Мазкур илмий мақолада рақамли далиллар тушунчасининг илмий-назарий асослари ҳамда унинг ҳуқуқий табиати таҳлил қилинган. Тадқиқотда “электрон далил” ва “рақамли далил” атамаларига нисбатан миллий ва хорижий олимларнинг қарашлари ўрганилиб, уларнинг ўхшаш ва фарқли жиҳатлари ёритилган. Рақамли далилларнинг суд ва тергов амалиётидаги аҳамияти, уларни йиғиш, сақлаш, текшириш ҳамда баҳолашнинг ўзига хос хусусиятлари очиб берилган. Шунингдек, халқаро стандартлар ва илғор хорижий тажрибалар асосида рақамли далилларнинг ҳуқуқий мақоми таҳлил этилган. Муаллиф томонидан мавжуд илмий ёндашувлар умумлаштирилиб, “рақамли далил” тушунчасига муаллифлик таърифи ишлаб чиқилган. Тадқиқот натижалари рақамли далиллар институтини такомиллаштириш ва уни ҳуқуқни қўллаш амалиётига самарали жорий этишга хизмат қилади.

Мақолада Совет ҳокимиятининг исломга нисбатан сиёса- тининг мураккаб тарихини кузатар эканмиз,биз куч, мафкура ва чидамли- ликнинг таъсирчан ҳикоясини топамиз. Совет Иттифоқи 1917-йилда ташкил топганидан то 1991-йилда парчаланишигача,диннинг роли билан, хусусан, мусулмон аҳолиси контекстида кураш олиб борди. Вақт бўйлаб жараён нафақат давлат томонидан қўлланиладиган ривожланаётган страте гияларни, балки бу сиёсатларнинг мусулмон жамоаларига чуқур таъсирини ва пост- совет ландшафтини шакллантиришда давом этаётган абадий меросни ҳам ёритади. Болшевиклар инқилоби ва унинг дастлабки йиллари ундан кейинги агрессив секуляризация кампанияси учун замин яратилганлиги таҳлил этилган.

Cardiac troponins (cTn), specifically troponin I (cTnI) and troponin T (cTnT), represent the most sensitive and specific biomarkers for myocardial injury. Their measurement has transformed the diagnostic landscape of acute coronary syndromes (ACS), enabling earlier recognition of myocardial infarction (MI), improved risk stratification, and better prognostic modeling. Modern high-sensitivity cardiac troponin (hs-cTn) assays can detect extremely low concentrations, allowing identification of myocardial injury even in subclinical states. This article provides an evidence-based synthesis of the biological basis of troponin release, analytical principles of troponin measurement, diagnostic thresholds, clinical algorithms, and limitations. By integrating data from clinical trials, pathology research, analytical validation studies, and international cardiology guidelines, this review aims to clarify how troponin measurement informs diagnosis and management in diverse clinical settings.

Gastric cancer (GC) remains one of the most significant global health challenges, ranking among the top causes of cancer mortality worldwide. Despite declining incidence in many high-income regions, gastric cancer continues to show substantial geographical variation, with East Asia, Eastern Europe, and parts of Latin America bearing the highest burden. The disease arises from a multifactorial interaction of environmental exposures, chronic infections—especially Helicobacter pylori—dietary habits, genetic predisposition, and socioeconomic determinants. This review synthesizes high-quality epidemiological evidence, incorporating global population-based registries, cohort studies, meta-analyses, and international cancer surveillance data. The article follows a hybrid systematic–narrative design to provide a comprehensive overview of incidence, mortality, risk factors, protective factors, histological patterns, and temporal trends. Special focus is given to the divergent patterns of non-cardia gastric cancer (NCGC) and cardia gastric cancer (CGC), the impact of H. pylori eradication, demographic transitions, and the influence of Western lifestyle patterns. The review highlights the persistent public health importance of gastric cancer and emphasizes that early detection, infection control, dietary modification, and molecularly targeted screening strategies remain essential for reducing disease burden. These findings underscore the need for region-specific preventive policies and strengthened cancer surveillance systems.

Hepatic fibrosis represents a dynamic wound-healing response of the liver that becomes pathologic when injury is persistent. Regardless of the cause—viral hepatitis, alcohol, NASH, autoimmune disease, or toxic injury—the process converges on a final common pathway: activation of hepatic stellate cells (HSCs) into contractile, ECM-producing myofibroblasts. This transition is driven by inflammatory cytokines, oxidative stress, and changes in the extracellular matrix environment. The article describes fibrosis as neither irreversible nor linear. Instead, it is a bidirectional process, where progression and regression depend on the balance between fibrogenic signals and mechanisms that promote matrix degradation. In regression, inactivated HSCs undergo apoptosis, senescence, or reversion to a quiescent phenotype, while matrix-remodelling enzymes reduce the dense collagen network. To build reliable conclusions, the review synthesizes findings from human trials, animal models (such as CCl₄ and bile-duct ligation), and mechanistic in-vitro studies. It selects studies with strong methodological design, appropriate fibrosis staging systems (like METAVIR or Ishak), and validated non-invasive assessment techniques including elastography. Overall, the aim is to integrate experimental and clinical evidence to clarify how fibrosis develops, how it can reverse, and which biological nodes represent the most promising therapeutic targets. The work emphasizes that modern understanding of liver fibrosis has shifted from viewing it as a static, end-stage scarring process to recognizing it as a modifiable, targetable disease state, opening new opportunities for anti-fibrotic therapy and early diagnosis.