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Fulminant Epstein-Barr virus (EBV)-driven clonal T-cell lymphoproliferative disorder (T-LPD) is rare and most patients are of Asian origin. The disease usually develops shortly after primary acute EBV infection and the mechanism remains poorly understood. Here we report such a rare case in a 28-year-old Caucasian female with systemic lupus erythematosus (SLE). Immunophenotypic and molecular studies revealed that the proliferating lymphoid cells displayed a CD8+ T-cell phenotype with clonal rearrangement of the T-cell receptor gamma gene. Epstein-Barr virus-encoded RNA was also observed in the clonal lymphoid cells by in situ hybridization. The patient subsequently developed fatal virus-associated hemophagocytic syndrome one month after the primary acute EBV infection. The case represents the first report of fulminant EBV-driven CD8+ T-LPD occurring in an immunocompromised Caucasian SLE patient. This study, along with studies of similar Asian cases reported in the literature, suggests that dysregulated immunity due to either acquired or genetically determined susceptibility may result in an abnormal response to primary EBV infection and contribute to the pathogenesis of EBV-mediated fatal T-LPD.
Epstein-Barr virus (EBV) is a member of the herpes virus family that infects B-cells in the majority of individuals during their early childhood in developing countries. Infants and young children with primary EBV infection are generally asymptomatic, but adolescents and adults usually develop infectious mononucleosis (IM), a self-limited lymphoid proliferation with a benign clinical course. This is due to regulated immune surveillance by the polyclonal proliferation of CD8+ cytotoxic T-cells which themselves are free of EBV [1, 2].
Fatal infectious mononucleosis (FIM) is an uncommon disease and is characterized by fever, rash, generalized lymphadenopathy, hepatosplenomegaly and blood cytopenia. FIM occurs sporadically in immunocompetent patients, but develops with high incidence in patients with X-linked lymphoproliferative disease (XLP, Duncan's disease) due to mutations in the SH2 domain-containing 1A gene (SH2D1A) [1–4]. Most FIM develops shortly after primary acute EBV infection and is almost always of T-cell lineage. Biologically, a defect in T-cell mediated immune regulation results in uncontrolled immune responses with extensive infiltration of lymphoid cells in marrow, lymph nodes, liver and spleen [5–9]. The lesion is often associated with cellular necrosis, histiocytic hyperplasia and virus-associated hemophagocytic syndrome (VAHS), which has been attributed to the defective or imbalanced cytotoxic T-cell response, as well as the vascular damage mediated by chemokines [10–11]. EBV is the virus most frequently found in VAHS, which occurs primarily in immunosuppressed patients and has a fatal outcome with a median survival of six weeks [5–8, 10, 12].
Fulminant EBV-driven clonal T-LPD in immunocompetent patients is very rare. Almost all reported cases were of Asian origin and some patients lacked serologic responses to infected virus, suggesting that geographic location and ethnicity associated with a specific vulnerability to EBV infection may play an important role [13–22]. The clinical presentation of this fulminant EBV+ clonal T-LPD significantly overlaps with the classical form of FIM, resulting in difficulties in differential diagnosis. The biological relationship of fulminant EBV+ clonal T-LPD to classical FIM remains undefined. In classical FIM, an antigen-specific CD8+ cytotoxic T-cell response is crucial to control EBV-infected B-lymphocyte proliferation [7]. However, the role and mechanism of EBV infection in the pathogenesis of fulminant EBV+ clonal T-LPD are poorly understood.
In addition to FIM, EBV infection has also been etiologically implicated in the development of a variety of human cancers, including Burkitt lymphoma [1], certain forms of natural killer (NK)-cell lymphomas [23], Hodgkin lymphoma [24–26], nasopharyngeal carcinoma [27], smooth muscle tumors and gastric cancers [28–30]. It has been particularly implicated as the causative agent in a wide range of B-cell lymphomas in immunocompromised patients, including post-transplant recipients and those with inherited or acquired immunodeficiencies [29, 31]. The clonal EBV infection has been confirmed in the tumor cells of these malignancies, supporting a causative role of EBV in tumorigenesis.
Here we report an EBV+ CD8+ clonal T-LPD in a 28-year-old Caucasian female with systemic lupus erythematosus (SLE) after primary acute EBV infection. The abnormal proliferation of T-cells was evaluated by immunohistochemistry, in situ hybridization, flow cytometry, cytogenetics and molecular analysis. To the best of our knowledge, this case represents the first report of a fulminant EBV+ clonal CD8+ T-LPD in a Caucasian SLE patient, and the results suggest that dysregulated immunity may contribute to the pathogenesis of EBV-mediated fatal T-LPD.
Tissues were fixed in 10% neutral buffered formalin, embedded in paraffin, and 4 µm sections were cut and stained with hematoxylin and eosin (H&E) for histological evaluation. Immunohistochemical stains were also performed on formalin-fixed, paraffin-embedded tissue sections. Briefly, after deparaffinization in xylene and rehydration in graded alcohols, endogenous peroxidase was blocked with 3% hydrogen peroxide. Antigen retrieval was performed in citrate buffer, pH 6.0, as appropriate for the antibodies. After rinsing in phosphate-buffered saline, antibodies against CD2 (DAKO), CD3 (Ventana Biotek), CD5 (Biocare), CD7 (DAKO), terminal deoxynucleotidyl transferase (Biocare), CD30 (Ventana Biotek), ALK-1 (Biocare) were employed for immunohistochemical stains. These stains were performed on a Ventana ES automated immunostainer (Ventana Biotek, Tucson, AZ) using an avidin-biotin-peroxidase complex method.
In situ hybridization for EBV-encoded RNA (EBER) was performed according to the manufacturer's instructions on a Ventana ES automated immunostainer using a streptavidin-biotin peroxidase detection system [32]. The optimum probe concentration was titrated to eliminate background staining while retaining good signal strength and contrast. Negative controls consisted of stains with omission of the EBV probes in the hybridization protocol. The quality of mRNA was estimated in tissue sections using poly A probes.
Bone marrow and lymph node specimens were processed using previously described methods [33]. At least 30,000 events were routinely acquired using a FACSCalibur (4-color) flow cytometer (Becton Dickinson [BD] Immunocytometry Systems, San Jose, CA) with CellQuest software (BD). All antibodies were purchased from BD Biosciences (except kappa and lambda light chains from DAKO) and were used according to manufacturer's recommendations. Monoclonal antibodies and fluorescent labels were specified as follows: fluorescein isothiocyanate-conjugated antibodies: CD5, CD7, CD8, CD103, TdT and kappa light chain; phycoerythrin-conjugated antibodies: CD19, CD22, CD23, lambda light chain and CD56; allophycocyanin-conjugated antibodies: CD2, CD4, CD10, CD11c, and CD38; peridinin chlorophyll protein-conjugated antibodies: CD3, CD20 and CD45. Fluorochrome-conjugated surface IgG1 monoclonal antibody was used as an isotypic control. Data were collected on FACSCalibur flow cytometer and cluster analysis was performed using Paint-a-Gate software (BD).
