Background/Objectives: Non-small-cell lung cancer (NSCLC) frequently metastasizes to the brain, significantly impacting patient prognosis and quality of life. Anlotinib, a novel tyrosine kinase inhibitor, has shown promise in treating NSCLC with brain metastasis. So, we aimed to evaluate the clinical efficacy of anlotinib and various types of radiotherapy combinations used to treat NSCLC patients with brain metastasis regarding overall survival and the treatment of internal and external lesions. Methods: A comprehensive literature search was conducted in the databases PubMed, Scopus, WoS, MedLine, and Cochrane Library up to April 2024. Studies assessing the efficacy of anlotinib combined with whole-brain radiotherapy (WBRT), stereotactic radiosurgery (SRS), or other radiotherapy modalities in NSCLC patients with brain metastasis were included. The primary outcomes were (a) the efficacy of anlotinib and radiotherapy on the intracranial lesions and OS and (b) the effectiveness of combined anlotinib and radiotherapy versus radiotherapy alone in NSCLC patients with brain metastasis. The secondary outcome was the efficacy of anlotinib and radiotherapy on extracranial progression. We used a combination of keywords and MeSH terms including ‘non-small cell lung cancer’ OR ‘NSCLC’, ‘brain metastases’, ‘anlotinib’, ‘radiotherapy’, ‘radiation therapy’, and ‘combined treatment’, among others. Boolean operators (AND, OR) were applied as appropriate to optimize the search strategy across databases. Results: Nine studies met the inclusion criteria, comprising 210 patients in the combination group and 228 patients in the radiotherapy alone group. The combination of anlotinib with radiotherapy showed a significant improvement in iPFS compared to radiotherapy alone, with a pooled risk ratio (RR) for iORR of 1.18 (95% CI: 1.00–1.39) and a pooled SMD for OS of 0.03 (95% CI: −0.29, 0.36). Radiotherapy combined with anlotinib also demonstrated enhanced intracranial and extracranial control rates. Conclusions: Anlotinib combined with radiotherapy, especially WBRT, offers a promising treatment strategy for NSCLC patients with brain metastasis, improving intracranial control. Further large-scale randomized controlled trials are needed to confirm these findings and optimize treatment protocols.

The human gut microbiome comprises a diverse community of bacteria whose interactions with the host range from beneficial mutualism to opportunistic pathogenicity. These interactions are shaped by genomic plasticity and ecological pressures that influence whether microbes support host health, remain conditionally harmless, or contribute to disease. Understanding the mechanisms underlying these shifts is essential for clarifying the balance between cooperation and pathogenicity within the gut ecosystem. This review explores the genomic and evolutionary mechanisms that shape microbial adaptation across the mutualism–pathogenicity spectrum in the human gut. Key processes, including horizontal gene transfer (HGT), host-mediated selection, and niche specialization, enable microbes to acquire, regulate, or retain traits that influence colonization, metabolic function, and virulence. These adaptive mechanisms allow gut bacteria to respond dynamically to ecological pressures such as inflammation, antibiotic exposure, and dietary change, resulting in context-dependent microbial behaviors. The review also considers how concepts from insect endosymbiosis may provide insight into gut microbial adaptation. While both systems exhibit host specialization, major differences in transmission mode, ecological flexibility, and genome evolution limit direct comparisons. Rather than following a fixed progression toward parasitism, gut microbes exhibit flexible adaptive strategies shaped by host and environmental conditions. By integrating ecological and evolutionary perspectives, this review presents a balanced framework for understanding how genomic adaptation influences microbial behavior in the gut. This perspective improves our understanding of dysbiosis and microbial pathogenesis and may support the development of microbiome-informed therapeutic strategies for maintaining host health.

