Ekstrak Purwaceng (Pimpinella Alpinna) sebagai Agen Kemopreventif dan Kemoterapi Kanker Paru (Kajian Antiproliferatif Serta Uji Apoptosis melalui Jalur P53,bcl-2,rb dan Caspase- 9)

Kanker paru merupakan kanker urutan ke-3 terbanyak dan penyebab kematian utama pada pria yang kemoterapinya memberikan banyak efek samping sehingga perlu dicari kemoterapi alternatif. Kumarin psoraldin diketahui memiliki efek kemotoksik pada sel kanker dan terkandung di dalam purwaceng (Pimpinella alpinna) namun efek ekstrak air Pimpinella alpinna sebagai agen antiproliferatif, sitotoksik, penginduksi apoptosis, dan jalur mekanismenya pada sel kanker belum diteliti secara ilmiah. Penelitian eksperimental murni dengan kultur sel kanker paru A549 ini menggunakan rentang dosis ekstrak purwaceng 1-10.000 μg/mLdan rentang dosis kontrol positif cisplatin 1-10 μg/mL yang direplikasi 6 kali serta dengan rentang waktu inkubasi 24-72 jam. Pada uji sitotoksik dengan inkubasi 24 jam yang dideteksi dengan pewarnaan MTT didapatkan IC50sebesar 3.862 μg/mL, sedangkan uji antiproliferasi dengan dosis 550 dan 275 μg/mL mampu menghambat kecepatan pertumbuhan sel 24 jam pertama dan kedua terhadap kontrol. Uji ANOVA satu jalan menunjukkan terdapat perbedaan bermakna rerata kadar ekstrak purwaceng terhadap variasi waktu (p<0.05). Uji apoptosis yang dideteksi menggunakan fluoresensi etidium bromide-acridine orange mendapatkan nilai EC50sebesar 5.271 μg/mL yang ditandai dengan penurunan ekspresi Rb dan bcl-2 serta peningkatan p53 dan caspase-9. Statistik Chi-Square menunjukkan proporsi efek IC50 pada ekspresi gen berbeda secara bermakna(p<0.05) terhadap kontrol. Dapat disimpulkan bahwa Pimpinella alpinna mempunyai efek antiproliferasi dan sitotoksik terhadap sel kanker paru A549 dan menginduksi apoptosis melalui Perubahan jalur apoptosis berupa penurunan ekspresi Rb dan bcl-2 serta peningkatan p53 dan caspase-9

A Phosphatidylinositol 3-Kinase/Protein Kinase B-independent Activation of Mammalian Target of Rapamycin Signaling Is Sufficient to Induce Skeletal Muscle Hypertrophy

Overexpression of Rheb activates mTOR signaling via a PI3K/PKB-independent mechanism and is sufficient to induce skeletal muscle hypertrophy. The hypertrophic effects of Rheb are driven through a rapamycin-sensitive (RS) mechanism, mTOR is the RS element that confers the hypertrophy and the kinase activity of mTOR is necessary for this event

Difference between Microscopic and PCR Examination Result for Malaria Diagnosis and Treatment Evaluation in Sumba Barat Daya, Indonesia

Microscopic examination is the backbone of malaria diagnosis and treatment evaluation in Indonesia. This test has limited ability to detect malaria at low parasite density. Inversely, nested polymerase chain reaction (PCR) can detect parasites at a density below the microscopic examination’s detection limit. The objective of this study is to compare microscopic and PCR results when being used to identify malaria in suspected patients and patients who underwent dihydroartemisinin–piperaquine (DHP) therapy in the last 3–8 weeks with or without symptoms in Sumba Barat Daya, Nusa Tenggara Timur, Indonesia. Recruitment was conducted between April 2019 and February 2020. Blood samples were then taken for microscopic and PCR examinations. Participants (n = 409) were divided into three groups: suspected malaria (42.5%), post-DHP therapy with fever (4.9%), and post-DHP therapy without fever (52.6%). Microscopic examination found five cases of P. falciparum + P. vivax infection, while PCR found 346 cases. All microscopic examinations turned negative in the post-DHP-therapy group. Conversely, PCR result from the same group yielded 29 negative results. Overall, our study showed that microscopic examination and PCR generated different results in detecting Plasmodium species, especially in patients with mixed infection and in patients who recently underwent DHP therapy

A review on the mechanisms of blood-flow restriction resistance training-induced muscle hypertrophy

It has traditionally been believed that resistance training can only induce muscle growth when the exercise intensity is greater than 65% of the 1-repetition maximum (RM). However, more recently, the use of low-intensity resistance exercise with blood-flow restriction (BFR) has challenged this theory and consistently shown that hypertrophic adaptations can be induced with much lower exercise intensities (<50% 1-RM). Despite the potent hypertrophic effects of BFR resistance training being demonstrated by numerous studies, the underlying mechanisms responsible for such effects are not well defined. Metabolic stress has been suggested to be a primary factor responsible, and this is theorised to activate numerous other mechanisms, all of which are thought to induce muscle growth via autocrine and/or paracrine actions. However, it is noteworthy that some of these mechanisms do not appear to be mediated to any great extent by metabolic stress but rather by mechanical tension (another primary factor of muscle hypertrophy). Given that the level of mechanical tension is typically low with BFR resistance exercise (<50% 1-RM), one may question the magnitude of involvement of these mechanisms aligned to the adaptations reported with BFR resistance training. However, despite the low level of mechanical tension, it is plausible that the effects induced by the primary factors (mechanical tension and metabolic stress) are, in fact, additive, which ultimately contributes to the adaptations seen with BFR resistance training. Exercise-induced mechanical tension and metabolic stress are theorised to signal a number of mechanisms for the induction of muscle growth, including increased fast-twitch fibre recruitment, mechanotransduction, muscle damage, systemic and localised hormone production, cell swelling, and the production of reactive oxygen species and its variants, including nitric oxide and heat shock proteins. However, the relative extent to which these specific mechanisms are induced by the primary factors with BFR resistance exercise, as well as their magnitude of involvement in BFR resistance training-induced muscle hypertrophy, requires further exploration