Genomic DNA was extracted from paraffin-embedded tissue sections using the QIAamp DNA Mini kit (QIAGEN, Valencia, CA). PCR for T-cell receptor (TCR) gamma gene and immunoglobulin heavy chain gene rearrangements was performed at the Mayo Medical Laboratories (Rochester, MN). Conventional cytogenetic analysis was performed on direct bone marrow cultures using standard techniques. Twenty metaphase cells from overnight and short-term cultures were analyzed using procedures described in The AGT Cytogenetics Laboratory Manual with modifications [34]. The karyotype was expressed according to the International System for Human Cytogenetic Nomenclature [35].
A 28-year-old woman with a history of SLE for nine years presented with fever, headache, splenomegaly and cervical lymphadenopathy. An acute IM was diagnosed and her medications for SLE (hydroxychloroquine, methotrexate and folic acid) were discontinued. She experienced partial improvement for one week, and then developed high fever and upper abdominal pain. A computerized tomographic scan revealed cholecystitis and diffuse lymphadenopathy. The patient underwent cholecystectomy. However, her fever and malaise persisted with decline of her hemoglobin and platelet count over the following days. The gall bladder was found to exhibit chronic cholecystitis, whereas the peri-cystic duct lymph node was initially diagnosed as "diffuse large cell lymphoma" at an outside hospital. A diagnosis of fulminant EBV+ clonal CD8+ T-LPD was made 7 days later at the University of Wisconsin Hospital and Clinics, where she was treated with allopurinol and two doses of Rituximab. Bone marrow biopsy at that time showed extensive involvement by fulminant EBV+ clonal CD8+ T-LPD. Treatment with antibiotics, fentanyl, hydrocortisone and supportive care was given. Her subsequent course was complicated by extensive disease progression, renal failure, coagulopathy, and respiratory distress symptoms. She expired two months after her initial presentation.
Laboratory findings on admission revealed a white blood cell count of 4.8 × 109/L (81% polymorphonuclear cells, 15% lymphocytes, 3% immature myeloid cells and 1% monocytes), hemoglobin 7.4 g/dL, hematocrit 22% and a platelet count of 88 × 109/L. Reticulocyte count was 10 × 109/L. Serum lactate dehydrogenase (LDH) was markedly elevated (5760 IU/L; normal reference range 105–230 IU/L). Liver function test was also abnormal with following results: total bilirubin, 8.4 mg/dL (normal: 0.0–0.4 mg/dL); direct bilirubin, 6.7 mg/dL (normal: 0.0–0.3 mg/dL); alkaline phosphatase (AP), 386 U/L (normal: 35–130 U/L); gamma glutamyl transferase (GGT) 245 U/L (normal: 0–40 U/L); aspartate transaminase (AST), 3618 U/L (normal: 0–40 U/L); and alanine aminotransferase (ALT), 849 U/L (normal: 0–65 U/L). Triglycerides were elevated at 385 mg/dL (normal: 3–149 mg/dL). Serum ferritin was >10,000 (normal: 20–300 ng/mL). Antibodies to EBV capsid (VCA), early (EA) and nuclear (EBNA) antigens showed IgG (+) for anti-VCA, anti-EA (−) and anti-EBNA (−), consistent with a primary acute infection. Antibody and quantitative PCR for CMV were negative. Antibodies for SLE, including anti-SSA, anti-SSB, anti-SM/RNP, anti-Smith, anti-cardiolipin and anti-ds DNA antibodies, were all negative.
The peri-cystic duct lymph node showed a complete effacement of the normal nodal architecture by small to intermediate-sized lymphoid cells. These lymphoid cells had round to slight irregular hyperchromatic nuclei and small prominent nucleoli. Scattered large cells with prominent nucleolus were also seen.
Occasional mitosis and apoptotic bodies were noted. Micro-foci of necrosis were also present (Figures 1A and 1B). The concurrent bone marrow biopsy was hypercellular with erythroid hypoplasia, left-shifted myeloid and dysmegakaryocytic hyperplasia. The atypical lymphoid cells constituted 30% of the cellular components and they were intermediate in size with higher nuclear to cytoplasmic ratio and dense chromatin (Figures 2A and 2B).
Immunohistochemistry showed these lymphoid cells were positive for CD2, CD3, CD5, CD7 and CD8; but were negative for CD4, CD20, BCL-2, BCL-6, cyclin D1, CD30, ALK-1, and TdT (Figures 1C-1F; Figure 2C). Partial loss of antigen expression was noted for CD5 and CD7 in the lymphoid cells. In situ hybridization confirmed that these T-cells were positive for EBV RNA (Figures 1G and 2D), and showed a nearly 100% proliferation index by Ki-67 immunostain (Figure 1H).
Flow cytometric immunophenotyping demonstrated a predominant population of mature CD8+ T-cells that express CD2, CD5 and CD7 with lower density CD3 expression compared to normal CD4+ T-lymphocytes (Figure 3A). Normal B-cells were nearly absent. Molecular studies performed at the Mayo Medical Laboratories showed a clonal T-cell receptor gamma gene rearrangement (Figure 3B). Immunoglobulin heavy chain gene rearrangement was polyclonal. Conventional cytogenetic analysis on the marrow aspirate revealed a normal female karyotype.
The liver was markedly enlarged (2,400 g) with infiltrates of mostly small lymphoid cells in the periportal and centrilobular areas. There were interspersed foci of hepatocyte necrosis with ghosted nuclei, cholestasis, macrovesicular steatosis and vascular congestion. Spleen was mildly enlarged (420 g) due to chronic congestion and prominent infiltration of atypical lymphoid cells in the parenchyma. Diffuse karyorrhexis was observed in the white pulp, mainly in the follicular areas. In contrast, the periarterial lymphoid sheath corresponding to the T-cell regions appeared to be hypocellular. The follicles of the spleen were essentially normal, some of which showed diminished germinal centers. No karyorrhexis was observed in the red pulp.
The bone marrow was hypercellular with extensive involvement by atypical lymphoid infiltrates. There was an increased mitotic index, and geographic foci of necrosis with much apoptotic debris. Generalized lymphadenopathy with atypical lymphoid proliferation was observed in all lymph nodes. Kidneys demonstrated acute tubular injury, necrosis and focal glomerulosclerosis with atypical lymphoid infiltrates. Strikingly increased histiocytes filled with apoptotic debris were observed in lymph nodes (Figure 2E and 2F) with similar changes present in the bone marrow, spleen and kidneys.
The gastric, intestinal, and colonic mucosae were diffusely hemorrhagic with bloody peritoneal fluid. Pulmonary parenchyma was severely edematous and hemorrhagic with bilateral pleural effusion. Brain dissection revealed atypical lymphoid infiltrates with a perivascular arrangement in the subarachnoid, bilateral temporal, basal cistern, and spinal nerve roots. Hemorrhagic lesions were also seen within the subarachnoid space of the left hippocampus, cerebellar vermis, and nerve roots of the spinal cord and cauda equine.
