Hepatocellular carcinoma (HCC) remains a leading cause of cancer-related deaths worldwide, with poor clinical outcomes due to challenges in early detection and limited efficacy of current treatments such as receptor tyrosine kinase inhibitors and immunotherapy. HCC exhibits significant heterogeneity at both histopathological and molecular levels, complicating its management but offering potential for personalized therapeutic approaches. This review outlines the morpho-molecular heterogeneity of HCC and summarizes various histological subtypes, including steatohepatitic, clear cell, macrotrabecular-massive, scirrhous, lymphocyte-rich, and fibrolamellar HCCs. Each subtype possesses distinct clinical, histological, and molecular features; for instance, steatohepatitic HCC is associated with metabolic dysfunction and shows IL-6/JAK/STAT activation, while clear cell HCCs often have IDH1 mutations and favorable prognosis. The macrotrabecular-massive subtype is linked to poor outcomes and TP53 mutations, whereas scirrhous HCCs express stemness markers and have TSC1/TSC2 mutations. Lymphocyte-rich HCCs are characterized by immune cell infiltration and better prognosis. CTNNB1-mutated HCCs show specific morphological features and may benefit from targeted therapies. Understanding these subtypes and associated molecular alterations is crucial for developing effective diagnostic and therapeutic strategies, including potential predictive biomarkers and personalized treatments. Additionally, the identification of patterns like vessels-encapsulatingtumor-clusters offers prognostic implications and may guide therapeutic decisions. Recent molecular studies have enhanced our comprehension of HCC heterogeneity, laying the groundwork for more personalized approaches. Pathologists play a vital role in recognizing these subtypes, aiding in prognosis prediction and treatment planning. Advances in digital pathology and artificial intelligence may further facilitate biomarker research, ultimately improving patient outcomes in HCC management.

Hepatocellular carcinoma (HCC) remains a leading cause of cancer-related deaths worldwide, with poor clinical outcomes due to challenges in early detection and limited efficacy of current treatments such as receptor tyrosine kinase inhibitors and immunotherapy. HCC exhibits significant heterogeneity at both histopathological and molecular levels, complicating its management but offering potential for personalized therapeutic approaches. This review outlines the morpho-molecular heterogeneity of HCC and summarizes various histological subtypes, including steatohepatitic, clear cell, macrotrabecular-massive, scirrhous, lymphocyte-rich, and fibrolamellar HCCs. Each subtype possesses distinct clinical, histological, and molecular features; for instance, steatohepatitic HCC is associated with metabolic dysfunction and shows IL-6/JAK/STAT activation, while clear cell HCCs often have IDH1 mutations and favorable prognosis. The macrotrabecular-massive subtype is linked to poor outcomes and TP53 mutations, whereas scirrhous HCCs express stemness markers and have TSC1/TSC2 mutations. Lymphocyte-rich HCCs are characterized by immune cell infiltration and better prognosis. CTNNB1-mutated HCCs show specific morphological features and may benefit from targeted therapies. Understanding these subtypes and associated molecular alterations is crucial for developing effective diagnostic and therapeutic strategies, including potential predictive biomarkers and personalized treatments. Additionally, the identification of patterns like vessels-encapsulatingtumor-clusters offers prognostic implications and may guide therapeutic decisions. Recent molecular studies have enhanced our comprehension of HCC heterogeneity, laying the groundwork for more personalized approaches. Pathologists play a vital role in recognizing these subtypes, aiding in prognosis prediction and treatment planning. Advances in digital pathology and artificial intelligence may further facilitate biomarker research, ultimately improving patient outcomes in HCC management.

Hyperbaric oxygen therapy (HBOT) was conducted on two male patients with chronic prostatitis/chronic pelvic pain syndrome who were resistant to conventional medical therapies. Both patients underwent 20 sessions of 100% oxygen inhalation (2.0 atmosphere absolute for 90 min/day, five days/week for four weeks) in a hyperbaric chamber. The follow-up period was three months. Although the patients reported a slight improvement in the pain domain of the National Institutes of Health-Chronic Prostatitis Symptom Index (NIH-CPSI) after HBOT, no changes were noted in the other domains of NIH-CPSI and International Prostate Symptom Score. No adverse events were encountered during or after HBOT.

