A lightweight CNN model for pepper leaf disease recognition in a human palm background.

The identification of pepper leaf diseases is crucial for ensuring the safety and quality of pepper yield. However, existing methods heavily rely on manual diagnosis, resulting in inefficiencies and inaccuracies. In this study, we propose a lightweight convolutional neural network (CNN) model for recognizing pepper leaf diseases and subsequently develop an application based on this model. To begin with, we acquired various images depicting healthy leaves as well as leaves affected by viral diseases, brown spots, and leaf mold. It is noteworthy that these images were captured against a background of human palms, which is commonly encountered in field conditions. The proposed CNN model adopts the GGM-VGG16 architecture, incorporating Ghost modules, global average pooling, and multi-scale convolution. Following training with the collected image dataset, the model was deployed on a mobile terminal, where an application for pepper leaf disease recognition was developed using Android Studio. Experimental results indicate that the proposed model achieved 100 % accuracy on images with a human palm background, while also demonstrating satisfactory performance on images with other backgrounds, achieving an accuracy of 87.38 %. Furthermore, the developed application has a compact size of only 12.84 MB and exhibits robust performance in recognizing pepper leaf diseases.

Experimental Study of Thermal Runaway Process of 18650 Lithium-Ion Battery.

This study addresses the effects of the SOC (State of Charge) and the charging-discharging process on the thermal runaway of 18650 lithium-ion batteries. A series of experiments were conducted on an electric heating and testing apparatus. The experimental results indicate that 6 W is the critical heating power for 40% SOC. With a 20 W constant heating rate, the thermal runaway initial temperature of the lithium-ion battery decreases with the increasing SOC. The final thermal runaway temperature increases with the SOC when the SOC is lower than 80%. However, a contrary conclusion was obtained when the SOC was higher than 80%. Significant mass loss, accompanied by an intense exothermic reaction, took place under a higher SOC. The critical charging current, beyond which the thermal runaway occurs, was found to be 2.6 A. The thermal runaway initial temperature decreases with the increasing charging current, while the intensity of the exothermic reaction varies inversely. Mass ejection of gas and electrolytes exists during thermal runaway when the charging current is higher than 10.4 A, below which only a large amount of gas is released. The thermal runaway initial temperature of discharging is higher than that of non-discharging.

Duplication of MER115 on chromosome 4 in patients with primary biliary cirrhosis.

BACKGROUND: Primary biliary cirrhosis (PBC) is a complex disease with genetic and environmental influences. The disease is more prevalent in families with PBC and candidate gene case-control studies have linked PBC with DRB1(*)08 human leucocyte antigen class II alleles. AIMS: The goal of this study was to characterize a MER115 intergenic region on chromosome 4 as a putative genetic variant associated with PBC. METHODS/RESULTS: This region was incidentally identified during investigations to discover candidate microbial agents using representational difference analysis (RDA) with liver samples from patients with PBC and primary sclerosing cholangitis (PSC). blast search analysis of all the RDA products from the PBC liver revealed genomic sequences, whereas Escherichia coli, mycoplasma and hepatitis B virus DNA were found in the PSC liver. We identified one of the PBC RDA products as an ancestral repeat, referred to as MER115. Southern blot analysis with the PBC product uncovered a restriction fragment length polymorphism in PBC patients' liver. Southern blot hybridization signal showed increased signal intensity in PBC vs. control patients' DNA (P<0.005) and slot blot hybridization studies confirmed a copy number variation of the MER115 in hepatic DNA of PBC vs. control patients (P=0.02). CONCLUSIONS: Further comparative genetic studies will be required to determine the extent of genomic duplication associated with MER115 and provide data on the possible copy number variants of genes close to this intergenic region in patients with PBC.

Ascitic fluid lactoferrin for diagnosis of spontaneous bacterial peritonitis.

