Family-based therapy for internet addiction among adolescents and young adults: A meta-analysis.

Background and aims: Internet addiction (IA) has been identified as a major public health problem that is more prominent in adolescents and young adults. Some researchers have indicated certain advantages of family-based therapy over other treatments in participants with IA, but no conclusive evaluation has been reported. The present meta-analysis aims to review the efficacy of family-based therapy on Internet addiction in adolescents and young adults. Methods: Relevant articles published from 1996 to February 15th, 2024, were searched from 14 databases, including three Chinese databases. A total of 19,590 articles were identified using a combination of three sets of search terms (Internet addiction, family therapy, and adolescents). Only RCTs and nonrandomized controlled trials were included. Results: 18 studies, most of which were conducted in Asian countries, were included in the final data analysis. The overall severity of Internet addiction in the family-based therapy group was significantly lower than that in the control group. However, significant heterogeneity was detected. Subgroup analysis showed a beneficial effect of family-based therapy when compared with non-intervention and when added to another psychological or behavioural therapy in psychiatric patients with co-medication. Few studies have examined secondary outcomes or follow-up effects. Discussion and Conclusions: Family-based therapy is most effective in reducing the severity of Internet addiction when combined with other therapies, especially medication treatments in psychiatric patients. It might also be helpful to relieve depression and enhance family functions, which needs further evidence. More studies following up on the post-intervention effects are recommended in the future.

Homologous or heterogenous vaccination boosters enhance neutralizing activities against SARS-CoV-2 Omicron BA.1 variant.

The SARS-CoV-2 Omicron BA.1 variant of concern contains more than 30 mutations in the spike protein, with half of these mutations localized in the receptor-binding domain (RBD). Emerging evidence suggests that these large number of mutations impact the neutralizing efficacy of vaccines and monoclonal antibodies. We investigated the relative contributions of spike protein and RBD mutations in Omicron BA.1 variants on infectivity, cell-cell fusion, and their sensitivity to neutralization by monoclonal antibodies or vaccinated sera from individuals who received homologous (CoronaVac, SinoPharm) or heterologous (CoronaVac-BNT162b2, BioNTech) and nonhuman primates that received a recombinant RBD protein vaccine. Our data overall reveal that the mutations in the spike protein reduced infectivity and cell-cell fusion compared to the D614G variant. The impaired infectivity and cell-cell fusion were dependent on non-RBD mutations. We also find reduced sensitivity to neutralization by monoclonal antibodies and vaccinated sera. However, our results also show that nonhuman primates receiving a recombinant RBD protein vaccine show substantial neutralization activity. Our study sheds light on the molecular differences in neutralizing antibody escape by the Omicron BA.1 variant, and highlights the promise of recombinant RBD vaccines in neutralizing the threat posed by the Omicron BA.1 variant.

Role of DLC2 and RhoA/ROCK pathway in formalin induced inflammatory pain in mice.

Deficiency of deleted in liver cancer 2 (DLC2), a novel domain to inhibit RhoA activity, plays an important role in inflammatory pain. However, the underlying mechanisms remain unclear. This study investigated the role of DLC2 and its downstream cascade of RhoA/ROCK in formalin-induced inflammatory pain using DLC2-knockout (DLC2-/-) mice and compared them with DLC2 wild-type (DLC2+/+) mice. Mechanical allodynia and thermal hyperalgesia were evaluated using von Frey filament aesthesiometer and Hargreaves test, respectively. The spinal cord dorsal horn (L3-L5) was selected for molecular and cellular identification by Western blot and immunofluorescence. DLC2-/- mice showed increased mechanical allodynia and thermal hyperalgesia. Expression of ROCK1, ROCK2 and IL-1ß was significantly higher in DLC2-/- mice. Intrathecal administration of RhoA inhibitor (C3 exoenzyme) or ROCK inhibitor (Y27632) significantly attenuated formalin-induced inflammatory hyperalgesia in DLC2-/- mice. ROCK2 and IL-1ß expression were reduced by C3 exoenzyme or Y27632. Spinal p38 activation was also inhibited by C3 exoenzyme or Y27632. Double-labelling immunofluorescence demonstrated co-localization of DLC2 with spinal dorsal microglia. The number of activated microglia in the spinal dorsal horn was significantly higher in DLC2-/- mice, but was reduced by Y27632. These findings indicate that DLC2 deficiency increased formalin-induced inflammatory hyperalgesia through regulating RhoA/ROCK2, and IL-1ß may be a downstream effector. Our results also suggest that RhoA/ROCK enhanced p38 activation plays an important role in formalin-induced inflammatory pain. The finding that DLC2 attenuated inflammatory pain through inhibiting RhoA/ROCK2 suggests that the DLC2/RhoA/ROCK2/p38/IL-ß pathway may be a potential therapeutic target to reduce inflammatory pain.