Coexisting Sickle Cell Anemia and Sarcoidosis: A Management Conundrum!

Sickle cell disease and Sarcoidosis are conditions that are more common in the African American population. In this report we share an unfortunate patient who had hepatic sarcoidosis but could not receive steroids since that precipitated acute liver failure. We have discussed potential therapy options but we need more options that improve mortality

IMPLEMENTASI WSN DENGAN PLUG AND PLAY SENSOR PADA TAMBAK UDANG VANNAMEI

Salah satu yang harus diperhatikan dalam budidaya udang vannamei adalah kualitas air. Kualitas air ini harus dicek secara berkala karena akan berpengaruh kepada kelulushidupan udang. Parameter-parameter yang mempengaruhi kualitas air tambak udang vannamei adalah keasaman (pH), Oksigen terlarut (DO), Salinitas (TDS), suhu air, ketinggian air, dan kekeruhan air. Data kualitas air tambak udang dapat dikirimkan secara wireless dan sensor dapat disebar keseluruh tambak dengan jenis sensor yang berbeda pada setiap nodenya. Node sensor akan mengirimkan hasil pembacaan dari masing masing sensor yang terpasang ke gateway dan kemudian dikirimkan dan diolah di server. Hal ini memudahkan pemilik tambak dalam mengakses data sensor dikarenakan udang vannamei sensitif terhadap perubahan kualitas air sehingga dengan ini bisa dilakukan tanggapan ketika data kualitas air tambak udang vannamei berubah. Untuk mengatasi hal tersebut maka dikembangkan alat WSN dengan plug dan play sensor. Alat WSN terdiri dari integrasi sensor keasaman (pH), Oksigen terlarut (DO), Salinitas (TDS), suhu air, ketinggian air, dan kekeruhan air (Turbidity) dengan topologi bintang. Hasil penelitian menunjukkan bahwa pada jarak 50 meter alat dapat mengirim data 250 byte ke server dalam rentang waktu dari 100 sampai 790 mikrodetik dengan protokol esp-now. Selanjutnya nilai kesalahan pembacaan sensor dalam rentang 0% - 4%

Post-Acute Sequelae of COVID-19 (PASC): Association with Inflammation and Autoimmunity

It has become increasingly evident that a high percentage of patients that recover from acute COVID-19 infection continue to suffer from a variety of persistent symptoms even months after viral clearance, the most common ones being fatigue, dyspnea, anosmia, dysgeusia, cognitive dysfunction, and psychological problems, including anxiety and depression. This syndrome, known as Post-acute sequelae of COVID-19 (PASC), can severely affect the life quality and represents an important health care concern. The exact causes for the symptoms observed in patients with PASC remain to be adequately characterized, but are likely to be associated with multiple factors, including residual disease and/or inflammation, organ damage, effects of hospitalization and/or prolonged ventilation, as well as effects of social isolation and stress. This mini-review discusses evidence that may link both inflammatory and auto-immune processes in the pathophysiology of PASC

Eosinophilic Heart Disease: A Case Report and Review of Literature (Poster).

Hypereosinophilic syndrome is a rare condition and present with nonspecific symptoms. Literature is limited. The involvement of myocardium has some peculiar features. Use of different diagnostic techniques such as echocardiography and MRI can help make the diagnosis of hypereosinophilic syndrome. We are presenting a case with review of the topic

Dermatologic Manifestations of Rheumatic Disease: Cutaneous Manifestations of Vasculitides

Cutaneous Manifestations of Vasculitides is a Powerpoint based learning module that begins with the definition of terms and findings often found in vasculitis, followed by a review of several systemic vasculitides, highlighting how characteristic cutaneous lesions may be predictive of the vessel of involvement as well as the associated histologic changes. Moreover, significant clinical and laboratory findings utilized to make the correct diagnosis will be emphasized. This module is not meant to be an exhaustive review of vasculitis, but to serve as an introduction to understanding disease processes and how systemic vasculitis and skin findings interrelate. It is part of the Dermatologic Manifestations of Rheumatic Disease project, which provides overviews of the identification, diagnosis, and workup for different rheumatologic diseases, with a focus on providing examples from persons of color (POC). The project is a tailored resource for medical learners that addresses a longstanding educational deficit in diverse representation. The OERs will enable us to train future physicians who are not only clinically astute, but also knowledgeable of and sensitive to inequities in healthcare. Ultimately, it is our hope that these OER will aid in fostering a generation of physicians who are truly patient-advocates

Perspectives on Adipose Tissue, Chagas Disease and Implications for the Metabolic Syndrome