Hepatocellular carcinoma (HCC) remains a leading cause of cancer-related deaths worldwide, with poor clinical outcomes due to challenges in early detection and limited efficacy of current treatments such as receptor tyrosine kinase inhibitors and immunotherapy. HCC exhibits significant heterogeneity at both histopathological and molecular levels, complicating its management but offering potential for personalized therapeutic approaches. This review outlines the morpho-molecular heterogeneity of HCC and summarizes various histological subtypes, including steatohepatitic, clear cell, macrotrabecular-massive, scirrhous, lymphocyte-rich, and fibrolamellar HCCs. Each subtype possesses distinct clinical, histological, and molecular features; for instance, steatohepatitic HCC is associated with metabolic dysfunction and shows IL-6/JAK/STAT activation, while clear cell HCCs often have IDH1 mutations and favorable prognosis. The macrotrabecular-massive subtype is linked to poor outcomes and TP53 mutations, whereas scirrhous HCCs express stemness markers and have TSC1/TSC2 mutations. Lymphocyte-rich HCCs are characterized by immune cell infiltration and better prognosis. CTNNB1-mutated HCCs show specific morphological features and may benefit from targeted therapies. Understanding these subtypes and associated molecular alterations is crucial for developing effective diagnostic and therapeutic strategies, including potential predictive biomarkers and personalized treatments. Additionally, the identification of patterns like vessels-encapsulatingtumor-clusters offers prognostic implications and may guide therapeutic decisions. Recent molecular studies have enhanced our comprehension of HCC heterogeneity, laying the groundwork for more personalized approaches. Pathologists play a vital role in recognizing these subtypes, aiding in prognosis prediction and treatment planning. Advances in digital pathology and artificial intelligence may further facilitate biomarker research, ultimately improving patient outcomes in HCC management.

Hyperbaric oxygen therapy (HBOT) was conducted on two male patients with chronic prostatitis/chronic pelvic pain syndrome who were resistant to conventional medical therapies. Both patients underwent 20 sessions of 100% oxygen inhalation (2.0 atmosphere absolute for 90 min/day, five days/week for four weeks) in a hyperbaric chamber. The follow-up period was three months. Although the patients reported a slight improvement in the pain domain of the National Institutes of Health-Chronic Prostatitis Symptom Index (NIH-CPSI) after HBOT, no changes were noted in the other domains of NIH-CPSI and International Prostate Symptom Score. No adverse events were encountered during or after HBOT.

Hepatocellular carcinoma (HCC) remains a leading cause of cancer-related deaths worldwide, with poor clinical outcomes due to challenges in early detection and limited efficacy of current treatments such as receptor tyrosine kinase inhibitors and immunotherapy. HCC exhibits significant heterogeneity at both histopathological and molecular levels, complicating its management but offering potential for personalized therapeutic approaches. This review outlines the morpho-molecular heterogeneity of HCC and summarizes various histological subtypes, including steatohepatitic, clear cell, macrotrabecular-massive, scirrhous, lymphocyte-rich, and fibrolamellar HCCs. Each subtype possesses distinct clinical, histological, and molecular features; for instance, steatohepatitic HCC is associated with metabolic dysfunction and shows IL-6/JAK/STAT activation, while clear cell HCCs often have IDH1 mutations and favorable prognosis. The macrotrabecular-massive subtype is linked to poor outcomes and TP53 mutations, whereas scirrhous HCCs express stemness markers and have TSC1/TSC2 mutations. Lymphocyte-rich HCCs are characterized by immune cell infiltration and better prognosis. CTNNB1-mutated HCCs show specific morphological features and may benefit from targeted therapies. Understanding these subtypes and associated molecular alterations is crucial for developing effective diagnostic and therapeutic strategies, including potential predictive biomarkers and personalized treatments. Additionally, the identification of patterns like vessels-encapsulatingtumor-clusters offers prognostic implications and may guide therapeutic decisions. Recent molecular studies have enhanced our comprehension of HCC heterogeneity, laying the groundwork for more personalized approaches. Pathologists play a vital role in recognizing these subtypes, aiding in prognosis prediction and treatment planning. Advances in digital pathology and artificial intelligence may further facilitate biomarker research, ultimately improving patient outcomes in HCC management.

Hyperbaric oxygen therapy (HBOT) was conducted on two male patients with chronic prostatitis/chronic pelvic pain syndrome who were resistant to conventional medical therapies. Both patients underwent 20 sessions of 100% oxygen inhalation (2.0 atmosphere absolute for 90 min/day, five days/week for four weeks) in a hyperbaric chamber. The follow-up period was three months. Although the patients reported a slight improvement in the pain domain of the National Institutes of Health-Chronic Prostatitis Symptom Index (NIH-CPSI) after HBOT, no changes were noted in the other domains of NIH-CPSI and International Prostate Symptom Score. No adverse events were encountered during or after HBOT.