BACKGROUND & AIMS: The diagnosis of spontaneous bacterial peritonitis (SBP) is based on a manual count of ascitic fluid polymorphonuclear cells (PMNs). This procedure is operator-dependent and lysis of PMNs during transport to the laboratory may lead to false-negative results. Furthermore, ascitic fluid culture is insensitive and leads to delays in diagnosis. The aim of this study was to assess the utility of ascitic fluid lactoferrin (AFLAC) for the diagnosis of SBP and to identify a cut-off level that can be used for future development of a rapid bedside test. METHODS: A total of 218 consecutive ascites samples from 148 patients (1-8 samples per patient) with cirrhosis at 2 tertiary care medical centers were examined for PMN count, bedside culture, and lactoferrin concentration. AFLAC concentrations were determined using a polyclonal antibody-based enzyme-linked immunosorbent assay. An ascitic fluid PMN count of 250 cells/mL or greater with or without a positive culture was used for diagnosis of SBP. RESULTS: Twenty-two (10.1%) samples fulfilled diagnostic criteria for SBP. Samples with SBP had a significantly higher lactoferrin concentration (median, 3744 ng/mL; 25th-75th percentiles [P25-P75], 788-9617) compared with non-SBP samples (median, 31 ng/mL; P25-P75, 12-67; P < .001). By using a cut-off level of 242 ng/mL, the sensitivity and specificity of the assay for diagnosis of SBP were 95.5% and 97%, respectively. The area under the receiver operating characteristic curve was 0.98. CONCLUSIONS: AFLAC can serve as a sensitive and specific test for diagnosis of SBP. Qualitative bedside assays for the measurement of AFLAC can be developed easily and may serve as a rapid and reliable screening tool for SBP in patients with cirrhosis.

Intramuscular hepatitis B immunoglobulin (HBIG) and nucleosides for prevention of recurrent hepatitis B following liver transplantation: comparison with other HBIG regimens.

UNLABELLED: High titer hepatitis B immunoglobulin (HBIG) has significantly reduced the recurrence of hepatitis B virus (HBV) infection after liver transplantation. We compared our experience with intramuscular (IM) HBIG prophylaxis to our earlier outcomes with intravenous (IV) HBIG and other regimens. METHODS: One hundred and twenty-three patients with acute or chronic hepatitis B underwent liver transplant at the Baylor Regional Transplant Center between July 1985 and July of 2005. Of these, 63 (43%) received long-term low-dose IM (n = 17) or high-dose IV (n = 46) HBIG. All patients in IM group also received a nucleoside before and after transplant. These patients were compared with those transplanted earlier who received either no prophylaxis (n = 16) or HBIG on day zero and one only (n = 44). RESULTS: HBV recurrence was significantly lower in patients who received long-term HBIG [9/38 (23.7%) for IV and 1/17 (5.9%) for IM] compared with patients who received no treatment (8/11; 72.7%) or only two doses of HBIG (32/40; 80.0%). Two-yr actuarial survivals were 89%, 88%, 54%, and 64%, respectively. Patients on long-term HBIG by either parenteral route survived as well as patients transplanted for other indications. Post-transplant recurrence of hepatitis B in the long-term HBIG groups was usually controlled by intensifying antiviral therapy. CONCLUSION: Long-term low-dose IM and high-dose IV HBIG are equally efficacious with similar survival and early hepatitis recurrence rates. Graft loss is usually avoidable when recurrence is discovered early and aggressively treated. The IM route is preferable to IV administration due to its ease of administration and lower cost.

Living donor liver transplantation for hepatitis C-related cirrhosis: no difference in histological recurrence when compared to deceased donor liver transplantation recipients.

The question of possible earlier and more aggressive recurrence of hepatitis C virus (HCV) infection after living donor liver transplantation (LDLT) compared to deceased donor liver transplantation (DDLT) remains unanswered. To address this issue we retrospectively reviewed virological, histological, and clinical data in 67 patients (52 DDLT and 15 LDLT) who underwent liver transplant for their HCV-related cirrhosis since April 2001. Our data indicate that there is no statistical difference between LDLT and DDLT groups in mean age, Child-Turcotte-Pugh score, model for end-stage liver disease score, and gender distribution. The mean follow-up was 749 +/- 371 days in LDLT and 692 +/- 347 days in DDLT. The predominant genotype in the LDLT and DDLT are genotype 1 (LDLT, 91%; DDLT, 70%). All patients with histologically confirmed recurrent HCV had detectable HCV-RNA in serum. The histological recurrence rate of hepatitis C was 58% at 4 months, 90% at 1 year, and 100% at 2 years in LDLT patients vs. 71% at 4 months, 94% at 1 year, and 95% at 2 years in DDLT patients (not significant) Comparison of the activity of inflammation and fibrosis score at all time points failed to show a statistical difference. Kaplan-Meier survival analysis showed similar patient and graft survival rates between the 2 groups. Our data indicate that histological recurrence of HCV is an early event and virtually universal 2 years' posttransplantation, regardless of modality of donor procurement.