Healthy young children are typically asymptomatic following primary EBV infection, but adolescents and adults usually develop IM. This is characterized by an integrated proliferation of cytotoxic T- and polyclonal B-cells through controlled immune responses including interferon production and neutralizing antibodies [1, 2]. FIM is associated with a defect in T-cell mediated immune regulation, resulting in aberrant cytotoxic T-cell activity, uncontrolled B-cell proliferation, and tissue damage [5–9]. A majority of the T-cell lymphomas associated with EBV appear to develop as a direct complication of EBV infection, usually in the setting of severe chronic active EBV infection (SCAEBV) [10, 36–44]. This type of T-LPD usually exhibits a CD4+ T-cell phenotype. In contrast, fulminant T-LPD is a less well-characterized and unique in that it usually develops shortly after primary acute EBV infection in immunocompetent individuals and typically presents with CD8+ T-cell phenotype. Almost all cases have been reported in Asian or Mexican population. Some patients lacked serologic responses to the viral infection, suggesting that ethnicity may be an important for predisposition to EBV infection. However, detailed evaluation of the phenotype and clonality of the lymphoid cells has only been performed in few cases [13–21]. The clinical presentation of fulminant EBV+ clonal CD8+ T-LPD shows significant overlap with the classical form of FIM, and its relationship to classic FIM remains elusive. Molecular, phenotypic and viral studies are often required to confirm the diagnosis. It should also be distinguished from dissemination of nasal type extranodal NK/T cell lymphoma.
We report here a rare case of fulminant EBV+ clonal CD8+ T-LPD arising in an immunocompromised Caucasian female with a history of SLE. The patient developed clonal CD8+ T-LPD one month after initial diagnosis of IM. To our knowledge, only 13 similar cases have been reported in the literature as summarized in Table 1 [13–21, 45, 46]. Nearly all reported cases were of Asian or Mexican origin and showed a diffuse growth pattern of atypical lymphoid cells in the bone marrow, lymph nodes and solid organs. The cytologic features in these cases are heterogeneous, possibly resulting from the combined effects of lymphokines released by transformed or activated T cells and genetic defects. Two characteristic histological features are recognized. One is the presence of atypical small or intermediate-sized lymphoid cells exhibiting coarsely stippled chromatin and inconspicuous nucleoli, which was present in four cases. The second feature is the presence of immunoblasts or immunoblast-like cells, found in nine cases. This type of cell has been shown in various types of EBV-associated lymphoproliferative disorders, such as IM and Hodgkin lymphoma. One case developed a large granular lymphocyte-type proliferation. The clinical behavior of fulminant EBV+ clonal CD8+ T-LPD was aggressive in all patients, and did not respond to intensive chemotherapy and supportive care. There were prominent systemic symptoms and signs in most patients. A characteristic finding was prolonged fever of unknown origin preceding the diagnosis. The interval from initial diagnosis of IM to fulminant clonal CD8+ T-LPD was variable, and ranged from 3 days to 19 months with a median survival of 1.7 months. The prognosis is significantly worse than that of EBV-negative peripheral T-cell lymphoma (18 months), and closely approaches that of human T-cell leukemia virus (HTLV-1)-positive adult T-cell lymphoma/leukemia (7 months) [47, 48]. In nine cases, T cell clonality was confirmed by Southern blot or PCR-based molecular analysis, whereas the remaining five cases were evaluated by conventional cytogenetics for hypertriploid abnormalities, or immunoblastic morphologic features only. All fourteen cases (including the current case) showed the presence of EBV, and ten of these cases revealed clonality of EBV genome, all with type A. Of fourteen fulminant CD8+ T-LPD cases, eleven cases had a complete analysis of EBV serology and the findings support primary acute infection in six cases, and possible chronic EBV infection in 3 cases (Table 1). Eight patients developed VAHS in the late stage of their clinical course. The current case demonstrated an extensive involvement of atypical lymphoid cells in the bone marrow, lymph nodes and solid organs. The lymphoid cells exhibited a CD8 T-cell phenotype and, most importantly, had clonal TCR gamma gene rearrangement. These observations support the contention that a fulminant EBV+ clonal CD8+ T-LPD can occur in an immunocompromised Caucasian patient, and suggest that dysregulated immunity resulted from an acquired immunologic disorder may result in an abnormal response to EBV infection and contribute to the pathogenesis [49–51].
Rare EBV+ clonal T-LPDs with a CD4+ phenotype developing as a direct complication of EBV infection have been reported; these diseases commonly occur in the setting of severe chronic active EBV infection (SCAEBV) (Table 2) [37, 38, 40–44]. Virtually all cases reported in the literature have occurred in Japanese children, and EBV infection had been present for several years before the development of the CD4+ clonal T-LPD. In comparison, the clinicopathologic features and outcome of the EBV+ CD4+ clonal T-LPD are significantly different from those seen in the fulminant EBV+ CD8+ T-LPD summarized in Table 1. It has been hypothesized that the high prevalence of EBV+T-LPDs in the Asian and Mexican populations may be due to a genetically determined susceptibility, possibly based on certain HLA types that result in an abnormal response to EBV infection [52, 53]. These observations suggest that EBV may infect precursor T-cells and that unique genetic defects may exist in different types of EBV+T-LPDs. The mechanisms that lead some patients to preferentially develop one type over the other have yet to be determined.
In situ and Southern blot hybridization have confirmed the clonotypic proliferation of EBV genomes in the neoplastic T cells of fulminant T-LPD, therefore, supporting an etiologic role of EBV in malignant transformation, as was previously demonstrated in B-cell and Hodgkin lymphomas [54, 55]. Molecular and serologic studies for anti-VCA and anti-EBNA of EBV show that fulminant EBV+ T-LPD occurs primarily in the setting of primary acute EBV infections and is rarely associated with chronic active EBV infection. The EBV-associated fulminant T-LPD develops mostly in healthy or immunocompetent individuals and exhibits a CD8 T-cell phenotype [46, 56–58]. The biological mechanism of EBV infection on primary T-cells, however, remains a point of contention. The EBV receptor (CD21) has been found to express primarily on immature precursor T-cells, and its expression declines markedly as the cells differentiate [59–61]. CD21 has also been shown to be expressed in a low percentage of neoplastic T-cells in CD4+ T-LPD [38]. Infection of thymocytes by EBV and the binding of EBV to CD8+ T-cells have also been reported [62, 63]. However, T cells infected with EBV have yet to be identified in the blood or tonsils of healthy individuals. It is possible that the expression of CD21 on the precursor T-cells or the neoplastic CD8+ T-cells may be transient, or cell-cycle specific, as was demonstrated in epithelial cells of nasopharyngeal carcinoma. Alternatively, infection of T-cells by EBV may be mediated through a receptor distinct from CD21 that has yet to be identified.
SLE is an idiopathic autoimmune disease characterized by basic defects in T- and B-lymphocytes, which result in immune dysregulation and production of autoantibodies, ultimately leading to organ damage. The risk of non-Hodgkin lymphoma was 3–4 fold higher compared with the risk in the general population, and B-cell lymphomas are the most common types [64–66]. Rare cases of anaplastic and peripheral T-cell lymphomas have also been reported [67, 68]. It has been postulated that this association is mediated by both genetic and exogenous factors by which uncontrolled lymphocyte activity leads to chromosomal translocations and malignant transformation. The immunological response to EBV has been found to be abnormal in individuals with SLE [49, 69]. Common findings in SLE patients include the presence of over 15-fold EBV viral burden, significantly elevated EBV antibodies and impaired EBV-specific cytotoxic cell function. Abnormal expression or function of CD21 is also found both in human and murine models of SLE [70, 71]. One can speculate that if patients with SLE release T cells from the thymus at a relatively immature state, these cells would be infected with increased frequency in the periphery. As a result, it might increase the risk for T-cell infection and the subsequent monoclonal expansion. It is possible that in compromised patients, the expanded T-cell populations become infected with EBV, and progress to fulminant T-LPD. This phenomenon appears similar to that seen in EBV-related B-LPD, in which there is progression from classical polyclonal B-cell expansion into an atypical oligoclonal phase and subsequent clonal malignant B-cell lymphoma. However, such a case has never been reported, and this may be partly due to the rarity of this disease.