Hyperbaric oxygen therapy (HBOT) was conducted on two male patients with chronic prostatitis/chronic pelvic pain syndrome who were resistant to conventional medical therapies. Both patients underwent 20 sessions of 100% oxygen inhalation (2.0 atmosphere absolute for 90 min/day, five days/week for four weeks) in a hyperbaric chamber. The follow-up period was three months. Although the patients reported a slight improvement in the pain domain of the National Institutes of Health-Chronic Prostatitis Symptom Index (NIH-CPSI) after HBOT, no changes were noted in the other domains of NIH-CPSI and International Prostate Symptom Score. No adverse events were encountered during or after HBOT.

Background: Femoral neck fractures need to be treated in their early stages with accurate reduction and stable fixation to reduce complications. The authors compared the early radiologic outcomes of femoral neck fractures treated with the recently introduced Femoral Neck System (FNS, Depuy-Synthes) with conventional cannulated screws (CS) in a multicenter design. Furthermore, the factors associated with early failure after FNS were analyzed. Methods: The FNS group included 40 patients treated between June 2019 and January 2020, and the CS group included 65 patients treated between January 2015 and May 2019. The operation was performed in 3 university hospitals. Patient demographics, fracture classification, postoperative reduction quality, sliding distance of FNS or CS, union and time to union, and complication rates were examined. Logistic regression analysis was performed on candidate factors for early failure of the FNS group. Results: The FNS group had a 90% union rate and a mean time to union of 4.4 months, while the CS group had similar results with an 83.1% union rate and a mean time to union of 5.1 months. In the subgroup analysis of Pauwels type III fractures, the union rates were 75.0% and 58.8% in the FNS and CS groups, respectively, and the time to union was significantly shorter in the FNS group with 4.8 months compared to 6.8 months in the CS group. Early failure rate within 6 months of FNS fixation was observed to be 10%, which included 3 reduction failures and 1 excessive sliding with a broken implant. Risk factors for early failure after FNS were identified as displaced fractures (Garden classification type III or IV), poor reduction quality, longer tip-apex distance, greater sliding distance, and 1-hole implants, of which sliding distance was the only significant risk factor in multivariate analysis. Conclusions In femoral neck fractures, FNS and CS did not show significant differences for short-term radiologic results. FNS resulted in shorter operative time than cannulated screw fixation and favorable outcomes in Pauwels type III femoral neck fractures.The FNS could be considered a reliable and safe alternative to CS when treating femoral neck fractures.

Background: Nonalcoholic steatohepatitis (NASH) is a liver disease caused by obesity that leads to hepatic lipoapoptosis, resulting in fibrosis and cirrhosis. However, the mechanism underlying NASH is largely unknown, and there is currently no effective therapeutic agent against it. DWN12088, an agent used for treating idiopathic pulmonary fibrosis, is a selective prolyl-tRNA synthetase (PRS) inhibitor that suppresses the synthesis of collagen. However, the mechanism underlying the hepatoprotective effect of DWN12088 is not clear. Therefore, we investigated the role of DWN12088 in NASH progression. Methods: Mice were fed a chow diet or methionine-choline deficient (MCD)-diet, which was administered with DWN12088 or saline by oral gavage for 6 weeks. The effects of DWN12088 on NASH were evaluated by pathophysiological examinations, such as real-time quantitative reverse transcription polymerase chain reaction, immunoblotting, biochemical analysis, and immunohistochemistry. Molecular and cellular mechanisms of hepatic injury were assessed by in vitro cell culture. Results: DWN12088 attenuated palmitic acid (PA)-induced lipid accumulation and lipoapoptosis by downregulating the Rho-kinase (ROCK)/AMP-activated protein kinase (AMPK)/sterol regulatory element-binding protein-1c (SREBP-1c) and protein kinase R-like endoplasmic reticulum kinase (PERK)/α subunit of eukaryotic initiation factor 2 (eIF2α)/activating transcription factor 4 (ATF4)/C/EBP-homologous protein (CHOP) signaling cascades. PA increased but DWN12088 inhibited the phosphorylation of nuclear factor-κB (NF-κB) p65 (Ser536, Ser276) and the expression of proinflammatory genes. Moreover, the DWN12088 inhibited transforming growth factor β (TGFβ)-induced pro-fibrotic gene expression by suppressing TGFβ receptor 1 (TGFβR1)/Smad2/3 and TGFβR1/glutamyl-prolyl-tRNA synthetase (EPRS)/signal transducer and activator of transcription 6 (STAT6) axis signaling. In the case of MCD-diet-induced NASH, DWN12088 reduced hepatic steatosis, inflammation, and lipoapoptosis and prevented the progression of fibrosis. Conclusion Our findings provide new insights about DWN12088, namely that it plays an important role in the overall improvement of NASH. Hence, DWN12088 shows great potential to be developed as a new integrated therapeutic agent for NASH.