An inertial range length scale in structure functions

It is shown using experimental and numerical data that within the traditional inertial subrange defined by where the third order structure function is linear that the higher order structure function scaling exponents for longitudinal and transverse structure functions converge only over larger scales, $r>r_S$, where $r_S$ has scaling intermediate between $\eta$ and $\lambda$ as a function of $R_\lambda$. Below these scales, scaling exponents cannot be determined for any of the structure functions without resorting to procedures such as extended self-similarity (ESS). With ESS, different longitudinal and transverse higher order exponents are obtained that are consistent with earlier results. The relationship of these statistics to derivative and pressure statistics, to turbulent structures and to length scales is discussed.Comment: 25 pages, 9 figure

Local properties of extended self-similarity in 3D turbulence

Using a generalization of extended self-similarity we have studied local scaling properties of 3D turbulence in a direct numerical simulation. We have found that these properties are consistent with lognormal-like behavior of energy dissipation fluctuations with moderate amplitudes for space scales $r$ beginning from Kolmogorov length $\eta$ up to the largest scales, and in the whole range of the Reynolds numbers: $50 \leq R_{\lambda} \leq 459$. The locally determined intermittency exponent $\mu(r)$ varies with $r$; it has a maximum at scale $r=14 \eta$, independent of $R_{\lambda}$.Comment: 4 pages, 5 figure

Strong Universality in Forced and Decaying Turbulence

The weak version of universality in turbulence refers to the independence of the scaling exponents of the $n$th order strcuture functions from the statistics of the forcing. The strong version includes universality of the coefficients of the structure functions in the isotropic sector, once normalized by the mean energy flux. We demonstrate that shell models of turbulence exhibit strong universality for both forced and decaying turbulence. The exponents {\em and} the normalized coefficients are time independent in decaying turbulence, forcing independent in forced turbulence, and equal for decaying and forced turbulence. We conjecture that this is also the case for Navier-Stokes turbulence.Comment: RevTex 4, 10 pages, 5 Figures (included), 1 Table; PRE, submitte

Amylase α-2A Autoantibodies: Novel Marker of Autoimmune Pancreatitis and Fulminant Type 1 Diabetes

OBJECTIVE— The pathogenesis of autoimmune pancreatitis (AIP) and fulminant type 1 diabetes remains unclear, although it is known that immune-mediated processes severely compromise the endocrine and exocrine functions in both diseases

BHLHA15-Positive Secretory Precursor Cells Can Give Rise to Tumors in Intestine and Colon in Mice

Background & Aims: The intestinal epithelium is maintained by long-lived intestinal stem cells (ISCs) that reside near the crypt base. Above the ISC zone, there are short-lived progenitors that normally give rise to lineage-specific differentiated cell types but can dedifferentiate into ISCs in certain circumstances. However, the role of epithelial dedifferentiation in cancer development has not been fully elucidated. Methods: We performed studies with Bhlha15-CreERT, Lgr5-DTR-GFP, Apc flox/flox , LSL-Notch (IC), and R26-reporter strains of mice. Some mice were given diphtheria toxin to ablate Lgr5-positive cells, were irradiated, or were given 5-fluorouracil, hydroxyurea, doxorubicin, or dextran sodium sulfate to induce intestinal or colonic tissue injury. In intestinal tissues, we analyzed the fate of progeny that expressed Bhlha15. We used microarrays and reverse-transcription PCR to analyze gene expression patterns in healthy and injured intestinal tissues and in tumors. We analyzed gene expression patterns in human colorectal tumors using The Cancer Genome Atlas data set. Results: Bhlha15 identified Paneth cells and short-lived secretory precursors (including pre-Paneth label-retaining cells) located just above the ISC zone in the intestinal epithelium. Bhlha15 + cells had no plasticity after loss of Lgr5-positive cells or irradiation. However, Bhlha15 + secretory precursors started to supply the enterocyte lineage after doxorubicin-induced epithelial injury in a Notch-dependent manner. Sustained activation of Notch converts Bhlha15 + secretory precursors to long-lived enterocyte progenitors. Administration of doxorubicin and expression of an activated form of Notch resulted in a gene expression pattern associated with enterocyte progenitors, whereas only sustained activation of Notch altered gene expression patterns in Bhlha15 + precursors toward those of ISCs. Bhlha15 + enterocyte progenitors with sustained activation of Notch formed intestinal tumors with serrated features in mice with disruption of Apc. In the colon, Bhlha15 marked secretory precursors that became stem-like, cancer-initiating cells after dextran sodium sulfate–induced injury, via activation of Src and YAP signaling. In analyses of human colorectal tumors, we associated activation of Notch with chromosome instability-type tumors with serrated features in the left colon. Conclusions: In mice, we found that short-lived precursors can undergo permanent reprogramming by activation of Notch and YAP signaling. These cells could mediate tumor formation in addition to traditional ISCs

Gallbladder adenocarcinoma with human chorionic gonadotropin: a case report and review of literature

<p>Abstract</p> <p>Background</p> <p>The case of adenocarcinoma with human chorionic gonadtropin (HCG), primary in the male gallbladder, is extremely rare. A Medline search has shown only a few similar cases reported.</p> <p>Methods</p> <p>We herein describe a case of primary gallbladder adenocarcinoma associated by ectopic HCG positive tumor cells in a 79-year-old male.</p> <p>Results</p> <p>Pathological examination showed a mixture of moderately and poorly differentiated adenocarcinoma with ectopic HCG and placental alkaline phosphatase (PlAP) in tumor cells, though the increase of serum or urinary HCG secretion was not confirmed. The literatures were also reviewed.</p> <p>Conclusions</p> <p>A case of gallbladder cancer with ectopic HCG production is quite rare in the literature, though many similar cases in other site, especially in GI tract, are reported. Embryological consideration suggests the increased frequency of similar cases more than being thought now.</p

Quantitative Analysis of Viral Load per Haploid Genome Revealed the Different Biological Features of Merkel Cell Polyomavirus Infection in Skin Tumor

Merkel cell polyomavirus (MCPyV) has recently been identified in Merkel cell carcinoma (MCC), an aggressive cancer that occurs in sun-exposed skin. Conventional technologies, such as polymerase chain reaction (PCR) and immunohistochemistry, have produced conflicting results for MCPyV infections in non-MCC tumors. Therefore, we performed quantitative analyses of the MCPyV copy number in various skin tumor tissues, including MCC (n = 9) and other sun exposure-related skin tumors (basal cell carcinoma [BCC, n = 45], actinic keratosis [AK, n = 52], Bowen’s disease [n = 34], seborrheic keratosis [n = 5], primary cutaneous anaplastic large-cell lymphoma [n = 5], malignant melanoma [n = 5], and melanocytic nevus [n = 6]). In a conventional PCR analysis, MCPyV DNA was detected in MCC (9 cases; 100%), BCC (1 case; 2%), and AK (3 cases; 6%). We then used digital PCR technology to estimate the absolute viral copy number per haploid human genome in these tissues. The viral copy number per haploid genome was estimated to be around 1 in most MCC tissues, and there were marked differences between the MCC (0.119–42.8) and AK (0.02–0.07) groups. PCR-positive BCC tissue showed a similar viral load as MCC tissue (0.662). Immunohistochemistry with a monoclonal antibody against the MCPyV T antigen (CM2B4) demonstrated positive nuclear localization in most of the high-viral-load tumor groups (8 of 9 MCC and 1 BCC), but not in the low-viral-load or PCR-negative tumor groups. These results demonstrated that MCPyV infection is possibly involved in a minority of sun-exposed skin tumors, including BCC and AK, and that these tumors display different modes of infection