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AbstractA Latin Square(LS) of order nis an arrangement of nsymbols in an n× nmatrix form so that each symbol occurs in each row and each column exactly once. The total number of Latin Squares LS(n) of order nincreases rapidly with n. This helps to design cryptosystems using Latin Squares with a very large key-space. We define encryption and decryption using simple operations on Latin Squares. Different schemes are designed to make the system secure and easy to implement. Use of keyed permutations and construction of large quasigroups ensure that the system is resistant to different practical cryptographic attacks. Computer implementations show the simplicity and power of these schemes for future cryptographic applications in resource-constrained networks or in mobile devices.

Clustering algorithms give general description of clusters, listing number of clusters and member entities in those clusters. However, these algorithms lack in generating cluster description in the form of pattern. From data mining perspective, pattern learning from clusters is as important as cluster finding. In the proposed approach, reduct derived from rough set theory is employed for pattern formulation. Further, reduct are the set of attributes which distinguishes the entities in a homogenous cluster, hence these can be clear cut removed from the same. Remaining attributes are then ranked for their contribution in the cluster. Pattern is formulated with the conjunction of most contributing attributes such that pattern distinctively describes the cluster with minimum error.

Clustering algorithms give general description of clusters, listing number of clusters and member entities in those clusters. However, these algorithms lack in generating cluster description in the form of pattern. From data mining perspective, pattern learning from clusters is as important as cluster finding. In the proposed approach, reduct derived from rough set theory is employed for pattern formulation. Further, reduct are the set of attributes which distinguishes the entities in a homogenous cluster, hence these can be clear cut removed from the same. Remaining attributes are then ranked for their contribution in the cluster. Pattern is formulated with the conjunction of most contributing attributes such that pattern distinctively describes the cluster with minimum error.

Introduction: Venous thromboembolism (VTE), including both pulmonary embolism (PE) and deep venous thrombosis (DVT) is often a silent disease, symptoms are often nonspecific, and the first manifestation may be fatal PE. The link between malignancy itself, and its treatment, type, stage and location, and clinical recurrent VTE has been well recognized since 1865, when Armed Trousseau first reported it. 10–20% of patients with acute VTE have malignancy. VTE may appear before the cancer has become symptomatic and may lead to an earlier diagnosis of cancer; the most common of them include those of the breast, colon, and lung. VTE is the 2nd leading cause of mortality in cancer patients, 2nd only to the cancer itself. Patients with concurrent VTE and malignancy have a more than 3-fold higher risk of recurrent VTE and death, and 4- to 8-fold higher risk of dying after an acute VTE than patients with VTE but no malignancy. Spiral computed tomography angiogram of chest (CTA) was first introduced in 1990s. It has the ability to study pulmonary vessels down to 2-3 mm in diameter and depict PE directly. Only 30–40% of all patients with suspected PE have a confirmed diagnosis. CTA can also provide significant additional information or an alternate diagnosis. Objectives: To determine the frequency of an incidental finding of occult malignancy by CTA of chest in patients highly suspected for PE. Materials and methods: 136 patients, suspected of having PE, were retrospectively studied. We included all the patients, examined by CTA of the chest to diagnose PE from October 2005 through April 2006 at BHMC. We used chart review to evaluate the contribution of CTA to the final clinical diagnosis. The baseline characteristic parameters included age, gender, CTA findings, and pathological examinations. Results: We studied both positive and negative CTA images for searching of evidence of occult malignancy.134 (97.8%) patients had at least one diagnostic finding. Of the 136 patients, highly suspected for PE, 33 (24.3%) patients were confirmed to have PE. A total of 11 (8.1% of total studied) patients were identified with new diagnosis of malignancies. Of these, cancer was detected in 3 (9.1%) patients with PE, and in 8 (7.8%) patients without PE. Thromboembolic risk factors were identified in 2 (66%) patients with positive PE and cancer (e.g. 14 hour flight, immobilization> 3 days). In 63.6% (#7) of patients cancer was diagnosed by initial CTA, and in 36.4% (#4) of patients with follow up studies and clinical evaluations for unresolved initial symptoms during a range of 1 to 7 months (mean of 3.4 months), 3 of the latter group being negative for PE. 72.8% (# 8) of patients had metastatic disease at the time of initial CTA. The most common cancers were gastric adenocarcinoma (# 3, 27.3%), and breast cancer (# 2, 18.2%) of all the patients with cancers. The most common alternative diagnosis other than malignancies, detected by CTA included pleural effusion in 53 (39%) and atelectasis in 48 (35.3%) patients. Only 3 (2.2%) CT angiograms were completely normal. Conclusion: CTA was able to identify occult malignancy in 8.1% of total patients, suspecting PE. Since screening for occult malignancies has been generally underutilized, cancer should be included in the differential etiologies of acute PE, and basic comprehensive evaluation to search for underlying cancer in high-risk patients should be considered.

