Changes in dry weight and projected area of human epidermal cells undergoing keratinization as determined by scanning interference microscopy

Cells, obtained from human leg by successive treatments with trypsin, were air dried on microscope slides before mounting in glycerol. Dry weights and projected areas of individual cells were measured using a Vickers M 86 scanning microinterferometer. The dry weights of cells varied from 100 pg for basal cells to 700 pg for large squames. Corresponding projected areas varied from 100 to 1500 μm².     

Hepatic Injury Due to Oxacillin Administration

Hepatotoxicity, in association with intravenous oxacillin therapy, is described and documented for the first time by liver biopsy in an illicit durg user suffering from acute staphylococcal endocarditis. Mild gastrointestinal symptomatology, fever, cosinophilia and abnormal liver enzyme abnormalities were nooted. Liver biopsy showed features consistent with a drug-induced hepatic injury. Cessation of therapy led to rapid reversal of clinical and biochemical changes and no further observation no evidence of chronic hepatic dysfunction was noted. A brief review of oxacillin hepatic injury is presented.     

Consensus approaches to best practice management of gastrointestinal stromal tumors

Gastrointestinal stromal tumors are rare mesenchymal tumors of the gastrointestinal tract. Progress in diagnosis has led to increased recognition of this disease, and the availability of effective, molecularly targeted therapy has revolutionised its management. Treatment of metastatic gastrointestinal stromal tumors with imatinib has led to unprecedented improvements in progression free and overall survival and there are ongoing investigations into the optimal pre‐operative and adjuvant use of imatinib. Second‐line sunitinib is now available for patients who develop resistance to imatinib, and third‐ and fourth‐line therapies are being investigated in clinical trials. In this ever‐changing environment, evidence from controlled clinical trials and the authors' experience were used to comprehensively outline current best practice management of patients with gastrointestinal stromal tumors.     

A phase II study of outpatient first-line paclitaxel, carboplatin, and bevacizumab for advanced-stage epithelial ovarian, peritoneal, and fallopian tube cancer

The purpose of this study was to assess the response rate and toxicity of paclitaxel, carboplatin, and bevacizumab (PCB) primary induction therapy for the treatment of advanced-stage ovarian carcinoma. Twenty patients were treated with paclitaxel (175 mg/m(2)), carboplatin (AUC of 5 IV), and bevacizumab (15 mg/kg) of body weight; q21 days for six cycles. Bevacizumab was administered at cycles two through six. Patients received 116 cycles of PCB chemotherapy (median = 6, range 2-6) and were evaluable for toxicity assessment. Grade 3 and 4 neutropenia developed in 23.3% and 25% of cycles, with no incidence of grades 3/4 thrombocytopenia or anemia. Prior to cycle six, one patient was removed from the study due to grade 3 neuropathy and another patient was excluded due to clinical deterioration. There was no incidence of gastrointestinal perforations, and only two patients demonstrated grade 3 hypertension (HTN). No grade 4 HTN was observed. Eighteen patients were evaluated for response following induction therapy. Six demonstrated a complete response (30%) and ten exhibited a partial response (50%), resulting in a total response rate of 80%. One patient exhibited stable disease (5%), and one demonstrated disease progression (5%). The lack of bowel perforations and wound complications should mitigate some concerns regarding these side effects. This study suggests that first-line treatment with PCB can be safely administered to previously untreated advanced-stage ovarian carcinoma patients. The favorable toxicity results and reasonable response rate warrant additional study in a larger patient population.     

Thrombocytopenia and bleeding in dental procedures of patients with Gaucher disease

Summary. The risk of bleeding during dental procedures may be increased in patients with Gaucher disease. We aimed to evaluate potential coagulation and platelet function abnormalities and targeted therapy accordingly. Patients with type 1 Gaucher disease who were treated at the Oral and Maxilo‐Facial surgery clinic at Sheba Medical Center between 2003 and 2010 comprised the study cohort. Data collected included disease history, enzyme treatment, platelet counts, dental therapy and outcome. Bleeding was defined as excessive bleeding during or immediately following procedure. Coagulation studies and platelet function tests including aggregometry were performed on all patients. Dental procedures (n = 14, including eight teeth extractions, two crown lengthening procedures, one cyst enucleation and three deep dental scaling) of seven patients were studied. Mean platelet count prior to procedure was 73 K ± 14.8 mm³. Patients bleeding risk score was calculated according to previous history of bleeding tendency, degree of thrombocytopenia, presence of comorbid coagulopathy and the type of dental procedure. Two patients with highest risk score received prophylactic platelet transfusions, three patients (medium‐risk) received DDAVP preprocedure and all received systemic tranexamic acid, which was the only systemic therapy for low‐risk patients. Meticulous surgical local haemostasis was applied. No excessive intra‐operative or postoperative bleeding occurred. Patients with Gaucher disease who have thrombocytopenia and abnormal platelet function tests may be safely treated if meticulous haemostasis is applied along with systemic therapy as required. Platelet transfusions are not mandatory and should be applied considering the procedure‐related risk and the patient’s calculated haematological risk for bleeding.     

Congenital afibrinogenemia; a study of some basic aspects of coagulation

In a study of three subjects with incoagulable blood due to congenital afibrinogenemia, information is presented regarding some basic aspects of coagulationindependent, of the fibrinogen-fibrin conversion mechanism. The following factshave been established: (1) Shortly after the blood is exposed to glass, the earliestdetectable changes are morphologic alteration in the platelets and their progressive agglutination and lysis. (2) Almost in parallel, plasma antihemophilicactivity, originally normal, declines rapidly and practically disappears. (3) Alsowithin minutes, SPCA evolves from its precursor in a normal manner. (4) Acglobulin is rapidly consumed. (5) These changes are well along before detectableamounts of prothrombin have disappeared. (6) Prothrombin consumption proceeds at normal velocity, or slightly faster than normal. (7) Thrombin additionto afibrinogenemic plasma induces platelet agglutination, but this does notoccur when thrombin is mixed with platelets alone. (8) The "natural" antithrombicactivity of afibrinogenemic plasma is normal. (9) The heparin co-factor ofantithrombic activity was demonstrable. (10) Quantitative data were obtainedrelating the one-stage prothrombin time with the fibrinogen concentration.

The theoretic and practical implications of the observations are discussed.

Submitted on July 17, 1953 Accepted on January 28, 1954     

The specificity and cellular origin of phenylethanolamine N-methyltransferase (PNMT)-like immunoreactivity in psoriatic skin

Phenylethanolamine N-methyltransferase (PNMT)-like immunoreactivity has been found in psoriatic skin and in this study, PNMT-like immunoreactivity was investigated in the involved and uninvolved skin of six patients with lichen planus and four patients with lichen simplex. No PNMT immunoreactivity was observed in these diseases. Studies were carried out using cultured fibroblasts from two patients with psoriasis from uninvolved and involved areas of skin and from two controls using antibodies to PNMT, as well as antibodies to the chemical messengers somatostatin, substance P, parathyroid hormone and peptide histidine isoleucine amide. No immunoreactivity to these substances was found, and fibroblasts are unlikely to be the cellular origin of the PNMT-like immunoreactivity as seen in psoriatic skin.