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This work investigates the feasibility of utilising the multilevel compressed block decomposition algorithm (MLCBD) to increase the efficiency of solving the matrix equation obtained from the finite-element method in the electromagnetic analysis. The MLCBD takes advantage of the low-rank approximation of each sub-matrix of the inverse matrix by truncating the information relative to the minor singular values. The choice of truncating tolerance will affect the accuracy and efficiency of the solution. Original MLCBD requires a small truncating threshold and uses a large amount of memory to yield a satisfying result. A novel technique is proposed to improve the solving efficiency by combining a less accurate truncating threshold in MLCBD with a rapid and cheap iterative refinement process. Numerical results are presented to demonstrate the accuracy and efficiency of the proposed technique.

No curative therapy available for MMM patients apart from allogeneic hemopoietic cell transplantation(HCT). There are high morbidity and mortality in traditional allogeneic HCT. We have gotten successful RIC allogeneic HCT for a MMM patient. A man, Chinese, 37 yrs. He had anemia and on dependent transfusion and was diagnosed idiopathic MMM according to bone marrow biopsy 7 years ago. He was hospitalized on May 10, 2007. Physical exam showed pale, pencytopenia without hepatosplenomegaly. The result of X-ray on chest and electrocardiography showed anemic cardiac disease. There were some teardrop-shaped red cells on blood. His Hb was 37g/L, WBC 5.9x 109/L, Plt 33x109/L. The total volume of red cell transfusion was about 8400ml. His serum Ferritin elevated 5110 (reference

Patient is a Chinese girl of 13 years. She had fever, weakness, headache, and was hospitalized on Feb 20th, 2003. There were 0.89 leukemic monocytes in her bone marrow smear at diagnosis. She was diagnosed acute monoblastic leukemia (M5b) according to FAB classification. The immunophenotyping of bone marrow cells showed CD13 0.579, CD15 0.289, CD33 0.78, cMPO 0.27. After the second remission, she underwent hyplo-identical, ABO-matched combination transplantation of bone marrow and peripheral blood stem cells of her donor mother with T-cell deletion in Aug. 2005. Her hemapoiesis recovered at +10d after transplantation. The while complete blood cell count recovered at +31d when the TCR-PCR DNA gene map was showed the chimera. The rejection appeared at +60d. Her blood picture showed Hb 63g/L, Plt 1.0×109/L, WBC 0.4×109/L. The bone marrow picture showed hypo-cellular as same as in severe aplastic anemia. The TCR-PCR DNA gene map showed the 3/16 locus of recipient. The schedule of treatment of delayed rejection was the combination of Cyclosporin A (CsA), Mycophemolate Mofeil (MMF) and Methylprednisolone (MP). She boosted the G-CSF-primed peripheral mononuclear cells of her mother. The cell dose was 4.3×108/kg without T-deletion. Then she received the stimulation of G-CSF 250 ug daily. One week later, she suffered from Herpes Zoster Virus (HZV) infection. There was characteristic HZV varicella in full right side of head, right face, right eye, and right hand with high fever, malaise. She felt severe postherpetic neuralgia. Only morphine or remain acupuncture can relieve her severe neuralgia. She had also severe pancytopenia, gastrointestinal bleeding. We had to transfuse backed red cell and platelet concentration every week. She received first TPE at +130d and second TPE at +137d after transplantation. Dramatic results were gotten after the two TPE. After TPE she did not need transfusion again. After the third TPE, she was discharged then had treated small dose of CsA for half year. The STR-PCR DNA gene map showed the gene type from her mother. At +311d she suffered from chronic graft versus disease (cGVHD). The skin lesion involved her whole body skin about was about 50% body surface area. The effect had not received after treatment with TPE. The cGVHD had not controlled after the basic treatment with CsA or Sirolimus (FK506), MMF, MP, and Thalidomide 100–400 mg/d. So we added with ultraviolet-B irradiation (UV-B) therapy with dose of narrowbank UV-B, twice a week. The lichenification planum was disappearing. The mechanism of TPE on delayed rejection in ABO-unmatched, allogeneic stem cell transplantation has been clear. But, it is still not clear in ABO-matched and hyplo-identical allogeneic stem cell transplantation. It may be cause humoral rejection as same as ABO-incompatible stem cell or solid organ transplantation. The antibodies have resulted from hyplo-identical allogeneic stem cell of her mother. The mechanism of cGVHD results from donor T-lymphocyte activated and involves skin, liver, gut and so on. It is effective of treatment of cGVHD with immune inhibitor drugs but with TPE. Recently reported ECP is effective because the method result in suppressing the activated T-lymphocyte in recipient.