In conclusion, we describe a fulminant EBV+ CD8+ clonal T-LPD in an immunocompromised Caucasian SLE patient following acute primary EBV infection. Biologically, the disorder represents a malignant proliferation of T cells that acquires the EBV genome as a crucial pathologic event. Patients with this type of lymphoid proliferation have very poor clinical outcomes with extensive lymphoid infiltration in the hematologic system, and often exhibit VAHS. Clinical, morphologic and immunophenotypic evaluation, along with molecular studies, are necessary to fully characterize such cases.
This study was supported by the Research and Development Funds from Gundersen Health Foundation and the Department of Pathology and Laboratory Medicine at the University of Wisconsin School of Medicine and Public Health. We thank Peggy Frickenstein, Joyce Johnson, Andrea Allen, Lynn Klein, John Beck and Susan M. LaRose for technical assistance.
PubMed Central Canada is a service of the Canadian Institutes of Health Research (CIHR) working in partnership with the National Research Council's national science library in cooperation with the National Center for Biotechnology Information at the U.S. National Library of Medicine(NCBI/NLM). It includes content provided to the PubMed Central International archive by participating publishers.


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Let's face it. I am no expert. I don't have a PhD in parenting. I don't have a PhD in childhood behavior. I don't have a PhD in therapy. The only PhD I have is that I am a Parent Holding Determination to find solutions to not yelling because it was destroying my kids' spirit. It was destroying me. So, I started getting creative. And a little wacky to keep from yelling. Here is my perhaps embarassing, hopefully helpful, list of the top 50 fun, silly, serious and other things I have done the last 100 days to keep from yelling. Consider it a cheat sheet for not yelling…or a source of entertainment. Either way I hope you enjoy it!
50 Alternatives to Yelling at your Kids:
Fun Alternatives (Added bonus: I don't yell and kids start laughing and changing behavior):
1. Run around the house (adrenaline boost)
2. Start talking jibberish (makes kids laugh and stop pummeling each other)
3. Start blowing bubbles (relaxes me, reminds me of childhood and that I should CHILL OUT)
4. Get the camera (forces me to see behavior wasn't so bad)
5. Laugh. Even if you don't want to. (laughter is good for the soul)
6. Bang arms on chest like a gorilla (a good release and a great entertainment for kids)
7. Put hand in front of mouth and pretend to "toot" a horn (great attention getter)
8. Do Jump and Jacks (releases positive chemicals or something like that!)
9. Do push ups (see above)
10. Start clapping and keep going until the kids have stopped annoying behavior (a good release)
11. Start drumming on table/counter until rage is gone (a REALLY good release)
12. Start the Hokey Pokey (silliness can snap anyone out of it)
13. Start a Dance Party (adrenaline + fun, what's not to love?)
14. Sing. I especially like "La la la, la la, la LAAAAA" (it's unexpected which works wonders)
15. Pretend to have Laryngitis (silence also works wonders)
"I look like a Fool" Alternatives:
16. Yell into a Closet (clothes don't have feelings)
17. Yell into a Kitchen Cabinet (cereal boxes don't have feelings either)
18. Open up the freezer and put head in (it cools me down and snaps me out of my mood and makes kids laugh)
19. Raise two hands in the air (it gets kids attention, like a warning signal that I'm about to blow)
20. Go to the bathroom and scream into the toilet, then flush it away ( um symbolic?)
21. Shake body, arms and legs (like The
Wiggles, Shake shake Shake your silly's out)
22. Get on back and put legs and arms in the air and howl like a Dog (yes, I did this,read here)
"I'll be considered a bad parent" Alternatives:
23. Put the TV on for longer than normally feels okay at moments that are especially dreadful (Sometimes TV is better than yelling, right?)
24. Have ice cream sundaes together (Fun family activity makes me want to have fun, not yell)
25. Start the day with Orange Yogurt (A very small food coloring goes a long way)
I don't know how to categorize Alternatives:
26. Go to The Orange Rhino Facebook page and yell there… (that's what the page is for!)
27. Text a friend announcing you're going to lose it (hopefully he/she will say "don't!!)
28. Set up phone calendar to notify you every 30 min to not yell. (annoying but helpful)
29. Stare at something in room that you love. (finding happy moments erases anger)
30. Ask your child WHY are you crying? (the response will make you give a hug instead)
31. Ask your child WHY are you doing that? (the response might make you understand behavior and make your desire to yell decrease)
32. Tell yourself "I won't yell. I won't yell." (Tricks you into believing you won't!)
33. Say "I love you. I love you. I love you." (Hard to yell when you realize you love someone).
More Serious/Expected Ideas
34. Count to 10. Or 100. Or 1000 until you calm down. (forces one to regroup and get perspective)
35. Walk away (more opportunity to gain perspective)
36. Take a deep breath (if one is breathing, one can't yell!)
37. Whisper (don't know why this works, it just does!)
38. Turn the Lights off (the shocking factor stops kids in tracks and adds calmness)
39. Eat (Food in mouth, mouth can't yell. major pros, major cons, um hello 5 pounds)
40. Keep a journal and write why you want to scream (paper is a great listener)
41. Grab your hands together and squeeze (a great release)
How I remind myself not to yell
42. Buy orange napkins and keep in the kitchen
43. Buy (or receive for Mother's Day!) orange kitchen towels
44. Wear more orange (necklace, clothes)
45. Put orange post it notes all over the house ESPECIALLY where one is apt to yell
46. Print out Orange Rhino Logo, attach popsicle sticks and have Kids hold it up when crankiness starts
47. Get kids involved! Have them yell "ORANGE RHINO!!!" when they sense the volcanic eruption coming!
48. Wear an orange hair elastic around wrist
49. Place orange flowers in a vase in kitchen
50. Serve Orange Foods (oranges, peaches, cheese, Cheez its, carrots)
So there you have it. 50 things I have tested in order to keep myself from yelling. Clearly, it has taken A LOT of creativity. And A LOT of patience. And A LOT of self control. But hey, my kids are worth it. They totally deserve to be raised in a more loving environment.
"I can't yell for 365 days...but I can still pick my nose!"
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While camera equipment itself does not take pictures -- photographers do that -- I am frequently asked as to what equipment I use. Here is a listing of my currently used gear. Don't go out and duplicate this list; buy the equipment you need to take the photographs you like. But be careful. Let me quote Jack Dykinga: "Cameras and lenses are simply tools to place our unique vision on film or sensor. Concentrate on equipment and you'll take technically good photographs. Concentrate on seeing the light's magic colors and your images will stir the soul."I use a Lowepro Pro Trekker photo backpack to carry equipment in the field. This large pack has the best harness and strap system of any backpack on the market, consequently it's comfortable to carry all day in the field. It's also a legal carry-on for airline travel within the US if you remove the outside pockets. When I'm working strictly from my vehicle I keep some gear in an shoulder bag and transfer equipment as needed to the Lowepro.
