A significant portion of newly diagnosed lung cancer cases occurs in populations exposed to air pollution. The World Health Organization has identified air pollution as a human carcinogen, prompting many countries to implement monitoring systems for ambient particulate matter (PM). PM is composed of a complex mixture of organic and inorganic particles, both solid and liquid, that are found in the air. Given the carcinogenic properties of PM and the high prevalence of lung cancer among exposed populations, exploring their connection and clinical implications is critical for effectively preventing lung cancer in this group. This review explores the relationship between ambient PM and lung cancer. Epidemiological studies have demonstrated a dose-response relationship between PM exposure and lung cancer risk. PM exposure induces oxidative stress, disrupts the body’s redox balance, and causes DNA damage, which is a crucial factor in cancer development. Recent findings on the strong correlation between ambient PM and adenocarcinoma highlight the importance of understanding the specific molecular and pathological mechanisms underlying pollution-related lung cancer. In addition to efforts to control emission sources at the international level, a more individualized approach is essential for preventing PM-related lung cancer.

A significant portion of newly diagnosed lung cancer cases occurs in populations exposed to air pollution. The World Health Organization has identified air pollution as a human carcinogen, prompting many countries to implement monitoring systems for ambient particulate matter (PM). PM is composed of a complex mixture of organic and inorganic particles, both solid and liquid, that are found in the air. Given the carcinogenic properties of PM and the high prevalence of lung cancer among exposed populations, exploring their connection and clinical implications is critical for effectively preventing lung cancer in this group. This review explores the relationship between ambient PM and lung cancer. Epidemiological studies have demonstrated a dose-response relationship between PM exposure and lung cancer risk. PM exposure induces oxidative stress, disrupts the body’s redox balance, and causes DNA damage, which is a crucial factor in cancer development. Recent findings on the strong correlation between ambient PM and adenocarcinoma highlight the importance of understanding the specific molecular and pathological mechanisms underlying pollution-related lung cancer. In addition to efforts to control emission sources at the international level, a more individualized approach is essential for preventing PM-related lung cancer.

A significant portion of newly diagnosed lung cancer cases occurs in populations exposed to air pollution. The World Health Organization has identified air pollution as a human carcinogen, prompting many countries to implement monitoring systems for ambient particulate matter (PM). PM is composed of a complex mixture of organic and inorganic particles, both solid and liquid, that are found in the air. Given the carcinogenic properties of PM and the high prevalence of lung cancer among exposed populations, exploring their connection and clinical implications is critical for effectively preventing lung cancer in this group. This review explores the relationship between ambient PM and lung cancer. Epidemiological studies have demonstrated a dose-response relationship between PM exposure and lung cancer risk. PM exposure induces oxidative stress, disrupts the body’s redox balance, and causes DNA damage, which is a crucial factor in cancer development. Recent findings on the strong correlation between ambient PM and adenocarcinoma highlight the importance of understanding the specific molecular and pathological mechanisms underlying pollution-related lung cancer. In addition to efforts to control emission sources at the international level, a more individualized approach is essential for preventing PM-related lung cancer.

A significant portion of newly diagnosed lung cancer cases occurs in populations exposed to air pollution. The World Health Organization has identified air pollution as a human carcinogen, prompting many countries to implement monitoring systems for ambient particulate matter (PM). PM is composed of a complex mixture of organic and inorganic particles, both solid and liquid, that are found in the air. Given the carcinogenic properties of PM and the high prevalence of lung cancer among exposed populations, exploring their connection and clinical implications is critical for effectively preventing lung cancer in this group. This review explores the relationship between ambient PM and lung cancer. Epidemiological studies have demonstrated a dose-response relationship between PM exposure and lung cancer risk. PM exposure induces oxidative stress, disrupts the body’s redox balance, and causes DNA damage, which is a crucial factor in cancer development. Recent findings on the strong correlation between ambient PM and adenocarcinoma highlight the importance of understanding the specific molecular and pathological mechanisms underlying pollution-related lung cancer. In addition to efforts to control emission sources at the international level, a more individualized approach is essential for preventing PM-related lung cancer.

A significant portion of newly diagnosed lung cancer cases occurs in populations exposed to air pollution. The World Health Organization has identified air pollution as a human carcinogen, prompting many countries to implement monitoring systems for ambient particulate matter (PM). PM is composed of a complex mixture of organic and inorganic particles, both solid and liquid, that are found in the air. Given the carcinogenic properties of PM and the high prevalence of lung cancer among exposed populations, exploring their connection and clinical implications is critical for effectively preventing lung cancer in this group. This review explores the relationship between ambient PM and lung cancer. Epidemiological studies have demonstrated a dose-response relationship between PM exposure and lung cancer risk. PM exposure induces oxidative stress, disrupts the body’s redox balance, and causes DNA damage, which is a crucial factor in cancer development. Recent findings on the strong correlation between ambient PM and adenocarcinoma highlight the importance of understanding the specific molecular and pathological mechanisms underlying pollution-related lung cancer. In addition to efforts to control emission sources at the international level, a more individualized approach is essential for preventing PM-related lung cancer.

