hemophagocytic syndrome (HPS), and to investigate the essentials of diagnosis and the genotype characteristics in adult onset patient.

METHODSThe definite diagnosis of HPS was made according to HLH-2004. Exons of PRF1, STX11, UNC13D, SH2D1A and RAB27A genes coding region were amplified using polymerase chain reaction.

RESULTSA 48-year-old man was admitted to our hospital because of recurrent fever, pancytopenia and lymph node enlargement. His laboratory test revealed bone marrow hemophagocytosis, elevated ferritin level (2000 µg/L), reduced level of NK cell activity (20.13%) and elevated soluble CD25 level (12277 U/ml). Based on the HLH-2004 diagnostic criteria, the patient was diagnosed as HPS. The patient had viral infection, and no other primary disease was identified that would cause HPS. The patient responded poorly to anti-viral therapy. DNA sequencing was used to confirm that perforin gene mutations might be one of the causes of the patient suffered from primary HPS.

CONCLUSIONSAlthough primary HPS usually affects infants and young children, it also occurred in teens and adults. It is essential to perform genetic screenings to patient whose illnesses recur with unknown causes. In addition, detection of molecular genetic alterations can be used to distinguish primary HPS from acquired HPS.

BACKGROUND: Previous findings demonstrated that the expression of cytotoxic effector molecules is increased in acute rejection of renal allografts. In the present study, we serially examined the gene expression of perforin, granzyme B and Fas ligand(FasL) in peripheral blood lymphocytes(PBLs) of renal allograft recipients to assess the potential of their expression as a marker of acute rejection. METHODS: PBLs were isolated from blood samples taken on days 2, 4, 6, 8, 10 and 12 after transplantation. Competitive PCR was performed to evaluate the abundance of mRNA of perforin, granzyme B and FasL. The mean value of each molecule plus 2 SD for the control group was set as a discriminatory level. RESULTS: When all measured samples were compared, perforin expression was significantly higher in patients with acute rejection than in the control group(1.84+/-3.01 versus 0.71+/-0.48, p=0.01). The percentage of perforin expression exceeding the discriminatory level was also significantly higher in patients with acute rejection(p=0.0003). Five patients in the rejection group(5/7, 71.4%) showed perforin expression exceeding the discriminatory level, while only 1 patient in the control group did so(1/8, 12.5%)(p= 0.02). Perforin expression of days 0 and 1 of rejection crisis was the highest over the study period. No consistent pattern of granzyme B and FasL expression was identified in relation to rejection crisis. CONCLUSION: Gene expression of perforin by PBLs was upregulated in accordance with acute rejection, thus offering the possibility that it may be utilized as a marker of acute rejection.
Allografts* ; Gene Expression ; Granzymes* ; Humans ; Kidney Transplantation ; Lymphocytes* ; Perforin ; Polymerase Chain Reaction ; RNA, Messenger

BACKGROUND: Natural killer (NK) cells constantly survey surrounding tissues and remove newly generated cancer cells, independent of cancer antigen recognition. Although there have been a number of attempts to apply NK cells for cancer therapy, clinical application has been somewhat limited because of the difficulty in preparing a sufficient number of NK cells. Therefore, ex vivo NK cell expansion is one of the important steps for developing NK cell therapeutics. METHODS: CD3+ depleted lymphocytes were cocultured with IL-2 and with feeder cells (peripheral blood mononuclear cells [PBMCs], K562, and Jurkat) for 15 days. Expanded NK cells were tested for cytotoxicity against cancer cell lines. RESULTS: We compared feeder activities of three different cells-PBMC, K562, and Jurkat. K562 expanded NK cells by almost 20 fold and also showed powerful cytotoxic activity against cancer cells. K562-NK cells remarkably expressed the NK cell activation receptors, NKG2D, and DNAM-1. K562-NK cells exhibited more than two-fold production of cytotoxic granules compared with Jurkat-NK cells, producing more perforin and granzyme B than naive NK cells. CONCLUSION: Our findings suggest that K562 are more efficient feeder cells than Jurkat or PBMCs. K562 feeder cells expanded NK cells by almost 20 fold and showed powerful cytotoxic activity against cancer cells. We herein propose an intriguing approach for a design of NK cell expansion.
Cell Line* ; Feeder Cells* ; Granzymes ; Humans ; Interleukin-2 ; Killer Cells, Natural* ; Leukemia, Myeloid* ; Lymphocytes ; Perforin

OBJECTIVE: To explore the synergistic immunomodulatory mechanism of interferon alpha-1b, interleukin-2 and thalidomide (ITI) regimen on patients with acute myeloid leukemia (AML). METHODS: Sixty eight untreated de novo or relapsed or refractory or maintenance therapy patients with AML admitted in the Affiliated Cancer Hospital of Zhengzhou University and the other 11 medical units from March 2016 to May 2019 were treated with ITI regimen. Peripheral blood specimen per patient was collected into EDTA-K3 anticoagulation vacuum tube before the administration of ITI and 3 months after the treatment; peripheral blood lymphocyte subsets and perforin and Granzyme B expression were analyzed by using flow cytometry; the levels of VEGF, IFN-γ, TNF-α and IL-6 in the plasma were detected by using a cytometric bead array. Thirty-five healthy subjects from the hospital physical examination centre were selected as normal controls. RESULTS: The ratio of CD4 CONCLUSION The ITI regimen can raise the ratio of CD4
CD8-Positive T-Lymphocytes ; Humans ; Interferon-alpha ; Interleukin-2 ; Leukemia, Myeloid, Acute/drug therapy* ; Perforin ; Thalidomide

OBJECTIVE: To detect genetic mutations in a child with late-onset hemophagocytic lymphohistiocytosis (HLH). METHODS: Clinical data of an 8-year-5-month-old girl with recurrent HLH and severe central nervous system disease was analyzed. Next-generation sequencing was used to detect mutation in the exons and adjacent introns of 17 genes associated with HLH. Suspected mutations were confirmed by Sanger sequencing. Influence of mutations on protein function was predicted with SIFT and PolyPhen-2 software. RESULTS: The child was found to carry compound heterozygous mutations of the PRF1 gene. Among these, the c.1349C>T (p.Thr450Met) mutation, with a SIFT predictive value of -4.921 (Deleterious variant) and a PolyPhen-2 predictive value of 1.000 (Probably damaging), was inherited from her father and known to be pathogenic. The c.1273dupT (p.Trp425fsX457) mutation was inherited from her mother and previously unreported, which resulted in the deletion of almost the entire C2 domain (amino acid residues 413 to 540) and carboxyl terminal of perforin, which seriously affected the function of the protein. CONCLUSION The c.1349C>T (p.Thr450Met) and c.1273 dupT (p.Trp425fsX457) compound heterozygous mutations of the PRF1 gene probably underlie the disease in this patient.
Central Nervous System Diseases ; Child ; Exons ; Female ; Humans ; Lymphohistiocytosis, Hemophagocytic ; Mutation ; Perforin