Here's what I currently use:
Camera bodies:Canon 1Ds Mark III Leaf Aptus 75sHasselblad H1 for film and digital with Leaf Aptus 75s. Hasselblad lenses: 35mm, 80mm, 50-110mm, 150mm and 210mm . Canon Lenses:14 mm f2.816-35mm f2.824-70mm f2.824mm f2.8 Tilt/Shift70-200mm f2.8 AF-IS100-400mm f4 AF-IS500mm f4 AF-ISCanon teleconvertersHeliopan circular polarizing filtersHeliopan Neutral DensityAccessories:Canon 580 TTL flash units + off-camera cordWalt Anderson's Better Beamer flash extenderCanon remote releasesPhotoflex LiteDisc diffusers and reflectors
Tripods: I normally photograph from a tripod. The number of handheld photos I take per year, aside from total flash shots, is miniscule. My standard 3 tripods: Gitzo G1228 , G1548 and GT3541 carbon fiber model with a Novoflex ClassicBall head complete with an quick release disk (all cameras and lenses have mini quick-release disksmounted on them). For long lens action photography with my 500mm I switch to a Wimberley head.
Photography Websites by BetterPhoto.com


text: Things at homefront and work has been real crazy for me, at least. Getting the year started with lots of activities going on at work, SKO, virtual learning, pipelines, business plans and what have you for a account manager is a rat race. Almost into the 2/3 completion of Q1 and hoping go start the year with good nos, has taken a toll on me. Constantly feeling the pressure and now seems to have the invisible Sun Wukong's head ring around me, tightening with each breathe in or each bend of the neck to pick up stuffs. Terrible feeling....... Tried to distress by baking and did a couple of baking projects. Praying the anxiety feeling goes away soon and good things awaits. Grace had a sprained right foot on Tuesday night after jumping off the bed, following the monkey business of her brother. Got us so worried how to handle the injury. We monitored her and kept her away from school. Thank God that today she's better and manage to walk and run even. Thus, concluded the very whiny, I cannot walk, I want to carry." stage. Hope you have a wonderful Friday to spend and enjoy the weekend!


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Kakopetria and Galata on the right called the guardians of the Byzantine churches. It is away from the beaten tracks in the Troodos Mountains preserved a truly unique architectural monuments of the Cyprus church - the church under a gable roof with ancient frescos.
In 2005 the treasury of the world cultural heritage by UNESCO joined the temple of the Holy Sozomenos in Galata, built on donations from the villagers in the XVI century. Temple vaulted, with a wooden roof. This is one of the few churches in Cyprus, which survived all the decoration of the whole. All the internal walls of the church frescoes. Decorated with frescoes, and the outer part of the north wall. Above the west entrance there ktitorskih inscription, which mentioned the names of the donors, the name of the artist (Simeon Aksenty) and year decoration church frescoes (1513 city).
In 2005 the treasury of the world cultural heritage by UNESCO joined the temple of the Holy Sozomenos in Galata, built on donations from the villagers in the XVI century. Temple vaulted, with a wooden roof. This is one of the few churches in Cyprus, which survived all the decoration of the whole. All the internal walls of the church frescoes. Decorated with frescoes, and the outer part of the north wall. Above the west entrance there ktitorskih inscription, which mentioned the names of the donors, the name of the artist (Simeon Aksenty) and year decoration church frescoes (1513 city).
Architectural composition of church structure is simple. It is traditional for the highlands basilica with semicircular apse to the east, a wooden ceiling and a steep gable roof, not only covering the central nave is the only building, but later Attached gallery surrounding the church on three sides. This building design has to save up to now virtually the only church in Cyprus, which is widely represented cycle plot tells about the life of the Virgin. Rich, beautifully preserved frescoes that adorn not only the interior but also the exterior walls of the church, give it a special charm and uniqueness.
It should tell you a bit about the Holy Sozomenos, which was erected in honor of the ancient church in the village of Galata. For more information about his righteous life are unknown to us, but the people preserved legends tell that on the island of Saint Sozomenos appeared at the beginning of the V century. Fleeing from the persecution of the Saracens, he was among the 300 Christians had to leave their native lands of Syria and move to Cyprus.
Not far from the abandoned Nicosia is now the village of Agios Sozomenos, near the village of Potamia is his cave dwelling.
The village is situated in 12 km from Nicosia, the island's capital, and a little away from the so-called "Green Line." Due to the fact that Cyprus is divided into two parts, the Greek and Turkish, was built between the buffer zone longer than 180 km, now known as the "Green Line." In 1964 of Major General Peter Young, commander of the peacekeeping forces, green crayon held on the map line, hence the name of the buffer zone.
So, in this village, on the slopes of the hill is carved in stone rocky monastery, where he lived a holy hermit Sozomenos (Sozomen). The cave cell preserved tomb of the saint and frescoes, the most ancient layers of which date back to X century.
In the few remnants of ancient murals Cypriot researchers have a better idea of the shape and operation of the saint. From flavored rock frescoes, scientists learned that many years of his life dedicated Sozomenos medicine and care of sick and infirm, treated for fever and wrote a book about Eastern Orthodoxy and religious beliefs.
The church, erected in his honor, on the outside wall of the building survived a unique painting, which depicted the seven ecumenical councils that unified the Ancient Church had not yet split into East and West, where Christianity has lived under the unwritten motto "Unity in diversity", and when in theological debates and discussions around the issues of faith consummated the triumph of Christianity. Thus, the frescoes of the church of St. Sozomenos immortalized unique scientifically subjects.
Interesting murals with images of women saints whose images do not often see in the ancient temples. This holy martyr Paraskeva, Kyriakos, Barbara and Catherine. Figures of young beautiful women in rich robes, embroidered with jewels and pearls decorate the lower and middle tiers of the south wall of the nave. The greatest interest is the image of the Holy Martyr Cyprian Kyriaki, whose name in Greek means the last day of the week - "Sunday". Holy Attire cover medallions, which faces personified the days of Holy Week. The idea of creating such an image pFolnostyu owned Cypriot artists and has its origins in the early Hellenistic traditions.
Church of Archangelos Michael, or Panagia Theotokos - a chapel with a wooden roof, situated right on the outskirts of the village. Its walls are completely covered with paintings of post-Byzantine style of the beginning of the XVI century.
The restored inn is of particular interest to fans of the original rural architecture of Cyprus.
The Church of Agios Georgios Perahoritis in the eastern part of the village is known for its very ancient wall paintings of the first half of the XVI century.
The church that once belonged to the monastery was built in the year 1502. The monastery was destroyed at the end of 19 century. The temple was built at the expense of the Greek Dimitrios1a de Corona, who was in the service of King James II. Its walls were not completely painted. Those that are, almost all were made at the same time when the temple was built. They are made in the Italo-Byzantine style.