Introduction: AML/MDS is usually diagnosed in older adults with median age of 64 in patients at time of diagnosis, after occupational exposure to organic solvents, such as benzene, or previous therapeutic exposure to alkylating agents, topoisomerase inhibitors, or ionizing radiation. We are presenting a case of AML/MDS in a young female without previous history of exposure to alkylating agents or ionizing radiation, but with history of exposure to jet fumes. Case Report: This is a 30-year old Carribean woman, chronic smoker, ethanol user, employed for eight years at the airport, working on the ground with heavy direct exposure to jet fumes, who presented with 2 weeks of progressive dyspnea, fatigue and bone pains. She was found to have pancytopenia, hemoglobin 2.8 gm/dL, platelets 37,000/mL, and neutrophils 1100/mL. Peripheral smear showed many nucleated red blood cells and blasts. Bone marrow aspiration was “dry” and bone biopsy revealed hypercellularity with dysplastic changes in erythrocyte, granulocyte and megakaryocytic lineages with 46% blasts. Flow cytometry of peripheral blood showed positivity for CD13, CD33, CD34, and CD117 and HLA-DR with complex cytogenetics showing deletions involving chromosomes 5q, 7q, 12p, 20q and loss of chromosome 17. Fluorescent in situ hybridization (FISH) studies were negative for t(15,17), MLL, t(8,21), inv(16) seen in classical de novo AML. FISH also did not show abnormalities in the probe regions 5q31, 7q31, 8cen and 20q12 of chromosomes 5, 7, 8 and 20 classically seen in de novo MDS. The blast cell morphology suggested acute myelocytic leukemia on a background of myelodysplasia. Precise FAB subtype was not possible in the absence of special stains like myeloperoxidase, and specific and non-specific esterase stains. The patient was treated with two induction courses of cytosine arabinoside and idarubicin. With persistence of 4.5% blasts on the peripheral blood and severe bone marrow aplasia, she was referred for allogeneic stem cell transplantation, in view of failed induction remission and complex cytogenetics at presentation. Conclusion: Case-control studies of leukemia demonstrated only slight increase in risk of disease after many years of occupational or chemical exposures. More studies to investigate leukemia incidence in airport employees, or even communities near airports are needed.

Introduction: The role of steroids in mammalian erythropoiesis has remained not well defined. At our institution, we have observed cases in which it appears that there is a synergism between Erythropoietin factor and glucocorticoids. In three cases, the patients were being treated for anemia that was slow to respond to erythropoietin, but then had a sudden quick rise in Hemoglobin following concomitant therapy with Glucocorticoids. Case #1 is a 32 year-old black female, with SLE for more than 20 years, lupus nephropathy, end-stage renal disease on maintenance Hemodialysis, for the last 5 years, chronic anemia secondary to renal failure, and thrombocytopenia due to lupus. The patient was treated with prednisone 20 mg daily as a maintenance therapy for her SLE and erythropoietin (procrit) 10,000 units injection three times a week, during each session of hemodialysis. On April 27th patient was switched over from prednisone 20mg daily to dexamethasone 6mg orally every 12 hours for 4 does followed by prednisone 40 mg orally every day for worsening thrombocytopenia. A robust rise in hemoglobin level was noticed, from 7.5gm/dl to 17.5 gm/dl within a month from the date started on high dose glucocorticoids a long with procrit. Complete work up for secondary polycythemia was all negative. Procrit was discontinued while prednisone 40mg/day was continued, hemoglobin level decreased to 14.8 g/dl, and platelet count remain stable above 150/CMM. Case #2. A 52 years old female who was diagnosed with stage 111B NSCLC treated with chemo radiation. During the period of chemo radiation hemoglobin level remained between 9–10gm/dl on procrit 40,000 units once per week. Before completion of the Chemotherapy patient developed brain metastasis treated with whole brain irradiation, Dexamethasone 4mg every 6 hours and Dilantin 100mg orally daily for seizure prophylaxis. Three weeks after starting dexamethasone hemoglobin level increased to 17 gm/dl without any obvious reason. Complete work up for secondary polycythemia was all negative. Case #3. is a 42 year old female, with HIV/AIDS (CD4<20) not on any HAART medications, Chronic anemia treated with procrit 10,000 units three times a week for six months and Feso4 325 mg tablets three times a day with hemoglobin base line around 8.00 gm/dl and Seizure. Was admitted on 12/28/05 with odynophagia, cough and shortness of breath was treated for oropharyngeal candidiasis and PCP pneumonia with Bactrim IV, Nystatin, Diflucan and Methylprednisolone 125 IV daily on 12/28/06 changed later to Prednisone 20mg orally once daily from 12/30/06 until 1/27/06. While the patient on both Glucocorticoids and procrit we notice the increased of hemoglobin from 7.7 gm/dl on 12/29/05 to 12gm/dl on 1/27/06. All other causes of secondary polycythemia have been ruled out. Conclusion: The reason for the inordinate rise in hemoglobin after starting corticosteriods could be explained by the action of corticosteriods on an immune component of the anemia, to a synergistic effect with erythropoietin on erythropoiesis through a shared mechanism or to a coincidental factor(s) unrelated to either drugs. Whatever the mechanism, When corticosteriods are prescribed for patient on erythropoietin they should be closely monitored for the development of erythrocytosis. Cautious use of glucocorticoids should be considered in patients who are refractory to erythropoietin.

