Be Hero For Zero Tuberculosis: Peran Remaja Melalui SIKRIBO dalam Mewujudkan "End TB": Be Hero for Zero Tuberculosis: The Role of Youth Through Sikribo in Realizing “End TB”

The TB case notification rate (CNR) in Semarang City has decreased from 2019 of 258 per 100,000 population to 155 per 100,000 population in 2020. The main focus in controlling tuberculosis cases is case detection in the community. The purpose was to increase TB knowledge and provide training on TB screening methods to adolescent cadres using the SIKRIBO application. The methods used in this community service are health education and Training of Trainers (ToT). The participants were 27 adolescent representatives from the Adolescent Integrated Healthcare Center working areas of the Sekaran Public Health Center, Semarang City. The results showed that adolescent cadres' average score knowledge about tuberculosis disease and screening improves after receiving TB health education and adolescent cadres can operate the application properly. The SIKRIBO application can be a means to facilitate the discovery of TB suspects in the community and is expected to be applied in various health facilities.   ABSTRAK Angka notifikasi kasus (CNR) TB di Kota Semarang mengalami penurunan dari tahun 2019 sebesar 258 per 100.000 penduduk menjadi 155 per 100.000 penduduk pada tahun 2020. Fokus utama dalam mengendalikan kasus TB merupakan penemuan kasus di masyarakat. Rendahnya penemuan kasus TB berdampak pada tingginya angka penularan TB. Tujuan pengabdian masyarakat ini untuk meningkatkan pengetahuan TB dan memberi pelatihan terkait cara skrining TB melalui aplikasi SIKRIBO pada kader remaja. Metode yang digunakan pada pengabdian masyarakat ini adalah penyuluhan kesehatan dan Training of Trainer (ToT). Jumlah partisipan sebanyak 27 remaja perwakilan dari Posyandu Remaja dan Posyandu Pesantren wilayah Puskesmas Sekaran, Kota Semarang. Hasil kegiatan bahwa terdapat peningkatan rata-rata skor pengetahuan terkait penyakit TB dan skrining TB pada kader remaja setelah diberi penyuluhan kesehatan TB dan kader remaja dapat mengoperasikan aplikasi SIKRIBO dengan baik. Aplikasi SIKRIBO dapat menjadi sarana untuk mempermudah penemuan suspek TB di masyarakat dan diharapkan dapat diterapkan di berbagai fasilitas kesehatan

The Combination of Alcohol and Cigarette Smoke Induces Endoplasmic Reticulum Stress and Cell Death in Pancreatic Acinar Cells

Background & aimsSmoking, an independent risk factor for pancreatitis, accelerates the development of alcoholic pancreatitis. Alcohol feeding of mice induces up-regulation of spliced X-box binding protein 1 (XBP1s), which regulates the endoplasmic reticulum (ER) unfolded protein response and promotes cell survival upon ER stress. We examined whether smoking affects the adaptive mechanisms induced by alcohol and accelerates disorders of the ER in pancreatic acinar cells.MethodsWe studied the combined effects of ethanol (EtOH) and cigarette smoke extract (CSE) on ER stress and cell death responses in mouse and human primary acini and the acinar cell line AR42J. Cells were incubated with EtOH (50 mmol/L), CSE (20-40 μg/mL), or both (CSE+EtOH), and analyzed by immunoblotting, quantitative reverse-transcription polymerase chain reaction, and cell death assays. Some cells were incubated with MKC-3946, an inhibitor of endoplasmic reticulum to nucleus signaling 1 (ERN1, also called IRE1) that blocks XBP1s formation. Male Sprague-Dawley rats were fed isocaloric amounts of an EtOH-containing (Lieber-DeCarli) or control diet for 11 weeks and exposed to cigarette smoke or room air in an exposure chamber for 2 hours each day. During the last 3 weeks, a subset of rats received intravenous injections of lipopolysaccharide (LPS, 3 mg/kg per week) to induce pancreatitis or saline (control). Pancreatic tissues were collected and analyzed by histology and immunostaining techniques.ResultsIn AR42J and primary acini, CSE+EtOH induced cell death (necrosis and apoptosis), but neither agent alone had this effect. Cell death was associated with a significant decrease in expression of XBP1s. CSE+EtOH, but neither agent alone, slightly decreased adenosine triphosphate levels in AR42J cells, but induced oxidative stress and sustained activation (phosphorylation) of eukaryotic translation initiation factor 2 alpha kinase 3 (EIF2AK3, also called PERK) and increased protein levels of DNA damage inducible transcript 3 (DDIT3, also called CHOP). CHOP regulates transcription to promote apoptosis. Incubation of AR42J or primary mouse or human acinar cells with MKC-3946 reduced expression of XBP1s, increased levels of CHOP, and induced cell death. In rats fed an EtOH diet, exposure to cigarette smoke increased ER stress in acinar cells and sensitized the pancreas to LPS-induced pathology.ConclusionsCigarette smoke promotes cell death and features of pancreatitis in EtOH-sensitized acinar cells by suppressing the adaptive unfolded protein response signaling pathway. It also activates ER stress pathways that promote acinar cell death