Cardiovascular disease (CVD) is increasingly recognized as a significant comorbidity in people living with HIV (PWH), contributing to increased morbidity and mortality. Epidemiological studies indicate that PWH have a 1.2–2-fold higher risk of myocardial infarction (MI) and other CVD events compared to HIV-negative individuals. While the mechanisms underlying HIV-associated CVD are not fully understood, they are likely to include a combination of cardiovascular-related adverse effects of HIV medications, vascular dysfunction caused by HIV-induced monocyte activation, and cytokine secretion, in addition to existing comorbidities and lifestyle choices. This comprehensive review examines the complex relationship between HIV infection and CVD, highlighting key pathophysiological mechanisms such as chronic immune activation, inflammation, endothelial dysfunction, and the role of antiretroviral therapy (ART) in promoting cardiovascular risk. Alongside conventional risk factors such as smoking, hypertension, and dyslipidemia, HIV-specific elements, especially metabolic abnormalities associated with ART, significantly contribute to the development of CVD. Prevention strategies are crucial, focusing on the early identification and management of cardiovascular risk factors as well as optimizing ART regimens to minimize adverse metabolic effects. Clinical guidelines now recommend routine cardiovascular risk assessment in PWH, emphasizing aggressive management tailored to their unique health profiles. However, challenges exist in fully understanding the cardiovascular outcomes in this population. Future research directions include exploring the role of inflammation-modulating therapies and refining sustainable prevention strategies to mitigate the growing burden of CVD in PWH.

Background/Objectives: Type 2 diabetes mellitus (T2DM) is increasingly recognized as a contributor to skeletal fragility despite patients often having a normal or even elevated bone mineral density (BMD), a phenomenon described as the “T2DM bone paradox.” This study aimed to use DEXA screening to explore how metabolic and demographic factors, particularly body mass index (BMI), age, sex, and glycated hemoglobin (HbA1c), influence Bone Mineral Density (BMD) among Saudi adults, a population where diabetes and obesity are highly prevalent. Methods: A retrospective cross-sectional study was conducted among 89 adults (mean age 61.1 years; 82% female) who underwent dual-energy X-ray absorptiometry (DEXA) at King Fahad Specialist Hospital in Tabuk, Saudi Arabia. Bone mineral density was evaluated at the lumbar spine, femoral neck, and total hip. Correlation and multiple regression analyses were conducted to assess how age, sex, body mass index (BMI), and glycated hemoglobin (HbA1c) were related to BMD T-scores. Results: The prevalence of osteopenia and osteoporosis was 43.8% and 23.6%, respectively, with women and older adults showing the highest rates of low bone mass. Participants had a mean age of 61.1 ± 12.1 years, average BMI of 32 kg/m², and mean HbA1c of 6.6 ± 1.8%. Females showed slightly lower T-scores at all skeletal sites compared with males (lumbar spine −1.81 vs. −1.55; femoral neck −1.15 vs. −0.76; total hip −0.62 vs. −0.12), indicating greater bone loss in women. BMI was consistently and positively associated with BMD across all skeletal sites (p < 0.05), whereas age and female sex were negative predictors at the femoral neck and hip. HbA1c showed a paradoxical positive relationship with BMD at weight-bearing sites, reflecting the complexity of metabolic effects on bone quality. The models explained up to 28% of the variance in BMD. Conclusions: Individuals with higher level BMI tended to have better bone mass, while older age and female sex were related to decreased BMD. The positive association between HbA1c and BMD supports the concept of the “diabetic bone paradox” and emphasizes the value of combining the evaluation of both metabolic and skeletal factors when assessing fracture risk in Middle Eastern populations.

Human metapneumovirus or HMPV is an important respiratory pathogen of public health significance that primarily affects the immunocompromised, the very old, and young infants. However, recent studies have long since dispelled the idea that healthy adults are not at risk for serious sequelae, though it seems that HMPV has a particular affinity to infect children rather than adults. HMPV was first identified in 2001 and is implicated in a range of respiratory illnesses, from less severe upper respiratory infections to more severe pneumonia. This review compiles the recent literature on the epidemiology, molecular virology, and clinical characteristics of HMPV with an emphasis on, importantly, the virus’s significant contribution to respiratory morbidity and the requirement for better diagnostic capabilities and public health measures against this very much underappreciated viral pathogen.