Liver cancer in Hidalgo State, Mexico: analysis of the status, risk factors and regional public health policy requirements: a cross-sectional correlational study

ABSTRACT BACKGROUND: In Latin America, liver cancer is one of the top causes of cancer mortality. It is the fifth most common cause of death among malignant tumors in Mexico and is the leading cause in Hidalgo State (43.8% of the population living in poverty). OBJECTIVE: To conduct a correlational analysis on the main risk factors for liver cancer in Hidalgo State, Mexico, including municipal disaggregation and comparison with the national level. DESIGN AND SETTING: Cross-sectional, correlational, descriptive and comparative epidemiological study using Mexican governmental databases covering 1990-2019. METHODS: A comprehensive review of the databases of the General Directorate of Health Information (DGIS) was performed to analyze official death figures, hospital discharges and national and municipal population projections, using specific search criteria defined in the Global Burden of Disease classification, based on the risk factors for liver cancer. RESULTS: Liver cancer rates showed an evident rise in Hidalgo (183%), moving from 21st place in Mexico in 1990 to 9th place in 2019. This increase was correlated with alcoholism. An increasing trend for liver cancer deaths, of 133.89%, is projected for 2030. Females and the population over 60 years of age are more affected. There are some critical regions with liver cancer death rates twice the national rate or more. CONCLUSION: Targeted effective public health strategies should be structured by identifying, characterizing and regionalizing critical marginalized municipalities that are vulnerable to alcoholism and other risk factors for liver cancer. This approach may be helpful for other states in Mexico or similar countries.

Liver cancer in Hidalgo State, Mexico: analysis of the status, risk factors and regional public health policy requirements: a cross-sectional correlational study.

BACKGROUND: In Latin America, liver cancer is one of the top causes of cancer mortality. It is the fifth most common cause of death among malignant tumors in Mexico and is the leading cause in Hidalgo State (43.8% of the population living in poverty). OBJECTIVE: To conduct a correlational analysis on the main risk factors for liver cancer in Hidalgo State, Mexico, including municipal disaggregation and comparison with the national level. DESIGN AND SETTING: Cross-sectional, correlational, descriptive and comparative epidemiological study using Mexican governmental databases covering 1990-2019. METHODS: A comprehensive review of the databases of the General Directorate of Health Information (DGIS) was performed to analyze official death figures, hospital discharges and national and municipal population projections, using specific search criteria defined in the Global Burden of Disease classification, based on the risk factors for liver cancer. RESULTS: Liver cancer rates showed an evident rise in Hidalgo (183%), moving from 21st place in Mexico in 1990 to 9th place in 2019. This increase was correlated with alcoholism. An increasing trend for liver cancer deaths, of 133.89%, is projected for 2030. Females and the population over 60 years of age are more affected. There are some critical regions with liver cancer death rates twice the national rate or more. CONCLUSION: Targeted effective public health strategies should be structured by identifying, characterizing and regionalizing critical marginalized municipalities that are vulnerable to alcoholism and other risk factors for liver cancer. This approach may be helpful for other states in Mexico or similar countries.

Isolation, identification and molecular docking as cyclooxygenase (COX) inhibitors of the main constituents of Matricaria chamomilla L. extract and its synergistic interaction with diclofenac on nociception and gastric damage in rats.

Chamomile (Matricaria chamomilla L., Asteraceae) is a medicinal plant widely used as remedy for pain and gastric disorders. The association of non-steroidal anti-inflammatory drugs (NSAIDs) with medicinal plant extracts may increase its antinociceptive activity, permit the use of lower doses and limit side effects. The aim was to isolate and identify the main chemical constituents of Matricaria chamomilla ethanolic extract (MCE) as well as to explore their activity as cyclooxygenase (COX) inhibitors in silico; besides, to examine the interaction between MCE and diclofenac on nociception in the formalin test by isobolographic analysis, and to determine the level of gastric injury in rats. Three terpenoids, α-bisabolol, bisabolol oxide A, and guaiazulene, were isolated and identified by (1)H NMR. Docking simulation predicted COX inhibitory activity for those terpenoids. Diclofenac, MCE, or their combinations produced an antinociceptive effect. The sole administration of diclofenac and the highest combined dose diclofenac-MCE produced significant a gastric damage, but that effect was not seen with MCE alone. An isobologram was constructed and the derived theoretical ED35 for the antinociceptive effect was significantly different from the experimental ED35; hence, the interaction between diclofenac and MCE that mediates the antinociceptive effect is synergist. The MCE contains three major terpenoids with plausible COX inhibitory activity in silico, but α-bisabolol showed the highest affinity. Data suggest that the diclofenac-MCE combination can interact at the systemic level in a synergic manner and may have therapeutic advantages for the clinical treatment of inflammatory pain.

Histamine augments beta2-adrenoceptor-induced cyclic AMP accumulation in human prostate cancer cells DU-145 independently of known histamine receptors.

Androgen-independent prostate cancer cells DU-145 express a number of G protein-coupled receptors, including histamine H1 receptors. There is evidence for the presence of beta-adrenoceptors in the human prostate, and in this work we set out to characterise the expression of beta-adrenoceptors by DU-145 cells, their linking to cyclic AMP (cAMP) formation and the possible modulation by histamine H1 receptors of beta-adrenoceptor function. Saturation [3H]-dihydroalprenolol binding indicated that DU-145 cells express moderate levels of beta-adrenoceptors (22.7+/-2.5 fmol/mg protein), which belong to the beta2-subtype as assessed by inhibition by the antagonists ICI-118,551 and CGP-20712A. Inhibition of [3H]-dihydroalprenolol binding by agonists (noradrenaline, adrenaline and isoproterenol) showed the presence of both high-(53-59%) and low-affinity binding sites. beta-Adrenoceptor stimulation with isoproterenol resulted in robust [3H]-cAMP accumulation (10-30-fold of basal, EC50 142 nM; pEC50 6.85+/-0.05). While not having effect of its own on basal [3H]-cAMP accumulation, histamine significantly augmented the beta2-adrenoceptor-induced response (overall effect 152+/-6% of isoproterenol alone) with EC50 1.35 microM (pEC50 5.87+/-0.06). This effect was independent of extracellular Ca2+, insensitive to antagonists/agonists at H1, H2 or H3/H4 receptors and mimicked by drugs containing an imidazole ring in their chemical structure and by imidazole itself. Taken together, our results show that in DU-145 cells histamine augments beta2-adrenoceptor-induced cAMP independently of the activation of known histamine receptors. The effect may involve other mechanisms such as allosteric modulation of beta2-adrenoceptors by the imidazole moiety of histamine.