The contribution of adipose tissue an autocrine and endocrine organ in the pathogenesis of infectious disease and metabolic syndrome is gaining attention. Adipose tissue and adipocytes are one of the major targets of T. cruzi infection. Parasites are detected 300 days postinfection in adipose tissue. Infection of adipose tissue and cultured adipocytes triggered local expression of inflammatory mediators resulting in the upregulation of cytokine and chemokine levels. Adipose tissue obtained from infected mice display an increased infiltration of inflammatory cells. Adiponectin, an adipocyte specific protein, which exerts antiinflammatory effects, is reduced during the acute phase of infection. The antiinflammatory regulator peroxisome proliferator activated receptor-γ (PPAR-γ) is downregulated in infected cultured adipocytes and adipose tissue. T. cruzi infection is associated with an upregulation of signaling pathways such as MAPKs, Notch and cyclin D, and reduced caveolin-1 expression. Adiponectin null mice have a cardiomyopathy and thus we speculate that the T. cruzi-induced reduction in adiponectin contributes to the T. cruzi-induced cardiomyopathy. While T. cruzi infection causes hypoglycemia which correlates with mortality, hyperglycemia is associated with increased parasitemia and mortality. The T. cruzi-induced increase in macrophages in adipose tissue taken together with the reduction in adiponectin and the associated cardiomyopathy is reminiscent of the metabolic syndrome

Trypanosoma cruzi Utilizes the Host Low Density Lipoprotein Receptor in Invasion

Trypanosoma cruzi, an intracellular protozoan parasite that causes Chagas disease in humans and results in the development of cardiomyopathy, is a major health problem in endemic areas. This parasite can invade a wide variety of mammalian cells. The mechanisms by which these parasites invade their host cells are not completely understood. Our study highlights, for the first time, that the Low Density Lipoprotein receptor (LDLr) is important in the invasion and the subsequent fusion of the parasitophorous vacuole with host lysosomes. We demonstrate that T. cruzi directly binds to LDLr, and inhibition or disruption of LDLr significantly decreases parasite entry. Additionally, we have determined that this cross-linking triggers the accumulation of LDLr and phosphotidylinositol phosphates in coated pits, which initiates a signaling cascade that results in the recruitment of lysosomes, possibly via the sorting motif in the cytoplasmic tail of LDLr, to the site of adhesion/invasion. Studies of infected CD1 mice demonstrate that LDLs accumulate in infected heart and that LDLr co-localize with internalized parasites. Overall, this study demonstrates that LDLr and its family members, engaged mainly in lipoprotein transportation, are also involved in T. cruzi entry into host cells and this interaction likely contributes to the progression of chronic cardiomyopathy

Thromboxane A2 is a key regulator of pathogenesis during Trypanosoma cruzi infection

Chagas' disease is caused by infection with the parasite Trypanosoma cruzi. We report that infected, but not uninfected, human endothelial cells (ECs) released thromboxane A2 (TXA2). Physical chromatography and liquid chromatography-tandem mass spectrometry revealed that TXA2 is the predominant eicosanoid present in all life stages of T. cruzi. Parasite-derived TXA2 accounts for up to 90% of the circulating levels of TXA2 in infected wild-type mice, and perturbs host physiology. Mice in which the gene for the TXA2 receptor (TP) has been deleted, exhibited higher mortality and more severe cardiac pathology and parasitism (fourfold) than WT mice after infection. Conversely, deletion of the TXA2 synthase gene had no effect on survival or disease severity. TP expression on somatic cells, but not cells involved in either acquired or innate immunity, was the primary determinant of disease progression. The higher intracellular parasitism observed in TP-null ECs was ablated upon restoration of TP expression. We conclude that the host response to parasite-derived TXA2 in T. cruzi infection is possibly an important determinant of mortality and parasitism. A deeper understanding of the role of TXA2 may result in novel therapeutic targets for a disease with limited treatment options

Chk1 phosphorylation of Metnase enhances DNA repair but inhibits replication fork restart

Chk1 both arrests replication forks and enhances repair of DNA damage by phosphorylating downstream effectors. Although there has been a concerted effort to identify effectors of Chk1 activity, underlying mechanisms of effector action are still being identified. Metnase (also called SETMAR) is a SET and transposase domain protein that promotes both DNA double-strand break (DSB) repair and restart of stalled replication forks. In this study, we show that Metnase is phosphorylated only on Ser495 (S495) in vivo in response to DNA damage by ionizing radiation. Chk1 is the major mediator of this phosphorylation event. We had previously shown that wild-type (wt) Metnase associates with chromatin near DSBs and methylates histone H3 Lys36. Here we show that a Ser495Ala (S495A) Metnase mutant, which is not phosphorylated by Chk1, is defective in DSB-induced chromatin association. The S495A mutant also fails to enhance repair of an induced DSB when compared with wt Metnase. Interestingly, the S495A mutant demonstrated increased restart of stalled replication forks compared with wt Metnase. Thus, phosphorylation of Metnase S495 differentiates between these two functions, enhancing DSB repair and repressing replication fork restart. In summary, these data lend insight into the mechanism by which Chk1 enhances repair of DNA damage while at the same time repressing stalled replication fork restart. Oncogene (2012) 31, 4245-4254; doi:10.1038/onc.2011.586; published online 9 January 2012NIH [CA92111, CA151367, NIDDK 1 T32 DK 0719-15, R01 GM084020, R01 CA100862, R01 CA102283, R01 HL075783, R01 CA139429]IU Cancer CenterWalther Oncology CenterAPRC [CA100862]Leukemia and Lymphoma Society SCOR [7388-06