Ask about this productRelated genes to: PMCH Blocking Peptide
- Gene:
- PMCH NIH gene
- Name:
- pro-melanin concentrating hormone
- Previous symbol:
- -
- Synonyms:
- MCH
- Chromosome:
- 12q23.2
- Locus Type:
- gene with protein product
- Date approved:
- 1991-11-08
- Date modifiied:
- 2015-11-23
Related products to: PMCH Blocking Peptide
Related articles to: PMCH Blocking Peptide
- Snakebite envenoming remains a significant yet neglected public health problem in tropical countries, particularly in rural South Asia. This study aimed to identify demographic characteristics, management practices, and the determinants of poor treatment outcomes among snakebite patients in Sindh, Pakistan. A prospective cohort study was conducted at Peoples Medical College Hospital (PMCH), Shaheed Benazirabad, Sindh, Pakistan, from July 1, 2023, to June 30, 2024. A non-probability purposive sampling technique was used for data collection, and all consecutive patients presenting with confirmed or suspected snakebite were included. Data were collected through a validated study tool on demographics, pre-hospital management, hospital care, and treatment outcomes. Categorical variables were tested with the Chi-square test, and Kaplan-Meier survival analysis was used to test the effect of exposure-to-reporting time and hospital stay time on outcomes using IBM SPSS V29. A total of 320 patients were included; 74.7% were male, and 98.4% were from rural areas. Most victims were aged 20-29 years (31.9%) and engaged in farming or manual labor (67.2%). Nearly half (49.7%) of the bites occurred during summer. Delayed hospital presentation was common, with 22.8% arriving after six hours of the bite. The overall poor-outcome rate was 10.9%, and mortality was 1.9%. A significant association was found between exposure-to-reporting time ( = 0.040) and hospital stay duration ( < 0.001) with treatment outcomes. Delayed presentation to the hospital and prolonged hospitalization were major predictors of poor outcomes following snakebite. Strengthening emergency referral systems, ensuring timely antivenom availability, and promoting community awareness are essential to reduce morbidity and mortality in snakebite-endemic regions of Pakistan. - Source: PubMed
Publication date: 2026/04/10
Kumar NarendarIshaqui Azfar AtharRajpoot Pushp LataMaqsood Muhammad BilalSultana RaziaKhaskheli Muhammad SalehIqbal AdnanTabassum ShahidaMuhammad Shaib - Chronic stress is a pivotal risk factor for the etiology of anxiety disorders. However, the molecular maladaptations within the medial amygdala (MeA) remain insufficiently characterized. Here, we investigated the MeA transcriptomic landscape to elucidate mechanisms underlying stress-induced anxiety and identify potential therapeutic targets. We established a mouse model using a 10-day chronic restraint stress paradigm, which resulted in robust anxiety-like phenotypes validated by multiple behavioral tests. RNA sequencing identified 193 differentially expressed genes. Bioinformatic analyses revealed a dominant upregulation of endoplasmic reticulum (ER) protein processing and chaperone-mediated refolding. This indicates a coordinated transcriptional upregulation of endoplasmic reticulum proteostasis components, consistent with an adaptive response to proteotoxic stress. Beyond proteostasis, the MeA transcriptome exhibited significant transcriptional reprogramming in neuroactive ligand-receptor interactions, synaptic organization, and lipid metabolism. Network analysis further pinpointed two functional modules: a highly connected ER chaperone hub centered on Hspa5 (BiP) and a neuropeptide signaling cluster involving Nms, Kng2, Agt, and Pmch. Importantly, site-specific pharmacological inhibition of Hspa5 within the MeA successfully attenuated CRS-induced anxiety-like behaviors. Collectively, these findings demonstrate that chronic stress orchestrates extensive transcriptomic reprogramming in the MeA characterized by the recruitment of proteostasis mechanisms and neuropeptide reorganization. Our study highlights Hspa5-mediated regulation as a promising mechanistic target with functional/causal evidence for the treatment of anxiety disorders. - Source: PubMed
Publication date: 2026/03/31
Hu ShengruZhang ZixuLi HaoTian YihanXie WeiMu Mingdao - To study the prevalence of LV systolic dysfunction measured using GLS in patients of CKD with normal LVEF and correlation of GLS with the biochemical parameters and to determine the incidence of all-cause mortality and its correlation with GLS. - Source: PubMed
Publication date: 2025/12/11
Kumar MuneshwarSingh SatyajitSingh Rathore VinayKumar Naik SurendraKumar AbhishekThakur Chandra PrakashVarshney Amratansh - Clinical case reports have linked isotretinoin to depressive symptoms. As acne incidence peaks in adolescence, we focused on adolescent exposure. However, prior studies on isotretinoin's effects in adolescents have yielded inconsistent results, and direct mechanistic evidence remains scarce. Here, we analyzed depressive-like behaviors in adolescent mice treated with isotretinoin. Pathological changes in the prefrontal cortex and hippocampus of isotretinoin-treated mice were observed. We characterized the metabolic and gene-expression signatures of the hippocampus and prefrontal cortex in isotretinoin-treated mice using RNA sequencing and untargeted metabolomics. The results show that isotretinoin induced depressive- and anxiety-like behaviors and caused significant pathological changes in the hippocampus and prefrontal cortex. In the prefrontal cortex, two differentially expressed genes (Nmb and Pmch) within the neuroactive ligand-receptor interaction pathway correlated positively with depressive-like behaviors; in the hippocampus, two genes (Pomc and Gh) within the same pathway correlated with anxiety-like behaviors. Six differential metabolites associated with the neuroactive ligand-receptor interaction pathway - Adenosine (hippocampus); Tyramine, Taurine, N-acetylaspartylglutamic Acid (NAAG), and ADP (prefrontal cortex); and Taurine (serum) - were associated with depressive-like behaviors. Taurine in the prefrontal cortex was also associated with anxiety-like behaviors. Finally, we reanalyzed metabolomics data from depressed patients to determine whether plasma Taurine levels are elevated. Our findings clarified the biological mechanisms underlying isotretinoin-induced depression and highlighted the neuroactive ligand-receptor interaction pathway, especially four genes (Nmb and Pmch in the prefrontal cortex; Pomc and Gh in the hippocampus) and one metabolite (Taurine in the prefrontal cortex) as potential targets for mitigating isotretinoin-induced depression and anxiety. - Source: PubMed
Publication date: 2025/11/20
Ren YiRen ZheZhao ShuangWu WentaoWang JiaolinHe FeiZhong QiZhang HanpingChen JianjunXu KeXie Peng - - Source: PubMed
Publication date: 2025/11/03
Rani JyotsnaSharma SushmitaDubey Sunita