Myelofibrosis with myeloid metaplasia(MMM) is a progenitor cell colony disease. The mechanism is not very clean. The prognosis is poor in MMM patients of the traditional treatment with Hydroxyurea, Interferne, Prednisone, transfusion. Thalidomide is a new anti-angiogenesis drug of inhibiting the genesis of fibrosis. Some reports presented that the cure method only is stem cell transplantation includes autologous and allogeneic bone marrow transplantation. Patient Sui, Man, 55 years, Chinese. He was hospitalized on Aug fifth, 2004, because he has had pale, severe weakness, for 5 months. T 36.C, HR 70, R 18/min, BP114/59 mmHg. Hb56g/L, WBC 5.7x109/L, Plt 72 x109/L.There were 0.66 plasma cell in bone marrow and his bone marrow aspiration with dry draw at the diagnosis,. The result of bone marrow biopsy was fibrosis. He received 4 courses of VAD regimens (VCR 0.4mg,d1–4; ADM 10mg,d1–4, DXM 40mg d1–4) before autologous peripheral stem cell (PBSCs) transplantation. The plasma cell count decreased from 0.66 before to 0.025 after the first course of VAD regimen in the bone marrow. The stem cell mobilization regimen was chemotherapy (cyclophosphamide, Cy, 2g/m2), high-dose methylprednisolone (MP), and G-CSF 250 ug, bid d1–5. The nucleated cell count of collection showed the a minimum of 4.17x108/kg per kg of body weight, CD34+ was 0.834x106/kg.The conditional regimen was melphalan 200mg/kg divided 2 times a day and cyclophosphamide 600mg VD. He received re-transfused PBSCs on March 25,2005. His neutrophil cell decreased 0 at +4 day after transplantation. He received platelet transfusion of single donor two times when his platelet decreased 7 x 109/L. his hemotopoietic recovered at +11d. He left transplantation ward +13 d. His platelet, WBC were normal, Hb 108g/L At+d. Bone marrow draw was no dry. There was 0.07 of plasma cell in his bone marrow. The result of reticulum protein stain was degree 3 after and 4 before PBSCT at +70d. Discussion: MM is incurable tumor because the tumor cells polluted in graft of bone marrow or peripheral blood stem cells. Some author considered the pollution tumor cell decreases with high-dose MP mobilization. Mobilization of stem cell in advanced MMM is difficulty, so we (1) increased the 3 times of mobilization, (2) added high-dose of MP to mobilization regimen of combination of Cy and G-CSF. The patient had received pre-transplantation of four courses of VAD chemotherapy regimen and the combination of west and Traditional Chinese Medicine to manage during stem cell transplantation. The patient had chronic gastric ulcer so we afraid of the condition result in relapse of it so we given the patient intravenous melphalan. Some researchers studied 21 cases of multiple myeloma were treated by autologous bone marrow transplantation. The condition regimen was melphalan 16 mg/kg. The role of allogeneic BMT as compared with autologous BMT is not yet defined. The patient had been followed up for 4 months, the result showed his plasma cell was 0.07 in his bone marrow. The degree of myeloid metaplasia had changed from degree 4 to 2. Conclusion: Intensive treatment with marrow rescue could induce complete remission of long duration in some patients and provided the basis for increased attempts to cure myeloma by intentive chemoradiotherapy and BMT. It is effective in multiple myeloma treatment with autologous stem cell transplantation. The curable method is only allogeneic stem cell maybe.

100 cases of aged non-hematological anemia patients hospitalized in our hospital since July 1, 2000, were analyzed for study on anemia etiology. The mean age was 72.08+/−10.86 (60–90) years (60~ 42; 70~ 39; 80~ 18; 90~ 3) at hospitalization. The etiology of anemia with known showed as followed: Malignant tumor 34: included digestive system malignant tumor 27 (gastric cancer 7, rectal carcinoma 7, colon cancer 6, liver cancer 3, cholangiocarcinoma 2, pencreatic duct cancer 2), lung cancer 3, urinary tract cancer 2, bone sarcoma 2. Iron deficiency anemia 47: digestive tract ulcer 16, hemorrhoid 14. The total number of iron deficiency anemia includes digestive tumors with bleeding. Single nutrition deficiency anemia, macrocytic anemia, i.e. vitamin B12 and/or folic acid deficiency (non-malignant, Non-iron deficiency anemia) 8. Inherited Anemia 10: Thalassemia 6, Glucose-6-phosphate dehydrogenase (G6PD) deficiency 4. Chronic diseases 23: Bone fracture 19, Stroke 18, infection 12, Diabetes 10, Kidney function failure 8, Gynecological bleeding 4. The etiology of anemia is unknown 29: it included some chronic diseases with anemia. Discussion: Incidence of malignant tumor is very high. The incidence of malignancy was 34% in the series of aged anemia. The chance of gene mutation increased as patients’ age getting older. When to diagnose aged anemia, we should better to consider that the primary disease is tumor maybe, and look for tumor carefully. Mechanism of anemia in patients with tumor Gastrointestinal tumor with chronic bleeding that can result in anemia. But, there is serious anemia without bleeding in our series. There were some different chronic diseases in 34 cases of tumor. Researchers have discovered that structural and metabolic disorders were detected in mature erythrocytes in patients with and without anemia in stomach cancer. Anemia development pathways were dependent on enhanced hemolysis of circulating erythrocytes and influx of immature cells from the bone marrow. Complication of etiology in aged anemia Etiological diseases of aged anemia is different and complicate. The major of aged anemia has two or more primary diseases. The primary presenting of gastrointestinal tumor maybe is iron deficiency anemia. The tumor with anemia can result from nutritional deficiency at advance. For example, there were vitamin B12 or/and folic acid 8 cases in our aged series. Some anemia patients in our series complicated cardiac disease, stroke, and bone fracture. 2 cases of G6PD deficiency had primarily diagnosed when they suffered from infection at very old age, 70 years or more in these aged anemia. There are 100 million G6PD in whole world, the incidence is very high especially in Africa and South China. Diagnosis should make as soon as possible. Many advanced tumors were incurable. About 20 per cent of patients with carcinoma of the colon or rectum present with metastatic disease. Surgeons are frequently asked to consider resection or other operative procedures in these patients for palliation. But, average survival was 11.2 months for operative patients versus 6.5 months for nonoperative patients (P < 0.05). So we should better discover tumor anemia and differentiate from other benign anemia in the aged anemia as soon as possible for curable section. To pay attention to treat of etiological diseases is very important for aged anemia patients.