During the period of Venetian rule in Cyprus church was built near the village of Panagia Podithou Galata. As the inscription on the outside is dedicated to the top of the west wall, the temple was built in 1502, and its founders were Coron Demetrios Greek officer in the service of King James II and his wife Elena. Although it is unknown when the church dedicated to the Virgin Mary, called Podithou, it is considered the main church of the monastery of the same name, has ceased to exist in the early XIX century.
The Church is not fully painted murals cover only the outside of the western wall, west wall inside the triangle, the triangle of the eastern wall, the apse and the eastern part of the northern and southern walls. Simultaneously with the creation of murals, was erected and a wooden iconostasis, gilding which was updated in 1783 city In the paintings of Panagia Podithou dated, mainly the beginning of the XV century. Evinces the Italian Renaissance to the exaltation of the image, its monumentality. Images of Christ, the Virgin Mary, the archangels and saints are presented simultaneously sublime and humanity, they are idealized and, at the same time filled with life. Ascetic religious painting gave way to the East is the place bright and cheerful colors of Western painting and its three-dimensional perception of body and space, striving to capture the movement and emotion artistic value of the frescoes is the interweaving of two traditions - Byzantine and Italian Renaissance.
Along with the image of Our Lady of the apse, the scene of the Communion of the Apostles is among the finest examples of Italian-Byzantine school on the island, which appeared in Cyprus in the late XV century, after the Venetians occupied the island in 1489 year. This school has combined classical elements with the peculiarities of the Byzantine tradition of the Italian Renaissance in its Venetian version, combining secular pompous and lofty spirituality.
A special grace of movement marked by the image of Mary in the scene of the Annunciation to the south of the wall of the apse. Seated Mary meets the gospel explosion of emotions swirl twists her body in the S-shaped bend, inherited from the Gothic expression. Unusually fine prescribed folds of his cloak with stars give the image a special charm and make it stand out in a series of iconographic images in the local fresco.
In the spirit of the local traditions of construction covers gable roof of flat tiles.
The temple is under the protection of UNESCO 1985 year.
In the small church of Agia Paraskevi on the old Kakopetria-Galata road frescoes 1514 years.
The Church of Agios Nikolaos tis Stegis (literally "the church of St. Nicholas with a roof") is located in 5 km north of the village of Kakopetria and once belonged to the monastery. Its walls are decorated with paintings fully XI - XVII centuries. It is considered one of the most interesting Byzantine churches on the island. The church got its name from the high, excessively steep wooden roof, which was built in such a way as to protect the church from adverse climatic conditions.
First dvuhkryshnoy Church in Cyprus was the Church of St. Nicholas in Kakopetria (Church of St. Nicholas under the double roof), located south of the village of Kakopetria, at the foot of the Troodos Mountains, built in XI century. in the name of St. Nicholas and the entrance sometime in the monastery complex of the same name.
Church of St. Nicholas under the double roof - is one of the most important religious monuments in Cyprus. The name "St. Nicholas under the double roof" because the temple was erected over the roof to protect it from rain and snow, so frequent in the mountainous region.
The well-preserved to this day the church of St. Nicholas - a typical Byzantine cross-domed church. Restoration work has repeatedly held it for centuries, somewhat changed its original form. At the beginning of the XII century. the cathedral built a narthex, domed, and the end of the century, the temple was covered with a steep gable roof, under which today lies krestovoobrazny vault and dome. The need for additional protection of the church original structure and its unique wall paintings from the damaging effects of snow, rain and wind, so frequent in the highlands, was obvious.
The monastery complex has flourished in the Byzantine period and during the domination of the Frankish kings of Cyprus. The interior of the church - its many ancient murals XI century and a large icon of St. Nicholas XIII c., Donated the temple of Frankish knights and embodying the images themselves and the donors to confirm this. Today, the icon of St. Nicholas on display in the Byzantine Museum Cultural Foundation Archbishop Makarios III in Nicosia. In 1633 year monastic buildings and church have been updated. The last monk, Father Gerasimos died in 1808 was, at the time the property and describe the structure of the monastery, and then rented out, what message is preserved in the old registration books of the Archbishopric of Cyprus.
The monastery was destroyed in the second half of the XIX century, but the monastery church survived. Just south of the church remained small two-story structure, which, in all probability, served as the residence of the last monk. The ruins around the church suggests that his best years in the monastery lived a significant number of monks. On the meadow called "Tomb of the bishops" in which scattered many stones, according to legend, buried the bishops, who died at the hands of the Ottomans. The interior of the church is called the "Museum of Byzantine art." This is one of the few places in Cyprus, where limited space frescoes XI - XVII centuries. The frescoes have been cleared at the initiative of the Department of Antiquities. Several murals have been transferred, and thus were found more ancient frescoes, which were under later, later added the XI century.
XI century paintings preserved in fragments. They stand saturation characteristics, the definition of curly shapes, color palette and severe internal spiritual way. Unfortunately, up to now only a few paintings we survived XI century. These include the traditional image in the apse (altar) of Our Lady surrounded by the archangels Michael and Gabriel, the Transfiguration and the Raising of Lazarus, fragments of a fresco of the Assumption and St. Nicholas, in the left corner which immortalized the image of the donor who paid for its creation. Panoramic composition "Forty Martyrs of Sebaste" dates back to the XII century and is dedicated to the first Christians were martyred. Skillfully using a system of scenic resources, a skilled artist, whose name is unknown to us, was able to vividly recreate a complete picture of the ancient Christian legend.
In the temple, except for the frescoes, and the text is prominent Russian traveler Vasili Barsky, as well as references to persons who have made gifts to the monastery.
The fresco with a rare iconographic type of Saint Mary, breast-feeding the child Divine, written to the right of the iconostasis, was founded in the XIV century. She kept the original color and paint and have never since inception are not restored. Church of the XVII century iconostasis separating the altar area from the whole of the temple, reflected the transition period in the formation of the modern. It combines the various structural elements: already leaving templon with cells for Byzantine icons and wall-barrier with the main icons of Christ and the Virgin Mary, placed on either side of the main entrance to the altar, closed curtain.
With 1985 the church is under the protection of UNESCO.
Today, next to the Church of St. Nicholas are placed buildings residential ensemble of the Archdiocese of Cyprus.