Fungal sinusitis is relatively rare, but it has become more common in recent years. When fungal sinusitis invades the orbit, it can cause proptosis, chemosis, ophthalmoplegia, retroorbital pain, and vision impairment. We present a case of an extensive orbital floor defect due to invasive fungal sinusitis. A 62-year-old man with hypertension and a history of lung adenocarcinoma, presented with right-side facial pain and swelling. On admission, the serum glucose level was 347 mg/dL, and hemoglobin A1c was 11.4%. A computed tomography scan and a Waters’ view X-ray showed right maxillary sinusitis with an orbital floor defect. On hospital day 3, functional endoscopic sinus surgery was performed by the otorhinolaryngology team, and an aspergilloma in necrotic inflammatory exudate obtained during exploration. On hospital day 7, orbital floor reconstruction with a Medpor Titan surgical implant was done. In principle, the management of invasive sino- orbital fungal infection often begins with surgical debridement and local irrigation with an antifungal agent. Exceptionally, in this case, debridement and immediate orbital floor reconstruction were performed to prevent enophthalmos caused by the extensive orbital floor defect. The patient underwent orbital floor reconstruction and received intravenous and oral voriconazole. Despite orbital invasion, there were no ophthalmic symptoms or sequelae.

Objective: Bipolar disorder displays a spectrum of manifestations, including manic, hypomanic, depressive, mixed, psychotic, and atypical episodes, contributing to its chronic nature and association with heightened suicide risk. Creating effective pharmacotherapy guidelines is crucial for managing bipolar disorder and reducing its prevalence. Treatment algorithms grounded in science have improved symptom management, but variations in recommended medications arise from research differences, healthcare policies, and cultural nuances globally. Methods: This study compares Korea’s bipolar disorder treatment algorithm with guidelines from the UK, Australia, and an international association. The aim is to uncover disparities in key recommended medications and their underlying factors. Differences in CYP450 genotypes affecting drug metabolism contribute to distinct recommended medications. Variances also stem from diverse guideline development approaches—expert consensus versus metaanalysis results—forming the primary differences between Korea and other countries. Results: Discrepancies remain in international guidelines relying on meta-analyses due to timing and utilized studies. Drug approval speeds further impact medication selection. However, limited high-quality research results are the main cause of guideline variations, hampering consistent treatment conclusions. Conclusion Korea’s unique Delphi-based treatment algorithm stands out. To improve evidence-based recommendations, large-scale studies assessing bipolar disorder treatments for the Korean population are necessary. This foundation will ensure future recommendations are rooted in scientific evidence.

Objective: This study investigated whether sleep and stress mutually interact to induce changes in white matter integrity. Methods: Diffusion tensor imaging (DTI) was conducted on 36 participants (male=22, female=14; mean age=38.33±12.78 years). Participants were divided into three groups depending on their sleep quality and stress levels: poor sleepers with stress, poor sleepers without stress, and good sleepers. Sleep quality and stress level were evaluated using the Pittsburgh Sleep Quality Index and the Life Experiences Survey, respectively. Fractional anisotropy (FA) values were calculated employing DTI tractography. Results: After controlling for age and sex, poor sleepers with stress exhibited a lower FA of the left inferior cerebellar peduncle (ICP) than did poor sleepers without stress (t=2.81, p=0.02). Poor sleepers without stress showed a higher FA of the right middle longitudinal fasciculus (MdLF) than did good sleepers (t=3.35, p=0.006). Conclusion The current study reports the effects of sleep, stress, and their interaction on the white matter integrities of the ICP and MdLF. ICP change seems to be associated with sleep disturbances related to stress, while MdLF change would be associated with sleep disturbances unrelated to stress.

Background and Objectives: This study aimed to investigate the protective effect of polydeoxyribonucleotide (PDRN) against skin flap necrosis in a murine skin flap model.Materials and Method Twenty mice with rectangular skin flaps on the dorsum were randomly divided into the PDRN (n=10) and pentobarbital sodium (PBS) (n=10) injection groups. PDRN (8 mg/kg) was subdermally injected at 12 different points immediately after the operation. After 7 days, the flap perfusions were evaluated using a laser speckle contrast imaging (LSCI) system, and specimens were collected for immunohistochemistry analysis. Results: The percentage of survival area relative to the total flap area was significantly higher in the PDRN group (60.87%±7.63%) than in the PBS group (45.23%±10.72%) (p<0.05). The mean LSCI perfusion signal of the distal part of the skin flap in the PBS group was 0.57±0.12, and that in the PDRN group was 0.74±0.13 (p<0.05). The PDRN group had a significantly lower interleukin 1 beta expression than the PBS group and higher vascular endothelial growth factor α expression than the PBS group (p<0.05). Conclusion These findings suggest that subdermally injected PDRN is more effective in enhancing flap survival during necrosis.