Nitrogenous uremic products in the blood have been considered responsible for uremia-related platelet dysfunction. Recent studies suggest uremic platelets are defective in thromboxane A2 metabolism, independent of plasma factors. In order to gain a better view on platelet dysfunction in uremia, we generated an animal model in rat by ligating bilaterally kidney hilar structure offset with a capillary tube (16- to 18-gauge) with a success rate of 72.2%. The resulted experimental uremic rats display elevated serum BUN and creatinine levels (112.7 ± 67.29 mg/dL, n =14, and 3.27 ± 0.95 mg/dL, n =14, respectively) on Day 7 after kidney ligation, compared to those sham operated controls (BUN: 16.7 ± 5.77 mg/dL, n =14, creatinine: 0.65 ± 0.33 mg/dL, n =14). Pathological examination of kidney sections from ligated rats reveals distended renal pelvis and dilated distal tubules with limited ischemic changes of tubular wall cells, consistent with hydronephrotic features. Semi-quantitative RT-PCR of whole kidney mRNA shows dramatic increase of kidney-injury molecule 1 (KIM-1) and reduced aquaporin-2 (Aqp2) message levels, indicating renal injuries by obstruction. Functions of uremic platelets were analyzed by an optical platelet aggregometer using separated platelets supplemented with control or uremic plasma after washing, in response to various concentrations of ADP. Uremic platelets in their homogeneous plasma (PlateletUremic/PlasmaUremic) demonstrated reduced aggregation in all ADP concentrations tested, with significant reductions at 5 and 10 uM of ADP (45.8 ± 11.9%, n =12, and 48.7 ± 12.0 %, n =12, respectively), compared to those of control platelets in control plasma (PlateletControl/PlasmaControl, 56.6 ± 10.1%, n =12, and 60.8 ± 7.9%, n =12, respectively). In plasma-exchanged aggregation studies, heterogeneous uremic or control plasma were used to resuspend control or uremic platelets. When control platelets supplemented with uremic plasma (PlateletControl/PlasmaUremic) and induced to aggregate with ADP, percentage aggregation achieved were reduced significantly at low concentrations of ADP (2.5 and 1.25 uM) to levels of 35.5 ± 13.9%, n =12, and 19.3 ± 16.9%, n =12, respectively, suggesting suppressing effects of uremic plasma on platelet aggregation. When platelets from uremic rats were tested in control plasma (PlateletUremic/PlasmaControl), aggregation was also decreased significantly at lower ADP concentration (1.25uM), to 18.7 ± 12.2%, n =12, compared with that of PlateletControl/PlasmaControl (34.7 ± 14.4%, n =12), revealing a hindered response of uremic platelets when activated by lower concentrations of exogenous ADP. Since our data from RT-PCR of platelet-derived total RNA did not support any reductions in the expression levels of platelet ADP receptor P2Y12 in uremic rats, the above response pattern of uremic platelets may suggest a decreased ADP storage or release during activation and warrant further investigations.