Hepatic B-cell non-Hodgkin's lymphoma of MALT type in the liver explant of a patient with chronic hepatitis C infection.

B-cell non-Hodgkin's lymphoma (B-NHL) is a well-documented complication of hepatitis C virus (HCV) infection. Marginal zone (mucosa-associated lymphoid tissue; MALT) lymphomas constitute a less common type of B-NHL. In this article, we report a case of liver MALT in a cirrhotic patient, incidentally discovered after liver transplantation (LT). We discuss pertinent diagnostic and management strategies in this clinical setting.

Does lamivudine prophylaxis eradicate persistent HBV DNA from allografts derived from anti-HBc-positive donors?

Transplantation of livers from anti-hepatitis B core antibody (anti-HBc)-positive donors into anti-HBc-negative recipients is associated with a high rate of viral transmission. We report a prophylaxis regimen based on virologic evaluation of the donor. Liver and serum from hepatitis B surface antigen (HBsAg)-negative, anti-HBc-positive donors were evaluated by polymerase chain reaction (PCR) for hepatitis B virus (HBV) DNA. All anti-HBc-negative recipients were given a single dose of hepatitis B immunoglobulin (HBIG) during the anhepatic phase of transplantation and were placed on maintenance lamivudine monotherapy. Recipients were followed up longitudinally monitoring intrahepatic HBV DNA as well as serologic HBsAg and HBV DNA by PCR. Between January 1999 and August 2001, 14 anti-HBc-negative recipients received liver transplants from anti-HBc-positive donors. All donor serum was negative for HBV DNA. In total, nine of 14 (64%) livers had detectable HBV DNA; 1 patient was initially PCR-negative and low levels of HBV DNA were detected in a posttransplantation liver biopsy. Mean follow-up was 33 months (range, 22 to 51), and patient and graft survival were each 93%. One case of de novo hepatitis B occurred in a patient noncompliant with lamivudine, although all other serial serum HBsAg assay results were negative. Single-dose HBIG followed by maintenance lamivudine monotherapy prevented de novo hepatitis B in compliant patients. For the cohort of compliant patients that were initially HBV DNA-positive, 7 of 8 (88%) now have undetectable virus in the hepatic allograft by PCR analysis. Nevertheless, there is no evidence to suggest that viral eradication occurs. Accordingly, all patients are maintained on continued lamivudine prophylaxis.

Does a betaretrovirus infection trigger primary biliary cirrhosis?

Patients with primary biliary cirrhosis develop progressive ductopenia associated with the production of antimitochondrial antibodies that react with a protein aberrantly expressed on biliary epithelial cells and peri-hepatic lymph nodes. Although no specific microbe has been identified, it is thought that an infectious agent triggers this autoimmune liver disease in genetically predisposed individuals. Previous serologic studies have provided evidence to suggest a viral association with primary biliary cirrhosis. Here we describe the identification of viral particles in biliary epithelium by electron microscopy and the cloning of exogenous retroviral nucleotide sequences from patients with primary biliary cirrhosis. The putative agent is referred to as the human betaretrovirus because it shares close homology with the murine mammary tumor virus and a human retrovirus cloned from breast cancer tissue. In vivo, we have found that the majority of patients with primary biliary cirrhosis have both RT-PCR and immunohistochemistry evidence of human betaretrovirus infection in lymph nodes. Moreover, the viral proteins colocalize to cells demonstrating aberrant autoantigen expression. In vitro, we have found that lymph node homogenates from patients with primary biliary cirrhosis can induce autoantigen expression in normal biliary epithelial cells in coculture. Normal biliary epithelial cells also develop the phenotypic manifestation of primary biliary cirrhosis when cocultivated in serial passage with supernatants containing the human betaretrovirus or the murine mammary tumor virus, providing a model to test Koch's postulates in vitro.