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text: 000 FXUS63 KIND 221813 AFDIND Area Forecast Discussion National Weather Service Indianapolis IN 213 PM EDT Fri Sep 22 2017 .UPDATE... The LONG TERM section has been updated below. && .SYNOPSIS... Issued at 235 AM EDT Fri Sep 22 2017 High pressure is expected across the area through the early parts of next week. A frontal system may affect the area towards the middle of next week. && .NEAR TERM /Rest of Today/... Issued at 1002 AM EDT Fri Sep 22 2017 Warm and hazy morning for most as the region remains firmly under the influence of surface high pressure and ridging aloft. 14Z temperatures had already risen into the mid and upper 70s. Astronomical Fall arrives later this afternoon but it will once again feel like the middle of the summer over central Indiana as the Ohio Valley resides under high pressure at the surface and aloft. Expect a very similar day to Thursday as temperatures will likely peak in the lower 90s in many locations this afternoon. Dewpoints in the upper 60s and lower 70s will once again give max heat indices in the mid and upper 90s. We will be in record watch mode this afternoon with the record high of 93 from 1895 for Indy. While the dry forecast has been maintained for the day with high pressure across the area and the presence of a high-based mid level cap...cannot entirely rule out a stray shower or storm this afternoon with a weakness in the upper ridge drifting southwest near the Ohio River. This mid level feature likely contributed to the isolated storm early this morning across southern Indiana and could see it tapping into the unstable airmass this afternoon to help produce a stray shower or storm over mainly southern counties. Confidence and coverage too low to include a mention in the forecast at this time but will continue to monitor. && .SHORT TERM /Tonight through Sunday night/... Issued at 235 AM EDT Fri Sep 22 2017 Model data suggest strong upper ridging aloft will hold across the local area through the weekend. This will result in dry and warm conditions through the period. Progged low level thicknesses suggest the GFS MOS temperature guidance may be on the cool side over the next couple of days. Will raise the guidance highs and lows a category or so through the period. && .LONG TERM /Monday Night Through Friday/... Issued at 213 PM EDT Fri Sep 22 2017 Models are close enough that the model blend initialization was accepted for most items. Warm conditions will continue early in the long term, then much cooler will move into the area to end the work week. Lingering upper ridging will keep the area dry Tuesday, but the cold front with the much cooler air behind it will move through on Wednesday bringing low chances for showers to parts of the area. Current timing puts the front moving through when there should be little instability, so continued to leave out any mention of thunder. There is still some uncertainty on timing of the front which could have impacts on rain chances if it changes. However, confidence is high for the much cooler air moving in by late next work week. && .AVIATION /Discussion for 221800Z TAF Issuance/... Issued at 1247 PM EDT Fri Sep 22 2017 With the exception of visibility restrictions from fog near daybreak...VFR conditions are anticipated. The region remains under the influence of high pressure aloft and at the surface. The result will be continued dry weather with little in the way of clouds. Despite a mid level cap...presence of strong surface heating and instability will generate some cu in the afternoon today and again on Saturday. Cannot entirely rule out an isolated shower or storm...but the threat is too low to consider for the terminals at this time. Will once again see brief visibility restrictions to IFR and lower at the outlying terminals from localized fog during the predawn hours through daybreak Saturday. Winds will be light and variable through the period. && .IND WATCHES/WARNINGS/ADVISORIES...NONE. && $$ SYNOPSIS...JAS NEAR TERM...Ryan SHORT TERM...JAS LONG TERM....50 AVIATION...Ryan


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Young Sensation Has All The Answers
The hip-hop world is a less than sensible place - lots of times, you're even required to clarify when bad means bad and when bad means good - so once a week we're going to get with a rapper and ask them to explain things. Have something you always wanted to ask a rapper? Email firstname.lastname@example.com.
This Week's Rapper: Young Sensation
This Week's Subject(s): MySpace; Uncle Luke; the Texans; Kanye West
Ask A Rapper: Okay, for this installment, we're going to empty the Ask A Rapper e-mailbag. These are questions that weren't meaty enough to carry an entire segment, but things that people took the time to email/Twitter/text us nonetheless. And you're off...
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Question No. 1: "Why are rappers still the only guys on MySpace anymore? It doesn't make any sense."
AAR: You're still on MySpace, right? Thoughts on this one?
Young Sensation: Man, cause boys tryna get it in. We gotta promo on any site to get notice. [I'm at] www.myspace.com/yungsensation. I got some new songs on there too [laughs].
Question No. 2: "Uncle Luke is coaching high school football now. Is there anything that could be less appropriate than Luke working with kids?"
YS [laughs]: Man, I can't hate on Luke. My major in school is kinesiology, so I am going to be coaching soon too [laughs]. We coach rappers [laughs].
Question No. 3: "What happened to the Texans this season? Weren't they supposed to contend? Why isn't Kubiak fired? And WHY ISN"T KUBIAK FIRED?"
YS: Naw, they gonna be alright, it's just our secondary is not the best. But we will be okay.
Note: Not the best? That's a nice way to put it. Those guys are pretty much the worst secondary in the entire league. It's like they all signed shoe deals with U.S. Concrete, Inc.
Question No. 4: "Did you see that 50 Cent and Soulja Boy were on the cover of XXL? Care to make a joke about that?"
YS: Pretty-boy gangsters [laughs].
Note: It seems like the commentary to make here would be some sort of parallel between 50's career and XXL's, but that'd be an unnecessarily cheap shot.
Question No. 5: "Kanye's album is out and you've written precious little about it. What gives? Is it awful or great?"
YS: Man, it is actually a very good album, but I am more of a College Dropout guy myself. People tell me it's a classic, so I'ono.
Note: It is a classic. Nobody on the planet is touching Kanye right now.
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A Greater Calling
Most who know me are aware of my current life journey. Looking to resolve the past and move forward to a great future. And trying my best to live life to the fullest, while on the journey. We are raised to not question God, whether your God is named Muhammad or Jesus, or Buddha they are considered all-powerful and it is not for us to question. But, I do question. I know my mere mortal mind is not meant to understand, but I do think a lot about life circumstances. I believe in past lives, so I understand we are all on our journey for a reason. I consider my not having children, to be payment for something from my past. Maybe I had children and didn't appreciate them or care for them. Maybe I was abusive to them. There is most certainly a reason for God to put so much pain in my heart. In this life, as in all past, I am paying for the "crimes" of the prior life. I don't want to keep repeating this cycle. Truth be told, I hope to not have to live another life. I feel blessed to have found my soul mate in this life, and although there is much I would like to accomplish, to be on this earth again, is not something I desire to go through. I question the justice in life when people lose their young children, you see the innocence of a life just beginning and you wonder in what way is it fair to snuff out that life? And what are those left on this earth grieving for that loss, supposed to do with this huge hole left in their hearts? What belief system would give them solace? I have never given birth, but I've lost my share of pregnancies and I still wonder what it would have been like, I guess I owe thanks to God for not allowing me to give birth and lose the child, because my psyche wouldn't have handled that! I would have went totally insane, I am sure. And would either be dead, in prison or in a padded room! When my brother died, I went immediately into denial. This year in September marks the 20th anniversary of his death. And over the years I have come to terms with certain details. Much of what I was told was lies, but in searching for the truth, I've dealt with much of it. I still struggle at times with why he died instead of me! My brother had great talent and potential in music and he was so popular, I was practically invisible, so why did he suffer so much? My brother was a schizophrenic, almost certainly! My parents blamed his problems on drugs, and while I am not denying that he may have had dealings in drugs, he was not a drug abuser. His body showed no signs of prolonged drug use and his body parts were made available for donation, and were donated. So, I guess that is part of my journey, trying to rectify what is my life purpose? I am a natural mother, but yet I'm not one! I love animals, yet I have yet to own