Nitrogenous uremic products in the blood have been considered responsible for uremia-related platelet dysfunction. Recent studies suggest uremic platelets are defective in thromboxane A2 metabolism, independent of plasma factors. In order to gain a better view on platelet dysfunction in uremia, we generated an animal model in rat by ligating bilaterally kidney hilar structure offset with a capillary tube (16- to 18-gauge) with a success rate of 72.2%. The resulted experimental uremic rats display elevated serum BUN and creatinine levels (112.7 ± 67.29 mg/dL, n =14, and 3.27 ± 0.95 mg/dL, n =14, respectively) on Day 7 after kidney ligation, compared to those sham operated controls (BUN: 16.7 ± 5.77 mg/dL, n =14, creatinine: 0.65 ± 0.33 mg/dL, n =14). Pathological examination of kidney sections from ligated rats reveals distended renal pelvis and dilated distal tubules with limited ischemic changes of tubular wall cells, consistent with hydronephrotic features. Semi-quantitative RT-PCR of whole kidney mRNA shows dramatic increase of kidney-injury molecule 1 (KIM-1) and reduced aquaporin-2 (Aqp2) message levels, indicating renal injuries by obstruction. Functions of uremic platelets were analyzed by an optical platelet aggregometer using separated platelets supplemented with control or uremic plasma after washing, in response to various concentrations of ADP. Uremic platelets in their homogeneous plasma (PlateletUremic/PlasmaUremic) demonstrated reduced aggregation in all ADP concentrations tested, with significant reductions at 5 and 10 uM of ADP (45.8 ± 11.9%, n =12, and 48.7 ± 12.0 %, n =12, respectively), compared to those of control platelets in control plasma (PlateletControl/PlasmaControl, 56.6 ± 10.1%, n =12, and 60.8 ± 7.9%, n =12, respectively). In plasma-exchanged aggregation studies, heterogeneous uremic or control plasma were used to resuspend control or uremic platelets. When control platelets supplemented with uremic plasma (PlateletControl/PlasmaUremic) and induced to aggregate with ADP, percentage aggregation achieved were reduced significantly at low concentrations of ADP (2.5 and 1.25 uM) to levels of 35.5 ± 13.9%, n =12, and 19.3 ± 16.9%, n =12, respectively, suggesting suppressing effects of uremic plasma on platelet aggregation. When platelets from uremic rats were tested in control plasma (PlateletUremic/PlasmaControl), aggregation was also decreased significantly at lower ADP concentration (1.25uM), to 18.7 ± 12.2%, n =12, compared with that of PlateletControl/PlasmaControl(34.7 ± 14.4%, n =12), revealing a hindered response of uremic platelets when activated by lower concentrations of exogenous ADP. Since our data from RT-PCR of platelet-derived total RNA did not support any reductions in the expression levels of platelet ADP receptor P2Y12 in uremic rats, the above response pattern of uremic platelets may suggest a decreased ADP storage or release during activation and warrant further investigations.

Introduction: Venous thromboembolism (VTE), including both pulmonary embolism (PE) and deep venous thrombosis (DVT) is often a silent disease, symptoms are often nonspecific, and the first manifestation may be fatal PE. The link between malignancy itself, and its treatment, type, stage and location, and clinical recurrent VTE has been well recognized since 1865, when Armed Trousseau first reported it. 10–20% of patients with acute VTE have malignancy. VTE may appear before the cancer has become symptomatic and may lead to an earlier diagnosis of cancer; the most common of them include those of the breast, colon, and lung. VTE is the 2nd leading cause of mortality in cancer patients, 2nd only to the cancer itself. Patients with concurrent VTE and malignancy have a more than 3-fold higher risk of recurrent VTE and death, and 4- to 8-fold higher risk of dying after an acute VTE than patients with VTE but no malignancy.

Introduction: The role of steroids in mammalian erythropoiesis has remained not well defined.

Isolated, also called idiopathic, splenic vein thrombosis (SVT) is a very rare clinical condition, which usually results in left-sided portal hypertension and isolated fundal varices. This syndrome is a rare cause of mostly upper, gastrointestinal bleeding. There are only a few hundreds of cases reported in the literature. Colonic varices are even much rarer, 0.07% post mortem autopsies, and 0.2% in a prospective large endoscopic trials. Pancreatic disorders, including malignancies are the most common underlying causes for SVT. Congenital aneurysm of the splenic vein is one of the theoretical explanations of the Isolated, Idiopathic SVT. Case report: A 53 year old Caucasian female with history of hypertension, and no history of smoking or alcohol abuse, presented with chronic lower gastrointestinal bleeding. Upper endoscopy and flexible colonoscopy revealed perigastric varices without any source of acute bleeding. A bleeding scan demonstrated marked splenomegaly and source of bleeding from left colon. Mesenteric angiogram during venous phase showed splenic vein thrombosis and extensive perigastric varices. In addition, a single large left colonic varix from the lower pole of the spleen was identified as the source of bleeding. The patient was treated with splenic artery embolization with coils, followed by splenectomy, without any major complication. Coagulation studies 8 weeks after the procedure did not show any hypercoagulable state. Conclusion: The Isolated, Idiopathic SVT, itself is a very rare syndrome. Our center has reported four cases of SVT, secondary to medical conditions, such as; pancreatic malignancy, MRSA sepsis, and multi-organ failure. Upper gastrointestinal bleeding has been more frequently reported than lower bleeding. Interestingly, in our case report, a single colonic varix secondary to SVT was proved to be the cause of chronic lower gastrointestinal bleeding. SVT should be suspected in any patient with a triad of gastric varices, splenomegaly, and normal liver function tests, who presents with gastrointestinal bleeding secondary to left sided or so called “sinistral” portal hypertension. Mesenteric angiography with venous phase is the gold standard for the diagnosis of SVT, as endoscopic studies may not be diagnostic of this syndrome. Splenectomy is the only and definitive procedure of choice in the patients with isolated SVT, followed by post splenectomy vaccination.

Isolated, also called idiopathic, splenic vein thrombosis (SVT) is a very rare clinical condition, which usually results in left-sided portal hypertension and isolated fundal varices. This syndrome is a rare cause of mostly upper, gastrointestinal bleeding. There are only a few hundreds of cases reported in the literature. Colonic varices are even much rarer, 0.07% post mortem autopsies, and 0.2% in a prospective large endoscopic trials. Pancreatic disorders, including malignancies are the most common underlying causes for SVT. Congenital aneurysm of the splenic vein is one of the theoretical explanations of the Isolated, Idiopathic SVT.

Pulmonary arterial hypertension secondary to vascular deposition is a rare presentation of Primary Amyloidosis. The natural history of pulmonary hypertension and concomitant right-sided cardiac failure is not very well understood and is associated with a very short median survival. This syndrome is a marker of advanced Amyloidosis Persistent pleural effusion is another much rarer presentation of pulmonary involvement in Primary Amyloidosis and is secondary to pleural infiltration, which sometimes is difficult to distinguish from the cardiomyopathic causes. The incidence of pleural effusion in primary Amyloidosis is 1–2%. This syndrome also has a very poor prognosis, and has limited response to treatment, however, pleurodesis has been temporarily useful in some cases. Case report: A 74 year old African American female, non-smoker, with history of hypertension, who presented with shortness of breath and persistent productive cough and 18 pounds weight loss for the last six months. The initial chest x-rays showed bilateral pleural effusion and a transudate fluid on analysis. Cardiac workup for an atypical chest pain revealed moderate to severe pulmonary hypertension without myocardial infiltration on 2-D echocardiogram, and normal coronary arteries on cardiac catheterization. Extensive workup did not show any secondary cause of pulmonary hypertension, however, the patient gradually developed nephrotic range proteinuria and kidney biopsy showed infiltration of 10 nm fibrils, involving 3+ segmental mesangium, and 2+ segmental glomerular basement membranes. This was consistent with renal Primary Amyloidosis, AL Lambda type. A random urine and serum sample for immunofixation also revealed an M- spike of 23 mg/dl in gamma region. A concomitant bone marrow biopsy revealed presence of monoclonal IgG lambda plasma cell (CD38 bright) population, without any B-cell or T-cell markers. Conclusion: Pulmonary hypertension and pleural effusion are two rare and lethal presentations of pulmonary involvements in Primary Amyloidosis, and it should be considered in the differential diagnosis of any patient presenting with pulmonary symptoms. There is no definite treatment of these syndromes, although combinations of steroids and melphalan, along with colchicines, vincristine, adriamycin, and thalidomide have been used with minimum satisfactory outcomes. Autologous stem cell transplantation (SCT) provides the opportunity to give higher doses of chemotherapy and may be of benefit in some cases.

Pulmonary arterial hypertension secondary to vascular deposition is a rare presentation of Primary Amyloidosis. The natural history of pulmonary hypertension and concomitant right-sided cardiac failure is not very well understood and is associated with a very short median survival. This syndrome is a marker of advanced Amyloidosis Persistent pleural effusion is another much rarer presentation of pulmonary involvement in Primary Amyloidosis and is secondary to pleural infiltration, which sometimes is difficult to distinguish from the cardiomyopathic causes. The incidence of pleural effusion in primary Amyloidosis is 1–2%. This syndrome also has a very poor prognosis, and has limited response to treatment, however, pleurodesis has been temporarily useful in some cases.