a ranch. I am charitable, but can't afford to give. I love to write, yet can't afford a literary agent to get manuscripts submitted. I love knowledge, but can't afford college. I know there is a purpose! I am working on it! Getting fit right now for my own health, but also to achieve another goal. Talked with my mate and we are seriously considering joining the National Guard once we think we can pass the fitness test. We haven't checked into it as far as knowing details about age limits or any of that, it's just something we feel passionate about. If we can't join the National Guard, then maybe we'll hook up with the Salvation Army to find out where we can go to help out during disasters (U.S) or things like that. I can't believe that I will NOT accomplish my goals! There isn't room in my life for negative results. I quit my job to achieve my goals. Working crazy hours was not accommodating to living a full life. There was no room for self discovery. Our business has yet to bring in any money, but we both feel we are in the development stage of our business where we are laying the groundwork. So, we're not worried. We probably should be by most people's standards. Could we lose all our belongings and end up on the street….YES! But I do believe it is well worth the gamble. I LOVE my life and I am enjoying the journey. There is no reason to pity me, because I am taking the chance, I am choosing to look for more instead of just allowing myself to be stagnant and settle! It is all so easy, to just say this is my lot in life and settle and not look for more, it is far more brave to take the risk! I look to examples like Picasso, one of the craziest artists of all time! His artwork is sought after and goes for millions! Yet in his lifetime he was a tortured soul, and penniless. I consider the fact that I have had no success, as being in good company! One must maintain a positive attitude while going through life, you can not allow yourself to be beaten down. I may end up leaving this world, accomplishing none of my goals, but I do hope to have done more good than harm. And if I accomplish that, well I can leave with a smile on my face. I will write this novel for my brother this year and I will enter it into the Amazon book contest next year. Will I write anymore after that, I can't be sure. But I will write this, not just for him, but for me. Writing is how I deal with my feelings, its great therapy. You know, I always wanted to be a nun….but I question too much. You have to have blind faith to be a nun. I believe in ALL beliefs, to a certain level. I applaud all those who are strong in their beliefs and convictions. If I was going to become a true believer in something, I would probably study Kabbalah, buddhism or hinduism. Because I am a spiritual person, I have a problem with some of the restrictions of some of the religions. I love the idea of confession, I think it's great to clear your conscience. I'm sure many find comfort in that. So, I am just rambling on. I have to take some time to figure out what I really want to accomplish with my BLOG(s). They say you are not supposed to treat them as a diary. There is supposed to be a theme. So, do I want to write about religion, fiction, poetry, animals, nature, fitness, what? Or do I want to just post pics of artwork and Lisa's photography? Maybe I want to write about Astrology and how it affects your life? I really don't know! I should write about our businesses… Franchise Consulting and being an Amway IBO. But, how much can be said? It's tough! There are things in life you would do if you were single, that once in a committed relationship you can't do. You have to consider the other person and how they feel. Somedays I think I'd like to just pack a backpack full of shit and just start walking and see where I end up! Life is a journey……..


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Stopping Windows Search ServiceBefore beginning the lab, I had to disable the Windows Search Service on this Vista machine. According to one of the lab "instructors", the Windows Vista Search Service was attempting to index the C: on the actual computers on which the labs where running. This made the virtual machines too slow to use.
Bill Detwiler has nothing to disclose. He doesn't hold investments in the technology companies he covers.
Full Bio
Bill Detwiler is Managing Editor of TechRepublic and Tech Pro Research and the host of Cracking Open, CNET and TechRepublic's popular online show. Prior to joining TechRepublic in 2000, Bill was an IT manager, database administrator, and desktop support specialist in the social research and energy industries. He has bachelor's and master's degrees from the University of Louisville, where he has also lectured on computer crime and crime prevention.


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A majority of the 3,400 species of frogs and toads worldwide are found in the tropics. Although Michigan plays host to a handful of these species, they are an important part of the wildlife found in the state. Frogs are extremely vocal during breeding season, which makes them easy to locate. Like the bull frog, the largest of Michigan frogs at 3 to 8 inches, each species is quite identifiable.
Blanchard's Cricket Frog
The Blanchard's cricket frog is only about one inch in length, usually brown or gray with dark bands on its legs, very warty, and quite often has a dark triangle between the eyes. The cricket frog is found in the southern part of the state and the western Lower Peninsula. It lives in the muddy or marshy edges of lakes, bogs and slow-moving bodies of water.
Northern Spring Peeper
This species is distinguishable by the dark brown "X" on its back. They reach 1 to 1 1/2 inches at adulthood and are often found in the soft mud near ponds during the winter. The frog's name derives from the "tinkling bell" call it produces during mating season.
Mink Frog
The mink frog is greenish or brownish. It looks a bit like the green frog, but rather than cross bands on its hind legs it has spots or blotches. Its belly is yellow and its upper lip is bright green. The mink frog is considered medium-sized at 2 to 3 inches in length. Its name comes from the mink-like, musky odor it emits when handled. It is found near permanent bodies of water.
Green Frog
The green frog is large, measuring from 2 1/2 to 4 inches in length. It has a fold of skin that runs from the eardrum down each side of the back. It sometimes has blotchy markings on its back and sides and its belly is white and often spotted with gray. In a male the throat is yellow, and in a female it is white. Its upper lip is green or yellow. The Green Frog is found near lakes, ponds, marshes and wooded swamps.
Gray Tree Frog
The color of the gray tree frog can actually change from gray to green or brown. It has large, sticky toe pads and the underside of its hind legs is yellow. This 1 1/2 to 2-inch long frog is found in swamps, woods and back yards. Because of the sticky toe pads, it is able to climb vertically or move horizontally.
Wood Frog
Found in woodlands and wooded swamps, the wood frog is either tan or brown in color with a dark band running through the eyes and a white stripe across the upper lip. It grows to be 2 to 2 1/2 inches.
Pickerel Frog
The 2 to 3-inch pickerel frog is squarish in shape. The inside of its hind legs is orange or bright yellow. It lives in pollution-free waters like clear ponds, bogs and streams.
Western Chorus Frog
The western chorus frog is small, measuring around 1 to 1 1/2 inches long. It is brownish in color with dark stripes on the back and a dark band that runs from its nose, through its eye, to the top of its front leg. It is generally only seen during breeding season in wet meadows, woodlands and marshes.
Northern Leopard Frog
The northern leopard frog is aptly named for the dark spots or bars that cover its legs and body. The body itself is green, brown or greenish-brown. It has a dark spot above each eye and on the snout. A white line stretches above the upper lip from its nose to shoulder. It is white underneath and grows to 2 to 3 1/2 inches in length. The Northern Leopard Frog is found at lake edges, wet meadows and grassy pond areas, although it may wander away from water sources after breeding season.
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- Photo Credit frog image by Leonie Pratt from Fotolia.com
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text: tag:blogger.com,1999:blog-10718266.post3056184229770845165..comments2017-01-06T15:26:17.094-05:00Comments on The BLAM! Blog: Setting up shop once again on the blogosphereTiny Fredhttp://email@example.com:blogger.com,1999:blog-10718266.post-60253057658466697712009-01-14T10:37:00.000-05:002009-01-14T10:37:00.000-05:00No more bows, they're for wussies, and we ain't wu...No more bows, they're for wussies, and we ain't wussying around anymore. Well, at least, I'm not.Christian Berntsenhttps://email@example.com:blogger.com,1999:blog-10718266.post-50296904869117961382009-01-13T23:41:00.000-05:002009-01-13T23:41:00.000-05:00But have you wrapped it up and put a bow on it? I'...But have you wrapped it up and put a bow on it? I've been wanting to say goodbye to 2005 for awhile now but it keeps stalking me. I can't go over to the left side of my house anymore. 2005 is there and it scares me.Erikhttps://email@example.com